The critical role of the kidney in maintaining fluid and electrolyte balance, and the disorders of homeostasis that are accompany diseases of the kidney and associated loss of renal function underscore the importance of this organ. Our increasing ability to both identify and modify the gene products that are responsible for maintaining normal homeostatic balance offers new and powerful approaches to examine the contributions of individual proteins to the maintenance of normal renal function and the consequences of loss of renal function. The objective of the Pittsburgh Center for Kidney Research is to both reinforce and expand interactions among investigators at the University of Pittsburgh and colleagues at Mount Sinai School of Medicine who have had a longstanding history of research in areas related to the identification and characterization of cellular processes within the kidney that are associated with normal physiology and with pathophysiological states, to develop new directions of investigation using electrophysiological, cell biological, molecular, and genetic tools, and to attract new investigators to renal-related research. The Center will be focused on four main cores, which will support the work of investigators at the University of Pittsburgh and Mount Sinai School of Medicine. Core A is a cellular physiology core, led by Dr. Johnson. Core B is a single nephron and organ physiology core, led by Drs. Jackson and Satlin. Core C is a urinary tract epithelial imaging core, led by Dr. Apodaca. Core D will focus on the use of model organisms to elucidate novel aspects of kidney function and is led by Drs. Brodsky and Hukriede. The Center will support three pilot and feasibility projects. An administrative core, led by Drs. Kleyman and Weisz, will provide administrative oversight of the core facilities, the pilot and feasibility project program and the instructional components of the center. All research cores are specifically structured to serve as nation-wide resources for investigators. Our Center is designed to realize our goal of continuing to advance our understanding of normal renal function, of cellular mechanisms that contribute to kidney disease, and of the myriad altered cellular functions that occur in the setting of renal insufficiency.
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| Balchak, Deidra M; Thompson, Rebecca N; Kashlan, Ossama B (2018) The epithelial Na+ channel ? subunit autoinhibitory tract suppresses channel activity by binding the ? subunit's finger-thumb domain interface. J Biol Chem 293:16217-16225 |
| Sun, Zhihao; Brodsky, Jeffrey L (2018) The degradation pathway of a model misfolded protein is determined by aggregation propensity. Mol Biol Cell 29:1422-1434 |
| Boyd-Shiwarski, Cary R; Shiwarski, Daniel J; Roy, Ankita et al. (2018) Potassium-regulated distal tubule WNK bodies are kidney-specific WNK1 dependent. Mol Biol Cell 29:499-509 |
| Kashlan, Ossama B; Kinlough, Carol L; Myerburg, Michael M et al. (2018) N-linked glycans are required on epithelial Na+ channel subunits for maturation and surface expression. Am J Physiol Renal Physiol 314:F483-F492 |
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| Ray, Evan C; Miller, Rachel G; Demko, John E et al. (2018) Urinary Plasmin(ogen) as a Prognostic Factor for Hypertension. Kidney Int Rep 3:1434-1442 |
| Jobbagy, Soma; Tan, Roderick J (2018) Nitrolipids in kidney physiology and disease. Nitric Oxide : |
| Joshi, Suhasini; Wang, Tai; Araujo, Thaís L S et al. (2018) Adapting to stress - chaperome networks in cancer. Nat Rev Cancer 18:562-575 |
| Jackson, Edwin K; Gillespie, Delbert G; Mi, Zaichuan et al. (2018) Adenosine Receptors Influence Hypertension in Dahl Salt-Sensitive Rats: Dependence on Receptor Subtype, Salt Diet, and Sex. Hypertension 72:511-521 |
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