BBSP Faculty

We are interested in determining the mechanisms involved in the beneficial modulation of the gut microbiota by prebiotics (functional foods that stimulate growth of gut native beneficial bacteria) and probiotics (live bacteria that benefit their host). Specifically, we aim to develop prebiotic and probiotic interventions as alternatives to traditional treatments for microbiota-health related conditions, and to advance microbiota-based health surveillance methods.

Our lab uses a combination of genetics, high-resolution cellular and animal imaging, animal tumor models and microfluidic approaches to study the problems of cell motility and cytoskeletal organization. We are particularly interested in 1) How cells sense cues in their environment and respond with directed migration, 2) How the actin cytoskeleton is organized at the leading edge of migrating cells and 3) How these processes contribute to tumor metastasis.

My lab uses a cognitive neuroscience approach to understand the neurobiology of drug addiction in humans. The tools we use include fMRI, cognitive testing, physiological monitoring, pharmacology, and genetic testing. We specifically seek to determine 1) how the brain learns new stimulus-response associations and replaces learned associations, 2) the neurobiological mechanisms underlying the tendency to select immediate over delayed rewards, and 3) the neural bases of addiction-related attentional bias.

We study the molecular mechanisms of HIV latency. Transcriptional silencing of HIV is a key mechanism of persistence in patients, and is a barrier to viral eradication, but little is known about the latent reservoir or the molecular mechanisms that regulate it. As such, our repertoire of drugs for targeting latently infected cells is limited. Some latency reversing agents (LRAs) have been developed, but these are typically reactivate only a minor subset of proviruses. This inefficiency is in part due to the reservoir not constituting a uniform target, but instead being a heterogeneous set of cells with diverse characteristics and restrictions to HIV expression. However, most analyses of latency use bulk cell cultures assays in which crucial information about the behavior of individual cells is lost. Also, latently infected cells in patient samples are exceedingly rare, making them very difficult to study directly. New technological breakthroughs in the field of single cell analysis as well as the development of primary cell models for HIV latency now open the possibility of observing how latently infected cells form and are maintained at single cell resolution. Our lab has developed tools to study the establishment, maintenance and reversal of HIV latency at single cell resolution using multi-omics methods. Furthermore, we combine these approaches with genetic perturbation, time-lapse microscopy and novel bioengineering tools to gain insight into how the host cell regulates HIV latency. We have recently discovered using single cell RNAseq (scRNAseq) that latency in primary CD4 T cells is associated with expression of a distinct transcriptional signature (Bradley et al 2018). Our hypothesis is that this signature represents part of a cellular program that regulates latency, and that this program is an exciting novel target for the development of LRAs. Ongoing projects in the lab involve the application of new technologies to our model systems, and testing/validation of the roles of host cell pathways we have identified in HIV latency. Our overall goal is to identify new targets for the development of drugs to clear the HIV reservoir.

A growing body of work in the biomedical sciences generates and analyzes omics data; our lab’s work contributes to these efforts by focusing on the integration of different omics data types to bring mechanistic insights to the multi-scale nature of cellular processes. The focus of our research is on developing systems genomics approaches to study the impact of genomic variation on genome function. We have used this focus to study genetic and molecular variation in both natural and engineered cellular systems and approach these topics through the lens of computational biology, machine learning and advanced omics data integration. More specifically, we create methods to reveal functional relationships across genomics, transcriptomics, ribosome profiling, proteomics, structural genomics, metabolomics and phenotype variability data. Our integrative omics methods improve understanding of how cells achieve regulation at multiple scales of complexity and link to genetic and molecular variants that influence these processes. Ultimately, the goal of our research is advancing the analysis of high-throughput omics technologies to empower patient care and clinical trial selections. To this end, we are developing integrative methods to improve mutation panels by selecting more informative genetic and molecular biomarkers that match disease relevance.

The Button lab in the Department of Biochemistry and Biophysics is part of the Marsico Lung Institute. Our lab is actively involved in projects that are designed to define the pathogenesis of muco-obstructive pulmonary disorders and to identify therapies that could be used to improve the quality of life in persons afflicted by these diseases. In particular, our research works to understand the biochemical and biophysical properties of mucin biopolymers, which give airway mucus its characteristic gel-like properties, and how they are altered in diseases such as Asthma, COPD, and cystic fibrosis.

Research in the Carelli laboratory is in the area of behavioral neuroscience. Our studies focus on the neurobiological basis of motivated behaviors, including drug addiction. Electrophysiology and electrochemistry procedures are used during behavior to examine the role of the brain ‘reward’ circuit in natural (e.g., food) versus drug (e.g., cocaine) reward. Studies incorporate classical and operant conditioning procedures to study the role of the nucleus accumbens (and dopamine) and associated brain regions in learning and memory, as they relate to motivated behaviors.

Developing and applying novel mass spectrometry (MS)-based proteomics methodologies for high throughput identification, quantification, and characterization of the pathologically relevant changes in protein expression, post-translational modifications (PTMs), and protein-protein interactions. Focuses in the lab include: 1) technology development for comprehensive and quantitative proteomic analysis, 2) investigation of systems regulation in toll-like receptor-mediated pathogenesis and 3) proteomic-based mechanistic investigation of stress-induced cellular responses/effects in cancer pathogenesis.

We study proteases that induce rapid changes in cell morphology, behavior, and identity. We are particularly interested in ones that play a role in myotube formation, muscular dystrophies, rhabdomyosarcoma, and cachexia. Our model systems include C2C12 cells, primary myoblasts, patient-derived iPSCs, and zebrafish. In addition to standard cell biology approaches, we make use of chemical biology and advanced microscopy techniques. Ultimately, we seek to identify a combination of protease inhibitors/activators that can cure musculoskeletal diseases.

The long-term goal of my research is to incorporate ‘omic (genomic, epigenomic, proteomic, etc.) measurements into environmental human health hazard identification, prioritization and risk assessment using a quantitative and interpretable biological systems framework. Thus, short-term goals have been to develop the molecular tools to investigate key biological events, and measurable biomarkers linked to those events, related to important disease processes that are impacted by environmental chemical exposures, such as liver and lung toxicity.  We have focused recent efforts on early-in-life genomic and epigenetic alterations and linkages to latent adverse outcome susceptibility due to commons exposures, genetics, and pre-existing conditions. Our laboratory uses cutting edge techniques such as gene editing tools including CRISPR-based methods; next generation nucleic acid-based sequencing to probe the genome and epigenome; advance, high-throughput microscopy; targeted RNA, DNA, and non-coding RNA measurements such as digital drop PCR and Fireplex; and advanced in vitro models.

The Chung lab is engineering immune cells, particularly T cells, to achieve maximum therapeutic efficacy at the right place and timing. We explore the crossroads of synthetic biology, immunology, and cancer biology. Particularly, we are employing protein engineering, next-gen sequencing, CRISPR screening, and bioinformatics to achieve our objectives:

(1) Combinatorial recipes of transcription factors for T cell programming.

(2) Technologies for temporal regulation and/or rewiring of tumor and immune signal activation (chemokine, nuclear, inhibitor receptors).

(3) Synthetic oncolytic virus for engineering tumor-T cell crosstalk.

Cross-talk between insulin like growth factor -1 and cell adhesion receptors in the regulation of cardiovascular diseases and complications associated with diabetes.

The Cohen Lab investigates how functional brain networks in humans interact and reconfigure when confronted with changing cognitive demands, when experiencing transformations across development, and when facing disruptions in healthy functioning due to disease. We are also interested in how this neural flexibility contributes to flexibility in control and the ability to learn, as well as the consequences of dysfunction in this flexibility. We use behavioral, neuroimaging, and clinical approaches taken from neuroscience, psychology, and mathematics to address our research questions.

My research aims to uncover the molecular aspects of protein aggregation diseases (also called PAD) which include neurodegenerative diseases (such as Alzheimer’s disease and Amyotrophic Lateral Sclerosis), myofibrillar myopathies (such as muscular dystrophies), as well as the formation of age-related cataracts.  Although very distinct, these disorders share a common underlying pathogenic mechanism.  Using a combination of biochemistry and in vitro approaches, cell biology, and primary cells / transgenic mouse models, we will investigate the post-translational modifications (PTMs) that drive these disease processes. Ultimately, this research will provide a platform for future drug discovery efforts against these devastating diseases.

Males and females differ in their prelevance, treatment, and survival to a diverse set of human disease states. This is exemplified cardiovascular disease, a disease that takes more lives than all forms of cancer combined. In cardiac disease, women almost uniformly fare far worse than men: as of 2007 one woman dying for cardiovascular disease in the US every minute. Our lab focuses on sex disparities in development and disease. For these studies, we use a highly integrated approach that incorporates developmental, genetic, proteomic, biochemical and molecular-based studies in mouse and stem cells. Recent advances by our past students (presently at Harvard, John Hopkins and NIH) include studies that define the cellular and molecular events that lead to cardiac septation, those that explore cardiac interaction networks as determinants of transcriptional specificity, the mechanism and function of cardiac transcriptional repression networks, and the regulatory networks of cardiac sexual dimorphism. Our lab has opening for rotation and PhDs to study these rapidly emerging topics.

With a particular interest in pediatric solid tumors, our lab aims to develop a mechanistic understanding of the role of aberrant or dysregulated transcription factors in oncogenesis.

Our lab studies brain network connectivity in the healthy brain and in neurological and neuropsychiatric patient populations. We focus on the organizational, dynamical, and computational properties of large-scale brain networks and determine how these properties contribute to human behavior in health and disease. We strive to advance the basic understanding of brain structure and function, while making discoveries that can be translated to clinical practice.

We use an integrated approach (genomics, proteomics, computational biology) to study the molecular mechanisms of hormone and drug desensitization. Our current focus is on RGS proteins (regulators of G protein signaling) and post-translational modifications including ubiquitination and phosphorylation.

The Elston lab is interested in understanding the dynamics of complex biological systems, and developing reliable mathematical models that capture the essential components of these systems. The projects in the lab encompass a wide variety of biological phenomena including signaling through MAPK pathways, noise in gene regulatory networks, airway surface volume regulation, and understanding energy transduction in motor proteins. A major focus of our research is understanding the role of molecular level noise in cellular and molecular processes. We have developed the software tool BioNetS to accurately and efficiently simulate stochastic models of biochemical networks

Our lab applies cutting edge genetic and proteomic technologies to unravel dynamic signaling networks involved in cell proliferation, genome stability and cancer. These powerful technologies are used to systematically interrogate the ubiquitin proteasome system (UPS), and allow us to gain a systems level understanding of the cell at unparalleled depth. We are focused on UPS signaling in cell cycle progression and genome stability, since these pathways are universally perturbed in cancer.

In the Ferris lab, we use genetically diverse mouse strains to better understand the role of genetic variation in immune responses to a variety of insults. We then study these variants mechanistically. We also develop genetic and genomic datasets and resources to better identify genetic features associated with these immunological differences.

Our goal is to revolutionize the treatment of psychiatric and neurological illness by developing novel brain stimulation paradigms. We identify and target network dynamics of physiological and pathological brain function. We combine computational modeling, optogenetics, in vitro and in vivo electrophysiology in animal models and humans, control engineering, and clinical trials. We strive to make our laboratory a productive, collaborative, and happy workplace.

The lab focuses on understanding how environmental exposures are associated with human disease with a particular focus on genomic and epigenomic perturbations. Using environmental toxicogenomics and systems biology approaches, we aim to identify key molecular pathways that associate environmental exposure with diseases. A current focus in the lab is to study prenatal exposure to various types of metals including arsenic, cadmium, and lead. We aim to understand molecular mechanisms by which such early exposures are associated with long-term health effects in humans. For example, we are examining DNA methylation (epigenetic) profiles in humans exposed to metals during the prenatal period. This research will enable the identification of gene and epigenetic biomarkers of metal exposure. The identified genes can serve as targets for study to unravel potential molecular bases for metal-induced disease. Ultimately, we aim to identify mechanisms of metal -induced disease and the basis for inter-individual disease susceptibility.

The Furey Lab is interested in understanding gene regulation processes in specific cell types, especially with respect to complex phenotypes, and the effect of genetic and environmental variation on gene regulation. We have explored these computationally by concentrating on the analysis of genome-wide open chromatin data generated from high-throughput sequencing experiments; and the development of statistical methods and computational tools to investigate underlying genetic and biological mechanisms of complex phenotypes. Our current projects include determining the molecular effects of exposure to ozone on chromatin, gene regulation, and gene expression in alveolar (lung) macrophages of genetically diverse mouse strains. We are also exploring genetics, chromatin, transcriptional, and microbial changes in inflammatory bowel diseases to identify biomarkers of disease onset, severity, and progression.

Our primary research is in the area of computational systems biology, with particular interest in the study of biological signaling networks; trying to understand their structure, evolution and dynamics. In collaboration with wet lab experimentalists, we develop and apply computational models, including probabilistic graphical and multivariate methods along with more traditional engineering approaches such as system identification and control theory, to current challenges in molecular biology and medicine. Examples of recent research projects include: prediction of protein interaction networks, multivariate modeling of signal transduction networks, and development of methods for integrating large-scale genomic data sets.

My group develops and deploys computational tools to predict physiological function and dysfunction. We are interested in a range of applications in medicine and biology, but our primary focus is the cardiovascular system. My group is actively developing fluid-structure interaction (FSI) models of the heart, arteries, and veins, and of cardiovascular medical devices, including bioprosthetic heart valves, ventricular assist devices, and inferior vena cava filters. We are also validating these models using in vitro and in vivo approaches. We also model cardiac electrophysiology and electro-mechanical coupling, with a focus on atrial fibrillation (AF), and aim to develop mechanistically detailed descriptions of thrombosis in AF. This work is carried out in collaboration with clinicians, engineers, computer and computational scientists, and mathematical scientists in academia, industry, and regulatory agencies.

I am a Pediatric Pulmonologist. My lab studies cell phenotype regulation in the context of lung fibrosis and lung development. We use in vitro and ex vivo models, mouse models, human tissue, and multi-omic approaches to explore fibroblast phenotypes in the formation of lung alveoli and in the pathologic modeling of lung fibrosis, and explore novel therapies for lung disease.

Possible Rotation Projects:

Markers of mechanotransduction in lung alveolar formation (immunofluorescence, bioinformatics)
Biological aging of the lung (DNA methylation)
Precision cut lung slice culture to model fibrosis and test therapies ex vivo
Fibroblast phenotype regulation in transgenic mice
Fibroblast-epithelial interactions in lung organoids

Dynamic control of signaling networks in living cells; Rho family and MAPK networks in motility and network plasticity; new tools to study protein activity in living cells (i.e., biosensors, protein photomanipulation, microscopy). Member of the Molecular & Cellular Biophysics Training Program and the Medicinal Chemistry Program.

My research interests involve the structure of inhibitory neuronal networks and how these networks change to produce adverse behavioral outcomes. My main interest is how the inhibitory neurotransmitter gamma-aminobutyric acid (GABA) regulates neuronal networks via both synaptic and extrasynaptic forms of inhibition and how alterations in inhibitory networks contribute to clinical conditions such as alcohol use disorder, nicotine, addiction, or stress. My work has focused primarily on three brain regions: the nucleus tractus solitaries (NTS), central and basolateral amygdala, and ventral tegmental area. In each of these areas I have identified local inhibitory networks that control overall excitability and that are dysregulated by exposure to acute and or chronic exposure to alcohol or nicotine.

Research in the Hicks lab focuses on development and implementation of mass spectrometric approaches for protein characterization including post-translational modifications, as well as the identification of bioactive peptides/proteins from plants. Keywords: proteins / peptides, proteomics, PTM, enzymes, analytical chemistry, mass spectrometry, separations / chromatography, plants, algae.

Our preclinical research is based on the concept that drugs of abuse gain control over behavior by hijacking molecular mechanisms of neuroplasticity within brain reward circuits. Our lab focuses on three main research questions: (1) Discover the neural circuits and molecular mechanisms that mediate the reinforcing and pleasurable subjective effects of alcohol and other drugs, (2) Identify the long-term effects of cocaine and alcohol abuse during adolescence, (3) Identify novel neural targets and validate pharmacological compounds that may be used to treat problems associated with alcohol and drug abuse. The lab culture is collaborative and dynamic, innovative, and team-based. We are looking for colleagues who share an interest in understanding how alcohol hijacks reward pathways to produce addiction.

While both genes and environment are thought to influence human health, most investigations of complex disease only examine one of these risk factors in isolation.  Accounting for both types of risk factors and their complex interactions allows for a more holistic view of complex disease causation.  The Kelada lab is focused on the identification and characterization of these gene-environment interactions in airway diseases, particularly asthma, a disorder of major public health importance.   /  / Additionally, to gain insight into how the airway responds to relevant exposures (e.g., allergens or pathogens), we study gene expression in the lung (particularly airway epithelia). Our goal is identify the genetic determinants of gene expression by measuring gene expression across many individuals (genotypes). / This “systems genetics” approach allows us to identify master regulators of gene expression that may underlie disease susceptibility or represent novel therapeutic targets. /

The Laederach Lab is interested in better understanding the relationship between RNA structure and folding and human disease. We use a combination of computational and experimental approaches to study the process of RNA folding and in the cells. In particular, we develop novel approaches to analyze and interpret chemical and enzymatic mapping data on a genomic scale. We aim to fundamentally understand the role of RNA structure in controlling post-transcriptional regulatory mechanisms, and to interpret structure as a secondary layer of information (http://www.nature.com/nature/journal/v505/n7485/full/505621a.html).  We are particularly interested in how human genetic variation affects RNA regulatory structure. We investigate the relationship between disease-associated Single Nucleotide Polymorphisms occurring in Human UTRs and their effect on RNA structure to determine if they form a RiboSNitch.

I am a mathematical biologist interested in the biochemical and biophysical aspects of blood clotting and emergent behavior in biological fluid-structure interaction problems. I especially love mathematical modeling, where creativity, biological knowledge, and mathematical insight meet. My goal is to use mathematical and computational modeling as a tool to learn something new about a biological system, not just to simply match model output to experimental data. My research paradigm includes an integration of mathematical and experimental approaches, together with statistical analyses and inference, to determine mechanisms underlying complex biological phenomena. This paradigm culminates in the contextualization of my findings to both the mathematical and biological communities. My research program is focused mainly on studying the influence of biochemical and biophysical mechanisms on blood coagulation, clot formation, and bleeding.

Dr. Macdonald is the Founder and Scientific Director of the new Metabolomic Facility and Co-Scientific Director of the joint UNC/NCSU/NOAA Marine MRI facility at Pivers Island near Beaufort NC. Dr. Macdonald’s research goal is to combine metabolomics and tissue engineering and apply these tools to quantitative biosystem analysis.

We are interested in the mechanisms by which histone protein synthesis is coupled to DNA replication, both in mammalian cell cycle and during early embryogenesis in Drosophila, Xenopus and sea urchins.

The Miller lab is working to improve the efficacy of immunotherapy to treat cancer. We aim to develop personalized immunotherapy approaches based on a patient’s unique cancer mutations. We have a particular interest in myeloid cells, a poorly understood group of innate immune cells that regulate nearly all aspects of the immune response. Using patient samples, mouse models, single-cell profiling, and functional genomics approaches, we are working to identify novel myeloid-directed therapies that allow us to overcome resistance and successfully treat more patients.

The Palmer lab investigates combination cancer therapy: understanding the mechanisms of successful drug combinations to inform the development of combinations with new cancer therapies. Our approach is a synthesis of experiments, analysis of clinical data, and modeling. Students can pursue projects that are experimental, computational, or a mixture of both. Our goals are to improve the design of drug combinations, the interpretation of clinical trials, and patient stratification to increase rates of response and cure through more precise use of cancer medicines in combinations.

It is estimated that less than 2% of the human genome codes for a functional protein.  Scattered throughout the rest of the genome are regulatory regions that can exert control over genes hundreds of thousands of base pairs away through the formation of DNA loops.  These loops regulate virtually all biological functions but play an especially critical role in cellular differentiation and human development. While this phenomenon has been known for thirty years or more, only a handful of such loops have been functionally characterized.  In our lab we use a combination of cutting edge genomics (in situ Hi-C, ATAC-seq, ChIP-seq), proteomics, genome editing (CRISPR/Cas), and bioinformatics to characterize and functionally interrogate dynamic DNA looping during monocyte differentiation.  We study this process both in both healthy cells and in the context of rheumatoid arthritis and our findings have broad implications for both cell biology as well as the diagnosis and treatment of human disease.

We study the behavior of individual cells with a specific focus on “irreversible” cell fate decisions such as apoptosis, senescence, and differentiation. Why do genetically identical cells choose different fates? How much are these decisions controlled by the cell itself and how much is influenced by its environment? We address these questions using a variety of experimental and computational approaches including time-lapse microscopy, single-molecule imaging, computational modeling, and machine learning. Our ultimate goal is to not only understand how cells make decisions under physiological conditions—but to discover how to manipulate these decisions to treat disease.

Heart failure is an increasingly prevalent cause of death world-wide, but the genetic and epigenetic underpinnings of this disease remain poorly understood. Our laboratory is interested in combining in vitro, in vivo and computational techniques to identify novel markers and predictors of a failing heart. In particular, we leverage mouse populations to perform systems-level analyses with a focus on co-expression network modeling and DNA methylation, following up in primary cell culture and CRISPR-engineered mouse lines to validate our candidate genes and identify potential molecular mechanisms of disease progression and amelioration.

We are interested in unraveling the molecular basis for human disease and discover new treatments focused on human and microbial targets. Our work extends from atomic-level studies using structural biology, through chemical biology efforts to identify new drugs, and into cellular, animal and clinical investigations. While we are currently focused on the gut microbiome, past work has examined how drugs are detected and degraded in humans, proteins designed to protect soldiers from chemical weapons, how antibiotic resistance spreads, and novel approaches to treat bacterial infections. The Redinbo Laboratory actively works to increase equity and inclusion in our lab, in science, and in the world. Our lab is centered around collaboration, open communication, and trust. We welcome and support anyone regardless of race, disability, gender identification, sexual orientation, age, financial background, or religion. We aim to: 1) Provide an inclusive, equitable, and encouraging work environment 2) Actively broaden representation in STEM to correct historical opportunity imbalances 3) Respect and support each individual’s needs, decisions, and career goals 4) Celebrate our differences and use them to discover new ways of thinking and to better our science and our community

Regulation of plant development:  We use techniques of genetics, molecular biology, microscopy, physiology, and biochemistry to study how endogenous developmental programs and exogenous signals cooperate to determine plant form.  The model plant Arabidopsis thaliana has numerous technical advantages that allow rapid experimental progress.  We focus on how the plant hormone auxin acts in several different developmental contexts.  Among questions of current interest are i) how auxin regulates patterning in embryos and ovules, ii) how light modifies auxin response, iii) how feedback loops affect kinetics or patterning of auxin response, iv) how flower opening and pollination are regulated, and v) whether natural variation in flower development affects rates of self-pollination vs. outcrossing.

The Robinson lab currently explores the neurodynamics of reinforcement pathways in the brain by using state-of-the-art, in vivo recording techniques in freely moving rats. Our goal is to understand the interplay of mesostriatal, mesocortical and corticostriatal circuits that underlie action selection, both in the context of normal development and function, and in the context of psychiatric disorders that involve maladaptive behavior, such as alcohol use disorder, adolescent vulnerability to drug use and addiction, cocaine-induced maternal neglect and binge-eating disorders.

Our lab uses a systems biology approach to study phenotypic heterogeneity in bacteria. We develop tools that quantify single cell bacterial transcription. We then compare dynamic measurements during vegetative growth and infection to identify regulators of gene expression and mechanisms that bacteria use to coordinate community organization. With this data we want to understand the role of heterogeneity and noise in infectious disease.

The Shiau Lab is integrating in vivo imaging, genetics, genome editing, functional genomics, bioinformatics, and cell biology to uncover and understand innate immune functions in development and disease. From single genes to individual cells to whole organism, we are using the vertebrate zebrafish model to reveal and connect mechanisms at multiple scales. Of particular interest are 1) the genetic regulation of macrophage activation to prevent inappropriate inflammatory and autoimmune conditions, and 2) how different tissue-resident macrophages impact vertebrate development and homeostasis particularly in the brain and gut, such as the role of microglia in brain development and animal behavior.

Dr. Shih is the Director of Small Animal Magnetic Resonance Imaging (MRI) at the Biomedical Research Imaging Center. His lab has implemented multi-model MRI techniques at high magnetic field to measure cerebral blood oxygenation, blood flow, blood volume, and oxygen metabolism changes in preclinical animal models. Dr. Shih’s lab is also developing simultaneous functional MRI (fMRI) and electrophysiology recording techniques at high spatial resolution to elucidate the pathophysiological mechanisms of neurovascular diseases. They will apply these techniques to (i) explore/validate functional connectivity network and neurovascular coupling in the rodent brain, (ii) study tissue characteristics after stroke, and (iii) investigate deep brain electrical stimulation, optogenetic stimulation, and pharmacogenetic stimulation in normal and Parkinsonian animal models.

Our laboratory is examining the role of histone post-translational modifications in chromatin structure and function.  Using a combination of molecular biology, genetics and biochemistry, we are determining how a number of modifications to the histone tails (e.g. acetylation, phosphorylation, methylation and ubiquitylation) contribute to the control of gene transcription, DNA repair and replication.

I study complex traits using linkage, association, and genetic epidemiological approaches.  Disorders include schizophrenia (etiology and pharmacogenetics), smoking behavior, and chronic fatigue.

Superfine’s group studies stimulus-responsive active and living materials from the scale of individual molecules to physiological tissues, including DNA, cells and microfluidic-based tissue models. We develop new techniques using advanced optical, scanning probe, and magnetic force microscopy. We pursue diverse physiological phenomena from cancer to immunology to mucus clearance in the lung. Our work includes developing systems that mimic biology, most recently in the form of engineered cilia arrays that mimic lung tissue while providing unique solutions in biomedical devices.

The Tarantino lab studies addiction and anxiety-related behaviors in mouse models using forward genetic approaches. We are currently studying a chemically-induced mutation in a splice donor site that results in increased novelty- and cocaine-induced locomotor activity and prolonged stress response. We are using RNA-seq to identify splice variants in the brain that differ between mutant and wildtype animals. We are also using measures of initial sensitivity to cocaine in dozens of inbred mouse strains to understand the genetics, biology and pharmacokinetics of acute cocaine response and how initial sensitivity might be related to addiction. Finally, we have just started a project aimed at studying the effects of perinatal exposure to dietary deficiencies on anxiety, depression and stress behaviors in adult offspring. This study utilizes RNA-seq and a unique breeding design to identify parent of origin effects on behavior and gene expression in response to perinatal diet.

We are a quantitative genetics lab interested the relationship between genes and complex disease. Most of our work focuses on developing statistical and computational techniques for the design and analysis of genetic experiments in animal models. This includes, for example: Bayesian hierarchical modeling of gene by drug effects in crosses of inbred mouse strains; statistical methods for identifying quantitative trait loci (QTL) in a variety of experimental mouse populations (including the Collaborative Cross); computational methods for optimal design of studies on parent of origin effects; modeling of diet by gene by parentage interactions that affecting psychiatric disease; detection and estimation of genetic effects on phenotypic variability. For more information, visit the lab website.

The Vincent laboratory focuses on immunogenomics and systems approaches to understanding tumor immunobiology, with the goal of developing clinically relevant insights and new cancer immunotherapies.  Our mission is to make discoveries that help cancer patients live longer and better lives, focusing on research areas where we feel our work will lead to cures. Our core values are scientific integrity, continual growth, communication, resource stewardship, and mutual respect.

We are actively engaged in multiple research arenas centered around understanding the associations between environmental exposures (primarily air pollution) and health outcomes. We use large clinical cohorts and electronic health records to understand associations between air pollution and health outcomes such as cardiovascular disease, metabolic disease, and aging. We use metabolomics and epigenetic data (primarily DNA methylation) to investigate molecular mechanisms, and highlight the integration of ‘omics data in a systems biology framework to better understand dysregulated pathways. Finally, we have projects centered around methods development and causal analyses to improve our understanding of the biology central to environmental health effects.

Our laboratory is focusing on developing and applying solution-state NMR methods, together with computational and biochemical approaches, to understand the molecular basis of nucleic acid functions that range from enzymatic catalysis to gene regulation. In particular, we aim to visualize, with atomic resolution, the entire dynamic processes of ribozyme catalysis, riboswitch-based gene regulation, and co-transciptional folding of mRNA. The principles deduced from these studies will provide atomic basis for rational manipulation of RNA catalysis and folding, and for de novo design of small molecules that target specific RNA signals. Research program in the laboratory provides diverse training opportunities in areas of spectroscopy, biophysics, structural biology, computational modeling, and biochemistry.