Stem Cells, Genomics, Aging, Muscle
Research in the Allen Lab is broadly focused on understanding the mechanisms of growth factor and morphogen signaling in development and disease. Specifically, we study the regulation of Hedgehog signaling during embryonic and postnatal development, as well as adult tissue homeostasis, repair and regeneration. Our research employs a wide range of approaches, including mouse genetics, chicken in ovo electroporations, biochemistry, and cell biology. The long-term goal of this work is to apply insights gained from the study of HH signaling in normal contexts to the treatment of a broad...
Our lab uses optical and electrophysiological techniques to study how hormone trafficking, signaling, and release are regulated in neurosecretory cells. We investigate these processes as they relate to stress and stress transduction at the sympatho-adrenal synapse.
Transcriptional regulation; genetic and molecular mechanisms of Mendelian disease
Diabetic Retinopathy and Stroke
Our lab uses cellular and mouse models to study protein folding and misfolding in pancreatic beta cells (proinsulin) and thyroid epithelial cells (thyroglobulin), in order to discover new treatments for conformational diseases that affect these cells of the endocrine system. Our lab has described the cellular and molecular basis for the human disease known as Mutant INS gene-induced Diabetes of Youth, caused in most cases by expression of misfolded mutant proinsulin.
The effects of sensory experience and sleep on neural circuits, mechanisms underlying nervous system plasticity and memory formation.
Protein quality control at eukaryotic membranes
chaperone action, chaperone discovery, directed evolution, nicotine addiction
RNA stability, RNA binding proteins, neurodegeneration, ALS, FTD
Enhancers, gene expression, developmental cell signaling
Neurogenetics, neural development, chromatin biology, cell fate, mouse and human brain organoids
Kidney disease, system biology, translational research.
Our research group aims to combine both computational and wet lab strategies to answer questions related to the transcriptional regulatory control of human genes. We believe that a complex regulatory control determines the fates of individual non-coding regulatory elements and that the integration of diverse genetic, epigenetic, and disease data is the best way to explore this control. Using innovative computational and wet lab approaches the lab both characterizes the function of these regulatory elements as well as examines the effect of genetic variation in these regions.
signal transduction, cardiac hypertrophy, heat failure, post-translational modifications
Our laboratory is interested in understanding how cells use nutrients and how excess nutrient flux, as occurs in obesity, and diabetes, triggers insulin resistance and inflammatory responses. We are also interested in how intrinsic exercise capacity and exercise training can alter metabolism. We use metabolomics profiling and other 'omics technologies to profile metabolism in animals and humans.
The Cadigan lab is interested in signal transduction and gene regulation in Drosophila and mammalian cells. Much of our research is focused on the Wnt/beta-catenin signaling pathway, but we are also exploring other pathways involved in cell specification during development and human disease.
Birth defects research, organogenesis, mouse models of human disease, neuroendocrine development and function, growth insufficiency
We study pathways involved in preserving genome stability as well as mechanisms of resistance to cancer chemotherapy.
ESCRT, endocytosos, autophagy, genetics, infection
Signal transduction pathways used by cytokine receptors and JAK tyrosine kinases; molecular actions of growth hormone; role of SH2-B adapter proteins in regulation of the cytoskeleton, gene expression and cellular differentiation and survival.
B cell responses to Transplantation. Co-evolution of TNFRSF13B polymorphisms with microbial adaptations. Immunotherapies. Mutable vaccines.
We are working on protein sorting and quality control in the yeast secretory pathway.
The Role of Nuclear Receptors in Obesity/Diabetes-Related Cardiovascular Complications.
T-cell leukemia, T-cell development, Notch, transcriptional genomics, protein-protein interactions
Dr. Chinnaiyan's laboratory has focused on functional genomic,proteomic and bioinformatics approaches to study cancer for the purposesof understanding cancer biology as well as to discover clinicalbiomarkers. He and his collaborators have characterized a number ofbiomarkers of prostate cancer including AMACR, EZH2 and hepsin. AMACRis being used clinically across the country in the assessment of cancerin prostate needle biopsies.
My lab is mainly focusing on biochemical and structural studies on kinetochore assembly, histone chaperones, and Sestrin-mediated mTORC1 regulation.
Our lab is interested in the proteolytic ECM remodeling of adipose tissues in development and obesity. Using 3-D adipocyte differentiation model and a series of genetically modified mice, we aim to define a molecular mechanism that links ECM remodeling to the regulation of organ function in development and diseases.
microtubule, motor proteins, cryo-EM
development, olfaction, neural circuits, genome evolution, sexual dimorphism
The Corfas Laboratory is interested in understanding the roles that interactions between neurons and glia-the two fundamental cell types of the nervous system-play in nervous system development, function and maintenance and in defining the molecular signals that orchestrate these interactions.
Tissue homeostasis, cell differentiation, genetic skin diseases, cancer, nucleus
Our research seeks to manipulate signaling pathways in T cells to understand their behavior. We are especially interested in how T cell recognize and respond to antigen. By applying our findings in the setting of cancer we aim to develop new immunotherapy strategies.
Cytoskeleton, Motor proteins, Microtubules, Dynein
Our lab concentrates on the molecular characterization of common and rare variants in genes associated with bleeding or thrombosis risk in humans. Through the study of large cohorts of human subjects, we and others have identified genetic variants associated with altered risk for disease. In our lab, we employ molecular and cellular techniques, such as mammalian cell culture, proteomic profiling, genome-wide CRISPR mediated knock-out screens, and mutagenesis libraries to functionally characterize the altered molecular genetic mechanisms contributing to disease risk.
Hedgehog-driven cancers, viral oncogenesis, non-melanoma skin cancers
Developmental biology, stem cells, epigenetics, kidney disease
Membrane traffic, Cell polarity, Protein interactions, Yeast, Organoids
Nutriepigenetics, metabolism, processed food, feeding behavior
Our lab focuses on the genetic determinants of thrombosis, atherosclerosis, and inflammation.
Our laboratory is interested in molecular mechanisms controlling epidermal growth and differentiation, including how this process is linked to host defense and autoimmunity. For this purpose, we utilize cell biology, organ culture, transgenic animals, genetic linkage analysis, and gene expression profiling.
Cancer genetics, gastrointestinal cancer, oncogenes, tumor suppressor genes, beta-catenin, Wnt signaling, developmental biology, CDX2, E-cadherin.
The role of growth factors in the pathogenesis and treatment of neurologic disorders.
Regulation of signal transduction by the conserved protein kinase mTOR, the mammalian target of rapamycin.