MSP 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
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	Full Member
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	Full Member
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	Full Member
Joshua D. Chandler, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology joshua.chandler@emory.edu \| Faculty Profile Assistant Professor, Division of Pulmonary Medicine, Department of Pediatrics, School of Medicine My laboratory studies mechanisms of lung diseases, such as cystic fibrosis, by analyzing the impact of pathological processes, such as lung inflammation, on the abundance and metabolism of metabolites involved in redox homeostasis, cell signaling, and bioenergetics, with an ultimate goal of identifying druggable pathways to halt disease advancement.	My laboratory studies mechanisms of lung diseases, such as cystic fibrosis, by analyzing the impact of pathological processes, such as lung inflammation, on the abundance and metabolism of metabolites involved in redox homeostasis, cell signaling, and bioenergetics, with an ultimate goal of identifying druggable pathways to halt disease advancement.Inflammation, or white blood cell infiltration into bodily tissues and activation of immune functions, impacts a range of human illnesses. Understanding the molecular basis of inflammatory tissue injury is key to preventing and resolving pathological outcomes. However, such mechanisms are complex, multifactorial, and change with time. The Chandler Laboratory focuses on elucidating the biochemical and metabolic causes and consequences of inflammatory pathology by utilizing a suite of small molecule, redox, metabolic, and biochemical-focused techniques. We also design experiments to test rational pharmacological interventions against inflammation that could improve human health. To date, we have placed major emphasis on myeloperoxidase (MPO), a heme enzyme, and its role in early-stage pathogenesis of cystic fibrosis. Neutrophils, the most abundant white blood cells in humans, secrete mature MPO after infiltrating tissues. MPO utilizes hydrogen peroxide to produce a range of oxidants, including hypochlorous acid (chlorine bleach) and a weaker, more selective oxidant, hypothiocyanous acid. Notably, changing the abundance of MPO substrates changes its output of oxidants, and differences in oxidant reactivity change the impacted biochemicals wherever MPO is present. Therefore, MPO substrates can be targeted as a means of controlling its activity and shifting oxidation reactions to different targets, a process I call "oxidant switching". My lab's research program is designed to build on previous successes in leveraging oxidant switching to improve lung health.[1-3] Due to the complexity of immune effector molecules, particularly promiscuous oxidants like hypochlorous acid, we use high-resolution, accurate-mass mass spectrometry to conduct metabolomics experiments (attempting to measure as many small molecules in a biological system as possible with a relatively unbiased method). This allows us to (1) quantify hundreds of validated compounds; (2) annotate and quantify hundreds more according to MS/MS fragmentation; and (3) potentially detect and quantify undiscovered compounds, all via nontargeted analysis of a single experiment. We also use stable isotope flux analysis to identify metabolic pathway activity and aid structure elucidation of novel compounds. Experiments can be set up to both generate and test hypotheses, depending on extent of a priori knowledge. Combining metabolomics and traditional biochemistry, we partnered with international colleagues to study bronchoalveolar lavage from clinically stable toddlers with cystic fibrosis. These samples are very difficult to acquire, and using them we determined that MPO is active in the earliest stages of cystic fibrosis, contributes to metabolite oxidation, and is closely associated with lung damage.[4, 5] Ongoing funded research aims to determine if it is also an important factor in disease risk, as well as the fate(s) and molecular impact of the MPO protein in the context of neutrophilic airway inflammation. Additional lines of research are focused on the ability to non-invasively monitor important metabolites in CF, and on the metabolic rewiring and metabolic signaling of neutrophils epithelial cells and circulating metabolites in cystic fibrosis and cystic fibrosis-related diabetes.[6] Citations 1. Chandler, J.D. and B.J. Day, Biochemical mechanisms and therapeutic potential of pseudohalide thiocyanate in human health. 2015. 49(6): p. 695-710. 2. Chandler, J.D., et al., Antiinflammatory and Antimicrobial Effects of Thiocyanate in a Cystic Fibrosis Mouse Model. American Journal of Respiratory Cell and Molecular Biology, 2015. 53(2): p. 193-205. 3. Chandler, J.D., et al., Selective Metabolism of Hypothiocyanous Acid by Mammalian Thioredoxin Reductase Promotes Lung Innate Immunity and Antioxidant Defense. 2013. 288(25): p. 18421-18428. 4. Chandler, J.D., et al., Myeloperoxidase oxidation of methionine associates with early cystic fibrosis lung disease. European Respiratory Journal, 2018. 52(4): p. 1801118. 5. Horati, H., et al., Airway profile of bioactive lipids predicts early progression of lung disease in cystic fibrosis. J Cyst Fibros, 2020. 19(6): p. 902-909. 6. Chandler, J.D., et al., Determination of thiocyanate in exhaled breath condensate. Free Radical Biology and Medicine, 2018. 126: p. 334-340. 7. Kim S.O., et al, Substrate-dependent metabolomic signatures of myeloperoxidase activity in airway epithelial cells: Implications for early cystic fibrosis lung disease. Free Radic Biol Med, 2023. S0891-5849(23)00508-7	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Chandler	Joshua		Full Member
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		Full Member
Huw M.L. Davies, PhD Full Member - Molecular and Systems Pharmacology hmdavie@emory.edu \| Faculty Profile \| Lab Website Asa Griggs Candler Professor, Department of Chemistry, Emory College of Arts and Sciences Member, Discovery and Developmental Therapeutics Research Program, Winship Cancer Institute Development of new synthetic methods in organic synthesis as enabling technologies for drug development.	Development of new synthetic methods in organic synthesis as enabling technologies for drug development.My group is involved in developing new synthetic methods in organic synthesis and using them as enabling technologies for drug development. I am involved in many collaborative projects in drug discovery that apply new enabling synthetic methods to design new classes of compounds to interact at novel biological targets. I am currently the Director of the NSF Phase II Center in Selective C-H Functionalization, which develops new synthetic tools for fine chemical synthesis and these tools are especially useful for drug discovery. This is a multi-site center and includes collaborators at 16 universities, such as Stanford University, Scripps Research Institute, University of Illinois, Princeton University, UCLA, Cal Tech and UC Berkeley. The pharmaceutical industry is especially interested in the enabling opportunities associated with the C-H functionalization technology, and several of the major pharmaceutical companies are actively engaged with the Center. In addition to my Center engagement and my own independent NIH and NSF grants, I am a collaborator in drug discovery projects focusing on cystic fibrosis and sickle cell disease.	MSPMolecular and Systems Pharmacology - Full Member	Davies	Huw		Full Member
Mike Davis, PhD Full Member - Molecular and Systems Pharmacology medavis@emory.edu \| Faculty Profile \| Lab Website Professor, Wallace H. Coulter Department of Biomedical Engineering, Emory University & Georgia Institute of Technology Director, Children's Heart Research and Outcomes (HeRO) Center, Department of Pediatrics, School of Medicine Associate Professor, Department of Medicine, School of Medicine Our laboratory focuses on various aspects of cardiac regeneration and preservation using molecular-based and biomaterials-based approaches to restoring function after cardiac injury.	Our laboratory focuses on various aspects of cardiac regeneration and preservation using molecular-based and biomaterials-based approaches to restoring function after cardiac injury.The major cause of heart failure is regional loss of myocardium following myocardial infarction. Because the loss of tissue is highly localized, and the endogenous response is not sufficient, recent efforts have focused on replacement of the lost cells using a variety of treatment options. These include, but are not limited to, cell therapy, gene therapy and biomaterial-based grafts. Gene therapy has been plagued by a variety of shortcomings including poor transfection efficiencies, inability to target specific cells and uncontrolled expression of the target gene/protein. Cell based therapies have been met with enthusiasm, however much debate still liners on the optimal delivery method of cells and exact cell type which holds the most promise. Indeed, many cells most likely diffuse away from the site of injection, making biomaterial-based grafts more feasible. These grafts, while promising have many shortcomings when combined with cell therapy including poor cell engraftment, survival and differentiation. Recently, a new phase of biomaterial design has come into favor: smart biomaterial engineering. Many studies have attempted to engineer the biomaterials to enhance the survival and retention of the cells to be implanted including modifying the biomaterials to contain adhesion sequences and loading the scaffolds with specific growth factors. Oxidative stress is greatly increased in the myocardium following infarction. The exact source of the free radical production has been examined and there are several candidates including cardiac fibroblasts, as well as invading neutrophils and myocytes. The increased superoxide following infarction not only increases damage to the local myocardium, but through dismutation to hydrogen peroxide may increase lipid peroxidation and cardiac fibrosis. Myocardial levels of the endogenous hydrogen peroxide scavenger catalase successively decrease in the weeks following infarction and its absence may also lead to incomplete regeneration by resident stem cells. Additionally, several therapies reported to improve cardiac function following infarction also increased catalase levels. Finally, oxidative stress initiates apoptosis in stem-cell derived cardiomyocytes and may play a role in the survival and efficacy of cardiac stem cells during aging. My research focuses on using biomaterials to deliver compounds to the highly vascularized myocardium that would otherwise be lost to diffusion. We currently are using polyketal particles, an exciting new class of polymers, to deliver small molecule signaling inhibitors to the myocardium to prevent fibrosis and dysfunction. We also are exmining delivery of superoxide dismutase and catalase, two important reactive oxygen species scavengers. It is our hope that we can achieve sustained inhibition or antioxidant therapy for the course of the post-infarct dysfunction and remodeling.	MSPMolecular and Systems Pharmacology - Full Member	Davis	Mike	Bioengineering Cardiology Pediatrics Pharmacology	Full Member
Ray Dingledine, PhD Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience rdingle@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Pharmacology and Chemical Biology, School of Medicine Role of neuroinflammation in chronic neurodegenerative disorders	Role of neuroinflammation in chronic neurodegenerative disordersWhy is the hippocampus so vulnerable to seizures and seizure-induced damage? What molecular and cellular changes underlie the gradual transition from a normal brain to a brain with epilepsy? How does neuroinflammation influence the development of epilepsy? These are some of the questions that drive research in our laboratory. A major research emphasis in our lab involves the identification of novel targets and pathways involved in the basic cellular and molecular mechanisms of epilepsy. Our recent work and that of others highlights a role for cyclooxygenase-2 (COX2) signaling pathways in the cognitive deficits, impaired synaptic inhibition, neuroinflammation and neurodegeneration caused by seizures. We have developed a mouse with COX2 conditionally ablated in principal forebrain neurons and are using this mouse to study the role of neuronal COX2 in epilepsy. We also employ a chemical biology approach to develop novel small molecule modulators of prostaglandin EP1 and EP2 receptors and are determining whether they interrupt the development of epilepsy. As a whole our work integrates information from a variety of experimental strategies to contribute to a better understanding of epilepsy, with broad implications for other brain disorders	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Dingledine	Ray	Electrophysiology Epilepsy Inflammation Molecular Biology Neuropharmacology Neuroscience	Full Member
Chris Doering, PhD (he/him) Full Member - Molecular and Systems Pharmacology cdoerin@emory.edu \| Faculty Profile Professor, Division of Hematology/Oncology, Department of Pediatrics, School of Medicine Member, Winship Cancer Institute Co-Founder, Expression Therapeutics Professor, Division of Hematology/Oncology, Department of Pediatrics, School of Medicine The development of cell, gene and protein-based therapies for pediatric blood diseases and cancers.	The development of cell, gene and protein-based therapies for pediatric blood diseases and cancers.The overall goal of our research is to develop better therapies for challenging blood disorders and cancers. Recently, the main areas of focus include 1) developing strategies to improve the design of vector genome cassettes in gene therapy, 2) use of genetically engineered immune cells from healthy donors to fight difficult to treat cancers, and 3) designing protein drugs with enhanced functionality. Research projects in these areas serve as training platforms for students and junior faculty.	MSPMolecular and Systems Pharmacology - Full Member	Doering	Chris		Full Member
Christine M. Dunham, PhD (she/her) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology cmdunha@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Chemistry, Emory College of Arts and Sciences Regulation of protein synthesis; ribosome structure & function; regulation by toxins, antibiotics, frameshifting elements, and quality control mechanisms.	Regulation of protein synthesis; ribosome structure & function; regulation by toxins, antibiotics, frameshifting elements, and quality control mechanisms.The Dunham laboratory studies how protein synthesis is regulated to alter critical aspects of cellular function essential for life. We use interdisciplinary approaches including structural biology (X-ray crystallography and single particle cryo-EM), biochemistry, molecular biology and microbiology to define molecular mechanisms of action.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Dunham	Christine		Full Member
Negar Fani, PhD, ABPP (she/her) Affiliate Member - Molecular and Systems Pharmacology Full Member - Neuroscience nfani@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Psychiatry and Behavioral Sciences, School of Medicine Negar Fani, PhD is a clinical neuropsychologist whose research is centered around obtaining multimodal biomarkers of Posttraumatic Stress Disorder (PTSD) and using innovative neurostimulation-based interventions to treat trauma-related conditions and enhance well-being.	Negar Fani, PhD is a clinical neuropsychologist whose research is centered around obtaining multimodal biomarkers of Posttraumatic Stress Disorder (PTSD) and using innovative neurostimulation-based interventions to treat trauma-related conditions and enhance well-being.Dr. Fani has expertise in using multi-modal methods (neuropsychological tests, affective paradigms, psychophysiology, functional and structural MRI, electroencephalography) to characterize heterogeneous manifestations of posttraumatic stress disorder (PTSD), with a focus on exploring disruptions in attention and emotion regulation marginalized populations. Her work has been conducted in the context of one of the longest-running studies of trauma in the nation, the Grady Trauma Project. Over the years she has observed observed unique neurophysiological adaptations to social adversity in this population, which has informed her intervention targets. Dr. Fani is testing the use of two novel non-invasive neurostimulation methods in healthy individuals and populations with PTSD. She is conducting a multisite clinical trial examining the use of sternal breath-synced vibration to examine effects on attention and interoceptive networks in a dissociative trauma-exposed population. She is also directing a new program of research centered around the use of temporal interference, a non-invasive transcranial electrical stimulation method to target subcortical regions and circuits involved with affect and cognition. Dr. Fani's laboratory is also developing community partnerships to: 1) disseminate science to the community and 2) collaboratively facilitate community resilience to psychosocial stressors. The following are active, funded projects in Dr. Fani's lab: 1) Neural mechanisms of device-augmented breath focused mindfulness in dissociative trauma-exposed people (Mechanistic Interventions and Neuroscience of Dissociation, MIND; https://www.negarfani.com/mind-study) 2) Identifying neural signatures of daily experiences of racial discrimination with data fusion (Neural Imprints of Racist Variable Experiences, NIRVE; https://www.negarfani.com/nerve-study) 3) Temporal interference non-invasive neuromodulation to enhance attention and emotion regulation	MSPMolecular and Systems Pharmacology - Affiliate Member NSNeuroscience - Full Member	Fani	Negar	Anxiety Disorders Biofeedback Inflammation Trauma	Affiliate Member
Haian Fu, PhD Full Member - Cancer Biology Full Member - Molecular and Systems Pharmacology hfu@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Pharmacology and Chemical Biology, School of Medicine Professor, Winship Cancer Institute Understanding cell growth regulation for drug discovery and translational research	Understanding cell growth regulation for drug discovery and translational researchOur research seeks to understand signal transduction pathways that control cell survival and death in normal and cancer cells. Based on the unraveled signaling mechanisms and tumor-addicted pathways, we employ the chemical biology approach to develop novel strategies for mechanistic understanding of tumorigenesis, small molecule drug discovery, and translational studies. • Cancer-specific protein-protein interactions (PPI) as therapeutic targets: Using systems biology approach, we aim to establish cancer-associated protein-protein interaction networks (OncoPPI network) to prioritize targets for therapeutic discovery and development. Specially, our research has led to the identification of mutated oncoprotein-mediated PPIs for mechanistic interrogation and therapeutic intervention. • Small molecule modulator identification for probe and drug discovery: We are designing mechanism-based bioassays for high throughput and high content screening (HTS/HCS) of compounds for the identification of cancer-specific PPI inhibitors, variant-directed PPI inducers to restore tumor suppressor functions, and anticancer immunity modulators. • Translational research. To translate our basic understanding of PPI network into clinic settings, we collaborate with physician scientists to develop novel therapeutic strategies for the treatment of cancer, which has been extended to Alzheimer's disease. Our collaborative project with physician scientists on lung cancer is such an example. On the other hand, we collaborate with chemists to develop new anticancer agents based on their action on survival pathways and move them into clinic.	CBCancer Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Fu	Haian	Biochemistry, Proteins Cancer Biology Genetics, Molecular Molecular Biology Oncology Pharmacology	Full Member
Thota Ganesh Full Member - Molecular and Systems Pharmacology tganesh@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Pharmacology and Chemical Biology, School of Medicine The overarching goal of my research is to develop small molecule tools and study them in in vitro culture systems and in vivo animal models to develop novel treatments for neurodegenerative diseases such as epilepsy, traumatic brain injury and Alzheimer’s disease.	The overarching goal of my research is to develop small molecule tools and study them in in vitro culture systems and in vivo animal models to develop novel treatments for neurodegenerative diseases such as epilepsy, traumatic brain injury and Alzheimer’s disease.Alzheimer's disease (AD) produces significant morbidity accompanied by substantial medical and societal burden. AD is the sixth leading cause of death in the USA without a way to prevent, treat, or even slow the disease progression. Currently about 5.4 million Americans (12% of those 65 or older) are living with AD, and the number is expected to triple by the year 2050 (www.alz.org). Approximately $ 200 billion per year is spent on all aspects of caring for AD patients in the USA, yet we remain powerless to stop its progression and no therapy is on the horizon that clearly alters the inevitable cognitive decline. Deposition of amyloid-β (Aβ)-plaques, neurofibrillary tangles, and loss of synapses are hallmarks of AD, and they begin to accrue many years before clinical symptoms are detectable. The last decade of drug discovery efforts for AD have mainly focused on the amyloid cascade hypothesis by targeting the removal of amyloid plaques from the brain of AD patients with active or passive immunization. However, this approach so far has failed to provide a clinical benefit, suggesting Aβ alone is not responsible for the development of the disease and anti-amyloids alone will not be therapeutically beneficial. The currently approved therapeutics offer minor symptomatic improvement and little, if any, modification of disease progression. Thus, identification of novel biological targets and drugs that work through novel mechanisms of action are crucial goals for future AD therapies. Increased COX-2 levels are found in the early stage of Alzheimer's brain and its levels are correlated with levels of Aβ-peptide. COX-2 levels are also correlated with neuronal atrophy and Aβ-plaque density in hippocampal neuronal structures. A maximal expression of COX-2 was found at very early onset of AD according to Braak-stages. A non-selective COX-2 inhibitor (NSAID, naproxen) reduced the incidence of the AD when it was given to the patients prior to the development of cognitive impairment, reinforcing the notion that Alzheimer's disease onset occurs several decades earlier than the clinical symptoms are diagnosed, and suggesting that a future anti-inflammatory therapy should start near the disease onset. However, chronic use of COX-2 drugs resulted in adverse cardiovascular effects, as a result, two COX-2 drugs (Vioxx and Bextra) have been withdrawn from the USA market, and future use of COX-2 drugs on AD patients will be limited because AD patients are already at increased risk for cardiovascular disease. COX-2 catalyzes the synthesis of five prostaglandins, which activate nine prostanoid (G protein- coupled) receptors. Each of these individual receptors plays a protective as well as a harmful role in a variety of disease conditions. For example, IP receptor (activated by PGI2) plays a cardioprotective role. Studies have now concluded that the adverse effects of COX-2 inhibitors are mediated through inhibition of IP receptor. Thus, targeting a specific pro-inflammatory prostanoid receptor would be an innovative and superior therapeutic strategy, rather than the generic block of the entire COX-2 cascade, for the suppression of Alzheimer's disease. We are the first to explore the EP2 receptor as a target for anti-inflammatory therapy using a pharmacological inhibition strategy. See Ganesh et al., J. Med. Chem., 2014, 57, 4173-4184; Rojas et al., Neuropharmacology. 2016, 110,419-430. My research is specifically geared towards the following specific aims. 1. We will develop a preclinical lead candidate by chemical synthesis and lead optimization to use in rodent models of Alzheimer's disease. 2. We will establish a proof of concept that our small molecule therapeutic will modify the progression of Alzheimer disease in transgenic mouse and rat models. 3. We will establish IND-related toxicology studies with our small molecules and seek FDA approval to use in humans.	MSPMolecular and Systems Pharmacology - Full Member	Ganesh	Thota		Full Member
Todd Golde, MD, PhD Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience todd.golde@emory.edu \| Faculty Profile Professor, Department of Pharmacology and Chemical Biology, School of Medicine Professor, Department of Neurology, School of Medicine Director, Center for Neurodegenerative Disease (CND), Goizueta Institute @ Emory Brain Health Dr. Golde research primarily focuses on the molecular pathogenesis of AD but has a broadening focus that extends to other neurodegenerative diseases, cancer, and links between the hypothalamic pituitary axis and metabolism.	Dr. Golde research primarily focuses on the molecular pathogenesis of AD but has a broadening focus that extends to other neurodegenerative diseases, cancer, and links between the hypothalamic pituitary axis and metabolism.I have led an internationally visible research laboratory for over 25 years, while taking on increasingly complex research administrative roles. Yet, above all, I remain deeply committed to conducting and supporting science that can yield insights into therapeutic strategies that may one day impact patients' lives. My own laboratory's long-standing research focus on Alzheimer's Disease (AD) and other neurodegenerative disorders has now expanded to include initiatives in cancer and stress-related disorders. Outlined below are areas of research that I am actively engaged in (https://med.emory.edu/departments/pharmacology-chemical-biology/labs/golde-lab/index.html): • Immune Modulation in Neurodegenerative Disease. My laboratory and close collaborators began studies on manipulating the immune system in neurodegenerative disease models before these studies were highly fashionable. Currently, we have been exploring AD immune targets identified both by inference from system level multi-omic data and by critical thinking about those data and known aspects of neuroimmune function. • Chimeric Phagocytic Receptors (CPRs) and Chimeric "Eat-Me" Antibody Fragments. We are evaluating whether rAAV-mediated delivery of i) transmembrane chimeric phagocytic receptors (CPRs) designed to enhance internalization and degradation of the target protein or ii) soluble chimeric antibodies fused to protein motifs that mediate phagocytosis might serve as effective approaches to proteinpathy reduction. • Amyloid Associated Proteins. We have identified many proteins that co-accumulate with amyloid in both human AD and our mouse models of Aβ deposition. We refer to these as Amyloid Associated Proteins (AAPs). Initial studies on two of these AAPs, midkine and pleiotrophin, demonstrate that they are integral components of the compact plaques and that their increased expression alters the spatiotemporal aspects and overall level of deposition of amyloid in mouse models. Further, as many of these are known extracellular signaling models, we are exploring the hypothesis that the accumulation of these proteins in plaques may mediate select aspects of cellular dysfunction observed in AD. • Slice Culture Models of Tauopathy - Tau-turnover and Mechanisms of Tau-induced Neurodegeneration. We have recently developed and published a novel, rapid and robust brain slice culture model of tau pathology and α-synucleinopathy. Subsequently, we used this model to demonstrate that tau aggregates turn over within cells. We are currently using these systems to explore how cells adapt to the presence of tau aggregates and to probe tau-induced mechanisms of cellular dysfunction and degeneration. • Targeting of the Hypothalamic Pituitary Adrenal Axis with an antibody to CRF. My lab began exploring links between stress, the Hypothalamic Pituitary Adrenal (HPA) axis, and AD about ten years ago. These studies led us to develop a monoclonal antibody that targets corticotropin releasing factor (CRF, aka CRH), the apex regulator of the HPA axis. This antibody mediates robust durable suppression of the HPA axis and has profound impacts on multiple organ systems. Indeed, we see beneficial impacts on metabolism with robust shifts in body composition. Work related to AD and brain aging is funded by an RF1 entitled "Immunotherapy targeting the HPA axis in Alzheimer's Disease". • Precision AAV-mediated Combinatorial Therapies (PACT). Underlying much of my laboratory's wet-bench research studies is the development and optimization of an extensive innovative rAAV vector "toolkit" that enables us to accelerate translational preclinical studies to advance both mechanistic and therapeutic target studies. This toolkit and our long-standing experience with using rAAV vectors is leveraged by others within and outside of our institution. Indeed, we make vectors and virus for many others, and provide guidance on experimental design using rAAV vectors. In this new initiative, we are exploring proof of concept studies that we believe may enable therapeutic approaches to many untreatable disease and disorders. We are developing paradigms whereby we can focally deliver tailored combinations of biotherapeutics. Indeed, the overriding rationale for these studies is that in many disease settings targeted combinations of therapeutics, delivered more focally to avoid systemic toxicities, are needed to significantly alter the course of disease.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Golde	Todd		Full Member
David Gordon, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology david.ezra.gordon@emory.edu \| Faculty Profile Assistant Professor, Department of Pathology and Laboratory Medicine, School of Medicine The Gordon laboratory utilizes high-throughput experimental genetics and mass spectrometry to build mechanistic models of biological functions.	The Gordon laboratory utilizes high-throughput experimental genetics and mass spectrometry to build mechanistic models of biological functions.Dr. David Ezra Gordon earned his Bachelor of Science in Biology from Cornell University, followed by an M.Phil. and Ph.D. in Clinical Biochemistry from the University of Cambridge. With a diverse research background encompassing cell and molecular biology, experimental genetics, virology, systems biology, mass spectrometry, and immunology, Dr. Gordon is recognized for his innovative and impactful contributions to biomedical science. As a graduate student at Cambridge, he utilized combinatorial experimental genetics to map redundant vesicle trafficking pathways in higher eukaryotes. During his postdoctoral fellowship at the University of California, San Francisco, Dr. Gordon pioneered high-throughput genetic interaction mapping to study HIV host-dependencies, and spearheaded the first peer-reviewed protein interaction maps for the highly pathogenic coronaviruses SARS-CoV-2, SARS-CoV-1, and MERS. At Emory University, the Gordon Laboratory builds upon these foundational studies to systematically dissect the biochemical mechanisms underlying immune regulation, particularly in the contexts of pathogen infection and the tumor microenvironment. Leveraging state-of-the-art mass spectrometry, the lab maps complex biochemical networks and employs high-throughput experimental genetics to pinpoint key nodes driving immune function and dysfunction. Collaboration is central to our approach—we partner widely to access the most physiologically relevant model systems for our research on immune responses, infectious diseases, and cancer. Our team specializes in the biochemical analysis and genetic modification of primary systems at scale, working closely with both academic and industry partners to advance the frontiers of immunology and therapeutic discovery.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Gordon	David	AIDS / HIV Biochemistry, Proteins Cancer Biology Genetics, Molecular Immunology Molecular Biology Neurodegenerative Disease Virology	Full Member
Shannon Gourley, PhD (she/her) Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience shannon.l.gourley@emory.edu \| Faculty Profile Associate Professor, Marcus Autism Center, Department of Pediatrics, School of Medicine I study neurobiology utilizing model organisms, cell- and circuit-specific manipulation, high-resolution microscopy, genetic and pharmacological strategies, and other techniques. I often focus on adolescent brain development, aiming to identify the building blocks necessary for adaptive decision-making behavior later in life and how they are impacted by stressors and addictive drugs.	I study neurobiology utilizing model organisms, cell- and circuit-specific manipulation, high-resolution microscopy, genetic and pharmacological strategies, and other techniques. I often focus on adolescent brain development, aiming to identify the building blocks necessary for adaptive decision-making behavior later in life and how they are impacted by stressors and addictive drugs.My group focuses on mechanistic factors controlling reward processing and reward-related behavior. We aim to understand mechanisms related to depression, such as blunted reward processing and poor capacity to prioritize or derive pleasure from reward, and addiction. My team marries classical and modern techniques to create a powerful research toolkit including: etiologically- and ethologically-based murine models for studying disease; behavioral pharmacology and appetitive conditioning; viral-mediated gene silencing and over-expression, neuromodulation and network tracing; high-resolution single-cell imaging and 3D reconstruction; and hypothesis-driven and discovery-based gene and protein quantification strategies. I have served on NIH and international study sections and reviewed manuscripts for >50 journals including Nature Neuroscience and Science. A major goal of my lab is to provide a training environment that emphasizes rigor and unbiased experimental design, where trainees learn to design experiments with optimal methods and analytical approaches. My goal is to aide and support trainees in identifying and transitioning into careers in the biomedical workforce. To date, I have mentored >30 post-doctoral fellows and PhD and MD/PhD students. I was awarded the Graduates in Neuroscience Faculty Person of the Year Award in 2017 and 2024, and the Emory Dept. Pediatrics Research Mentor of the Year Award in 2018. Recently, I was awarded the Emory University School of Medicine Mentorship Award, which recognized 3 faculty persons among the entire School of Medicine faculty.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Gourley	Shannon		Full Member
Kathy K. Griendling, PhD Full Member - Molecular and Systems Pharmacology kgriend@emory.edu \| Faculty Profile \| Lab Website Professor, Division of Cardiology, Department of Medicine, School of Medicine Executive Associate Dean for Faculty Affairs and Professional Development, Emory University School of Medicine, School of Medicine The role of reactive oxygen species derived from NADPH oxidases in smooth muscle differentiation, migration and proliferation using molecular and cellular techniques as well as animal models of vascular disease.	The role of reactive oxygen species derived from NADPH oxidases in smooth muscle differentiation, migration and proliferation using molecular and cellular techniques as well as animal models of vascular disease.Dr. Griendling's research program has centered on the role of reactive oxygen species and related signaling in vascular function. Her lab concentrates on the cellular events responsible for regulation of the oxidative state of the cell, focusing primarily on the vascular NADPH oxidases. Over 20 years ago, they were one of the first to show that vascular smooth muscle cells contain novel NADPH oxidases that are responsible for the majority of the superoxide produced by these cells. Activation of these oxidases not only increases intracellular superoxide, but also results in the accumulation of H2O2, which in turn regulates a number of signaling pathways that regulate growth, differentiation and migration. In collaboration with Dr. David Lambeth, her laboratory cloned two novel catalytic subunits of these enzymes, Nox1 and Nox4 from vascular cells. They have investigated the functions of Nox1 and Nox4 and explored their individual roles in vascular growth and differentiation, cell migration and pathophysiology. They have studies their activators, their subunit composition, the specific signaling pathways that they modify, their roles in migration, differentiation, growth and cytoskeletal reorganization, and their roles in hypertension and diabetic vascular disease. More recently, they discovered, cloned and characterized the first known regulator of Nox4, Poldip2. Poldip2 has turned out to be a very interesting protein, because it has multiple binding partners and many roles in vascular pathology and physiology. They made a knockout mouse and showed that it has stiffer arteries, a reduced capacity to generate arterial force and increased collagen deposition. they have also discovered roles for Poldip2 in cell migration and proliferation as well as collateral formation and neointimal formation. Their recent focus has shifted to endothelial cells, based on a profound phenotype of decreased endothelial permeability in a murine model of cerebral ischemia. Poldip2 is a universal regulator of endothelial permeability, making it an excellent therapeutic target for diseases such as stroke and acute respiratory distress syndrome (ARDS). The lab's current efforts are directed towards investigating the role of Poldip2 in ARDS. The lab is adept at molecular studies, cell signaling, pharmacology, cell biology (including confocal microscopy studies), and the use of animal models.	MSPMolecular and Systems Pharmacology - Full Member	Griendling	Kathy	Cell Biology Pulmonary Medicine Reactive oxygen species Vascular Disease	Full Member
Randy A. Hall, PhD Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience rhall3@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Pharmacology and Chemical Biology, School of Medicine Mechanisms of signal transduction by neurotransmitter and hormone receptors.	Mechanisms of signal transduction by neurotransmitter and hormone receptors.My laboratory's research is focused on the activation and regulation of G protein-coupled receptors in the nervous system. We have a special interest in studying disease-associated mutations to human receptors that perturb receptor signaling and/or trafficking. Such studies are of significant clinical importance because they shed light on genetic diseases, and also because they provide fundamental new insights into the basic biology of G protein-coupled receptors. Furthermore, we have a strong interest in screening understudied G protein-coupled receptors to identify novel ligands. G protein-coupled receptors are extremely common targets for therapeutic pharmaceuticals, and thus the identification of new ligands acting on disease-relevant receptors provides leads that may eventually be developed into novel therapeutics.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Hall	Randy	Neuroscience Pharmacology Receptors	Full Member
Laura Hansen, PhD Full Member - Molecular and Systems Pharmacology laura.hansen2@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Division of Cardiology, Department of Medicine, School of Medicine My lab studies vascular growth in the context of peripheral artery disease specifically focusing on skeletal muscle satellite cells in exercise therapy and as a cell therapy.	My lab studies vascular growth in the context of peripheral artery disease specifically focusing on skeletal muscle satellite cells in exercise therapy and as a cell therapy. Dr. Hansen's lab studies the interactions between satellite cells and the vasculature. Satellite cells are skeletal muscle progenitor cells that are known to play an important role in muscle repair after injury and adaptation to exercise. However, the Hansen lab focuses on a previously underexplored role of satellite cells in vascular growth. They have found that satellite cells, when activated, produced a number of chemoattractant growth factors that drive the migration of vascular smooth muscle and endothelial cells which in an important factor in the growth and development of blood vessels. This area is of particular interest in the context of peripheral artery disease (PAD), where patients suffer from ischemic tissue damage but treatment options are still limited. The lab has shown that ischemia stimulates satellite cells and are exploring ways to harness their angiogenic properties in vivo or through therapeutically delivered cells. Current work in the lab is determining the effects of satellite cell growth factor production using in vitro assays as well as determining what factors are critical to these vascular effects. We also working to optimize satellite cell delivery and further develop therapeutic strategies. Our newest project explores the biology satellite cells in response to exercise. We are utilizing a mouse model in which we can selectively ablate satellite cells. Additionally, we are exploring the changes in expression and heterogeneity of satellite cells after exercise in both our murine models and human patient biopsies using single cell sequencing.	MSPMolecular and Systems Pharmacology - Full Member	Hansen	Laura		Full Member
C. Michael Hart, MD (he/him) Full Member - Molecular and Systems Pharmacology michael.hart3@va.gov \| Faculty Profile Professor, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, School of Medicine Associate Chief of Staff for Research & Development, Atlanta VA Medical Center Assistant Dean for VA Research, Atlanta VA Medical Center Molecular targets in the pathogenesis and therapy of pulmonary and systemic vascular disease.	Molecular targets in the pathogenesis and therapy of pulmonary and systemic vascular disease.The Hart lab focuses on vascular cell biology to examine how alteration in gene expression and metabolism contribute to the pathogenesis of systemic and pulmonary vascular disease. We are particularly interested in developing novel strategies for intervention that might permit more effective treatments. For example, we have demonstrated that activation of the nuclear hormone receptor, peroxisome proliferator-activated receptor gamma (PPARg), using anti-diabetic thiazolidinedione medications, can reduce pulmonary hypertension (PH) in animals. We are in the planning stages to perform a small clinical trial to test this approach in patients with PH. Recent work shows that majors effects of these medications are related to their regulation of mitochondrial structure and function in vascular wall cells. Collectively, our findings indicate that targeting the PPARg receptor provides a novel strategy to attenuate vascular disease. Ongoing studies employ molecular, cell, and whole animal approaches to define the mechanisms by which PPARg activation regulates vascular function and disease.	MSPMolecular and Systems Pharmacology - Full Member	Hart	C.	Biology, Molecular Cell Biology Hypertension Metabolism MicroRNAs Pulmonary Medicine Respiratory Disorders Tissue Culture Vascular Disease	Full Member
John R. Hepler, PhD Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience jhepler@emory.edu \| Faculty Profile \| Lab Website Professor and Vice Chair for Academic Affairs, Department of Pharmacology and Chemical Biology, School of Medicine Executive Committee, NS Cell signaling mechanisms of synaptic transmission and synaptic plasticity.	Cell signaling mechanisms of synaptic transmission and synaptic plasticity.The Hepler lab studies how brain cells communicate with one another to modulate synaptic signaling and brain physiology. To do so, our lab employs a variety of modern multidisciplinary experimental approaches including cellular signaling and imaging, molecular biology, protein biochemistry, bioinformatics/genomics, proteomics, and genetic mouse models. More specifically, our research focuses on identifying key brain signaling proteins (RGS proteins, G proteins, receptors and linked signaling proteins) to understand how these proteins work together to propagate neurotransmitter and neuromodulator signals to regulate neuronal and glial functions. These cellular functions are critical for normal cognitive functions, learning and memory as well as tissue regeneration following brain injury (e.g., stroke). Impairment of these processes contributes to cognitive decline associated with neurodegenerative diseases (e.g., Alzheimer 's disease and others) and aging. Current research focuses on identifying roles for RGS proteins and their binding partners in regulating synaptic signaling and plasticity in neurons relating to learning, memory and cognition. Complimentary studies focus on identifying human mutations and genetic variations within the RGS protein family relating to variable human traits and disease states. Ongoing work seeks to determine the functional consequences of de novo RGS protein variants/missense mutations with the goal of understanding the impact of these protein variants on physiology and disease. Relating to this, we also seek to define the functional consequences of genetic variation in the general population by identifying RGS protein gene regions intolerant to change, and identify candidate genes that contribute to multifactorial human traits and as risk factors for diseases. This information will help guide our efforts and those of others in the development of new small molecule inhibitors or mimetics of RGS protein functions that will dissect/define RGS roles in cell physiology and serve as lead compounds for future drug development.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Hepler	John	Biochemistry, Proteins Cell Biology Hormones Neurochemistry Neuropharmacology Neurophysiology Receptors	Full Member
Ellen J. Hess, PhD Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience ellen.hess@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Pharmacology and Chemical Biology, School of Medicine Professor, Department of Neurology, School of Medicine Abnormal dopamine signaling in Parkinson's disease and dystonia; understanding the neuronal mechanisms underlying sex differences in the presentation and response to treatment in Parkinson's disease and dystonia	Abnormal dopamine signaling in Parkinson's disease and dystonia; understanding the neuronal mechanisms underlying sex differences in the presentation and response to treatment in Parkinson's disease and dystoniaThe goal of our research is to better understand and treat neurological disorders by using a true bench to bedside approach. We are specifically interested in the movement disorders dystonia and Parkinson's disease. Our focus is on abnormal dopamine signaling with the striatum to understand the abnormalities underlying these disorders with the ultimate goal of developing better treatments. Questions include 1) Why does low dopamine cause Parkinson's disease in some people, but dystonia in others; 2) Are there gene expression patterns in brain that distinguish Parkinson's disease from dystonia? 3) Are there patterns of striatal neuron activity that distinguish Parkinson's disease from dystonia?; 4) Can we correct the abnormal signaling pathways with existing drugs or newly developed compounds? A major focus is understanding the neuronal mechanisms that underlie sex differences in Parkinson's disease and dystonia because understanding sex differences has important implications for prognosis and treatment. Although it has been known for decades that biological sex is a risk factor for both Parkinson's disease and dystonia, very little work has focused on the underlying mechanisms. We are filling this gap in knowledge by addressing the following questions: 1) What is the role of ovarian hormones in the presentation of Parkinson's disease and dystonia? 2) How does the molecular signature (transcriptome) of Parkinson's disease and dystonia differ between males and females and what is the role of ovarian hormones? 3) How does neuronal activity (in vivo calcium imaging) in Parkinson's disease and dystonia differ between males and females and what is the role of ovarian hormones? At the basic science level, we use molecular, genetic, anatomical, neurochemical, physiologic, pharmacologic and behavioral approaches. We manipulate specific subpopulations of neurons using genetically engineered mice, viral vectors or region-specific drug injections by targeting ion channels, receptors or neurotransmitters to induce or ameliorate Parkinson's disease or dystonia. Then, we assess the effects of these manipulations on neurochemistry, anatomy, neurotransmission, physiology and behavior, allowing us to pinpoint the molecular or cellular source of the dysfunctional signal. The results of our studies in mice are then used to develop and test novel small molecule compounds for the treatment of movement disorders. This leads directly into our clinical work in patients under the direction of Dr. Jinnah, which includes more precise characterizations of clinical phenotypes, exploring genotype-phenotype relationships, and clinical trials of promising new treatments.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Hess	Ellen	Basal Ganglia Dystonia / Tremor Molecular Biology Movement Disorders Neuroanatomy Neurochemistry Neuropharmacology	Full Member
Ilanit Ronen Itzhaki, PhD Full Member - Molecular and Systems Pharmacology IRONENI@emory.edu \| Faculty Profile Assistant Professor, Children's Heart Research and Outcomes (HeRO) Center, Department of Pediatrics, School of Medicine Our research aims to investigate age and sex differences with respect to sex hormones’ impact on mechanisms responsible for the initiation and termination of cardiac arrhythmias, with the intent of contributing to the identification of molecular antiarrhythmic therapeutic targets, drug repurposing, and the development of drug screening platforms.	Our research aims to investigate age and sex differences with respect to sex hormones’ impact on mechanisms responsible for the initiation and termination of cardiac arrhythmias, with the intent of contributing to the identification of molecular antiarrhythmic therapeutic targets, drug repurposing, and the development of drug screening platforms.Our research aims to investigate age and sex differences with respect to sex hormones' impact on mechanisms responsible for the initiation and termination of cardiac arrhythmias, with the intent of contributing to the identification of molecular antiarrhythmic therapeutic targets, drug repurposing, and the development of drug screening platforms.	MSPMolecular and Systems Pharmacology - Full Member	Itzhaki	Ilanit		Full Member
Hanjoong Jo, PhD Full Member - Molecular and Systems Pharmacology hjo@emory.edu \| Faculty Profile \| Lab Website Professor and Coulter Distinguished Chair Professor, Wallace H. Coulter Department of Biomedical Engineering, Emory University & Georgia Institute of Technology Professor, Division of Cardiology, Department of Medicine, School of Medicine Associate Chair for Emory Biomedical Engineering, Emory University Director of Cardiovascular Biomechanics Graduate Training Program, Emory University and Georgia Tech Cardiovascular Mechanobiology, Therapeutics, and Nanomedicine Lab	Cardiovascular Mechanobiology, Therapeutics, and Nanomedicine LabI direct the Cardiovascular Mechanobiology and MechanoTherapeutics Lab at Emory University. My group studies how blood flow regulates vascular endothelial biology and cardiovascular disease, especially atherosclerosis and aortic valve disease. My lab's current emphasis is on identifying mechanosensitive genes (e.g., mRNAs, microRNAs, long noncoding RNAs) and epigenetic mechanisms that are regulated by blood flow (shear stress) and how they regulate vascular biology and diseases using both mouse models and in vitro systems as well as single cell RNA sequencing and single cell ATAC sequencing. Based on these mechanosensitive genes and miRNAs, we develop novel gene/drug therapeutics to prevent and inhibit atherosclerotic diseases and aortic valve diseases. In addition, we have been developing novel ways to deliver gene therapy and drugs using nanoparticles and ultrasound-guided methods to treat cardiovascular diseases with minimum side effects.	MSPMolecular and Systems Pharmacology - Full Member	Jo	Hanjoong	Atherosclerosis	Full Member
Dean P. Jones, PhD Full Member - Molecular and Systems Pharmacology dpjones@emory.edu \| Faculty Profile Professor, Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, School of Medicine Research in precision medicine uses redox systems biology, proteomics, transcriptomics and clinical metabolomics in human and model systems. Impacts of the exposome on human disease	Research in precision medicine uses redox systems biology, proteomics, transcriptomics and clinical metabolomics in human and model systems. Impacts of the exposome on human diseaseCurrent research in precision medicine involves a mixture of human, animal, and cell and molecular model systems, with specific experimental studies focused on redox biology and sequencing the exposome. Within this broad spectrum of research, we have grant funding in exposome pharmacology, pulmonary toxicity, microbiome and aging, mitochondrial signaling in cancer, deployment-associated exposure surveillance in military personnel (DOD), metabolomics of aging and Alzheimers disease. We have additional collaborations on environmental exposures and preterm birth, biologic responses to air pollution, and metabolomics of HIV-1 infection and tuberculosis. Mitochondrial mechanisms of disease: We have used studies of mitochondrial function, redox proteomics, transcriptomics and high-resolution metabolomics to develop integrated omics models. Oxidative stress and redox systems biology. My research group provided the seminal finding that glutathione and cysteine redox couples are not in redox equilibrium; this led to ongoing research on subcellular redox systems and development of methods in quantitative redox proteomics. Current projects address low-dose environmental toxicity, aging, inflammation and lung disease. High-resolution metabolomics. During the past two decades, we have focused on transforming personalized (precision) medicine through development of low cost, high-throughput and high capacity clinical chemistry analytical platforms. We use dual liquid chromatography with ultra-high resolution mass spectrometry and advanced data extraction algorithms for routine measurement of >20,000 chemicals in microliter volumes of human plasma. We have more recently developed untargeted gas chromatography high-resolution mass spectrometry to measure thousands of environmental chemicals. The relatively low cost enables global evaluation of the exposome, metabolism and disease. Methods are routinely applied to clinical, epidemiologic and model systems studies.	MSPMolecular and Systems Pharmacology - Full Member	Jones	Dean	Drug Metabolism Ischemia Nutrition / Dietetics Toxicology	Full Member
Sumin Kang, PhD Full Member - Cancer Biology Full Member - Molecular and Systems Pharmacology smkang@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Hematology and Medical Oncology, School of Medicine Director, Division of Basic and Translational Science, Department of Hematology and Medical Oncology, School of Medicine Protein kinase and metabolic signaling in tumor metastasis and therapy resistance using translational and preclinical studies.	Protein kinase and metabolic signaling in tumor metastasis and therapy resistance using translational and preclinical studies.Our research interests are focused on how intricate molecular communication networks evolve to control proliferation, differentiation, movement, organization, and death processes in human cells, and how disruption of these processes leads to oncogenesis. In particular, our laboratory is interested in understanding how protein kinases, metabolic signaling, and immune system promote therapy resistant tumor progression and tumor metastasis. The ultimate goal of our research is to translate the insights that we obtain in basic research to clinical treatment that will improve the clinical outcome for patients. Three main directions are as below. (1) Identification and characterization of protein kinases that are important in cancer progression and metastasis: Uncontrolled kinase activity is a frequent cause of cancers, therefore oncogenic protein kinases and their critical signaling effectors are attractive therapeutic targets in cancer treatment. We combined phospho-proteomics, genome-wide screening strategies to identify and characterize novel protein kinases that play a critical role in tumorigenesis, tumor growth, and tumor metastasis. (2) Targeting cancer metabolism as a novel and timely therapeutic strategy: Metabolic alteration is one of the well-known hallmarks of cancer. However, detailed mechanisms by which tumor cells control metabolism and how crucial this is for tumorigenesis, tumor growth, and metastasis remain unknown. We identified several metabolic enzymes including GDH1, LDHA, and 6PGD contributes to tumor growth and metastasis and validate its signaling pathway as a therapeutic target in the treatment of relevant cancers. We are currently performing metabolome-wide RNAi screening to identify novel metabolic enzymes that contribute to cell invasion and anoikis resistance. These studies will enable us to find novel metabolic enzymes which could be potential targets to treat cancers. (3) Identification and characterization of metabolic pathways, post-translational modifications, and immune signaling required for therapy resistance in human cancers: The treatment of solid tumors with chemotherapy or immunotherapy often results in the development of resistance leading to therapeutic failure, but the mechanisms causing this resistance in cancers remain unclear. Through customized RNAi screening, we identified and currently uncovering the molecular mechanism of kinases and metabolic factors that act as synthetic lethal partners of cisplatin, pemetrexed, and anti-PD1 antibodies. These studies will provide not only insights into the underlying mechanism of resistance but also make an impactful contribution to improving medical treatment of cancer patients who are resistant to current anticancer therapy.	CBCancer Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Kang	Sumin	Biology, Cellular Biology, Molecular Cancer Biology Cell Biology	Full Member
Baek Kim, PhD Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology baek.kim@emory.edu \| Faculty Profile \| Lab Website Professor, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine Director, Center for Drug Discovery HIV-1 and influenza research.	HIV-1 and influenza research.Our laboratory has been working on the molecular and cellular biology of HIV-1 replication, mutagenesis, evolution and viral escape by employing both biochemical and virological approaches. Recently, we have launched new projects designed to understand cell signal pathways that are hijacked by HIV-1 for the establishment of long-living HIV-1 macrophage reservoirs. We also focus on understanding the cellular metabolic changes made by HIV-1 infection for maintaining long-term survival of macrophage reservoirs and persistent viral production. In addition, through the support of the New York Influenza Center of Excellence, our laboratory began exploring the mechanisms involved in the replication and mutagenesis of swine and avian influenza viruses, which contribute to viral host switch and adaptation between animals and humans. The titles of the current research subjects in the Kim laboratory are: 1) Mechanistic understanding of highly error prone HIV-1 reverse transcriptase 2) Cell type-specific HIV-1 mutagenesis and evolution 3) Long-living HIV-1 macrophage reservoirs and PI3K/Akt cell survival pathway 4) Metabolomics of HIV-1 macrophage and resting memory T cell reservoirs 5) Kinetic and mechanistic analysis of influenza virus replication machinery	MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Kim	Baek		Full Member
Tom Kukar, PhD (he/him) Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience thomas.kukar@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Pharmacology and Chemical Biology, School of Medicine Associate Professor, Department of Neurology, School of Medicine Associate Professor, Center for Neurodegenerative Disease, School of Medicine Our lab studies the pathogenesis of neurodegenerative diseases to guide development of novel therapeutics. We focus on Alzheimer's disease (AD), frontotemporal dementia (FTD), and Amyotrophic lateral sclerosis (ALS).	Our lab studies the pathogenesis of neurodegenerative diseases to guide development of novel therapeutics. We focus on Alzheimer's disease (AD), frontotemporal dementia (FTD), and Amyotrophic lateral sclerosis (ALS).The goal of my laboratory is to develop new therapies to treat neurodegenerative diseases. We aim to understand the pathogenesis of these diseases by deciphering their molecular causes in order to identify new drug targets and ultimately therapeutic compounds. We use a multidisciplinary approach ranging from cell culture, chemical biology, high-throughput screening, animal models, human Induced Pluripotent Stem Cell (iPSC) models (neurons, microglia, organoids), AAV-based gene therapies, clinical samples, and multi-omics (including proteomics, metabolomics, and lipidomics). One of our major projects is to understand how mutations in the GRN gene, which cause loss of function of the progranulin (PGRN) protein, cause neurodegeneration. GRN mutations cause frontotemporal dementia (FTD) and neuronal ceroid lipofuscinosis (NCL), a lysosome storage disease. Variants in the GRN gene also increase the risk of developing Alzheimer's disease (AD) and Parkinson's disease (PD). Thus, understanding the function of PGRN is important for multiple neurodegenerative diseases. Our lab discovered that PGRN is a lysosomal protein and is made into small peptides called granulins in the lysosome. Recent work in the lab is focused on determining the function of granulins in the lysosome, how granulins are made, understanding how loss of PGRN causes neuroinflammation (activation of microglia and astrocytes) which are associated with neuron loss. We are also developing PGRN-replacement therapies to treat FTD and other disorders like AD and PD where decreased levels of PGRN are associated with neurodegeneration.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Kukar	Tom	Aging Alzheimer's Disease Biochemistry, Proteins Cell Biology Dementia Disease Model Drug Design Growth Factors Immunology Molecular Biology Neurodegenerative Disease	Full Member
Sang-Ho Lee, PhD Affiliate Member - Molecular and Systems Pharmacology sangho.lee@emory.edu \| Faculty Profile Assistant Professor, Division of Cardiology, Department of Medicine, School of Medicine The goal of my research is to develop novel treatments for cardiovascular diseases using stem cell technology.	The goal of my research is to develop novel treatments for cardiovascular diseases using stem cell technology.Cardiovascular diseases are the most frequent cause of mortality. The main cause of this clinical entity is the loss of blood vessels. Therefore, therapies should target regeneration of endothelial cells. Many clinical therapies have been tried using stem or progenitor cells. However, to date, any trial was not satisfactory due to the complexities and problems. Recent discovery of iPSCs opened the possibility of direct reprogramming to target cells from somatic cells. Thus, I have successfully induced reprogrammed endothelial cells (rECs) directly from fibroblasts by the overexpression of a single transcription factor, ETV2. Continuously, I have been optimizing the various conditions for generating rECs with higher efficiency and developing new strategies to increase clinical applicability of rECs. During this study, I also identified reprogrammed lymphatic endothelial cells (rLECs) among reprogrammed ECs. Hence, I will endeavor to use these rLECs to target lymphatic vessel regeneration for treating lymphedema, which is the most prevalent lymphatic disease and characterized by chronic swelling of tissue due to the lack of fluid drainage. Additionally, I am developing ETV2 gene direct delivery as a therapeutic approach for promoting neovascularization to treat cardiovascular diseases and lymphedema. 1. Lee S, Park C, Han JW, Kim JY, Cho K, Kim EJ, Kim S, Lee SJ, Oh SY, Tanaka Y, Park IH, An HJ, Shin CM, Sharma S, Yoon YS (2017) Direct reprogramming of human dermal fibroblasts into endothelial cells using ER71/ERV2, Circ. Res., 2017 Mar; 120(5):848-861 PMID: 28003219 PMCID: PMC5336520. * equally contributed 2. CakirB,XiangY,TanakaY,KuralMH,ParentM,KangY-J,ChapetonK,PattersonB, Yuan Y, He C-S, Raredon MSB, Dengelegi J, Kim K-Y, Sun P, Zhong M, Lee S, Patra P, Hyder F, Niklason LE, Lee S-H, Yoon Y-s, Park I-H, Development of human brain organoids with functional vascular-like system, Nat. Methods, 2019, 16(11):1169-1175 PMID:31591580 PMCID:PMC6918722 DOI: 10.1038/s41592-019-0586-5	MSPMolecular and Systems Pharmacology - Affiliate Member	Lee	Sang-Ho		Affiliate Member
Rebecca D. Levit, MD (she/her) Full Member - Molecular and Systems Pharmacology rlevit@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Division of Cardiology, Department of Medicine, School of Medicine My lab is built upon translational studies to understand inflammation in cardiovascular disease with a focus on innate inflammation. We are especially focused on the detrimental actions of neutrophils and their ability to release neutrophil extracellular traps (NETs). We have demonstrated the importance of NETs in direct cardiac injury, as well as identify an endogenous regulator of NETs, adenosine (Shin E, JAHA, 2018; Xu K, J Leuk Biology, 2019). We have developed adenosine producing hydrogel designed specifically to combat neutrophilic inflammation in the heart and peripheral limb ischemia (Sayegh M, ATVB, 2021). We have developed large animal hind limb ischemia model as well as a method and device to deliver hydrogels through the heart through the pericardial space (Deppen J, under review; Garcia J, JACC: BTS, 2017). In summary my lab has expertise in the study of the pathophysiology of cardiac innate immunology and experience to design, develop and test novel therapeutic strategies.	My lab is built upon translational studies to understand inflammation in cardiovascular disease with a focus on innate inflammation. We are especially focused on the detrimental actions of neutrophils and their ability to release neutrophil extracellular traps (NETs). We have demonstrated the importance of NETs in direct cardiac injury, as well as identify an endogenous regulator of NETs, adenosine (Shin E, JAHA, 2018; Xu K, J Leuk Biology, 2019). We have developed adenosine producing hydrogel designed specifically to combat neutrophilic inflammation in the heart and peripheral limb ischemia (Sayegh M, ATVB, 2021). We have developed large animal hind limb ischemia model as well as a method and device to deliver hydrogels through the heart through the pericardial space (Deppen J, under review; Garcia J, JACC: BTS, 2017). In summary my lab has expertise in the study of the pathophysiology of cardiac innate immunology and experience to design, develop and test novel therapeutic strategies. I am both a practicing cardiologist and basic science researcher. My lab is built upon translational studies to understand clinically relevant pathophysiology, and the studies needed to move forward the development of new therapeutic strategies. Our recent research focus has been on understanding the early innate immune response in cardiac reperfusion injury. We are especially focused on the detrimental actions of neutrophils in this sterile inflammatory setting, specifically their ability to release neutrophil extracellular traps (NETs). We have been able to demonstrate the importance of NETs in direct cardiac injury, as well as identify an endogenous regulator of NETs, adenosine (Shin E, JAHA, 2018; Xu K, J Leuk Biology, 2019). Working in conjunction with collaborators we have developed adenosine producing purinergic hydrogel designed specifically to combat neutrophilic inflammation in the heart and peripheral limb ischemia (Sayegh M, ATVB, 2021). These gels build off of prior work with biomaterials and their capability to improve cardiac targeted cell therapies (Levit RD, JAHA, 2013). While many of these therapeutics work well in rodents, we have been dedicated to studying their efficacy in large animal models. We have developed a novel large animal hind limb ischemia model as well as a method and device to deliver hydrogels through the heart through the pericardial space (Deppen J, under review; Garcia J, JACC: BTS, 2017). During the COVID-19 pandemic, we have been able to apply our knowledge of neutrophils and NETs to the study of human infection with SARs-CoV-2. Partnering with the Yerkes Primate Research center we have defined the early acute role of neutrophils and NETs in COVID-19 infection as well as tested the ability of the JAK kinase inhibitor baricitinib to target this pathway (Hoang TN, Cell, 2021). These investigations have also lead to novel observations of the effects of COVID-19 on the heart and autonomic nervous system. We have the expertise and protocols in place to work with COVID-19 primate samples with the focus on the cardiac disease manifestations and innate inflammatory response. In summary my lab has expertise in the study of the pathophysiology of cardiac innate immunology as well as the tools and experience to design, develop and test novel therapeutic strategies in small and large animal models.	MSPMolecular and Systems Pharmacology - Full Member	Levit	Rebecca		Full Member
Yona Levites, PhD Affiliate Member - Molecular and Systems Pharmacology Affiliate Member - Neuroscience yona.levites@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Pharmacology and Chemical Biology, School of Medicine I study neurodegeneration for over 20 years. My passion has always been to develop a therapy or a drug that will be able to reverse or prevent these devastating diseases. But more I investigate and learn about them; more I understand how far we are from having a cure. So one of the most intriguing questions I have been puzzled by is why neurons die and what is the reason for selectivity of neuronal death in different diseases, such as Parkinson’s, Alzheimer’s, ALS, etc.	I study neurodegeneration for over 20 years. My passion has always been to develop a therapy or a drug that will be able to reverse or prevent these devastating diseases. But more I investigate and learn about them; more I understand how far we are from having a cure. So one of the most intriguing questions I have been puzzled by is why neurons die and what is the reason for selectivity of neuronal death in different diseases, such as Parkinson’s, Alzheimer’s, ALS, etc.I study neurodegeneration for over 20 years. My passion has always been to develop a therapy or a drug that will be able to reverse or prevent these devastating diseases. But more I investigate and learn about them; more I understand how far we are from having a cure. So one of the most intriguing questions I have been puzzled by is why neurons die and what is the reason for selectivity of neuronal death in different diseases, such as Parkinson's, Alzheimer's, ALS, etc. Recombinant immunotherapy Since then, my research was primarily focused on development novel recombinant antibodies against varieties of neurodegenerative disorders, utilizing resources for novel antibodies as well as pioneering discoveries in the aspects of adeno-associated virus delivery tools available at the University of Florida. A common feature of many neurodegenerative diseases is believed to be an accumulation of misfolded proteins in the brain, initiating a cascade of neurotoxic and inflammatory events leading eventually to brain organ failure. There are no current therapies against most of these diseases. In the recent years immunotherapeutic approach, specifically targeting misfolded proteins' accumulation in the CNS has been very promising, although is facing many challenges in clinic. I have utilized my prior expertise with anti-amyloid beta immunotherapy to clone variable regions from newly developed antibodies against these proteins, modify them to increase their stability and efficacy and further test these novel therapeutics in vitro, cell culture, as well as in various mouse models. Although I started Recombinant Immunotherapy as a specific project, cloning variable regions from anti-Abeta and anti-tau hybridomas during my postdoctoral training, over the time I developed the approach and was able to apply it to my independent funded projects, as well as to earn a reputation in the field of an expert in design, characterization, and delivery of recombinant scFvs against a variety of misfolded proteins and neurodegenerative conditions. Another approach that we took was to stabilize single chain fragments and increase their avidity. The project turned out to be technically very challenging, as a lot of scFvs, especially the ones we targeted intracellularly, lost the parental antibody binding properties, did not fold or express as expected. Although this project did not yield a large number of publications, Marshall became an accomplished antibody engineering scientist and is applying acquired expertise in the biotech industry. AAV My most impactful line of research to date, is probably development of most efficient routs of viral delivery and expression. Adeno-associated virus has been the focus of gene therapy field for many years now, but limited expression and spread are the main obstacles encountered by the scientists trying to develop new models of neurodegenerative diseases or new therapies. We have been both developing and characterizing new viral capsids in collaboration with UF AAV experts, as well as testing various methods of delivery into the brain, spinal cord, muscle, ganglion. I was a lead of the team who developed and coined the term "somatic brain transgeniesis" for neonatal AAV delivery and consulted many collaborators and colleagues in the field on this technique. Amyloid Associated proteins Another project that budded from a collaboration with Emory Department of Biochemistry and Emory ADRC, is looking into the roles Amyloid Associated proteins play in development of pathology in Alzheimer's Disease. My expertise to overexpress genes in the brains of mice and assess their effects on Alzheimer's pathology led to a collaborative project that resulted in MPI RF1 funding. I hope to continue this line of research here at Emory. In addition to main projects, I collaborate with a number of researchers at UF and outside, utilizing my knowledge of Alzheimers Disease mouse models and AAV delivery into the CNS. For example, I was a co-I on a NIH funding, in collaboration with Dr. Rangachary from USM looking into the effects of soluble Amyloid beta oligomers on AD pathology and cerebral amyloid angiopathy in the transgenic mouse model. We plan to obtain additional funding to continue this project.	MSPMolecular and Systems Pharmacology - Affiliate Member NSNeuroscience - Affiliate Member	Levites	Yona	Alzheimer's Disease Immunotherapy Neurodegenerative Disease	Affiliate Member
Lian Li, PhD (she/her) Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience lli5@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Pharmacology and Chemical Biology, School of Medicine Vice Chair, Department of Pharmacology and Chemical Biology, School of Medicine Neurodegenerative disease pathways and therapeutic target discovery	Neurodegenerative disease pathways and therapeutic target discoveryResearch in my laboratory is aimed at understanding the molecular basis of brain function in health and disease with an emphasis on cellular and molecular mechanisms of signal transduction, vesicular trafficking, and neurodegeneration. We are using an innovative, multi-faceted approach that combines proteomics, glycoproteomics, cell biology, systems biology, network pharmacology, and animal model studies with translational research in human patient specimens to discover and study signaling mechanisms, pathogenic pathways, and therapeutic targets for combating Alzheimer's disease, Parkinson's disease, and other brain disorders. The Li laboratory has identified and characterized many novel regulators of neuronal signaling and protein trafficking, and our studies have provided new insights into the fundamental mechanisms controlling synaptic vesicle exocytosis, endosomal trafficking, mitochondrial dynamics, and cellular signal transduction mediated by protein post-translational modifications, including ubiquitination, phosphorylation, and glycosylation as well as their dysregulation in neurodegenerative diseases. Furthermore, we have discovered a number of new molecular pathways linking dysregulated protein trafficking and signaling to the pathogenesis of Alzheimer's disease, Parkinson's disease, and peripheral neuropathy. Through our ongoing research, we aim to identify new molecular targets and therapeutic compounds for treating Alzheimer's disease, Parkinson's disease, and other age-related neurodegenerative diseases.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Li	Lian	Biochemistry, Proteins Brain Tumors Cell Biology Disease Model Dystonia / Tremor Genetics, Molecular Movement Disorders Neurodegenerative Disease Neuropharmacology Neuroscience Parkinson's Disease	Full Member
Zhiyong Lin, PhD (he/him) Full Member - Molecular and Systems Pharmacology zhiyong.lin@emory.edu \| Faculty Profile Associate Professor, Division of Cardiology, Department of Medicine, School of Medicine My research focuses on the molecular mechanisms that govern vascular homeostasis and inflammation.	My research focuses on the molecular mechanisms that govern vascular homeostasis and inflammation.The broad scope of my research program seeks to understand the fundamentals of cardiovascular function. Specifically, I am interested in the molecular mechanisms that govern vascular homeostasis and how the breakdown of these mechanisms significantly contributes to the onset and progression of many vascular pathologies. My lab uses a variety of techniques, including, cellular and molecular biology, biochemistry, and mouse models to study vascular diseases, including atherosclerosis, aortic aneurysm, thrombosis and peripheral artery disease, with the ultimate goal geared toward the development of strategies for disease prevention and treatment. Regulation of important cardiovascular signaling pathways has become an active pursuit of pharmacological intervention for disease treatment. However, nodal determinants that regulate signaling changes in the cardiovasculature are not well understood. Toward that end, our ongoing research efforts have been focused on the signaling events that control vascular inflammation and remodeling. Current efforts in the lab center on dissecting the regulatory roles of two important signaling regulators: Cellular Communication Network (CCN) factor proteins and Protein phosphatase 2A (PP2A) in cardiovascular function. CCN proteins are secreted matricellular proteins that interact with growth factors, the extracellular matrix (ECM), cell surface integrins and other receptors to promote ECM-intracellular signaling. Our published and unpublished work has led to the appreciation that CCN3 serves as an important regulator of vascular health. We found that that CCN3 mitigates the formation and progression of aortic aneurysm (AA) in both thoracic and abdominal regions of aorta. Our recent data points toward CCN3 deficiency as a major contributor to 1) endothelial dysfunction and 2) the loss of barrier integrity, both instrumental in driving the pathology of thoracic aortic aneurysm. We have also shown that bone marrow-derived CCN3 is atheroprotective. Our ongoing work also substantiates the importance of CCN3 in the promotion of angiogenesis and vascular blood flow recovery after hind limb ischemia (HLI) induction. Mechanistic studies suggest that impaired HIF1a signaling and diminished VEGF-induced angiogenesis likely contribute to the loss of functional collateral blood flow in the context of CCN3 deficiency-induced ischemic injury. Despite significant progress, there still remains significant unanswered questions, namely – what is the precise physiological role of CCN from different cellular origins in vivo? And what are the fundamental mechanisms responsible for CCN's action? Answers to these important questions will help fill in our knowledge gap of CCN and potentially guide therapy development. Another area of interest for my lab is the role of protein phosphatase 2A (PP2A) in cardiovascular biology. PP2A is a potent de-phosphorylating enzyme within mammalian cells. It is a critical serine/threonine phosphatase that has been implicated in the regulation of many signaling pathways. Nascent observations from my laboratory revealed a profound loss of PP2A activity in murine models of heart failure, atherosclerosis and aortic aneurysms. This is supported by studies that show PP2A activation by the orally bioavailable small molecule activators of PP2A (SMAPs) markedly suppresses multiple pathologic conditions, including 1) cardiac remodeling in a murine model of heart failure, 2) plaque formation in atherosclerosis models and 3) aortic aneurysm progression. Building on these exciting findings, our overarching goal is to leverage both pharmacologic and genetic approaches to dissect the molecular basis and functional consequences of PP2A activation/inactivation in the above referenced disease settings.	MSPMolecular and Systems Pharmacology - Full Member	Lin	Zhiyong		Full Member
Dennis Liotta, PhD (he/him) Full Member - Molecular and Systems Pharmacology dliotta@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Chemistry, Emory College of Arts and Sciences Co-Director, Center for New Medicine, Emory University Board Member, Scientific Advisory Board, Emory NCI-CBC Center Chair, Advisory Committee, Drug Innovation Ventures at Emory Chair, Scientific Advisory Committee, Emory Institute of Drug Development Over 90% of HIV-infected persons in the US take or have taken a drug invented by Professor Liotta. In addition, lamivudine, the first hepatitis B drug, was invented by him.	Over 90% of HIV-infected persons in the US take or have taken a drug invented by Professor Liotta. In addition, lamivudine, the first hepatitis B drug, was invented by him.In his decades-long career at Emory University, Dr. Dennis Liotta has dramatically improved the longevity and quality of life of millions worldwide. His accomplishments are not limited to just one significant discovery. Dr. Liotta has been directly involved in the discovery and development of multiple lifesaving therapeutic agents. As a successful entrepreneur and visionary leader, he has also created or fostered many businesses in the biopharmaceutical industry and pioneered new approaches to drug development in academia. Dr. Liotta's research focuses on the discovery and development of novel antiviral, anticancer, and anti-inflammatory agents. He has authored over 300 peer-reviewed publications, cited by scientists around the globe tens of thousands of times. These publications fundamentally shaped modern medicinal chemistry and profoundly influenced countless young researchers. An inventor of over 110 issued US patents, Dr. Liotta initiated the development of 18 lifesaving, FDA-approved therapies and is recognized as a premier discoverer of novel therapeutics. While Dr. Liotta's biggest impact has come from the HIV/AIDS therapeutics he developed, he has also made important contributions to other therapeutic fronts, such as oncology and neurological diseases, creating many clinical therapeutic agents to address unmet medical needs. and improve human health. Dr. Liotta embodies the finest qualities of a scientist dedicated to improving human health through original research in medicinal chemistry. More recently, Dr. Liotta initiated a new program to develop cannabidiol prodrugs and analogs as therapeutics for epilepsy, pain and depression.	MSPMolecular and Systems Pharmacology - Full Member	Liotta	Dennis		Full Member
Zixu Mao, MD, PhD Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience zmao@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Pharmacology and Chemical Biology, School of Medicine Professor, Department of Neurology, School of Medicine Mechanisms of neuronal stress response in health and neurological diseases.	Mechanisms of neuronal stress response in health and neurological diseases.We study the critical decision processes by which neural cells respond to stress signals. We are particularly interested in the roles of key subcellular organelles in regulating these central processes. In this context, we want to determine how neurons process specific signals, how these signals are relayed to key sites by mediators, and how cellular processes are modulated in response. Our work involves neuroinflammation, miRNA biology, autophagy, mitochondrial function, and ER homeostasis. We use a combination of approaches including molecular, cellular, animal models, and human tissues in our studies to delineate the roles of these processes in heath and diseases. For additional details, please visit our lab website at http://www.pharm.emory.edu/zmao/	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Mao	Zixu	Neurodegenerative Disease Parkinson's Disease	Full Member
Nael A. McCarty, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology namccar@emory.edu \| Faculty Profile \| Lab Website Professor, Division of Pulmonary Medicine, Department of Pediatrics, School of Medicine Adjunct Associate Professor, School of Biological Sciences, College of Sciences, Georgia Institute of Technology Adjunct Associate Professor, School of Chemistry and Biochemistry, College of Sciences, Georgia Institute of Technology Program Director, MSP Systems biology of chronic lung diseases; Links between immunology and lung disease; Pathophysiology in cystic fibrosis; Epithelial biology; Structure, function, evolution, and pharmacology of ion channels and ATP-binding cassette (ABC) transporters; Regulation of CFTR ion channel by lipids and lipid-mediated signaling.	Systems biology of chronic lung diseases; Links between immunology and lung disease; Pathophysiology in cystic fibrosis; Epithelial biology; Structure, function, evolution, and pharmacology of ion channels and ATP-binding cassette (ABC) transporters; Regulation of CFTR ion channel by lipids and lipid-mediated signaling.Cystic Fibrosis (CF) is a complex lethal disorder, which is the second most common genetic disease in the U.S. and affects people of all ethnic groups. CF is manifest in multiple tissues of epithelial origin. Mutations in the gene encoding the Cystic Fibrosis Transmembrane conductance Regulator (CFTR) result in abnormal secretion in exocrine glands, due to dysfunctional ion channels and/or improper regulation of ion channels. This laboratory is actively engaged in research addressing three aspects of CF: 1) Systems biology approaches to understand mechanisms underlying disease progression in chronic lung diseases, including CF, especially focusing on the biogeography of infection, inflammation, and injury in the lung. Our team within the Center for CF and Airways Disease Research considers the airway as an ecosystem, comprised of many different cell types plus a variety of pathogens, all of which play important roles in pulmonary function. We believe that it is only by studying this ecosystem in situ, relying on samples of airway fluid and cells from CF patients themselves, that we will ever fully understand this disease and identify the means to control it. Many collaborators at Emory, Georgia Tech, and Children's Healthcare of Atlanta contribute to this team, led by N McCarty as Director of the Center. This work also allows us to be involved in the development of novel therapies and devices for CF patients. This multifaceted approach keeps our efforts focused upon issues relevant to this disease and its treatment. 2) Impact of mutations in the CFTR gene on the interactions between airway epithelial cells and transmigrating neutrophils, which are the source of damage leading to bronchiectasis and death in people with CF. 3) The impact of systemic hyperglycemia as found in CF-related diabetes - the most common comorbidity in CF - on the management of airway glucose and the regulation of innate immunity in the airway. New work from our lab his identified an impact of mutant CFTR on insulin-dependent glucose transport, the first evidence of this sort. We are now determining the mechanism underlying this defect in the CF airway. 4) The biophysics, regulation, and pharmacology of the CFTR chloride channel. CFTR forms a low-conductance Cl channel which is controlled in a novel way. A major effort in this lab involves performing structure/function experiments to: (a) determine how CFTR evolved channel function from its molecular ancestors, all of which function as transporters; (b) determine how mutant CFTR impacts the innate immune system in the airway; (c) determine how lipids and lipid-mediated signaling alter function and pharmacology; and (d) identify novel therapeutic small molecules that repair the defects in mutated CFTR channels as found in our patients. This has led to the identification of several novel potentiators of mutant CFTR function.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	McCarty	Nael	Cell Biology Electrophysiology Membrane Biology Molecular Biology Pediatrics Physiology Respiratory Disorders	Full Member
Lefteris Michailidis, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology emicha7@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine Curriculum Committee, BCDB Seminars Committee, MMG Our research program focuses on understanding the interaction between viruses and the host using a set of biochemical, cell-based and in vivo methods. In particular, we are interested in hepatitis B virus (HBV) and the development of eradication strategies that involve state-of-the-art primary hepatocyte systems and humanized liver chimeric mice. These systems expand the scope of our research beyond viral hepatitis to other liver-related diseases and fields including fatty liver disease and liver immunometabolism. In addition, we have a strong interest in antiviral mechanisms carried out by interferon-stimulated genes and other host proteins but also small molecule inhibitors in regards to mechanisms of action and resistance. In this direction our main focus has been HIV, HBV, and SARS-CoV-2. To accomplish these goals we use medium and high-throughput genetic screens (gene overexpression and CRISPR knockout) across different cell systems and in some cases in humanized mice.	Our research program focuses on understanding the interaction between viruses and the host using a set of biochemical, cell-based and in vivo methods. In particular, we are interested in hepatitis B virus (HBV) and the development of eradication strategies that involve state-of-the-art primary hepatocyte systems and humanized liver chimeric mice. These systems expand the scope of our research beyond viral hepatitis to other liver-related diseases and fields including fatty liver disease and liver immunometabolism. In addition, we have a strong interest in antiviral mechanisms carried out by interferon-stimulated genes and other host proteins but also small molecule inhibitors in regards to mechanisms of action and resistance. In this direction our main focus has been HIV, HBV, and SARS-CoV-2. To accomplish these goals we use medium and high-throughput genetic screens (gene overexpression and CRISPR knockout) across different cell systems and in some cases in humanized mice. The Michailidis laboratory is interested in understanding the molecular and cellular mechanisms that drive virus-host interactions, how viruses lead to human diseases, and the strategies we can develop to control them. In particular, we are interested in hepatitis B virus (HBV), its target cells, the hepatocytes, and the crosstalk between innate immunity and metabolism in the liver. With physiologically relevant in vitro and in vivo systems and state-of-the-art technologies ranging from single-cell transcriptomics to whole-genome CRISPR editing, there is a great potential to uncover the mechanisms that govern chronic hepatitis B and ultimately cure this deadly disease. Furthermore, using similar strategies we want to extend our knowledge across multidisciplinary fields, including other hepatotropic infections, liver-related diseases and liver functions. The innate immune response, driven by interferon (IFN), protects cells against invading viral pathogens. The workhorses that mediate this defense are the products of hundreds of IFN-stimulated genes (ISGs). Our previous work with HBV, Zika virus and multiple coronaviruses, including SARS-CoV-2, has revealed a set of ISGs that have a drastic effect on viral replication. Our objective is to characterize the mechanism of action of these ISGs and inform the development of new antiviral strategies. Towards this goal we employ a diverse set of molecular, cellular, and biochemical tools.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Michailidis	Lefteris	Cell Biology Liver Diseases Virology	Full Member
Eric J. Miller, PhD Affiliate Member - Molecular and Systems Pharmacology ejmill2@emory.edu \| Faculty Profile Assistant Professor, Department of Pharmacology and Chemical Biology, School of Medicine We develop chemical probes and novel therapies to understand and control drug, protein, and cell localization.	We develop chemical probes and novel therapies to understand and control drug, protein, and cell localization.As highlighted by the maturation of proteolysis targeting chimeras (PROTACs), antibody-drug conjugates (ADCs), and targeted radionuclides (e.g., 177Lu-PSMA-617), a new era of bifunctional molecules is upon us. While many of these agents are designed to bring two binding partners into close proximity using linkers that are stable under experimental conditions (e.g., PROTACs), others take advantage of cleavable linkers for activation in response to specific stimuli, which can be either exogenous (e.g., photons) or endogenous (e.g., acidic pH in endosomes). For example, ADCs function via antibody binding to a cell surface protein that is overexpressed on the cell type of interest. This facilitates cell type-selective localization of the associated drug, often a potent cytotoxin, which is inactive when conjugated to the linker. However, internalization of the ADC-antigen complex into endosomes leads to linker cleavage under endosomal conditions (e.g., reduced pH) and subsequent intracellular release of the associated drug. Although these bifunctional molecules have significant therapeutic potential, few agents have achieved regulatory approval. Perhaps the largest barrier to successful clinical translation is the need for exquisitely fine-tuned linker chemistry. This is exemplified by the first FDA-approved ADC Mylotarg, which features a cleavable linker designed for acid-catalyzed hydrolysis in endosomes. Although Mylotarg demonstrated reduced toxicity relative to the unconjugated cytotoxin, it was withdrawn from the market due to toxicities driven partially by poor plasma stability. This is just one example highlighting the need for rigorous investigation, development, and innovation in the field of linker chemistry, which is the core focus of our research. We seek to discover chemical tools and novel therapeutic agents that probe, perturb, and control the localization of drugs, proteins, and cells. While projects in the lab revolve around this central theme, the objectives of each are unique. For example, using cleavable linker chemistry, we explore (1) the localization and activation of nucleoside-based therapeutics, (2) protein-protein interactions with spatial and temporal resolution, and (3) the physiological trafficking of immune cells. Through this lens, we are focused on providing members of the lab with cutting-edge training in biomedical research at the interface of biology and chemistry, the scientific community with new chemical biology tools, and the medical community, patients, and caregivers with novel therapeutic agents to address unmet medical needs.	MSPMolecular and Systems Pharmacology - Affiliate Member	Miller	Eric		Affiliate Member
Xiulei Mo, PhD Full Member - Cancer Biology Full Member - Molecular and Systems Pharmacology xiu-lei.mo@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Pharmacology and Chemical Biology, School of Medicine Understanding the molecular circuitry underlying tumor initiation, progression, and therapeutic response towards anti-cancer target and drug discovery.	Understanding the molecular circuitry underlying tumor initiation, progression, and therapeutic response towards anti-cancer target and drug discovery.My long-term goal is to understand the molecular basis underlying tumor initiation, progression and drug resistance, and to bridge the gap between vast cancer genomic dataset and unmet clinical need using system biology and chemical biology approaches. A major focus of my research is to leverage high-through screening technologies for biological target identification and drug discovery. As a key investigator in the Molecular Interaction Center for Functional Genomics Center (MicFG) of Emory University, I have innovated multiple cutting-edge technologies to identify cancer associated protein-protein interactions as therapeutic target, and leveraged chemical biology tools for therapeutic discovery. I have built the foundation for the proposed research by developing several HTS technology platforms for PPI detection, such as TR-FRET, BRETn and NanoPCA, aiming towards systematic target identification on a cancer genomic scale, as well as for small molecule screening campaign for anti-cancer agent discovery and development as documented in the following publications. Specifically related to this proposal, I have developed the quantitative high-through differential screening (qHT-dS) platform based on the BRETn live-cell PPI detection technology to systematically discover mutated residue-directed neoPPIs in cancer. My work led to the discovery of novel protein binding partners for MYC and Hippo signaling pathway proteins, as well as other novel PPI targets, such as STK11-CDK4, MKK3- MYC, GATAD2B-MYC and AXL-RAS, that are important in tumorigenesis, metastasis and drug resistance. I also conducted and actively contributed to the target-based small molecule screening campaign for discovery of inhibitors for potential oncogenic PPI targets, such as PRAS40-PRAS40 dimer and NSD3-MYC. As a logical extension in order to interrogate some immunotherapy associated PPI targets, I led the development of the High-Throughput immunomodulator Phenotypic (HTiP) screening platform that recapitulates the complex in vivo tumor-immune network using in vitro immune- and cancer cell co-culture system. My work has led to the discovery of several IAP inhibitors as potential small molecule immunomodulator hits with desired properties in enhance the anti- tumor immunity in reversing the oncogenic mutation-induced immunosuppressive microenvironment. To interrogate the often-neglected tumor suppressor space for drug discovery, I led the discovery of small molecule mutant SMAD4-PPI inducers (MuSMADid) through innovative TR-FRET HTS screening, orthogonal PPI-detection assays and functional assays validation. My work has led to the discovery of bisindolylmaleimide derivatives with desired MuSMADid properties in induce the mutant SMAD4-SMAD3 PPI, restore the TGb/SMAD4 signaling, and re-sensitize the cancer cells response to TGFb induced growth inhibition.	CBCancer Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Mo	Xiulei		Full Member
Eric Ortlund, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology eortlun@emory.edu \| Faculty Profile \| Lab Website Professor, Department of Biochemistry, School of Medicine Director of Emory Integrated Metabolomics and Lipidomics Core Facility (EIMLC), Department of Biochemistry, School of Medicine Structural biology (X-ray and CryoEM), drug design, and molecular evolution of receptors, transporters and other drug targets. Deep mutational scanning to characterize protein-protein interfaces.	Structural biology (X-ray and CryoEM), drug design, and molecular evolution of receptors, transporters and other drug targets. Deep mutational scanning to characterize protein-protein interfaces.Our mission is to make fundamental discoveries relating to hormone signaling, transcriptional control and host-pathogen interactions. We leverage these discoveries to pursue drug design as treatments for viral infections and chronic inflammatory diseases. We use a range of sophisticated biological techniques including cryo-electron microscopy, x-ray crystallography, mass spectrometry, deep mutational scanning and in silico simulations. Our primary research interests include lipid-mediated signaling and transport, development of LRH-1 modulators to treat metabolic disease, characterization of anti-inflammatory steroids and molecular evolution. We have ongoing drug development efforts in these areas. With the outbreak of SARS-CoV-2, we were well-placed to redirect our expertise to investigate detection and neutralizing antibodies using Cryo-EM, and to predict antibody escape using deep mutational scanning (DMS). Working closely with the RADx initiative, our methods have proven useful to multiple companies seeking FDA approval for their novel COVID-19 diagnostic methods. Currently we are expanding our technology to tackle other arising infectious diseases of concern and to design new therapeutic proteins.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Ortlund	Eric	Biochemistry, Lipids Biochemistry, Nucleic Acids Biochemistry, Proteins Diabetes Digestive Disease & Disorders Drug Design Endocrinology Hormones Metabolism	Full Member
Mike Owens, PhD Full Member - Molecular and Systems Pharmacology Affiliate Member - Neuroscience mowens@emory.edu \| Faculty Profile Professor, Department of Psychiatry and Behavioral Sciences, School of Medicine Interactions between neuropeptides and clinically efficacious psychotropic drugs; neuropsychopharmacology.	Interactions between neuropeptides and clinically efficacious psychotropic drugs; neuropsychopharmacology.I am interested in the cellular and molecular underpinnings of complex psychiatric diseases and their pharmacotherapy. These include depression, anxiety disorders, bipolar disorder and schizophrenia with the ultimate goal of development of novel therapeutics and/or increasing the efficacy of current treatments. To address these issues, we have used a variety of molecular, cellular, pharmacological, behavioral and imaging techniques in laboratory animals and humans. Most recent interests have focused on: 1) clinically-relevant design of pharmacotherapy studies in laboratory animals, 2) modeling of in utero medication exposure and the response of the transcriptome and epigenome in offspring, and 3) development of methodologies to easily assess transporter occupancy of antidepressant medications in clinical populations with the goal of quickly and easily identifying patients who are non-responders due to inadequate dosing. I have long been committed to mentoring a new generation of scientists interested in neuropharmacology.	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Affiliate Member	Owens	Mike	Emotions / Mental Disorders Neurochemistry Neuroendocrinology Neuropharmacology Pharmacology Receptors	Full Member
Anupam Patgiri, PhD (he/him) Full Member - Biochemistry, Cell and Developmental Biology Full Member - Molecular and Systems Pharmacology anupam.patgiri@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Pharmacology and Chemical Biology, School of Medicine Member, Discovery and Developmental Therapeutics Research Program, Winship Cancer Institute My lab studies the pathophysiology of mitochondrial and metabolic diseases to develop novel therapies. We use LCMS-based metabolomics, chemical probe development, therapeutic protein engineering, animal models, and molecular and cell biology techniques.	My lab studies the pathophysiology of mitochondrial and metabolic diseases to develop novel therapies. We use LCMS-based metabolomics, chemical probe development, therapeutic protein engineering, animal models, and molecular and cell biology techniques.We study how defective mitochondria contribute to common and rare diseases to develop potential therapy. Our lab uses a multidisciplinary approach that includes therapeutic protein engineering, LCMS-based metabolomics, small molecular probe development, and AAV-based gene therapy in animal models. Three of our ongoing are: Project 1. Pre-clinical testing of an engineered enzyme therapy for mitochondrial electron transport dysfunction (Patgiri et al. Nat Biotech, 2020), Project 2. Development of chemical strategies to restore mitochondrial homeostasis in disease, and Project 3. Novel strategies to modulate metabolism in the tumor-immune microenvironment to boost the cytotoxicity of CAR T cells and tumor-associated macrophages. For more information, please visit https://patgirilab.org/	BCDBBiochemistry, Cell and Developmental Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Patgiri	Anupam	Biochemistry, Proteins Cell Metabolism Drug Design Enzymology Immunotherapy Metabolic Diseases Metabolism Neurodegenerative Disease	Full Member
Cassandra L. Quave, PhD (she/her) Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology cquave@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Dermatology, School of Medicine Associate Professor, Emory Center for the Study of Human Health, Emory College of Arts and Sciences Natural products drug discovery for novel inhibitors of bacterial pathogenesis and virulence pathways.	Natural products drug discovery for novel inhibitors of bacterial pathogenesis and virulence pathways.Dr. Quave's research is focused on drug discovery efforts from natural products derived from medicinal plants and fungi to improve treatment options for drug‐resistant bacterial infections. The Quave lab team uses the ethnobotanical approach to drug discovery. This involves conducting field research in which traditional medical practices for the treatment of infectious diseases are documented in the field, and later assessed in the lab. Specifically, medicinal plants are brought back to the lab for chemical extraction and analysis, followed by testing using a series of anti‐bacterial bioassays and tests for mammalian toxicity. In particular, research efforts are focused on blocking pathogenesis and virulence pathways rather than bacterial growth. Simply put, by using natural products to turn off bacterial defense mechanisms (i.e. biofilms), the organisms can be made more susceptible to antibiotics and host immune factors. Likewise, by turning off bacterial communication (quorum sensing) mechanisms, which are responsible for the production of a suite of toxins, the damage inflicted by pathogens to the host can be reduced. To date, there are no anti‐virulence drugs available on the pharmaceutical market for S. aureus infection, though many agree that such drugs are desperately needed. As a graduate student, Quave documented the use of plants in the treatment of skin and soft tissue infection in traditional south Italian folk medicine. She was the first to document the quorum‐quenching effects of medicinal plant products in a staphylococcal model. She then spent 3 years as a postdoctoral fellow in microbial pathogenesis at UAMS, where she concentrated on the bioassay‐guided fractionation of natural product extracts, testing them against other pathogenesis targets such as biofilms, in particular. This work on staphylococcal pathogenesis targets led to UAMS filing a patent to protect the discovery of an antibiofilm agent, known in the literature as "220D‐F2". Dr. Quave and her lab team continue these research efforts at Emory University by developing novel solutions to the issue of skin and soft tissue infection. Their core approach in these efforts is based on the study of medicinal plants for their capacity to target pathogenicity and virulence pathways. Here is a short description of a few of the major projects currently underway in the Quave lab: 1) Quorum quenchers for Staphylococcus aureus.Quave studies natural products from medicinal plants that block staphylococcal quorum‐sensing in the staphylococcal accessory gene regulator system (agr), types I‐IV. We are examining the translational potential of these compounds as part of the hit to lead discovery and development process. 2) Biofilm inhibitors for multiple pathogens from the Elmleaf Blackberry: The Quave lab is working on the chemical characterization of the compounds present in the highly bioactive natural products composition "220D‐F2". In collaboration with other Emory investigators, we are also investigating the breadth of activity of this composition against other important human pathogens. 3) Other projects underway include expansion of the QNPL (Quave Natural Products Library) with a highly biodiverse collection of extracts derived from plants and fungi, and screening of these compounds for bioactivity against high priority multidrug resistant pathogens. We are also exploring the use of plant natural products as resistance modifying agents against ESKAPE pathogens and others. 4) Chemical and pharmacological characterization of plant natural product extracts. We leverage orthogonal techniques (MS, NMR, SXRD) as well as emerging technologies (MicroED, aka 3DED) to resolve structures of novel natural products.	MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Quave	Cassandra	Antibiotics Dermatology Drug Resistance Microbiology Pharmacology Skin Diseases	Full Member
Sunil S. Raikar, MD (he/him) Full Member - Cancer Biology Full Member - Molecular and Systems Pharmacology sraikar@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Aflac Cancer and Blood Disorders Center Developing chimeric antigen receptor (CAR) T cells for pediatric blood cancers.	Developing chimeric antigen receptor (CAR) T cells for pediatric blood cancers.The overall goal of the Raikar laboratory is to develop novel therapeutics for pediatric blood cancers through (i) development of innovative cellular immunotherapies utilizing chimeric antigen receptors, (ii) production of novel recombinant protein-based therapeutics such as L-asparaginase and (iii) identifying new therapeutic targets in rare leukemias utilizing advanced bioinformatic tools. The specific diseases I investigate include acute lymphoblastic leukemia (ALL), acute myeloid leukemia (AML) and mixed phenotype acute leukemia (MPAL). While the survival of pediatric leukemia patients has greatly improved with the intensification of chemotherapy, relapsed disease still accounts for high rate of mortality among childhood cancer patients. Thus, a need exists to develop novel alternative approaches to target relapsed disease with lesser side effects. In recent years, chimeric antigen receptor (CAR) T-cell immunotherapy for relapsed/refractory B-cell acute lymphoblastic leukemia (B-ALL) has been a revolutionary breakthrough in pediatric cancer. In this form of therapy, the patient's own immune cells (T cells) are genetically modified to express receptors called CARs, which enable them to specifically target B cells. While CAR T-cell therapy is extremely successful in targeting B-cell cancers, the same approach has not been successful in targeting T-cell cancers such as T-cell acute lymphoblastic leukemia (T-ALL), which has a higher rate of relapse and is more difficult to cure compared to B- ALL. One of Dr. Raikar's main research aims is centered on adapting this novel CAR technology to T-cell disease. Given the lack of a tumor specific antigen in T-cell malignancies, utilizing CAR-based immunotherapy in this disease has been extremely challenging as it can result in (i) fratricide (self-killing) of CAR T cells, (ii) long-standing immunosuppression from T-cell aplasia and (iii) product contamination from accidental transduction of malignant T cells. Dr. Raikar is exploring several different approaches to overcome these challenges, including the use of unique immune cells such as natural killer cells and gamma delta T cells. As an extension of this work, Dr. Raikar is now also exploring the use of cellular therapy in acute myeloid leukemia (AML), a more aggressive form of childhood blood cancer with survival around 60-70%. Dr Raikar's laboratory also has interest in developing novel chemotherapeutics through protein engineering. A current ongoing project is the development of a novel humanized L-asparaginase drug candidate utilizing an innovative protein drug discovery and optimization platform called ancestral sequence reconstruction (ASR). L-asparaginase has been a critical component of the chemotherapy armamentarium used to treat acute lymphoblastic leukemia (ALL) for several decades. However, current L-asparaginases are bacterial in origin, derived from either Escherichia coli and Erwinia chrysanthemi, and hence are highly immunogenic with reactions ranging from silent inactivation to severe anaphylaxis. Additionally, these drugs have a high level of liver and pancreatic toxicity, thus limiting its widespread use. Recent data has shown that discontinuation of L-asparaginase results in poorer prognostic outcomes in ALL. Thus, development of a more humanized and less immunogenic asparaginase is essential to overcome the major deficiencies of the current bacterial L-asparaginase products. We are currently utilizing the ASR platform to identify and characterize potential less toxic L-asparaginase candidates. As a physician-scientist, Dr. Raikar is also a member of the clinical leukemia/lymphoma team at the Aflac Cancer and Blood Disorders Center at Children's Healthcare of Atlanta and spends his clinical time taking care of children with blood cancers. Through his national involvement with the Children's Oncology Group (COG), where he serves on the T-ALL and MPAL (mixed phenotype acute leukemia) disease committees, Dr. Raikar also maintains a strong presence in the concept, design and implementation of clinical studies in these high-risk leukemia populations.	CBCancer Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Raikar	Sunil		Full Member
Renee D. Read, PhD (she/her) Full Member - Molecular and Systems Pharmacology Full Member - Neuroscience renee.read@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Department of Pharmacology and Chemical Biology, School of Medicine Associate Professor, Department of Hematology and Medical Oncology, School of Medicine Co-Leader, Cellular and Molecular Biology Research Program, Winship Cancer Institute My research program focuses on genetic, epigenetic, and developmental mechanisms that drive initiation and progression of primary brain tumors, including high-grade gliomas and schwannomas, in both children and adults.	My research program focuses on genetic, epigenetic, and developmental mechanisms that drive initiation and progression of primary brain tumors, including high-grade gliomas and schwannomas, in both children and adults.Our research focuses on high-grade gliomas, the most common primary malignant brain tumors, and other primary glial tumors. These tumors are thought to arise from mutations that disrupt developmental and homeostatic processes in neuro-glial stem and progenitor cell types in the brain and central nervous system. The goals of my lab are to determine how insights into the cell and developmental biology of these tumors and how a greater understanding of the tumor neural microenvironment can be harnessed to develop new and improved treatments for patients. Currently, our research program employs a multidisciplinary approach to study the function of developmental pathways and mechanisms in tumorigenesis. Our approach uses several brain tumor model systems, including mouse genetic model systems, primary patient-derived human tumor stem cells, and human organoid models of adult and pediatric high-grade gliomas. Much of our research focuses on receptor tyrosine kinases (RTKs) and their downstream signaling effectors, including their transcriptional targets, and their function in oncogenic neuro-glial stem/progenitor cells as well as interactions between different cell types within tumors and the neural microenvironment. Our research is supported by productive collaborations with other neuro-oncology researchers in the Departments of Pediatrics, Neurosurgery, Human Genetics, and Pathology, including clinical neurosurgical faculty, neuropathology faculty, and other faculty with interests in this dynamic field. Through our efforts, our team has contributed to the development of new therapies targeting RTK effector pathways in high-grade gliomas, including the YAP and TAZ transcription factors. Our work has included investigator-initiated clinical trials of a YAP/TAZ inhibitor in adult brain tumor patients. Current funded and exploratory projects in our lab include research on the roles of RTK fusion variants in tumor initiation from neuro-glial stem/progenitor cells, mechanisms of drug response and drug resistance in adult and pediatric high-grade gliomas, and the functions of innate immunity signaling pathways cell-cell interactions in gliomas and schwannomas. We welcome trainees interested in developmental and molecular neurobiology, cancer stem cell biology, drug target identification and drug discovery, neurologic diseases, and related disciplines to join us in our journey to identify new and effective therapeutic strategies for these diseases. See our lab website to learn more: https://www.reneereadlab.org/	MSPMolecular and Systems Pharmacology - Full Member NSNeuroscience - Full Member	Read	Renee		Full Member
Amir Rezvan, MD, MS Full Member - Molecular and Systems Pharmacology arezva2@emory.edu \| Faculty Profile Assistant Professor, Division of Cardiology, Department of Medicine, School of Medicine My research focuses on the role of disturbed flow on endothelial cell activation and interaction with the immune system and its effect on atherosclerosis.	My research focuses on the role of disturbed flow on endothelial cell activation and interaction with the immune system and its effect on atherosclerosis.Our lab and collaborators have developed various in vitro and in vivo models to study the mechanisms underlying atherosclerosis, including the endothelial cell response to disturbed flow. We have also developed a mouse model to help us understand the contribution of liver inflammation and fibrosis to cardiovascular inflammation and atherosclerosis. The current main project in our lab (NIH funded) is understanding the role of the transcription factor ZBTB46 in endothelial cells and its contribution to preventing atherosclerosis. Our results showed that this factor is expressed in arterial endothelial cells, is regulated by shear stress both in vitro and in vivo, and affects endothelial cell proliferation and cell cycle. Knockout mice that don't express ZBTB46 in their endothelial cells are more prone to atherosclerosis. We are also exploring the role of liver fibrosis and the role of the liver as an immune organ on atherosclerosis in collaboration with Dr. Arash Grakoui (funded by AHA 2017-2018) with preliminary data suggesting that research fibrosis contributes to atherosclerosis.	MSPMolecular and Systems Pharmacology - Full Member	Rezvan	Amir		Full Member
Stefan Sarafianos, PhD Full Member - Biochemistry, Cell and Developmental Biology Full Member - Microbiology and Molecular Genetics Full Member - Molecular and Systems Pharmacology ssarafi@emory.edu \| Faculty Profile \| Lab Website Professor, Laboratory of Biochemical Pharmacology, Department of Pediatrics, School of Medicine Drug discovery, drug resistance, replication mechanisms in HIV, HBV, SARS-CoV-2, MPox, Nipah virus, Ebola and emerging pathogens using virology, structural biology, microscopy, biochemistry, and high-throughput technologies.	Drug discovery, drug resistance, replication mechanisms in HIV, HBV, SARS-CoV-2, MPox, Nipah virus, Ebola and emerging pathogens using virology, structural biology, microscopy, biochemistry, and high-throughput technologies.Our research aims to unravel fundamental mechanisms of drug action, drug resistance, and other aspects of the life cycles of viruses that cause severe diseases. In turn, we apply this knowledge in the design of novel antiviral approaches toward the development of therapeutics. Our drug discovery efforts leverage collaborations with world leading laboratories and use of state-of-the-art multidisciplinary tools, including virological approaches, microscopy methods (super-resolution, single-molecule, and confocal approaches), structural (crystallographic and now cryo-electron microscopy), biochemical (pre-steady state kinetics), biophysical (thermophoresis, surface plasmon resonance), high-throughput and high-content screening as well as structure-based drug design (molecular modeling). Our efforts have led to the development of EFdA, a highly promising long-acting antiviral, currently in Phase III clinical trials for the treatment of HIV infection. Additional funded research interests include SARS-CoV-2, Hepatitis B Virus (HBV), MonkeyPox Virus (MPOXV, Nipah Virus (NiV). Other viruses studied include Ebola Virus, Hepatitis C Virus (HCV), Zika Virus, Foot-and-Mouth Disease Virus (FMDV). For detailed description of currently funded research, please follow link: https://projectreporter.nih.gov/Reporter_Viewsh.cfm?sl=12EECC0B4C8ECFDE7598B8961CAA4A01A2FFCEB861BF Some projects (with selected publications) are also listed below: -Development of EFdA as a weekly oral dosing and once-yearly slow-release dosing anti-HIV drug (PNAS 113:9274-9, 2016; J Biol Chem. 289: 24533-48, 2014) (with Dr. Mitsuya, NIH, Kumamoto Univ). Studies continue on the mechanism of EFdA activation and resistance in clinical settings (R01 AI076119). -Virological, biochemical, and structural studies of HIV capsid with host factors and capsid-targeting antivirals (Science 349: 99-103, 2015) (with Z. Wang, Univ of Minnesota) (R01 AI120860). -Molecular mechanisms of HIV Drug resistance (Antimicrob Agents Chemother. 61, 2017; Viruses. 6 (9), 3535-3562, 2015) (with U Neogi and A Sonnerborg, Karolinska Institutet) (R01 GM118012). -Novel antiviral discovery and drug resistance studies for SARS-CoV-2. Using our recently developed replicon systems, we are screening nucleoside analog compounds for the discovery of anti-SARS-CoV-2 hits, which upon hit-to-lead optimization can become COVID-19 drug candidates (R01 AI167356). To explore the mechanisms of resistance to the antiviral component of Paxlovid, nirmaltrevir (NIR), we have designed mutations in our replicons to impair NIR binding (bioRxiv. 2023 Jan 3:2022.12.31.522389). -Novel antivirals for Mpox Virus (MPXV). Through our collaboration with the lab of Dr. Haian Fu, we are performing high throughput screening (HTS) and high content screening (HCS) using Modified Vaccinia Ankara virus (MVA) as an initial screening system, and by validating identified hits in an MPXV cell culture system, thus leading into downstream lead candidate development (Rapid Synergy: Monkeypox, Emory SoM/WHSC I3 Award). - Novel antivirals for Nipah Virus (NiV). We have been using our first-generation Nipah mini-genome replication system to screen a unique nucleoside analog library that our collaborators in the Schinazi lab have been building over the course of decades. By leveraging minigenome (MG) replicon-based approaches, we aim to identify compounds that demonstrate potent antiviral activity against NiV, which can serve as the basis for the development of novel antiviral therapies. -Interactions of HIV with host factors-APOBEC3-HIV RT interactions. To block reverse transcription, cells express APOBEC3 (A3) family of restriction factors that suppress infection. Co-investigator Malim (King's college) has shown that HIV evades A3-mediated inhibition through the action of its Vif protein. While it has been established that A3s block HIV primarily through their cytidine deaminase activity, which causes hypermutation and genetic inactivation, they also inhibit RT itself (Nature Microbiol. Nov 20. 2017), through a mechanism that is poorly understood. As the co-Director of the HIV Interactions in Viral Evolution Center (HIVE) (http://hive.scripps.edu/index.html), a Center for AIDS molecular interactions and evolution studies, I am leading efforts to characterize the RT-A3 interactions (U54 GM103368). -HIV eradication studies through novel techniques for visualization of viral RNA, DNA and protein. We recently published a novel microscopy-based method (MICDDRP or Multiplex Immunofluorescent Cell-based Detection of DNA, RNA and Protein) (Nature Commun. 8:1882. 2017) that should facilitate investigations on fundamental biology of HIV or other viruses, including the specific role of host factors on integration, transcription, and latency, and also provide critical advances in elucidating mechanisms of antiviral inhibition at the level of single cell, single viral genome, and single integration site. -Novel antivirals targeting the RNase H activity of HIV (PLoS Pathogens 9: e1003125, 2013; J Med Chem. 60: 5045-5056, 2017) (with Z. Wang, and R. Ishima, Univ of Pittsburgh) (R01 AI100890 NCE). -Novel antivirals for treatment of HBV infection. We are targeting HBV through the development and characterization of antivirals that block HBV by targeting its capsid, reverse transcriptase, or RNase H active sites (PLoS Pathog. 2013 Jan;9(1):e1003125; Antimicrob Agents Chemother. 61, e00245-17, 2017; Hepatology 62:1024-36, 2015; ). We are also developing cutting-edge microscopy-based and molecular biology based approaches to study HBV biology (R01 AI121315). References 1: Puray-Chavez M, Tedbury PR, Huber AD, Ukah OB, Yapo V, Liu D, Ji J, Wolf JJ, Engelman AN, Sarafianos SG. Multiplex single-cell visualization of nucleic acids and protein during HIV infection. Nature Commun. 2017 Dec 1;8(1):1882. doi: 10.1038/s41467-017-01693-z. PubMed PMID: 29192235; PubMed Central PMCID: PMC5709414. 2: Gres AT, Kirby KA, KewalRamani VN, Tanner JJ, Pornillos O, Sarafianos SG. STRUCTURAL VIROLOGY. X-ray crystal structures of native HIV-1 capsid protein reveal conformational variability. Science. 2015 Jul 3;349(6243):99-103. doi: 10.1126/science.aaa5936. Epub 2015 Jun 4. PubMed PMID: 26044298; PubMed Central PMCID: PMC4584149. 3: Salie ZL, Kirby KA, Michailidis E, Marchand B, Singh K, Rohan LC, Kodama EN, Mitsuya H, Parniak MA, Sarafianos SG. Structural basis of HIV inhibition by translocation-defective RT inhibitor 4'-ethynyl-2-fluoro-2'-deoxyadenosine (EFdA). Proc Natl Acad Sci U S A. 2016 Aug 16;113(33):9274-9. doi: 10.1073/pnas.1605223113. Epub 2016 Aug 3. PubMed PMID: 27489345; PubMed Central PMCID: PMC4995989. 4: Lan S, Neilsen G, Slack RL, Cantara WA, Castaner AE, Lorson ZC, Lulkin N, Zhang H, Lee J, Cilento ME, Tedbury PR, Sarafianos SG. Nirmatrelvir Resistance in SARS-CoV-2 Omicron_BA.1 and WA1 Replicons and Escape Strategies. bioRxiv [Preprint]. 2023 Jan 3:2022.12.31.522389. doi: 10.1101/2022.12.31.522389. PMID: 36656782; PMCID: PMC9844013.	BCDBBiochemistry, Cell and Developmental Biology - Full Member MMGMicrobiology and Molecular Genetics - Full Member MSPMolecular and Systems Pharmacology - Full Member	Sarafianos	Stefan	AIDS / HIV Biochemistry, Nucleic Acids Drug Design Drug Resistance Virology	Full Member
Mala Shanmugam, PhD Full Member - Cancer Biology Full Member - Molecular and Systems Pharmacology mala.shan@emory.edu \| Faculty Profile Associate Professor, Department of Hematology and Medical Oncology, School of Medicine The Shanmugam lab is studying how cancer cells alter their metabolism to evade programmed cell death, promote immune evasion and foster cooperative metabolic heterogeneity in invasion and metastasis.	The Shanmugam lab is studying how cancer cells alter their metabolism to evade programmed cell death, promote immune evasion and foster cooperative metabolic heterogeneity in invasion and metastasis.The central interest of my lab is to elucidate metabolic alterations in multiple myeloma (MM) cells that promote survival, growth, proliferation and resistance to therapy. We also examine how altered metabolism promotes invasion vs proliferative phenotypes of lung cancer cells. My translational goal is to identify metabolic vulnerabilities with diagnostic, prognostic and/or therapeutic significance. We engage in drug discovery/drug repurposing and identifying synthetic lethal combination strategies. More specifically, we investigate: 1) how drug sensitivity can be improved by targeting altered cellular metabolism; 2) elucidate molecular mechanisms contributing to apoptosis sensitivity following inhibition of specific metabolic pathways; 3) the prognostic significance of altered cancer metabolism; 4) explore targeting tumor metabolism to improve immune surveillance and adoptive T cell therapy and lastly; 5) investigate how metabolites regulate collective non-small cell lung cancer cell invasion in a collaboration with the Marcus lab. Relevant references: i) Targeting glutamine metabolism in multiple myeloma enhances BIM binding to BCL-2 eliciting synthetic lethality to ABT-199. Bajpai R, Matulis SM, Wei C, Nooka, AK, Von Holen JE, Lonial Sagar, Boise, LH, Shanmugam M. Oncogene (2016) 35(30):3955-3964 PMID: 26640142. PMCID: PMC5025767 ii) Electron transport chain activity is a predictor and target for venetoclax sensitivity in multiple myeloma. Bajpai R, Sharma A, Achreja A, Edgar CL, Wei C, Siddiqa AA, Gupta VA, Matulis SM, McBrayer SK, Mittal A, Rupji M, Barwick BG, Lonial S, Nooka AK, Boise LH, Nagrath D, Shanmugam M. Nat Commun. 2020 Mar 6;11(1):1228. iii) Therapeutic targeting of mitochondrial stress-induced proteasome inhibitor resistance in multiple myeloma. Sharma A, Nair R, Achreja A, Mittal A, Gupta P, Balakrishnan K, Edgar CL, Animasahun O, Dwivedi B, Barwick BG, Gupta VA, Matulis SM, Bhasin M, Lonial S, Nooka AK, Wiita AP, Boise LH, Nagrath D, Shanmugam M. Science Advances 8: Issue 39 2022 PMID: 36170375 iv) Cancer Metabolism and the Evasion of Apoptotic Cell Death.Sharma, A, Boise, L and Shanmugam M Invited Review: Cancers 2019, 11(8), 1144 (selected as "Editors' Choice" article) 2. Metabolic heterogeneity drives collective lung cancer cell invasion. We have identified that metabolically heterogeneous subpopulations of cells facilitate collective lung cancer cell invasion by maintaining distinct phenotypes in the collective invasion pack. We have investigated how this metabolic heterogeneity fosters a cooperative biology and consequently warrants a co-targeting therapeutic approach to inhibit metastasis. Relevant reference: 1. R. Commander# C. Wei#, A. Sharma, D. Mahboubi, R.J. Peterson, J. Konen, J.K. Mouw, W. Zhou, Y. Du, H. Fu, M. Shanmugam, A.I. Marcus (* Co-senior authors; #Co-first authors). Subpopulation targeting of pyruvate dehydrogenase and GLUT1 decouples metabolic heterogeneity during collective cancer cell invasion. Nat Communications 2020;11(1):1533. We use metabolite profiling, metabolite flux and cellular bioenergetics assays in the context of biochemical, cellular and molecular interventions to investigate these questions in cell line, patient sample and in vivo models. We are also developing high throughput screening platforms to identify inhibitors that can synergize with BH3 mimetics and immunotherapy. My long-term goals are thus to better understand the functional implications of altered cellular metabolism in cancer; to elucidate how nutrient metabolism signals to promote cancer cell survival and metastasis; to investigate cancer metabolism as a conduit to understanding therapy resistance that can be perturbed to orchestrate potent strategies of synthetic lethality with existing therapy. Please visit us at http://shanmugamlab.com/ for more details. Complete List of Published Work in MyBibliography: http://www.ncbi.nlm.nih.gov/sites/myncbi/1lGu15CbE_yQg/bibliography/44947922/public/?sort=date&direction=descending	CBCancer Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Shanmugam	Mala	Biology, Cellular Cancer / Carcinogenesis Metabolism Molecular Biology	Full Member
Vivien Sheehan, MD, PhD (she/her) Full Member - Molecular and Systems Pharmacology vivien.sheehan@emory.edu \| Faculty Profile \| Lab Website Associate Professor, Division of Hematology/Oncology, Department of Pediatrics, School of Medicine Director, Translational Sickle Cell Disease Research, School of Medicine I develop biomarkers to assess pharmacologic and gene-based therapies for individuals with sickle cell disease (SCD), using red cell function devices and multi-omics strategies.	I develop biomarkers to assess pharmacologic and gene-based therapies for individuals with sickle cell disease (SCD), using red cell function devices and multi-omics strategies.My research focus is on developing new therapies for individuals living with sickle cell disease, and improving the use of existing or emerging therapies. I chose this field when I was a third-year medical student at Emory; I was motivated by the inspiring patients, bravely living with an inherited, painful disease that shortened their lives, by a fascinatingly complex disease that was different in each individual, despite being caused by the same genetic mutation, and by the healthcare and research disparities experienced by this primarily Black population. My independent research began with genomics, identifying and using genetic differences between patients to discover new drug targets to turn on fetal hemoglobin, a type of hemoglobin that does not sickle. Increasing levels are known to improve the health of people living with sickle cell disease. I took this project from finding an association between variants in a gene and fetal hemoglobin levels, to confirming the association in cell culture, to a clinical trial in individuals with SCD, which I completed in July of 2020, identifying a drug that increased fetal hemoglobin and is safe in pregnancy. I continue to use genomics collaboratively with other scientists across the country to better understand why our patients develop certain complications, in order to develop new, targeted therapies. A newly funded omics project is understanding why some individuals with SCD develop alloantibodies when transfused. One of the most distressing aspect of sickle cell disease is that after years of episodic pain crises, usually 3-4 a year lasting up to 2 weeks, over half of our patients begin to have pain every day. This chronic pain is often not relieved by morphine type medications, and may be the result of cells called microglia getting permanently turned on, sending the nerves a signal of tissue injury all the time, even when there is no sickle cell blockage causing lack of oxygen and tissue death. My lab is investigating genetic reasons for the development of chronic pain, and biomarkers to help distinguish chronic from acute pain, in collaboration with behavioral psychologists and neuroradiologists. I screen drug compounds in a cell -based assay of chronic pain to develop effective therapies to treat daily pain in people with sickle cell disease. I also analyze the transcriptomes of patients with SCD that have acute pain only, or chronic pain, as well as longitudinally collected transcriptomes of the same patients at steady state, in a pain crisis, and in recovery, to find biomarkers that may help us distinguish between acute and chronic pain. I also develop biomarkers to determine if therapies are improving the quality and function of an individual's red cells. Sickle hemoglobin polymerizes into rigid rods, making the red cell inflexible, causing it to block small blood vessels and break open easily, resulting in pain crises and organ damage. My work with a device, oxygen gradient ektacytometry, which measures red cell flexibility and tolerance of low oxygen levels proved to be very timely, as the pharmaceutical industry has developed new drugs that affect different aspects of sickle cell disease, some that cannot be monitored by our conventional clinical lab tests. Other biomarkers in development are dense red blood cells, and adhesion index. I collaborate with Dr. Wilbur Lam to translate his research-based devices like adhesion microfluidics for use in SCD clinical trials and patient care. These same biomarkers are essential to evaluating gene-based therapies in individuals with sickle cell. The primary endpoint for all current gene-based therapy trials is reduction in the number of pain events. While this is an important and valuable goal, it does not mean the person is cured. I proposed that the definition of a cure should be red cell function that is at least as good as an individual with sickle cell trait. This idea is supported by NHLBI's Cure Sickle Cell Initiative, and have been included in Beam Therapeutics, St Jude and Novartis's ongoing gene-based therapy trials. My lab is the reference lab for these multi-site trials. I believe my work will raise the bar for industry and academic groups engaged in gene-based therapy trials to optimize their strategies beyond pain reduction, and into prevention of organ damage from abnormal red blood cells, which is the true source of early death in our patients. Another barrier to successful gene-based therapy for individuals with SCD is the recent discovery that two subjects in a lentiviral based gene addition trial developed AML. Individuals with SCD develop clonal hematopoiesis at younger ages, and have higher rates of hematologic malignancies outside of cell-based therapies. This has raised concern that stem cells from individuals with SCD have a higher risk of malignant transformation than those from healthy individuals, and that the stress of transplant and rapid expansion in the bone marrow exacerbates this risk. My lab is investigating on-and off target effects of CRISPR/Cas9 editing that may contribute to malignancy risk, and developing a mouse model to identify drivers of malignant transformation using SCD CD34+ cells.	MSPMolecular and Systems Pharmacology - Full Member	Sheehan	Vivien		Full Member
Hailing Shi, PhD Full Member - Genetics and Molecular Biology Full Member - Molecular and Systems Pharmacology hailing.shi@emory.edu \| Faculty Profile \| Lab Website Assistant Professor, Department of Human Genetics, School of Medicine The Shi lab studies spatial gene regulation mechanisms in brain health and diseases by integrating nucleic acid chemistry and spatial genomics.	The Shi lab studies spatial gene regulation mechanisms in brain health and diseases by integrating nucleic acid chemistry and spatial genomics.Gene expression in the nervous system is tightly regulated at the RNA level during development and function through processes such as RNA localization, modifications, and alternative splicing. In addition, the dysregulation of RNA-binding proteins has been implicated in various neurodegenerative and neurological disorders, further highlighting the importance of RNA regulation in brain health. The brain's spatial organization, diverse cellular microenvironments, and intricate cell morphologies pose significant challenges to studying RNA biology with cell-type-specific and subcellular-compartment resolution. Spatial transcriptomics provides a powerful solution by enabling high-throughput RNA profiling while preserving spatial context, empowering the study of cellular, pathogenic, and therapeutic RNAs within their native tissue environments. The Shi Lab is dedicated to uncovering the principles of context-dependent RNA regulation underlying brain physiology and pathology, ultimately aiming to modulate gene expression in a context-specific manner. By integrating nucleic acid chemistry, spatial genomics, and machine-learning-assisted computation, the lab pursues several interrelated research programs: Program 1: Advancing spatial genomics tools. Building on imaging-based spatial transcriptomics, we aim to enable tools to profile various aspects of RNA biology in complex tissues at cell-type- and subcellular-level resolution. These tools will allow the analysis of RNA localization, dynamics, and modifications in unprecedented detail and inform the design of effective gene delivery strategies. Program 2: Elucidating molecular mechanisms in tissue biology. Spatial omics technology bridges genomics and histology by capturing gene expression information while maintaining the native tissue architecture. Combining spatial omics with reporter engineering, we aim to understand the molecular foundations of brain health and disease by combining spatial molecular mapping with phenotypic and functional explorations, such as cell differentiation and migration during brain development and region-specific vulnerability of neurodegenerative diseases. Program 3: Modulating gene delivery and expression. Effective and cell-type-specific gene delivery remains highly desired for both fundamental studies of gene functions and clinical applications. Spatial profiling of gene delivery vectors in situ opens opportunities to characterize vector biodistribution, expression, and cellular impact in specific cell types and tissue microenvironments. We aim to enable multiplexed in situ evaluation of various carriers for mechanistic disease understandings and therapeutics optimization.	GMBGenetics and Molecular Biology - Full Member MSPMolecular and Systems Pharmacology - Full Member	Shi	Hailing		Full Member