Our 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
Mohamed Abdel Hakeem, PhD Full Member - Cancer Biology Full Member - Immunology and Molecular Pathogenesis m.hakeem@emory.edu \| Faculty Profile Assistant Professor, Department of Pathology and Laboratory Medicine, School of Medicine Affiliate Member, Emory Vaccine Center Faculty Member, Winship Cancer Institute Affiliate Scientist, Emory National Primate Research Center Dissecting modules and molecular programs of exhausted T cells (Tex). Characterizing impact of pre-existing exhaustion on subsequent immune responses.	Dissecting modules and molecular programs of exhausted T cells (Tex). Characterizing impact of pre-existing exhaustion on subsequent immune responses.Exhausted T cells (Tex) are a hallmark of cancer and chronic viral infection induced by persistent antigenic stimulation, and results in progressive loss of function and failure to clear tumors and viruses. Tex possess unique cellular, transcriptional, metabolic, and epigenetic profiles distinct from effector/memory T cells (Teff/Tmem) generated during acute infection. Therapeutically targeting Tex to reverse their dysfunction by immune checkpoint blockade (ICB) of inhibitory receptors such as PD1 revolutionized cancer immunotherapy. However, not all patients benefit from immunotherapy, and ICB does not have the same success rate in all indications. Even successful ICB is not durable in all cases, due to lack of modulation of the epigenetic landscape of Tex by immunotherapy. My previous work shows that even cure of chronic disease does not achieve significant modulation of the Tex epigenetic program in resting/recovering Tex. Thus, a deeper understanding of other molecular pathways underlying development and reversal of T cell exhaustion is needed. My research focuses on dissecting molecular mechanisms of development of the T cell exhaustion program, as well as potential mechanisms underlying recovery of Tex from the different aspects of exhaustion within the context of different cancer types and chronic viral infection. The main research directions of Hakeem Lab include; 1. Dissecting intrinsic modules and molecular programs of Tex, including specific exhaustion modules downstream individual inhibitory receptor interactions, as well as genetic validation of the roles of specific epigenetic loci identified in my previous work. 2. Studying the impact of extrinsic factors on shaping the T cell exhaustion program, including differential signaling by cytokine modulation, and impact of differential metabolites associated with dysbiosis of gut microbiota in chronic disease. 3. Defining the impact of a pre-existing exhaustion environment on subsequent acute and chronic immune responses. For these studies, we employ an integrated systems immunology approach dissecting the phenotypic, transcriptional, epigenetic, and proteomic profiles of T cells, as well as their impact on Tex functionality. We use therapeutic and molecular approaches for modulating different pathways to decipher the mechanisms underlying observed changes from our profiling data. Experimentally, we use both mouse models that enable deeper insights into mechanisms and allow manipulation of specific pathways, in addition to human samples that will be examined directly ex-vivo and in vitro to confirm the translational significance of our mouse findings. For animal studies, we use the well-established LCMV mouse model of viral infection, and several tumor models that reflect the potential biology of hot and cold tumors, such as B16 and MC38. We collaborate with all our colleagues at the Division of Pathology Advanced Translational Research Unit (PATRU) headed by Dr. Rafick Sekaly. We also collaborate with several research laboratories within the Emory Vaccine Center (EVC) headed by Dr. Rafi Ahmed, including Dr. Ahmed, Dr. Arash Grakoui, Dr. Haydn Kissick, and Dr. Tomas Garzon. As well as many research and clinical groups at Emory Winship Cancer Center and Emory University at large. For human studies, samples are acquired through collaborations with Dr. Arash Grakoui and Rafick-Pierre Sekaly at Emory, the Gastrointestinal Oncology Division at Emory Winship Cancer Center, and Dr. Naglaa Shoukry at the University of Montreal. These studies will enhance our understanding of immunological and molecular mechanisms of Tex development and recovery, and have the potential to identify novel therapeutic strategies for recovery and reinvigoration of more functional T cells. This will have major implications on the treatment of cancer and chronic viral infection.	CBCancer Biology - Full Member IMPImmunology and Molecular Pathogenesis - Full Member	Abdel Hakeem	Mohamed	Epigenetics Immunology Immunotherapy Infectious Diseases / Agents
Rafi Ahmed, PhD Full Member - Immunology and Molecular Pathogenesis Full Member - Microbiology and Molecular Genetics rahmed@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Microbiology and Immunology, School of Medicine Director, Vaccine Center, Emory National Primate Research Center Immunology and pathogenesis of chronic viral infections; immunological memory and vaccine development.	Immunology and pathogenesis of chronic viral infections; immunological memory and vaccine development.The mechanism of viral persistence remains a major unresolved problem and our goal is to understand how viruses evade or suppress the immune response and persist in vivo. We are using two natural models of viral persistence. 1) Infection of mice with lymphocytic choriomeningitis virus provides an excellent model for studying the interaction between the virus and the immune system of its natural host, and in defining conditions that lead to viral clearance or persistence. We are also using this system to address fundamental questions about immunological memory. 2) Infection of rabbits with Shope papillomavirus allows one to examine the immune response during various stages of neoplasia; during papilloma development, during spontaneous regression, and during progression to carcinoma. Our approach is to combine the disciplines of virology and immunology to attain a better understanding of virus vs. host interaction.	IMPImmunology and Molecular Pathogenesis - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Ahmed	Rafi	Immunology Infectious Diseases / Agents Microbiology Vaccine Development Virology
John D. Altman, PhD Full Member - Immunology and Molecular Pathogenesis jaltman@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Microbiology and Immunology, School of Medicine Affiliate Scientist, Emory National Primate Research Center Associate Professor, Vaccine Center, Emory National Primate Research Center T-cell immune responses to viral and bacterial infection; vaccine development; development of T-cell memory.	T-cell immune responses to viral and bacterial infection; vaccine development; development of T-cell memory.During my postdoctoral work with Dr. Mark Davis at Stanford University, I developed an important new technology to directly identify antigen-specific T cells by staining with tetrameric forms of soluble MHC/peptide complexes that have enhanced avidity for cells bearing specific T cell antigen receptors (TCR). Since coming to Emory, I have developed several research programs, all centered around use of this new technology to investigate many aspects of CD8+ T cell mediated immune responses to viral infections. These include basic studies in mouse models designed to answer questions about the factors contributing to the development of antigen-specific T cell repertoires, clinically relevant studies to assess immune function in HIV-infected individuals on potent anti-retroviral therapy, and applied studies to assess AIDS vaccine efficacy in a rhesus macaque model. Together with Rafi Ahmed, we are employing the LCMV model to investigate the basis of T cell memory and the development of the LCMV-specific T cell repertoires. In B6 mice, there are three immunodominant CD8+ T cell epitopes within LCMV, all restricted by H-2Db; we have successfully prepared and tested MHC tetramers for each of these epitopes. For the strongest epitope, the NP396 peptide, costaining with Vb antibodies shows that the primary response is diverse , with the participation of at least four distinct TCR Vb regions. We have also shown that there are both conserved and non-conserved responses, suggesting that we will have to follow repertoire development over time in individual mice. Studies of LCMV infection in BALB/c mice show very similar results. The Vb repertoire specific for the single immunodominant epitope NP118 is diverse and not completely conserved between individual mice. We also plan to investigate the lifespan of memory T cells in these non-transgenic mice, and we have developed methods to costain T cells with MHC tetramers and antibodies to detect incorporation of BrdU. The tetramers were originally developed to study CD8+ responses to HIV, and the initial reagents were based on two HIV-peptide complexes with HLA-A*0201. The most surprising finding of those studies was that the frequency of CD8+ T cells for a specific epitope was as high as 2% of all CD8+ T cells. We plan to follow up these studies to examine the effects of highly active antiretroviral therapy (HAART) on the frequency and function of HIV-specific CD8+ T cells. The questions that we will address concern the contribution of chronic antigen stimulation to maintaining the specific cells at high frequency and the effect it has on function. In many patients with high viral burdens, we have found that the HIV-specific CD8+ T cells die upon in vitro stimulation with peptide and IL2. We plan to investigate this further to determine if this antigen induced cell death is relevant in vivo and if it represents an important mechanism used by the virus to escape the immune response. Finally, we plan to use the MHC tetramers to assess vaccine development studies in the rhesus macaque model; this work is part of a program project grant from the Emory Vaccine Center, led by Dr. Harriet Robinson. Together with a team including Drs. Brian Barber and Kelly MacDonald from the University of Toronto, Francois Villinger from Emory, and Janet McNicholl from the CDC, we plan to map CD8+ T cell epitopes from SIV and SHIV viruses in the macaques in our colony at the Yerkes Primate Center. We will also receive important information from Dr. David Watkins at the Wisconsin Primate Center, who will be conducting parallel studies. Once the relevant epitopes are mapped, we will prepare tetramers based upon the macaque MHC molecules which present them, and we will study the effectiveness of a number of planned vaccination strategies at inducing sizable SHIV-specific CD8+ T cell responses. These studies hope to provide insight into the potential correlates of protective immunity to SHIV infection in macaques, with potential extension of the model to humans.	IMPImmunology and Molecular Pathogenesis - Full Member	Altman	John	Immunology Microbiology
Francisco J. Alvarez, PhD Full Member - Neuroscience francisco.j.alvarez@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Cell Biology, School of Medicine Development and plasticity of synaptic circuits in functional networks. Focus on inhibitory synapses and interneurons of the spinal cord motor circuits; their origin, specification and maturation during development and alterations following injury or neurodegenerative disease.	Development and plasticity of synaptic circuits in functional networks. Focus on inhibitory synapses and interneurons of the spinal cord motor circuits; their origin, specification and maturation during development and alterations following injury or neurodegenerative disease.Our lab focuses on spinal motor circuit assembly during development and how they change after injury in adult or in neurodegenerative diseases. In our developmental projects we study the formation of spinal circuits capable of adult motor behaviors, including locomotion. Within these circuits our main interest is on the specification and maturation of the neurochemical and electrophysiological properties of inhibitory interneurons (like Renshaw cells and Ia inhibitory interneurons) that modulate and pattern the activity of motoneurons and how they become integrated in synaptic circuits. These projects seek a circuit mechanistic explanation of the maturation of motor function and locomotion after birth and may have implications for many neonatal motor syndromes including cerebral palsy and spinal muscular atrophy. This basic understanding of motor development constitutes the knowledge foundation to analyze how these circuits are modified after injury or during neurodegenerative disease in adults. In another project we study how spinal premotor circuits are modified by peripheral nerve injury in adults and what prevents them from recovery. The goal of this study is to elucidate the circuit changes in the spinal cord that are induced by the nerve injury, for example abolition stretch reflexes, and that linger in patients with peripheral nerve injuries and explain lack of recovery of fine motor control after the nerve regenerates and motor and sensory axons reinnervate muscle. To provide a mechanistic explanation to synapse deletions within spinal motor circuitry after nerve injury we analyze the role of microglia and neuroinflammation, specifically we focus on the microglia reaction in the ventral horn and the contributions of the innate and adaptive immune system to synapse reorganizations in spinal motor circuits. We are also interested in the progressive transformation of some inhibitory circuits in motor neurodegenerative diseases like amyotrophic lateral sclerosis. The goal here is to provide mechanistic explanations on the progression of symptoms and uncover synaptic level processes that might enhance motor dysfunction and/or the motoneuron demise. Finally, we are also analyzing the role of GABA/Glycine synapses on motoneurons axotomized after nerve injuries and their role in maintaining or even enhancing the regenerative phenotype to regrow motor axons towards the denervated muscles.	NSNeuroscience - Full Member	Alvarez	Francisco	Animal Physiology / Morphology Cell Biology Motor Systems Neonatal Neuroanatomy Neuroscience Physiology Spinal Disorders
Rama Amara, PhD (he/him) Full Member - Immunology and Molecular Pathogenesis ramara@emory.edu \| Faculty Profile \| Lab Website Charles Howard Candler Professor, Department of Microbiology and Immunology, School of Medicine Professor, Vaccine Center, Emory National Primate Research Center The goal of our lab is to develop vaccines and therapies for infectious diseases such as HIV, HCV, SARS-CoV-2, influenza and TB.	The goal of our lab is to develop vaccines and therapies for infectious diseases such as HIV, HCV, SARS-CoV-2, influenza and TB.My laboratory is focused on developing vaccines against infectious diseases. We have more than 27 years of research experience with immunology, pathogenesis, and vaccine development for infectious diseases. We are currently developing vaccines against HIV, SARS-CoV-2, HCV, TB and influenza using the mouse and non-human primate models. Over the past 18 years, we mastered how to effectively educate the host immune system to induce a potent humoral and cellular immunity both in systemic and mucosal sites that is optimal for a specific disease condition. We employ a combination of a variety of vaccine delivery platforms (such as DNA, mRNA, MVA, recombinant proteins, and a probiotic Lactococcus lactis), molecular and synthetic adjuvants (such as GM-CSF, CD40L, alum, 3M-052, dmLT, and AS03), and routes of immunization (intramuscular, intradermal, and oral needle-free vaccination). A major part of our research is focused on understanding the pathogenesis and immune correlates for HIV/AIDS to develop novel vaccines to prevent HIV infection and therapies to cure HIV. My laboratory played a major role in the preclinical development of the AIDS vaccine that completed Phase 2a human clinical trials in the US. As a co-Program Director, Dr. Amara leads the Emory Consortium for Innovative AIDS Research (ECIAR) for over 12 years. ECIAR is one of the two consortia established by NIH and constitutes multiple investigators at and outside of Emory aimed at developing novel vaccines and cure strategies for HIV/AIDS. Dr. Amara is also working with collaborators in India to develop an HIV vaccine that could be used to control AIDS on the Indian subcontinent. In addition to the development of preventive vaccines, Dr. Amara's laboratory develops approaches to treat HIV infection by combining PD-1 checkpoint blockade therapy with vaccination. When the COVID-19 pandemic emerged, we quickly developed COVID-19 vaccines within few months using our 20+ years of knowledge in HIV/AIDS vaccine work, and showed their efficacy in mice and NHPs. Dr. Amara received a grant from the National Institute of Allergy and Infectious Diseases (NIAID) for this research and was recently featured talking about his COVID-19 vaccine in the season 2 opening episode of "Your Fantastic Mind". Dr. Amara published over 150 peer-reviewed manuscripts in high-impact journals, serves as a reviewer for multiple high-impact scientific journals, served on multiple NIH study sections including as a chair for a few of them, serves on multiple leadership/advisory committees at Emory and outside of Emory (include NIH) in an advisory role. Dr. Amara received his doctorate in molecular biology and immunology from the Indian Institute of Science in Bangalore, India. His thesis on the immunopathogenesis of Mycobacterium tuberculosis, the causative agent of tuberculosis, received the prestigious "Best Thesis Award for 1999". He completed his postdoctoral training in the lab of Dr. Harriet Robinson at the Emory Primate Center.	IMPImmunology and Molecular Pathogenesis - Full Member	Amara	Rama	Immunology Vaccine Development
Jimena Andersen, PhD (she/her) Full Member - Genetics and Molecular Biology Full Member - Neuroscience jimena.andersen@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Human Genetics, School of Medicine My research goal is to understand the processes that shape the development and function of the motor system and identify vulnerable links that predispose it to disease.	My research goal is to understand the processes that shape the development and function of the motor system and identify vulnerable links that predispose it to disease.The generation of region-specific 3D cultures or organoids derived from pluripotent stem cells provides a unique opportunity to study previously inaccessible complex human cell- to-cell interactions, and to start to shed light on some of the mechanisms that underlie disease pathophysiology. During my postdoctoral work, excited about this potential, I focused on developing and characterizing new organoid-based models to study human nervous system assembly and disease. As part of these efforts, I pioneered the generation of cortico-motor assembloids, a versatile and innovative organoid-based platform to model human cortico-spinal-muscle assembly and function in vitro for the first time. Damage or degeneration of the cortico-motor pathway in spinal cord injuries, amyotrophic lateral sclerosis (ALS) or autoimmune disorders results in severe motor dysfunction, yet translation of findings from animal models to humans has been largely unsuccessful, emphasizing the need for such a model. Importantly, cortico-motor assembloids can be used to trace anatomical and functional connectivity, can be maintained long-term to capture cellular and functional changes such as myelination and motor neuron maturation, and can be manipulated optogenetically or pharmacologically at multiple levels to control human muscle contraction. Ultimately, this platform provides an exciting opportunity to ask questions about previously inaccessible features of human cortico-motor development, connectivity, and function in both physiological and disease conditions. My research goal is to integrate my expertise in cell and developmental biology, stem cell biology, neuroscience and organoid and assembloid models of disease to understand, at a cellular and tissue levels, the fundamental processes that shape the development and function of the spinal cord and motor system and identify vulnerable links that predispose it to disease. My particular focus will be on studying the contribution of extrinsic factors or cell-to-cell interactions in this context, by leveraging the modular nature of the cortico-motor assembloid system. As such, research in my lab will aim to answer two general questions: 1) how do cell-to-cell interactions regulate the development and function of the human spinal cord and motor system, and 2) how do aberrations in cell-to-cell interactions contribute to diseases such as ALS in the motor system. In addition, work in my lab will continue to innovate and develop novel assembloid models that incorporate other regions of the motor system. To answer these questions, my lab will use stem cell-derived organoid and assembloid technologies in combination with state-of-the-art molecular and functional techniques, including genome engineering, single cell omics, viral tracing, calcium imaging and optogenetics. Ultimately these efforts will shed light on human-specific aspects important for the development and function of motor pathways, and will allow us to dissect cell type-specific contributions to motor neuron susceptibility in ALS and other motor neuron disorders while providing candidate mechanisms as potential therapeutic targets.	GMBGenetics and Molecular Biology - Full Member NSNeuroscience - Full Member	Andersen	Jimena	Biology, Developmental Cell Biology Neurodegenerative Disease Spinal Disorders
Larry James Anderson, MD (he/him) Full Member - Microbiology and Molecular Genetics larry.anderson@emory.edu \| Faculty Profile Professor, Division of Infectious Disease, Department of Pediatrics, School of Medicine Pathogenesis of respiratory virus infections, syncytial virus and rhinovirus, to develop antiviral drugs and vaccines.	Pathogenesis of respiratory virus infections, syncytial virus and rhinovirus, to develop antiviral drugs and vaccines.Pathogenesis of Respiratory Syncytial Virus (RSV) Disease. Our laboratory is focusing on pathogenesis of respiratory syncytial virus (RSV) disease related to vaccine development and anti-viral treatment. RSV is the single most important cause of serious lower respiratory tract disease in the infant and young children and a high priority for vaccine development. Unfortunately, efforts to develop RSV vaccines have failed. The first vaccine, formalin inactivated RSV (FI-RSV), actually led to enhanced disease when recipients were later infected with RSV. Multiple live virus vaccines have also been developed but none has proven safe and effective. These experiences suggest we need a better understanding of virus induced host responses associated with disease and those associated with protection. Our laboratory is using the BALB/c mouse and a human airway epithelial cell line (polarized and non-polarized cells) plus human peripheral blood mononuclear cell (PBMC) cell culture system to explore virus induced host responses that contribute to disease and ways to prevent these responses. For the last 15 years, we have focused on the RSV G protein and its CX3C chemokine motif. The G protein and this motif appear to contribute to induction of a Th-2 type T cell response, enhanced pulmonary inflammatory after RSV infection, FI-RSV vaccination, and dampening of the host adaptive immune response. For example, administration of a monoclonal antibody that bind G near the CX3C motif and blocks binding to CX3CR1 before or after challenge decreases the pulmonary inflammatory response in naïve or FI-RSV vaccinated mice and improves the host antibody responses and directs a more Th1 biased T cell response. We are using G peptide vaccines, anti-G monoclonal antibodies, clinical RSV isolates associated with different phenotypes, and genetically engineered viruses to 1) understand pathogenesis of RSV disease and especially that associated with the G protein and 2) develop novel approaches to making a safe and effective RSV vaccine. Pathogen and Biomarker Detection. We are collaborating on studies to biomarkers in upper respiratory tract specimens to identify biomarkers associated with severity of RSV disease in children and coughed droplets captures on a filter to detect pathogens and biomarkers of disease state in patients with lung disease.	MMGMicrobiology and Molecular Genetics - Full Member	Anderson	Larry
Rustom Antia, PhD Full Member - Immunology and Molecular Pathogenesis Full Member - Population Biology, Ecology, and Evolution rantia@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Biology, Emory College of Arts and Sciences Modeling the dynamics of immune responses and infections.	Modeling the dynamics of immune responses and infections.My research interests encompass a broad area of theoretical and empirical studies of the interaction between pathogens and the immune response. I use mathematical models and computer simulations in conjunction with experimental work to: understand the complex and often counter-intuitive dynamics of pathogens and immune responses in vivo; estimate important biological parameters that are not directly measurable by experimentation; and generate empirical tests of different models and hypotheses. Almost all my theoretical work is based on experiments, mostly done in collaboration with other experimental immunologists at Emory, and some done in my laboratory. Some areas I am interested in are: (i) the measurement of birth and death rates of immune cells; (ii) the generation of a theoretical framework to understand immune memory; (iii) theory and modeling to describe the dynamics of viral and bacterial infections; (iv) the use of antimicrobial agents to control infections; and (v) the evolution of pathogens and their hosts.	IMPImmunology and Molecular Pathogenesis - Full Member PBEEPopulation Biology, Ecology, and Evolution - Full Member	Antia	Rustom
Michal Arbilly, PhD Affiliate Member - Population Biology, Ecology, and Evolution michal.arbilly@emory.edu \| Faculty Profile Assistant Teaching Professor, Department of Biology, Emory College of Arts and Sciences Teaching biology with a focus on quantitative methods; evolution and evolutionary genetics; behavioral ecology.	Teaching biology with a focus on quantitative methods; evolution and evolutionary genetics; behavioral ecology.I use computer models to simulate the evolution of learning in social animals, in an attempt to shed light on variations in learning and in degree of social interaction we see in nature. I am especially interested in the interaction between sociality and cognition, and how they co-evolve to produce complex cognitive abilities, like theory of mind. My simulations combine behavioral ecology models of animal interaction with population genetics models, and with models of cognitive processing. I am also interested in the biologically wired traits that promote the evolution of culture, and shape its complexity.	PBEEPopulation Biology, Ecology, and Evolution - Affiliate Member	Arbilly	Michal
Dave Archer, PhD Full Member - Immunology and Molecular Pathogenesis darcher@emory.edu \| Faculty Profile Associate Professor, Division of Hematology/Oncology, Department of Pediatrics, School of Medicine Stem cell therapy for the treatment of inherited and acquired diseases.	Stem cell therapy for the treatment of inherited and acquired diseases.The lab is focused on the pathogenesis of sickle cell disease, the development and testing of new therapies, and the use of cellular therapies. Our aim is to investigate stem cell therapy in murine models with defects in their hematopoietic and immune systems. The major project in the lab is the potential treatment of b-thalassemia which is one of the most common inherited disorders in man and has an increasingly global distribution. Current conventional therapies for this debilitating hemoglobinopathy are complicated, expensive, and are not curative. Hematopoietic stem cell (HSC) transplantation may cure b-thalassemia, but transplant-related morbidity and mortality is substantial. Additionally, stem cell transplantation is limited by the lack of suitable histocompatible stem cell donors. We are trying to pursue the opportunity to evalute in utero therapy for hemoglobinopathies, immunodeficiency disorders and metabolic diseases. Transplantation in utero has the potential to increase the donor pool by circumventing the immunological barriers associated with post-natal transplantation of mismatched cells, and would also allow for treatment before the onset of serious pathological episodes.	IMPImmunology and Molecular Pathogenesis - Full Member	Archer	Dave
Nicholas Au Yong, MD, PhD Full Member - Neuroscience nicholas.au.yong@emory.edu \| Faculty Profile Assistant Professor, Department of Neurosurgery, School of Medicine Assistant Professor, Department of Cell Biology, School of Medicine Assistant Professor, Wallace H. Coulter Department of Biomedical Engineering, Emory University & Georgia Institute of Technology Development of neurorestoration strategies to restore motor and autonomic function in paralyzed patients.	Development of neurorestoration strategies to restore motor and autonomic function in paralyzed patients.I am a neurosurgeon-scientist with a translational neurophysiology laboratory centered on developing novel strategies to restore or rescue motor and autonomic function in patients with severe paralysis following spinal cord or brain injury/disease. To accomplish this, my laboratory is focused on understanding key motor control neuronal circuits and how to engage with them to restore functions. To this end, my laboratory's research portfolio spans several motor control research domains described below. I am the site-PI for a multi-institution Braingate 2 clinical trial (https://www.braingate.org) to study the use of cortically implanted micro-electrode arrays in human subjects for brain-machine interface (BMI) purposes. Along with my close collaborator, Chethan Pandarinath PhD (Biomedical Engineering), we are working on developing the next generation BMI for restoring motor control and speech using modern artificial intelligence neural networks. A second project in my lab is centered on spinal cord neuronal networks. My lab has expertise in using high-channel count multi-electrode arrays for in-vivo intraspinal recording. We are particularly interested in spinal cord network activity during resting state and locomotor behavior. A key motivating question for this project is how neuronal networks drives the flexible but dependable timing and coordination involved in locomotor behaviors. Additionally, we are studying how neuronal networks processes sensory information. A greater understanding of these key issues will help guide therapeutic development for paralysis. Principles from this project is being leveraged in a translational research project to develop a treatment for Freezing of gait (FOG), a common symptom in patients with Parkinson's disease (PD) where the ability to walk is abruptly interrupted, often described as if their feet were suddenly "glued" to the floor. A third project is based on restoring breathing function following cervical spinal cord injury. Life expectancy of ventilator-dependent cervical spinal cord injury (cSCI) patients is significantly reduced by respiratory complications. Despite recent advances in pulmonary medicine, including phrenic nerve stimulation and diaphragm pacing, there are no long-term solutions for cSCI- induced ventilator dependency. This project addresses this profound therapeutic gap by testing and developing translational principles to amplify diaphragm contraction strength via selective neuromodulation of phrenic sympathetic innervation to reduce or eliminate ventilator dependency. We are also investigating neuromodulation approaches to selectively augment sympathetic tone. Resultant treatments are applicable in spinal cord injury patient with a labile autonomic system.	NSNeuroscience - Full Member	Au Yong	Nicholas	Basal Ganglia Bioengineering Neurophysiology Spinal Cord Injuries
Byron Au-Yeung, PhD (he/him) Full Member - Immunology and Molecular Pathogenesis byron.au-yeung@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Division of Rheumatology, Department of Medicine, School of Medicine Immune responses mediated by T cells are promoted by signals stimulated by the T cell receptor (TCR). We are interested in understanding how variations in TCR signal intensity and duration encode information that influences how T cells become activated.	Immune responses mediated by T cells are promoted by signals stimulated by the T cell receptor (TCR). We are interested in understanding how variations in TCR signal intensity and duration encode information that influences how T cells become activated.Biochemical signals triggered by the TCR are required for the activation of T cell responses. Work from our group and others suggests that TCR signals can vary in their intensity and duration, or strength, and that variations in TCR signal strength can influence T cells to behave differently. We are interested in understanding the information encoded by variations in TCR signal strength, and how this information can be used to influence T cell-mediated immune responses. Signal transduction by the T cell receptor requires the function of ZAP-70, a tyrosine kinase. Genetic, cellular, and biochemical studies all highlight a central role for ZAP-70 in T cell activation and function. We believe that targeting ZAP-70 would be an effective strategy for blocking destructive T cell-mediated immune responses. However, to date, effective inhibitors of ZAP-70 have not yet been optimized or approved but he FDA for use as a therapy in humans. To study how inhibiting ZAP-70 would impact T cell functions, we have developed a model system where a mutant ZAP-70 with a single amino acid substitution gains sensitivity to a pharmacologic inhibitor. This experimental tool allows us to model how inhibiting ZAP-70 kinase function in a time or dose-dependent manner influences cellular behavior. We also have an interest in studying the how TCR signals in response to self-antigens in vivo (aka "tonic" or "basal" TCR signals) influence T cell behavior. The strength of tonic TCR signaling varies broadly between individual T cells. Our recent work has focused on understanding how the strength of tonic TCR signals affects how naive T cells respond to stimulation by foreign antigens. In our lab, we can visualize the strength of TCR signals indirectly with a reporter transgene called Nur77-GFP in which the Green Fluorescent Protein is transcribed and translated under the control of the gene encoding Nur77 (Nr4a1). In T cells, Nur77 is expressed in proportion the the strength of TCR stimulation. This experimental system enables us to identify T cells that have previously experienced weak or strong tonic TCR signals. Our work suggests that T cells that experience weak tonic TCR signals respond more robustly to stimulation by foreign antigens, whereas T cells that experienced strong tonic TCR signals are less responsive. Therefore, we propose that tonic TCR signals "program" naive T cells differentially. This is a fundamental property of T cells that is potentially relevant to normal T cell homestasis and tolerance, or to diseases mediated by T cell responses.	IMPImmunology and Molecular Pathogenesis - Full Member	Au-Yeung	Byron
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
Ben Barwick, PhD Full Member - Cancer Biology Full Member - Genetics and Molecular Biology bbarwic@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Hematology and Medical Oncology, School of Medicine My lab leverages genomic and epigenomic tools to understand disease pathology, therapeutic resistance, and immune responses.	My lab leverages genomic and epigenomic tools to understand disease pathology, therapeutic resistance, and immune responses.My research seeks to better understand basic mechanisms of cancer and translate findings to better health outcomes. My major focus areas currently include genetic, epigenetic, and gene regulatory mechanisms of normal and malignant hematopoiesis. This research program leverages my expertise as both a computational biologist and wet-bench scientist trained in genetics, molecular biology, immunology, and cancer biology. Currently, I have two major research directions focused on the plasma cell malignancy multiple myeloma. My first research direction stems from studies where we helped characterize multiple myeloma genomic alterations. We identified immunoglobulin lambda (IgL) translocations as prognostic of poor outcome and reduced responses to immunomodulatory imide drugs (IMiDs). IMiDs function by inducing degradation of the transcription factors, Ikaros and Aiolos. These transcription factors are bound to the IgL enhancer at some of the highest levels in the myeloma epigenome, and in IgL-translocated myeloma, this enhancer drives the expression of juxtaposed oncogenes, most commonly MYC. To better understand myeloma IMiD responses, we are investigating Ikaros and Aiolos function using a variety of methods, which present learning opportunities for GDBBS students. First we are characterizing myeloma cell line IMiD responses using cellular and molecular assays. These include RNA-seq to identify gene expression changes resulting from IMiD treatment. These data are being paired with the genomic binding sites of Ikaros and Aiolos using Cleavage Under Targets & Tagmentation (CUT&Tag) to help discriminate direct versus secondary effects of IMiDs. Additionally, we are studying the individual functions of Ikaros and Aiolos by disrupting their function using CRISPR/Cas9 genome editing. Computational biology approaches are being used to integrate omic data from both IMiD-treated and CRISPR/Cas9-edited cells to better understand how each transcription factor contributes to myeloma cell survival and IMiD responses. Finally, we are in the process of acquiring a mouse model of myeloma (Vk*MYC), which will be used to better understand the immunological impact of IMiDs in the context myelomagenesis. These work are supported by a Woodruff Early Independence Award and an NCI K22. The second research direction in the lab focuses on understanding the role of DNA methylation in myeloma pathogenesis. We have generated DNA methylation by whole genome bisulfite sequencing on several hundred samples from the MMRF CoMMpass trial. These data revealed a dramatic hypomethylation of myeloma as compared to other hematopoietic and B lineage cells including plasma cells from healthy donors. These hypomethylation occurred in late replicating regions of the genome, indicating cellular division is imprinted on the epigenome. However, DNA methylation changes were not uniform between myeloma subtypes. In particular, two high-risk myeloma subtypes had divergent changes in DNA methylation. First, myeloma with t(4;14) translocations had higher levels of DNA methylation, specifically in the late replicating domains of the genome. This subtype of myeloma is associated with worse outcomes and we are currently exploring the hypothesis that higher levels of DNA methylation in these late replicating domains where a lot retrotransposons exist, results in reduced immunogenicity. The second subtype with distinctive DNA methylation programming is the proliferation subtype, which is also associated with worse outcomes, but is an amalgamation of different geneic subtypes. Here, we are exploring the hypothesis that DNA hypomethylation supports the proliferative phenotype observed in this class of myeloma. We are using next-generation CRISPR/Cas9 systems (Cas9-DNMT3L-DNMT3A and Cas9-Tet1) to perform site-specific epigenetic editing as well as overexpression and gene knock-out models in myeloma cell line models to further test these hypotheses. This work is supported by a Riney Foundation grant, a Myeloma Solutions Fund award, and an R21. The above projects will provide excellent training opportunities for students to learn about cancer biology, genetics, molecular and cellular biology, computational biology, and even some immunology, while also contributing to and leading high-impact research. With current funding and my start-up package I hope to recruit 1-2 students to help create and vibrant lab environment that is collegial and inclusive.	CBCancer Biology - Full Member GMBGenetics and Molecular Biology - Full Member	Barwick	Ben
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
Georgii Bazykin, PhD Full Member - Population Biology, Ecology, and Evolution gbazyki@emory.edu \| Faculty Profile Visiting Professor, Department of Biology, Emory College of Arts and Sciences I use comparative genomics and bioinformatics to investigate sequence variation and evolution, and theory to interpret the observed patterns.	I use comparative genomics and bioinformatics to investigate sequence variation and evolution, and theory to interpret the observed patterns.We perform computational analysis of biological evolution in a broad range of biological systems – from viruses to humans. We develop and apply methods to measure and disentangle the roles of evolutionary forces – mutation, selection, gene flow, recombination and genetic drift – in shaping evolution and variation. We use comparative genomics and bioinformatics to investigate different aspects of sequence variation and evolution, and theory to interpret the observed patterns. Current research in the lab falls into three general directions: Inference of Natural Selection and Genetic Interactions from Genomic Data. Mutations may be advantageous or deleterious. Whether a particular mutation harms the cell carrying it, or does it good, may be inferred from its rate of spread, which can in turn be inferred from sequencing data. Moreover, interactions between mutations shape the phenotype. We develop approaches for inference of selection forces and interactions from genetic data, and apply them to a broad range of organisms. Mutations in Germline and in Cancer. Mutations arise due to a wide range of processes. Changes in these processes, e.g. exposure to ultraviolet rays or a modification of a protein involved in handling of DNA, may increase the rate of mutations and/or change their character. We infer changes in mutagenesis from changes in the mutation rates and patterns observed in large-scale sequencing data. Ultimately, such approaches might improve understanding of heritable mutagenesis and cancer diagnosis and treatment. Predicting Evolutionary Dynamics of Pathogens. Evolution of pathogens allows them to evade host immune system, contributing to disease and death caused by them. We are trying to predict such dynamics, notably in Influenza A and SARS-CoV-2.	PBEEPopulation Biology, Ecology, and Evolution - Full Member	Bazykin	Georgii
Chris Beck, PhD (he/him) Affiliate Member - Population Biology, Ecology, and Evolution cbeck@emory.edu \| Faculty Profile \| Lab Website Professor of Pedagogy, Department of Biology, Emory College of Arts and Sciences Approaches to scientific teaching; Effects of resource quality on life history traits; Effects of plant secondary compounds on insect microbiomes	Approaches to scientific teaching; Effects of resource quality on life history traits; Effects of plant secondary compounds on insect microbiomesnull	PBEEPopulation Biology, Ecology, and Evolution - Affiliate Member	Beck	Chris
George Richard Beck Jr., PhD Full Member - Cancer Biology gbeck2@emory.edu \| Faculty Profile Associate Professor, Division of Endocrinology, Metabolism, and Lipids, Department of Medicine, School of Medicine Research Biologist, Atlanta VA Medical Center Cellular response to changes in inorganic phosphate and how these changes alter disease progression, with a focus on cancer and bone metabolism.	Cellular response to changes in inorganic phosphate and how these changes alter disease progression, with a focus on cancer and bone metabolism.Inorganic phosphate regulated proliferation, transformation and tumorigenesis: Inorganic phosphate (Pi) is critical to the human body on many levels. At the cellular level it is required as a component of energy metabolism, kinase signaling and in the formation and function of DNA and lipids. Traditionally, Pi has been thought of as a passive, required ion for these processes, however, recent data suggests a more active role for this ion in the regulation of cell function. Our in vitro results have revealed that exposure of a variety of cell types to elevated Pi will alter growth properties, specific signal transduction pathways, and gene expression, including cancer and metastasis related factors such as osteopontin (OPN), c-fos, Egr1 and Cox-2 (1, 2). Our in vivo results corroborate the in vitro studies and suggest that the levels of serum Pi alter tumorigenesis in the two-stage model of skin carcinogenesis. The main source of serum Pi is from dietary intake and due, in part, to the increased consumption of processed foods, the amount of Pi in the American diet continues to rise above levels already considered high by the FDA. Although it is becoming increasingly apparent that diet can have profound effects on functional genomics, to date the molecular and cellular responses to changes in serum Pi levels have only begun to be investigated. We are currently investigating the hypothesis that; the increased consumption of inorganic phosphate alters the growth and transformation potential of cells through specific cellular and molecular regulatory signals and circulating factors. Biological Actions and Cellular Targeting of Nanoparticles for Medical Applications: The skeleton is extremely dynamic and bone is regenerated throughout life in a process by which old bone is resorbed by osteoclasts and new bone synthesized by osteoblasts, a process termed bone remodeling. Factors that destabilize bone regeneration lead to osteoporosis, a serious medical condition that dramatically increases the risk of bone fractures. The unique combination of semi-structured extracellular matrix, biomechanical properties, and active remodeling makes bone a unique tissue particularly suited for targeting by nanoparticles. We are investigating the molecular and cellular mechanisms by which specific silica-based nanoparticles regulate bone cell metabolism including the identification of specific intracellular mechanisms by which the particles influence cell behavior. One particular novel nanoparticle formulation possesses a potent stimulatory effect on the formation of osteoblasts, the cells responsible for bone formation, and concomitant inhibitory effect on the formation of osteoclasts, the cells responsible for bone breakdown (resorption). This nanoparticle therefore, may have the potential to be developed into a powerful dual anticatabolic and proanabolic agent for the treatment of numerous osteoporotic diseases.	CBCancer Biology - Full Member	Beck	George	Biology, Molecular Biomaterials / Cell Lines Cancer Biology Nutrition / Dietetics Osteoporosis
Jessica A Belser, PhD Adjunct Member - Microbiology and Molecular Genetics jbelser@cdc.gov \| Faculty Profile Microbiologist, Influenza Division, National Center for Immunization and Respiratory Diseases, Centers for Disease Control and Prevention Pathogenesis, transmission, and tropism of Influenza A viruses.	Pathogenesis, transmission, and tropism of Influenza A viruses.Overall objectives: 1. Determine the pathogenicity, transmissibility, and tropism of wild-type influenza viruses in mice and ferrets, notably those within the H7 virus subtype. 2. Delineate the human risk posed by ocular exposure to influenza viruses of all subtypes by the use of in vitro and in vivo ocular models. 3. Identify genetic determinants responsible for the ocular tropism detected among selected H7 subtype influenza viruses using in vitro and in vivo models. Specific examples of recent/ongoing research towards these objectives: 1. Development and validation of a novel aerosol in vitro inoculation method to expose human cultured cells to a defined influenza virus aerosol inoculum, an approach that will enhance ongoing studies of influenza virus tropism in human cells throughout the respiratory tract and ocular surface. 2. Establishment of several in vivo models (mouse and ferret) employing ocular inoculation with influenza viruses, permitting the identification of host properties which do/do not confer infectivity by the ocular route and assessment of existing and novel vaccine/antiviral agents to prevent or reduce infection following ocular exposure. 3. Expanding aerobiology-based approaches to study the contribution of aerosolized influenza virus in modulating virus pathogenicity and transmissibility in vivo and in vitro, studies which further our understanding of assessing the pandemic risk of novel influenza viruses. The research described above occurs within the umbrella of the Pathogenesis Laboratory Team (Immunology and Pathogenesis Branch, Influenza Division, CDC). The overarching goals of the team are: 1) assess virus-host interactions, 2) monitor the pathogenicity and transmission properties of novel influenza strains as they emerge in the US and other parts of the world, 3) identify molecular and biologic correlates of virulence and the pandemic potential of influenza viruses; 4) assess immunogenicity and identify correlates of protection in appropriate animal models and bridge to human vaccine studies, and 5) vaccine safety testing. Recent publications: Kieran TJ, Sun X, Maines TR, Beauchemin CAA, Belser JA. 2024. Exploring associations between viral titer measurements and disease outcomes in ferrets inoculated with 125 contemporary influenza A viruses. Journal of Virology. 98(2):e0166123. Belser JA, Lash RR, Garg S, Tumpey TM, Maines TR. 2018. The eyes have it: influenza virus infection beyond the respiratory tract. Lancet Infectious Diseases. 18(7):e220-e227. Creager HM, Kumar A, Zeng H, Maines TR, Tumpey TM, Belser JA. 2018. Infection and replication of influenza virus at the ocular surface. Journal of Virology. 92(7): e02192-17. Creager HM, Zeng H, Pulit-Penaloza JA, Maines TR, Tumpey TM, Belser JA. 2017. In vitro exposure system for study of aerosolized influenza virus. Virology. 500:62-70.	MMGMicrobiology and Molecular Genetics - Adjunct Member	Belser	Jessica
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
Jacob E. Berchuck, MD Full Member - Cancer Biology jberchuck@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Hematology and Medical Oncology, School of Medicine Medical Oncologist, Department of Hematology and Medical Oncology, Winship Cancer Institute My research focuses on using cell-free DNA-based liquid biopsy tools to study molecular correlates of treatment response and resistance in cancer.	My research focuses on using cell-free DNA-based liquid biopsy tools to study molecular correlates of treatment response and resistance in cancer.Improving outcomes for people living with advanced cancer will require developing clinical tools to optimize therapeutic decision-making for individual patients, understanding mechanisms of treatment resistance, and discovering the next generation of effective anti-cancer drugs. Progress towards these goals has been impeded by the intractable challenges of obtaining tumor tissue specimens. Liquid biopsies – studying tumor cell-free (cf)DNA circulating in the bloodstream – present an unprecedented opportunity to interrogate an individual patient's tumor molecular features in real-time, and longitudinally across their disease course. Further, the minimally-invasive nature of a blood draw compared to a tumor biopsy, allows for sample collection and analysis at unprecedented scale. We believe that liquid biopsy technologies are poised to revolutionize cancer research, propelling unprecedented scientific breakthroughs, and transforming patient care into a new era of precision and hope. Our lab has made several contributions to advancing the field of liquid biopsy, including pioneering novel methods to profile epigenomic features in cell-free cfDNA, demonstrating the power of epigenomic liquid biopsies for non-invasive cancer detection, establishing the ability of liquid biopsies to deliver precision medicine for patients with advanced cancer, developing epigenomic cfDNA-based diagnostic tests to detect clinically actionable mechanisms of therapeutic resistance, and highlighting the power of integrated multiomic cfDNA profiling to maximize insights into tumor biology. Building upon this work, we are deploying a rapidly evolving suite of liquid biopsy tools to generate predictive biomarkers to determine in real-time which treatments will be most, and least, likely to benefit individual patients, understand mechanisms of treatment resistance, and nominate novel therapeutic strategies for patients with advanced cancer.	CBCancer Biology - Full Member	Berchuck	Jacob
Gordon J. Berman, PhD (he/him) Full Member - Neuroscience gordon.berman@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Biology, Emory College of Arts and Sciences Graduate Field Member, Department of Physics, Emory College of Arts and Sciences Program Faculty, Biomedical Engineering, Wallace H. Coulter Department of Biomedical Engineering, Emory University & Georgia Institute of Technology Data-driven theory, analysis, and modeling of animal movements and their underlying neurobiology.	Data-driven theory, analysis, and modeling of animal movements and their underlying neurobiology.My lab uses theoretical, computational, and data-driven approaches to gain quantitative insight into entire repertoires of animal behaviors, aiming to make connections to the neurobiology, genetics, and evolutionary histories that underlie them. In particular, we are interested in not just the precise physical and physiological mechanisms behind the performance of a single behavior or motion. Instead, we primarily focus on the intricate interactions that underlie the temporal ordering, control, and evolution of an organism's movements, attempting to unearth general organizing principles that apply across species. Publications: https://scholar.google.com/citations?user=rPGn0XYAAAAJ&hl=en	NSNeuroscience - Full Member	Berman	Gordon
Gregory S. Berns, MD, PhD Affiliate Member - Neuroscience gberns@emory.edu \| Faculty Profile Distinguished Professor of Neuroeconomics, Department of Psychology, Emory College of Arts and Sciences Director, Facility for Education and Research in Neuroscience (FERN), Emory College of Arts and Sciences Relationship of neural systems to decision making in people and other animals (dogs & cattle).	Relationship of neural systems to decision making in people and other animals (dogs & cattle).My research was previously aimed at understanding the neurobiological basis for individual preferences and how neurobiology places constraints on the decisions people make -- a field now known as neuroeconomics. To achieve this goal, we use functional MRI to measure the activity in key parts of the brain involved in decision making. We then link these activity traces to various phenotypes of decision making. For example, we have linked the pattern of activity in the striatum with the differential processing of risk and reward. More recently, we have used this activity to predict the commercial success of popular songs – the first prospective demonstration in neuromarketing. More recently we have used fMRI to study canine cognitive function in awake, unrestrained dogs. My current interests are focused on the psychology sustainability and how cattle think.	NSNeuroscience - Affiliate Member	Berns	Gregory	Animal Physiology / Morphology Bioengineering Imaging Mathematical Modeling Neuroscience
Ranjita Sandeep Betarbet, PhD Adjunct Member - Neuroscience rbetarb@emory.edu \| Faculty Profile Assistant Professor, Department of Neurology, School of Medicine Influences of genetic and environmental factors on Parkinson's disease pathogenesis.	Influences of genetic and environmental factors on Parkinson's disease pathogenesis.My research interests are in the pathogenesis and pathology of neurodegenerative diseases including Parkinson's (PD) and Alzheimer's disease (AD). More specifically, the interactions between PD/AD-related genetic factors and external stressors, including mitochondrial impairment, oxidative stress, proteasomal inhibition, and their involvement in protein trafficking pathways in neurodegeneration. My recent interests are to accelerate development of AD therapeutic compounds through the open development and distribution of experimental tools necessary to catalyze robust in vitro and preclinical evaluation of their potential roles in AD through the Emory-Sage-SGC TREAT-AD Center funded by NIA.	NSNeuroscience - Adjunct Member	Betarbet	Ranjita	Basal Ganglia
Tyler S Beyett, PhD (he/him) Full Member - Cancer Biology Full Member - Molecular and Systems Pharmacology tbeyett@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Pharmacology and Chemical Biology, School of Medicine The Beyett lab uses structural and chemical biology to discover and develop new therapeutic strategies targeting kinase signaling in cancer.	The Beyett lab uses structural and chemical biology to discover and develop new therapeutic strategies targeting kinase signaling in cancer.We are generally interested in kinases and phosphatases, which play opposing roles in maintaining the balance in many signaling cascades and are often mutated or dysregulated in cancer. Using a combination of structural and chemical biology, we aim to develop chemical probes/tools that can be used to identify new therapeutic strategies for these proteins. Our research is focused on two areas with high translational potential. First, we aim to advance the concept of "dual-targeting" or "double-drugging" as a viable therapeutic strategy for kinases, especially for drug-resistant variants. Second, we aim to characterize and modulate protein-protein interactions (PPIs) that regulate phosphatases in growth and development signaling pathways.	CBCancer Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Beyett	Tyler	Biochemistry, Proteins Biophysics Cancer Biology Chemotherapy Drug Design Drug Resistance Pharmacology X-Ray Crystallography
Manoj Bhasin, PhD Full Member - Cancer Biology manoj.bhasin@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Division of Hematology/Oncology, Department of Pediatrics, School of Medicine Associate Professor, Department of Biomedical Informatics, School of Medicine My lab has deep interest in defining the mechanisms of disease using innovative AI-based data analysis and cutting-edge single and spatial omics approaches.	My lab has deep interest in defining the mechanisms of disease using innovative AI-based data analysis and cutting-edge single and spatial omics approaches.Bhasin lab uses cutting edge single-cell omics approaches and developing machine learning-based bioinformatics algorithms to understand disease pathophysiology for the identification of novel disease diagnosis and therapeutic biomarkers. We have developed tissue, urine, and blood-based biomarkers for diagnosis and prognosis of cancers using publicly available genome-level data in conjunction with Artificial intelligence approaches. Currently, our main areas of interest are immune landscape mapping of cancers and therapies, precision medicine personalized cancer vaccines, drug repurposing, and complementary and alternative medicine. In the area of bioinformatics, we are developing a platform for the analysis of single-cell profiling data for the transformation of digital data into biologically meaningful data. Our group is also developing tools for integrative analysis of single cell genomics, proteomics and metabolomics data for understanding diseases heterogeneity and pathophysiology. Please visit http://bhasinlab.org for further details.	CBCancer Biology - Full Member	Bhasin	Manoj
Fikri Birey, PhD Full Member - Genetics and Molecular Biology Full Member - Neuroscience fikri.birey@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Human Genetics, School of Medicine Our group is interested in understanding the fundamental principles that govern the assembly of human brain during development and how genetic aberrations that can perturb these processes contribute to disease using state-of-art stem cell-based models.	Our group is interested in understanding the fundamental principles that govern the assembly of human brain during development and how genetic aberrations that can perturb these processes contribute to disease using state-of-art stem cell-based models.We are broadly interested in functional interactions within neurobiological systems and various disease states that emerge from their disturbance by genetic factors. During my doctoral work, I described previously unknown roles of oligodendrocyte progenitor cells in maintaining neuronal and astrocytic functions in the adult mouse frontal cortex, a bidirectional crosstalk which is adversely affected by social stress. My postdoctoral research was focused on investigating how pathological gene variants perturb the development of human cortex in various disease states at a molecular, cellular and systems scales. Due to the lack of functional access to human brain tissue, progress in gaining insights into mechanistic interactions between variants and cellular phenotypes in patients has been slow. To address this issue, I developed a human induced pluripotent stem cell (hiPSC)-derived in vitro model called "forebrain assembloids" to reliably model key aspects of human forebrain development and uncovered novel disease phenotypes in Timothy Syndrome, a neurodevelopmental disorder characterized by autism and epilepsy and caused by a mutation in a L-type calcium channel subunit. This approach has been widely recognized as a major advancement in the newly emerging field of 3D human neural cultures, has been named one of the top research highlights of 2017 by NIH and has now been adopted across several labs. My group at Emory University works at the intersection of stem cell biology, developmental biology, and neurobiology, where we combine the ever-improving assembloid platform with state-of-the-art techniques, such as CRISPR gene editing, microscopy and single-cell RNA sequencing. We will seek to study the. Our scientific interests are diverse but share the broader goal of better understanding mechanistic interactions underlying human brain development at various scales (molecular, cellular, population) to uncover unifying biological principles behind clinically disparate classes of disorders. Our ultimate ambition is to discover novel, cross- modal disease signatures to better diagnose and treat disorders of brain development that lead to neurodevelopmental and neuropsychiatric disorders later in life.	GMBGenetics and Molecular Biology - Full Member NSNeuroscience - Full Member	Birey	Fikri
Jeffrey H. Boatright, PhD Full Member - Neuroscience jeffboatright@emory.edu \| Faculty Profile Professor, Department of Ophthalmology, School of Medicine We explore the causes of and develop treatments for retinal neurodegenerative diseases.	We explore the causes of and develop treatments for retinal neurodegenerative diseases.Neuroprotectants in treatment of retinal degenerations and glaucoma. Development of new animal models of retinal degeneration. Exercise preconditioning as retinal protectant therapy. Role of metabolic regulation in retinal health, damage, and disease.	NSNeuroscience - Full Member	Boatright	Jeffrey	Animal Physiology / Morphology Biochemistry, Nucleic Acids Biological Response Modifiers Biology, Molecular Electrophysiology Imaging Molecular Biology Neurodegenerative Disease Neuropharmacology Ophthalmology
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
Michael R. Borich, DPT, PhD (he/him) Full Member - Neuroscience michael.borich@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Rehabilitation Medicine, School of Medicine Program Faculty, Biomedical Engineering, Wallace H. Coulter Department of Biomedical Engineering, Emory University & Georgia Institute of Technology Vice-Chair of Research, Department of Rehabilitation Medicine, School of Medicine To understand the adaptive capacity of the human nervous system using multimodal neuroimaging and neurostimulation approaches to develop effective (p)rehabilitation strategies.	To understand the adaptive capacity of the human nervous system using multimodal neuroimaging and neurostimulation approaches to develop effective (p)rehabilitation strategies.My primary research focus has been to understand the neural substrates of motor learning in healthy individuals and patients after stroke. This work has utilized cutting-edge neuroimaging techniques to evaluate both human brain anatomy (structure) and physiology (function). It remains unclear how the brain recovers from neurologic insult and, therefore, rehabilitation strategies aimed at ameliorating functional impairments following injury are currently suboptimal. My work aims to understand how best to measure brain recovery after injury and how best to stimulate optimal restoration of function. Prior to joining the Department in Rehabilitation Medicine at Emory University, I was a postdoctoral research fellow in the Brain Behavior Laboratory at the University of British Columbia. During my appointment, we successfully translated a cutting-edge magnetic resonance imaging technique to non-invasively quantify specific structural properties (e.g. myelin) in vivo in white matter of the human brain after stroke. This work built upon our previous diffusion-weighted magnetic resonance imaging (dw-MRI) work showing relationships between white matter tract structural integrity with motor behavior and response to motor skill training in individuals with chronic stroke. We also demonstrated the potential benefits of noninvasive brain stimulation paired with motor training for motor and sensory function in correlational approaches to infer brain behavior after stroke. It is now possible to combine brain imaging and stimulation techniques in real-time to infer causal relationships between regional brain activity. Using this 'online' stimulation-imaging paradigm, we initiated a preliminary electroencephalography (EEG) to characterize changes in effective brain connectivity and how these changes may relate to motor behavior in chronic stroke. This project is currently ongoing and is foundation for initial work in my lab at Emory. In my labs, the Neural Plasticity Research Laboratory (NPRL) and Precision Neuromodulation Laboratory (PNEL), we utilize real-time EEG recording during non-invasive brain stimulation using transcranial magnetic stimulation (TMS) to characterize causal relationships between regional activity in human brain and motor behavior in neurotypical individuals and those with neurologic conditions. We also utilize MRI to evaluate white and grey matter structure and functional network connectivity. We also utilize robotics to evaluate sensorimotor control and to study sensorimotor learning processes The NPRL and PNEL are composed of ~2000 sq. ft. space, configured as two large brain stimulation and neurophysiology testing laboratories with a smaller connected lab for quiet behavioral testing. The lab also contains a semi-immersive virtual reality system, motor and sensory testing equipment and custom-designed platforms for assessing motor learning and functional ability. The lab is located in the Emory Rehabilitation Hospital on the same floor at the MOTIONS and Neuromechanics laboratories (PIs Dr. Kesar and Dr. Ting). These labs conduct leading edge motion analysis and motor control research in health and disease. The close proximity and shared common interests offer numerous opportunities for collaboration and resource sharing. This research environment provides training opportunities in human subjects research and offers excellent avenues for cross-discipline collaboration. Taken together, the overall objective of my research is to understand the neural mechanisms of sensorimotor control and learning by exploiting advanced multimodal brain imaging approaches towards developing effective rehabilitation strategies that restore function and enhance quality of life for individuals with and without neurologic conditions.	NSNeuroscience - Full Member	Borich	Michael	Motor Systems Rehabilitation Stroke
Steven E Bosinger, PhD (he/him) Full Member - Immunology and Molecular Pathogenesis Full Member - Microbiology and Molecular Genetics steven.bosinger@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Pathology and Laboratory Medicine, School of Medicine Director, Non Human Primate Genomics Core, Vaccine Center, Emory National Primate Research Center Associate Director, Systems Immunology Core, Center for AIDS Research Interferon in HIV pathogenesis and cure; Single-cell RNA sequencing technologies for immunology; Genomics of AIDS-resistant non-human primates	Interferon in HIV pathogenesis and cure; Single-cell RNA sequencing technologies for immunology; Genomics of AIDS-resistant non-human primatesDespite 30 years of intense research, the basis by which HIV causes immunodeficiency is still poorly understood. The interferon system (IFN) was under debate as being a culprit for disease since the 1980's. In early work, we observed that in cynomolgus macaques undergoing pathogenic SIV infection, there was a widespread induction of antiviral genes, specifically, Interferon Stimulated Genes (ISGs), however, despite the impressive breadth of this response, there was no apparent effect on viral load. We next made the observation that African monkey species that do not develop AIDS after SIV infection and rapidly down-regulate their IFN system, whereas humans and AIDS-susceptible monkey species maintain a high level of the IFN system indefinitely. The decreased IFN state observed in non-human primates was also observed in HIV-infected "Viremic Non-Progressors" – patients that remain asymptomatic despite long-term high viral load. Collectively, these studies demonstrated that uncontrolled, persistent IFN production in chronic HIV infection is harmful. A central focus of my laboratory is to develop therapies targeting the IFN response and test them in the SIV/NHP model. Another area of interest of the laboratory is in the development and application of singlecell RNA-Sequencing technology for immunology and vaccinology. B cells comprise a major component of the immune system function primarily by secreting antibodies that bind and neutralize pathogens. Antibodies are produced by the paired expression of a "heavy chain" (IgH) immunoglobulin gene and a "light chain" (IgL) immunoglobulin gene. The unique combination of heavy and light chain genes defines the immunological activity of a B cell and also its identity, also referred to as its clonotype. In order to deal with the near infinite array of pathogenic structures that may face the immune system, B cells exhibit an incredible level of diversity, mostly by recombining multiple gene segments to form functional mature antibody genes. The advent of Next Generation Sequencing and single-cell RNA-Seq transcriptomics now make it possible to obtain the clonotype and transcriptional of each individual cell in a population of antigen-specific B cells. My laboratory developed a computational algorithm that can accurately reconstruct the recombined antibody gene sequences in B cells. This algorithm, BALDR – "BCR Assignment of Lineage using De novo Reconstruction allows us to identify clonotypes and combine them with gene expression data in individual cells. Ongoing research is deploying single-cell RNA-Seq and BALDR analysis in a number of clinical and pre-clinical trial studies for HIV, SIV and HCV, and for antibody cloning. Lastly, a major focus of my laboratory for several years has been in understanding the biology of African natural host primate species and their ability to avoid AIDS. SIV infection of natural hosts, such as sooty mangabeys (Cercocebus atys, SM), is typically non-pathogenic despite high viremia. This is in stark contrast to HIV infection in humans and experimental SIV infection in rhesus macaques (Macaca mulatta, RM) that progress to AIDS unless treated with antiretroviral therapy. Over the past 15 years, the main virological and immunological features of natural SIV infection in SMs have been described in studies that compared and contrasted this infection with the pathogenic infections of HIV and SIV in humans and RMs. These studies have demonstrated that non-pathogenic infection is dependent on maintenance of low levels of immune activation during the chronic phase of the infection, downregulation of the interferon (IFN) system after infection, and the ability to achieve compartmentalization of virus replication that preserves central- and stem-cell memory CD4+ T cells as well as follicular T helper cells. Despite this progress, however, the ultimate molecular mechanisms responsible for the lack of pathogenicity in natural SIV hosts remain poorly defined. Elucidation of AIDS resistance factors in natural host species would provide remarkable insight into the molecular sequelae that drive pathogenesis and provide tractable drug targets for treating the HIV-associated immune dysfunction. In previous studies, we have used high throughput transcriptomics to characterize SIV infection in SMs and other natural hosts. These studies have identified the IFN system as a critical determinant of pathogenesis, and have initiated a series of studies designed to test the clinical utility of targeting the IFN system. With the advent of next-generation sequencing technology, the ability to study non-human primates at a genome-wide level has undergone a remarkable explosion in recent years, and draft assemblies for several species are now available. We sequenced the genome of the Sooty Mangabey and developed a novel pipeline to identify novel factors regulating primate lentiviral pathogenesis. We identified a C-terminal frameshift in the TLR4 gene of SMs that enabled an elongated C-terminus. This frameshift in TLR4 was also found in several other African natural SIV hosts such African green monkeys (AGM), colobus monkeys and drills. Subsequent analyses determined this mutation to render sooty mangabeys less responsive to bacterial LPS, thought to be a major driver of AIDS pathogenesis. In future studies, my laboratory will use 3rd Generation sequencing technology to sequence the genomes of additional African natural host NHPs.	IMPImmunology and Molecular Pathogenesis - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Bosinger	Steven
Jeremy M. Boss, PhD (he/him) Full Member - Genetics and Molecular Biology Full Member - Immunology and Molecular Pathogenesis jmboss@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Microbiology and Immunology, School of Medicine Member, Vaccine Center, Emory National Primate Research Center Associate Dean for Basic Research, Emory University Chair, Department of Microbiology and Immunology, School of Medicine Studies seek to understand the global and specific mechanisms involved in lymphocyte differentiation and gene expression.	Studies seek to understand the global and specific mechanisms involved in lymphocyte differentiation and gene expression.My lab has explored mechanisms by which epigenetics and gene expression control immune responses. Our studies are based in model systems and on human tissues. Studies are split into understanding how single genes are regulated and global mechanisms of immune cell differentiation. For single genes we study the regulation of the major histocompatibility complex class II gene system and its super enhancers, and the regulation of human programmed cell death-1 (PD-1) gene expression in T cells. In each of these gene systems, we have identified complex circuits of transcription factors and epigenetic modulators that orchestrate expression of each of these genes. We are keenly interested in how B cells differentiate into antibody secreting cells. Our work has defined precise mechanisms that tie cell fate decisions and epigenetic processes to cell division that is critical for the process. Our work employs a full set of genomics-based assays. Here, we are also taking advantage of novel CRISPR/Cas9 systems to edit the genomes of cells and derive novel culture systems as well as animal models to dissect the pathways that lead to plasma cells and to memory B cells. We are also focused on understanding what goes wrong with B cell immunity in autoimmune disorders such as systemic lupus erythematosus (SLE), where a subset of B cells are pathogenic. These studies have linked epigenetic mechanisms to the development of disease.	GMBGenetics and Molecular Biology - Full Member IMPImmunology and Molecular Pathogenesis - Full Member	Boss	Jeremy	Biochemistry, Nucleic Acids Genetics, Molecular Immunogenetics Immunology Molecular Biology
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
Nick Boulis, MD (he/him) Full Member - Neuroscience nboulis@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Neurosurgery, School of Medicine Strategies for neuroprotection and control of neural activity and synaptic transmission through gene delivery.	Strategies for neuroprotection and control of neural activity and synaptic transmission through gene delivery.The Boulis laboratory was launched over my first two years at the Cleveland Clinic Foundation (CCF). While my K award was funded on arrival to the CCF, funding began at the beginning of my second year and extended to year six, when I departed for Emory University. I received grants from a variety of foundations, to supplement my start-up package and K award. Despite having a nominal mentor, I was independent from my arrival, receiving my true mentorship from my prior mentors at Harvard and Michigan. During this time, I developed the concept proposed in my K Award, that gene delivery could be used to control synaptic and neural activity. First, I published manuscripts on the application of the gene for glutamate decarboxylase to upregulate the production of the neurotransmitter, GABA, to inhibit focal neural targets. Next, I explored the application of genes encoding the enzymatic fragments of Clostridial Neurotoxins to inhibit synaptic vesicle release as a means to inhibit synaptic transmission within spinal cord and brain targets. My team went on to publish applications of this gene-based neuromodulation approach to epilepsy and anxiety. The earlier work in motor neuron neuron gene delivery was extended at the CCF. After recognizing that retrograde transport of the wildtype non-neurotropic vector capsids was too weak to deliver sufficient genes for therapy in larger mammals, I embarked on an effort to alter the coats of viruses to enhance their uptake into the nervous system. This led to the discovery of novel peptides that bind to axon terminals and undergo enhanced uptake into the nervous system. We subsequently demonstrated that this peptide could be used to enhance the uptake of AAV vectors, while lyssavirus glycoproteins could be used to enhance the uptake of lentiviral vectors. My work on spinal cord growth factor gene therapy in ALS, led to a collaboration with Clive Svendsen PhD, who was working to develop an ex-vivo gene therapy approach to ALS that utilized lentiviral vectors to engineer fetal stem cells to secrete the growth factor GDNF for use in spinal cord stem cell transplantation. To make this approach practical, I embarked on the development of devices and techniques for safe and accurate stem cell transplantation into the spinal cord. These devices were tested and refined in pigs, leading to the patents for the Floating Spinal Cannula and Stabilized Spinal Cord Instrumentation & Therapeutics Delivery Platform. This program culminated in the first three spinal cord stem cell transplantation programs including: NeuralStem Phase 1, NeuralStem Phase 2, The Italian Phase 1 trial Vescovi/Mazzini, and the CIRM funded trial by Dr Svendsen at Cedar Sinai. Since my arrival to Emory in 2007, I have continued to work on gene and cell therapies for neurodegenerative disease in both the laboratory and clinical trials. I built on my success as the site-PI of Ceregene's first Phase 2 CERE120 PD trial, launching sites for the subsequent CERE110 stereotactic gene therapy trial to treat Alzheimer's Disease, and the CERE120 stereotactic gene therapy trial to treat PD. As a consultant for Ceregene, I became the CERE120 trial's lead surgeon, reviewing the stereotactic planning for all sites in the trial. In addition, the pig work begun at the CCF was brought to human application in the first human spinal cord stem cell transplantation, performed at Emory in 2010. Because of my patents, I was deemed conflicted by the Emory COI Committee. For this reason, I asked Jon Glass MD/PhD to be the Principle Investigator on the trial. However, I remained a Co-PI on the RO1 grant awarded to fund the Phase 2 trial. These human trials remain the standard for intraparenchymal spinal cord therapeutics. Additionally, I acted as an advisor to the Italian and Cedars teams, teaching the surgeons to perform the surgeries on pigs, and flying to Italy to proctor the initial lumbar and cervical operations. I also trained the surgeons at the University of Michigan and Massachusetts General Hospital for the multicenter Phase 2 NeuralStem Trial. Finally, I trained the surgeons at the University of California San Diego to use my devices for the NeuralStem Chronic Spinal Cord Injury trial. As the laboratory grew, I divided the group into a large animal/late stage translational team to do IND enabling studies for academic and biotech collaborators and translational work that required large scale anatomy or the immune system of higher mammals, and a proof-of-principle team that does molecular biology, vector construction, and tests therapeutics in cell culture and rodent transgenic models. The small animal team has continued to work on means for motor neuron gene delivery and gene-based neuromodulation. We discovered that intrathecal injections of new AAV serotypes could efficiently deliver genes to motor neurons diffusely throughout the spinal cord. We later published intracerebroventricular delivery as a means for widespread gene delivery to the brain. CSF injection of AAV6 and 9, has become one of the most widely employed means for gene delivery in the nervous system for experimental and translational studies. It will be employed for the trial to treat Cerebral Mucopolysaccharidosis (RegenXBio), and forms the basis for the ongoing NINDS funded Giant Axonal Neuropathy trial. The small animal team has explored a variety of other therapeutic approaches and animal models for motor neuron disease. This large animal team was awarded a CDMRP grant from the DOD, to overcome critical practical barriers in spinal cord transplantation, including tracking the delivery and survival of cells in the cord, and the tolerance of the cord for multiple injections and volume of the injected therapeutic. The team is currently supporting two new spinal cord surgical gene therapy programs for ALS expected to file IND's in 2019 (Above and Beyond, and Voyager Therapeutics). Both of these trials will use my devices and techniques for spinal cord surgery. In addition, the team is supporting the development of stereotactic cerebellar gene therapy for Freidrich's Ataxia (PTC). The team is also supporting large animal experiments that extend foundational work by the small animal team. For example, the team demonstrated that AAV9 CSF mediated gene delivery can be scaled up for both ventricular and intrathecal injection. Currently the team is studying augmented collagen nanofibers as grafts for enhanced nerve repair. This work is a collaboration with GA Tech, funded by an RO1 for which I am Co-PI. In addition, we have developed a pro-oncogenic lentiviral vector based pig model for Glioblastoma Multiforme. We anticipate using this model to aid in the development of a variety of surgical, stem cell, exosome, and immunotherapeutic approaches to this brain tumor. In the last three years, I have become increasingly convinced that the creation of actual therapies requires the creation of companies. To this end, I have founded two biotechs. The first, Coda, received series A funding for $10 Million in 2017 and extended series A for another $24 million. The company controls the intellectual property for chemogenetics, which employs the delivery of the genes for mutant neurotransmitter receptors engineered to respond to small molecule ligands, but not their native neurotransmitters. These ligand drugs are selected for their capacity to enter the CNS and PNS without side effects. This approach will be a disruptive technology that we expect to replace the implantation of electrodes as the dominant clinical approach to therapeutic neuromodulation over the next 20 years. I intend to continue continue my work in gene-based neuromoduation through collaboration with CODA. My second company, Above and Beyond (A&B) was founded in 2014, to develop novel ALS Therapies at an accelerated pace. A&B was angel investor funded for $15 Million Dollars to date, with an open-ended commitment for further funding from the sponsor. A&B initially launched 6 translational programs, subjecting them to rigorous accelerated therapeutic development. Of these, two became human therapies. The first involves the use of intrathecal pumps to deliver the drug Riluzole, which taken orally prolongs survival by 3 months in ALS patients. Our method increases the spinal cord concentration by an order of magnitude. This therapy has now received approval for a Phase 1 Clinical Trial in Australia. Dr. Boulis is working hard to raise the money to open the trial in 2025. The second program utilized robotic high throughput screening of patient iPS derived motor neurons to look for phenotypic correction using a library of FDA approved compounds. This precision medicine approach identified commercially available drugs that appeared to have therapeutic effects on a patients own motor neurons. Currently, the laboratory has ongoing projects in glioma modeling in rodents and pigs in both the spinal cord and brain. We have used lentiviral vectors carrying known oncogenes and shRNA for tumor suppressors to create both high and low grade gliomas. Ongoing projects are working to develop convection enhanced chemotherapy delivery to spinal cord glioma as a clinical trial for these patients. We are attempting to create low grade glioma (already identified in pig spinal cord) in the pig brain. These models are being applied in collaboration with industry to test new therapies. In addition, we continue to work toward chemogenetic approaches for spasticity in the laboratory, with work to refine a rodent spasticity model and testing of inhibitory chemogenetic viral vectors to inhibit hindlimb motor function through spinal cord gene delivery. In addition, we are working on the use of stem cell derived motor neurons to create new neuromuscular junctions in denervated endplates in both pigs and rodents. This approach can be used to create neuronal relays for enhanced peripheral nerve repair, and to prevent atrophy. Finally, we have ongoing collaboration with the laboratory Younan Xia PhD and GA Tech on the application of augmented engineered collagen grafts for nerve repair.	NSNeuroscience - Full Member	Boulis	Nick
Sarah Bowden, PhD Adjunct Member - Population Biology, Ecology, and Evolution sebowdenphd@gmail.com \| Faculty Profile Data Scientist Contractor, Office of Innovation, Development, Evaluation, and Analytics, Division of Global Migration and Quarantine, Centers for Disease Control and Prevention I use machine learning, mathematical and statistical modeling, and spatial analysis to address questions at the interface of ecology and public health.	I use machine learning, mathematical and statistical modeling, and spatial analysis to address questions at the interface of ecology and public health.My research uses quantitative techniques, such as machine learning, mathematical and statistical modeling, and spatial analysis, to address questions at the interface of ecology and public health. My interests lie mostly within the realm of vector-borne and zoonotic diseases. I am also interested in how data science can be applied within ecology and public health, as well as which analytic tools and platforms can best support reproducibility and open science research. Some important themes and questions of my research include: (1) How do trans-boundary ecosystem effects alter infectious disease transmission? Some species, such as mosquitoes, undergo an ontogenetic niche shift where they spend part of their life cycle (egg, larval, and pupal stages) in the aquatic environment and the remainder of their life cycle (adult stage) in the terrestrial environment. This niche shift makes it possible for interactions during the aquatic life stages (e.g., biotic interactions like interspecific competition and abiotic interactions like temperature) to impact population dynamics of the terrestrial life stage -- a phenomenon known as trans-boundary ecosystem effects. The ability of mosquitoes to produce such effects is of interest to both ecologists and epidemiologists because many mosquito species serve as disease vectors during the adult life stage. My research in this area includes laboratory microcosm experiments to measure the effect of interspecific competition on the vital rates of three important vector mosquito species, which showed a competitive hierarchy among these species. I have also studied the sensitivity of these vital rates to temperature and interspecific competition simultaneously, showing that a vector's thermal niche can be altered by competitive interactions in the larval stage. (2) Which locations and/or animals are likely to give rise to infectious disease spillover? The current approach to disease outbreaks is fully reactive, where a response is mounted only after an outbreak is detected. Using machine learning algorithms borrowed from the field of computer science, I am interested in how we can move toward a proactive approach to disease outbreaks by determine where and from which species outbreaks are most likely to occur. I have collaborated on research in this area that includes implementing a supervised learning algorithm to determine which rodent species are most likely to be undiscovered or future reservoirs of zoonotic pathogens, as well as which bat species are likely to be undiscovered or future reservoirs of filoviruses, based on trait similarity to known reservoir species. My postdoctoral research took this methodology and added a temporal component where I attempted to predict the probability that a county would see human West Nile virus cases in a given year based on past land cover changes in that county. In my research at the CDC, I am also implementing these algorithms on large socio-demographic and public health datasets. (3) How can scientists make our research more open and reproducible? As a data scientist, I spend a lot of time thinking, learning, and teaching others about data, quantitative methods, and how to combine them to get interpretable results. New methods for analyzing data are constantly being developed, so keep up to date on how to implement new methodologies and sharing that information with my colleagues is very important. Finally, joining data with an appropriate method to extract and communicate new insights is what research is all about. I do this using code in the R language and RStudio development environment. While I have been using R for over a decade, I thoroughly enjoy learning new things on a daily basis, as well as creating presentations and workshops to share with scientists at all career stages to help them optimize the analysis, visualization, and communication of their research.	PBEEPopulation Biology, Ecology, and Evolution - Adjunct Member	Bowden	Sarah
Doug Bremner, MD Full Member - Neuroscience jdbremn@emory.edu \| Faculty Profile Professor, Department of Psychiatry and Behavioral Sciences, School of Medicine Professor, Department of Radiology and Imaging Sciences, School of Medicine Neuroimaging in PTSD, anxiety and depression; neuroreceptor imaging; PET; MRI, cardiac imaging, mechanisms of stress and depression in cardiovascular disease	Neuroimaging in PTSD, anxiety and depression; neuroreceptor imaging; PET; MRI, cardiac imaging, mechanisms of stress and depression in cardiovascular diseaseOur work followed up animal studies showing that stress is associated with deficits in memory and alterations in morphology of the hippocampus, a brain area which plays a critical role in learning and memory. In the first neuroimaging study ever performed in PTSD, we used magnetic resonance imaging (MRI) to measure volume of the hippocampus in combat veterans with PTSD and healthy controls, and found an 8% reduction of volume of the hippocampus. We also found significantdeficits in hippocampal-based memory in PTSD. These findings were replicated in childhood abuse-related PTSD by our group, and have since been replicated by five independent studiesat various sites. We also demonstrated a failure of activation of the hippocampus during memory tasks as measured with positron emission tomography (PET) in PTSD. Other studies developed methods for quantitation of neuroreceptors, and showed a decrease in frontal lobe binding of benzodiazepine receptors in the prefrontal cortex in PTSD and panic disorder. Functional PET imaging studies showed deficits in prefrontal cortical activity during stimulation of PTSD symptoms or induction of depressive relapse in depression. Current studies are developing neuroreceptor compounds for assessment of serotonin and dopamine receptors in human brain for application to anxiety and depression, and assessing mechanisms by which stress and depression mediate increased mortality in patients with heart disease.	NSNeuroscience - Full Member	Bremner	Doug	Neuroscience Psychiatry
Yana Bromberg, PhD Full Member - Genetics and Molecular Biology Full Member - Population Biology, Ecology, and Evolution yana.bromberg@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Biology, Emory College of Arts and Sciences The lab is currently working on implementing machine learning-based models for understanding of what protein function aspects (if any) are captured by large language models, whether metagenome functionality can be inferred from sequencing reads, and how genome variants impact molecular function in association with disease.	The lab is currently working on implementing machine learning-based models for understanding of what protein function aspects (if any) are captured by large language models, whether metagenome functionality can be inferred from sequencing reads, and how genome variants impact molecular function in association with disease.The primary focus of the research in my lab can be summarized two words – molecular function. Where does the molecular functional machinery of life come from? Why and how does it run? Is there a minimum set of the functional gears that represents a viable entity? Biological machinery is a complex system of many molecular interactions, both within and outside a single cell. I believe that the DNA blueprint of this machinery, the understanding of which is currently being improved with increasingly high-throughput techniques, holds many of the answers to our questions. Thus, my long-term goal is to understand how biological functionality is encoded in genomic data, whether by a single gene, a genome, a metagenome, or some combination of these. To this end, my lab develops computational, machine learning, and network- based methods for annotation and analysis of molecular functions. My research aims to explore the origins and details of protein function and to make sense of the available genome and metagenome data. Specifically, we are: (1) Correlating genome variation to phenotype, (2) Identifying the specifics of sequence-encoded molecular functions, and (3) Elucidating complex microbial community (and host) interactions. Functional effects of genomic variants. Nearly 20 years ago, we developed SNAP, a neural network- based method for predicting non-synonymous variant functional effects. Since then, despite the rapid proliferation of variant effect prediction tools, there remains a crucial gap in our understanding of variants within the molecular function context. Pioneering positive-unlabeled learning approaches, we propose to improve existing tools by extracting significantly larger variant effect training sets directly from genome data, with potential implications for disease diagnostics and treatment. Recent advances in protein and DNA language models (LLMs) also provide an unsupervised manner for improving our prediction techniques. Whole-genome variation in disease. We've discovered that common non-synonymous variants, often dismissed as irrelevant, actually often carry more functional effects than rare variants. Based on this inference, we've developed AVA,Dx, an SVM-based model that maps whole-genome variation to functional changes associated with diseases like Crohn's Disease, Tourette Syndrome, and Chronic Obstructive Pulmonary Disease. While we are investigating other applications and improvements of AVA,Dx, we're also actively exploring other methods for identifying the molecular function failures that underlie various disorders. Exploring unknown functionality of microbes and microbiomes. Our lab has developed network- based classifiers, such as fusionDB, pEffect, mi-faser, and LookingGlass to identify microbial bacterial functionality. These tools have been instrumental in uncovering microbiome functional signatures in diverse environmental conditions. Currently, we're working on expanding these tools to annotate microbiome functions directly from reads and exploring emergent bacterial functional abilities encoded in metagenomic data. Furthermore, we also recently proposed a novel way of identifying microbial proteins of similar function, without defining the function itself. This approach opens new avenues for exploration of bacterial functionality, particularly as related to environmental preferences, microbial evolution, and microbe-host interactions. Evolution of function at the origins of life. Our expertise lies in studying protein evolutionary timelines, common origins of transition metal-binding structures, and the ancient evolution of peptides. Tools like sahle and mebipred have been developed for structural analysis, identifying protein structural repeats, and exploring the history of life on Earth and potentially other planets. We are currently building tools that would allow discovery of previously unseen proteins, likely deep in the oceanic metagenomes, carrying out well known functions. These functions, we propose, lie at the origins of life on this planet, and possibly others.	GMBGenetics and Molecular Biology - Full Member PBEEPopulation Biology, Ecology, and Evolution - Full Member	Bromberg	Yana
Lou Ann Brown, PhD (she/her) Full Member - Molecular and Systems Pharmacology lbrow03@emory.edu \| Faculty Profile Professor, Division of Neonatology, Department of Pediatrics, School of Medicine Co-Director, Alcohol and Lung Biology Center, School of Medicine Director, Postdoctoral Office, School of Medicine Impact of chronic oxidative stress (adult and fetal) on pulmonary cellular phenotype and function.	Impact of chronic oxidative stress (adult and fetal) on pulmonary cellular phenotype and function.Recently, a history of chronic alcohol abuse has been shown to be the first co-morbid variable that significantly increases the incidence and severity of Acute Respiratory Distress Syndrome (ARDS). Despite modest decreases in the plasma glutathione of non-cirrhotic patients, decreased availability for pulmonary transport resulted in an 80% decrease in glutathione in the fluid lining the alveolar surface. In an ethanol-fed rat model, chronic ethanol ingestion increased susceptibility sepsis-induced acute lung injury. Although many different cell types are likely altered by chronic ethanol exposure, we initially focused on the type II cell because of the many different roles this cell type plays in pulmonary function and repair. The glutathione pool in type II cells was decreased by 60% after 16 weeks of ethanol ingestion. Although the cytosolic glutathione pool was decreased during ethanol ingestion, the mitochondrial glutathione pool was dramatically decreased as a result of ethanol inhibition of mitochondrial glutathione uptake. Decreased mitochondrial glutathione then resulted in increased mitochondrial production of reactive oxygen species, particularly when sepsis was superimposed on ethanol ingestion. Increased mitochondrial reactive oxygen species generation then resulted in mitochondrial dysfunction, sensitization of the cell to the cytotoxins up regulated during sepsis and increased apoptosis and necrosis. The role of mitochondrial glutathione in this process was supported by the differential capacities of glutathione precursors to restore the mitochondrial glutathione pool and decrease the risk of sepsis-induced reactive oxygen species generation and type II cell apoptosis and necrosis. The alteration of mitochondrial ATP generation by chronic ethanol exposure is currently under intense study. Another hallmark of alcohol abuse is a high risk of respiratory infections. Since alcohol depletes the glutathione pool of the alveolar epithelial lining fluid, we proposed a similar depletion of the glutathione pool in the alveolar macrophages bathed by this pool. In alveolar macrophages from ethanol mice and clinical samples, we demonstrated glutathione depletion which is an underlying mechanism for impaired Nrf2 signaling, chronic oxidant stress and immune suppression. Glutathione repletion restored the Nrf2 and immune responses; thereby restoring the capacity for bacterial and viral clearance. Clinical trials with glutathione precursors are underway to determine if the immune responses of alveolar macrophages are restored. Subjects that are HIV+ are also at high risk for pneumonia and TB, chronic oxidant stress and immune suppression of alveolar macrophages. Similar clinical trials with glutathione precursors are underway for HIV+ subjects as a therapeutic strategy to decrease the risk of respiratory infections. These studies have also been extended to determine if chronic alcohol exposure in utero increases the risk of acute lung injury when superimposed on a second insult such as sepsis, mechanical ventilation or oxygen therapy. Using a preterm guinea pig model and a fetal mouse model, we demonstrated that fetal ethanol exposure decreased glutathione availability in the fluid lining the lung and alveolar macrophages. Such dramatic decreases in these important glutathione pools were associated with increased risk of pulmonary oxidative injury during oxygen therapy. In addition to altered glutathione homeostasis, chronic ethanol exposure in utero resulted in immune suppression and increased respiratory infections in experimental models of bacterial or viral pneumonia. In a recent clinical study of premature low birthweight newborns, maternal alcohol ingestion of at least 7 drinks per week prior to pregnancy or during the first two trimesters increased the risk of sepsis within the first week of life. Fetal alcohol exposure also increased the risk of all poor outcomes associated with premature delivery of a very low birthweight newborn.	MSPMolecular and Systems Pharmacology - Full Member	Brown	Lou Ann	AIDS / HIV Alcohol / Alcoholism Antioxidants Asthma Neonatal Pulmonary Medicine Toxicology
Zachary Buchwald, MD, PhD Full Member - Cancer Biology zachary.scott.buchwald@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Radiation Oncology, School of Medicine We study ways to enhance the anti-tumor immune response, checkpoint blockade and other novel immuno-modulatory approaches.	We study ways to enhance the anti-tumor immune response, checkpoint blockade and other novel immuno-modulatory approaches.The overarching theme of my translational research is understanding and maximizing the radiation induced anti- tumor immune response to control and eventually cure locally advanced and metastatic cutaneous malignancies. During my post-doctoral fellowship, I confirmed that radiation can act as an in-situ vaccine and stimulate an anti- tumor immune response at a distant unirradiated site (abscopal effect). I went on to show that radiation stimulates a subset of T-cells (stem-like CD8+ T-cells) important for the anti-PD-1 response in the tumor-draining lymph node (TDLN). Disruption of the TDLN impairs the radiation stimulated anti-tumor immune response. These observations form a cornerstone of one of the three main areas of research in my lab: (1) Determining the importance of TDLN stem-like T-cells in the abscopal effect; (2) Determining the impact of dexamethasone on the abscopal response; (3) Interrogating the effect of pre-operative stereotactic radiosurgery on the immune niche in brain metastases. Project (1) is currently the focus of two submitted/pending grants, a K08 and a Melanoma Research Alliance YIA with the initial data published in Journal for ImmunoTherapy of Cancer in 2020. It is known that prognosis is poor for patients diagnosed with locally advanced melanoma. Survival outcomes are improved with checkpoint blockade in the neoadjuvant, adjuvant and unresectable setting. Dual checkpoint blockade further enhances outcomes, but often at the cost of significant clinical toxicity. However, despite this progress, for the more than 40% of patients who do not respond, outcomes remain dismal. Radiotherapy (RT) is used for locally advanced melanoma in the adjuvant setting to improve local control. Interestingly, RT is also now known to occasionally have distant anti-tumor effects outside the radiation field. This process is known as the abscopal effect. RT mediates this, in part, by acting as in-situ vaccine liberating tumor antigens and generating an inflammatory milieu that enhances the CD8+ T-cell anti-tumor response. Based on pre-clinical and clinical studies, this effect can synergize with single agent checkpoint blockade with limited toxicity. Combined RT and αPD-1 treatment has now shown clinical potential, however, the abscopal effect still occurs in only a minority of patients and there remains an urgent need to improve response rates. Our lab has demonstrated that RT may stimulated the abscopal effect by activating a T-cell subset in the tumor-draining lymph node (TDLN). To further evaluate this, we are developing a transgenic mouse model to specifically deplete this T-cell subset to determine the role of tumor resident and TDLN stem-like CD8+ T-cells in the abscopal effect. We also have an on-going collaboration with Dr. Susan Thomas at Georgia tech using nanoparticles to evaluate whether Tumor-RT combined with αPD- 1 and adjuvanted nanoparticle targeting of the TDLN leads to abscopal enhancement. Finally, we have a pilot clinical trial in development supported by the Melanoma Working Group to determine whether neoadjuvant Tumor-RT with αPD-1 is associated with increased stem-like CD8+ T-cell infiltration in locally advanced melanoma. From this study both primary tumor and TDLN will be collected for RNA seq and flow cytometric analysis. Project (2) progress is reflected by a manuscript nearing submission with a grant submission to follow. Despite less toxicity with combined RT and αPD-1 than dual checkpoint blockade, immune related adverse events (IRAE) can still develop. Corticosteroids, specifically glucocorticoids, are a potent immunosuppressant used to treat IRAE, pre-existing auto-immune disease, and symptomatic cerebral edema secondary to brain metastases. In current clinical practice, when a patient requires corticosteroids, αPD-1 therapy is either stopped or not initiated due to a presumed counteraction of αPD-1's immune-stimulation. This delay or cessation in αPD-1 treatment worsens outcomes due to cancer progression. Therefore, we are investigating the impact of glucocorticoids on both the αPD-1 and the RT stimulated anti-tumor T-cell response. We have preliminary data demonstrating preferential impact of dexamethasone, a potent glucocorticoid, on specific T-cell subsets. In our model system, dexamethasone actually suppresses tumor growth and enhances the abscopal response by both tumor direct and indirect effects on regulatory T-cells. We have developed both a glucocorticoid receptor KO cell line and performed CD4 T-cell depletion experiments to further isolate the direct effects of dexamethasone on the CD8 T-cell response. Project (3) is currently funded by an institutional K12 award. A manuscript is planned for submission in December 2020. It is being executed in collaboration with Dr. Haydn Kissick. The Kissick lab previously demonstrated that the density of an immune niche of stem-like T-cells and antigen presenting cells in renal cell carcinoma is prognostic for longer progression free survival. We are now investigating this niche in brain metastases and determining whether (a) it is prognostic for outcomes and (b) whether radiation to brain metastases influences the intra-tumoral immunologic architecture. This study includes both 7-color multiparametric immunofluorescence which was optimized and is being performed in my lab of FFPE brain metastases that were either resected up-front or pre-treated with radiation and then resected. . It also includes a prospective clinical trial undergoing final IRB review which will evaluate the impact of dexamethasone dose and radiation on this immunologic architecture and T-cell phenotype in brain metastases by flow and RNA sequencing.	CBCancer Biology - Full Member	Buchwald	Zachary
Cathrin M. Buetefisch, MD, PhD Affiliate Member - Neuroscience cathrin.buetefisch@emory.edu \| Faculty Profile Professor, Department of Neurology, School of Medicine Mechanisms and modulation of motor system plasticity with the clinical translational aspect of formulating treatment strategies.	Mechanisms and modulation of motor system plasticity with the clinical translational aspect of formulating treatment strategies. Motor cortex reorganization plays a major role in the adult healthy brain and in many neurological diseases affecting the motor performance such as post-stroke recovery or movement disorders. It is currently a is primary therapeutic target for people with neurological diseases affecting the the motor cortex such as rehabilitation of impaired hand function after stroke, people with writer's cramp or Parkinsons disease. Mechanisms that modify synaptic efficacy, such as long-term potentiation (LTP) are thought to be involved in this process. In my lab, we study mechanisms and means to modulate motor cortex reorganization in the intact and injured brain using neuroimaging techniques, such as functional and structural MRI, and electrophysiological techniques such as transcranial magnetic stimulation (TMS) and pharmaceutical interventions.	NSNeuroscience - Affiliate Member	Buetefisch	Cathrin	Dystonia / Tremor Movement Disorders Neurology Neurophysiology Rehabilitation Stroke
Kevin Bunting, PhD Full Member - Cancer Biology kevin.bunting@emory.edu \| Faculty Profile Professor, Division of Hematology/Oncology, Department of Pediatrics, School of Medicine Cytokine signaling in normal and leukemic hematopoiesis.	Cytokine signaling in normal and leukemic hematopoiesis.Dr. Bunting's research is focused on understanding the biology of the latent transcription factor STAT5, in particular its roles in normal hematopoietic stem cell function and its aberrant activation associated with a variety of hematologic malignancies. Activation of STAT5 by phosphorylation is required at tightly regulated levels for normal hematopoiesis but its persistent activation is prevalent in adult and pediatric leukemias. A major focus of the Bunting lab is to identify key STAT5 downstream target genes associated with both normal and leukemic hematopoietic cell function and to utilize this knowledge to develop novel approaches to manipulate STAT5 activity in a therapeutic setting. In leukemia therapy, the goal is to disengage leukemic cell survival and to facilitate leukemia cell sensitivity in combination with other targeted agents. In hematopoietic stem cell transplantation, the goal is to develop innovative forms of conditioning based on STAT5 signaling inhibition. Dr. Bunting also studies the Grb2-associated binding (Gab) family of adapter proteins and their role in PI3K-AKT-mTOR activation in hematopoietic and immune cell biology. The Gab family of scaffolding adapter proteins are synergistic with STAT5 in controlling hematopoietic stem cell self-renewal and leukemogenesis and thus represent an attractive cooperative signaling node in which to focus on therapeutics targeting both STAT5 and AKT mediated signals.	CBCancer Biology - Full Member	Bunting	Kevin
Vince D. Calhoun, PhD Full Member - Neuroscience vince.calhoun@emory.edu \| Faculty Profile \| Lab Website Professor, Wallace H. Coulter Department of Biomedical Engineering, Emory University & Georgia Institute of Technology Distinguished University Professor, Psychology, Georgia State University Founding Director, Center for Translational Research in Neuroimaging and Data Science (TReNDS) Professor, Depts. of Neurology, Psychiatry, and Pediatrics Professor, School of Electrical and Computer Engineering, College of Engineering, Georgia Institute of Technology Develops methods to analyze complex multimodal neuroimaging data, including MRI, EEG, MEG, as well as genomics, and DNA methylation, with an emphasize on human neuroimaging, biomarker development to study normative development and aging, mental illness, and neurological disease.	Develops methods to analyze complex multimodal neuroimaging data, including MRI, EEG, MEG, as well as genomics, and DNA methylation, with an emphasize on human neuroimaging, biomarker development to study normative development and aging, mental illness, and neurological disease.In my lab we have been focused on ways to apply engineering principles to extract knowledge from brain imaging data through developing and optimizing methods and software to study human brain imaging with particular focus on the study of the disordered brain. This focus manifests in contributions to multiple areas of science including data-driven medical imaging analysis, functional connectivity, data fusion of multimodal imaging data, imaging genetics, and neuroinformatics among others. To list just a few of the contributions I am proud of: • Established a 'first of its kind' multi-institutional neuroimaging and data science center (TReNDS) • Among the first to develop centralized data sharing and neuroinformatics infrastructure. This include implementation of fully automated 'cloud-based' neuroimaging facility at the center for advanced brain imaging (CABI; http://cabi.gsu.edu) which I direct, fueled by COINS (http://coins.trendscenter.org) and BrainForge (https://brainforge.trendscenter.org/) automated analysis tools developed at GSU. • Published over 1000 peer-reviewed journal papers published, and over 1000 conference papers. • Developed a brain network estimation approach (group ICA), which has since become a widely used tool in the field and is a large part of various national and international projects including the NIH funded human connectome project. Our toolbox, GIFT, implements many dozens of approaches and algorithms and is among the most widely used in the field) • One of the first applications of a multivariate network approach to study mental illness including schizophrenia and bipolar disorder. • First to develop joint blind source separation approaches to identify multimodal markers of brain disorders (including multimodal imaging and imaging- genomics) • An early strong advocate for single-subject classification approaches including one of the first classification studies in schizophrenia, multiple review articles, and a highly cited special issue in neuroimage on the topic. • First to develop techniques to study whole brain dynamic connectivity (his introduction of techniques for this essentially launched a whole new direction in the field and was highlighted by the National Institutes of Mental Health Director in the 'best of the year' list) • Introduced a family of multivariate analyses of imaging (epi)genomic data and identified some key links between structural/functional brain networks and genomic patterns. • One of the first to introduce and validate deep learning approaches for neuroimaging, including a high turnout symposium and educational session at the OHBM meeting on the topic. • Developed methods to study spatial dynamics (spatially varying nodes) within network/multivariate modeling approaches. Prior to this point spatial dynamics was essentially ignored. • Broad and deep application of the above approaches to many areas including mental and neurological disorders, normative development, healthy aging, and more. • First to introduce algorithms and to develop tools (e.g., COINSTAC, http:// https://coinstac.trendscenter.org/) for federated learning from large scale brain imaging. • Prolific software developer including the widely used GIFT (group ICA of fMRI and EEG) & FIT (data fusion) software packages, the COINS neuroinformatics tools in use by dozens of imaging facilities around the world, the COINSTAC federated analysis platform, and the BrainForge automated neuroimaging portal (developed at GSU). • Discovery of deficiencies in communication efficiency between the 'default mode network' in the brain and other networks in patients with schizophrenia. Follow up studies are evaluating cross- domain entropy approaches to try to improve upon existing models of schizophrenia. • Active in tech transfer work, including multiple patents and small business grants for predicting medication class response to antidepressants or mood stabilizers in emerging youth and for scaling up of cloud-based neuroinformatics tools for data capture, management, and sharing. • First to show deep learning methods can outperform standard machine learning in terms of their prediction accuracy, while also be used in a way that can provide interpretable output, moving beyond black box modeling approach.	NSNeuroscience - Full Member	Calhoun	Vince
John W. Calvert, PhD Full Member - Molecular and Systems Pharmacology jcalver@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Division of Cardiothoracic Surgery, Department of Surgery, School of Medicine DGS (Y3-), MSP Cardioprotective signaling mechanisms.	Cardioprotective signaling mechanisms.The central theme of my research program is to define cardiac signaling events initiated in response injury. Specifically, I am interested in understanding how cardiomyocytes maintain homeostasis during period of stress through the activation or induction of protective signaling cascades. As such, my lab focuses on the molecular and cellular events initiated within hours to days following the onset of myocardial infarction. Our hope is that the knowledge gained from our studies will identify novel therapeutic targets that will lead to new treatment options aimed at reducing the risk of cardiovascular disease or improve the quality of life of patients whom have experienced a heart attack or have heart failure. Over the past several years, studies detailing our findings have been published in high impact journals including Circulation, Circulation Research, Diabetes, Atherosclerosis, Thrombosis, and Vascular Biology, Circulation Heart Failure, and Cell.	MSPMolecular and Systems Pharmacology - Full Member	Calvert	John	Cardiovascular Disease Diabetes
Tamara Caspary, PhD (she/her) Full Member - Genetics and Molecular Biology Full Member - Neuroscience tcaspar@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Human Genetics, School of Medicine Mammalian genetics, cilia-dependent signaling.	Mammalian genetics, cilia-dependent signaling.Our work centers around the role of the primary cilium, the slender protrusion found on virtually all eukaryotic cells, including neurons and glia. Through mouse genetic screens, we have identified several genes enriched in cilia and mutated in patients with ciliopathies. We use a combination of genetic, molecular and cell biological approaches to dissect apart the mechanism through which signaling pathways are coupled to the primary cilium. Through these approaches we are figuring out fundamentally novel mechanisms important to processes from neural development, kidney cytogenesis and obesity.	GMBGenetics and Molecular Biology - Full Member NSNeuroscience - Full Member	Caspary	Tamara	Biology, Cellular Biology, Developmental Biology, Molecular Birth / Congenital Defects Cell Biology Cloning of Genes Disease Model Genetics, Molecular Molecular Biology Neuroscience Spinal Disorders
Mike Caudle, PhD (he/him) Full Member - Neuroscience william.m.caudle@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Environmental Health, Rollins School of Public Health Director of Graduate Studies, Environmental Health Sciences, Department of Environmental Health, Rollins School of Public Health Investigating the role of environmental toxicants on the development of neurological disorders. Lab website: caudlelabemory.weebly.com	Investigating the role of environmental toxicants on the development of neurological disorders. Lab website: caudlelabemory.weebly.comMy work is focused on examining the effect of exposure to environmental toxicants on the development of neurological disorders. The over arching goal of our research is to elaborate our current knowledge of the neurotoxic effects of the environment and further elucidate the influence of the environment on the etiopathogenesis of neurodegenerative and neurobehavioral disorders. To accomplish these goals we utilize progressive in vitro and in vivo model systems and couple these techniques with our expertise in cellular and molecular neuroscience, neuropathology, and toxicology. Additionally, we also draw upon our collaborations with epidemiologists and exposure scientists in order to establish a comprehensive understanding and human relevance of our effects. A large part of our research has been specifically directed towards understanding the effects of flame retardant and pesticide compounds on the central nervous system and their impact risk for development of neurological disease. Our current work elaborates upon these findings by investigating the specific cellular mechanisms responsible for these deficits as well as evaluating the neurotoxic potential of other environmental toxicants currently being used, for which little or no neurotoxicological information is available.	NSNeuroscience - Full Member	Caudle	Mike	Autism Neurodegenerative Disease Neuroscience Parkinson's Disease
Luisa Cervantes-Barragan, PhD (she/her) Full Member - Immunology and Molecular Pathogenesis Full Member - Microbiology and Molecular Genetics lcervantes@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Microbiology and Immunology, School of Medicine The gastrointestinal tract is one of the primary sites of exposure to pathogens, but it is also the niche of the largest collection of commensal microbes in the body. Studies in recent years started to reveal the extensive influence microbiota and intestinal immune system have on each other and how this constant interplay impacts human health. The study of this very dynamic interaction is the main focus of our lab.	The gastrointestinal tract is one of the primary sites of exposure to pathogens, but it is also the niche of the largest collection of commensal microbes in the body. Studies in recent years started to reveal the extensive influence microbiota and intestinal immune system have on each other and how this constant interplay impacts human health. The study of this very dynamic interaction is the main focus of our lab.Mucosal immune system-microbiota interactions Cervantes Lab, Department of Microbiology and Immunology. The gastrointestinal tract is one of the primary sites of exposure to pathogens, but it is also the niche of the largest collection of commensal microbes in the body. Studies in the recent years started to reveal the extensive influence that microbiota and intestinal immune system have on each other and how this constant interplay impacts immune responses to pathogens and the development of chronic inflammation. The study of this very dynamic interaction is the main focus of our lab. Using in vivo models harboring different microbiota as well as using diverse agents to perturb microbiota homeostasis, we can determine which immune cell populations are affected by the presence or absence of microbial species or their metabolic products, as well as discover new microbiota- immune system interactions. Moreover, using genetically modified models we can study the function of these immune populations or molecules expressed on them, and how they impact our ability to control pathogens or preserve the intestinal barrier. Recently, using these approaches we discovered how a population of intraepithelial T cells, the CD4+CD8αα+ T cells (DP IEL); require the presence of Lactobacillus reuteri to develop. We showed that CD4 intraepithelial T cells use the Aryl hydrocarbon receptor (AhR) to sense indole-3-lactic acid, produced by L. reuteri metabolism of dietary tryptophan, to convert into DP IELs1. Furthermore, using genetically modified models we could determine that CRTAM, an adhesion molecule expressed on DP IELs, is essential for their permanence at the epithelial cell layer2. While intraepithelial T cells are some of the most abundant immune cell populations that reside in the intestine, and their location at the epithelial cell layer makes them some of the first to interact with microbiota, pathogens and dietary antigens, the function and mechanism of action of some of these T cells populations, like the DP IELs is largely unknown. We aim to discover the role of this population in intestinal homeostasis, response to pathogens or control of inflammation, and to discover novel interactions between intestinal microbiota members and immune populations in the intestinal intraepithelial space. 1 Cervantes-Barragan L. et al . Science 2018. 2 Cortez VS, Cervantes-Barragan L. et al. JEM 2014.	IMPImmunology and Molecular Pathogenesis - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Cervantes-Barragan	Luisa
Ann Chahroudi, MD, PhD Full Member - Immunology and Molecular Pathogenesis Full Member - Microbiology and Molecular Genetics ann.m.chahroudi@emory.edu \| Faculty Profile Professor, Department of Pediatrics, School of Medicine Staff Physician, Ponce Family and Youth Clinic, Infectious Diseases Program, Grady Health System Attending Physician in Infectious Diseases, Children's Healthcare of Atlanta Affiliate Scientist, Emory National Primate Research Center The primary research focus of my laboratory is to find a cure for HIV using nonhuman primate models to investigate HIV/SIV reservoirs.	The primary research focus of my laboratory is to find a cure for HIV using nonhuman primate models to investigate HIV/SIV reservoirs.My research focus is centered on HIV pathogenesis, transmission, and cure. We aim to identify cellular and anatomic HIV/SIV reservoirs that represent the key obstacle(s) to an HIV cure. Using nonhuman primate models to interrogate these reservoirs in the setting of fully suppressive antiretroviral therapy allows us to more completely assess the potential sources of viral persistence. In addition, the model of SIV infection and antiretroviral treatment of rhesus macaques allows for testing of novel interventions to disrupt persistent reservoirs. My lab is focused on testing cure strategies in both infant and adult rhesus macaques. Ultimately, we hope to contribute to the development of a cure for HIV.	IMPImmunology and Molecular Pathogenesis - Full Member MMGMicrobiology and Molecular Genetics - Full Member	Chahroudi	Ann
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
Jae Won Chang, PhD Full Member - Molecular and Systems Pharmacology jae.won.chang@emory.edu \| Faculty Profile Assistant Professor, Department of Pharmacology and Chemical Biology, School of Medicine Assistant Professor, Department of Hematology and Medical Oncology, School of Medicine Member, Discovery and Developmental Therapeutics Research Program, Winship Cancer Institute Developing of novel chemical probes for profiling poorly characterized protein activities and drugs.	Developing of novel chemical probes for profiling poorly characterized protein activities and drugs.Large-scale profiling methods have uncovered numerous gene and protein expression changes that correlate with tumorigenesis. However, determining the relevance of these expression changes and which biochemical pathways they affect has been hindered by our incomplete understanding of the proteome and its myriad functions and modes of regulation. Activity-based profiling platforms enable both the discovery of cancer-relevant enzymes and selective pharmacological probes to perturb and characterize these proteins in tumor cells. When integrated with other large-scale profiling methods, activity-based proteomics can provide insight into the metabolic and signaling pathways that support cancer pathogenesis and illuminate new strategies for disease diagnosis and treatment. Overall goal of our lab is to understand how alterations in the function of proteins contribute to human disease and to identify individual proteins and cognate biochemical pathways that can be pharmacologically targeted for human disease. Therefore, our laboratory is mainly focused on developing of novel chemical probes for profiling poorly characterized protein activities and drugs for prevention, diagnosis, treatment, and cure of diseases like cancer.	MSPMolecular and Systems Pharmacology - Full Member	Chang	Jae
Lih-Shen Chin, PhD Affiliate Member - Neuroscience lchin@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Pharmacology and Chemical Biology, School of Medicine Elucidation of the molecular pathogenic mechanisms of Parkinson's disease.	Elucidation of the molecular pathogenic mechanisms of Parkinson's disease.My research focuses on the molecular pathogenic mechanisms of Parkinson's disease (PD). We are using molecular, cellular, proteomic, and biochemical approaches to delineate the molecular pathways by which the mutations in familial PD proteins DJ-1, Parkin, and PINK1 lead to neurodegeneration and to identify additional proteins and new pathways involved in PD pathogenesis. By using a redox proteomic approach, we are characterizing protein targets of oxidative damage in idiopathic PD brains and investigating the gene-environment interactions in PD pathogenesis. We are also studying the role of ubiquitination and aggresome formation in PD pathogenesis. Our goal is to use the mechanistic insights gained from these studies for developing new intervention strategies to treat PD.	NSNeuroscience - Affiliate Member	Chin	Lih-Shen