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One or more keywords matched the following properties of Ko, Benjamin S.
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overview Dr. Ko is a dedicated physiologist and teacher who studies sodium and calcium transport in the kidney, especially as they pertain to kidney stone disease. His integrated approach to scholarship and investigation spans basic science and translational research, with a focus on understanding the molecular mechanisms of renal tubular transport of cations in humans. Using urinary exosomal analyses, small but discrete packages of transporter proteins extruded from the epithelial cell into the urinary space, and a variety of molecular and biochemical techniques he is able to characterize the complex regulation of sodium and calcium homeostasis. His current projects include an examination the molecular mechanisms underlying calcium kidney stone formation and determining the hormonal regulators of the sodium chloride co-transporter. Dr. Ko has been heavily involved for a number of years in medical education including pre-med, medical, resident and fellow trainees. He is a fellow of the Academy of Distinguished Medical Educators and the co-director of the Tissues, Cell and Organ Physiology Course at the Pritzker School of Medicine. Nationally, he serves as the director for the American Society of Nephrology’s Tutored Research and Education of Kidney Scholars (TREKS) program at the University of Chicago.
One or more keywords matched the following items that are connected to Ko, Benjamin S.
Item TypeName
Concept Sodium
Concept Sodium Chloride, Dietary
Concept Sodium Chloride Symporter Inhibitors
Concept Epithelial Sodium Channels
Concept Sodium Chloride Symporters
Academic Article Phorbol ester stimulation of RasGRP1 regulates the sodium-chloride cotransporter by a PKC-independent pathway.
Academic Article Molecular physiology of the thiazide-sensitive sodium-chloride cotransporter.
Academic Article RasGRP1 stimulation enhances ubiquitination and endocytosis of the sodium-chloride cotransporter.
Academic Article Parathyroid hormone (PTH) regulates the sodium chloride cotransporter via Ras guanyl releasing protein 1 (Ras-GRP1) and extracellular signal-regulated kinase (ERK)1/2 mitogen-activated protein kinase (MAPK) pathway.
Academic Article A new model of the distal convoluted tubule.
Academic Article Sex differences in proximal and distal nephron function contribute to the mechanism of idiopathic hypercalcuria in calcium stone formers.
Academic Article Aldosterone acutely stimulates NCC activity via a SPAK-mediated pathway.
Academic Article Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.
Academic Article Interleukin-17A Regulates Renal Sodium Transporters and Renal Injury in Angiotensin II-Induced Hypertension.
Academic Article The sodium chloride cotransporter (NCC) and epithelial sodium channel (ENaC) associate.
Academic Article CD8+ T cells stimulate Na-Cl co-transporter NCC in distal convoluted tubules leading to salt-sensitive hypertension.
Academic Article Parathyroid hormone and the regulation of renal tubular calcium transport.
Academic Article Nedd4-2 modulates renal Na+-Cl- cotransporter via the aldosterone-SGK1-Nedd4-2 pathway.
Academic Article Zinc deficiency induces hypertension by promoting renal Na+ reabsorption.
Academic Article The Pharmacological Inhibition of CaMKII Regulates Sodium Chloride Cotransporter Activity in mDCT15 Cells.
Academic Article The IFN?-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension.
Academic Article Interleukin 6 mediated activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron.
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  • Sodium