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.
Understanding the role of mitophagy in colon cancer iron regulation, and investigating metabolic regulations of ER-mitochondria contact sites in cancer.
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.
Using optogenetics, investigate the spatiotemporal regulation of small GTPase RhoA and how it orchestrates actin cytoskeletal dynamics responsible for junctional remodeling and cytokinesis in vertebrate epithelial tissues.
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
Understanding the role of NETs in neutrophil-mediated immune functions as well as the intercellular signaling cascade surrounding this process.
I am studying the H. pylori virulence factor vacuolating cytotoxin A (VacA). Using single-particle cryo-EM, I am determining VacA's pore-form and characterizing its membrane interactions.
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.
I study the mechanisms of neurodegeneration in Niemann-pick type C disease, an autosomal recessive lysosomal storage disorder
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.
I study the biosynthetic trafficking of G-protein-coupled receptors (GPCRs). GPCR localization to the the cell surface is critical for functional coupling to both extracellular agonists and G-protein effectors on the plasma membrane. Despite the functional importance of GPCR localization to the plasma membrane, relatively little is known about the biosynthetic trafficking of these receptors to the cell surface. I would like to understand how the trafficking of these receptors to the cell surface is regulated and how we can target receptors to the surface to increase signaling.