Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype. - Wikidata - awgldk - TriplyDB

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

http://www.wikidata.org/entity/Q34251618

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Nedd4-2 and the regulation of epithelial sodium transport Serum and Glucocorticoid Regulated Kinase 1 in Sodium Homeostasis Roles of Akt and SGK1 in the Regulation of Renal Tubular Transport Ubiquitylation and control of renal Na+ balance and blood pressure Serum- and Glucocorticoid-Inducible Kinase-1 (SGK-1) Plays a Role in Membrane Trafficking in Caenorhabditis elegans Epithelial sodium transport and its control by aldosterone: the story of our internal environment revisited Na+-sensitive elevation in blood pressure is ENaC independent in diet-induced obesity and insulin resistance Nephron-specific deletion of the prorenin receptor causes a urine concentration defect.Endocytic regulation of alkali metal transport proteins in mammals, yeast and plants.Aldosterone regulates a 5' variant sgk1 transcript via a shared hormone response element in the sgk1 5' regulatory region A gene-based analysis of variants in the serum/glucocorticoid regulated kinase (SGK) genes with blood pressure responses to sodium intake: the GenSalt Study.Renal tubular NEDD4-2 deficiency causes NCC-mediated salt-dependent hypertension mTORC2 regulates renal tubule sodium uptake by promoting ENaC activity.Alternatively spliced proline-rich cassettes link WNK1 to aldosterone action Regulation of the renal Na+-Cl- cotransporter by phosphorylation and ubiquitylation.Possible role for nephron-derived angiotensinogen in angiotensin-II dependent hypertension.Low SGK1 expression in human adrenocortical tumors is associated with ACTH-independent glucocorticoid secretion and poor prognosis.Renal Deletion of 12 kDa FK506-Binding Protein Attenuates Tacrolimus-Induced Hypertension.SGK1 regulation by miR-466g in cortical collecting duct cells.Activation of mTORC1 in collecting ducts causes hyperkalemia.Therapeutic potential of serum and glucocorticoid inducible kinase inhibition.Regulation of transport across cell membranes by the serum- and glucocorticoid-inducible kinase SGK1.Dietary potassium and the renal control of salt balance and blood pressure.Activation of mineralocorticoid receptor in salt-sensitive hypertension.Regulation of the epithelial Na+ channel by the mTORC2/SGK1 pathway.Molecular Mechanisms of Sodium-Sensitive Hypertension in the Metabolic Syndrome.The sodium chloride cotransporter (NCC) and epithelial sodium channel (ENaC) associate.Coordinated Control of ENaC and Na+,K+-ATPase in Renal Collecting Duct.A regulated NH2-terminal Sgk1 variant with enhanced function is expressed in the collecting duct.Associations of the Serum/Glucocorticoid Regulated Kinase Genes With BP Changes and Hypertension Incidence: The Gensalt Study.SPAK and OSR1 play essential roles in potassium homeostasis through actions on the distal convoluted tubule.Renal tubular SGK1 deficiency causes impaired K+ excretion via loss of regulation of NEDD4-2/WNK1 and ENaC.Ubiquitylation and the pathogenesis of hypertension.Rab-GAP TBC1D4 (AS160) is dispensable for the renal control of sodium and water homeostasis but regulates GLUT4 in mouse kidney.Mice carrying ubiquitin-specific protease 2 (Usp2) gene inactivation maintain normal sodium balance and blood pressure.SGK1-dependent ENaC processing and trafficking in mice with high dietary K intake and elevated aldosterone.Distal convoluted tubule.

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P2860

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

http://www.wikidata.org/entity/Q34251618

description

2012 nî lūn-bûn

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2012 թուականի Փետրուարին հրատարակուած գիտական յօդուած

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2012 թվականի փետրվարին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@ast

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@en

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

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type

label

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@ast

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@en

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@nl

prefLabel

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@ast

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@en

Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

@nl

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AJPRENAL.00535.2011

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American Journal of Physiology - Renal Physiology

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Inducible kidney-specific Sgk1 knockout mice show a salt-losing phenotype.

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P2093

Adil Ismailji

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Aniko Náray-Fejes-Tóth

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Anne Debonneville

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Dagmara Lagnaz

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Geza Fejes-Toth

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Marc Maillard

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Nourdine Faresse

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Olivier Staub

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P2860

The Nedd4-like protein KIAA0439 is a potential regulator of the epithelial sodium channel

Sgk kinases and their role in epithelial transport

Significance of SGK1 in the regulation of neuronal function

Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expression

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

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

Vasopressin induces phosphorylation of the thiazide-sensitive sodium chloride cotransporter in the distal convoluted tubule

Cell-specific expression of epithelial sodium channel alpha, beta, and gamma subunits in aldosterone-responsive epithelia from the rat: localization by in situ hybridization and immunocytochemistry

A novel mouse Nedd4 protein suppresses the activity of the epithelial Na+ channel

WNK kinases regulate thiazide-sensitive Na-Cl cotransport

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10.1152/AJPRENAL.00535.2011

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2012-02-01T00:00:00Z

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22301619

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