BCDB Faculty

The three types of GDBBS membership are Full Graduate Faculty, Affiliate Graduate Faculty, and Adjunct Faculty. The definition of membership rights and responsibilities are as follows:

Full graduate faculty members have full rights and privileges, including the right to act as Dissertation Advisors, to serve on any GDBBS Committee, or in an administrative position. Full members must be faculty at Emory in good standing. They should be engaged in research, research funding, and peer reviewed publication in the biological and biomedicals sciences. To assure a stable training environment, full members must have independent funding, or likelihood of obtaining funding in the near future, and sufficient research space.

Full members are reported as doctoral faculty for the purpose of institutional research and evaluation that is both internal and external to the University.

Affiliate graduate faculty members should have at least a 50% appointment at Emory. Affiliate members have the privileges of Graduate Faculty except: (1) they may only serve as co-advisors; (2) they are not eligible to serve in LGS governance bodies; and (3) they are not eligible to serve on LGS competitive fellowship/funding committees. Their level of participation in curricular design and governance of the graduate program is subject to the program’s discretion. Generally, this membership is for faculty who contribute to the mission of the graduate program but are not in a position to directly serve as an advisor for new students in their research group, or those who have been judged to be non-participatory during the annual program review of participation.

Affiliate members are not reported as Graduate Faculty for the purpose of institutional research and evaluation that is both internal and external to the University.

Adjunct faculty members are faculty or staff of another research institution (e.g., Center for Disease Control, Georgia Tech) who have credentials similar to those of full members. They have all the rights and privileges of full members, except that they may only serve on University or GDBBS committees in an unofficial capacity and they may only serve as dissertation co-advisors. Adjunct members do not count toward the minimum number of required Emory dissertation committee members.

Adjunct members are not reported as graduate faculty for the purpose of institutional research and evaluation that is both internal and external to the University.

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Faculty Listing
Faculty Member	Research	Program
Fikri Avci, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Immunology and Molecular Pathogenesis favci@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Biochemistry, School of Medicine We are an interdisciplinary research group at the interface of immunology and glycobiology. Our objective is to explore the treatment of and protection from infectious diseases, autoimmune diseases, and cancer by understanding key molecular and cellular interactions between the immune system and glycan/glycoprotein antigens associated with microbes or cancers.	We are an interdisciplinary research group at the interface of immunology and glycobiology. Our objective is to explore the treatment of and protection from infectious diseases, autoimmune diseases, and cancer by understanding key molecular and cellular interactions between the immune system and glycan/glycoprotein antigens associated with microbes or cancers.I joined the faculty at Emory University School of Medicine on July 1st, 2022. Before that, I worked as an Assistant Professor (2013 – 2019) and Associate Professor (2019 – 2022) in the Department of Biochemistry and Molecular Biology at the University of Georgia. In the past nine years as a principal investigator, I have established a highly productive and interdisciplinary research group addressing problems at the interface of immunology and glycobiology. My postdoctoral studies laid the foundation for my independent research program addressing questions on immune interactions of carbohydrate antigens in health and disease. As part of my postdoctoral work (Avci et al., Nature Medicine, 2011; Avci et al., Nature Protocols, 2012), my colleagues and I described the molecular and cellular mechanisms for T-cell recruitment by glycoconjugate vaccines. This work has been highlighted in various print and online media and has had direct and indirect impacts on novel strategies for vaccine development. While the strength of my research group has been rooted in exploring mechanisms of effector immune responses induced by bacterial and viral pathogens through their known and novel surface glycoconjugates, in the past five years, we have made significant progress in our cancer immunology and immunoregulation through gut microbiome research projects. Our research has direct relevance to the design of a new generation of vaccines against devasting pathogens. In one study, we identified new T cell-specific immune mechanisms induced by HIV envelope glycoprotein, which offered a foundation for developing a protective AIDS vaccine (Nature Comm, 2020). In another discovery, we demonstrated that host protein glycosylation can be detrimental to nucleic acid vaccine design (PNAS, 2020). More recently, we elucidated the impact of immune suppressants used clinically on SARS-CoV-2 vaccine efficacy (Vaccine, 2022). Our work on bacterial polysaccharides and conjugate vaccines against bacterial pathogens yielded many important discoveries published in reputable journals such as mBio, JBC, JI, IAI, and Glycobiology. We identified and developed a pneumococcal polysaccharide-degrading enzyme, which is currently being investigated in preclinical studies as a biological antibacterial drug through a federally and privately funded startup company I founded. Our research in infectious diseases and vaccine research could not have been more relevant and important during the COVID-19 pandemic. We also have exciting new findings in cancer immunology and gut microbiome research. Below is the list of the current ongoing projects at Avci Lab. - Molecular Mechanisms for Carbohydrate Presentation to CD4+ T cells by MHCII Pathway. - Adaptive Immune Mechanisms Induced by HIV Envelope Glycoprotein. - Aberrant Tumor Glycosylation Modulates the Immune Response. - Immunomodulatory roles of Tn-expressing, symbiotic bacteria inhabiting host gastrointestinal tract. - Structural and Functional Characterization of the Protein Glycosylation in S. pneumoniae. We have established a sustainable research platform to ensure future funding, discoveries/inventions and publications, and the training of a new generation of scientists. Our research program serves as an important bridge between the fields of immunology and glycobiology to provide knowledge-based solutions to infectious diseases and cancers by utilizing the power of carbohydrate antigens.	BCDBBiochemistry, Cell and Developmental Biology - Full Member IMPImmunology and Molecular Pathogenesis - Full Member	Avci	Fikri		Full Member
Gary J. Bassell, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology Full Member - Neuroscience gary.bassell@emory.edu \| Faculty Profile \| Lab Website Charles Howard Candler Professor, Department of Cell Biology, School of Medicine Chair, Department of Cell Biology, School of Medicine RNA dysregulation and synapse dysfunction in genetic neurodevelopmental, neurodegenerative and neuropsychiatric disorders	RNA dysregulation and synapse dysfunction in genetic neurodevelopmental, neurodegenerative and neuropsychiatric disordersThe research interests of our laboratory are to understand the diverse and critical roles played by mRNA binding proteins and associated factors in the posttranscriptional regulation of gene expression in the nervous system, and investigate how these processes go awry in neurodevelopmental and neurodegenerative disorders. We investigate the normal mechanism, function and regulation of mRNA binding proteins in mRNA transport and local protein synthesis needed for neuronal development and synaptic plasticity. We investigate pathomechanisms for Fragile X syndrome (FXS), related autism spectrum disorders, myotonic dystrophy and amyotrophic lateral sclerosis (ALS). We are using mouse models of neurological diseases to assess the function of mRNA regulation and local protein synthesis in axon guidance, synapse development and neuronal signaling. Efforts are also underway to evaluate different therapeutic modalities in mouse models of neurological diseases and iPSC derived neurons and 3D organoids. Our research utilizes an integrated multi-disciplinary approach that involves cellular, molecular, biochemical, physiological, and behavioral methods and paradigms. These studies are expected to reveal new mechanisms important for neuronal development and function, and targeted approaches for therapeutic intervention that treat underlying molecular defects in SMA, Fragile X syndrome and autism spectrum disorders.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member NSNeuroscience - Full Member	Bassell	Gary	Autism Cell Biology MicroRNAs Neurodegenerative Disease Neuroscience	Full Member
Guy M. Benian, MD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology pathgb@emory.edu \| Faculty Profile Professor, Department of Pathology and Laboratory Medicine, School of Medicine Professor, Department of Cell Biology, School of Medicine Muscle and cytoskeleton in C. elegans.	Muscle and cytoskeleton in C. elegans.We use the powerful model genetic organism, C. elegans, to discover new conserved aspects about muscle assembly, maintenance and regulation. Although our work is basic science, it has relevance to human diseases of muscle including cardiomyopathies and muscular dystrophies. Our main projects are: (1) The structures and functions of giant polypeptides in muscle, >700,000 Da, that consist of multiple Ig and Fn domains and one or two protein kinase domains. One focus is to determine the substrates for these kinases, and how they are activated (normally autoinhibited). One hypothesis being tested is that activation occurs by small pulling forces that result in removal of one or more autoinhibitory tails away from the kinase domains. These studies are in collaboration with structural biologist Olga Mayans (Univ. of Konstanz), biomedical engineer Hang Lu (Georgia Tech), and biophysicists Laura Finzi and David Dunlap (Emory's Physics Dept.). Recently, we have discovered that UNC-89 (human "obscurin") kinase activity is required for proper mitochondrial organization and function. This has initiated a collaboration with Jennifer Kwong in Emory's Pediatrics Dept. (2) The molecular mechanism by which the muscle contractile units (sarcomeres) are attached to the muscle cell membrane and transmit force. This involves "integrin adhesion complexes" (IACs) consisting of the trans-membrane protein integrin and many other proteins. C. elegans muscle has 3 structurally-distinct types of IACs, and through mutant screens, we discovered assembly or maintenance of muscle IACs requires a GEF for Rac (PIX-1), a GAP for Rac (RRC-1) and a class 9 unconventional myosin (HUM-7), all of which have human orthologs. (3) An additional collaboration with Jennifer Kwong has led to our discovery that cardiac-specific KO of the PIX-1 ortholog in mice called beta-PIX results in a dilated cardiomyopathy. We are exploring the mechanisms by which cardiomyopathy develops. (4) In collaboration with biophysicist Andres Oberhauser (UTMB), we are studying the mechanisms by which the conserved myosin head chaperone, UNC-45 folds or re-folds myosin heads, and we have recently discovered a role for UNC-45 in muscle aging (sarcopenia). (5) We have a long-term collaboration with Dan Kalman in Emory's Pathology Dept. to study the beneficial effects of indoles produced by the gut microbiome that promote healthspan, including the attenuation of sarcopenia.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Benian	Guy	null null Biochemistry, Proteins Biology, Cellular Biomechanics Biophysics Cardiomyopathy Cell Biology Genetics, Molecular Molecular Biology Muscular Disorders	Full Member
Larry Boise, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Cancer Biology Full Member - Immunology and Molecular Pathogenesis lboise@emory.edu \| Faculty Profile Professor, Department of Hematology and Medical Oncology, School of Medicine Professor, Department of Cell Biology, School of Medicine The basis mechanisms of apoptosis and translation to better define the mechanism(s) of action of therapeutic agents in multiple myeloma.	The basis mechanisms of apoptosis and translation to better define the mechanism(s) of action of therapeutic agents in multiple myeloma.An area of interest in the lab is to try to understand how the biology of being a plasma cell can be exploited in the therapeutic treatment of the plasma cell malignancy, multiple myeloma. Plasma cells are the antibody producing cells found in the bone marrow. They are long lived and have extensive endoplasmic reticulum (ER) for the production and constitutive secretion of antibodies into the bloodstream. Myeloma is a disease of transformed plasma cells and unlike many other malignancies, myeloma plasma cells retain most of the characteristics of their normal counterparts however they gain proliferative capacity. We have taken the approach that maintenance of the normal plasma cell phenotype could provide opportunities for therapeutic intervention. One drug that is FDA-approved for treatment of myeloma is the proteasome inhibitor bortezomib. We reasoned that these cells may be sensitive to proteasome inhibition because of extensive protein production and demonstrated that the unfolded protein response (UPR) and ER stress pathways are activated by proteasome inhibitors in these cells. We also reasoned that the oxidative process of protein folding may render these cells susceptible to oxidative stress and have published several papers on their response to arsenicals, including a clinical trial. Finally we can now target the survival of these cells with Bcl-2 inhibitors and are determining the factors that regulate sensitivity to one such molecule. We continue to study the apoptotic pathways induced by all of these cellular stresses and have also started to study aspects of the UPR in normal plasma cell differentiation. A second interest in the lab is understanding what the intrinsic and extrinsic signals are that control myeloma cell survival, how they are regulated and can influence therapeutic response. Our focus on intrinsic signals are primarily on the BCL2 family of apoptotic regulators. We study what determines why some cells may be dependent on one family member for survival and other cells on a different family member. This can be influenced both genetic (chromosomal translocations) and epigenetic (differentiation state) of the cell. Moreover, it can also be influenced by signals from other cells in the bone marrow micro-environment such as mesenchymal derived stromal cells or cytokines (IL6). We study how these and other signals influence BCL2 dependency and cell survival and influence response to therapy. This includes modern immunotherapy such as CAR-T cells.	BCDBBiochemistry, Cell and Developmental Biology - Full Member CBCancer Biology - Full Member IMPImmunology and Molecular Pathogenesis - Full Member	Boise	Larry	Biology, Cellular Cancer Biology Cell Biology	Full Member
Charles Bou-Nader, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology cbounad@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Biochemistry, School of Medicine We focus on mechanistic studies of R-loops and RNP complexes to understand how these assemblies control gene expression and genomic integrity in human health and diseases.	We focus on mechanistic studies of R-loops and RNP complexes to understand how these assemblies control gene expression and genomic integrity in human health and diseases.Our lab uses cutting edge biochemical, biophysical, and structural methods (such as cryo-EM and X-ray crystallography) to mechanistically understand how RNAs and RNP assemblies control gene expression and genomic integrity in human health and diseases. We are especially interested in defining the rules behind R-loop formation and recognition by proteins and how R-loop deregulation causes diseases such as neurological disorders, cancers, and autoimmune disorders. To tackle this gap in knowledge, we are also developing new molecular biology tools to manipulate R-loops in vitro and in vivo. Current topics investigated in the lab include: • The immunogenicity of nucleic acids and how R-loops contribute to immunity or viral infectivity. • Mechanistic studies of toxic R-loops, RNAs, and other nucleic acids in neurological disorders. • Understanding how RNA structures organize chromatin architecture and how R-loops regulate DNA-repair pathways. Collectively, our innovative studies will not only reveal new paradigms of genomic instability and R-loop functions, but will also create new methodologies for other researchers to study R-loops more broadly and build the foundation to design new therapeutics to extend the healthy and active years of life.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Bou-Nader	Charles	Autoimmunity Biochemistry, Nucleic Acids Biochemistry, Proteins Biophysics Cancer Biology Cryo-Electron Microscopy Enzymology Microscopy Molecular Biology Neurodegenerative Disease Radiocrystalography X-Ray Crystallography	Full Member
Joshua D. Chandler, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology joshua.chandler@emory.edu \| Faculty Profile Assistant Professor, Division of Pulmonary Medicine, Department of Pediatrics, School of Medicine My laboratory studies mechanisms of lung diseases, such as cystic fibrosis, by analyzing the impact of pathological processes, such as lung inflammation, on the abundance and metabolism of metabolites involved in redox homeostasis, cell signaling, and bioenergetics, with an ultimate goal of identifying druggable pathways to halt disease advancement.	My laboratory studies mechanisms of lung diseases, such as cystic fibrosis, by analyzing the impact of pathological processes, such as lung inflammation, on the abundance and metabolism of metabolites involved in redox homeostasis, cell signaling, and bioenergetics, with an ultimate goal of identifying druggable pathways to halt disease advancement.Inflammation, or white blood cell infiltration into bodily tissues and activation of immune functions, impacts a range of human illnesses. Understanding the molecular basis of inflammatory tissue injury is key to preventing and resolving pathological outcomes. However, such mechanisms are complex, multifactorial, and change with time. The Chandler Laboratory focuses on elucidating the biochemical and metabolic causes and consequences of inflammatory pathology by utilizing a suite of small molecule, redox, metabolic, and biochemical-focused techniques. We also design experiments to test rational pharmacological interventions against inflammation that could improve human health. To date, we have placed major emphasis on myeloperoxidase (MPO), a heme enzyme, and its role in early-stage pathogenesis of cystic fibrosis. Neutrophils, the most abundant white blood cells in humans, secrete mature MPO after infiltrating tissues. MPO utilizes hydrogen peroxide to produce a range of oxidants, including hypochlorous acid (chlorine bleach) and a weaker, more selective oxidant, hypothiocyanous acid. Notably, changing the abundance of MPO substrates changes its output of oxidants, and differences in oxidant reactivity change the impacted biochemicals wherever MPO is present. Therefore, MPO substrates can be targeted as a means of controlling its activity and shifting oxidation reactions to different targets, a process I call "oxidant switching". My lab's research program is designed to build on previous successes in leveraging oxidant switching to improve lung health.[1-3] Due to the complexity of immune effector molecules, particularly promiscuous oxidants like hypochlorous acid, we use high-resolution, accurate-mass mass spectrometry to conduct metabolomics experiments (attempting to measure as many small molecules in a biological system as possible with a relatively unbiased method). This allows us to (1) quantify hundreds of validated compounds; (2) annotate and quantify hundreds more according to MS/MS fragmentation; and (3) potentially detect and quantify undiscovered compounds, all via nontargeted analysis of a single experiment. We also use stable isotope flux analysis to identify metabolic pathway activity and aid structure elucidation of novel compounds. Experiments can be set up to both generate and test hypotheses, depending on extent of a priori knowledge. Combining metabolomics and traditional biochemistry, we partnered with international colleagues to study bronchoalveolar lavage from clinically stable toddlers with cystic fibrosis. These samples are very difficult to acquire, and using them we determined that MPO is active in the earliest stages of cystic fibrosis, contributes to metabolite oxidation, and is closely associated with lung damage.[4, 5] Ongoing funded research aims to determine if it is also an important factor in disease risk, as well as the fate(s) and molecular impact of the MPO protein in the context of neutrophilic airway inflammation. Additional lines of research are focused on the ability to non-invasively monitor important metabolites in CF, and on the metabolic rewiring and metabolic signaling of neutrophils epithelial cells and circulating metabolites in cystic fibrosis and cystic fibrosis-related diabetes.[6] Citations 1. Chandler, J.D. and B.J. Day, Biochemical mechanisms and therapeutic potential of pseudohalide thiocyanate in human health. 2015. 49(6): p. 695-710. 2. Chandler, J.D., et al., Antiinflammatory and Antimicrobial Effects of Thiocyanate in a Cystic Fibrosis Mouse Model. American Journal of Respiratory Cell and Molecular Biology, 2015. 53(2): p. 193-205. 3. Chandler, J.D., et al., Selective Metabolism of Hypothiocyanous Acid by Mammalian Thioredoxin Reductase Promotes Lung Innate Immunity and Antioxidant Defense. 2013. 288(25): p. 18421-18428. 4. Chandler, J.D., et al., Myeloperoxidase oxidation of methionine associates with early cystic fibrosis lung disease. European Respiratory Journal, 2018. 52(4): p. 1801118. 5. Horati, H., et al., Airway profile of bioactive lipids predicts early progression of lung disease in cystic fibrosis. J Cyst Fibros, 2020. 19(6): p. 902-909. 6. Chandler, J.D., et al., Determination of thiocyanate in exhaled breath condensate. Free Radical Biology and Medicine, 2018. 126: p. 334-340. 7. Kim S.O., et al, Substrate-dependent metabolomic signatures of myeloperoxidase activity in airway epithelial cells: Implications for early cystic fibrosis lung disease. Free Radic Biol Med, 2023. S0891-5849(23)00508-7	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Chandler	Joshua		Full Member
Charles J. Cho, MD, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology charles.j.cho@emory.edu \| Faculty Profile Assistant Professor, Division of Digestive Diseases, Department of Medicine, School of Medicine I am interested in understanding unique features of differentiated cells in the gastrointestinal tract, including acinar cells in the pancreas and chief cells in the stomach.	I am interested in understanding unique features of differentiated cells in the gastrointestinal tract, including acinar cells in the pancreas and chief cells in the stomach.My lab is interested in characterizing unique features of fully differentiated cells in the gastrointestinal (GI) tract. The GI tract serves as an excellent example of an organ system that supports a wide variety of differentiated cells, including digestive enzyme-secreting acinar cells in the pancreas, salivary gland and chief cells in the stomach corpus, and hepatocytes in the liver. We are just beginning to understand the unique characteristics of these differentiated cells, which so far include: 1) cellular quiescence, in which these cells seldom enter the cell cycle unless injured; 2) a disproportionately high abundance of ribosomes and endoplasmic reticulum with active translation; and 3) the existence of abnormal ploidy (e.g., polyploidy or multinucleation). These unique features of fully differentiated cells not only enable them to perform specialized functions, distinguishing them from undifferentiated and constantly proliferating somatic stem cells, but also makes them prone to cancer, especially in the context of injury. Using in vivo models is the best, and perhaps only, way to study these unique features. We employ a variety of mouse models and skillsets to investigate ribosome dynamics, translation, and ploidy status in various GI organs, in combination with the injury models that can faithfully mimic inflammatory diseases (e.g., acute and chronic pancreatitis) and subsequent metaplasia in humans. Our ultimate goal is to gain a more comprehensive understanding of how these differentiated cells utilize shared mechanisms to cope with injury and restore homeostasis through a recently described process known as "paligenosis". This will ultimately provide unique targets to address unresolved questions in the realms of facilitating tissue regeneration and treating cancer.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Cho	Charles		Full Member
Hyojung Choo, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology hyojung.choo@emory.edu \| Faculty Profile Assistant Professor, Department of Cell Biology, School of Medicine The role of muscle stem cells in craniofacial muscle pathologies	The role of muscle stem cells in craniofacial muscle pathologiesThe objective of my research is to examine the function and maintenance of skeletal muscle stem cells in relation to muscle physiology. Within skeletal muscle tissues, there exist specialized stem cells known as satellite cells. Normally dormant, these satellite cells are activated in response to muscle tissue injury and play a crucial role in regenerating the muscle structure. Additionally, skeletal muscles contain fibroadipogenic progenitors, a type of mesenchymal progenitor, which interact with satellite cells to facilitate efficient muscle regeneration. However, these fibroadipogenic progenitors can also contribute to fibrosis or the accumulation of fat within muscle tissues, particularly in cases of chronic muscle pathology. In our studies, we have focused on satellite cells and fibroadipogenic progenitors in pharyngeal muscles, which are responsible for the process of swallowing. We have utilized mouse models, including those with oculopharyngeal muscular dystrophy (OPMD), to investigate the role of defective autophagy in pharyngeal satellite cells, which may explain the specific pathology observed in OPMD affecting pharyngeal muscles. To gain insight into the muscle pathology specific to OPMD using patient cells, we have developed a novel protocol for generating craniofacial muscle myogenic cells from human induced pluripotent stem cells. Additionally, we have discovered that hepatocyte growth factor, derived from fibroadipogenic progenitors, can activate pharyngeal satellite cells even without injury and the essential role of fibroadipogenic progenitors in maintaining pharyngeal muscle function and mass. To improve functional assessment of swallowing muscles for drug screening in animals and non-invasive, continuous diagnosis of dysphagia patients, we are collaborating with bioengineers and clinicians to develop surface EMG sensors. Currently, our focus lies in investigating the impact of fibroadipogenic progenitor-derived growth factors on the maintenance of upper airway skeletal muscles in the context of obesity. Obesity is a significant contributing factor to obstructive sleep apnea, as it leads to increased volume and weakened tone of the tongue and pharyngeal muscles. This line of research aims to lay the groundwork for the development of therapeutics targeting obstructive sleep apnea.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Choo	Hyojung	Cell Biology	Full Member
Graeme Conn, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics gconn@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Biochemistry, School of Medicine Faculty Member, Emory Antibiotic Resistance Center Molecular mechanisms of antibiotic resistance (via RNA modification and drug efflux) and RNA-mediated regulation of the human innate immune system .	Molecular mechanisms of antibiotic resistance (via RNA modification and drug efflux) and RNA-mediated regulation of the human innate immune system .We use modern biochemical, biophysical, computational and structural biology (e.g. single-particle cryoEM) methods to study the structures, interactions and biological functions of biomedically important RNA and protein molecules. Current topics include mechanisms of bacterial antibiotic resistance through ribosomal RNA modification and drug efflux systems, and RNA-mediated regulation of host cell innate immune responses. In both areas, we are developing small molecule regulators of these processes and avenues to novel therapeutic interventions. Our research is also complemented by extensive interactions and collaborations with other groups at Emory and world-wide.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Conn	Graeme	Antibiotics Biochemistry, Nucleic Acids Biochemistry, Proteins Biophysics Drug Resistance Molecular Biology	Full Member
Anita Corbett, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology acorbe2@emory.edu \| Faculty Profile \| Lab Website Samuel C. Dobbs Professor, Department of Biology, Emory College of Arts and Sciences Senior Associate Dean of Research, Emory College of Arts and Sciences Understanding how mutations in genes that encode ubiquitously expressed RNA binding proteins or proteins that regulate gene expression cause tissue-specific disease such as intellectual disability, pontocerebellar hypoplasia and cancer	Understanding how mutations in genes that encode ubiquitously expressed RNA binding proteins or proteins that regulate gene expression cause tissue-specific disease such as intellectual disability, pontocerebellar hypoplasia and cancerDr. Corbett's lab seeks to understand the movement of macromolecules between the nucleus and the cytoplasm with a primary focus on understanding how mRNA processing the nucleus is coupled to export to the cytoplasm to ensure accurate gene expression. Current studies are focused on elucidating the function of ubiquitously expressed RNA binding/processing factors that are linked to human disease ranging from intellectual disability to muscular dystrophy and cancer. These studies are highly collaborative and exploit numerous models including budding yeast, Drosophila (collaboration with Moberg lab), mice, and cultured cells to address fundamental questions related to gene expression, post-transcriptional RNA processing, and disease mechanisms. Approaches include genetics, cell biology, structural biology (collaborations), and biochemistry.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Corbett	Anita	Biochemistry, Proteins Cancer / Carcinogenesis Cell Biology Genetics, Molecular Molecular Biology	Full Member
Biplab Dasgupta, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Cancer Biology biplab.dasgupta@emory.edu \| Faculty Profile Professor, Division of Hematology/Oncology, Department of Pediatrics, School of Medicine We work at the interface of nutrient and energy sensing, signaling and tumor metabolism to examine metabolic genes and environment that regulate cancer development.	We work at the interface of nutrient and energy sensing, signaling and tumor metabolism to examine metabolic genes and environment that regulate cancer development.Research Projects in the Dasgupta Lab laboratory Understanding dynamic regulation of nutrient and energy sensing in cancer. AMP activated protein kinase (AMPK) is an evolutionarily conserved energy sensor. Active AMPK inhibits the biosynthetic kinase and nutrient sensor mTORC1. For decades AMPK was though to exert tumor suppressive role. Through comprehensive genetic and pharmacologic studies, we showed that AMPK is a key regulator of tumor bioenergetics and is required for brain tumor growth. These studies have been published in PNAS, Nature Cell Biology, Molecular Cancer Therapeutics, Nature Communications and Trends in Pharmacological Sciences. A major project in our lab is to examine the role of AMPK in adult brain tumor signaling and metabolism. Metabolic Dependencies in Pediatric High-Grade Glioma. An active project in our laboratory is to understand the gene-metabolite interactome of an incurable childhood brain tumor called diffuse intrinsic pontine glioma (DIPG). We performed the first untargeted metabolomics of several patient-derived DIPG lines. Current studies (in review) are underway to integrate and map gene-metabolite interactome in DIPG, perform in-depth validation studies in orthotopically xenografted human tumors, and in brainstem tumors in genetically engineered mice. Examining passenger mutation vulnerability in human cancer. We are testing the hypothesis that human cancer subtypes have unique in-built, yet unexplored vulnerabilities that could potentially be harnessed for novel therapy. For example, we discovered that Stearoyl Co-A desaturase (SCD), a gene crucial for membrane flexibility is inadvertently and hemizygously co- deleted as a passenger to PTEN in a subset of human cancers such as glioblastoma, melanoma and prostate cancer. These studies have been published in Science Advances, and Cancer Research. We are currently examining SCD inhibitor resistance mechanisms in cancer. Identifying biomarkers ('molecular beacons') to stratify patients for improved biguanide sensitivity in human cancer. Mitochondrial inhibitors such as metformin are in clinical trials and some of them may exert therapeutic benefit in certain cancers. The lack of accumulation in cells at therapeutic concentrations is a significant problem with metformin therapy due to inconsistent cell permeability. We are investigating cancer molecular subtypes that may elicit therapeutic response at low metformin accumulation inside tumors and may greatly improve metformin-based targeted therapy. Investigating mechanisms by which hyperglycemia increases risk for cancer development and progression. Meta-analysis of several epidemiological studies has confirmed that hyperinsulinemia, hyperglycemia, obesity and diabetes (metabolic syndrome) elevate the risk of malignant neoplasms in various organs. This raises the compelling question whether any component of metabolic syndrome enable fixation of deleterious mutations (that otherwise would be eliminated by the DNA repair system), and whether integrative management of diabetes can significantly prevent/delay cancer onset and improve cancer prognosis. Despite strong epidemiological evidence, the molecular link between these two widespread diseases is not known. Besides being used as an energy source, glucose is used for post-translational modification of cellular enzymes and lipids through the hexosamine pathway – a pathway which is highly active in cancer cells. Aberrant glycosylation in the diabetic environment causes vascular dysfunction, cardiac pathology, nephropathy and oxidative stress. A key question we aim to address is whether excess tissue glucose utilization causes aberrant glycosylation and misregulation of proteins to cause epithelial cell hyperplasia. To address this question, we made a model of hyperglycemia in C57BL/6J mice (unpublished). We are replicating this model in genetically engineered mouse models of epithelial cancer to examine the cooperation between hyperglycemia and cancer-causing mutations. We formed collaboration with a renowned research hospital in India to perform retrospective and prospective human studies in patients with diabetes with or without breast and colon cancer.	BCDBBiochemistry, Cell and Developmental Biology - Full Member CBCancer Biology - Full Member	Dasgupta	Biplab		Full Member
Paul A Dawson, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology paul.dawson@emory.edu \| Faculty Profile Professor, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Department of Pediatrics, School of Medicine Physiologic and molecular mechanisms controlling bile acid signaling in the gut-liver-kideny axis and their contribution to hepatic, gastrointestinal, renal, and metabolic disease.	Physiologic and molecular mechanisms controlling bile acid signaling in the gut-liver-kideny axis and their contribution to hepatic, gastrointestinal, renal, and metabolic disease.My lab is focused on developing new therapies and preventive measures for diseases associated with the gut-liver axis. The scope of the problems that we are trying to solve ranges from rare monogenic disorders such as Progressive Familial Intrahepatic Cholestasis (PFIC) to the common finding of nonalcoholic fatty liver disease (NAFLD) in the pediatric and adult populations. Included in that spectrum are biliary atresia, the most common indication for pediatric liver transplantation, Cystic fibrosis-associated liver disease, sickle cell-associated liver disease, acquired forms of cholestatic diseases such as Primary Biliary Cholangitis and Primary Sclerosis Cholangitis, and forms of bile acid malabsorption. Broadly, the strategy is to exploit novel bile acid-based therapeutics targeting the gut-liver axis. Towards that end, we are using a range of experimental approaches, including genomics, metabolomics, gnotobiotics, novel mouse models, novel chemistry, and clinical trials. The discoveries pioneered by my laboratory and supported by the NIH laid the groundwork for development of the Ileal Bile Acid Transporter (IBAT) inhibitors, which were approved by the US FDA and European Medicines Agency (EMA) in 2021 as the first medical therapy for the treatment of pediatric cholestatic liver disease. A major project in the lab is to elucidate the molecular mechanisms and regulation of hepatobiliary, renal and intestinal bile acid transport. Bile acids are natural detergents that function to drive bile flow and facilitate the digestion and absorption of nutrients in the gut. In addition, bile acids also act as signaling molecules to regulate glucose homeostasis, lipid metabolism, and energy expenditure. The signaling potential of bile acids in compartments such as the systemic circulation is regulated in part by an efficient enteronephrohepatic circulation that functions to conserve and channel the pool of bile acids within the intestinal and hepatobiliary compartments. For these studies, we are using bile acid transporter-expressing cell lines, mouse models engineered to constitutively or conditionally knockout the transporters, and studying patients with inherited or acquired defects in bile acid metabolism. A second major project in the lab is to determine the mechanisms by which bile acids are cytotoxic to the epithelium. The cellular and molecular mechanisms of hepatocyte injury caused by retention of hydrophobic bile acids in cholestatic disease have been the subject of intensive study. However less is known regarding the mechanisms and signaling pathways underlying the cytotoxic effects of bile acids in intestinal, biliary, and renal proximal tubule epithelium. For these studies, we are using bile acid transporter-expressing cell lines, mouse models engineered to constitutively or conditionally knockout the transporters. Included in this work are studies of novel bile acid transport inhibitors, designer bile acid analogs, and development of novel intracellular bile acid sensors. Much of this project is focused on elucidating the role of bile acids in the development of liver disease-associates kidney injury (Cholemic Nephropathy). This includes working with pre-clinical models to elucidate the mechanisms and therapeutic potential of targeting renal bile acid transport to treat liver and kidney disease. These studies are funded by the NIH and industry partners and conducted in close collaboration with investigators here at Emory University and Georgia Tech, and with international collaborators in Europe.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Dawson	Paul	Cell Biology	Full Member
Robert A. Dick, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics robert.dick@emory.edu \| Faculty Profile Assistant Professor, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine The Robert Dick Lab uses a combination of structural biology, biochemistry, and tissue culture to understand virus assembly and structure. Cryo-Electron Microscopy and Tomography are uniquely suited to this work, providing quanternary and tertiary protein information. The lab is active in training graduate students and postdoctoral researchers, in all aspects of sample preparation, data acquisition, and data processing. We also recruit and train undergraduate students.	The Robert Dick Lab uses a combination of structural biology, biochemistry, and tissue culture to understand virus assembly and structure. Cryo-Electron Microscopy and Tomography are uniquely suited to this work, providing quanternary and tertiary protein information. The lab is active in training graduate students and postdoctoral researchers, in all aspects of sample preparation, data acquisition, and data processing. We also recruit and train undergraduate students.Inositol hexakisphosphate (IP6) With our expertise in retrovirus assembly and structure, we work to determine how to disrupt these elements with the goal of developing new antivirals. Previously, we demonstrated that the small cellular molecule IP6 is essential for the assembly and maturation of HIV-1, the causative agent of AIDS. This observation led to the development of new tools to study the assembly process. To this end, we are actively working with collaborators in the field of HIV biology to describe how compounds that inhibit HIV assembly, maturation, and infectivity specifically interact with and effectively kill the virus. Endogenous retroviruses Over evolutionary history, retroviruses have infected mammalian cells many times, and thereby have left copies of viral genes in the cellular genome. Of particular interest to us is how organisms have 'domesticated' what were originally viral proteins. By identifying and studying these endogenous retroviral proteins, we hope to learn how cells have come to use such proteins for their own functions. Paramyxoviruses We are applying many of the tools developed for the study of retrovirus structure and assembly to paramyxoviruses, including the emerging zoonotic virus, Nipah Virus (NiV). With a high mortality rate and transmissibility between animals and humans, NiV represents a virus of significant concern. We are working in a close collaboration with the lab of Dr. Hector Aquilar- Carreño (Department of Microbiology and Immunology, Cornell) to determine the structures and arrangement of NiV proteins in virus particles to better understand the mechanisms of a) virus assembly and release and b) virus-mediated fusion.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Dick	Robert		Full Member
Lizzy Draganova, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics elizabeth.draganova@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Biochemistry, School of Medicine Assistant Professor, Department of Microbiology and Immunology, School of Medicine Biophysics of herpesvirus capsid assembly, packaging and nuclear egress; structural biology; virology; light scattering; antivirals.	Biophysics of herpesvirus capsid assembly, packaging and nuclear egress; structural biology; virology; light scattering; antivirals.Herpesviruses are some of the most complex and interesting viruses infecting humans. These viruses can establish lifelong dormant infections - many of us are infected with at least one type of herpesvirus, and do not even know it. Unfortunately, these viruses can have detrimental effects on the immunocompromised, yet there is no universal vaccine or cure. We are focused on Herpes Simplex Virus Type 1 (HSV-1), a neuroinvasive virus infecting ~60% of the human population. Currently, we combine a variety of biophysical tools, along with chemistry and virology, to understand how capsid-centric processes contribute to viral replication. The goal of our work is to provide new insights into how we can more effectively combat this virus. Capsid assembly: All herpesviruses require the assembly of a capsid shell to protect the viral genome. This process is essential for successful viral replication and is an attractive therapeutic target. We aim to develop novel biophysical methodologies using light scattering and mass spectrometry to dissect the HSV-1 capsid assembly pathway, informing the design of assembly inhibitors and provide new tools for other virologists. Capsid packaging: Herpesviral capsids overcome amazing biological feats, capable of housing a viral genome under extreme amounts of pressure, while trafficking through the cellular milieu. Despite these forces, the capsid shell stays intact. We seek to understand how they achieve such feats and understand the limits of these properties. Capsid nuclear escape: Herpesvirus replication, including capsid assembly and packaging, occurs in the nucleus. Here, capsids face yet another obstacle - escaping the nucleus to become mature virions in the cytoplasm. The large size of herpesviral capsids precludes nuclear pore transport and instead, capsids bud out of the nucleus, in a process termed nuclear egress. Budding is mediated by the viral nuclear egress complex (NEC), a virally encoded budding machine, essential for viral replication. We are currently designing various inhibitors to block NEC activity, both as therapeutic and functional tools.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Draganova	Lizzy		Full Member
Christine M. Dunham, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology cmdunha@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Chemistry, Emory College of Arts and Sciences Regulation of protein synthesis; ribosome structure & function; regulation by toxins, antibiotics, frameshifting elements, and quality control mechanisms.	Regulation of protein synthesis; ribosome structure & function; regulation by toxins, antibiotics, frameshifting elements, and quality control mechanisms.The Dunham laboratory studies how protein synthesis is regulated to alter critical aspects of cellular function essential for life. We use interdisciplinary approaches including structural biology (X-ray crystallography and single particle cryo-EM), biochemistry, molecular biology and microbiology to define molecular mechanisms of action.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Dunham	Christine		Full Member
Victor Faundez, MD, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Neuroscience vfaunde@emory.edu \| Faculty Profile Professor, Department of Cell Biology, School of Medicine Cellular and molecular mechanisms of neuropsychiatric disorders.	Cellular and molecular mechanisms of neuropsychiatric disorders.Our laboratory studies the cellular and molecular mechanisms of rare neurological disorders characterized by neurodegeneration and neurodevelopmental disorders of the childhood. We focus on the 22q11.2 microdeletion syndrome, Menkes disease, CDKL5-deficiency and Rett syndrome. We have gained insight into novel and fundamental cellular and molecular mechanisms necessary for neuronal development and homeostasis studying these rare neurological disorders utilizing molecular systems biology and genetic approaches.	BCDBBiochemistry, Cell and Developmental Biology - Full Member NSNeuroscience - Full Member	Faundez	Victor	Biochemistry, Proteins Cell Biology Disease Model Electrophysiology Neuroscience Psychiatry	Full Member
Yue Feng, MD, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology yfeng@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Pharmacology and Chemical Biology, School of Medicine RNA biology in neuron and glia function in normal brain development and brain diseases	RNA biology in neuron and glia function in normal brain development and brain diseasesUsing a multidisciplinary strategy based on molecular, cellular, genetics and pharmacological approaches, we are investigating how RNA homeostasis and cellular behavior govern normal brain development and function and how RNA malfunction in distinct brain cell types leads to human brain disorders. 1) Non-coding RNA in human brain diseases We investigate novel mechanisms that regulate the biogenesis and function of regulatory non-coding RNAs (ncRNAs), including long noncodoing RNAs (lncRNAs), circular RNAs (circRNAs), and microRNAs (miRNAs), in human neuronal and glial development and how their dysregualtion leads to neuropsychiatric and neurodegenerative disorders, represented by schizophrenia and Alzheimer's disease. Using human neuronal and glial cells as well as mopuse models, we employ genetic and biochemical approaches to elucidate the functional interplay of cnRNAs with various RNA binding proteins that control broad gene networks involved in brain disorders. 2) Alternative splicing, homeostasis and translation of mRNAs in brain diseases We currently focus on the selective RNA-binding protein QKI, a key factor controlling proliferation and differentiation of myelin producing glia and myelin formation via regulating pre-mRNA splicing, biogenesis of non-coding RNAs, as well as mRNA stability and translation. Emerging evidence indicated the involvement of QKI function in several human diseases, including myelin repair in multiple sclerosis, white matter defects in schizophrenia, and glioma tumorigenesis. We have established molecular, cellular and animal models to investigate mRNA targets and cellular mechanisms that underlie QKI-dependent myelinogenesis and axonal protection. Genetic and pharmacological approaches are employed to manipulate QKI function to promote myelination.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Feng	Yue	Biochemistry, Nucleic Acids Biochemistry, Proteins Cell Biology Genetics, Molecular Mental Retardation MicroRNAs Molecular Biology Neuroscience	Full Member
Judith L. Fridovich-Keil, PhD (she/her) Affiliate Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology jfridov@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Human Genetics, School of Medicine Human genetics and metabolic disease.	Human genetics and metabolic disease.The principal focus of our research is galactose metabolism and the role(s) galactose metabolites play in normal development and disease. Specifically, we are working to understand the role(s) of galactose metabolism in normal embryogenesis and homeostasis, and the pathophysiology of inherited galactosemias using a combination of model systems and patient studies. We are also working to identify modifiers of outcome and using a rat model of classic galactosemia to explore novel strategies for improved intervention.	BCDBBiochemistry, Cell and Developmental Biology - Affiliate Member GMBGenetics and Molecular Biology - Full Member	Fridovich-Keil	Judith	Biochemistry, Proteins Cell Biology Genetics, Medical Metabolic Diseases Molecular Biology	Affiliate Member
Homa Ghalei, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology homa.ghalei@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Biochemistry, School of Medicine My laboratory studies RNA-mediated mechanisms that control gene expression in both normal biology and disease. A major focus of our research is uncovering how RNA-protein complexes involved in ribosome biogenesis are assembled, and how disruptions in the spatial and temporal regulation of ribosomal RNA modification and processing contribute to altered gene expression in human disease. We employ a diverse range of approaches, including biochemical techniques, structural biology, and genetics.	My laboratory studies RNA-mediated mechanisms that control gene expression in both normal biology and disease. A major focus of our research is uncovering how RNA-protein complexes involved in ribosome biogenesis are assembled, and how disruptions in the spatial and temporal regulation of ribosomal RNA modification and processing contribute to altered gene expression in human disease. We employ a diverse range of approaches, including biochemical techniques, structural biology, and genetics.Role of ribosomal RNA modifications for ribosome biogenesis and translational control Ribosomes are responsible for producing all cellular proteins. Because of their critical role in defining the cellular proteome, defects associated with the ribosome production, function or regulation have detrimental outcomes and can cause serious human diseases, termed ribosomopathies. In human cells, bulk of the ribosomal mass accounts for ribosomal RNA (rRNA) that is chemically modified at over 200 nucleotides. These modifications are required for ribosome production and function and their dysregulation affects the efficiency and accuracy of protein synthesis and can lead to human diseases. How cells control their rRNA modification pattern or the ribosomal epitranscriptomic marks to ensure the quality and quantity of their proteins remains elusive. A major goal of our lab is to reveal the contribution of rRNA modifications to the structure and function of the ribosome. Mechanism of snoRNP assembly In eukaryotes, the majority of rRNA modifications are added by evolutionarily conserved small nucleolar ribonucleoprotein (snoRNP) complexes. These snoRNP complexes are composed of a set of essential proteins and a small nucleolar non-coding RNA (snoRNA). The formation of snoRNP complexes is tightly regulated by transiently acting assembly factors. This regulation controls the production of active snoRNP complexes and coordinates the snoRNP assembly process with other cellular events such as transcription, splicing, and ribosome biogenesis. snoRNP complex formation also maintains the steady-state levels of snoRNAs by protecting them from ribonuclease degradation. This is important as dysregulation of snoRNA levels can result in several human diseases and alter gene expression. Although the main regulatory factors involved in snoRNP assembly have been identified, how they exert their functions, and how their dysregulation causes cellular defects is unclear. A key area of research in our lab is focused on deciphering the mechanisms that regulate the formation of snoRNP complexes for rRNA modification and processing. This is a crucial step towards a more comprehensive understanding of translational control in eukaryotes. Dysregulation of snoRNAs and impaired snoRNP assembly in disease Changes in rRNA modification pattern or the expression of snoRNAs have severe functional outcomes: In yeast, deletion of individual snoRNAs affects adaptation of cells to stress and drug resistance. In zebrafish, inhibition of snoRNA expression leads to severe morphological defects. In humans, snoRNA dysregulations and changes in rRNA modification pattern are linked to several diseases including oncogenesis in breast, lung, prostate, and colorectal cancers. How deregulation of snoRNA levels or snoRNP assembly results in human diseases is largely unknown and constitutes a major area of research in our laboratory.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Ghalei	Homa		Full Member
David Gordon, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology david.ezra.gordon@emory.edu \| Faculty Profile Assistant Professor, Department of Pathology and Laboratory Medicine, School of Medicine The Gordon laboratory utilizes high-throughput experimental genetics and mass spectrometry to build mechanistic models of biological functions.	The Gordon laboratory utilizes high-throughput experimental genetics and mass spectrometry to build mechanistic models of biological functions.Dr. David Ezra Gordon earned his Bachelor of Science in Biology from Cornell University, followed by an M.Phil. and Ph.D. in Clinical Biochemistry from the University of Cambridge. With a diverse research background encompassing cell and molecular biology, experimental genetics, virology, systems biology, mass spectrometry, and immunology, Dr. Gordon is recognized for his innovative and impactful contributions to biomedical science. As a graduate student at Cambridge, he utilized combinatorial experimental genetics to map redundant vesicle trafficking pathways in higher eukaryotes. During his postdoctoral fellowship at the University of California, San Francisco, Dr. Gordon pioneered high-throughput genetic interaction mapping to study HIV host-dependencies, and spearheaded the first peer-reviewed protein interaction maps for the highly pathogenic coronaviruses SARS-CoV-2, SARS-CoV-1, and MERS. At Emory University, the Gordon Laboratory builds upon these foundational studies to systematically dissect the biochemical mechanisms underlying immune regulation, particularly in the contexts of pathogen infection and the tumor microenvironment. Leveraging state-of-the-art mass spectrometry, the lab maps complex biochemical networks and employs high-throughput experimental genetics to pinpoint key nodes driving immune function and dysfunction. Collaboration is central to our approach—we partner widely to access the most physiologically relevant model systems for our research on immune responses, infectious diseases, and cancer. Our team specializes in the biochemical analysis and genetic modification of primary systems at scale, working closely with both academic and industry partners to advance the frontiers of immunology and therapeutic discovery.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Gordon	David	AIDS / HIV Biochemistry, Proteins Cancer Biology Genetics, Molecular Immunology Molecular Biology Neurodegenerative Disease Virology	Full Member
Dave Gorkin, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology david.gorkin@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Biology, Emory College of Arts and Sciences My research uses genomic tools to understand how the cell’s epigenetic machinery contributes to gene regulation in development, and dysregulation in disease.	My research uses genomic tools to understand how the cell’s epigenetic machinery contributes to gene regulation in development, and dysregulation in disease.Mammalian development relies on a complex interplay between genetic and epigenetic factors to create trillions of highly specialized cells from a single genetic blueprint. Each cell has essentially the same set of genes encoded in its DNA, but cells express different subsets of genes at the RNA and protein levels depending on developmental and environmental cues. This cell-specific gene expression is orchestrated, at least in part, by epigenetic processes that add layers of information on top of the DNA sequence. Mammalian genomes contain hundreds of epigenetic regulators -- collectively referred to as the "epigenetic machinery" -- which are responsible for reading, writing, and erasing epigenetic information in the form of chemical modifications to the DNA and associated packaging proteins. This epigenetic machinery is critical for development, as evidenced by the fact that >60% of genes encoding components of the epigenetic machinery lead to embryonic lethality or subviability when knocked out in mouse – more than twice the background rate of all genes tested. In humans, mutations of the epigenetic machinery cause or contribute to a variety of diseases including pleiotropic Mendelian syndromes, neurodevelopmental disorders, and cancer. Research in my lab seeks to understand how the epigenetic machinery works, and how its dysfunction leads to disease. Current directions in the lab seek to answer the following key questions about the epigenetic machinery: 1. What are the specific regulatory DNA sequences and target genes influenced by components of the epigenetic machinery, and in what cell types/contexts? 2. How are components of the epigenetic machinery recruited to specific regions of the genome (e.g. regulatory sequences) in specific cellular contexts? 3. By what mechanisms do disease-causing mutations in components of the epigenetic machinery cause phenotypes at the molecular, cellular, and organismal levels. To answer these questions, we use a variety of tools including epigenomics, genome-editing, single-cell genomics, and computational biology, with a focus on mouse developmental and human cell culture models.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Gorkin	Dave	Cell Biology	Full Member
Marcin Grabowicz, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics marcin.grabowicz@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Microbiology and Immunology, School of Medicine Modern medicine relies on infection control provided by effective antibiotic therapy. Escalating antibiotic resistance threatens public health. Gram-negative pathogens are particularly problematic. These bacteria envelope their cell with an outer membrane (OM) that serves as a potent permeability barrier, blocking entry of many available antibiotics and preventing their clinical use. Escherichia coli is responsible for the most global deaths due to antibiotic resistant infections. Our lab uses genetics, biochemistry, and modeling to unravel how E. coli and other Gram-negative pathogens build their OM barrier. Our goal is to empower ongoing efforts to discover new, effective antibiotics.	Modern medicine relies on infection control provided by effective antibiotic therapy. Escalating antibiotic resistance threatens public health. Gram-negative pathogens are particularly problematic. These bacteria envelope their cell with an outer membrane (OM) that serves as a potent permeability barrier, blocking entry of many available antibiotics and preventing their clinical use. Escherichia coli is responsible for the most global deaths due to antibiotic resistant infections. Our lab uses genetics, biochemistry, and modeling to unravel how E. coli and other Gram-negative pathogens build their OM barrier. Our goal is to empower ongoing efforts to discover new, effective antibiotics.Antibiotic resistance is a particularly acute problem for Gram-negative infections. Indeed, Escherichia coli is responsible for the most global deaths due to antibiotic resistant infections. These bacteria build an outer membrane (OM) barrier that prevents entry of many antibiotics, limiting clinical options. Even recently discovered novel antibiotics all fail to penetrate the OM. No new drugs with clinical efficacy against Gram-negatives have been discovered since the 1960s. We aim to understand OM biogenesis and exploit that knowledge to develop therapeutics which disrupt this barrier. Such drugs would kill Gram-negative bacteria because the OM is a conserved and essential organelle, or such drugs could be used to permeabilize bacteria to existing antibiotics. OM assembly is a fascinating biological problem. All OM components are made inside the cell, are then secreted, and must be assembled into a contiguous membrane barrier. In recent years, several essential pathways that assemble the OM have been identified. Our work aims to understand how these processes occur, how they are regulated, and how they are coordinated to ensure that the OM antibiotic barrier is always impenetrable. We use a combination of genetics, biochemistry, modeling, and high-throughput sequencing techniques to investigate the OM of diverse Gram-negative bacteria, including Escherichia coli, Pseudomonas aeruginosa, Acinetobacter baumannii, and others. Our translational goal is to find new strategies for novel antibiotic discovery that are effective against pan-antibiotic resistant Gram-negative pathogens.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Grabowicz	Marcin		Full Member
Adam Gracz, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology agracz@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Division of Digestive Diseases, Department of Medicine, School of Medicine We study how transcription factors and chromatin modifications contribute to cellular identity, especially in the context of stem cell biology.	We study how transcription factors and chromatin modifications contribute to cellular identity, especially in the context of stem cell biology.Epithelial tissues are often highly proliferative and exposed to dynamic cellular environments, which can include potential toxins, infectious material, and sources of physical injury. Epithelial stem cells maintain tissue function by balancing differentiation and self-renewal via precisely regulated gene expression programs. Additionally, many partially-differentiated or mature epithelial cells can reacquire functional stemness in the setting of injury to the endogenous stem cell pool. Maintenance of epithelial homeostasis therefore demands a complex balance of (1) rapid proliferation, (2) differentiation into diverse functional lineages, and (3) "plastic" cellular phenotypes that can de-differentiate in the setting of injury. Our lab studies how gene regulatory mechanisms are integrated and deployed in a context-specific manner to fulfill these requirements. We utilize two model systems with distinct functional characteristics: intestinal and biliary epithelia. While the intestinal epithelium is rapidly proliferative throughout adult life, the biliary epithelium is largely quiescent unless damaged. The long-term goal is to advance our mechanistic understanding of regulatory programs in rare stem cell populations across organ systems, in order to improve therapeutic approaches relevant to regenerative medicine and cancer biology. I. Chromatin in intestinal homeostasis and disease. Emerging data demonstrate a significant degree of cellular plasticity following epithelial injury in the intestine. It is unknown what role DNA/histone modifications and chromatin-modifying enzymes play in generating stable and metastable ISC/progenitor states. This portion of our research program focuses on understanding the role of chromatin in ISC identity, specifically how chromatin and chromatin modifying enzymes maintain the stem cell "state" and contribute to differentiation. II. Biliary epithelial cell identity. Biliary proliferation is associated with liver injury and cancer, and BECs contribute to hepatocyte regeneration following severe or chronic liver injury. However, the genetic identity of BEC subpopulations remains elusive, and the precise cell populations responsible for normal biliary function and post-damage regeneration remain unknown. Ongoing work in our lab seeks to define: (1) genetic characteristics of BEC subpopulations and (2) induction and maintenance of BEC identity by Sox9.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Gracz	Adam	Biology, Developmental Cell Biology Chromatin Gastrointestinal Disorders Genetics, Molecular Liver Diseases	Full Member
Criss Hartzell Jr., PhD (he/him) Emeritus Member - Biochemistry, Cell and Developmental Biology criss.hartzell@emory.edu \| Faculty Profile Professor Emeritus, Department of Cell Biology, School of Medicine Ion channel regulation and signal transduction.	Ion channel regulation and signal transduction.The Hartzell Lab in the Department of Cell Biology at Emory University School of Medicine studies the molecular mechanisms that cells use to regulate the movement of ions like sodium, potassium, calcium, and chloride across their membrane. Our focus is ion channel proteins that form aqueous pores across cell membranes. They are vital to the cell's ability to maintain and regulate the cell's internal ionic composition because ions do not easily cross the oily cell membrane. Ion channel pores are selective for different species of ions; that is, they have structures that allow only one or a few kinds of ions to enter them. Ion channels also have gates that open and close to control ion movement across the membrane. Channel gating can be controlled by various factors including membrane potential, chemicals and neurotransmitters, mechanical stretch, and heat. Ion channels are important in probably every physiological process, from the heart beat to the immune response. Our lab is interested in understanding the roles that ion channels in cell physiology and the molecular machinery that determines how channels open and close and conduct ions. Presently, our main interest is devoted to chloride channels. It is possible that more people have been killed by diseases that affect chloride channels than any other disease, because cholera, diarrheal diseases of infancy, and cystic fibrosis involve chloride channel function. Chloride channels are essential for fluid and salt secretion from epithelia, play a role in sensory transduction, regulate both cytosolic pH and the pH of intracellular organelles, control neuronal and cardiac excitability, and contribute to bone resorption by osteoclasts. In addition to cystic fibrosis and secretory diarrheas, a wide variety of diseases including cystic fibrosis, myotonias, osteopetrosis, deafness, kidney disorders, and neurodegenerative diseases are linked to defects in chloride channel function. Recent inteersts are focusing on non-traditional roles of ion channel protein families. website: www.emory.edu/HEARTCELL	BCDBBiochemistry, Cell and Developmental Biology - Emeritus Member	Hartzell	Criss	null Biophysics Cardiology Neuroscience Physiology	Emeritus Member
Peijian He, PhD Full Member - Biochemistry, Cell and Developmental Biology phe3@emory.edu \| Faculty Profile Assistant Professor, Division of Digestive Diseases, Department of Medicine, School of Medicine Mitochondrial dysfunction, oxidative stress and iron metabolism in the pathogenesis of metabolic diseases.	Mitochondrial dysfunction, oxidative stress and iron metabolism in the pathogenesis of metabolic diseases.Iron metabolism is the hub of the research studies in my lab. Centering around the "iron" focus, we have developed multiple projects that are related to liver and metabolic diseases (see below). We utilize the state-of-art techniques including omics analysis, multiplex fluorescence imaging, and in vivo perfusion and staining, as well as a variety of model systems including knockout and knock-in mouse strains, diet induced disease models, 3D organoid and 2D primary and cell line culture, and specimens of healthy and diseased human subjects. Project 1: Deciphering the role of perturbed iron metabolism and mitochondrial dysfunction in the pathogenesis of metabolic dysfunction-associated steatotic liver diseases (MASLD). MASLD is a metabolic disorder and the most prevalent chronic liver diseases. MASLD comprises a spectrum of conditions including simple steatosis, steatohepatitis, fibrosis, and cirrhosis. The pathogenesis of MALSD remains not well understood. Our recent study suggested a potentially critical role of the altered iron metabolism in MASLD pathogenesis. Hepatocellular iron metabolism is regulated at different levels including iron import, trafficking, utilization, and storage. We identified that the expression of frataxin, a mitochondrial iron chaperone, is markedly decreased in the liver of MASLD in mice and humans. We have generated the FXN knockout and knock-in models and will address how FXN deficiency impacts the progression of MASLD as well as defining the underlying molecular mechanisms. Project 2: In-depth understanding of the specific role of iron metabolism in alcohol-associated liver diseases (ALD). Hepatic iron deposition is frequently reported in patients with ALD and, traditionally, considered a strong risk factor for ALD progression to the more advanced stage - alcoholic cirrhosis, which currently has no cure expect for liver transplantation. Our recent findings in mouse model (Gao-Binge model) of alcoholic liver injury and in ALD patients led us a completely new recognition that absolute and functional hepatocellular iron deficiency plays a crucial role in exacerbating alcoholic liver injury. Iron transport/chaperone proteins including DMT1, mitoferrin 1 and frataxin that play important roles in mitochondrial iron import/utilization are significantly decreased in alcoholic steatohepatitis and alcoholic cirrhosis. We are excited interrogate how functional iron deficiency is caused and, in turn, promotes the progression of ALD by utilizing several lines of genetically engineered mouse models. Project 3: Defining an autonomous role of the hepatocytes in regulating systemic iron metabolism. Hepatocytes are the major site of iron deposition when systemic iron is in excess and are responsible for production of hepcidin which suppresses dietary iron absorption and macrophage-dependent iron recycling. Much effort has been devoted into defining a critical role of liver sinusoidal endothelial cells (LSECs) in hepcidin induction. However, the mechanism of hepcidin regulation in liver injury remains poorly understood. Our recent study revealed a previously unappreciated autonomous role of the hepatocytes in suppressing hepcidin expression in liver injury models. In this scenario, LSECs failed to impose a stimulatory effect on hepcidin expression, despite the elevations in circulating iron and the production of BMP ligands. By utilizing mice with autophagy deficiency and diet/drug induced liver injury, we will elucidate that the altered epigenetic program due to oxidative stress accounts for hepatocyte's autonomous control of hepcidin expression.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	He	Peijian		Full Member
Xin Hu, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology xin.hu2@emory.edu \| Faculty Profile Assistant Professor, Department of Environmental Health, Rollins School of Public Health Assistant Professor, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, School of Medicine We develop and employ systems biology methods to study lung development and how it is affected by early-life environmental factors.	We develop and employ systems biology methods to study lung development and how it is affected by early-life environmental factors.I was trained in inhalation toxicology for my PhD and continued to study pulmonary molecular biology during my post-doctoral training. Through my research, I have gained extensive experience working with a variety of molecular and cell biology approaches with different pulmonary experimental models. A new field that I embarked on in my post-doc research is untargeted metabolomics when trained with Dr. Dean Jones at Emory. Metabolomics, when integrated with other omics platforms, has become an important foundation for my research approach, which relies heavily on systems biology theories, methods and study design. My major focus is to study development of mammalian respiratory airway system and how this process is perturbed by maternal exposure to environmental toxicants. Lung developmental biology is fascinating to me as it spans multiple life stages, from fetal organogenesis to late childhood. My current funded R01 project uses metabolomics and single- cell multiomics to study whether pyrimidine metabolism is a critical pathway in airway formation. This project uses murine embryonic lung explants to study branching morphogenesis. This is a finely regulated biological program with complex and rapidly changing molecular signaling to support cell growth and differentiation. By employing metabolomics, fluxomics and single-cell genomics, we aim to capture this delicate crosstalk and understand the vulnerable targets for environmental stressors. Teaming up with the Emory Stem Cell Core, we are working to move the model to human lung organoids to recapitulate the effects in humans. My second arm of research is to characterize molecular signatures for respiratory subclinical dysfunction and other disease. We use high-resolution LC-MS and GC-MS to deep phenotyping the chemical exposure as well as small-molecule metabolites. For example, we are developing a project to characterize environmental contaminants in cannabis products which may contain a broad spectrum of toxic contaminants depending on how cannabis is grown, processed, and consumed. We are also working with a range of epidemiologists in asthma and cancer to understand how metabolism serves as a proxy for cell function and potentially a driver for pathogenesis. An important component of my research team is to develop and apply computational tools to integrate large-scale, high-dimensional datasets including various omics data, clinical data and even imaging data to construct the landscape of molecular aberrations in disease processes. We recently identified sexual dimorphism in metal induced respiratory dysfunction. Based on this interesting data, our next project will be to investigate the role of sexual hormone and steroid receptors in environmental origins of asthma. Elucidation of sexual dimorphism in environmental toxicology provides opportunities to identify a common mechanism linking respiratory outcomes to a wide range of early-life, modifiable risk factors that disrupt the endocrine system. Further, it may lead to development of intervention strategies that are more targeted towards susceptible populations, making the most impactful translational findings. Taken together, my vision for research is to embrace the complexity and multiplicity of interactions among biological processes and environmental factors. Integrative systems biology tools hold promises to advance knowledge of the interactions in a more comprehensive and efficient way.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Hu	Xin	Biology, Developmental Cell Biology Cell Metabolism Environmental Effects	Full Member
Young C. Jang, PhD Full Member - Biochemistry, Cell and Developmental Biology young.jang@emory.edu \| Faculty Profile Associate Professor, Department of Orthopaedics, School of Medicine Our research integrates biomedical engineering, stem cell biology, and physiology to understand the mechanisms of aging and age-related diseases.	Our research integrates biomedical engineering, stem cell biology, and physiology to understand the mechanisms of aging and age-related diseases.My academic training and research experiences in integrative cell physiology and stem cell biology, combined with innovative bioengineering approaches, have uniquely positioned my research program to undertake challenging research questions in aging and regenerative medicine. Since starting a faculty position in 2014, I have established an internationally recognized, interdisciplinary research program focusing on skeletal muscle biology, specifically in the context of sarcopenia (age-associated muscle loss and function). My laboratory has made significant progress toward understanding the aging process and developed new technologies to enhance the therapeutic potential of stem cells in regenerative medicine applications. My primary goal in teaching and mentoring is to guide and motivate students to think logically and systematically but also have the ability to look at the big picture and to think outside of the box in tackling scientific questions or solving problems. I have been implementing this philosophy in my lectures, and my efforts in teaching have been recognized with the 2021 Georgia Tech CTL/BP Teaching Excellence Award and student evaluation average score of 4.8 for being an "overall effective instructor", which placed me in the top 3% of the College of Science at Georgia Tech. Along with my research and teaching, I have been an advocate for the local, national, and international research communities. I've served on a variety of committees both within Georgia Tech and in the broader scientific community. Collectively, I am fully committed to developing a successful research program, maintaining a high standard of teaching, and serving the Emory and national and international research communities. By the year 2030, more than one out of five individuals will be over the age of 65, and the majority of these individuals will suffer from one or more age-related diseases in the United States. Needless to say, the healthcare costs to treat age-associated diseases will increase dramatically, and this number is estimated to reach 4 trillion dollars by 2030. Moreover, in the last two decades, the incidence of a major disease that causes mortality in aged individuals, such as cardiovascular disease and cancer, is on a downward trend due to advances in medical care. However, other age-related disorders, such as Alzheimer 's disease and dementia-related neurodegenerative disease, frailty, hearing loss, and musculoskeletal disorders, age-acquired diseases that influence everyday life and a loss of independence, are increasing exponentially. Thus, the long-term goals of my research program are to understand the cellular and molecular mechanisms of these age-acquired defects, with particular emphasis on age-associated musculoskeletal dysfunction, and develop therapeutic strategies to alleviate muscle-wasting and provide the basis for improving quality of life and rehabilitation strategies for frailty and sarcopenia (Figure 1). My research program aims to achieve these goals by combining innovative approaches in stem cell biology, bioengineering, and physiology to better understand how stem cells interact/communicate with their local microenvironment (niche) and systematic environment to maintain skeletal muscle homeostasis and how these processes are disrupted and dysregulated during aging and in pathophysiological conditions.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Jang	Young		Full Member
Sohail Khoshnevis, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics sohail.khoshnevis@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Biochemistry, School of Medicine The Khoshnevis Lab utilizes RNA/protein biochemistry, yeast genetics, structural biology and cell- based assays to understand post-transcriptional regulation of gene expression in human fungal pathogens and applies this knowledge to identify novel targets for therapeutic development.	The Khoshnevis Lab utilizes RNA/protein biochemistry, yeast genetics, structural biology and cell- based assays to understand post-transcriptional regulation of gene expression in human fungal pathogens and applies this knowledge to identify novel targets for therapeutic development.The overarching goal of Khoshnevis laboratory, within the Department of Biochemistry at Emory University, is to define the molecular mechanisms of post-transcriptional regulation of the virulence in the human fungal pathogen Candida albicans. C. albicans is a prevalent human fungal pathogen, a leading cause of nosocomial infection, and the cause of an estimated 700,000 severe cases of candidiasis per year with a mortality rate of 40%. C. albicans is a commensal organism found in the gastrointestinal tract, mouth, skin, and female reproductive tract that can cause superficial mucosal infection. These infections can be life-threatening in immunocompromised patients, including organ transplant recipients, cancer and HIV/AIDS patients. The current treatments are mostly restricted to polyenes, azoles, and echinocandins. The use of these antifungals is limited by toxicity, drug-drug interactions, and the emergence of resistance, underscoring the importance of identifying novel therapeutic targets and the need for new treatment approaches. C. albicans can undergo a morphological transition from single oval cells (yeast) to elongated cells (hyphae); this process is important for its pathogenicity. Understanding the molecular basis for yeast-to- hyphae transition is, therefore, of great importance to find new ways to combat Candida infections. A long-term goal of our laboratory is to identify the post-transcriptional mechanisms that regulate protein synthesis and understand their contribution to fungal pathogenicity. We focus on two areas of post- transcriptional gene regulation: mRNA modifications and translational control. These two areas represent a significant gap in our knowledge of how these processes can rapidly affect cellular plasticity in response to the changes in environmental cues in C. albicans. Translational control of cell-type switching in C. albicans: One of the main goals of our research is to address the role of translation machinery in controlling cell plasticity in C. albicans. Our efforts are currently focused on two translation factors: eIF3 and eEF3. The eukaryotic translation initiation factor 3 (eIF3) has emerged as a master player in translation regulation by promoting or suppressing the translation of a subset of mRNAs. However, how this key initiation factor controls cell plasticity is not understood. Similarly, the eukaryotic translation elongation factor 3 (eEF3), an AAA-ATPase that is fungal-specific, is important in pathogenesis but its role in cell plasticity remains unknown. Through a combination of biochemical, structural, and cell-based approaches we aim to characterize the role of eEF3 in morphological transition in C. albicans and target it to design new classes of antifungals. The role of post-transcriptional modifications in the pathogenicity of C. albicans: A second area of research in our lab is focused on understanding how RNA modifications regulate cell plasticity in C. albicans. By combining novel genetic tools and reagents that we have developed with biochemical assays, proteomics, and next-generation sequencing we aim to answer two key questions: 1) What is the mechanism of m6A deposition on mRNAs during cell-type switching in C. albicans? and 2) How do RNA modifications contribute to cell-type switching and pathogenicity in C. albicans? By answering these questions, we hope to provide significant insights into the mechanisms of post-transcriptional control of cell plasticity in C. albicans that will aid in understanding how dysregulation of these processes contributes to pathogenicity.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Khoshnevis	Sohail		Full Member
Michael Koval, PhD Full Member - Biochemistry, Cell and Developmental Biology mhkoval@emory.edu \| Faculty Profile \| Lab Website Professor, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, School of Medicine Professor, Department of Cell Biology, School of Medicine Program Director, BCDB Molecular basis for intercellular communication and barrier function in lung health and disease.	Molecular basis for intercellular communication and barrier function in lung health and disease.The lung provides a barrier that enables the exchange of oxygen and carbon dioxide between the atmosphere and bloodstream. The part of the barrier which faces the atmosphere (airspace) is covered by epithelial cells with different characteristics, depending upon the location in the lung. The terminal airspace (alveolus), where gas exchange occurs is covered by a layer of cells collectively known as the alveolar epithelium. Cell-cell contacts between alveolar epithelial cells contain distinct elements which contribute to their function. These include tight junctions and gap junctions. Tight junctions are the primary mechanism that regulates whether the epithelium is tight or leaky. This is due to claudin-family proteins that form a seal to both restrict paracellular diffusion and permit specific transport of ions between cells across the epithelial barrier. There are nearly twenty different claudins, and cells simultaneously express several claudins. However, the mechanisms that regulate claudin intermixing are poorly understood at present. Also, it is not know how cells use multiple claudins to regulate epithelial barrier function. A primary goal of my laboratory is to use molecular and cell biological approaches to define roles for different claudins in normal lung barrier function and in pathologic conditions such as acute respiratory distress syndrome (ARDS). A long term goal is to develop methods to augment alveolar barrier function as a means to improve the outcome of patients with ARDS and other forms of lung injury. Gap junctions consist of channels which interconnect cells in a tissue. This enables the direct transfer of small signaling molecules and metabolites between adjacent cells. There are almost two dozen different gap junction proteins (called connexins) and cells regulate the specificity of intercellular communication by expressing different connexins. The mechanisms which regulate the assembly of connexins into gap junction channels remain poorly understood. In contrast to most transmembrane protein complexes, connexins oligomerize after exit from the endoplasmic reticulum (ER) in different aspects of the Golgi apparatus. This suggests that a novel post-ER mechanism for the control of protein assembly may exist. We have recently employed a system using connexins fused to ER retention/retrieval motifs to trap assembly intermediates and to identify key steps in connexin-specific assembly pathways. One goal of the lab is to identify chaperones that participate in this process, using ER-retained connexins as "bait" to bind potential chaperones. We are also identifying connexin domains that control sorting and gap junction channel assembly, using fluorescence microscopy to examine the behavior of transfected mutant connexin constructs containing domains from multiple connexins. Finally, we are currently developing cell culture and animal models where gap junctional communication is disrupted to define roles for gap junctional communication in lung function and diseases, particularly Cystic Fibrosis.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Koval	Michael	Alcohol / Alcoholism Biochemistry, Proteins Biology, Cellular Cardiovascular Disease Cell Biology Membrane Biology Molecular Biology Pulmonary Medicine Respiratory Disorders	Full Member
Jennifer Kwong, PhD Full Member - Biochemistry, Cell and Developmental Biology jennifer.kwong@emory.edu \| Faculty Profile Assistant Professor, Division of Cardiology, Department of Pediatrics, School of Medicine The central theme of my research program is to define the molecular mechanisms by which mitochondria function as signaling organelles, with a specific focus on the contribution of mitochondrial dysfunction and altered metabolism to cardiac disease and development.	The central theme of my research program is to define the molecular mechanisms by which mitochondria function as signaling organelles, with a specific focus on the contribution of mitochondrial dysfunction and altered metabolism to cardiac disease and development.The central theme of our research program is to define the molecular mechanisms by which mitochondria function as signaling organelles, with a specific focus on the contribution of mitochondrial dysfunction and altered metabolism to cardiac disease and development. Mitochondria are uniquely positioned at the tipping point between life and death as they are central to both energy and death pathways. Maintaining this balance has special relevance in the heart, where mitochondria are the major energy source for contraction, yet mitochondria-mediated death contributes significantly to cardiac disease. Therapies limiting death and enhancing energy would be extremely beneficial. Pursuit of such strategies however, is restrained by the current limited knowledge of how mitochondria decode environmental signals (particularly Ca2+) to engage physiological versus pathological responses, and the signaling mechanisms utilized to communicate dysfunction. The goal of our laboratory is to try to understand how cardiac mitochondria sense and integrate environmental information to make cellular life and death decisions. Currently, our research is directed towards two main lines of research: 1) mitochondrial energetics and retrograde signaling in the heart, and 2) the role of mitochondria in cardiac development and congenital heart disease. 1. Mitochondrial energetics and retrograde signaling in the heart Mitochondrial dysfunction is a hallmark of cardiac diseases ranging from heart failure to diabetic cardiomyopathy. This link between energy dysfunction and cardiac dysfunction is further underscored by the fact that mutations in the mitochondrial ATP synthesis machinery cause mitochondrial disorders that often present with cardiomyopathy. Strategies to mitigate energy dysfunction would be highly beneficial, but such development is limited by our incomplete understanding of how impaired energy leads cardiac disease. To tackle this issue, we have developed an in vivo model of cardiac mitochondrial energy dysfunction and we are deploying this model to investigate pathways activated upon cardiac mitochondrial energy deficit, with the ultimate goal of identifying signals that convey energetic crisis in the heart. 2. Mitochondria and the development heart. The heart is a high-energy tissue that relies on mitochondria to supply the majority of energy needed to fuel cardiac excitation-contraction coupling. Thus, establishing mature mitochondrial energy systems is critical for cardiac development. Our research focuses on the impact of mitochondrial dysfunction in cardiac ventricular morphogenesis and delineating the molecular mechanisms that need to be engaged in cardiac metabolic maturation.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Kwong	Jennifer	Cell Biology	Full Member
Steven W. L'Hernault, PhD Affiliate Member - Biochemistry, Cell and Developmental Biology Affiliate Member - Genetics and Molecular Biology bioslh@emory.edu \| Faculty Profile Professor, Department of Biology, Emory College of Arts and Sciences Chair, Department of Biology, Emory College of Arts and Sciences Developmental genetics; cell and molecular biology of C. elegans spermatogenesis and fertilization.	Developmental genetics; cell and molecular biology of C. elegans spermatogenesis and fertilization.My laboratory is interested in the proteins and processes required to assemble a fertilization-competent cell surface on spermatozoa. We study spermatogenesis and fertilization in the nematode Caenorhabditis elegans because of its superior genetic and reproductive biological tools. Like mammals, the C. elegans spermatid surface must be remodeled by secretory vesicle fusion in order for cell-cell fusion to occur during fertilization. Consequently, we focus on mutants that are either directly defective in fertilization or defective in the sperm secretory vesicles (analogous the the acrosome in mammalian sperm) that must fuse to generate a fertilization-competent surface. These sperm secretory vesicles fuse with the sperm plasma membrane during activation, when spermatids acquire motility and become fertilization-competent. So far, at least four transmembrane proteins reside in sperm secretory vesicles are placed onto the sperm surface, where they are required to create a fertilization-competent sperm. We have shown that one, SPE-45, is orthologous to mammalian Izumo, which is known to be required for sperm-egg fusion in mammals. We have used CRISPR genome engineering to analyze SPE-45/Izumo chimeric proteins for fertilization competence in C. elegans spe-45 null mutant backgrounds and found that much of the human Izumo-derived Ig domain can functionally replace the SPE-45 Ig domain. We are currently exploiting this "humanized" worm to search for potential male birth control compounds via a high-throughput screen of small molecule libraries. In parallel, we continue to explore C. elegans sperm expressed proteins required for fertilization as, despite 1 billion years since nematodes and humans last shared a common ancestor, at least three of these proteins have convincing orthologs in humans.	BCDBBiochemistry, Cell and Developmental Biology - Affiliate Member GMBGenetics and Molecular Biology - Affiliate Member	L'Hernault	Steven		Affiliate Member
Dorothy Lerit, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology dlerit@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Cell Biology, School of Medicine Centrosomes are microtubule-organizing centers that build the mitotic spindle required for error-free mitosis. Our research interests include understanding how centrosome activity is regulated in space and time, and how centrosome regulation contributes to cell and animal viability.	Centrosomes are microtubule-organizing centers that build the mitotic spindle required for error-free mitosis. Our research interests include understanding how centrosome activity is regulated in space and time, and how centrosome regulation contributes to cell and animal viability.REGULATION OF CENTROSOME ACTIVITY IN DEVELOPMENT AND DISEASE Precise control of cellular proliferation is essential to prevent tissue degeneration or tumorigenic expansion. Tasked with ensuring proper cell division in most animal cells is a small organelle called the centrosome. Centrosomes function to nucleate and assemble microtubules (MTs) that contribute to cellular form and function. As the MT-organizing centers, centrosomes build the bipolar mitotic spindle that segregates the duplicated genome into two daughter cells during cell division. In addition, centrosomes orchestrate numerous critical tasks during non- proliferative stages, including cell polarization, ciliogenesis, cell migration, and intracellular trafficking. The essential determinant of MT-organizing activity is the pericentriolar material (PCM), a matrix of numerous proteins that envelops the central pair of centrioles residing at the centrosome center. Deregulation of centrosome activity is often detrimental, leading to mitotic catastrophe and/or genome instability, which are hallmarks of cancer cells. Centrosome dysfunction is also a major cause of human recessive primary microcephaly, a hereditary neurodevelopmental disorder characterized by abnormally small brain and head size. Other centrosome disorders are associated with obesity, sterility, and polycystic kidney disease. Therefore, understanding how cells regulate centrosome activity remains a critical question of profound human health significance. To address how centrosome activity is regulated in space and time, our lab couples cutting-edge microscopy with modern molecular biology, genetics, and cell biology approaches. As a result, we have provided valuable mechanistic insight into the functions of several human disease genes. For example, we showed the ortholog to Pericentrin (Pcnt), Pcnt-like-protein (PLP), is a critical regulator of centrosome activity control in the neural stem cells and rapidly dividing early embryos of the powerful model organism, Drosophila. Our data lay the groundwork toward understanding how deregulation of human Pcnt leads to microcephaly and contributes to cancers of the lung, breast, and colon. Additionally, we defined an intimate regulatory network between PLP and another microcephaly protein, CDK5RAP2/Centrosomin (Cnn), providing an important mechanistic link to disease etiology. More recently, we showed that localization of Plp mRNA to the centrosome is important for centrosome function and genome stability. Our laboratory is at the forefront of examining the roles of the select mRNAs that localize to the centrosome. Because mRNA localization coupled to translational regulation is an efficient and highly conserved paradigm used to acutely regulate diverse cellular behaviors, we investigate which RNAs localize to centrosomes, how they get there, whether they are translated locally, and what happens if the RNA is unable to localize. To address these questions, we leverage the rapidly dividing and transcriptionally quiescent Drosophila early embryo. However, we are expanding this work into other tissues, as well as cell culture models. Our goal is to define how centrosomes are controlled in healthy and diseased cells. By investigating novel paradigms of centrosome regulation, we aim to uncover mechanisms of centrosome activity control, aspects of which may be deregulated in diseases such as microcephaly, neurodegeneration, sterility, and cancer. Selected Key Publications: Fang, J.* , Tian, W., Quintanilla, MA, Beach, J.R., and Lerit, DA (2025) The PCM scaffold enables RNA localization to centrosomes. Molecular Biology of the Cell. 36(6):ar75. PMID: 40305119 Ryder, P.V., Fang, J., and Lerit, D.A. (2020) centrocortin RNA localization to centrosomes is regulated by FMRP and facilitates error-free mitosis. Journal of Cell Biology. 219(12): e202004101. equal contributions	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Lerit	Dorothy	Cell Biology	Full Member
Bo Liang, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics bo.liang@emory.edu \| Faculty Profile Associate Professor, Department of Biochemistry, School of Medicine Co-Scientific Director, Robert P. Apkarian Integrated Electron Microscopy Core, Emory University Our principal goal is to scrutinize high-resolution structural details and understand the molecular mechanisms of large assemblies, including ribonucleoprotein complexes and membrane proteins, using integrated approaches of cryo-EM and X-ray crystallography.	Our principal goal is to scrutinize high-resolution structural details and understand the molecular mechanisms of large assemblies, including ribonucleoprotein complexes and membrane proteins, using integrated approaches of cryo-EM and X-ray crystallography.Structure and Regulation of Non-Segmented Negative-Sense RNA Virus Polymerases The Liang Laboratory is focused on integrating the power and advantages of different imaging system modalities, including those using electrons, x-rays, and visible lights, to scrutinize how macromolecular machinery functions in various biological processes in real-time and at unprecedented resolution. Capitalizing on breakthroughs in detector technology and image processing algorithms, the Liang laboratory is particularly interested in using cryo-electron microscopy (cryo-EM) as a primary tool to visualize macromolecular complexity. Cryo-EM is especially well suited for molecular systems traditionally challenging for structural characterization, including membrane proteins and large and heterogeneous assemblies. In addition, we employ X-ray crystallography and fluorescence light microscopy to provide complementary structural and dynamic information for challenging systems of significant biological importance. One such challenging system is the RNA synthesis machinery of a class of pathogenic and sometimes deadly non-segmented negative-sense (NNS) RNA viruses, including Rabies, Measles, Ebola, Marburg, and Respiratory Syncytial Virus (RSV). RNA synthesis is central to the life of these viruses, and it is carried out by RNA polymerase (a multifunctional enzyme). The structural basis of the RNA synthesis machinery remains largely unclear. The Liang laboratory is dedicated to understanding the structure and function of the RNA synthesis machinery of RSV, the top leading cause of severe pediatric respiratory tract diseases in the United States and worldwide. RNA synthesis by the RNA polymerase of RSV is essential for viral pathogenesis in infants and children. The Liang laboratory will establish an RNA synthesis platform for RSV, elucidate how this RNA synthesis machine functions, and identify potential antiviral therapeutic targets for more effective treatment. Our immediate research goal would be to decipher the molecular architecture of the RNA synthesis machinery of these viruses using cryo-EM and x-ray crystallography. This could lead to developing effective antiviral drugs to block RSV activity. Such drugs would result in a substantial reduction in serious RSV infections in infants and children and provide a major achievement for human health. References • Cao D., Gao Y., Chen Z., Gooneratne I., Roesler C., Mera C., D'Cunha P., Antonova A., Katta D., Romanelli S., Wang Q., Rice S., Lemons W., Ramanathan A., Liang B.* Structures of the promoter-bound respiratory syncytial virus polymerase. Nature (2023). DOI: 10.1038/s41586-023-06867-y \| PMID: 38123676. • Xu E., Park S., Calderon J., Cao D., Liang B.* In Silico Identification and In Vitro Validation of Repurposed Compounds Targeting the RSV Polymerase. Microorganisms 11, (2023). DOI: 10.3390/microorganisms11061608 \| PMID: 37375110. • Gao Y., Raghavan A., Deng B., Lee J., Liang B.* Optimal Conditions for In Vitro Assembly of Respiratory Syncytial Virus Nucleocapsid-like Particles. Viruses 15, (2023). DOI: 10.3390/v15020344 \| PMID: 36851557. • Cao D., Gooneratne I., Mera C., Vy J., Royal M., Huang B., Park Y., Manjunath A., Liang B.* Analysis of Template Variations on RNA Synthesis by Respiratory Syncytial Virus Polymerase. Viruses 15, (2022). DOI: 10.3390/v15010047 \| PMID: 36680087. • Cao D., Gao Y., Roesler C., Rice S., D'Cunha P., Zhuang L., Slack J., Antonova A., Romanelli S., Liang B.* In vitro primer-based RNA elongation and promoter fine mapping of the respiratory syncytial virus. J Virol (2020) \| 10.1128/JVI.01897-20. • Gao Y., Cao D., Pawnikar S., John K., Ahn H. M., Ha J. M., Parikh P., Ogilvie C., Yang A., Bell A., Salazar A., Miao Y., Liang B. Structure of the human respiratory syncytial virus M2-1 protein in complex with a short positive-sense gene-end RNA. Structure (2020) \| 10.1016/j.str.2020.07.001. • Cao D., Gao Y., Roesler C., Rice S., D'Cunha P., Zhuang L., Slack J., Domke M., Antonova A., Romanelli S., Keating S., Forero G., Juneja P., Liang B.* Cryo-EM structure of the respiratory syncytial virus RNA polymerase. Nat Commun 11, 368 (2020) \| 10.1038/s41467-019-14246-3. • Gao Y., Cao D., Ahn H. M., Swain A., Hill S., Ogilvie C., Kurien M., Rahmatullah T., Liang B.* In vitro trackable assembly of RNA-specific nucleocapsids of the respiratory syncytial virus. The Journal of Biological Chemistry (2019) \| 10.1074/jbc.RA119.011602.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Liang	Bo		Full Member
Xu Liu, PhD Full Member - Biochemistry, Cell and Developmental Biology xu.liu@emory.edu \| Faculty Profile Assistant Professor, Department of Biochemistry, School of Medicine My research focuses on the structure and function of macromolecular interactions, specifically targeting hormone receptors and their influence on biological processes.	My research focuses on the structure and function of macromolecular interactions, specifically targeting hormone receptors and their influence on biological processes.Mineralocorticoid receptor (MR) has traditionally been studied in the renal epithelium for its role in regulating potassium balance after activation by aldosterone. Recent studies found that overactivation or inappropriate activation of MR in non-epithelial cells increase inflammation, fibrosis and oxidative stress. Therefore, dysregulation of MR signaling leads to the development of chronic kidney disease, hypertension, fatty liver disease and major depressive disorder. MR antagonists are of great use in combating these pathological conditions. However, their development is largely lagging compared to modulators targeting its homologs, such as glucocorticoid, estrogen and androgen receptors. We envision to develop two research programs centered on MR biochemistry and biology as follows: Program 1: A massive gap of knowledge on the Ligand Binding Domain (LBD) and DNA Binding Domain (DBD) of MR is the allostery between them. MR has the largest disordered N-terminal domain (NTD) and hinge region; and the study of their roles in regulating transcription is limited and urgently needed. Only with detailed understanding of each domain in the context of full-length MR will we be able to understand the pathologies resulting from its dysregulation and to design modulators to circumvent those defects. For this program, we plan to understand how the NTD and hinge region regulate MR transcription by condensate formation. Biomolecular condensates (or droplets) are membrane-less organelles that have no fixed stoichiometry and are often formed by the physical process of liquid-liquid phase separation (LLPS). We have published work on how LLPS regulates GR-mediated transcription by forming condensates and driving the recruitment of distinct transcriptional coregulators (such as G9a and MED1) and will expand this study to MR on its biomolecular condensate formation with distinct coregulators and nucleotides. We will also study the mechanism of regulation of MR transcription by allostery, including the interdomain allostery between DBD and LBD and the intradomain allosteric communication from ligand binding site to AF-2 coregulator binding site. We will determine the quaternary structure of MR/coregulator/DNA complex underlying the interdomain allostery and use a function-centered deep mutational scanning approach to discover the MR hotspot residues that play key roles in allosteric signaling and determine proper coregulator binding in response to aldosterone, eplerenone and finerenone. Results generated from this theme will significantly advance the field of MR antagonist development by enabling a series of previously unexplored opportunities, including targeting the 'undruggable' disordered domain. Program 2: Duchenne Muscular Dystrophy (DMD) is a chronic devastating muscular dystrophy with an incidence rate of 1 in 5000 boys and an average life expectancy below 30 years. Hypertrophic cardiomyopathy followed by end-stage dilated cardiomyopathy and heart failure are major factors in mortality in patients. Recent studies show that vamorolone has cardiac protection by acting on MR in DMD mouse model. While our study of vamorolone's mechanisms targeting GR has been published, its action on MR and its potential antihypertensive efficacy remain unexplored and are the focus here. We will set up to understand how vamorolone drives MR function from both atomic and genomic scales. We will leverage structural and biochemical approaches to build a multidisciplinary group that will determine how vamorolone acts as an MR antagonist. We have solved the structures of MR LBD in complex of cortisol (endogenous ligand), prednisolone (agonist) and vamorolone (antagonist) and am currently characterizing how vamorolone drives MR function compared to the other ligands. We will complement the structural and biochemical insights by leveraging multi-OMICS (ATAC-seq, ChIP-seq, RNA-seq and metabolomics) to provide a complete picture of vamorolone's mechanism of action. Our understanding of mechanism that connects molecular interactions to clinical outcomes will revolutionize our ability to design new GR/MR modulators for DMD and other inflammatory disorders.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Liu	Xu		Full Member
Dave Lynn, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics Full Member - Population Biology, Ecology, and Evolution dlynn2@emory.edu \| Faculty Profile \| Lab Website Asa Griggs Candler Professor, Department of Chemistry, Emory College of Arts and Sciences HHMI Professor, Department of Chemistry, Emory College of Arts and Sciences Rhizosphere/human brain comparisons, symbiotic interactions and neuroscience, intelligent materials and the living/non-living continuum, origins of complex molecular functions.	Rhizosphere/human brain comparisons, symbiotic interactions and neuroscience, intelligent materials and the living/non-living continuum, origins of complex molecular functions.During the last century the view of the living cell as a collection of machines driving metabolic cycles was both developed and rejected, as the layers of cellular diversity and complexity were uncovered. Most remarkable has been our realization that phenomenally complex biological structures are capable of spontaneous self-assembly. From protein folding, to vesicle formation, to the organogenesis of multicellular organisms, a genome clearly encodes not only the information for synthesizing the biological macromolecules, but instructions for their precise 3D self-assembly. Increasingly, genomics and proteomics methods are enabling the large-scale analysis of biological macromolecules such that the energies of supramolecular self-assemblies might now be understood and extended into new materials. Several specific systems are currently being studied: 1. Parasitic angiosperms have developed novel developmental strategies that enable avoidance of host defenses. The molecular basis and evolution of these strategies are studied, 2. Agrobacterium tumefaciens is the only organism that employs lateral gene transfer to eukaryotic cells as a routine adaptive strategy; the molecular basis and evolution of this strategy are of interest, 3. Amyloid diseases, or mis-folding diseases, offer unique opportunities to analyze tertiary and quaternary structure formation. In 2002, I was awarded one of 20 inaugural Howard Hughes Medical Institute Professorships nationwide and pioneered several new educational strategies including science/arts collaborations for communicating science. These efforts culminated with the initiation of the annual Atlanta Science Festival that brought science to over 45,000 people last year and the new Gordon Research Conference on Systems Chemistry.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member PBEEPopulation Biology, Ecology, and Evolution - Full Member	Lynn	Dave		Full Member
Cheryl L. Maier, MD, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Immunology and Molecular Pathogenesis cheryl.maier@emory.edu \| Faculty Profile Assistant Professor, Department of Pathology and Laboratory Medicine, School of Medicine My research focuses on the intersection of hemostasis and immunology, including understanding the mediators of thromboinflammation and alloimmunization and ways to mitigate or prevent associated pathology to ultimately improve patient outcomes.	My research focuses on the intersection of hemostasis and immunology, including understanding the mediators of thromboinflammation and alloimmunization and ways to mitigate or prevent associated pathology to ultimately improve patient outcomes.My long-standing research interests have centered on the multifaceted interplay between the immune system with the vascular and hemostatic systems. Specifically, before COVID, this included work on T cell-vascular cell interactions, alloimmunization to transfused blood products, and platelet immunology. Amid the pandemic, I was uniquely poised to expand my research to include mechanisms driving thromboinflammation. Early in the pandemic I participated in a large multidisciplinary care team dedicated to understanding COVID-associated-coagulopathy, which is now regarded as the major mechanism of organ failure and death in patients with SARS-CoV- 2 infection, and led the team that made the novel observation of blood hyperviscosity in critically ill patients. Since then, my research has focused on understanding the relationship between inflammation, clotting and alterations in blood rheology. Through multiomics and multidisciplinary collaboration, with adult and pediatric specialists, biochemists, pathologists and bioengineers, we uncovered a unique mechanism whereby pathologically-elevated fibrinogen induces red blood cell aggregation that mechanically injures the vascular endothelium. This finding is impactful not only for understanding COVID pathogenesis, but also for understanding the importance of blood rheology in many diseases hallmarked by thromboinflammation, including malignancy, sepsis, sickle cell disease and pre-eclampsia. Understanding how elevated fibrinogen alters blood rheology is a current major focus of the laboratory, in addition to defining mediators driving fibrinogen expression and the consequences of fibrinogen modification on clot formation and breakdown. Finally, we have been using electron microscopy and MALDI-mass spectrometry to better understand the composition of blood clots retrieved from various patient populations with stroke. We have found increased levels of a particular variant fibrinogen isoform, and are currently exploring its role in clot formation and lysis, as well as its role in promoting red blood cell aggregation and endothelial perturbation. Overall, our work strives to better understand thrombosis in order to develop better therapeutics for patients with coagulopathy.	BCDBBiochemistry, Cell and Developmental Biology - Full Member IMPImmunology and Molecular Pathogenesis - Full Member	Maier	Cheryl		Full Member
Adam Marcus, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Cancer Biology aimarcu@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Hematology and Medical Oncology, School of Medicine Director, Integrated Cellular Imaging Core, Winship Cancer Institute Mechanisms guiding cancer cell invasion and metastasis.	Mechanisms guiding cancer cell invasion and metastasis.I have an extramurally funded research laboratory that focuses on the cytoskeletal mechanisms guiding cancer cell invasion and metastasis. My laboratory combines cutting-edge cellular imaging with molecular biology to understand cancer cell motility. We are using these methodologies to generate mechanistic data that is being tested in the pre-clinical and clinical settings. Our work has focused on the lung cancer tumor suppressor protein and epithelial signaling protein, LKB1. This serine/threonine kinase is mutated in 30% of patients with non-small cell lung cancer; however, the functional significance of LKB1 loss is unknown. We now show that LKB1 plays a central role in cancer cell migration by behaving as a dynamic, actin-associated protein that regulates the canonical cdc42 cell polarity pathway. We show that LKB1 associates with the active form of cdc42 and its downstream binding partner PAK. LKB1 loss results in inhibition of cdc42 activation, lack of cdc42 cellular recruitment, and complete disruption of lung cancer polarity. Since aberrant cell polarity is proposed to be a trigger for cancer cell invasion, these results suggest that LKB1 is an upstream regulator of both cdc42 activity and localization, and that LKB1 loss triggers aberrant lung cancer cell polarity. We are further dissecting the LKB1-cdc42-PAK pathway and have projects underway to decipher the temporal and spatial regulation of this interaction. Specifically, we are determining how LKB1 interacts with PAK and cdc42, if LKB1 serves as a PAK kinase, and at what point LKB1 interacts with cdc42-PAK in the polarity pathway. Since we show that LKB1 is a dynamic actin-associated protein that migrates to the cellular leading edge, we are continuing in vivo cytoskeletal trafficking studies of LKB1 using photoactivatable fluorescent proteins and fluorescent recovery after photobleaching (FRAP) live cell imaging techniques. We are also investigating the LKB1 co-factor STRAD, and have generated data on complex regulation as well as LKB1-independent functions of STRAD. This project has three long-term research objectives. First, we want to determine if LKB1 loss triggers cancer metastasis in lung cancer patients. We will use our epithelial to mesenchymal transition (EMT) patient biomarker analysis to investigate the impact of LKB1 loss on EMT then we will work with our biostatistics team to determine if LKB1 mutational status correlates with disease progression and appearance of metastatic disease. We will also work in pre-clinical mouse models to further test our mechanism and hypothesis that LKB1 loss triggers metastatic disease. Second, our work has elucidated a novel pathway but we still do not understand how perturbation of this pathway triggers cancer invasion. Our preliminary data indicate this occurs through modifications of cell adhesion; however we want to fully decipher this and precisely determine how LKB1 triggers cancer invasion. Third, we want to expand these findings into other tumor types. We have preliminary data showing that the LKB1 gene is homozygously deleted in another tumor type and are currently performing laser capture microdissection of clinical tissue samples to confirm this deletion in patient samples. Within the past two years we have also focused on developing an anti-metastatic cancer chemopreventative strategy. This work, which was based upon our basic cell biology findings, has identified a completely novel agent and target that is critical for cancer cell migration. We are collaborating with the Emory Department of Chemistry to develop this therapeutic for use in the anti-metastatic chemopreventative setting. We envision that this agent can be used in high-risk metastatic patients and can be combined with traditional cytotoxics to inhibit both metastasis and tumor growth. Lastly, we also are focused on the physical mechanisms driving glioblastoma invasion. We use 3-D spheroid invasion models in combination with live cell imaging to study the bi-directional communication between invading cells and the extracellular matrix.	BCDBBiochemistry, Cell and Developmental Biology - Full Member CBCancer Biology - Full Member	Marcus	Adam	Cell Biology	Full Member
Nael A. McCarty, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology namccar@emory.edu \| Faculty Profile \| Lab Website Professor, Division of Pulmonary Medicine, Department of Pediatrics, School of Medicine Adjunct Associate Professor, School of Biological Sciences, College of Sciences, Georgia Institute of Technology Adjunct Associate Professor, School of Chemistry and Biochemistry, College of Sciences, Georgia Institute of Technology Program Director, MSP Systems biology of chronic lung diseases; Links between immunology and lung disease; Pathophysiology in cystic fibrosis; Epithelial biology; Structure, function, evolution, and pharmacology of ion channels and ATP-binding cassette (ABC) transporters; Regulation of CFTR ion channel by lipids and lipid-mediated signaling.	Systems biology of chronic lung diseases; Links between immunology and lung disease; Pathophysiology in cystic fibrosis; Epithelial biology; Structure, function, evolution, and pharmacology of ion channels and ATP-binding cassette (ABC) transporters; Regulation of CFTR ion channel by lipids and lipid-mediated signaling.Cystic Fibrosis (CF) is a complex lethal disorder, which is the second most common genetic disease in the U.S. and affects people of all ethnic groups. CF is manifest in multiple tissues of epithelial origin. Mutations in the gene encoding the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) result in abnormal secretion in exocrine glands, due to dysfunctional ion channels and/or improper regulation of ion channels. This laboratory is actively engaged in research addressing three aspects of CF: 1) Systems biology approaches to understand mechanisms underlying disease progression in chronic lung diseases, including CF, especially focusing on the biogeography of infection, inflammation, and injury in the lung. Our team within the Center for CF and Airways Disease Research considers the airway as an ecosystem, comprised of many different cell types plus a variety of pathogens, all of which play important roles in pulmonary function. We believe that it is only by studying this ecosystem in situ, relying on samples of airway fluid and cells from CF patients themselves, that we will ever fully understand this disease and identify the means to control it. Many collaborators at Emory, Georgia Tech, and Children's Healthcare of Atlanta contribute to this team, led by N McCarty as Director of the Center. This work also allows us to be involved in the development of novel therapies and devices for CF patients. This multifaceted approach keeps our efforts focused upon issues relevant to this disease and its treatment. 2) Impact of mutations in the CFTR gene on the interactions between airway epithelial cells and transmigrating neutrophils, which are the source of damage leading to bronchiectasis and death in people with CF. 3) The impact of systemic hyperglycemia as found in CF-related diabetes - the most common comorbidity in CF - on the management of airway glucose and the regulation of innate immunity in the airway. New work from our lab his identified an impact of mutant CFTR on insulin-dependent glucose transport, the first evidence of this sort. We are now determining the mechanism underlying this defect in the CF airway. 4) The biophysics, regulation, and pharmacology of the CFTR chloride channel. CFTR forms a low-conductance Cl channel which is controlled in a novel way. A major effort in this lab involves performing structure/function experiments to: (a) determine how CFTR evolved channel function from its molecular ancestors, all of which function as transporters; (b) determine how mutant CFTR impacts the innate immune system in the airway; (c) determine how lipids and lipid-mediated signaling alter function and pharmacology; and (d) identify novel therapeutic small molecules that repair the defects in mutated CFTR channels as found in our patients. This has led to the identification of several novel potentiators of mutant CFTR function.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	McCarty	Nael	Cell Biology Electrophysiology Membrane Biology Molecular Biology Pediatrics Physiology Respiratory Disorders	Full Member
Gregory B. Melikian, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics gmeliki@emory.edu \| Faculty Profile \| Lab Website Professor, Division of Infectious Disease, Department of Pediatrics, School of Medicine Molecular mechanisms of enveloped virus entry into cells.	Molecular mechanisms of enveloped virus entry into cells.Enveloped viruses initiate infection by merging their membrane with the target cell membrane. Our research is aimed at understanding the molecular mechanisms of enveloped virus entry into cells, including HIV, influenza virus, Ebola virus and others. Our main experimental approaches are functional assays with the primary focus on advanced imaging techniques, such as real-time single virus tracking. Virus co-labeling with fluorescent membrane, content and/or core markers enables the detection of lipid mixing (hemifusion) and viral content and core release (fusion pore formation) during viral entry. Novel labeling and imaging strategies enable the visualization of transport, fusion and uncoating of HIV cores en route to the nucleus. We are also interested in delineating the mechanisms of antiviral activity of host restriction factors that target the viral fusion, such as SERINC5 and IFITM3, and in identifying novel small molecule inhibitors of virus fusion.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Melikian	Gregory	Biophysics Cell Biology Imaging Membrane Biology Virology	Full Member
Lefteris Michailidis, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology emicha7@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine Curriculum Committee, BCDB Seminars Committee, MMG Our research program focuses on understanding the interaction between viruses and the host using a set of biochemical, cell-based and in vivo methods. In particular, we are interested in hepatitis B virus (HBV) and the development of eradication strategies that involve state-of-the-art primary hepatocyte systems and humanized liver chimeric mice. These systems expand the scope of our research beyond viral hepatitis to other liver-related diseases and fields including fatty liver disease and liver immunometabolism. In addition, we have a strong interest in antiviral mechanisms carried out by interferon-stimulated genes and other host proteins but also small molecule inhibitors in regards to mechanisms of action and resistance. In this direction our main focus has been HIV, HBV, and SARS-CoV-2. To accomplish these goals we use medium and high-throughput genetic screens (gene overexpression and CRISPR knockout) across different cell systems and in some cases in humanized mice.	Our research program focuses on understanding the interaction between viruses and the host using a set of biochemical, cell-based and in vivo methods. In particular, we are interested in hepatitis B virus (HBV) and the development of eradication strategies that involve state-of-the-art primary hepatocyte systems and humanized liver chimeric mice. These systems expand the scope of our research beyond viral hepatitis to other liver-related diseases and fields including fatty liver disease and liver immunometabolism. In addition, we have a strong interest in antiviral mechanisms carried out by interferon-stimulated genes and other host proteins but also small molecule inhibitors in regards to mechanisms of action and resistance. In this direction our main focus has been HIV, HBV, and SARS-CoV-2. To accomplish these goals we use medium and high-throughput genetic screens (gene overexpression and CRISPR knockout) across different cell systems and in some cases in humanized mice. The Michailidis laboratory is interested in understanding the molecular and cellular mechanisms that drive virus-host interactions, how viruses lead to human diseases, and the strategies we can develop to control them. In particular, we are interested in hepatitis B virus (HBV), its target cells, the hepatocytes, and the crosstalk between innate immunity and metabolism in the liver. With physiologically relevant in vitro and in vivo systems and state-of-the-art technologies ranging from single-cell transcriptomics to whole-genome CRISPR editing, there is a great potential to uncover the mechanisms that govern chronic hepatitis B and ultimately cure this deadly disease. Furthermore, using similar strategies we want to extend our knowledge across multidisciplinary fields, including other hepatotropic infections, liver-related diseases and liver functions. The innate immune response, driven by interferon (IFN), protects cells against invading viral pathogens. The workhorses that mediate this defense are the products of hundreds of IFN-stimulated genes (ISGs). Our previous work with HBV, Zika virus and multiple coronaviruses, including SARS-CoV-2, has revealed a set of ISGs that have a drastic effect on viral replication. Our objective is to characterize the mechanism of action of these ISGs and inform the development of new antiviral strategies. Towards this goal we employ a diverse set of molecular, cellular, and biochemical tools.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Michailidis	Lefteris	Cell Biology Liver Diseases Virology	Full Member
Ken Moberg, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology kmoberg@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Cell Biology, School of Medicine 1) Control of cell proliferation and survival in developing Drosophila epithelia by the Hippo, Ecdysone and dFbw7 pathways 2) Neurodevelopmental roles of a conserved Drosophila RNA binding protein whose human equivalent is lost in heritable form of intellectual disability.	1) Control of cell proliferation and survival in developing Drosophila epithelia by the Hippo, Ecdysone and dFbw7 pathways 2) Neurodevelopmental roles of a conserved Drosophila RNA binding protein whose human equivalent is lost in heritable form of intellectual disability.My lab uses the fruit fly Drosophila melanogaster to model fundamental aspects of metazoan development and disease, with a main focus on (i) cancer cell biology and an (ii) development of the invertebrate central nervous system. Cancer cell biology This portion of the lab studies regulatory inputs into the Hippo pathway, which was discovered in Drosophila but plays critical roles in developmental, pathogenic (e.g. cancerous), and regenerative growth in vertebrates. One current project centers on a physical complex between the Hippo transcription factor Yki/Yap1 and the Taiman/AIB1 protein, which functions as a transcriptional coactivator for steroid hormone receptors in flies (e.g. the ecdysone receptor) and humans (e.g. the estrogen and androgen receptors). A second project is focused on a role for Taiman in regenerative growth after wounding, and a third project is focused on an anti-growth feedback loop that inhibits Yki/Yap in cells lacking the tumor suppressor protein dFbw7. Neurodevelopment This portion of the lab is focused on neurological roles of the conserved poly(A) RNA binding protein dNab2/ZC3H14, which is mutated in a heritable form of autosomal recessive intellectual disability in humans. One current project focuses on a physical complex between dNab2 and the Fragile-X mental retardation protein that links dNab2 to translational repression of key neuronal mRNAs, such as CamKII. A second project is pursing an exciting link between dNab2 and post-transcriptional N6-methylation of RNA (m6A), and a third project is aimed at identifying mRNAs that are bound by dNab2 and encode factors that control axon guidance via the planar cell polarity pathway.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Moberg	Ken	Biology, Developmental Cancer Biology Cell Biology Genetics, Molecular Neuroscience	Full Member
Chris Neufeldt, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics c.neufeldt@emory.edu \| Faculty Profile Assistant Professor, Department of Microbiology and Immunology, School of Medicine With a limited number of proteins, viruses can cause significant reorganization within cells to create environments conducive to replication. By studying the mechanisms through which viruses manipulate host cells, we can both determine how viral processes can be attenuated and use this manipulation as a tool to investigate fundamental cellular processes. Building on previous work with positive-strand RNA viruses, which comprise a large portion of human infections and are among the strongest candidates for emerging diseases, our research program focuses on novel discoveries at the virus-host interface, with the overarching goal of understanding how virus infection modulates cellular systems to facilitate infection. With a specific focus on arborviruses and coronavirus, we are pursuing the investigation of conserved and divergent mechanisms of cellular membrane reorganization. Our program is aimed at providing insight into how viruses engage and manipulate ER membrane systems, as well as uncovering novel cell biology involving ER membranes.	With a limited number of proteins, viruses can cause significant reorganization within cells to create environments conducive to replication. By studying the mechanisms through which viruses manipulate host cells, we can both determine how viral processes can be attenuated and use this manipulation as a tool to investigate fundamental cellular processes. Building on previous work with positive-strand RNA viruses, which comprise a large portion of human infections and are among the strongest candidates for emerging diseases, our research program focuses on novel discoveries at the virus-host interface, with the overarching goal of understanding how virus infection modulates cellular systems to facilitate infection. With a specific focus on arborviruses and coronavirus, we are pursuing the investigation of conserved and divergent mechanisms of cellular membrane reorganization. Our program is aimed at providing insight into how viruses engage and manipulate ER membrane systems, as well as uncovering novel cell biology involving ER membranes.Our research program specifically focuses on determining mechanisms by which viruses utilize ER membrane-shaping proteins and cellular vesicle trafficking pathways, to better understand virus infection and characterize fundamental cellular functions of the ER and ER-associated proteins. All studied positive-strand RNA viruses replicate in host membranes with the majority requiring the ER for formation of their replication organelles. Although the morphology of virus-induced membrane rearrangements has been characterized, the mechanisms underlying ER membrane alterations are still poorly understood. The ER is the largest cellular organelle that extends throughout the cytoplasm and is involved in connecting numerous cellular processes. Mapping connections between the ER and other cellular organelles or processes, as well as understating the functional significance of these connections, is vital for our basic understanding of the cell and many diseases. Studying virus-induced manipulation of the ER represents a unique opportunity to understand both virology and host processes that are linked to a variety of genetic diseases or disorders. Additionally, uncovering conserved host pathways utilized by different viruses has a broad therapeutic potential. To address these questions, our research uses a diverse set of tools and methodologies ranging from fundamental biochemical analysis to advanced microscopy and gene manipulation techniques, all aimed at determining molecular processes and mechanisms functioning at the virus-host interface. We have three core areas of research encompassing a wide range of questions. 1. Functional characterization of ATLs in virus infection: a mechanistic and comparative analysis. We have recently demonstrated a central role for Atlatsin proteins in the flavivirus infection cycle. Though we have done the preliminary analysis of ATL function in flavivirus infection, there are still many questions regarding the specific role of ATLs in flavivirus replication. The first goal of this project is to investigate the role of ATLs in other positive strand RNV virus infection, such as Coronaviruses, HCV, Poliovirus, or Chikungunya virus. The second is to acquire a more mechanistic understanding of Atlastin protein in flavivirus infection. Finally, building on the mutational analysis from our recent publication, we would explore the possibility of developing inhibitors that could be used to selectively modulate Atlastin functions and manipulate different aspects of virus infections. With this work, we aim to provide mechanistic insight into ATL function, determine how these functions utilized by different viruses, and investigate the therapeutic potential of ATLs for both virus infection and for genetic diseases linked to ATLs. 2. Characterization of ER proteins associated with positive-strand RNA virus infection. Our initial analysis using proteomics and RNAi based screening identified several other proteins linked to ATLs that are also involved in DV infection. The goal of this project is to further characterize these candidates by evaluating function or location changes caused by virus infection. The resulting information would be used to understand how these factors generally coordinate ER structure and how alterations in the context of virus infection are used to reshape host cellular membranes. These studies rely on super-resolution light microscopy and specialized EM techniques for structural analysis as well as proteomics and RNAi screening for functional analysis. Through this analysis we aim to define the protein components and molecular structures required for virus-mediated membrane alterations as well as further defining how the ER network organizes cellular and viral processes. 3. Connecting the ER to vesicle trafficking and innate immune signaling. In our recent study, we describe a link between ATL3 and retrograde trafficking, specifically in internalization of molecules at the plasma membrane. This observation has a broad impact for many cellular transport pathways including immune signaling, which often relies on receptor uptake and endosomal recycling pathway. Additionally, we have recently connected cGAS-STING activation to the initiation of pro-inflammatory responses induced by SARS-CoV-2 infection. This activation leads to a selective NF-kB response that could initiate the hyper-inflammation observed in severe COVID-19 cases. Moreover, we found that STING translocation from the ER to the Golgi may be inhibited by the virus, leading to a selective pro-inflammatory response. The goal of this project is to characterize the role of the ER factors in innate immune activation and to determine how virus infection manipulates these cellular responses leading to pathogenesis. With these studies, we aim to elucidate details pertaining to how the ER is involved in connecting and regulating other cellular pathways, such as membrane lipid dynamics, endosomal trafficking and immune signaling, and how these functions can be utilized or manipulated by pathogens. Through a better understating of these fundamental cellular and viral process we can progress towards the development of effective antiviral therapies.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Neufeldt	Chris	Cell Biology	Full Member
Shoichiro Ono, PhD Full Member - Biochemistry, Cell and Developmental Biology sono@emory.edu \| Faculty Profile Associate Professor, Department of Pathology and Laboratory Medicine, School of Medicine Associate Professor, Department of Cell Biology, School of Medicine Member, Winship Cancer Institute Regulation of cytoskeletal dynamics.	Regulation of cytoskeletal dynamics.My primary research interest is the mechanisms that regulate dynamic rearrangement of the actin cytoskeleton during various cellular events including development, cell movement, cytokinesis, and human diseases. We have been studying this problem using the nematode Caenorhabditis elegans as a model system. C. elegans has been used to study many aspects of development, because of its relative simplicity in the body patterning, and application of genetics, molecular biology, biochemistry, and cell biology. We are especially interested in the functions of the actin depolymerizing factor (ADF)/cofilin family of actin-binding proteins, which are required for enhancement of actin filament dynamics. We found that two ADF/cofilin proteins that are generated from the unc-60 gene have different actin-regulating activities. Mutation and expression analyses demonstrated that one of the two ADF/cofilin isoforms (UNC-60B) was specifically required for organized assembly of actin filaments in muscle. ADF/cofilin promotes depolymerization and severing of actin filaments, but tropomyosin inhibits this effect by stabilizing filaments. The other ADF/cofilin isoform (UNC-60A) is highly expressed in early embryos and regulates cytokinesis and embryonic patterning. In addition, we found that actin-interacting protein 1 (AIP1) is a new regulator of muscle actin filaments. AIP1 (UNC-78) specifically interacts with ADF/cofilin-bound actin filaments and enhances filament depolymerization. We also found that the gene product of sup-12 (an RBM24 homolog) regulates alternative splicing of the unc-60 gene and is required for generation of the unc-60B mRNA. We are currently studying functions of these proteins and other regulators of actin dynamics in several developmental aspects in C. elegans.	BCDBBiochemistry, Cell and Developmental Biology - Full Member	Ono	Shoichiro	Cell Biology Genetics, Molecular Muscular Disorders	Full Member
Eric Ortlund, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology eortlun@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Biochemistry, School of Medicine Director of Emory Integrated Metabolomics and Lipidomics Core Facility (EIMLC), Department of Biochemistry, School of Medicine Structural biology (X-ray and CryoEM), drug design, and molecular evolution of receptors, transporters and other drug targets. Deep mutational scanning to characterize protein-protein interfaces.	Structural biology (X-ray and CryoEM), drug design, and molecular evolution of receptors, transporters and other drug targets. Deep mutational scanning to characterize protein-protein interfaces.Our mission is to make fundamental discoveries relating to hormone signaling, transcriptional control and host-pathogen interactions. We leverage these discoveries to pursue drug design as treatments for viral infections and chronic inflammatory diseases. We use a range of sophisticated biological techniques including cryo-electron microscopy, x-ray crystallography, mass spectrometry, deep mutational scanning and in silico simulations. Our primary research interests include lipid-mediated signaling and transport, development of LRH-1 modulators to treat metabolic disease, characterization of anti-inflammatory steroids and molecular evolution. We have ongoing drug development efforts in these areas. With the outbreak of SARS-CoV-2, we were well-placed to redirect our expertise to investigate detection and neutralizing antibodies using Cryo-EM, and to predict antibody escape using deep mutational scanning (DMS). Working closely with the RADx initiative, our methods have proven useful to multiple companies seeking FDA approval for their novel COVID-19 diagnostic methods. Currently we are expanding our technology to tackle other arising infectious diseases of concern and to design new therapeutic proteins.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Ortlund	Eric	Biochemistry, Lipids Biochemistry, Nucleic Acids Biochemistry, Proteins Diabetes Digestive Disease & Disorders Drug Design Endocrinology Hormones Metabolism	Full Member
Anupam Patgiri, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology anupam.patgiri@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Pharmacology and Chemical Biology, School of Medicine Member, Discovery and Developmental Therapeutics Research Program, Winship Cancer Institute My lab studies the pathophysiology of mitochondrial and metabolic diseases to develop novel therapies. We use LCMS-based metabolomics, chemical probe development, therapeutic protein engineering, animal models, and molecular and cell biology techniques.	My lab studies the pathophysiology of mitochondrial and metabolic diseases to develop novel therapies. We use LCMS-based metabolomics, chemical probe development, therapeutic protein engineering, animal models, and molecular and cell biology techniques.We study how defective mitochondria contribute to common and rare diseases to develop potential therapy. Our lab uses a multidisciplinary approach that includes therapeutic protein engineering, LCMS-based metabolomics, small molecular probe development, and AAV-based gene therapy in animal models. Three of our ongoing are: Project 1. Pre-clinical testing of an engineered enzyme therapy for mitochondrial electron transport dysfunction (Patgiri et al. Nat Biotech, 2020), Project 2. Development of chemical strategies to restore mitochondrial homeostasis in disease, and Project 3. Novel strategies to modulate metabolism in the tumor-immune microenvironment to boost the cytotoxicity of T cells and tumor-associated macrophages. For more information, please visit https://patgirilab.org/	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Patgiri	Anupam	Biochemistry, Proteins Cell Metabolism Drug Design Enzymology Immunotherapy Metabolic Diseases Metabolism Neurodegenerative Disease	Full Member
Maureen A. Powers, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Cancer Biology mpowers@emory.edu \| Faculty Profile Associate Professor, Department of Cell Biology, School of Medicine Structure and function of the nuclear pore.	Structure and function of the nuclear pore.The research interests of my laboratory center on the function of the Nuclear Pore Complex (NPC) and its component proteins, the nucleoporins (Nups). The NPC is responsible for movement of proteins and RNAs between nucleus and the cytoplasm, a fundamental activity of the eukaryotic cell. This process is mediated by the NPC along with an extensive series of cargo receptors, the alpha and beta karyopherin families. Our long term goal is to understand how NPC function is regulated and tightly integrated with other cellular processes including nuclear organization, cell division and transcription. We have largely, but not exclusively, focused on the unique nucleoporin, Nup98, which plays key roles both on and off the NPC. We showed that Nup98 moves dynamically between the NPC and the nucleoplasm and its mobility is linked to ongoing transcription. At the NPC, Nup98 is located at the center of the structure and plays roles in trafficking and, we propose, in the exclusion of non-nuclear proteins from the nucleus – the permeability barrier of the pore. More recently, Nup98 was shown to regulate transcription of a subset of genes in Drosophila. We are particularly interested in the mechanism of such regulation in vertebrate cells and the interaction of Nup98 with chromatin. We expect to extend this in the future to the interaction between other nucleoporins and chromatin. The NPC is remarkably integrated with other key nuclear functions, in particular with mitosis. We have shown that Nup98 regulates microtubule dynamics within the mitotic spindle through an affect on the microtubule depolymerizing kinesin, MCAK. We have also shown that this influence is regulated in part by mitotic phosphorylation of Nup98. An additional interest is the mechanism by which chromosomal translocations involving Nup98 lead to Acute Myelogenous Leukemia. In these translocations, the N-terminal nucleoporin repeat domain of Nup98 is fused to the C-terminus of one of a variety of nuclear proteins. This fusion partner is most often a member of the homeobox transcription factor family. The fusion proteins lead to aberrant transcriptional activation of genes, particularly HoxA9 and Meis, and this in turn contributes to leukemogenesis. We have shown that the leukemogeneic proteins have a novel localization within the nucleus during interphase and are targeted to kinetochores during mitosis. Additionally, the leukemogenic fusions can interact with and relocalize the endogenous Nup98. These activities may be additional factors in the ability of the fusion proteins to induce cancer. Our work employs a variety of complementary approaches: biochemical assays, in vitro reconstitution of mitotic and interphase nuclear function using Xenopus egg extract, and sophisticated imaging analyses in both fixed and living cells. Through the combination of these approaches, we have made important contributions to novel facets of NPC function including nucleoporin dynamics, links to transcription, and regulation of mitosis. As increasing connections between nucleoporin mutations and disease, including leukemias, cardiac disease, and neurodegenerative diseases, continue to emerge, it is essential to understand how alterations in nucleoporins can impact nuclear transport and other functions to which nucleoporins make important contributions.	BCDBBiochemistry, Cell and Developmental Biology - Full Member CBCancer Biology - Full Member	Powers	Maureen	Cell Biology	Full Member
Daniel Reines, PhD Emeritus Member - Biochemistry, Cell and Developmental Biology Emeritus Member - Genetics and Molecular Biology dreines@emory.edu \| Faculty Profile Professor Emeritus, Department of Biochemistry, School of Medicine Biochemistry and molecular genetics of RNA polymerase II transcription and RNA-binding proteins.	Biochemistry and molecular genetics of RNA polymerase II transcription and RNA-binding proteins.Current research is focusing on the biochemistry and molecular biology of gene expression. The Reines lab is using yeast to study the fundamental mechanisms of transcription elongation and termination. We are focusing on the transcription termination machinery composed of RNA-binding proteins Nab, Nrd1, and Sen1 (NNS). We have been studying the interesting assembly properties of the Nab3 protein (Nrd1 shows this as well) which contains a polyglutamine-rich region that enables the protein to polymerize. The domain is essential and drives the protein to a specialized subnuclear compartment under specific conditions. Similar regions of low sequence complexity are found in many RNA binding proteins and play a role in neuropathologies in which they aggregate. This feature appears to be important for the protein's function as a termination factor and its switch to a protein that marks RNAs for degradation. The behavior of the NNS complex, and its formation are linked to nutrient availabiilty, cell signaling pathways, and the entry of dividing cells into the cell cycle. We are examining the metabolic control of the complex and the resulting change in the cell's transcriptome that guides cell proliferation.	BCDBBiochemistry, Cell and Developmental Biology - Emeritus Member GMBGenetics and Molecular Biology - Emeritus Member	Reines	Daniel	Biochemistry, Proteins Genetics, Molecular Molecular Biology	Emeritus Member
Blaine Roberts, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Neuroscience blaine.roberts@emory.edu \| Faculty Profile Associate Professor, Department of Biochemistry, School of Medicine Scientific Director, Molecular Interactions, Emory Glycomics and Molecular Interactions Core, School of Medicine We work to understand the role of proteins, and metals in neurodegenerative diseases and apply this to the development of biomarkers and therapies.	We work to understand the role of proteins, and metals in neurodegenerative diseases and apply this to the development of biomarkers and therapies.Nearly everything we study in biology and disease is the product of protein function. Whether it is normal enzymatic function or aberrant functions, proteins have a central role in the manifestation of the pathologies and phenotypes. The goal of my research program is to apply cutting-edge analytical technology and mass spectrometry to assist in the early diagnosis and treatment of neurodegenerative diseases. Specifically, we work to understand the mechanism of action for the toxic effects of neurological proteins (e.g. Amyloid-beta, alpha-synuclein, Cu, Zn-superoxide dismutase) and to translate this information into clinical outcomes. To do this we have developed and applied advanced analytical mass spectrometry tools to discover and measure metalloproteins (metalloproteomics). We have applied these tools to amyotrophic lateral sclerosis, and this has contributed to a first-in-class clinical trial for ALS and Parkinson's disease (NCT02870634 & NCT03204929). Our ongoing research aims to investigate; (1) the role of metalloproteins in biology (2) how post-translation modifications of proteins (e.g. dityrosine, nitrotyrosine, metal cofactors) contribute to protein function (3) the natural history of Ab and APOE in Alzheimer's disease (4) blood-based diagnostics for neurodegenerative diseases. As detailed below a major focus in my lab is to utilize the advanced mass spectrometry technologies to discover, validate and qualify biological molecules (e.g. proteins, metals) as disease biomarkers. Our Alzheimer research aims to answer some basic questions about the role of amyloid beta in the disease. Our work, and others, demonstrate that the neurotoxic peptide amyloid beta accumulates in the brain for 20 years before someone develops clinical symptoms. We have shown that the reason for the accumulation of the peptide is due to a reduction in the clearance of the peptide from the brain. We reasoned that a post translational modification of the peptide could be the reason for amyloid accumulation. To investigate this, we applied ion mobility mass spectrometry to compare the amyloid beta peptides in AD brain to controls. Ion mobility mass spectrometry measures the shape of a molecule in addition to the standard mass spectrometry information (e.g. m/z, peptide sequence). We discovered that over 60% of the amyloid beta peptide in AD brain was isomerized making it the predominate form of the peptide in AD brain. The isomerization of amyloid beta reults in a peptide with a different shape and handedness this has implications for ability of proteases to clear the peptide and for antibody therapies that target amyloid beta to recognize the peptide. Currently, we aim to determine the biochemical consequences of isomerization in AD brain. Neurodegenerative disease has a long history that implicates a role of copper, iron and zinc in the pathophysiology of Alzheimer's, Parkinson's, and amyotrophic lateral sclerosis. However, most of the investigations have relied on measurement of the total amount of metal in disease tissue vs control tissues. Although informative, it does not yield mechanistic detail on the pathways or proteins that directly use the metals as cofactors. We have developed proteomic techniques that allow the direct measurement of the proteins and metal cofactor. These techniques are being used to unlock the mechanistic link between changes in bulk levels of trace elements (e.g. Fe, Cu, Zn) to specific proteins and metabolic pathways. We are one of the few laboratories in the world dedicated to the measurement and characterization of metalloproteins in neurodegenerative disease. In particular we are excited to understand the role of metalloproteins in biology and disease. The results from are investigations in metalloproteins and mechanism of neurotoxic proteins in neurodegeneration are often useful for detection and diagnosis of disease. We use a range of bioanalytical techniques from the next generation ELISA systems (e.g. Quanterix SIMOA) and quantitative mass spectrometry to translate our findings into clinically relevant biomarkers. Our goal is to improve the outcomes for those suffering from neurodegenerative diseases. Two recent publications selected from 55 peer reviewed articles published since 2015: 1. McAllum, E.J., Hare, D.J., Voltakis, I., McLean, C.A., Finkelstein, D.I., Roberts, B.R. Regional iron distribution and ferroprotein profiles in healthy human brain. Progress in Neurobiology (2020) Mar;186:101744 2. Mukherjee, S., Fang, M., Kok, W.M., Kapp, E.A., Thombare, V., Huguet, R., Hutton, C.A., Reid, G., Roberts, B.R. Establishing Signature Fragments for Identification and Sequencing of Dityrosine Cross-linked Peptides using Ultraviolet Photodissociation Mass Spectrometry. Analytical Chemistry (2019) 91, 19, 12129-12133	BCDBBiochemistry, Cell and Developmental Biology - Full Member NSNeuroscience - Full Member	Roberts	Blaine		Full Member
Stefan Sarafianos, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology ssarafi@emory.edu \| Faculty Profile \| Lab Website Professor, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine Drug discovery, drug resistance, replication mechanisms in HIV, HBV, SARS-CoV-2, MPox, Nipah virus, Ebola and emerging pathogens using virology, structural biology, microscopy, biochemistry, and high-throughput technologies.	Drug discovery, drug resistance, replication mechanisms in HIV, HBV, SARS-CoV-2, MPox, Nipah virus, Ebola and emerging pathogens using virology, structural biology, microscopy, biochemistry, and high-throughput technologies.Our research aims to unravel fundamental mechanisms of drug action, drug resistance, and other aspects of the life cycles of viruses that cause severe diseases. In turn, we apply this knowledge in the design of novel antiviral approaches toward the development of therapeutics. Our drug discovery efforts leverage collaborations with world leading laboratories and use of state-of-the-art multidisciplinary tools, including virological approaches, microscopy methods (super-resolution, single-molecule, and confocal approaches), structural (crystallographic and now cryo-electron microscopy), biochemical (pre-steady state kinetics), biophysical (thermophoresis, surface plasmon resonance), high-throughput and high-content screening as well as structure-based drug design (molecular modeling). Our efforts have led to the development of EFdA, a highly promising long-acting antiviral, currently in Phase III clinical trials for the treatment of HIV infection. Additional funded research interests include SARS-CoV-2, Hepatitis B Virus (HBV), MonkeyPox Virus (MPOXV, Nipah Virus (NiV). Other viruses studied include Ebola Virus, Hepatitis C Virus (HCV), Zika Virus, Foot-and-Mouth Disease Virus (FMDV). For detailed description of currently funded research, please follow link: https://projectreporter.nih.gov/Reporter_Viewsh.cfm?sl=12EECC0B4C8ECFDE7598B8961CAA4A01A2FFCEB861BF Some projects (with selected publications) are also listed below: -Development of EFdA as a weekly oral dosing and once-yearly slow-release dosing anti-HIV drug (PNAS 113:9274-9, 2016; J Biol Chem. 289: 24533-48, 2014) (with Dr. Mitsuya, NIH, Kumamoto Univ). Studies continue on the mechanism of EFdA activation and resistance in clinical settings (R01 AI076119). -Virological, biochemical, and structural studies of HIV capsid with host factors and capsid-targeting antivirals (Science 349: 99-103, 2015) (with Z. Wang, Univ of Minnesota) (R01 AI120860). -Molecular mechanisms of HIV Drug resistance (Antimicrob Agents Chemother. 61, 2017; Viruses. 6 (9), 3535-3562, 2015) (with U Neogi and A Sonnerborg, Karolinska Institutet) (R01 GM118012). -Novel antiviral discovery and drug resistance studies for SARS-CoV-2. Using our recently developed replicon systems, we are screening nucleoside analog compounds for the discovery of anti-SARS-CoV-2 hits, which upon hit-to-lead optimization can become COVID-19 drug candidates (R01 AI167356). To explore the mechanisms of resistance to the antiviral component of Paxlovid, nirmaltrevir (NIR), we have designed mutations in our replicons to impair NIR binding (bioRxiv. 2023 Jan 3:2022.12.31.522389). -Novel antivirals for Mpox Virus (MPXV). Through our collaboration with the lab of Dr. Haian Fu, we are performing high throughput screening (HTS) and high content screening (HCS) using Modified Vaccinia Ankara virus (MVA) as an initial screening system, and by validating identified hits in an MPXV cell culture system, thus leading into downstream lead candidate development (Rapid Synergy: Monkeypox, Emory SoM/WHSC I3 Award). - Novel antivirals for Nipah Virus (NiV). We have been using our first-generation Nipah mini-genome replication system to screen a unique nucleoside analog library that our collaborators in the Schinazi lab have been building over the course of decades. By leveraging minigenome (MG) replicon-based approaches, we aim to identify compounds that demonstrate potent antiviral activity against NiV, which can serve as the basis for the development of novel antiviral therapies. -Interactions of HIV with host factors-APOBEC3-HIV RT interactions. To block reverse transcription, cells express APOBEC3 (A3) family of restriction factors that suppress infection. Co-investigator Malim (King's college) has shown that HIV evades A3-mediated inhibition through the action of its Vif protein. While it has been established that A3s block HIV primarily through their cytidine deaminase activity, which causes hypermutation and genetic inactivation, they also inhibit RT itself (Nature Microbiol. Nov 20. 2017), through a mechanism that is poorly understood. As the co-Director of the HIV Interactions in Viral Evolution Center (HIVE) (http://hive.scripps.edu/index.html), a Center for AIDS molecular interactions and evolution studies, I am leading efforts to characterize the RT-A3 interactions (U54 GM103368). -HIV eradication studies through novel techniques for visualization of viral RNA, DNA and protein. We recently published a novel microscopy-based method (MICDDRP or Multiplex Immunofluorescent Cell-based Detection of DNA, RNA and Protein) (Nature Commun. 8:1882. 2017) that should facilitate investigations on fundamental biology of HIV or other viruses, including the specific role of host factors on integration, transcription, and latency, and also provide critical advances in elucidating mechanisms of antiviral inhibition at the level of single cell, single viral genome, and single integration site. -Novel antivirals targeting the RNase H activity of HIV (PLoS Pathogens 9: e1003125, 2013; J Med Chem. 60: 5045-5056, 2017) (with Z. Wang, and R. Ishima, Univ of Pittsburgh) (R01 AI100890 NCE). -Novel antivirals for treatment of HBV infection. We are targeting HBV through the development and characterization of antivirals that block HBV by targeting its capsid, reverse transcriptase, or RNase H active sites (PLoS Pathog. 2013 Jan;9(1):e1003125; Antimicrob Agents Chemother. 61, e00245-17, 2017; Hepatology 62:1024-36, 2015; ). We are also developing cutting-edge microscopy-based and molecular biology based approaches to study HBV biology (R01 AI121315). References 1: Puray-Chavez M, Tedbury PR, Huber AD, Ukah OB, Yapo V, Liu D, Ji J, Wolf JJ, Engelman AN, Sarafianos SG. Multiplex single-cell visualization of nucleic acids and protein during HIV infection. Nature Commun. 2017 Dec 1;8(1):1882. doi: 10.1038/s41467-017-01693-z. PubMed PMID: 29192235; PubMed Central PMCID: PMC5709414. 2: Gres AT, Kirby KA, KewalRamani VN, Tanner JJ, Pornillos O, Sarafianos SG. STRUCTURAL VIROLOGY. X-ray crystal structures of native HIV-1 capsid protein reveal conformational variability. Science. 2015 Jul 3;349(6243):99-103. doi: 10.1126/science.aaa5936. Epub 2015 Jun 4. PubMed PMID: 26044298; PubMed Central PMCID: PMC4584149. 3: Salie ZL, Kirby KA, Michailidis E, Marchand B, Singh K, Rohan LC, Kodama EN, Mitsuya H, Parniak MA, Sarafianos SG. Structural basis of HIV inhibition by translocation-defective RT inhibitor 4'-ethynyl-2-fluoro-2'-deoxyadenosine (EFdA). Proc Natl Acad Sci U S A. 2016 Aug 16;113(33):9274-9. doi: 10.1073/pnas.1605223113. Epub 2016 Aug 3. PubMed PMID: 27489345; PubMed Central PMCID: PMC4995989. 4: Lan S, Neilsen G, Slack RL, Cantara WA, Castaner AE, Lorson ZC, Lulkin N, Zhang H, Lee J, Cilento ME, Tedbury PR, Sarafianos SG. Nirmatrelvir Resistance in SARS-CoV-2 Omicron_BA.1 and WA1 Replicons and Escape Strategies. bioRxiv [Preprint]. 2023 Jan 3:2022.12.31.522389. doi: 10.1101/2022.12.31.522389. PMID: 36656782; PMCID: PMC9844013.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Sarafianos	Stefan	AIDS / HIV Biochemistry, Nucleic Acids Drug Design Drug Resistance Virology	Full Member
Lindsey Seldin, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Genetics and Molecular Biology lseldin@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Cell Biology, School of Medicine Assistant Professor, Department of Dermatology, School of Medicine My lab studies molecular mechanisms that modulate epithelial stem cell fate during development, homeostasis, and tumorigenesis in the mammalian epidermis and its sub-appendages.	My lab studies molecular mechanisms that modulate epithelial stem cell fate during development, homeostasis, and tumorigenesis in the mammalian epidermis and its sub-appendages.Epithelial tissues, composed of adherent polarized cell sheets, serve a critical barrier function throughout the body. Such tissues, which include the skin, intestine, and mammary gland, harbor stem cells that can proliferate extensively as well as generate diverse cell types. These features, which are essential to maintain tissue architectural and functional integrity, can also promote tumor formation. Epithelia do not exist in a vacuum. They are surrounded by a complex microenvironment consisting of many distinct cell populations that impact stem cell behavior. The Seldin Lab uses the mouse epidermis and its subappendages (which include the hair follicle and mammary gland) to understand how extrinsic signals dictate epithelial stem cell function in developmental, damage and disease contexts. The themes of inquiry we focus on include: 1) Tumor Microenvironment - How do diverse cell types impact epithelial stem cell behavior during cancer development?; 2) Inflammasome Biology - What stimuli promote inflammasome activation in diverse cell types, and how may this link to disease?; 3) Stem Cell Fate - What intrinsic/extrinsic signals dictate stem cell fate decisions, and what factors cause stem cell fate mis- specification?; 4) Damage Responses - How do epithelia respond to different types of damage?; 5) Lineage Dynamics - How do stem cell lineage trajectories evolve throughout development and tumorigenesis?; and, 6) Mechanistic Conservation - What stem cell regulatory mechanisms are conserved among distinct epithelial tissues? The primary project in our lab currently focuses on the role of the microenvironment in skin cancer development. Cutaneous skin carcinomas, which include basal and squamous cell carcinoma, are the most commonly occurring cancers in humans. Despite their prevalence, however, the mechanisms that promote the development of these cancers remain poorly understood. We are applying confocal imaging, organoid culture, cancer mouse models, primary human specimens, and RNA sequencing to understand how non-epithelial populations that reside within the skin dermis impact epidermal stem cell function to promote tumorigenesis. The overarching goal of our research is to exploit the microenvironment to develop more targeted regenerative and cancer therapies.	BCDBBiochemistry, Cell and Developmental Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Seldin	Lindsey	Biology, Cellular Biology, Developmental Biology, Molecular Breast Imaging Cancer / Carcinogenesis Cancer Biology Cell Biology Chemotherapy Chromatin Cloning of Genes Cytometry Dermatology Disease Disease Model Epigenetics Genetic Manipulation Genetics, Molecular Growth Factors Imaging Imaging Technology Immune System Disorders Immunology Inflammation Molecular Biology Oncology Organ & Tissue Transplantation Skin Diseases Tissue Culture Transgenic Technology Wound Healing	Full Member