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.
Our objective is to obtain a better understanding of the development and function of neurons and glia in the peripheral nervous system using human genetics, molecular and cellular biology, and zebrafish transgenesis. The major end goal of these studies is to characterize how these cell types are affected in patients with peripheral neuropathies.
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.
RNA stability, RNA binding proteins, neurodegeneration, ALS, FTD
Enhancers, gene expression, developmental cell signaling
Discovery of new genes for human developmental brain disorders highlights the genes essential for brain development. The disease mechanisms associated with these genes are modeled using patient induced pluripotent stem cells and mice to understand the associated molecular pathology.
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.
The Brody lab is broadly focused on the molecular signals that underlie cardiac disease onset and progression. We have a specific interest in understanding how intracellular signaling is compartmentalized and regionally controlled by lipid modifications that modulate the function of signaling molecules in various cell types of the heart to control cardiac physiology and pathogenesis. Our laboratory utilizes a combination of mouse genetics, biochemistry, and molecular and chemical biology techniques to gain insight into pathophysiological signaling mechanisms that contribute to human...
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.
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.
We study the communications between transcription factors that result in epigenetic modifications at super-enhancers of oncogenes. These changes drive the development of normal lymphocytes , but also the generation of cancer stem cells in childhood leukemia. By targeting specific, synthetic lethal interactions responsible for the context dependence of transcription factors in cancer, we might combat the cancer functions of transcription factors without potential adverse consequences of total inhibition.
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.
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.
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.
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.
The Dressler lab utilizes genetic and biochemical approaches to understand the development of the kidney and reproductive tract. The lab has identified multiple epigenetic and cell signaling pathways that control epithelial cell lineage specification and differentiation. These pathways also contribute to chronic and acute renal disease and cancer, for which novel therapeutics are being developed.
Membrane traffic, Cell polarity, Protein interactions, Yeast, Organoids
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.