TRAINING FACULTY

We focus on the genetic regulation of bone mass and the genetic causes of bone disease from the point of view of bone formation and strength. We use both forward and reverse genetics studies to interrogate the genetic causes of phenotypes critical to understanding bone quality that cannot be readily studied in human populations. These phenotypes of interest include bone composition, bone formation and mineralization by the osteoblast. In addition, we participate in many human cohort studies aimed at understanding the etiology of musculoskeletal disease wherein we determine the biological function of genes found to be associated with musculoskeletal traits. Lastly, we study the diagnosis of and the consequences of postoperative infection, with an emphasis on an infection associated with spinal instrumentation.

Without being conscious of it, our motor system is constantly solving computationally challenging problems in ways that astonish both roboticists and neuroscientists. We develop computational models of animal movement to understand how the brain generates movement and design novel rehabilitation therapies and assistive devices for patients with movement disorders. We collaborate closely with neuroscientists, clinicians and roboticists to study the brain and help patients achieve a better quality of life.

​Dr. David Albers lab focuses on advancing biomedicine using: -data assimilation of both clinician and patient collected data to forecast physiology and compute new phenotypes -health care process modeling and analysis -temporal-focused spectral analysis and information theoretic tools -mechanistic physiologic models using clinical data -discovering phenotypes using temporal information within clinical data -visualizing patient health evolution in an intensive care setting -deconvolving biases present in clinical data -computational machinery based on variational inference to discover features that can be used to define phenotypes and other clinically actionable quantities

The Alberti lab is working to better understand the genetic and molecular basis of splicing factor gene mutations in the initiation, development, and progression of clonal hematopoiesis and myeloid malignancies, such as myelodysplastic syndromes (MDS).

Dr. Alper's laboratory is focused on understanding the regulation of the innate immune response, particularly as it relates to the basis for inflammatory disease.

Our major focus over the last five years has been to understand the role of the hexose transporter Glut1 in mammary tumorigenesis.

We employ cutting-edge approaches including mouse genetics, optogenetics, viral circuit tracing, ex vivo slice electrophysiology, CRISPR/cas9 genome editing, single-cell RNA-sequencing and super-resolution microscopy to investigate how disease-relevant synaptic molecules are utilized in a cell-type- and synapse-specific manner in neural circuits implicated in neuropsychiatric disorders and addiction.

We investigate the genetic, molecular and cellular basis of brain development and myelination using zebrafish as a model system.

Despite including many different proteins, macromolecular complexes often display minimal enzymatic activity. This suggests that conformational changes and interactions are fundamental to their molecular mechanism. My group uses cryo-electron microscopy to characterize the structure, conformational states and interactions of macromolecular complexes involved in essential cellular processes. We correlate that structural information with biochemical and functional data to establish the mechanism of these remarkable cellular machines.

Our work is focused in two main areas. First, we are interested in the molecular mechanisms of transcriptional regulation using the nuclear receptor superfamily as a model system. We use a blend of biophysical, structural and cell biological approaches to dissect the various protein-DNA and protein-protein interactions critical to transcriptional activation, and then use this information to synthesize and predict overall behavior. Our second focus is on characterizing the molecular interactions of therapeutic proteins, especially at high concentrations and under formulation/delivery conditions. This work is primarily directed toward monoclonal antibodies, but we are also interested in therapeutic peptides and vaccines.

We are interested in the molecular mechanisms of sensory transduction in the brain. One of the goals of our work is to understand somatosensation: the process through which the body (Skin, cornea, etc.) experience the external environment. This can be broken down into three major components: mechanosensation (touch or sensing of pressure), thermosensation (sense of heat or cold), and nociception (sense of pain).

We use in vivo molecular genetic mouse models, and in vitro taste organoids derived from adult lingual stem cells to understand how taste buds renew during normal homeostasis, and how this regenerative process is impacted by cancer therapies that cause taste dysfunction in patients.

The Barton lab studies RNA viruses - viral RNA replication - and host-pathogen interactions involving viral RNA and endoribonucleases.

Understanding how ion channels contribute to morphological development and microtubules are regulated for brain development.

Our field is molecular and cellular neuroscience. Specifically, we are interested in the molecular and cellular mechanisms underlying learning, memory and cognition.

My lab investigates intracellular calcium signals, which play essential roles including the activity-dependent regulation of gene expression in diverse cell types, muscle contraction, and neuronal plasticity. We use a variety of techniques including molecular biology, electrophysiology, biochemistry, and analysis of structure.

My laboratory focuses on an understanding of the enzymes that synthesize cell surface carbohydrates, the glycosyltransferases. In addition, characterization of the carbohydrate structures themselves and development of new methods for elucidation of these molecules is ongoing.

The Benninger lab is a multi-disciplinary team of scientists who are guided by engineering principles and technologies to study the endocrine pancreas (islets of Langerhans). With mechanistic knowledge underlying the dynamics of islet function and hormone release, we can develop diagnostics and therapeutic interventions to effectively manage, cure and prevent diabetes. Towards this goal the lab combines novel optical imaging and ultrasound imaging approaches to study the function of the islets of Langerhans over multiple levels of organization, and how function is disrupted in diabetes.

Our research asks how the RNA polymerase II transcriptional machinery and RNA processing factors work together to achieve coordinated synthesis and maturation of messenger RNA (mRNA).

Intermuscular adipose tissue, myosteatosis, lipidomics, triglyceride, insulin sensitivity, insulin resistance.

Dr. Bitler is committed to the fight against cancer through his work to elucidate the impact of cancer-related signaling and epigenetic regulation.

My lab studies how cells use epigenetics to control gene amplifications. We have identified epigenetic pathways that cells use to create transient increases in gene copy number. These copy number changes play roles in tumor development, progression and drug resistance. By understanding the fundamental mechanisms that govern copy number control we hope to allow better cancer therapies.

The Bonetto Lab investigates the molecular mechanisms responsible for abnormal muscle, bone and liver crosstalks in cachexia due to cancer and/or anticancer treatments. In order to achieve our goals, we leverage different in vitro and in vivo models, paired with a set of comprehensive molecular, metabolic, and pharmacologic tools to dissect the causes of musculoskeletal abnormalities associated with cancer.

My research focuses on clinical interventions combined with mechanistic investigations by using primary human cell culture models. Most recently, we have developed a model for investigating human intrauterine phenotype development using umbilical cord-derived mesenchymal stem cells (MSCs). In the context of obesity in pregnancy, these infant stem cells demonstrate greater adiposity and metabolic dysfunction consistent with the adult obesity phenotype. It is our goal to further our understanding of how maternal obesity or diabetes impact the infants born to these mothers by evaluating the epigenetic and metabolic outcomes in the infant MSCs. Moreover, longitudinal assessments of the children from which the MSCs were derived will clarify the potential role of umbilical cord MSC phenotype for predicting obesity or diabetes risk in the children.

My research interests focus on hormone/growth factor signaling and cancer. Specifically, our laboratory is studying the role of selective protein kinase C (PKC) isoforms in the modulation of cell growth and death in endometrial cancer.

The Breuss laboratory is interested in genomic and cellular mosaicism. We assess its impact on human disease and utilize it as a tool to unravel brain and germline development.

My primary research interests are focused toward: 1) understanding the regulation of alveolar epithelial cell maturation during lung development and 2) determining the molecular regulation of surfactant pool sizes in the postnatal and adult lung, with particular interest in diseases associated with surfactant dysfunction.

We are interested in uncovering the mechanisms that regulate mammalian retinal development and applying this knowledge to inform novel stem cell based treatments that restore vision. We primarily use the mouse as a model system, as its development is similar to human, and because there is a wealth of genetic resources we can utilize.

Research in our laboratory leverages our expertise in immunology, molecular biology and model systems of liver disease to explore the early and late events that influence the progression of chronic liver disease.

Our group aims to understand how mitochondria reprogramming in tumors impact cellular behaviors that drive progressive and lethal cancer. We use a broad repertoire of biochemistry, cell biology, live cell imaging and animal models to study the impact of mitochondria shape, number and subcellular distribution in metastatic dissemination.

My research interests include pharmacokinetic and pharmacodynamic therapeutic drug monitoring, clinical biochemistry, biochemical toxicology, and drug metabolism. My research has focused on the interactions between energy metabolism, mitochondrial metabolism and the mTOR pathway. This includes the toxicodynamic interactions between calcineurin and mTOR pathway inhibitors, ageing, metabolic diseases, oxidative stress, ischemia/ reperfusion injury and drug-coated coronary stents and balloons.

The Christie Lab endeavors to understand the neural-circuit-mechanisms that underlie the learning-dependent optimization of behavior. The lab’s approach mainly focuses on the cerebellum, a brain region that guides adaptive updating of simple reflexive movements as well as experience-driven refinement of high-order brain function (e.g., thinking, planning, and decision making).

My lab is interested in understanding the molecular basis of essential processes that regulate gene expression. We use biophysical, biochemical methods, and structural methods, including X-ray crystallography. Our insights into these fundamental mechanisms will contribute to a better understanding and ability to regulate gene expression processes involved in human diseases and will assist in drug development efforts. Our studies focus on the following questions: (1) How is chromatin structure modulated for DNA-dependent processes? and (2) How do transcription factors and pioneering factors activate gene expression?

Deciphering the mechanisms underlying increased risk of brain metastases in young women with triple negative breast cancer. These include ovarian estrogen effects on reactive astrocytes that results in paracrine activation of EGFR and TRKB signaling in brain metastatic cells.

The Clark lab investigates bacterial-driven immune modulation in the respiratory tract. The upper respiratory tract is home to a diverse microbial community that includes both commensal and opportunistic bacterial pathogens. Research in the lab explores how exposure to these bacteria influences upper and lower respiratory tract inflammation and disease, with a focus on the innate immune response to acute infection.

My research focuses broadly on personalizing medicine, using genetic information and biomarkers for tailored treatment, in relation to pharmacogenomics as well as understanding the ethical, cultural, and social implications of genomic research with populations historically underrepresented in health research. My current research includes studying cytochrome P450 genetic variation in Indigenous communities (e.g., American Indian and Alaska Native peoples), with a focus on CYP2A6 variation in relation to nicotine metabolism and smoking cessation, as well as understanding the ways in which adaptations to diverse local environments may have impacted modern pharmacogenomic variation and evolutionary medicine. My other projects include exploring the perspectives of tribal members on genetic research with tribes and developing guidelines and policies in partnership with tribes. All of my projects strive to use community based participatory research approach and include cultural and Indigenous knowledge.

Neural crest cells (NCCs) arise at the junction between the neural and non-neural ectoderm before moving ventrally around the embryo along the entire rostro-caudal axis. Cranial NCCs form most of the bone and cartilage in the face, explaining why defects in early NCC patterning are so devastating to human facial development. Our lab uses a number of cutting edge molecular and cellular techniques and approaches in both mouse and zebrafish models to dissect signaling networks that decide the fate of NCCs. We then use this information to better understand the basis for human birth defect syndromes affecting the face for which a genetic basis has not been established.

We are a computational group using large-scale human genomics as a tool to learn more about diet’s role in the body and in human health, with a focus on cardiometabolic disease.

Within the broad scope of systems biology, my lab focuses on 3 research areas: 1) Network inference for identifying drug targets, 2) Predicting drug sensitivity from -omics datasets, and 3) Modeling temporal effects of drug combinations.

We are a translational research lab focusing on inborn errors of metabolism such as pyridoxine-dependent epilepsy (PDE), glutaric aciduria type I (GA I), and vitamin B6 metabolism. We are committed to scientist - advocate collaborations with the goal to ensure scientific advances are relevant and patient-centered. We partner with families, clinicians, and scientists to study the natural history of these neurologic disorders and the impact of therapies on clinical outcomes.

Prostate Cancer Tumor Suppressors, Stem Cells, Tumor Initiating cells, Signal Transduction, Receptor Signaling.

The control of cerebral blood flow by ion channels and calcium signaling in the pericytes, endothelial cells, and smooth muscle cells that constitute the parenchymal microcirculation, and use this information to combat brain diseases with a vascular component.

Research interests include: (1) CAR T and engineered T cell therapies of autoimmune diseases; (2) Mechanisms of T cell mediated metal hypersensitivities; (3) Mechanisms of T cell recognition of autoantigens in Type 1 diabetes and RA; and (4) Redox signaling and drug design in the immune diseases and infectious diseases.

Exploring the conditions that foster somatic evolution and discovering cancer vulnerabilities.

My laboratory’s specific research in the area of neuropharmacology focuses on understanding how cAMP and calcium second messenger signaling pathways are organized at the postsynaptic specializations of excitatory neuronal synapses.

Dr. Peter Dempsey's program focuses on the role of ADAM metalloproteinases in regulating extracellular signaling events involved in normal tissue homeostasis of the gastrointestinal tract and during injury/inflammation and cancer pathogenesis.

We are interested in how populations of neurons generate sensory perceptions. We use quantitative psychophysics, in vivo electrophysiology, in vivo imaging, circuit tracing, and computational methods to study the dynamics of populations of single neurons. We are also focused on how neural interactions specifically - within areas and distributed across the brain - generate successful perceptions.

The Dias Lab is broadly interested in the genetics of neurodevelopment. We are interested in better understanding the molecular mechanisms of neurodevelopmental disorders, including autism and intellectual disability. In order to do this, we are tackling two major challenges in the field- cellular and clinical heterogeneity.

My laboratory studies how dysregulation of pathogenic and protective T cells causes autoimmunity. We are specifically interested in the mechanisms underlying the autoimmune diseases Type 1 Diabetes and Systemic Sclerosis/Scleroderma. We focus on identifying the factors and pathways that enable autoreactive T cells to escape immune regulatory checkpoints and cause tissue damage, with the goal of using this knowledge for the development of innovative immunotherapies.

The overall interest of the Doran Lab is the study of host - pathogen interactions in the central nervous system and the female reproductive tract. Our studies focus on major human pathogens including Streptococcus agalactiae (also known as Group B Streptococcus, GBS), a leading cause of invasive disease in newborns and certain adult populations including pregnant women. We seek to elucidate the mechanisms by which GBS colonizes the vaginal tract during pregnancy and penetrates the blood-brain barrier in the newborn to cause meningitis, as well as characterize host response to infection and colonization.

The Duerkop lab studies bacterial viruses (bacteriophages or phages) and their interactions with their hosts. The long-term goal of the Duerkop lab is to understand how phages and other forms of mobile DNA contribute to host-microbe interactions in the intestine and their overall impact on human health.

The Eisenmesser lab takes a unique approach to understand protein function, and particularly enzyme function, by utilizing molecular engineering methods to control both structural interactions and the underlying movements that underlie their conformational changes. The ultimate goal of the Eisenmesser lab is to fully characterize molecular interactions at both atomic resolution and biological levels with a particular emphasis on medically relevant systems that may be exploited to either block or promote events underlying disease progression.

Our group focuses on epigenetic mechanisms regulating normal hematopoiesis and leukemia focusing on MLL-family histone methyltransferases.

Cytoplasmic mRNA regulation is very important during oogenesis, early embryogenesis, and during stem cell divisions that occur throughout development. The mechanisms that regulate cytoplasmic mRNAs and that tie this control to the development of living cells are poorly understood. Recent studies hint that the mechanisms are similar in many animals and that they are important for various human diseases. We are exploring this problem in the small nematode worm, Caenorhabditis elegans.

A fundamental question in developmental biology is how cells communicate with one another and the environment. Receptor tyrosine kinases (RTKs) contribute to this communication by binding to growth factors at the cell surface and activating various intracellular signaling pathways to elicit responses with broad roles in developmental cellular processes. A subset of RTK families has been shown to regulate the activity of neural crest cells (NCCs) and the development of their derivatives in mammalian systems. NCCs are migratory, multipotent cells that play a critical role in vertebrate development. Cranial NCCs originate from the forebrain to the hindbrain and populate the frontonasal prominence and pharyngeal arches 1-4. These cells give rise to the bone and cartilage of the frontonasal skeleton, among other derivatives. Our lab is focused on investigating the mechanism and function of signaling through a particular RTK family, the platelet-derived growth factor (PDGF) receptor family, in development of the cranial NCC-derived craniofacial skeleton.

My lab is interested in how the nervous system makes and acts upon decisions. We use electrophysiological, behavioral, pharmacological, molecular, and computational methods to study how sensory representations are transformed into plans for motor output. We are interested in how these processes occur in the normal brain, as well as how they are affected by pathological conditions.

A major emphasis in my laboratory is on questions concerning the development and organization of these systems in several vertebrate models. Three major areas are under investigation at present: 1) morphology and function of solitary chemosensory cells (see Finger et al. PNAS 2003) in protection of the airways and gut, 2) the cellular organization and development of taste buds (see Finger et al, Science 2005, and 3) regulation of feeding behavior by taste and other oropharyngeal chemoreceptors.

Our lab examines how neuromodulators are encoded in the mesolimbic and nigrostriatal systems and how circuit dysfunctions in these areas contribute to neurological and psychiatric disorders.

Our laboratory focuses on a specific family of homeoproteins, the Six family, and their transcriptional cofactors, Eya and Dach. The Six1 homeobox gene is overexpressed in 50% of primary breast cancers and 90% of metastatic lesions, and its overexpression.

Our lab seeks to define out epitranscriptomic changes impact specificity in protein synthesis across an array of contexts including pediatric bone marrow failure and oncogenesis predisposition.

The cerebral cortex is the control center of most of our higher-level brain functions, including thought, language, memory and emotion. During cortical development, billions of neurons and glia must be precisely specified and assembled into the intricate circuits that underlie these complex tasks. Disruption of these processes is associated with many devastating human neurological disorders, including epilepsy, schizophrenia, autism and intellectual disability. Our lab studies several processes involved in the formation and function of neural circuits in the cerebral cortex.

Research in my laboratory has focused on improving treatments for Parkinson's disease. In 1988, we performed the first transplant of dopamine-producing brain cells into an American patient with Parkinson's. We have done more brain cell transplants than any other group. While the transplanted cells can replace the need to take drugs like L-DOPA, they do not stop the relentless progression of the underlying disease. In 2006, we began the search for a drug to stop Parkinson’s and have found phenylbutyrate. In animal testing, phenylbutyrate can prevent Parkinson’s from advancing. We are now testing phenylbutyrate in patients and should know in the next few years if it is able to stop the progression of Parkinson's disease in people.

We are interested in understanding how the immune system is dynamically regulated through cellular interactions and environmental cues. Using methods including in vivo microscopy and flow cytometry our goals are to elucidate mechanisms of immune activation and tolerance in autoimmunity, with the goal of developing therapeutic approaches for regulating the immune response.

My lab has investigated biological roles and molecular regulations of 1) IL-1, inflammasomes and autoinflammation in human melanoma and skin diseases; 2) IL-37 and immune tolerance; 3) Tumor heterogeneity and plasticity in melanoma and its therapeutic resistance; and 4) ALDH2 and melanocyte activation and melanoma.

Mechanisms of iNKT cell development and antigen recognition.

The overall focus of the Garcia Lab is to better understand the unique adaptations governing pathological cardiac remodeling, exercise intolerance, and the progression to heart failure in pediatric patients with complex congenital heart disease, including hypoplastic left heart syndrome and other single ventricle defects. The ultimate goal of this research is to develop the critical knowledge base and infrastructure necessary to identify efficacious therapies for improving outcomes in this vulnerable group. The lab utilizes several unique tools to address the mechanisms of cardiac dysfunction including whole animal and cell culture-based models, as well as access to a meticulously preserved Pediatric Tissue and Blood Bank here at the University of Colorado Anschutz Medical Campus.

Professor Gibson's lab conducts multidisciplinary research at the intersection of photonics and neuroscience. Our lab develops novel optical devices using multiphoton, superresolution and structured illumination microscopy applied to living systems with the goal of aiding basic neuroscience research and development of clinical tools.

We leverage human genetic diversity to gain a better understanding of the architecture of complex traits, using a mixture of epidemiological and population genetic methods. We have worked extensively on questions regarding human population structure, admixture, and other components of ancestry critical to modern human genetic research, as well as examined their impact on quantitative traits and disease.

My laboratory studies maternal effects on the immune system and development of allergic diseases, with a particular focus on asthma. Maternal effects are defined as influences of maternal environment, genotype or phenotype on the phenotype of the offspring. Maternal effects have been observed in a number of species, including mice and humans, for several environmental factors and in several tissues and systems of the offspring, including their immune system. Maternal effects may be beneficial, increasing offspring adaptation to changes in the environment and preventing a disease, and harmful, leading to a disease. List of maternally-influenced diseases includes asthma.

My research focuses on a specific type of cancer called high-grade glioma, an aggressive brain tumor affecting both children and adults. We focus especially on two pediatric subtypes called diffuse intrinsic pontine glioma and pediatric glioblastoma. I work in the lab to find new treatments for these tumors; we then study the treatments in laboratory models of the tumors, including mouse models, and then bring the treatments most likely to be successful to clinical trials in children.

We focus on bringing together publicly available big data, developing new computational methods to analyze that data, and creating tools to put those resources into the hands of every biologist.

Our lab is interested in understanding the complexities of humoral immunity against rapidly evolving viruses. Our lab has three major interests: (1) Manipulating host factors to improve humoral immunity; (2) Zoonotic Influenza Viruses and Broadly Protective Humoral Immunity; and (3) Co-evolution of humoral immunity and influenza viruses.

My laboratory’s goals include understanding how the nuclear proteins Early B cell Factor (EBF) and Pax5 (B cell-specific activator protein) regulate B lineage specification, commitment and the immune response to antigens.

The extracellular matrix (ECM) provides structural scaffolding and mediates signaling in the extracellular space. According to our findings, approximately 75-85% of the fibrillar ECM resides in a chaotrope resistant insoluble ECM fraction (iECM), making proteomic characterization difficult without additional chemical digestion. We have developed optimized protocols for extraction of ECM that have been refined using samples from many systems, allowing for molecular-scale assessment of iECM proteome composition and architecture. We currently use these methods with the help of collaborators to assess ECM remodeling in pulmonary hypertension, anti-aging models, and tumor progression.

How does the structure of a genome evolve over time? Our research investigates the molecular causes and phenotypic consequences of the broadly defined family of genomic features known as structural variations (SVs). SVs like aneuploidy, loss-of-heterozygosity, and copy number alteration are pervasive, yet poorly understood genomic elements which contribute significantly to the genotypic and phenotypic diversity of eukaryotic populations. Our current work is addressing many fascinating and important biological questions focused on understanding how SVs arise in the genome, and how these variations contribute to genome stability and evolution, phenotypic diversity, and cellular and organismal fitness.

My lab investigates signaling networks involving RTKs, GPCRs, and chemokine/cytokine receptors that function as oncogene drivers and acquired/intrinsic resistance pathways to targeted therapeutics in lung cancer, head and neck cancer and mesothelioma. Our approach blends in vitro and in vivo functional genomics approaches with human and murine cancer cell line models to define both cancer cell autonomous signals as well as tumor microenvironment-derived signals that contribute to the overall sensitivity of these cancers to targeted drugs and immune therapies.

Dr. Henson's primary areas of study are Cell biology, Inflammation, Apoptosis, Immunology and Phagocytosis. His Cell biology research incorporates themes from Receptor, Phosphatidylserine and Apoptotic cell clearance. His biological study spans a wide range of topics, including Tumor necrosis factor alpha, Immune system, Macrophage and Cytokine.

We are a research laboratory of RNA biologists, technology developers, and data analysts focused on discovering and translating fundamental principles of RNA regulation. A major effort in the lab is to understand how RNA damage and repair are integrated with stress responses by combining method development, bioinformatics, genetics, biochemistry, and cell biology.

The Hopp lab studies the functional role of immune cells on PKD progression. Specifically, the lab researches the role of T cells in PKD, their interplay with other immune cells and the cystic epithelium, and their impact on cyst initiation and progression. She believes that these studies will provide novel insights into the pathomechanisms of disease/disease heterogeneity, and give rise to new therapeutic approaches.

Research in the Horswill laboratory is focused on the physiology and pathogenesis of Staphylococcus aureus. We are also interested in commensal bacterial interactions with S. aureus, development of new treatment approaches, and we’re starting projects on Gram negative pathogens.

Our lab addresses mechanistic and translational questions in human immunology using high-dimensional single-cell mass cytometry and ex-vivo cellular manipulation. Our goal is to enable a deeper understanding of normal immune function, and dysregulated immune processes in immunodeficiency, autoimmunity, and the overlap between the two.

The Huang laboratory studies transplantation immunology with a focus on developing clinically relevant protocols for the establishment of transplantation tolerance. Dr. Huang's research involves using basic immunologic approaches to develop clinically relevant strategies for regulating inflammation, overcoming transplant rejection and improving tumor immunotherapy.

Function and regulation of the DNA damage response.

The long-term goals of our work is to understand how neuron-glial interactions modulate brain function and contribute to pathology in neurodegenerative disease. Towards this goal, we study the interactions of oligodendrocyte lineage cells with neurons in the adult cerebral cortex.

My research interests involve the development and application of advanced computational techniques to biomedicine, particularly the application of machine learning and statistical inference techniques to high-throughput molecular assays. I am also interested in automated processing of biomedical texts, anatomically realistic models of neural computation, and neurobiologically and evolutionarily informed computational models of cognition.

The goal of the Preterm Labor Research Laboratory (Hurt Lab) is to understand reproductive physiology and apply those findings to improve the health of women and infants.

My laboratory is interested in understanding how a network of proteins called the cytoskeleton regulates the migration and cell-cell interactions of lymphocytes. In particular we focus on how the cytoskeleton generates the mechanical forces and shape changes required for lymphocyte migration and trafficking during homeostasis and disease.

Our lab studies how cells detect and degrade aberrant RNAs, and how dysregulation of this surveillance process contributes to human muscle development and disease.

His primary areas of study are Immunology, Acquired immunodeficiency syndrome, Internal medicine, Vaccination and Viral disease. His Immunology research is mostly focused on the topic Immune system. His work carried out in the field of Immune system brings together such families of science as Antibody and Antigen.

My research is focused on mechanisms of repair following acute and chronic lung injury. This includes studying how lung collectins influence alveolar macrophage phenotype, function, and fate in healthy lungs and during inflammation. I am also interested in the role that bone-marrow-derived stem cells (including endothelial progenitor cells) play in recovery from lung injury.

Mechanism and targeting of aggressive properties of pediatric sarcomas.

Our work focuses on the formation and regulation of chromatin domains and their ultimate roles in epigenetic genome regulation. We are particularly interested in the mechanisms of heterochromatin establishment and function.

Research in my lab uses NMR spectroscopy, X-ray crystallography, molecular biology and biophysical approaches to answer the fundamental questions of how mediators of signal transduction interact with proteins of neuronal signaling pathways.

Dr. Jordan serves as the Chief of the Hematology Division and directs a research program focused on the development of novel therapies for the treatment of leukemia.

Dr. Julian's research focuses primarily on the mechanisms underlying human adaptation to the chronic hypoxia of high altitude and, in particular, how these processes influence maternal vascular adaptation to pregnancy, pregnancy outcome and the long-term health of of affected offspring.

Dr. Karam’s laboratory is focused on basic and translational research related to head and neck and pancreatic cancer.

Our research focuses on the development and application of statistical and computational methods for analyzing omics data sets.

Our lab is interested in this curious boundary between the innate and adaptive immune systems and seeks to elucidate signals and pathways emanating from the various families of innate receptors most efficiently mediate the transition to the adaptive cellular immune response. In doing so, we seek to determine not only the basic rules of immunity, many of which remain elusive, but also to identify practical methods of intervention for the purposes of vaccine discovery, development and design.

The major focus of my research program is to elucidate pathways of innate immunity that can distinguish harmless microbes from pathogens, thereby enabling the host to mount responses that are commensurate with the threat.

We study how synapses in the central nervous system are modified by experience, with the ultimate goal of understanding how these mechanisms contribute to normal cognitive function and how they break down in various brain diseases and disorders.

Adipocyte biology.

Our laboratory studies the mammalian sound localization pathway, a circuit in the auditory brainstem which is involved in telling us “where” in space a sound is coming from. This circuit is important for an animal or human to localize sound, but it is also important to help us spatially separate multiple simultaneous and competing sounds from each other, and thus help us function in typical “cocktail party” situations. We would like to understand how this circuit operates in the healthy auditory system, and how it changes in medical conditions such as central hearing loss or autism spectrum disorder (ASD).

Investigating the mechanisms leading to cellular reprogramming and aging, as well as induced Pluripotent Stem Cell (iPSC)-associated cellular rejuvenation.

The effects of advanced age and alcohol misuse on inflammatory responses after burn trauma or infection.

Our goal is to enable biomedical researches to effectively reuse massive collections of publicly-available data — e.g., omics, knowledgebases, unstructured text, genetic associations — to gain nuanced insights into the molecular mechanisms underlying heterogeneous traits and disease.

Dr. Kuhn’s research program focuses upon understanding mechanistic connections between the gut mucosa and joints in the development of spondyloarthritis and rheumatoid arthritis.

The Kumar Laboratory investigates all aspects of gonadotropin biology, including gonadotrope development and tumori​genesis, mechanisms of pituitary gonadotropin subunit gene expression and post-transcriptional regulation, gonadotropin biosynthesis with a focus on age-dependent glycosylation, gonadotropin secretion and action with one focus on somatic cell development and regulation in the gonads and the other on osteoclasts in the bone.

Research in my group focuses on the molecular mechanisms of epigenetic regulation and phosphoinositide signaling. We apply high field NMR spectroscopy, X-ray crystallography and a wide array of biochemical and molecular biology approaches to characterize the atomic-resolution structures and functions of chromatin- and lipid-binding proteins implicated in cancer and other human diseases.

Our lab is interested in developing mass spectrometry and computational methods to understand protein dynamics in health and disease. Current projects include developing multi-omics strategies to quantify protein alternative isoforms; investigating the role of ER stress and protein glycosylation in cellular stress responses; and identifying the trends and focuses of research topics in the biomedical literature.

The focus of research in the Lampe lab is understanding the role of drug metabolism and pharmacokinetics (DMPK) in drug efficacy within special population groups, with a particular emphasis on cytochrome P450 enzymes (CYP).

We are interested in the regulation and function of protein turnover, homeostasis, and secretion in development, senescence, and diseases. Our work leverages advances in proteomics, bioinformatics, and human induced pluripotent stem cell (iPSC) models.

We study mechanisms of immune subversion and immune regulation during bacterial infections and other disease settings. We dissect strategies that microbes have evolved to thwart or manipulate immune responses and work to define host immune regulatory circuits that are manipulated by pathogens. Our studies focus on innate immune responses during mucosal and systemic infections. We are actively pursuing translation of information from our studies towards improved therapies for infectious, inflammatory, cancerous, and other diseases.

Role of PI3K/PTEN/AKT pathway in HNSCC progression.

Dr. Lyons laboratory focuses on mechanisms of lymphatic mediated metastasis of breast cancer. Specifically, utilizing mouse models to investigate developmentally regulated programs of inflammation and lymphangiogenesis that are utilized in the adult mammary gland and may be hijacked by breast tumor cells. The results of these translational studies have the potential to instruct therapy aimed at prevention of breast cancer metastasis.

Our research focuses on the following topics: (1) Signaling mechanisms that regulate oligodendrocyte differentiation and myelination; (2) The impact of ischemia on actively myelinating oligodendrocytes; (3) Demyelination induced by antibodies cloned from multiple sclerosis patients; and (4) Identification of small molecules that enhance oligodendrocyte differentiation.

Dr. MacLean's research in women’s health has included studies of mammary gland development and its function during lactation, perinatal metabolic programming, the menopausal transition, and the risk for breast cancer.

The focus of the work in the Majka laboratory is to understand how the normal and reparative function of resident lung mesenchymal progenitor cells (MPC) is altered during the development and course of lung diseases (including pulmonary hypertension, fibrosis, emphysema and TSC/LAM).

Research in the Protein Stability, Folding, and Aggregation Laboratory is currently focused on understanding the fundamental physical mechanisms of protein stability, folding, and aggregation of disease-related and model proteins. Current research projects include studying the (1) biophysics of dystrophin and utrophin, and (2) alcohol and antimicrobial preservative-induced protein aggregation. The research group utilizes various biophysical and structural techniques that include optical spectroscopy (CD, fluorescence, and absorbance) and NMR.

The research in my laboratory has been continuously funded by the NIH/NIDDK, and we use a variety of “state-of-the-art” techniques including survival rodent surgeries, retrograde fluorescent tracers, pharmacogenetic modulation of neuronal and glial function by DREADDs, immunohistochemistry, awake cystometry, in vitro contractility studies, patch clamp recordings, cell cultures, transcriptomic and proteomic approaches, imaging and behavioral experiments. The laboratory also provides resources and support for training undergraduate and graduate students, residents and postdoctoral fellows interested in urological research.

Our laboratory is interested in the basic biology of lymphocytes and application of knowledge about lymphocytes to human disease. Much of our work concentrates on T cells and their peculiar ability, via their aß T cell receptors (TCRs), to react with foreign antigens when these are bound as peptides to major histocompatibility complex proteins (MHC) of the host. We are interested in the structural reasons for this bias, the role of evolution in creating the bias, and the ability of T cells to distinguish between different alleles of MHC proteins, an ability which affects the health of the host and rejection of transplants.

Our growing team studies perinatal determinants of female fertility with a special focus on the relationship between establishment of architecture and functional differentiation of the mammalian ovary.

Epigenetic regulation of heart failure; signaling and transcriptional mechanisms of muscle disease.

Dr. McManaman’s current research interests are related to the cellular and systems physiology of lipid metabolism with particular emphasis on mammary gland function, neonatal metabolic health and obesity.

Our research focuses on identifying molecular mechanisms underlying the assembly of macromolecular complexes, with a focus on multisubunit complexes formed by septin proteins. All cellular processes require the function of multisubunit complexes, and while much attention has been given to solving the final structures of such assemblies, comparatively little is known about how individual subunits adopt oligomerization-competent conformations and find their partner subunits in the crowded, dynamic cellular milieu.

Research in the laboratory focuses on the study of molecular mechanism underlying vascular calcification. Vascular calcification is recognized as an independent predictor of cardiovascular morbidity and mortality, particularly in subjects with chronic kidney disease (CKD).

Molecular regulation of the microtubule network in cell division and disease.

Emerging infections are a global public health threat. In the 21st century alone, we already have experienced devastating outbreaks of infectious disease, including diseases caused by mosquito-borne (e.g., chikungunya and Zika viruses) and respiratory RNA viruses (e.g., SARS-CoV-2). Our laboratory seeks to improve our knowledge of the molecular pathogenesis of these infections (i.e., what are the critical host-pathogen interactions that contribute to protection or pathology?) by addressing questions at the interface of immunology and virology/parasitology.

The aim of our lab's research is to understand how cells acquire their fates during development and how these processes go wrong in congenital disease. As principal model, we use the zebrafish (Danio rerio) to investigate the cell fate control of mesodermal lineages, in particular of the lateral plate mesoderm (LPM).

Systems Biology of Human RNA Regulatory Networks.

Her research strives to understand the mechanism of initiation of anti-beta cell autoimmunity. She focuses on the tri-molecular complex consisting of antigen, major histocompatibility complex (MHC), and T cell receptor (TCR) that could be a key component for the development of T1D. Her laboratory explores antigen specificity of autoreactive T cells having different functions (i.e. pathogenic vs regulatory T cells) that target pancreatic beta cells; the role of T cells expressing specific TCRs in the development of T1D using an animal model; the potential of TCR sequences to be used as T cell biomarkers to predict the development of type 1 diabetes as well as recurrence of hyperglycemia after clinical therapeutic trials; lastly, exploring the mechanism of transplantation failure in T1D patients.

Our recent work has identified multiple loci within the nervous system that may be relevant for driving habituation learning. We are investigating whether and how activity within these neuronal populations changes during learning and how activity is disrupted in animals that cannot learn.

My laboratory is focused on examining molecular pathways that regulate the progression and metastasis of lung cancer.

We are interested in the mechanisms that keep development on track, even when cells are faced with deleterious changes like genetic mutations.

The Norman lab researches immunogenetics, which is the study of polymorphic molecules that have critical roles during infection control, reproduction, cancer, and immune-mediated disease. We study the genetic and functional immune diversity of indigenous groups worldwide, including African hunter-gatherers, Australians and Pacific Islanders. We also study ancient humans, and perform comparative evolutionary analyses of multiple other species. The Lab focuses on the co-evolution of the HLA molecules that are expressed by healthy cells, and the KIR, which are Natural Killer (NK) cell receptors that interact with HLA to control immune cell activity.

I perform clinical and translational research focusing on lifestyle interventions, including dietary, to reduce risk of cardiovascular disease and kidney disease progression in patients with kidney diseases including autosomal dominant polycystic kidney disease (ADPKD) and chronic kidney disease (CKD). I also conduct research on the mechanisms of vascular dysfunction in kidney diseases, as well as on novel therapeutics to alleviate such dysfunction.

We use advanced optical imaging techniques to examine the spatiotemporal mechanisms that govern activity-dependent excitatory and inhibitory synaptic and circuit plasticity in the developing cortex.

Fungi are normal members of the human gut microbiome that are benign commensals in people. However, fungi can become pathogenic when the microbiome or immune system is perturbed. Candida species dominating the gut fungal community are notorious opportunistic pathogens capable of causing life-threatening disseminated infections. Candida species can also drive pathogenic inflammation in the gut and are associated with worsened inflammatory bowel disease in people. It is still largely a mystery as to how these fungi reside peacefully in the gut of most people. The goal of the Ost lab is to uncover the immune forces that constrain these fungi to a commensal state to prevent disease.

Delineating the effects of HIV infection on T cell function.

Our research focuses on the development of regenerative medicine approaches for bone and cartilage tissues, with a particular interest in treating growth plate (physeal) cartilage injuries, which represent a significant clinical problem in children.

Centrosome and cilia biology in cell division, motility, and disease.

Our lab is interested in uncovering the molecular pathways that guide the development, selection and activation of autoreactive and non-autoreactive B cells and that, thus, lead to the generation of the naïve B cell repertoire.

Our lab studies host-pathogen interactions with the goal of defining host and bacterial pathways involved in bacterial persistence. Bacterial interactions with the host involve dynamic exchanges where heterogeneity from both sides can lead to many different outcomes. Persistence occurs when the pathogen evades the host immune response and the host is unable to clear the invading pathogen, resulting in stable bacterial colonization. Individuals with persistent infections often do not respond to long-term or repeated appropriate antibiotic treatment and, importantly, serve as reservoirs for the development of antibiotic resistance.

We have an exquisite sense of hearing, where we are able to encode over 12 orders of magnitude in intensity and discriminate between two tones that differ in only 0.2% in frequency. These abilities originate from the auditory periphery’s ability to detect sound. A key process in the detection lies in the mechano-electrical transduction (mechanotransduction) process that happens in the stereocilia hair bundle (highlighted in middle image above). Failures of this process lead to multiple causes of genetic deafness and likely underlie some forms of noise induced and age related hearing loss. In our lab, we are interested in the molecular mechanisms of the mammalian auditory mechanotransduction process. We use state-of-the-art technology to elucidate these mechanisms.

Abigail Person's laboratory studies the contribution of the cerebellum to motor control, focusing on circuit mechanisms that support smooth, precise movement. A central idea in cerebellar physiology is that the position of the body is monitored via copies of motor commands conveyed by "corollary discharge pathways". By combining physiology, optogenetics, anatomical methods, and behavior we address how cerebellar circuitry makes movements precise. These topics are at the heart of the role of the cerebellum as a sensorimotor integrator. Disorders of this circuitry are hypothesized to contribute to some aspects of disorders such as autism and schizophrenia as well as broad motor disturbances seen in cerebellar ataxias.

Preclinical behavioral pharmacology using rodent self-administration models of addiction, optogenetic and chemogenetic dissection of neural circuit function, neural circuitry and mechanisms underlying extinction memory, and the intersection of aversion and reward in systems neuroscience.

We aim to study the chemical ecology of environmental and host-derived microbiome communities by developing broadly accessible experimental approaches. We accomplish this goal by combining modern and classical tools and techniques from a variety of scientific fields, including chemistry, microbiology, cell biology, molecular biology, and biochemistry.

Interplay between inflammation and metabolism as a driver of leukemia development; targeting of pre-malignant and malignant blood-forming stem cells.

His research group investigates the roles that cellular proteins play in viral replication cycles, and innate immune system factors that mediate frontline antiviral defenses and prevent cross-species virus transmission. They are interested in cellular systems that sense and respond defensively to viral RNA and DNA and also prevent autoimmunity to self nucleic acids.

Protein, RNA, and other functional molecules that exist in living organisms are the product of millions of years of evolution. The substitutions that have occurred over the years had to have been compatible with the constraints of structure and function, and thus the evolutionary record provides critical data for understanding macromolecular structure/function/sequence relationships. In our laboratory, we use the techniques of molecular evolution, computational biology, and evolutionary genomics to exploit this record to make inferences about past biological events and to make testable predictions about the effects of mutations.

Our team is working on the creation of normative statistical models of cranial growth that can be used as references to study developmental abnormalities quantitatively. Based on such models, we are creating new methods to identify and quantify abnormal developmental patterns associated with specific pathologies and genetic factors. Those methods will help us better understand developmental cranial disorders and create more informed and targeted treatments.

G-protein linked receptors and their regulation; regulation of mRNA stability.

Neurodegenerative diseases and Down Syndrome.

Regulation of cell division, cell polarity and cell migration.

One major focus of the lab is to understand the molecular basis for pacemaker activity within individual sinoatrial node myocytes (SAMs). To this end, we use patch clamp electrophysiology to record spontaneous action potentials and membrane currents from isolated SAMs from mice. We also use advanced patch clamp techniques like AP clamp and dynamic clamp to isolate and manipulate individual currents in SAMs.

The Quillinan laboratory studies excitability and plasticity changes in the brain following cerebral ischemia. We are particularly interested in cerebellar networks that are affected by stroke and cardiac arrest. We also investigate the role of sex hormones and their receptors in acute neuronal injury and longterm hippocampal function.

My research interests are focused broadly on precision medicine approaches for preventing and treating obesity, diabetes, and their complications, particularly cardiovascular disease. We use electronic health record data and genetic data as tools to understand the heterogeneity of the diabetes patient population and variability in response to interventions, to identify novel risk factors for cardiometabolic diseases, and to build risk models optimized to real-world patient populations in health systems. Our ultimate goal is to build evidence that guides individualized targeting of preventive and treatment interventions for obesity, diabetes, and diabetes complications.

The long-term goal of the Ramachandran Lab is to understand how distinctive chromatin landscapes that reflect cellular identity are established and maintained.

We develop general-purpose computational approaches that integrate large-scale heterogeneous public datasets that lead to the mechanistic understanding of microbial genotypes, phenotypes, and diseases.

Dr. Judy Regensteiner is the director of the Ludeman Family Center for Women's Health Research and distinguished professor of medicine in the divisions of internal medicine and cardiology at the University of Colorado Anschutz Medical Campus. Dr. Regensteiner leads an interdisciplinary team of researchers who focus on women's health and sex differences research.

​The long-term goal of our research is to expand our understanding of the following five areas: 1) The cellular and molecular events that influence allergic disease susceptibility and initiation; 2) The mechanisms regulating immunity to parasites as a foundation for vaccine development; 3) The role and relationship between follicular T helper (Tfh), T-helper 2 (Th2), and follicular regulatory (Tfr) cells in the development/suppression of allergic and infectious disease, 4) The role of group 2 innate lymphoid cell (ILC2) subsets in mucosal barrier immunity, and 5) The mechanisms driving interferon-mediated autoinflammatory diseases.

Our lab is working on three main projects: (1) Identify pathways within the fat body that control organismal fat; (2) Determine the role in body fat regulation of a putative nutrient-responsive modifier of physical activity; and (3) Develop a functional map of neuronal control of body fat.

This laboratory's research is focused on hair cells of the vestibular system. The vestibular system of the inner ear senses accelerations of the head and interacts with other systems to produce the sensation of balance. It is estimated that more than one third of adults in the US experience vestibular dysfunction at some time in their life. However the mechanisms underlying normal and abnormal processing of vestibular sensory signals are not well understood. Our research aims to elucidate how signals are processed in the peripheral vestibular system using rodent models.

I am a systems neuroscientist with a background in physics studying sensory decision making and neurological disorders using novel genomics, transcriptomics, computational neuroscience, automated behavioral testing, advanced neurophotonics and multielectrode arrays. I believe that diversity, equity and inclusion are key in neuroscience inquiry.

Dr Judy Regensteiner and I are trying to understand the molecular underpinnings of decreased functional exercise capacity in youth and adults with uncomplicated type1 and type 2 diabetes. We have clinical interventions ongoing to see if medications can improve exercise function in people with diabetes. In addition, we are actively working to better understand sex-differences in exercise capacity on people with and without diabetes and differences in response to exercise training.

Regulation of Cell Death by the Protein Kinase C Family: Implications for Tissue Damage and Tumorigenesis.

The focus of my research is on the role of estrogen and progesterone receptors in breast and gynecological cancers, mechanisms of resistance to hormone therapy, and the differences between hormone dependent and independent breast cancer.

The major areas of our research currently are: 1. Understanding how metabolism contributes to cancer chemoresistance and developing approaches to overcome chemoresistance; 2) Investigating MCJ as a target to enhance CD8 T cell mitochondrial metabolism and efficacy of CAR-T immunotherapy.

Our goal is to understand how translation impacts mRNA stability, and to place gene regulation in the contexts of broader biological processes.

One of the longest running goals of the Rozance Laboratory has been to develop a better understanding how the fetus translates nutrient and hormonal signals from the placental into anabolic signals for fetal growth with a focus on the fetal anabolic growth factor, insulin.

The Russo lab is interested in understanding how bacterial pathogens interact with their hosts. As a model, we investigate the pathogenesis of Shigella flexneri, which infects cells of the colon and causes diarrhea in humans.

We utilize and develop systems genetics tools to explore biological mechanisms responsible for disease.

Our lab uses zebrafish to study transcriptional and epigenetic control of key transitions during embryogenesis. We are particularly interested in understanding the onset of zygotic transcription at the maternal-to-zygotic transition, ​and in unraveling the transcription orogram driving neural cell fates beginning during gastrulation.

The Sandoval Lab conducts a variety of research studies focused on the role of the gut-brain-axis on regulating body weight and metabolism with the aim to gain a better understanding the role of the gut-brain axis in physiology and in the pathophysiology of obesity and Type 2 diabetes mellitus. We use a combination of techniques including genetic mouse models, bariatric surgery, and in depth metabolic phenotype including in vivo assessment of glucose and lipid metabolism.

Our laboratory studies the interplay between the innate and adaptive immune response against retroviruses to conceptually advance vaccine and cure strategies against HIV/AIDS. We are specifically interested in “restriction factors” – host proteins that could directly inhibit retroviruses but we discovered also play critical roles in shaping adaptive immune responses. These factors could be regulated by Type I interferons, thus highlighting possibilities for clinical translation.

We are interested in how life experience guides the development and adaptation of the mammalian nervous system. We recently discovered that, in mice, olfactory experience regulates the relative birthrates of the > 1000 distinct olfactory sensory neuron subtypes in an odor-specific manner. These findings have led us to hypothesize that life-long olfactory sensory neurogenesis performs an unknown adaptive role, in addition to the known reparative one. We are currently investigating the mechanism and function of this phenomenon. These studies are anticipated to elucidate fundamental aspects about how the olfactory system develops, adapts, and frequently loses function with age and disease.

Our laboratory studies the role of hormone receptors (estrogen, progesterone, glucocorticoid, etc.) in breast cancer gene regulation and progression to endocrine resistance and metastasis.

Our lab is interested in understanding mechanisms and function of brain circuits involved in processing olfactory information. Our focus is on two structures, the olfactory bulb and the piriform cortex, asking basic questions about what neurons are present, how they are connected, and how groups of neurons work to effect a particular circuit output.

My research focuses on genetics and genomics of pulmonary fibrosis, gene discovery in innate immunity and epigenetics of environmental lung disease.

The focus of my lab is to identify novel molecular targets relevant to papillary and anaplastic thyroid cancer (PTC and ATC) with the ultimate goal of advancing these studies to clinical trials for thyroid cancer patients who do not respond to standard treatment.

My research focuses on three major areas; i) Copy Number Variation in Human Disease, ii) Genome Instability and Mechanisms of Rearrangement and iii) Discovery and Functional Characterization of Candidate Disease Genes.

Our lab is interested in pigment-producing cell in health and disease, with the ultimate aim from bench-to-bedside for melanoma, pigmentation disorders and aging.

Our lab specializes in translational research on multiple myeloma, a debilitating and incurable blood cancer. We are focused on developing new therapies, including both large-molecule immunotherapies and small-molecule pathway inhibitors. We are also developing approaches to personalize treatment through real-time monitoring of drug resistance development using ex vivo drug sensitivity testing.

Our lab studies the interplay between the CNS and its vital support structures the meninges and the brain vasculature. We have meninges and brain vascular projects in CNS development, the adult brain and CNS injury and disease.

The overall goal of the Sikora Laboratory is to understand mechanisms of response and resistance to steroid hormones and anti-estrogen therapies in breast cancer, with a special emphasis on invasive lobular carcinoma of the breast.

Using an animal model for colon cancer, we are determining what substitutions in tumor antigen peptides improve antitumor immunity.

Research in our lab is focused on understanding how the excitability of neurons is regulated by excitatory and inhibitory synaptic plasticity. Many neuropsychiatric diseases and brain pathologies exhibit alterations in neuronal excitability in key brain regions associated with learning and memory. Our goal is to understand the molecular mechanisms of how excitatory and inhibitory synapses function together to maintain appropriate excitability of the neuron, and how this is disrupted in diseases such as autism and schizophrenia. To reach this goal we image both excitatory and inhibitory synapses using cutting-edge microscopy, including super-resolution imaging, supported by electrophysiology and biochemical analysis.

The Smith Lab focuses on how B-cells escape tolerance mechanisms to contribute to autoimmune disorders, such as type 1 diabetes.

The goal of research in our lab is to understand mechanisms governing cardiac lineage commitment and pathogenesis of cardiomyopathies, which forms bases to develop therapeutic strategies for heart disease. We actively collaborate with scientists in the field with the long-term goal of improving human health.

My research examines the role of the gut microbiome in obesity and cardiometabolic disease.

The Su Lab’s primary research focus is to better understand the molecular mechanisms underlying abnormal placental blood flow and function. One common finding in placentas from pregnancies complicated by severe FGR is maldevelopment of the placental vascular tree as a consequence of impaired angiogenesis. We are investigating cellular and molecular derangements from human placental endothelial cells isolated from pregnancies complicated by severe FGR that underlie compromised endothelial cell migration. More recently, we have begun to study the role of the placental microenvironment, with focus on the placental villous stroma and on placental endothelial cell-extracellular matrix interactions. The ultimate goal of our research is to understand mechanisms underlying aberrant placental function in severe FGR that will lead to prevention strategies and treatment modalities.

Our main goal is to identify potential new therapeutic agents for the treatment of heart failure.

The main focus of the Sussel lab is to understand the complex transcriptional networks that regulate development, differentiation and function of the pancreas.

We study how the expression of genetic information is spatially regulated within a cell.

The Tamburini lab focuses on understanding how immune cells interact and traffic through the lymphatic vasculature to facilitate an appropriate immune response. We are also interested in the trafficking of small molecules and antigens through the lymphatic vasculature and into draining lymph nodes during infection, vaccination or during chronic disease such as non-alcoholic steatohepatitis, alcohol related liver disease and primary schlerosing cholangitis.

Genetics studies of inherited cardiomyopathies, polycystic kidney disease, intellectual disabilities, hereditary vascular diseases, Barth syndrome, Danon disease, and lysosomal storage diseases.

The overall goal of the Theiss Lab is to elucidate the role and mechanism whereby mitochondrial signaling pathways in intestinal epithelial cells contribute to gastrointestinal diseases, specifically inflammatory bowel diseases (IBD), colitis-associated cancer, and colorectal tumorigenesis.

The role of T-type (low-voltage-activated, LVA) calcium channels in the molecular mechanisms of anesthesia and analgesia.

The role of auditory environmental experience, both normal and abnormal, on the development and maintenance of auditory function.

We have a long-standing interest in investigating the mechanisms by which B lymphocytes develop and subsequently mount antibody responses to foreign antigens and pathogens. In the recent past we have particularly focused on understanding how the distinct B cell populations that exist in humans and mice act in concert to provide humoral immunity. To address these issues, we rely on molecular, genetic and biochemical in vitro and in vivo approaches that often rely on genetically-engineered mouse models. More recent work in our lab has revealed that a bioactive lipid, lysophosphatidic acid (LPA), is able to suppress signaling by both B and T lymphocyte antigen receptors and specifically upon engagement with the LPAR5 receptor.

My research focuses on molecular mechanisms and physiological functions of transporters and ion-channels, particularly those in mitochondria. We approach questions using a wide range of tools, including membrane-biochemistry, electrophysiology, cryo-electron microscopy, animal models, and imaging.

Research in the Tucker Lab focuses on developing new tools to sense and manipulate the intracellular environment, and using these tools to understand dynamic cellular processes. A major focus is in developing ways that we can inducibly regulate and control fundamental molecular events such as protein trafficking, proteolysis, gene expression, and intracellular signaling using inducers such as light (optogenetic tools) or chemicals.

His laboratory uses a variety of neurotropic viruses, including reoviruses, Enterovirus D-68, and Flaviviruses (West Nile, Japanese encephalitis and Zika) to study the pathogenesis of viral CNS infections. A particular interest has been in understanding the nature of specific cellular pathways (signaling, gene expression, apoptosis) that are activated during neurotropic viral infections and that lead to neuronal injury and death. The laboratory uses primary cell cultures, ex vivo slice cultures of brain and spinal cord, and murine models to study virus-cell interactions.

Our lab studies the cellular mechanisms of injury and stress responses in the heart. We are particularly interested in the innate immune system and how inflammation impacts wound healing, fibrosis, and tissue remodeling in beneficial as well as adverse ways. We use the mouse as our primary model, which allows us to interrogate gene functions and signaling pathways, perform genetic lineage tracing, and mimic complex cardiovascular pathology in a mammalian system. Our goal is to understand the regulatory mechanisms of cardiac wound healing and discover novel approaches to repair or even rejuvenate the damaged heart. Our approach, first and foremost, is driven by a shared lab culture of teamwork, discovery, and high-quality science.

The van Dyk lab studies the interactions between virus and host in health and disease. Specifically, our work focuses on gammaherpesviruses.

I am interested in neurometabolic diseases that causes seizures, in particular in non-ketotic hyperglycinemia. I study the genetic basis, the clinical spectrum, the prediction of outcome including the relation between genotype and phenotype, the pathogenesis in animal models and human patients and the development of new treatments for this condition. I am also interested in pyridoxine dependent epilepsy and related metabolic causes of seizures. I am interested in the development of appropriate clinical tests for mitochondrial energy disorders, in the identification and proof of new genetic causes as well as the development of new treatments. Disorders of lipoate metabolism are a particular focus.

The research in the Vázquez-Torres lab uses state-of-the-art biochemical, genetic and molecular biology approaches to understand the molecular mechanisms by which reactive species mediate resistance of macrophages against intracellular bacteria, as well as the adaptive strategies that boost antioxidant and antinitrosative defenses of pathogenic bacteria.

My research studies are aimed at developing cellular therapy to reduce leukemia recurrence by enhancing immune recovery and by more effectively treating sites of leukemia (with a newly developed method of bone marrow irradiation).

My research focuses on genetic mechanisms by which normal brain cells become cancerous and how these genetic differences can be used to better diagnose and treat children with brain tumors,

We are a lab that works on cholinergic signaling in the mammalian brain. Cholinergic systems, via the actions of released acetylocholine, are thought to play an essential role in behaviors involving attention, learning and memory. Impairment of cholinergic signaling is implicated in many neurodegenerative diseases likes Alzheimer's and Parkinson's; and in psychiatric disorders like schizophrenia. However, we know very little about mechanisms underlying signaling by this important neurotransmitter. Our lab strives to remedy this deficit in our knowledge.

We use mice and primary mouse and human cell culture to study how multiciliated cells adopt their cell fate, build cilia and orient the cilia for directional clearance. We investigate the pathways that drive these processes during normal development and regeneration and study how they are misregulated in human disease. Our research has the potential to develop novel biomarkers and therapeutics for individuals suffering from chronic airway diseases.

We develop NMR methods and apply them together with other biophysical methods to study biologically relevant systems at atomic resolution: Diverse dynein motor adaptors and their cargos, allostery in key cell regulator Pin1, Olduvai domains involved in brain function and disease, and various RNA and DNA segments.

Mycobacterium tuberculosis survival during latent disease.

We are specifically focused on the following research: (1) Reproducible software for processing high-dimensional microscopy readouts; (2) Microscopy representations of cell state; (3) Drug screening for pediatric diseases; and (4) New models of pediatric disease to aid drug screening.

Our laboratory focuses on vascular biology, with particular emphasis on smooth muscle cell (SMC) signaling and understanding the regulation of SMC phenotypic modulation in disease.

Dr. Welle’s BIOElectrics Lab investigates how neurological medical devices interact with the nervous system. We dissect circuit-level structural and functional implications of neuromodulatory and brain-computer-interface devices using optogenetics, chronic electrophysiology and longitudinal in-vivo imaging in animal models. Our goal is to understand the dynamic interactions between devices and neural circuits in the context of translational neurotechnology.

Dr. Wesolowski’s primary research is aimed to understand the effects of intrauterine growth restriction (IUGR) using integrative approaches in physiology and metabolism combined with novel molecular techniques in cell biology, epigenetics, and metabolomics. Her current studies are focused on understanding the mechanisms for the early activation of fetal hepatic glucose production and development of hepatic insulin resistance, specifically the role of reduced glucose versus oxygen supply to the fetus, both key features of placental insufficiency and resulting IUGR. In addition, she is involved in projects investigating the effects of maternal high fat diet and obesity on offspring metabolism, specifically the early development of non-alcoholic fatty liver disease (NAFLD) and immune cell reprogramming. Dr. Wesolowski’s long-term goal is to understand how altered nutrient supply programs fetal metabolism and how these changes may persist after birth and increase susceptibility to adult metabolic disease.

I am interested in Reproductive Endocrinology, Neuroendocrinology, Pituitary Disease, Disorders of Adolescence and Menopause and Hypogonadism in Men and Women.

Transcriptional regulation of mouse embryonic development.

My current research is focused on determining mechanisms underlying age and sex differences in subcellular cardiomyocyte function.

My research program uses genetics, transcriptomics, epigenomics and animal/cell models of disease to enhance early detection, predict outcome, develop biomarkers, and design personalized therapeutic strategies in lung disease. Specific current disease areas of interest include asthma and allergy in underrepresented minority populations, pulmonary fibrosis, and sarcoidosis.

We develop statistical machine learning for single-cell omics to study inflammatory disease for translational medicine.

RNA Polymerase II (Pol II) pausing is a unique transcription regulation mechanism in higher eukaryotes. We found that release of paused Pol II, phosphorylation of CTD-Pol II by CDK9, and cleavage of arginine methylated histone tails on + 1 nucleosome by JMJD5, are intrinsically coupled. We are trying to elucidate the underlying mechanism.

My lab focuses on developing technologies that enable tracking the full life cycle of proteins in real time with high spatiotemporal resolution in their native intracellular environments. This will help us understand when, where, and how proteins are synthesized, folded, modified, and degraded in both healthy and diseased cells.

My lab studies the role of the Six1/Eya transcriptional complex and splicing in cancer. We are also developing small molecule or RNA-based approaches to target the Six1/Eya complex or splicing as potential cancer therapeutics.

The biological functions of a cell are heavily influenced by its surrounding environment. This influence is achieved mostly through membrane proteins that mediate various informational exchange between the two bodies. Thus, it is vitally important to understand how these membrane proteins function, which is the overarching goal of our research. The main tools we use in the laboratory are cryo electron microscopy and X-ray crystallography.

My research interest in cancer immunotherapy focuses on 1) identifying novel immune checkpoints, 2) characterizing pathways that limit intratumoral T cell infiltration.

The central focus of our research can be divided programmatically into three parts: 1) Study of the pathological impact of obesity on the skeleton, particularly bone and joint health and fracture healing, 2) Elucidating the role of the gut microbiome in posttraumatic and obesity-associated osteoarthritis, and 3) Development of disease-modifying treatments to address joint degeneration in osteoarthritis. Our work spans from bench to bedside, involving basic molecular-cellular biology and microbiology in microbial and cell culture systems, state-of-the-art animal models of disease, and human clinical trials. Our aim is to pursue a basic study of skeletal homeostasis and disease, using information gained from that work to develop therapeutic strategies addressing key orthopedic challenges including fracture non-union, osteoporosis, and osteoarthritis.