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UT Southwestern Endowed Scholars Committee
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Director, Nancy B. and Jake L. Hamon Center for Basic Research in Cancer
Dr. Olson's lab studies muscle cells as a model for understanding how cell differentiation and morphogenesis are controlled during development. Using a combination of biochemistry and genetics, Dr. Olson and his colleagues discovered a network of genes that directs heart formation in mammals and the fruit fly. Dr. Olson's work has also had a direct impact on understanding the pathophysiology of heart failure since many of the same transcription factors and regulatory mechanisms that control heart development are deployed within the adult heart as a consequence of pathological stress.
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Investigator, Howard Hughes Medical Institute
Dr. Deisenhofer's Nobel-winning research used X-ray crystallography to elucidate the three-dimensional structure of a large membrane-bound molecule. This structure helped explain the process of photosynthesis, by which sunlight is converted to chemical energy. In addition, his work has provided key information about the structure and function of proteins involved in disease and serves as a basis for the design of mutants and drugs.
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Joseph L. Goldstein, M.D.
Regental Professor and Chair, Department of Molecular Genetics
Drs. Goldstein's and Brown's Nobel-winning research identified low-density lipoprotein receptors on the surface of cells that recognize, bind to, and admit LDL cholesterol into cells. High LDL, or "bad" cholesterol, is a major risk factor for heart disease, heart attack, and stroke. Since winning the Nobel Prize, these researchers have discovered a family of membrane-bound proteins, called SREBPs (sterol regulatory element-binding proteins) that regulate cholesterol synthesis and control the number of LDL receptors in the body.
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Investigator, Howard Hughes Medical Institute
Dr. Hobbs is interested in how dysregulation of the uptake and trafficking of dietary lipids contribute to human diseases, in particular coronary atherosclerosis and the metabolic syndrome. Her work has led to the identification of the genes defective in two autosomal recessive forms of severe hypercholesterolemia (autosomal recessive hypercholesterolemia [ARH] and sitosterolemia), which are both associated with premature coronary artery disease. She has recently shown that sequence variations with major effects are collectively more common than expected and contribute significantly to low plasma levels of HDL and LDL in the population.
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Professor and Chair, Department of Pharmacology
Investigator, Howard Hughes Medical Institute
Dr. Mangelsdorf's research is directed at understanding the function of nuclear hormone receptors, a family of ligand-dependent transcription factors that govern diverse physiologic processes ranging from reproduction to nutrient metabolism. His laboratory discovered the ligands and signaling pathways for several orphan nuclear receptors, including the oxysterol receptors (LXRs), bile acid receptor (FXR), and DAF-12, the nematode receptor that regulates reproduction, development, and longevity. By exploiting their ligand dependency, his work has highlighted the potential of these receptors as novel therapeutic targets for diseases such as atherosclerosis, cholesterol gallstone disease, cancer, and parasitic nematode infections.
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Dr. Parada is a developmental biologist with interests in neural development and its links to cancer and disease. Using genetic mouse models, the Parada laboratory focuses on the roles of Trk receptors and neurotrophins in the development of the brain, in neurogenesis, and in behavioral outcomes of manipulating these molecules as they may relate to psychiatric disorders. In addition, the laboratory studies the NF1 tumor suppressor which is responsible for neurofibromatosis and is implicated in cancers of the peripheral and central nervous system. Mouse models are used to examine the cell of origin in glioblastoma and the nature of cancer stem cells.
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Investigator, Howard Hughes Medical Institute
Dr. Rosen’s lab studies the molecular mechanisms by which extracellular signals control the structure and dynamics of the actin cytoskeleton, a filament network that provides mechanical stability and spatial organization to the cell. Using a combination of structural biology and biochemical reconstitution, he has discovered how information flows from the Rho family GTPase, Cdc42, to the Wiskott-Aldrich Syndrome Protein (WASP) to the Arp2/3 complex, leading to formation of branched actin networks. He has also shown how the physical properties of WASP enable complex integrative behaviors, including noise filtering and molecular memory. These findings have laid the foundations for understanding the many human diseases that involve defects in actin regulation including cancer, immunodeficiencies and bacterial/viral pathogenesis.
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Sam G. Winstead and F. Andrew Bell Distinguished Chair in Biochemistry
The McKnight lab at UT Southwestern Medical Center studies the relationship between metabolism and biological regulation. Our simple thesis holds that cells exist in metabolic states that are both specialized and dynamic, and that metabolic state feeds back to help establish the regulatory state of the cell or tissue. Of the systems under study, the most robust is a “yeast metabolic cycle” (YMC) adopted by prototrophic yeast when grown in a chemostat under high density. Upon such conditions, yeast cells enter into a metabolic cycle 4-5 hours in length. The culture can be observed to rhythmically progress between three metabolic states designated oxidative (OX), reductive building (RB), and reductive charging (RC). Different cellular processes are stringently proportioned in time, such that they are undertaken solely in one of these three states. DNA replication and cell division, for example, are tightly gated to the RB phase of the YMC.
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Instructions for Endowed Scholar Nominations
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