Mark A. Knepper
National Institutes of Health
16 Papers
173 Citations
Mark A. Knepper is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Aquaporin 2 & Vasopressin. The author has an hindex of 9, co-authored 16 publications. Previous affiliations of Mark A. Knepper include Georgetown University & Aarhus University.
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Papers
Hypokalemia-induced downregulation of aquaporin-2 water channel expression in rat kidney medulla and cortex.
TL;DR: Hypokalemia, like lithium treatment, results in a decrease in AQP2 expression in rat collecting ducts, in parallel with the development of polyuria, and the degree of downregulation is consistent with the level ofpolyuria induced, supporting the view that there is a causative link.
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Expression of VAMP-2-like protein in kidney collecting duct intracellular vesicles. Colocalization with Aquaporin-2 water channels.
Søren Nielsen,David Marples,Henrik Birn,M Mohtashami,Nils Ole Dalby,M Trimble,Mark A. Knepper +6 more
TL;DR: VAMP2, a component of the neuronal SNARE complex, is expressed in vesicles carrying AQP2, suggesting a role in vasopressin-regulated vesicle trafficking of AQP1 water channels.
Syntaxin-4 is localized to the apical plasma membrane of rat renal collecting duct cells: possible role in aquaporin-2 trafficking.
TL;DR: The demonstrated localization of syntaxin-4 in the apical plasma membrane of collecting duct principal cells, coupled with previous demonstration of syntaxIn-4's putative cognate receptor VAMP2 in aquaporin-2-containing vesicles, supports the view that these proteins could play a role of aquaporIn-2 vesicle targeting to the apicals plasma membrane.
Concentrating defect in experimental nephrotic syndrome: Altered expression of aquaporins and thick ascending limb Na+ transporters
Patricia Fernández-Llama,Peter M. Andrews,Peter M. Andrews,Peter M. Andrews,Carolyn A. Ecelbarger,Carolyn A. Ecelbarger,Carolyn A. Ecelbarger,Søren Nielsen,Søren Nielsen,Søren Nielsen,Mark A. Knepper,Mark A. Knepper,Mark A. Knepper +12 more
TL;DR: The concentrating defect in adriamycin-induced nephrotic syndrome in rats is a consequence of multiple defects in water and solute transporter expression, which would alter both the generation of medullary interstitial hypertonicity and osmotic equilibration in the collecting duct.
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Reduced renal medullary water channel expression in puromycin aminonucleoside--induced nephrotic syndrome.
E Apostol,Carolyn A. Ecelbarger,James Terris,A. D. Bradford,Peter M. Andrews,Mark A. Knepper +5 more
TL;DR: PAN-nephrosis is associated with an extensive downregulation of collecting duct water channel expression despite increased circulating vasopressin, providing an explanation for the concentrating defect associated with the nephrotic syndrome.