The Gould Laboratory studies vesicles, known as exosomes and microvesicles (EMVs), that can be taken up by neighboring cells, completing a pathway of intercellular vesicle traffic. Our laboratory studies the molecular mechanisms of EMV biogenesis and uptake, and their contributions to cell polarity, cell-to-cell interactions, and intercellular signaling. We also examine the ways in which HIV and other retroviruses use the exosome biogenesis pathway for the formation of infectious virions, and the consequences of their EMV origin.

Research in the Claypool Lab is focused on defining how lipids and membrane proteins interact to establish and maintain normal mitochondrial function and how derangements in this complex relationship result in pathophysiology. We have demonstrated that yeast lacking tafazzin recapitulates all of the phospholipid abnormalities observed in human patients and many of the mitochondrial defects. Another major project in our lab focuses on the mitochondrial ADP/ATP carrier that is required for oxidative phosphorylation. Researchers are studying how these novel interactions help establish normal mitochondrial function, the biochemical details of these associations, and whether disturbances in these assemblies can contribute to mitochondrial dysfunction.

The research in the Svetlana Lutsenko Laboratory is focused on the molecular mechanisms that regulate copper concentration in normal and diseased human cells. Copper is essential for human cell homeostasis. It is required for embryonic development and neuronal function, and the disruption of copper transport in human cells results in severe multisystem disorders, such as Menkes disease and Wilson's disease. To understand the molecular mechanisms of copper homeostasis in normal and diseased human cells, we utilize a multidisciplinary approach involving biochemical and biophysical studies of molecules involved in copper transport, cell biological studies of copper signaling, and analysis of copper-induced pathologies using Wilson's disease gene knock-out mice.

The Seth Blackshaw Lab uses functional genomics and proteomics to rapidly identify the molecular mechanisms that regulate cell specification and survival in both the retina and hypothalamus. We have profiled gene expression in both these tissues, from the start to the end of neurogenesis, characterizing the cellular expression patterns of more than 1,800 differentially expressed transcripts in both tissues. Working together with the lab of Heng Zhu in the Department of Pharmacology, we have also generated a protein microarray comprised of nearly 20,000 unique full-length human proteins, which we use to identify biochemical targets of developmentally important genes of interest.

Current research in the Sean T. Prigge Lab explores the biochemical pathways found in the apicoplast, an essential organelle found in malaria parasites, using a combination of cell biology and genetic, biophysical and biochemical techniques. We are particularly focused on the pathways used for the biosynthesis and modification of fatty acids and associated enzyme cofactors, including pantothenate, lipoic acid, biotin and iron-sulfur clusters. We want to better understand how the cofactors are acquired and used, and whether they are essential for the growth of blood-stage malaria parasites.

The Jeremy Nathans Laboratory is focused on neural and vascular development, and the role of Frizzled receptors in mammalian development. We use gene manipulation in the mouse, cell culture models, and biochemical reconstitution to investigate the relevant molecular events underlying these processes, and to genetically mark and manipulate cells and tissues. Current experiments are aimed at defining additional Frizzled-regulated processes and elucidating the molecular mechanisms and cell biologic results of Frizzled signaling within these various contexts. Complementing these areas of biologic interest, we have ongoing technology development projects related to genetically manipulating and visualizing defined cell populations in the mouse, and quantitative analysis of mouse visual system function.

Research in the Clifton O. Bingham III Lab focuses on defining clinical and biochemical disease phenotypes related to therapeutic responses in rheumatoid arthritis and osteoarthritis; developing rational clinical trial designs to test new treatments; improving patient-reported outcome measures; evaluating novel imaging modalities for arthritis; and examining the role of oral health in inflammatory arthritis.

Dr. Sidhaye is interested in improving the care of persons with cystic fibrosis, type 1 diabetes mellitus and hospitalized person with diabetes. research topics include bone health of persons with CF undergoing lung transplant, CF-related diabetes mellitus, Care of persons with type 1 diabetes mellitus transitioning from pediatrics to adult specialty clinics, Management of hospitalized persons with diabetes.

Research in the Nicola Heller Lab focuses on the immunobiology of macrophages. Our team explores how these cells impact diseases with an inflammatory element, such as cancer, cardiovascular disease and obesity. Using a variety of techniques, including molecular and cellular biology, biochemistry, mouse models and more, we study the role of IL-4/IL-13 signaling in asthma and allergic disease, as well as the role of alternatively activated macrophages (AAM) in the pathogenesis of allergic inflammation. Currently, we are researching the links between asthma and obesity, with a focus on the roles of gender and race.

Ion channels are pore-forming membrane proteins gating the flow of ions across the cell membrane. Among their many functions, ion channels regulate cell volume, control epithelial fluid secretion, and generate the electrical impulses in our brain. The Qiu Lab employs a multi-disciplinary approach including high-throughput functional genomics, electrophysiology, biochemistry, and mouse genetics to discover novel ion channels and to elucidate their role in health and disease.