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Hypertension: the missing WNKs.

Hypertension: the missing WNKs.

http://www.wikidata.org/entity/Q37139457

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Emerging Targets of Diuretic Therapy.Potassium: friend or foe?The evolving field of salt transport regulation in the Steve Hebert Lecture.

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Hypertension: the missing WNKs.

http://www.wikidata.org/entity/Q37139457

description

article científic

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article scientifique

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articolo scientifico

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artigo científico

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bilimsel makale

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scientific article published on 23 March 2016

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vedecký článok

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vetenskaplig artikel

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videnskabelig artikel

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vědecký článek

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name

Hypertension: the missing WNKs.

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Hypertension: the missing WNKs.

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type

label

Hypertension: the missing WNKs.

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Hypertension: the missing WNKs.

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prefLabel

Hypertension: the missing WNKs.

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Hypertension: the missing WNKs.

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AJPRENAL.00358.2015

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American Journal of Physiology - Renal Physiology

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Hypertension: the missing WNKs.

@en

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Chou-Long Huang

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Hashem A Dbouk

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Melanie H Cobb

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P2860

Cloning, characterization, and chromosomal location of a novel human K+-Cl- cotransporter

Heart Disease and Stroke Statistics--2015 Update: A Report From the American Heart Association

Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure

WNK3 kinase is a positive regulator of NKCC2 and NCC, renal cation-Cl- cotransporters required for normal blood pressure homeostasis

MO25 is a master regulator of SPAK/OSR1 and MST3/MST4/YSK1 protein kinases

KLHL3 mutations cause familial hyperkalemic hypertension by impairing ion transport in the distal nephron

WNK3 positively regulates epithelial calcium channels TRPV5 and TRPV6 via a kinase-dependent pathway

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

Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2

The WNK-regulated SPAK/OSR1 kinases directly phosphorylate and inhibit the K+-Cl- co-transporters

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F16-27

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scholarly article

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10.1152/AJPRENAL.00358.2015

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