Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells. - Wikidata - wikimedia - TriplyDB

Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

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Regulatory Crosstalk by Protein Kinases on CFTR Trafficking and Activity.Short-term nonpressor angiotensin II infusion stimulates sodium transporters in proximal tubule and distal nephron.Hypertension: the missing WNKs.WNK signalling pathways in blood pressure regulation Revisiting the NaCl cotransporter regulation by with-no-lysine kinases.Mini-review: regulation of the renal NaCl cotransporter by hormones.Characterization of constitutive and acid-induced outwardly rectifying chloride currents in immortalized mouse distal tubular cells Potassium Supplementation Prevents Sodium Chloride Cotransporter Stimulation During Angiotensin II Hypertension.A novel function of calcitonin gene-related peptide in body fluid Cl- homeostasis Zebrafish as a Model System for Investigating the Compensatory Regulation of Ionic Balance during Metabolic Acidosis.

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Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

http://www.wikidata.org/entity/Q35274077

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Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

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Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

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type

label

Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

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Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

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prefLabel

Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

@ast

Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

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AJPRENAL.00465.2014

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American Journal of Physiology - Renal Physiology

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Mechanisms of angiotensin II stimulation of NCC are time-dependent in mDCT15 cells.

@en

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Abinash Mistry

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Benjamin Ko

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Lauren Hanson

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Rickta Mallick

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Robert S Hoover

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P2860

Gitelman's variant of Bartter's syndrome, inherited hypokalaemic alkalosis, is caused by mutations in the thiazide-sensitive Na-Cl cotransporter

Molecular pathogenesis of inherited hypertension with hyperkalemia: the Na-Cl cotransporter is inhibited by wild-type but not mutant WNK4

Angiotensin II signaling increases activity of the renal Na-Cl cotransporter through a WNK4-SPAK-dependent pathway

WNK4 enhances the degradation of NCC through a sortilin-mediated lysosomal pathway

The Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure: the JNC 7 report

The Na+:Cl- cotransporter is activated and phosphorylated at the amino-terminal domain upon intracellular chloride depletion

Angiotensin II induces phosphorylation of the thiazide-sensitive sodium chloride cotransporter independent of aldosterone

Molecular cloning, primary structure, and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney

WNK kinases regulate thiazide-sensitive Na-Cl cotransport

Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension

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10.1152/AJPRENAL.00465.2014

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