I work on the evolution of species interactions in plants and insects, and the evolution and genomics of pregnancy in mammals. I integrate diverse approaches, from molecular biology to ecology.

My laboratory aims to understand the molecular events controlling early events of HIV infection. We are interested in the functions of the viral capsid and its interactions with host factors, with an view toward developing novel antiviral therapies targeting it.

Dr. Alexander’s laboratory is focused on the role of adaptive immunity in the pathogenesis of hypertension and associated cardiovascular disease. Current projects are focused on the role of counter-regulatory immune mechanisms in hypertension, including the role of novel regulatory T cell subsets in the pathogenesis of hypertension and microvascular dysfunction. We perform cutting edge basic and translational research integrating vascular biology and immunology using a variety of approaches including molecular biology, physiology, highly dimensional single cell analysis, and human genetics.

Projects in Dr. Algood’s lab focus on pathogen – host interactions in chronic infections and during chronic inflammation. Her projects investigate how T cell cytokines influence gastric epithelial cells responding to infection but also even more broadly how T cell cytokines activate other cells to protect the epithelial cells and the mucosal barrier they maintain. The main model system the laboratory uses to address these processes is H. pylori, but she is interested in many processes in mucosal immunology.

Our lab studies reproductive immunology with a focus on bacterial infections that complicate pregnancy. We primarily examine host-microbe interactions in the pathogenesis of chorioamnionitis, a major cause of preterm birth and stillbirth. Group B Streptococcus is the primary pathogen our lab studies. Join us!

We study the post-transcriptional networks that govern gene expression during the innate immune activation of cells. We use and develop an inherently multidisciplinary set of tools to answer our questions including: biochemistry, chemical biology, transcriptomics, proteomics, and computational biology.

Our research focuses on the use of functional genomic and epigenetic approaches to understand gene regulation. Our interests range from detailed mechanistic studies of the interferon-gamma gene, a key cytokine produced by cells of the innate and adaptive immune system, to the use of these approaches to gain new insights into human disease. In addition, we have begun to focus our attention on long noncoding RNAs (lncRNAs) and other species of RNAs that do not code for proteins. We have developed model organisms, computational and analytic pipelines to dissect enhancer function and functions of these newly identified RNA species in biologic systems.

My lab is interested in gut-brain interactions that play a role in the maintenance of energy homeostasis. We focus on local effects of the gut hormone glucagon-like peptide-1 (Glp1) in the gut and both the peripheral and central nervous systems that regulate nutrient intake and energy expenditure. Our approaches include using transgenic mice, metabolic phenotyping, behavioral assays and opto/chemogenetics.

The Vanderbilt Laboratory for Biosynthetic Studies (Bachmann, P.I.) studies and harnesses the biosynthetic capabilities of living systems in order to radically accelerate the discovery of new bioactive compounds and revolutionize how molecules are synthesized. By studying pathways and enzymes involved in secondary metabolism, we create new biochemical knowledge, and apply it toward the generation of new bioactive molecules. Our precision-medicine drug discovery subgroup uses a single cell chemical biology paradigm on patient-derived cells to drive the discovery of secondary metabolites as cures for cancer.

Our laboratory is focused on improving treatment oucomes in breast cancer (particularly triple-negative breast cancer) as well as in other solid tumors. To accomplish this, we integrate data from genomic and molecular profiling studies with molecular biology and signal transduction methodologies to translationally identify altered pathways in cancer, the functional consequences of these alterations, and ways to directly target them in patients to improve clinical outcomes and survival.

My lab studies cellular and molecular mechanisms of lung alveolar capillary barrier function in sepsis and acute respiratory distress syndrome. We use state of the art cell and mouse models to define the key cellular processes that drive disruption of the alveolar capillary barrier. Mechanistic studies are complemented by translational studies in human models of lung injury.

We study colorectal carcinogenesis and metastasis biology. Our recent work has identified a previously unrecognized role of TGFbeta signaling in controlling epithelial inflammation, and links this role with tumor suppression. Our lab also seeks to identify novel therapeutic targets and molecular biomarkers.

Experimental Evolution and Population Genetics of Microbes. Our lab is interested in how genetic variation is introduced into a bacterial population and bacteria diversify as they colonize a novel environment. The phenotypes associated with this diversification often include biofilm formation, antimicrobial susceptibility, resource utilization, pH tolerance, changes in mutation rate, etc. We examine these questions on an individual (mutation accumulation), population (batch culture), and community (metagenomics) level. For more information see our lab’s website: http://www.behringerlab.wixsite.com/index

Generally, I am interested in developing and applying computational methodologies to further our understanding of the genetic basis of human disease. Specifically, I focus on development of novel strategies for identifying and confirming genetic risk factors to complex traits including blood lipid levels, diabetes, obesity, Alzheimer’s disease, cardiovascular disease, and metabolic traits via ascertainment of dense genetic (specifically, whole genome/exome sequenced and whole genome imputed datasets) and phenotypic data.

Jada Benn Torres, PhD, is a genetic anthropologist , Associate Professor, and Director of the Genetic Anthropology and Biocultural Studies Laboratory ​at Vanderbilt University in Nashville, Tennessee, USA. ​For the past 17 years, Dr. Benn Torres  has researched the population genetics of Caribbean communities in order to examine their ancestry, colonial, and post-colonial experiences. Her second emerging research interest combines the tools and methods of genetic epidemiology with anthropology in order to holistically examine women’s health disparities across human populations.

The Blind Lab uses structural biology, molecular genomics and chemical biology to discover new ways nuclear lipid signaling controls gene expression. We apply these discoveries to the design and implementation of novel drug screens, developing therapeutics for diabetes, cancer and fatty liver.

Our overarching goal is to identify mechanisms by which autoantigen-specific B lymphocytes breach immune tolerance barriers to drive autoimmune disease. We apply cutting-edge hybridoma and single-cell RNAseq/CITEseq/BCRseq technology to study this process in type 1 diabetes, myositis, and immune checkpoint inhibitor-induced autoimmunity.

We endeavor to understand the principles that shape interactions between animals, microbes, and viruses and the basic and translational outcomes of these interactions. We employ hypothesis-driven approaches to study two forms of animal-microbe associations: intimate symbioses (between animals, obligate intracellular bacteria and bacteriophages) that impact animal reproduction and vector control, and facultative associations (between free-living organisms) that shape genome and microbiome evolution across the tree of life.

Polyunsaturated fatty acids (PUFA) are easily oxidized, and enzymes (“oxygenases”) take advantage of this to form lipid signaling mediators such as the prostaglandins and leukotrienes. The focus of Alan Brash’s research is the mechanism of biosynthesis of these oxygenated lipids and their biological role. We employ a wide variety of analytical methods on tissues and cells and recombinant enzymes, with structural analysis of enzymic products by HPLC, UV-Visible spectroscopy, mass spectrometry, and NMR.

Pharmacology and Physiology of Prostaglandin Receptors especially as it relates to blood pressure control, diabetes mellitus and Alzhheimer’s Disease.

We pursue the genetic dissection of nervous system development, function and adaptive plasticity, to understand the molecular mechanisms by which neural circuits mediate behavior. We generate genetic models of heritable neurological disorders, including autism spectrum disorders, intellectual disabilities and neurodegeneration states, in order to discover underlying causes and design cures. Our work spans from genes to behavior with molecular biology, biochemistry, light and electron microscopy, electrophysiology and behavioral output studies.

Mitochondrial protein-protein interactions and assembly are necessary for maintaining proper human health. Unfortunately, there are numerous painful, debilitating, and life-threatening diseases that occur due to genetic mutations that prevent proper protein assembly. Our approach is to use X-ray crystallography and other complementary biochemical techniques to understand how these various mutations lead to changes in protein structure and function, thus preventing proper macromolecular assembly.

The Burkewitz lab is interested in combating age-onset diseases like neurodegeneration, cardiovascular disease, cancer and diabetes by understanding and targeting their common risk factor: the aging process itself.  A combination of molecular genetic, biochemical and imaging approaches allows us to study interventions such as dietary restriction, which extends lifespan in a variety of animal models. In particular, we focus on understanding aging and longevity at the level of organelle function and cell architecture.

We focus on the following areas: 1) The cell biology of heart muscle cells (i.e., cardiomycoytes). 2) How both cardiomyocytes and cancer cells generate the forces driving their function. 3) Combining “omics” technologies with high resolution and high content microscopy.

Our group uses a multidisciplinary approach combining microbiology, molecular biology, cell biology, immunology and pathology to try to understand how inflammation-dependent changes in gut epithelial metabolism can result in gut dysbiosis and increased risk to non- communicable disease. Specifically, we used a variety of mouse models, including diet-induced-obesity, chemical-induced colitis, infectious gastroenteritis (Salmonella enterica serovar Typhiumurium), and germ-free animals with the goal to identify metabolic pathways in the gut bacteria and in the host response to microbiota-induced metabolites that will aid in prevention of human disease.

The interplay between rapid, temporally specific neuronal activation and longer-term changes in transcription is of critical importance in the expression of appropriate or, in the case of disease, inappropriate behaviors. Together, my research seeks to understand how information about stimuli is encoded in the brain. Developing new approaches to understand how activity-dependent changes are stored within particular cells and circuits at the level of the epigenome will allow us to understand adaptive and maladaptive processes in reward, motivation, and associative learning.

Our group studies mechanisms of neurodegeneration in the visual system. Our objective is to probe the therapeutic potential of novel targets for intervention based on neuroprotection, repair, rehabilitation and regeneration.

We study the molecular mechanisms regulating the development of the peripheral nervous system. Specifically, we focus on the regulation of neuronal apoptosis by the neurotrophins, the mechanisms by which the apoptotic neurons are cleared and the functional interplay between neurons and glia.

My lab explores the use of ultrasound for therapy and imaging. We have been developing magnetic resonance imaging-guided methods to use ultrasound for applications, such as neuromodulation, drug delivery, and immunomodulation.

Our lab studies host-pathogen interactions during invasive bacterial infections, with a specific focus on osteomyelitis. We are also interested in how inflammation and the microbiome impact skeletal cell biology. Finally, we study interconnections between the vertebrate immune and skeletal systems.

We have a broad range of interests, using the concepts and approaches of structural biochemistry to address key questions in medicine and biology. Three key factors govern our research: (1) a deep commitment to working with human proteins; (2) fascination with the mechanics of multi-protein machinery in genome maintenance and innate immunity; (3) firm belief in the power of collaboration and multi-disciplinary team science.

Current focus of our lab is to investigate how receptor tyrosine kinase signaling in tumor cells affects glutamine metabolism and tumor immunity. We also study how tumor blood vessel normalization affect anti-tumor immune cells recruitment and activation.

We are interested in elucidating the molecular mechanisms underlying 1) pancreatic islet cell function and dysfunction, 2) communications between islet cells and other organs/tissues, and 3) tumorigenesis. We hope to use the new knowledge for treatment of diabetes and cancer.

The Chiang lab is interested in how neurochemically distinct neurons are generated and how they contribute to associative motor learning, a process whereby the cerebellum learns an association between two sensory stimuli from the environment. Dysfunction in this process has been linked to neuropsychiatric disorders in humans such as autism. Another interest in the lab is to identify molecular and epigenetic mechanisms that contribute to medulloblastoma, the most common pediatric brain tumors in the cerebellum.

1. Defining the risk factors for gastric cancer development 2. Understanding progression and evolution of dysplastic stage to cancer as a key transition state in gastric carcinogenesis 3. Targeting the early stages of Ras-induced cancer

The Colbran Lab (https://lab.vanderbilt.edu/colbran-lab/) is focused on understanding the mechanisms controlling excitatory synaptic transmission and structure under physiological and pathophysiological conditions. We focus on calcium/calmodulin-dependent protein kinase II (CaMKII), an abundant postsynaptic signaling molecule with a unique auto-regulatory mechanism that mediates many downstream responses in neuronal dendrites. We are testing the over-arching hypothesis that direct interactions with diverse CaMKII-associated proteins modulate the activity, localization and/or substrate-specificity of CaMKII to confer specific downstream actions that have unique roles in modulating synaptic function and behavior.

We study the of specific neurotransmitter receptors in regulation of transmission and signaling in brain circuits involved in psychiatric and neurological disorders.   From this, we endeavor to develop new treatment strategies for brain disorders and engage in full drug discovery efforts aimed at advancing new drug candidates into clinical development with industry partners.

Over six billion base pairs of DNA must be copied rapidly and accurately trillions of times in a human lifetime. My lab studies how this happens, the consequences of errors for human disease, and how we can intervene to improve health. We are particularly focused on how cells respond and repair DNA damage in the context of the cell division cycle.

Research projects in the Cover laboratory are focused on bacterial infections, bacteria-host interactions, and the role of microbes in development of cancer. We are particularly interested in the bacterium Helicobacter pylori and its role as a causative agent of stomach cancer.

The Cox lab develops methods for integrating genome variation with genome function and applies these methods in BioVU, the biobank at Vanderbilt University Medical Center. Our goal is to identify the genetic components to common human diseases and use that information to improve the health and well being of our patients.

Advanced human immunology studies of the response to infectious diseases

Role of endogenous bioactive lipids including N-acyl-ethanolamides and isolevuglandins in physiology and metabolic diseases . Role of lipids derived from gut microbiota in physiology and disease. Diseases of focus include obesity, diabetes, and cardiovascular disease.

In the Davis Lab, we are driven to understand how polygenic liability, rare variant effects, and environment interact to affect the health of human populations. We study a wide range of traits including psychiatric and non-psychiatric chronic disease. Many of our projects are focused on identifying and understanding the biological and clinical linkages between mental health and physical health.

I am a physician-scientist. My research focuses on development and testing of novel therapeutics to enhance the regenerative capacity of kidneys after injury (using a Zebrafish screen and mouse models of injury), as well as the analysis of retinoic acid signaling and macrophage function after kidney injury. We have been continuously funded since 2002, and have recently been successful in obtaining a new DOD drug discovery grant to identify new therapeutic approaches to prevent chronic kidney disease progression after acute kidney injury (AKI). I am committed to teaching and mentoring in biomedical sciences. I have trained 6 PhD graduate students, 1 MD PhD and 1 Master’s student in my lab since 2000. I am a member of the Department of Cell and Developmental Biology Graduate Steering Committee and Director of the Vanderbilt Program in Molecular Medicine (VPMM). I am research area director for bench research immersion projects, which is a requirement for 3rd year medical students at Vanderbilt University Medical School. I am also Director of the Education and Outreach Program for the Vanderbilt Center for Kidney Disease, Director of the Summer Research Training Program (SRTP) in Kidney Disease, and the Vanderbilt Mouse Kidney Injury Workshop.

The Dean lab seeks to understand how nutritional and other environmental factors affect pancreatic islet cell function and proliferation. Islet alpha cells secrete glucagon in response to hypoglycemia leading to increased glucose output by liver, but persons with diabetes often have hyperglucagonemia further contributing to hyperglycemia. We recently described a novel hepatic-pancreatic islet alpha cell axis that we believe is important in diabetes. We are currently interested in 1) defining the mechanism of how amino acids are sensed by alpha cells to stimulate proliferation and glucagon secretion and 2) investigating the role of amino acids on alpha cell dysfunction in diabetes.

We employ state-of-the-art techniques in ion channel electrophysiology and drug discovery to develop the molecular pharmacology of clinically important potassium and anion channels.

The Dewar lab studies DNA replication, telomeres, and DNA damage responses. We use cell extracts that allow us to apply biochemical approaches to complex cellular processes, such as DNA replication. We aim to uncover cellular mechanisms that impact cancer and aging.

Genetic epidemiology of complex human traits using large-scale resources

Research in the Eichman laboratory uses X-ray crystallography and other high-resolution structural and biochemical approaches to investigate the molecular mechanisms of DNA repair and replication machines. Current work focuses on base excision repair of bacterial genotoxins and interstrand crosslinks by DNA glycosylases, repair of stalled replication forks by structure-specific DNA translocases, and priming of DNA synthesis during eukaryotic replication.

The research interests of our laboratory focus on the cellular and molec­ular processes under­ly­ing neuronal com­mun­i­ca­tion in nor­mal and patho­phys­i­o­log­ic disease states. Spe­cif­ically, we are examining the molecular mechanisms involved in the editing of RNA transcripts encoding proteins critical for mammalian nervous system function.

The Ess lab does basic and translational research to study brain development and neurological dysfunction. We use several human genetic diseases as model systems. We employ human stem cell and transgenic mouse models for this work.

My area of interest is understanding cancer metastasis. We are particularly interested in mechanisms that tumor cells appear to have copied from immune cells, such as using cytokine receptor signaling to alter metabolism and adapt to new environments.

Our work focuses on mechanisms of progression of chronic kidney disease. Our new work studies how even mild tubula rinjury senstizes glomeruli to a second hit. We are studying the role of changes in podocyte progenitor cells in this process, using various mice and cell culture models.

Lung cancer is the largest single contributor to cancer deaths worldwide: 85% of lung cancers are classified as non-small cell lung cancer (NSCLC), and for patients who present with locally advanced stage IIB/III disease the standard of care is concurrent chemoradiation therapy. Unfortunately, this approach only yields a median survival of 17 months. Dr. Michael L. Freeman of the Department of Radiation Oncology at Vanderbilt University School of Medicine and Cumberland Emerging Technologies have partnered to develop a formulated version of a novel radio and chemo sensitizing compound that targets NPM1 for the treatment of NSCLC stage IIB/III disease. Dr. Freeman’s lab is using various approaches to develop a clinically efficacious formulation.

The Friedman lab uses the yeast Saccharomyces cerevisiae as a model system to study basic mechanisms of DNA replication and DNA repair, with a particular emphasis on telomere biology. We use genetic and biochemical approaches to identify regulatory mechanisms affecting DNA repair pathway choice at double-strand breaks. Recent work has identified sites in the yeast genome that serve as “hotspots” of de novo telomere addition following a chromosome break.

We use mouse models to study the role of signaling pathways on formation, differentiation and morphogenesis of the developing eye. Another focus in the lab is ocular regeneration; we are determining the molecular and cellular mechanisms controlling the regenerative capacity of the retinal pigment epithelium. Among other pathways, we are specifically studying the role of Wnt signaling during development and regeneration.

Our research program aims to reveal new molecular mechanisms involved in regulating cell fate. The lab focuses on three main lines of research: 1) Mechanisms by which mitochondrial biology regulates normal and cancer stem cell fate – role of the BCL-2 family of proteins modulating mitochondrial morphology/function, stem cell self-renewal, pluripotency and differentiation; 2) Examining the role of MCL-1 in early human neural development using three dimensional systems (embryoid bodies, neural rosettes and brain organoids; 3) Function of the ubiquitin ligase CUL9 in the transition from a stem cell to a neural progenitor cell.

Our laboratory studies transcription factors and signaling pathways that regulate the differentiation, proliferation, survival, and function of the different cell types in the pancreas. We use genetically engineered mouse models, as well as primary pancreatic cells from non-human primates and human donors. Our studies have implications for diseases such as diabetes and pancreatic cancer.

At the interface of immunology and virology, recent computational advances have allowed us to better understand the interactions between antibodies and antigen, to design immunogens capable of eliciting target antibody specificities, and to optimize antibodies as clinical products. Research efforts in the Georgiev laboratory aim to utilize the power of computation to increase our understanding of fundamental questions in immunology and virology and to develop novel ways of using this understanding to fight diseases. For the translational component of our research, we apply structure-based protein design approaches to the development of new vaccine and antibody product candidates against a number of viruses of biomedical interest.

The Giorgio lab conducts curiosity-driven research focused on important unmet needs aligned with our capabilities and interests. Our projects are interdisciplinary and we engage collaborators with synergistic expertise and compatible approaches. We are currently developing new materials for modulation of immunity and devices for sensing and pathogen extraction.

Our lab is interested in understanding the mechanisms regulating intestinal immunity and what leads to dysregulation and disease as well as how gut microbes shape the mucosal immune system. In particular the cytokine interleukin-23 (IL23) is required for the development of many experimental models of inflammatory bowel disease (IBD) in mice and mutations in IL23 receptor (IL23R) have been identified as susceptibility or resistance factors for Crohn’s disease. We have developed several murine strains that will facilitate investigations into the role of IL23R signaling in a cell-specific manner using experimental models of IBD and inflammation-associated carcinogenesis.

The Goldenring lab has multiple interests in Epithelial Biology and Cancer biology including 1) the role of membrane trafficking and recycling in polarity, 2) the cellular basis of congenital diarrheas, 3) the cell of origin for pre-cancerous metaplasia in the stomach and the immune cell drivers of stomach carcinogenesis and 4) the role of AKAP350 in organizing the pericentrosomal material.

Development and applications of magnetic resonance imaging for neuroscience applications including understanding the biophysical basis of functional MRI and diffusion MRI of brain and spinal cord. Integration of MRI and electrophysiology and other techniques to understand brain function in rodents and non-human primates. Basic physics of MRI signals and physiological factors affecting MR images.

The Gould laboratory conducts foundational research on the molecular basis of cell division, a highly conserved process central to development and tissue maintenance. The laboratory takes a multi-disciplinary approach employing genetics, biochemistry, phosphoproteomics, and microscopy. Our ultimate goal is to obtain a comprehensive mechanistic understanding of the exquisite spatial and temporal control of cell division in eukaryotes.

The research goals of the Graham laboratory are to understand the molecular mechanisms underpinning vesicle-mediated protein transport and membrane biogenesis. Defects in these processes lead to a number of human diseases, including diabetes, cardiovascular disease, neurodegenerative diseases and cancer.

The goal of the Grueter lab research program is to advance the current understanding of the nucleus accumbens (NAc), a brain region responsible for integrating information from diverse inputs and modifying complex motivated behaviors, including its involvement in adaptive responses to rewarding and aversive stimuli. Specifically, we strive to elucidate the molecular constituents in the NAc that are necessary and sufficient to drive complex motivated behaviors.

We study how organisms made optimally functional beta cells to reduce the risks of diabetes. Our focuses are the genetic pathways and epigenetic modifications involved in the process. We use mouse models and human islets for our studies.

The Guelcher laboratory designs and develops biomaterials and drug delivery systems that enhance healing of tissue damaged by trauma or disease. Current projects include design of injectable tissue grafts for healing bone in challenging environments, including weight-bearing anatomic sites, defects contaminated by bacteria, and large tissue voids resulting from extremity and craniofacial trauma.

The Guengerich laboratory is interested in the enzymes involved in the activation and processing of xenobiotic chemicals (i.e., those not normally found in the body, such as drugs and carcinogens), as well as steroids and vitamins. The work is focused on the enzymology of two major groups of enzymes, cytochromes P450 and DNA polymerases.

We are studying the role of the signaling mechanisms regulated by G protein-coupled receptor kinases and arrestins in brain diseases.

We study structure and biological functions of arrestin proteins. Arrestins are key regulators of G protein-coupled receptor signaling and several receptor-independent pathways that affect life and death of cells. Our ultimate goal is to create designer arrestins that bind the receptors we want and activate the pathways of our choosing.

We study G protein signaling in mouse brains and human platelets. Current projects relate to G protein coupled receptor pharmacology and signaling. We seek to discover small molecules that inhibit the protease-activated receptor PAR4 for antiplatelet and antithrombotic therapy. We also study regulation of secretion by Gi/o-coupled receptors and Gbg. We have discovered a novel interaction between Gbg and the SNARE complex and have generated a mouse that disables this interaction. Phenotyping this mouse has given us insight into the role of Gbg SNARE interaction and inhibition of exocytosis in metabolism and physiology.

Nutritional factors that impact Alzheimer’s disease pathogenesis, including high fat diet and vitamin C deficiency. The lab uses behavioral and molecular biochemical methods to study altered learning and memory in a range of mutant mouse models.

We study how obesity impacts health. The growing worldwide obesity epidemic is frequently linked to hyperlipidemia, inflammation, and insulin resistance leading to increased risk of diabetes and cardiovascular disease. The long-term goal of our laboratory is to determine mechanisms by which obesity increases risk for and pathophysiological consequences of these devastating diseases. Macrophages are part of the innate immune system that infiltrate white adipose tissue (fat) in obese rodents and humans, and produce most of the inflammatory cytokines and chemokines secreted from adipose tissue. In addition, their presence has been shown to be temporally associated with the development of insulin resistance. Our current research focus is threefold: to determine mechanisms by which macrophages accumulate in adipose tissue, to determine the role of resident macrophages in normal adipose tissue function, and to determine how other immune cells like eosinophils and T cells also contribute to adipose tissue function.

My laboratory studies molecular and cellular mechanisms of cardiac tissue repair after myocardial infarction and in diabetic cardiomyopathy. At the cellular level, we investigate the role of endothelial and cardiovascular stem cells in tissue repair and regeneration. At the molecular level, we focus on the role of BMP signaling in inflammation after injury and in the growth and differentiation of various adult stem cell populations.

Our research is focused on interventional approaches to regulate uterine contractions for either the management of preterm labor or postpartum hemorrhage. Our laboratory has established a drug discovery strategy to identifying novel regulators of uterine myometrial contractility. We are equipped for high-throughput screening of small-molecules, prioritization of hits into leads using secondary assays and pre-clinical in vivo testing in mouse models.

Using CRISPRs coupled with HDR DNA repair to engineer endogenous genes for deep genomic and proteomic analysis. This allows us to define transcription targets and networks for mechanistic studies.

The Hillyer Lab investigates aspects of mosquito immunology and physiology related to their ability to transmit diseases such as malaria.  The lab focuses on the mechanical and molecular bases of hemolymph (blood) propulsion, the immunological interaction between mosquitoes and pathogens in the hemocoel (body cavity), and the effect of life history on immune competence.

The Hinton Lab utilizes SBF-SEM and FIB-SEM to investigate the molecular mechanisms that regulate molecule transfer and morphology changes between the mitochondria and the endoplasmic reticulum and how these mechanisms are altered during pathophysiological states diabetes, obesity, and cardiovascular disease.

Primary research in the Hodges lab is focused on DNA methylation and non-coding gene regulatory variation in evolution, development and disease. In particular, we study dynamic changes in the epigenome during cellular fate transitions using innovative genomic and bioinformatic approaches.

The Computational Neurogenomics lab leverages advanced statistical approaches and computational ‘omics to identify novel treatment targets for Alzheimer’s disease (AD). We primarily focus on identifying the molecular drivers of resilience to AD, and identifying sex-specific genetic predictors of AD.

Aging is the major risk factor for common illnesses that account for most human morbidity and mortality. My lab uses the nematode Caenorhabditis elegans to study the role of a conserved insulin-like growth factor signaling pathway in development, metabolism, and aging. We seek to reveal insights into basic mechanisms of aging that may lead to new strategies to prevent and manage prevalent diseases such as diabetes and cancer.

The goal of our laboratory is to reduce the death and suffering caused by prostate cancer. Cancer localized to the prostate is often curable with treatments such as surgery or radiation therapy; however, once prostate cancer has spread beyond the prostate to other organs or to bone, it is an incurable disease. Our lab focuses on identifying both cancer cell-autonomous and non-cancer cell-autonomous genetic and molecular pathways that promote lethal prostate cancer and cause therapy resistance.

The Hutson lab is interested in understanding the cell-level forces that drive epithelial morphogenesis and wound healing. Current projects include the following: measurement of cellular forces in vivo — both via laser manipulations and image-based force inference; understanding how these forces are perturbed after exposure to chemicals with developmental toxicity; and investigations of the calcium signaling pathways by which cells detect and respond to wounds. Projects include both experimental and computational approaches.

We use imaging and flow cytometry to understand the signaling events driving normal stem cell commitment in the brain and the disruption of this process in disease. We work in animal models and in human tissue specimens to directly study neural stem cells and brain tumors of all grades.

Graduate thesis projects in the Irish lab are tailored to fit student interests. Active research areas include: (1) programming immune cell identity, (2) computational biology & machine learning cell identity, and (3) neural stem cells, neuroimmunology, and brain tumors. Graduate projects may be entirely computational, basic cell biology, or human disease oriented, although most projects blend all these elements. Rotations begin with training in relevant technologies, such as mass cytometry (CyTOF), computational tools, and methods for human tissue research. Graduate students craft their projects in regular mentoring meetings with Dr. Irish and are supported by a team science environment including expert lab staff, postdocs, clinical fellows, and collaborators at Vanderbilt and institutions around the world.

Research in the Iverson laboratory focuses on the basis for information encoding in proteins, which may manifest as molecular recognition and cellular communication. We use a combination of structural techniques to understand these processes.

The Jackson lab studies membrane trafficking pathways, which are the Fedex system of eukaryotic cells. We investigate structures and functions of protein complexes to understand how key proteins assemble and are regulated. We use a range of techniques, including structural biology, biochemistry, biophysics, and cell biology to understand both fundamental cellular processes and disease implications.

The Jacobson lab focus is on the mechanisms that influence pancreatic islet calcium homeostasis and hormone secretion under physiological and diabetic conditions. The goal is to identify pathways that can be therapeutically targeted to reduce pancreatic islet dysfunction and restore euglycemia in patients with diabetes. The primary models employed in these projects include: human islets, rodent islets, pancreatic slices and cultured cells. The research utilizes cutting edge approaches in molecular biology, fluorescent microscopy (both widefield and confocal), electrophysiology, biochemistry, virus mediated expression of genetically encoded indicators for calcium and membrane potential, and transgenic models.

The Vanderbilt Memory & Alzheimer’s Center is an interdisciplinary research program advancing our understanding of risk factors, early diagnostic markers, and prevention and treatment methods for memory loss and abnormal cognitive aging, including Alzheimer’s disease, cerebral small vessel disease, and neurodegeneration in older adults. Our innovative research portfolio includes initiatives (1) examining vascular health intersections with Alzheimer’s disease and neurodegeneration to identify risk factors and prevention targets, (2) identifying tools for early detection of unhealthy cognitive aging, and (3) elucidating factors underlying resilience to the clinical manifestation of Alzheimer’s disease. Trainees gain knowledge and skills working with a comprehensive, longitudinal study of older adults, including but not limited to multi-modal neuroimaging, cardiac imaging, blood and cerebrospinal fluid biomarkers, genomics and proteomics, neuropsychological assessment, and lifestyle factors.

My lab studies lipid and lipoprotein metabolism. We are interested in how lipids alter intracellular processes and how lipid and protein structures interact to determine lipoprotein function. These studies combine microscopy, biochemistry, molecular genetics and molecular modeling to provide robust data sets.

Our lab is interested in breast cancer dormancy and metastasis to the bone marrow. We investigate mechanisms of tumor recurrence and tumor cell entry / exit from dormancy. Our particular interest is in how cytokine signaling and hypoxia regulates these processes.

Organisms and even single cells have endogenous biological “clocks” that allow them to tell the time of day. Research in our laboratory is directed towards understanding the cellular and molecular bases of these fascinating timing mechanisms in a variety of organisms: bacteria, plants, and animals. Another major emphasis is understanding the evolution of these clocks by studying the fitness advantage conferred by these clocks, as well as experimentally evolving clocks in cells that don’t already have them! We cover many fields in this quest: biochemistry, neurobiology, biophysics, microbiology, evolutionary biology, and genetics.

We apply the principles and techniques of organic chemistry to create new reagents and reactions. These developments are driven by their potential to solve longstanding problems in small molecule and peptide synthesis. We collaborate with colleagues at Vanderbilt and elsewhere to advance our understanding of disease pathways using small molecule tools, ultimately aimed at early stage drug development.

Adjuvant and vaccine design and mechanism/s of action

The Kang Laboratory is interested in understanding the role of GABAergic signaling in disease conditions as well as in normal brain development. Currently, lab staff members are investigating the molecular pathophysiology of genetic variations/mutations in GABAA receptor subunits and GABA transporter 1, two major components of GABAergic signaling and common pediatric disorders: epilepsy, autism and intellectual disability. The goal is to understand how a single nucleotide change like a mutation could define the whole life of a child and identify the most effective precision treatments for those who have these disorders in order to improve their life outcome.

My laboratory is interested in understanding the molecular mechanism of calcium signaling at the ER-mitochondria contact sites. Our goal is to uncover the molecular mechanisms underlying the activity and regulation of key protein complexes involved in calcium signaling at the ER-mitochondria contact sites using innovative structural biological methods including X-ray crystallography and cryo-electron microscopy (cryo-EM) together with biophysical, biochemical and functional methods.

The long term goal of our laboratory is to uncover fundamental mechanisms of gene expression by exploiting the interactions of viruses with their host.

Our group studies mechanisms underlying presynaptic function and its impact on neuronal signaling.

Microtubules are dynamic biopolymers, which serve as major trafficking highways in cells. Microtubule-dependent transport is critical for physiology of all cell types, and disturbance of microtubule networks underlies many human diseases, from neurodegeneration to diabetes. Kaverina laboratory uses high-end microscopy combined with molecular and computational approaches to target basic cell biology of microtubules as well as the role of microtubules in pancreatic beta cell physiology and diabetes.

The Kim lab (KIM LAB AT VUMC-HEM/ONC) is in the division of Hematology/Oncology, the department of Medicine at Vanderbilt University Medical Center. The Kim lab is also affiliated with Vanderbilt Center for Immunobiology (VCI) and Vanderbilt Institute for Infection, Immunology and Inflammation (VI4). Dr. Kim (PI) is a physician who treats leukemia/lymphoma/myeloma patients using chemotherapy and stem cell transplantation. Dr. Kim is also an immunologist who is interested in tumor (Cancer) immunology, checkpoint immunology (beyond PD-1 and PD-L1) and transplant immunology. We are looking for enthusiastic students and post-doctoral fellows.

Research in my laboratory focuses on understanding the interaction between oxidative stress and inflammation in the genesis of cardiovascular disease. We are studying the role of excess dietary salt in inducing activation of the innate immune system leading to hypertension via formation of the fatty acid oxidation products known as isolevuglandins. We are also studying the impact of excess dietary salt on the gut microbiome.

As a cancer biologist and radiation oncologist, we study new approaches for combining X-ray radiation treatment and other treatments, such as chemotherapy, targeted drug therapy, and immunotherapy. We are investigating the interactions and mechanisms for improved therapeutic effects of combination treatments involving X-ray radiation therapy. Our research work, models, and projects are geared toward translation to the clinical setting. We leverage combination approaches to provide enhanced cancer treatment and understand the biological pathways involved.

We want to be able to accurately predict the phenotype of any and all genetic variants. Our approach is to collect as much phenotype information–at high and low resolution–as is feasible for the largest number of variants and then leverage experimental and computational structural biology to fill in the details for yet uncharacterized variants. To develop this methodology, we are starting with ion channels involved in the heart contraction cycle.

– Our discovery of ADAMTS10 causing open angle glaucoma in dogs led us to form the microfibril hypothesis of glaucoma. – We use a variety of animal models, including mice, pigs and zebrafish to investigate the mechanisms of glaucomatous optic neuropathy. – We use state-of-art imaging and electrophysiology technology, such as optical coherence tomography, electroretinogram, atomic force microscopy, electron microscopy, confocal microscopy and polarized light microscopy to study mechanisms of optic nerve damage at the cellular and tissue levels.

Pathogenic bacteria have evolved a diverse array of mechanisms for delivering toxins and other virulence factors into the interior of host cells. Studying the molecular structures of these virulence factors alone and in complex with host receptors, membranes, and inhibitors can lend insight into how these delivery processes occur and how these processes can be exploited or prevented. Current research in the Lacy laboratory is primarily focused on the structure and function of large clostridial cytotoxins, including the two toxins responsible for symptoms in Clostridium difficile infection. Structural biology is combined with cellular, tissue, and animal models of intoxication and infection to understand the toxin-host interaction at the molecular level. In addition, we aim to identify new toxin inhibitors using both rational design and high-throughput screening approaches.

The MASI research laboratory concentrates on analyzing large-scale cross-sectional and longitudinal neuroimaging data. Specifically, we are interested in population characterization with magnetic resonance imaging (MRI), multi-parametric studies (DTI, sMRI, qMRI), and shape modeling.

We are interested in understanding how signal transduction pathways maintain function during homeostasis and how these processes are disrupted in various disease etiologies, which include breast cancer, infection and chemotherapy-induced cardiac toxicity. To study these questions we employ a variety of techniques, which include modern molecular biology and biochemistry, enzyme kinetics, novel assay development, high throughput screening, drug development, quantitative microscopy, various animal models, novel patient-derived explant cultures, patient-derived xenografts and bioinformatics.

The Lau lab considers every one of the 30 plus trillion cells in the body to be unique, thus, utilizes state-of-the art technologies to profile tissues at the single-cell resolution. Resulting “big data” consisting of thousands of data points and dimensions are analyzed by data science-driven computational techniques.

Research in the Lea lab sits at the intersection of evolutionary biology, genomics, and human health research. Much of our work focuses on two questions: (i) what are the molecular mechanisms that connect environmental challenges (e.g., social or nutritional stress) experienced across the life course with compromised health? and (ii) why do health outcomes vary among individuals exposed to the same environmental challenge? Our primary study systems are small-scale, subsistence-level populations that are currently transitioning to more urban and market-integrated lifestyles. We focus on subsistence-level populations because they experience socioecological variation representative of human evolutionary history, and because they provide opportunities to investigate how major, ongoing environmental shifts-namely urbanization and market-integration-impact health.

Our lab is interested in the basic mechanism of Wnt signal transduction, a pathway that plays critical roles in the early development of multicellular organisms and the maintenance of intestinal stem cells in adults. Misregulated Wnt signaling is often implicated in human diseases such as colorectal cancer. We use biochemistry, chemical biology, cell biology, and developmental biology to study the Wnt pathway.

We study the developmental biology of the mammalian retina, from the initial patterning events through the formation of the multiple retinal cell types. We also study retinal regeneration as a way to repair damaged tissue resulting from injury or disease.

Our research focuses on understanding the neurobiology underlying cognitive and social impairments in neuropsychiatric disorders. We are particularly interested in neurodevelopmental disorders such as schizophrenia and autism and their effects on hippocampal function. Our goal is to use a “bedside to bench” approach, starting with robust, replicable findings in human patient populations and applying cutting edge neuroscience techniques in rodent models to understand underlying pathophysiology.

My resource is focused on developing statistical models and computational tool to understand genetic basis of human complex disease, with a particular focus on neuropsychiatric disorders. We integrate multifaceted functional genomics data (DNA, RNA, epigenomics) data to dissect the mechanisms of genes implicated in complex diseases on a genome-wide scale.

My diverse laboratory develops and applies advanced technologies and approaches to identify novel and unexpected genes and proteins involved in the fundamental process of protein translation and immune responses. Selected genes are functionally and mechanistically pursued using a diverse array of experimental approaches and model organisms.

The Linton laboratory pursues basic science and clinical translational investigations of inherited disorders of lipoprotein metabolism, macrophage biology, and atherosclerosis. Dr. Linton pioneered the use of bone marrow transplantation (BMT) as an approach to investigate the impact of genes expressed by bone marrow-derived cells, including macrophages, on the development of atherosclerosis in murine models. A major area of interest is the role of HDL function in human disease. We also are actively involved in clinical cardiovascular outcome trials of lipid lowering drugs, including a recent gene therapy study in familial hypercholesterolemia.

Our lab seeks to model, understand, and treat neurodegenerative disease, with a particular focus on neurovascular function and crosstalk. We operate at the intersection of engineering and regenerative medicine, and our projects span a wide variety of disciplines. We employ a number of techniques to carry out our work, including human induced pluripotent stem cell differentiation, genetic engineering, biomaterial and microdevice fabrication, high throughput screening, and molecular selection.

Structure of biological regulatory networks, dynamics, and noise. Method development, parameter estimation, machine learning, data science, AI, and simulations across scales.

Research in the Lovly lab focuses on two major themes: 1) stratification of lung tumors into clinically relevant molecular subsets, with a particular interest in those tumors which harbor EGFR mutations, ALK gene rearrangements, and small cell lung cancer and 2) determination of the molecular mechanisms leading to primary and acquired resistance to anti-cancer therapies. We work from the ground up to understand the key genetic and molecular events contributing to the development and progression of lung cancer, utilizing a variety of techniques, including genomic and proteomic studies, in silico modeling, and high throughput / high content imaging screens in order to obtain deep mechanistic insights into these events. Our entire team is excited to welcome new members and share our passion for translational lung cancer research!

In our laboratory, we utilize computational methods to study the properties and behavior of biomacromolecules and ligand-biomacromolecule complexes, and to aid in the design of small molecule ligands with desired binding properties for targeted receptors. Techniques used include quantum mechanical calculations, molecular dynamics and Monte Carlo simulation, and free energy perturbation methods. Computational methods complement experimental techniques and can enhance our understanding of biomacromolecular function.

We use a wide range of cutting-edge technologies, from single-molecule imaging to mouse models, to investigate how epithelial cells polarize and organize into tissues, and how these processes are disrupted in cancer. We use the mammary gland as a model, and study the role of stem cells and progenitors in responses to tissue damage, and mechanisms of homeostasis.

We are broadly interested in understanding how eukaryotic cells regulate membrane trafficking and protein degradation decisions and how these pathways are dysregulated in disease states. We investigate these regulatory pathways using biochemistry, proteomics, and live cell imaging in yeast and mammalian cells with the long-term goal of harnessing the intrinsic protein degradation machinery of eukaryotic cells as a therapeutic strategy for treatment of disease.

The Madhur lab seeks to elucidate inflammatory mechanisms in hypertension and vascular disease. There is growing evidence that cardiometabolic diseases have an inflammatory basis. We use cell culture, mouse models, bioinformatics, mass cytometry, flow cytometry, and human blood and tissues to investigate inflammatory pathways and identify novel therapeutic targets.

The Magnuson Laboratory uses genetically-altered mice, next generation sequencing, and bioinformatics to study the gene regulatory network (GRN) that underpins pancreatic endocrine cell identity and function. Our current studies are focused on analyzing the effects of a chronic elevation in intracellular Ca2+ (excitotoxicity) on the GRN in mature beta-cells, and the role of several zinc finger transcription factors in these networks. In addition, we are interested in determining how Sox17 gene expression is controlled during early development, and are using CRISPR mutagenesis and embryonic stem cells to identify the key transcriptional factors that regulate formation of both the definitive endoderm and vascular endothelial cells.

Our lab spans molecular probe development, including tracers for positron emission tomography (PET) imaging and drug development. Much of our work is related to precision cancer medicine.

The Markham Lab investigates C. difficile bacterial toxin pathogenesis and the mechanisms of microbially influenced colorectal cancer tumorigenesis. Our long-term goal is to understand how changes in the human microbiome affect epithelial cell signaling events and inflammatory responses in colorectal cancer.

Inborn Errors of Immunity (IEI) are diseases characterized by impaired immune development or function, leading to severe infection, autoimmunity, and cancer. Our lab uses a combination of human genetics, human immunology, bioinformatics, and molecular biology to identify and functionally characterize disease-causing mutations in these patients. This work paves the way to provide genetic diagnosis and personalized treatment for patients and allows us to identify new mechanisms of human immunity.

Our research focuses on how the androgen receptor control the growth of the prostate gland and prostate cancer

The focus of our research is the use of molecular modeling tools to understand and predict the thermodynamic and transport properties of biological systems, nanomaterials and complex fluids. These tools include molecular dynamics and Monte Carlo simulations as well as molecular theory. Current projects include using molecular simulation to provide insight into the barrier function of skin lipids and to understand the differences between healthy and diseased skin.

The McDonald lab investigates linked metabolic-epigenetic programs that drive metastasis, which is by far the most common cause of cancer deaths. We utilize patient tissue samples, 3D organoid cultures, clonal cell lines, and mouse models to investigate how these non-genetic drivers are naturally selected to accelerate metastatic spread during disease evolution. Discoveries are translated into new therapies targeting metabolic reactions that reprogram the cancer genome into an epigenetic state that facilitates metastasis.

Our research focuses on the design, construction, and application of advanced technologies for structural mass spectrometry, in particular, for studies in systems, synthetic, and chemical biology. We primarily focus on the comprehensive, untargeted, and rapid characterization of molecules directly from complex biological samples, generating signals for 10,000 to 100,000 molecules in approximately 1 minute. We utilize high performance deep learning tools to rapidly let the data inform us what is important about the sample system under investigation. These tools are then applied to a variety of biological systems with funding from the Department of Defense, the National Institutes of Health, the Environmental Protection Agency, and the Intelligence Advanced Research Project Agency.

Research in our laboratory seeks to fuse computational and experimental efforts to investigate proteins, the fundamental molecules of biology, and their interactions with small molecule substrates, therapeutics, or probes. We develop computational methods with three major ambitions in mind. A) To enable protein structure elucidation of membrane proteins the primary target of most therapeutics and large macromolecular complexes such as viruses; B) Design proteins with novel structure and/or function to explore novel approaches to protein therapeutics and deepen our understanding of protein folding pathways. C) Understand the relation between chemical structure and biological activity quantitatively in order to design more efficient and more specific drugs. Crucial for our success is the experimental validation of our computational approaches which we pursue in our laboratory or in collaboration with other scientists.

The Merrikh lab has two major interests: 1) the mechanistic, physiological, and evolutionary outcomes of the collisions between the DNA replication and transcription machineries, and 2) characterization and inhibition of the molecular mechanisms that promote the evolution of antibiotic resistance. Our laboratory uses a wide variety of techniques to studies these topics, ranging from in vivo single molecule imaging, to biochemical, molecular, and genetic methods, as well as genomics, and bioinformatics approaches. Our research utilizes a wide variety of bacterial species, including the model organisms Bacillus subtilis and Escherichia coli, and important pathogens including Salmonella typhimurium, Mycobacterium tuberculosis, and Pseudomonas aeruginosa.

The Miller lab uses the model organism C. elegans to investigate neural development and function. Research topics include mechanisms of synaptic specificity, neuronal remodeling and dendrite morphogenesis. The goal of this work is to identify molecular pathways that control these events and to establish the cell biological mechanism of each process.

Dr. Monteggia’s work focuses on the molecular and cellular basis of neural plasticity as it pertains to neuropsychiatric disorders. Her research seeks to elucidate the mechanisms underlying antidepressant efficacy and depression. She has also been investigating the role of Methyl-CpG-binding protein 2 (MeCP2), the gene linked to the autism spectrum disorder, Rett syndrome, in CNS function .

My laboratory studies regulation of the immune system in autoimmune disease and organ transplantation. Our primary focus is on T cell-B cell actions and interactions during Type 1 diabetes and islet transplantation. We use a variety of cellular and molecular immunology techniques to uncover the mysteries of immune function.

The Morgan Engineering and Imaging in Epilepsy Lab works closely with the departments of Neurology and Neurosurgery to develop Magnetic Resonance Imaging (MRI) methods to improve neurosurgical outcomes, particularly for patients with epilepsy. Ultimately, we aim to fully characterize the spatial and temporal impacts of seizures across brain networks using MRI to optimize management of epilepsy patients.

Our goal is to understand the biophysics of learning and memory. We use structural biology, in particular cryo-EM, to reveal the functional mechanism of macromolecular complexes critical for synaptic plasticity, a cellular mechanism underlying learning and memory. We also use transgenic mouse models that are deficient in learning and reveal the underlying synaptic pathology using electrophysiology.

Quantitative and predictive understanding of dynamic signal transduction and gene regulation of the coding and the non-coding genome in model organisms and human disease.

The Neul lab is interested in understanding the pathophysiology and developing therapies for Rett syndrome and other neurodevelopmental disorders using animal and cellular models.

Our lab studies how sex hormones regulate inflammatory pathways in asthma using mouse models and human samples.

The Ng lab is interested in research related to the genetics of type 2 diabetes, the complications of diabetes (e.g. diabetic kidney disease and cardiovascular disease), and contributors to diabetes (e.g. obesity, insulin resistance and insulin secretion) in African Americans and other populations. We apply a wide range of genomics (genome-wide association, exome sequencing, polygenic risk scores) approaches and integrate with metabolomics to dissect the genetic architecture of diabetes and related phenotypes. We lead the MEDIA consortium, a GWAS meta-analysis study of type 2 diabetes in African Americans. We collaborate extensively with national and international consortia including AAGILE, AMP-T2D, CHARGE, DIAMANTE, T2D-GENES, TOPMed and MVP for genomic studies of various cardiometabolic phenotypes.

The Niswender lab investigates the basic biology of and develops fundamentally new treatments for neurodevelopmental disorders such as Rett syndrome, MECP2 Duplication syndrome, Pitt Hopkins Syndrome, and Neurofibromatosis Type I. We use a combination of molecular, biochemical, electrophysiological, and behavioral techniques in mouse models of these diseases for our studies. Additionally, as part of the Vanderbilt Center for Neuroscience Drug Discovery, we are evaluating the therapeutic potential of new drug candidates in these models and hope to advance our findings into clinical development to impact the lives of children and families affected by a neurodevelopmental disorder. In addition to being part of the VCNDD, we are also members of the Vanderbilt Kennedy Center for Intellectual Disability and the Vanderbilt Institute of Chemical Biology.

We are interested in understanding the molecular pathophysiology of obesity, diabetes, and cardiovascular disease. We work to identify attractive therapeutic targets and develop novel approaches for therapeutic intervention. Much of our work, has as an underpinning, the neurobiological basis of metabolic disease.

Regulation of genome duplication requires exquisite control to ensure proper transmission of genetic material from mother cell to daughter cell and to prevent the genome aberrations that are associated with cancer cells. Importantly, the replication machinery must respond to changes in chromatin structure and cell cycle parameters that are associated with cellular differentiation to maintain genome integrity. We are using a combination of proteomic, genomic, cell biological, genetic and biochemical approaches to uncover and characterize fundamental aspects of genome duplication and stability.

We use bacterial pathogens to probe innate immune responses in the lung in an effort to identify a means of inducing enhanced antibacterial lung defenses.

Our lab is interested in two proteins, G6PC2 and ZnT8, that when mutated reduce the risk of type 2 diabetes in humans. We are working to understand the function of these proteins in vivo and we are developing inhibitors that target these proteins as novel therapies to prevent type 2 diabetes.

Research in the Ogden lab is focused on understanding mechanisms by which segmented, double stranded RNA viruses, including rotavirus and reovirus, acquire genetic diversity and impacts of this diversity on virus and host populations. Rotavirus is an important cause of diarrheal disease that results in the deaths of hundreds of thousands of infants and young children each year, and reovirus is an oncolytic virus that infects many mammalian species, including humans, but causes disease only in newborn animals. Themes we are currently exploring in our laboratory include (i) the frequency and dynamics of genome segment reassortment during co-infection, (ii) the composition and effects of defective viral genome segments, and (iii) effects of rotavirus outer-capsid antigenic diversity on antibody-mediated viral neutralization.

Two fundamental questions my lab aims to address are: how does the cell use mechanical forces to drive biochemical processes across lipid bilayers and how does the nucleus sense and transform mechanical force into biochemically meaningful signals that influence cellular development and function? In particular, we aim to create new methods to visualize and manipulate force transduction pathways that span the nuclear envelope.

Our laboratory studies mucosal immunology of the intestines. In particular, we are studying the role of lymphoid cells present in the intestinal epithelium during normal and disease conditions. Our goal is to determine the impact of these cells in intestinal diseases such as ulcerative colitis and Crohn’s disease.

The intertwining of the two strands of the DNA helix presents a number of topological problems that the cell must be able to overcome in order to maintain its genetic information. Consequently, the enzymes that modulate the topological state of nucleic acids, the DNA topoisomerases, play a crucial role in controlling the physiological functions of DNA. The type II enzyme alters nucleic acid topology by passing an intact double helix of DNA through a transient double-stranded break made in a second DNA helix. Because these enzymes cleave DNA, they also have the potential to fragment the genome. As a result, they are targets for some of the most widely prescribed anticancer and antibacterial drugs. We are very interested in how type II topoisomerases function and how they interact with drugs.

Our lab is interested in basic science questions about how tissues are formed and how they are repaired. Current projects center on how cells detect a nearby wound, basement membrane repair, and extracellular signaling controlling stem cell functions. Most of our experiments are performed in the fruitfly Drosophila melanogaster whose biology is surprisingly similar to our own.

Epithelial cells respond immediately to a wound (at 0 sec) by increasing intracellular calcium (imaged with GCaMP6m).

The Park Lab uses genetic approaches to identify, validate and develop new targets for therapy as well as diagnostic tests to help guide clinical decision making for breast cancer. Using human somatic cell gene editing, we create and exploit isogenic cell lines to achieve these aims. Our goal is to then translate these laboratory findings for clinical trials and patient benefit and have accomplished this using plasma tumor cell-free DNA as a biomarker for residual tumor burden.

Disease can be defined as a state in which the body’s ability to maintain homeostasis of molecular and cellular processes within their physiologically “normal” range is compromised. We use state of the art approaches including genomics, high resolution imaging, and systems biology to study mitochondrial homeostasis. Our short-term is to provide fundamental insights into mechanisms of mitochondrial homeostasis and the consequences of its breakdown, while our long-term goal is to provide an evolutionary framework for understanding why and under what physiological circumstances mitochondrial homeostasis collapses.

Our lab is specifically interested in the role of endogenous cannabinoids as mediators of stress resiliency and have extramurally funded research projects in areas of endocannabinoid synaptic biology, endocannabinoid-based therapeutics development, and investigation of circuit-level mechanisms by which endocannabinoids promote resiliency to stress.

The Patton lab is an RNA biology lab with projects that focus on retina regeneration and colon cancer. For retina regeneration, we use zebrafish as a model organism to study how an adult stem cell (Muller glia) can respond to injury to replace any lost cell type. For colon cancer, we are studying how cell-cell signaling can be mediated by extracellular vesicles that deliver proteins, RNAs, and lipids and are key to interactions in the tumor microenvironment and metastasis.

Our lab focuses on the mechanisms that regulate lung inflammation, predominantly viral-induced and allergic-mediated inflammatory processes. We have a particular interest in how eicosanoids and cytokines modulate lung inflammatory responses.

Our laboratory is focused on microbially-induced gastric carcinogenesis with the overarching theme being delineation of the signaling events initiated by bacterial:epithelial cell contact that regulate carcinogenic phenotypes using complementary model systems. Our group utilizes ex vivo gastric organoid systems that closely recapitulate cellular organization in the stomach to examine aberrant responses to oncogenic H. pylori strains. We also developed robust and reproducible rodent models of H. pylori-induced gastric cancer and continually extend our observations into human populations.

Dr. Penn’s research focuses on the molecular and cellular characterization of retinal vascular inflammation and angiogenesis with emphasis on biomarker identification and development of targeted therapies and novel mechanisms of drug delivery to the eye. His work specifically impacts several prevalent causes of irreversible vision loss, including retinopathy of prematurity, diabetic retinopathy and age-related macular degeneration. Penn’s lab partners closely with drug companies to develop pre-clinical efficacy data for investigational new drug applications to the FDA.

My research spans the full range of molecular imaging, from imaging system design to in vivo preclinical and clinical research studies. A particular emphasis of my lab is the application of semiconductor radiation detector technology to the development of high-resolution SPECT.

The work in my lab focuses on the development of technology for drug delivery and biomarker imaging. This is a hybrid lab of medicinal chemistry and molecular imaging, and thus multdisciplinary efforts are under taken to achieve our objective.

The Philip Lab seeks to understand how the immune system interacts with developing cancers from the first mutation initiating carcinogenesis through progression to late-stage and metastatic tumors. We use clinically-relevant genetic cancer mouse models to understand the molecular and epigenetic regulatory mechanisms underlying tumor-specific T cell dysfunction and to design and test cutting-edge strategies to override T cell dysfunction to improve cancer immunotherapy.

I study the genetic risk and immunopathogenesis of severe T-cell mediated adverse drug reactions using advanced multi-omic and single cell technologies

Our research uses multidisciplinary approaches in chemical biology and proteomics to profile transient protein complexes. The goal is to understand how protein-protein interaction networks are dynamically regulated in diverse cellular processes, such protein folding and secretion, or during viral infections. We leverage new insights on the dysregulation of protein interactions networks in disease states to guide the development of therapeutic strategies.

Inflammatory and autoinflammatory diseases have high morbidity, limited diagnostic specificity and suboptimal treatments. In the Pua lab, we study how non-coding RNAs (particularly microRNAs) regulate inflammatory programs to uncover novel molecular networks in immune disease. We investigate both the cell-intrinsic roles of these regulatory RNAs as well as how they are communicate signals between cells when secreted into the extracellular space using mouse models, cell culture systems, molecular biology and high throughput sequencing.

The Quaranta laboratory combines theory and experimentation to understand cancer as a complex system, capable of evolving by a variety of genetic and non-genetic means in order to adapt to and evade treatment. The laboratory is comprised of a mix of experimentalists, engineers, statisticians, and mathematicians iteratively combining experimental and modeling tools towards a systems-level understanding of the basic principles governing cancer, with a specific focus on melanoma, lung and breast cancer. The Quaranta laboratory has made key contributions to developing single-cell methodologies that merge automated time-lapse microscopy with image analysis and computational modeling, in order to evaluate the dynamics of cancer cell response to targeted therapy.

The Rafat Lab works at the interface of engineering and cancer biology. We examine the biological, chemical, and physical cues that influence cancer metastasis and recurrence. Current studies focus on the effect of radiation and surgery on tumor and immune cell migration dynamics, the molecular profiles of tissues wounded from therapy, and the biomechanical properties of tissues following therapy.

We study the regulation of metabolism in T cells and how metabolic pathways direct inflammatory and anti-tumor responses. Using human and mouse models as well as genetic tools our work identifies new targets to modulate T cell differentiation and function.

Fully processed eukaryotic mRNAs are exported to the cytoplasm where translation occurs. We determine the sequence and mechanism of events that prepare nuclear mRNA for export and investigate how mRNA export is altered in human disease.

We are investigating mechanisms and therapies for complex neurodegenerations of the visual system. We use dietary, pharmacologic, gene therapy and cell therapy approaches to provide neuroprotection and neuroregeneration in models of glaucoma and neurotrauma. We also have a clinical study to understand the physiological basis for self-reported sensory dysfunction in TBI patients and develop quantitative diagnostics for their symptoms.

The Reynolds laboratory combines molecular and biochemical approaches with 3D (organoid) culture and mouse models of colon and breast cancer to examine roles of p120-catenin (p120) in cadherin-mediated cell-cell adhesion, tumorigenesis and metastasis. A recent focus involves p120 signaling to the nucleus through Kaiso (aka ZBTB33), a p120-associated transcription factor involved in genetic and epigenetic regulation of stem-cell function and tissue differentiation. The lab is interested in defining the nuclear functions of Kaiso and p120 using state of the art next generation sequencing technologies, including ChIPseq, PROseq and ATACseq.

We research bone tumors and how they affect the bone microenvironment and immune compartment. Our protein of interest is the Gli2 transcription factor and how it contributes to osteolytic destruction in primary and metastatic bone tumors. We also seek to understand how the bone microenvironment affects cancer cell signaling, and to design novel therapeutics aimed at blocking bone resorption and tumor growth.

The research in my lab focuses on developing new approaches for cancer therapeutics that combine targeted therapies and immune therapy using a precision medicine approach.

Dr. Riess’ research focuses on intracellular mechanisms of cardio- and neuroprotection pertaining to cardiac arrest, heart attacks and stroke, especially the role of mitochondrial function as a trigger and effector of cellular protection. He has presented over 120 abstracts at national and international meetings and has authored more than 70 book chapters and papers in peer-review journals.

Our lab is focused on various aspects of DNA damage. We specialize in the site-specific synthesis of oligonucleotide modified with DNA damaging agents. These modified oligonucleotides are valuable substrates for subsequent biochemical, cellular, and structural studies.

Our research team develops cutting-edge quantitative proteomics and lipidomics approaches based on mass spectrometry. These approaches are applied to study health disparities in Alzheimer’s disease and sepsis, to understand the role of the periphery in these diseases, and to identify potential biomarkers useful for diagnosing disease.

We are interested in understanding the role of genetic variation in two distinct domains: in susceptibility to abnormal heart rhythms and response to antiarrhythmic therapies, and in the broader question of how genetic variation modulates drug responses. We use models from iPS cells to large scale studies in BioVU, Vanderbilt’s biobank.

In the Rokas lab, we study the DNA record to gain insight into the patterns and processes of evolution, focusing on three major questions: I. What are the molecular foundations of the fungal lifestyle? II. How can we elucidate the tree of life? III. How did human pregnancy evolve? We are working with several eukaryotic lineages, but mainly with mammals and fungi. Because, many of the computational and experimental approaches we employ are novel and unfamiliar to many biologists, we also investigate their utility for studying the function and evolution of the genomes of non-model organisms.

We study host and pathogen interactions between two chytrid fungi and susceptible amphibians. The research involves studies of lymphocyte-mediated responses, skin microbial communities, and antimicrobial skin peptide defenses. Field and laboratory studies also examine possible effects of climate change on amphibian immune defenses.

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Our group is at the intersection of genomics, biomedical informatics and psychiatry and has two broad research interests. 1) Capturing and extracting information to aid in elucidating genetic etiology of behavioral health traits and psychiatric diagnoses. 2) Utilizing genetics/genomics to understand biological mechanism and interventional strategies of psychiatric disorders

The Samuels group works in the area of genetic research using large scale electronic medical records. We have a special emphasis on mitochondrial function in medicine.

The Sanders Lab uses the tools of Biochemistry, Structural Biology, and Chemical Biology to determine how defects in membrane proteins cause human diseases.

Trillions of distinct synaptic connections assemble into stereotyped circuits during mammalian brain development. Our laboratory examines the mechanisms of synaptic circuit formation, refinement, and maintenance using a combination of cellular and molecular, electrophysiological, and imaging approaches.

We study biotransformations of small molecules with relevance to human health and disease in vitro and in vivo. We determine the structures of novel metabolites (LC-MS, NMR), analyze enzymes and reaction mechanisms involved in their formation, and quantify their abundance in animals and humans. We investigate the biological activity of the newly identified metabolites using cell culture and animal models.

Immunotherapies to improve systemic and localized host defense in preexisting conditions, such as diabetes and aging

We study the regulation of rhodopsin endocytosis in Drosophila photoreceptors. We investigate the real-time trafficking using transgenic flies expressing GFP or mCherry tagged rhodopsin or arrestin. We believe that insights into light-regulated rhodopsin endocytosis will further better understanding of GPCR trafficking in vivo.

A major focus of the lab is to understand the neural mechanisms of individual differences in decision making – that is, why do behavioral responses vary even when given the same experience. For example, although a large portion of the population will be exposed to alcohol, only some will go on to develop an alcohol use disorder. We develop behavioral procedures in rodents to model these phenomena, allowing us to determine the pre-existing differences that may contribute to individual differences as well as how they change with experience. By combining these models with various recording and manipulation techniques we dissect the circuitry of maladaptive decision making.

We study how environmental factors, such as nutrition and hormones, impact the development of neural circuits that control behavior and metabolism, in order to better understand how early events in an individual’s life influence behavior and metabolic physiology. We discovered that the fat-derived hormone leptin is a major developmental signal that participates in metabolic programming of the hypothalamus. Using genetically targeted fluorescent labels, and both in vitro and in vivo conditional regulation of gene expression, we are determining if manipulations of genes known to participate in brain development also influence development of leptin-sensitive pathways that mediate hypothalamic responses to changes in energy balance. Utilization of light sheet microscopy to visualize large tissue volumes, and in vivo calcium imaging to record network activity, we are interrogating the functional significance of metabolically programmed changes in neural architecture, with direct implications for the developmental origins of obesity and diabetes.

Our lab studies receptor tyrosine kinase (RTK) signaling in human health and disease with an emphasis on epidermal growth factor receptor (EGFR) signaling. The research may broadly be divided into two areas: 1. Trafficking of EGFR ligands in polarized epithelial cells: Spatial cues to regulate EGFR signaling are best appreciated in three-dimensional (3D) cultures (e.g. Transwell, type I collagen, and Matrigel cultures) than conventional 2D plastic cultures, where EGFR ligands are delivered and secreted in a polarized manner (apical vs basolateral trafficking). A major focus within this area is to understand the loss of epithelial polarity induced by loss of polarized trafficking of the EGFR ligand, epiregulin, and role of novel epiregulin-interacting proteins in the observed phenotypes. 2. Cetuximab resistance in colorectal cancer: Using 3D cultures of colorectal cancer (CRC) cells, we study novel resistance mechanisms to cetuximab, which is an FDA-approved EGFR neutralizing monoclonal antibody. We have discovered two non-genetic modes of cetuximab resistance and identified means to overcome this resistance by addition of a dual MET/RON RTK inhibitor, crizotinib. We are committed to elucidating the mechanistic underpinnings of this mode of cetuximab resistance, its scope in human CRC, and the therapeutic benefit of combined blockade of EGFR with RTKs, MET and RON. This multi-disciplinary and collaborative research integrates approaches like molecular cell biology, live or fixed (confocal) microscopy, comparative RNA-seq (single-cell or bulk), proteomic analysis, pre-clinical models (patient-derived xenografts and organoids, PDXs/PDOs), and small-animal imaging.

We study the impact of nutrition on the outcome of infectious diseases with a focus on both sides of the host-pathogen interaction.

Our group investigates the heritable origin of prostate cancer through study of men with a strong family history of the disease. We also study the genetic determinants of prostate cancer severity, distinguishing men with an indolent from an aggressive disease course. We use advanced genomic technologies and analytic approaches to discover and to understand causal genetic mechanisms.

We have established a method to grow, identify and immortalize IgE encoding B cells from peripheral blood of allergic and helminth infected individuals. With this technology we can generate and study, for the first time, naturally-occurring human IgE monoclonal antibodies specific to clinically important allergens and parasitic worms. These studies will provide novel insights into the pathogenesis of allergic diseases for the development of new therapeutics and the natural immunity to helminth infection to assist with the rational design of vaccines.

Our group is focused on peripheral innervation of visceral organs specifically the intestine and lower urinary tract.  We are working to define the gene networks that control lineage specification and differentiation of neural crest stem cells as they give rise to the innervation of these organ systems.  Our team uses mouse models in transgenic and gene-targeted strategies in combination with bioinformatic approaches in human and mouse datasets to dissect the pathways that regulate gastrointestinal motility and bladder function.

Structural biology of the immune response and host pathogen interactions.

Our lab aims to define and target pathways that give rise to cardiovascular disease with obesity and diabetes. We study liver metabolism in vivo, how obesity alters lipoprotein metabolism, and male female differences in metabolic and cardiovascular risk. We use cutting-edge tracer approaches to define glucose and lipid metabolism. We do functional studies of HDL and its ability to protect from heart disease. We use mouse and human studies.

Chemistry and Biology of DNA Damage

We are interested in understand how mutations in transcription factors and chromatin remodeling enzymes contribute to malignancy. We are also interested in the genomic landscape of cancers, and how both permanent and transient alteration in the enhancer landscape contribute to malignancy.

Sulikowski’s research interests are on the design and development of chemical syntheses of complex molecules, specifically bioactive natural products and molecular probes. Over time his interests have expanded to the chemical synthesis of molecular tools with application in biological research and therapeutic lead development.

MYC is an oncoprotein and transcription factor that features in the death of 100,000 people each year in the United States alone. We are interested in understanding how MYC works, and how it can be targeted for new therapies in cancer cells.

We study the interactions of hosts and their microbial communities through a combination of molecular, ecological, and evolutionary perspectives. Particular lab interests include host co-infection with multiple parasites, immune system evolution, and immune system function in wild populations. We use a combination of field work, wet lab work, and mathematical and computational modeling.

Cellular and molecular mechanism that result in autoimmunity.

Deciphering how human milk maintains homeostasis over dysbiosis.

The human body is composed of hundreds of distinct cell types that take on unique morphologies to serve specific physiological tasks. The Tyska laboratory is focused on understanding of how cell morphology is controlled by regulated assembly of the actin cytoskeleton.

Dr. Vago is the director of research at the Osher Center for Integrative Medicine where he also directs the Contemplative Neuroscience and Integrative Medicine laboratory. Dr. Vago’s research interests broadly focus on utilizing translational models to identify and characterize neurobiological substrates that constitute adaptive mind-body interactions, to better predict outcomes and potential biologically-based diagnostic and therapeutic strategies for those suffering with mental illness and chronic pain. Dr. Vago and his research team use mixed research methods of systems biology, neuroimaging, predictive computational modeling, connectomics, genomic and neuroendocrine science, innovation, cognitive-behavioral and first-person phenomenological analyses.

Our research is broadly focused on interactions between the immune and metabolic systems, an emerging field referred to as immunometabolism. We employ a variety of mouse models of disease, including multiple sclerosis, type 1 and type 2 diabetes, inflammatory bowel disease, infection, cancer, and cardiovascular disease.

Our lab focuses on evaluating the genetic and environment risk factors associated with women’s health and reproductive outcomes, as well as genetic diseases with significant racial/ethnic disparities. We have an ongoing grants to study the genetic determinants of uterine fibroid risk and to evaluate the role of race and ancestry on risk for keloids. We also have a repository of biospecimens from participants in the Right from the Start pregnancy cohort to be used for genetic epidemiology studies examining uterine fibroid and the role drug exposures in adverse pregnancy outcomes. Our lab has significant expertise in fibroid epidemiology and genetics and next-generation sequencing (DNA and RNA sequencing).

Our research focuses on understanding the role of protein kinase/phosphatase modules in the control of normal cellular signaling. We are exploiting complementary biochemical, immunological, and genetic strategies to better understand the structure, function, and regulation of these signaling modules in normal biology and disease. More recently, we have taken advantage of the unique immune system of alpacas, and have incorporated a “bench to farm and back again” approach to target these key signaling proteins.

The Walker lab uses machine learning and statistics to solve difficult problems in chemical biology. We build our machine learning models based on the wealth of available sequences and structures of biomolecules. After a machine learning model is developed, we experimentally verify our computational predictions and use experimental data to further optimize our models.

Our lab is interested in determining the molecular mechanisms that drive viral infections. We do this by studying how viruses infect cells using a variety of approaches including structural biology and biophysics. We are specifically interested in negative-sense RNA viruses such as Ebola and rabies viruses.

My research focuses on mechanisms of organ dysfunction in critical illness with an emphasis on acute lung injury, sepsis and acute kidney injury. We currently are focused on how cell-free hemoglobin, a potent oxidant, can injure the lung epithelium and endothelium and contribute to the pathogenesis of acute lung injury.

We are interested in the regulation of glucose metabolism during health and disease. Insulin, exercise, and pharmacological agents are used to study physiological processes in mice with selective gene mutations.

Our laboratory focuses on the discovery and development of drug-like potassium ion channel modulators. We use molecular biology, high-throughput screening, automated electrophsiology, medicinal chemistry, and rodent disease models to better understand the function of potassium channels in search of new therapies for epilepsies and other CNS disorders.

The Weaver laboratory studies the role of extracellular vesicles, including exosomes, in driving cell migration, and cellular communication in cancer, in the brain, and other biological systems. We use a variety of approaches, including biochemical purification, molecular manipulation of cells, microscopy (including live cell and tissue imagine), mouse models, and working with human patient samples.

The Weiss laboratory is focused on understanding the molecular and immunologic mechanisms of thyroid cancer invasion and metastasis. While most thyroid cancer patients respond well to standard therapy, there are few options for those with widely metastatic or recurrent disease. Predicting which patients will have aggressive disease and treating those patients is an important goal in the field. The goal of the laboratory is to understand the signaling mechanisms and immune microenvironment responsible for the aggressive malignant behaviors of metastatic and recurrent disease. Projects include defining the role of Wnt signaling within the current molecular landscape of papillary thyroid carcinoma. The laboratory also uses computational immunogenomics to define the immunologic microenvironment within aggressive thyroid cancer subtypes to improve treatment and malignancy risk prediction at the time of biopsy.

The Williams Lab decodes intestinal epithelial repair programs in inflammatory bowel disease and colitis-associated carcinoma. We have a particular interest in chromatin regulation, protection from ROS mediated injury, and junctional signaling in wound healing

Our laboratory investigates gastrointestinal mucosal immunology, inflammation, and carcinogenesis. We focus on two diseases, Helicobacter pylori infection of the stomach and the link to gastric cancer, and inflammatory bowel disease and the link to colon cancer. Through basic and translational studies, using many mutant mouse lines, human tissues, and a variety of techniques we aim to assess factors such as alterations in immunometabolism in disease that can serve as opportunities for disease prevention.

We study mechanisms of stress-reward interaction in the brain.

Our long-term goal is to provide insight into the molecular, genetic and cell-biological mechanisms that coordinate development of complex organ systems, which has relevance to human congenital birth defects, and overt and cryptic susceptibilities to disease or inherited syndromes. All of these processes can be analyzed using either single-cell or bulk methods such as ATAC-Seq, single-molecule-FISH, epigenetic analysis, real-time/time-lapse video- and super-resolution microscopy, 3D tissue-clearing immunolabeling approaches, and many others.

My main research interests are the development and validation of advanced magnetic resonance imaging techniques to probe tissue microstructures non-invasively and assess the ability of our new imaging techniques to address unmet clinical needs.

By integrating physical simulation and data-driven modeling, we develop and apply computational platforms to evaluate, understand, predict, and design biomolecules for uses in catalysis, immunology, and environmental degradation.

The overall goal of my lab is to develop novel metabolic engineering approaches to measure, understand, and control cellular metabolism. We use metabolic flux analysis and mathematical modeling to investigate research questions of relevance to medicine and biotechnology.

The research in our group is focused on understanding how inflammatory signaling contributes to the development, progression and treatment of cancers; including ovarian, breast, lung and skin. Cell culture and transgenic mouse model approaches are providing insights into effects within specific cell types and interactions between tumor and infiltrating immune cells that are informing our strategies to develop new therapies based on pharmacologic or nanoparticle approaches.

We investigate the role of mitochondrial function in cell fate decisions and the implications of this regulation in physiology. Importantly, we are focused on identifying how altered mitochondrial function leads to pathology.

Microtubules are dynamic intracellular polymers vital for cell shape, motility and cell division. Our lab uses an interdisciplinary approach, combining molecular and cell biology, biochemistry, engineering and physics, to elucidate the molecular mechanisms driving the dynamic architecture of the microtubule cytoskeleton. Our ultimate goal is to provide a fundamental understanding of how cells engineer large-scale, dynamic structures essential for life.

Cell-extracellular matrix interactions in health and disease from structure to function. Primary focus is on integrins in epithelial cells utilizing transgenic mice, cell biology and structural approaches..

Cell-to-cell communication is crucial for multicellular organisms because it allows organisms to coordinate the activity of their cells. Using structural biology techniques including cellular cryo-electron tomography (cryo-ET) combined with optical imaging and electrophysiological methods, we are investigating the molecular mechanisms of vesicle-mediated cell-to-cell communication in the central nervous system. A broad long-term goal is to apply knowledge gained from above mechanistic studies to investigate how dysfunction in certain aspects of neurotransmitter release and neuronal development contributes to brain disorders.

We study the impact of programmed cell death and mitochondrial function on hematopoietic stem cell function and progression to bone marrow failure or leukemia. An additional focus is on identifying correlations between genetically regulated variations in gene expression and human blood disease.