Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3 - Test2 - elhamkhani - TriplyDB

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

http://www.wikidata.org/entity/Q35140143

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Cul3-KLHL20 ubiquitin ligase: physiological functions, stress responses, and disease implications Nephron-specific deletion of the prorenin receptor causes a urine concentration defect.Generation of WNK1 knockout cell lines by CRISPR/Cas-mediated genome editing.KLHL3 regulates paracellular chloride transport in the kidney by ubiquitination of claudin-8.Ca(2+) is a Regulator of the WNK/OSR1/NKCC Pathway in a Human Salivary Gland Cell Line.Hypertension-causing Mutations in Cullin3 Protein Impair RhoA Protein Ubiquitination and Augment the Association with Substrate Adaptors.Alternatively spliced proline-rich cassettes link WNK1 to aldosterone action Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia.Cell-specific regulation of L-WNK1 by dietary K.Degradation by Cullin 3 and effect on WNK kinases suggest a role of KLHL2 in the pathogenesis of Familial Hyperkalemic Hypertension Generation and analysis of knock-in mice carrying pseudohypoaldosteronism type II-causing mutations in the cullin 3 gene.Possible role for nephron-derived angiotensinogen in angiotensin-II dependent hypertension.The CUL3/KLHL3-WNK-SPAK/OSR1 pathway as a target for antihypertensive therapy Hypertension: the missing WNKs.Cullin-3 mutation causes arterial stiffness and hypertension through a vascular smooth muscle mechanism.Multistep regulation of autophagy by WNK1 WNK signalling pathways in blood pressure regulation Revisiting the NaCl cotransporter regulation by with-no-lysine kinases.Kelch-like 3/Cullin 3 ubiquitin ligase complex and WNK signaling in salt-sensitive hypertension and electrolyte disorder.PPARγ Regulation in Hypertension and Metabolic Syndrome.Association between Cullin-3 Single-Nucleotide Polymorphism rs17479770 and Essential Hypertension in the Male Chinese Han Population.ROMK expression remains unaltered in a mouse model of familial hyperkalemic hypertension caused by the CUL3Δ403-459 mutation.Physiological role of SLC12 family members in the kidney.Paracellular transport in the collecting duct.Ubiquitination and the Regulation of Membrane Proteins.Potassium depletion stimulates Na-Cl cotransporter via phosphorylation and inactivation of the ubiquitin ligase Kelch-like 3.SPAK and OSR1 play essential roles in potassium homeostasis through actions on the distal convoluted tubule.Mutant Cullin causes cardiovascular compromise.Phosphorylation by PKC and PKA regulate the kinase activity and downstream signaling of WNK4.Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport.Mutant Cullin 3 causes familial hyperkalemic hypertension via dominant effects.Potassium Sensing by Renal Distal Tubules Requires Kir4.1.WNK-Cab39-NKCC1 signaling increases the susceptibility to ischemic brain damage in hypertensive rats.The evolving field of salt transport regulation in the Steve Hebert Lecture.Endothelial transcriptomics reveals activation of fibrosis-related pathways in hypertension.Mechanisms and controversies in mutant Cul3-mediated Familial Hyperkalemic Hypertension.A novel mutation in exon 9 of Cullin 3 gene contributes to aberrant splicing in pseudohypoaldosteronism type II.WNK pathways in cancer signaling networks

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P2860

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

http://www.wikidata.org/entity/Q35140143

description

2014 nî lūn-bûn

@nan

2014 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

@hyw

2014 թվականի սեպտեմբերին հրատարակված գիտական հոդված

@hy

2014年の論文

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2014年論文

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2014年論文

@zh-hant

2014年論文

@zh-hk

2014年論文

@zh-mo

2014年論文

@zh-tw

2014年论文

@wuu

name

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

@ast

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

@en

type

label

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

@ast

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

@en

prefLabel

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

@ast

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

@en

P1433

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P1433

Journal of Clinical Investigation

P1476

Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3

@en

P2093

Aljona Borschewski

http://www.w3.org/2001/XMLSchema#string

Belinda McCully

http://www.w3.org/2001/XMLSchema#string

Bethzaida Yarbrough

http://www.w3.org/2001/XMLSchema#string

Brittney Davidge

http://www.w3.org/2001/XMLSchema#string

Chao-Ling Yang

http://www.w3.org/2001/XMLSchema#string

Chong Zhang

http://www.w3.org/2001/XMLSchema#string

Eduardo R Argaiz

http://www.w3.org/2001/XMLSchema#string

Hae J Park

http://www.w3.org/2001/XMLSchema#string

James A McCormick

http://www.w3.org/2001/XMLSchema#string

Jeffrey D Singer

http://www.w3.org/2001/XMLSchema#string

P2860

Cullin-3 targets cyclin E for ubiquitination and controls S phase in mammalian cells

Ubiquitination of Keap1, a BTB-Kelch substrate adaptor protein for Cul3, targets Keap1 for degradation by a proteasome-independent pathway

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

Impaired KLHL3-mediated ubiquitination of WNK4 causes human hypertension

Kelch-like 3 and Cullin 3 regulate electrolyte homeostasis via ubiquitination and degradation of WNK4

WNK3 and WNK4 amino-terminal domain defines their effect on the renal Na+-Cl- cotransporter

A molecular update on pseudohypoaldosteronism type II

Structural Basis for Cul3 Protein Assembly with the BTB-Kelch Family of E3 Ubiquitin Ligases

Pathophysiology of functional mutations of the thiazide-sensitive Na-Cl cotransporter in Gitelman disease

Constitutive turnover of cyclin E by Cul3 maintains quiescence

P304

4723-4736

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scholarly article

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10.1172/JCI76126

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P407

P433

11

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P478

124

http://www.w3.org/2001/XMLSchema#string

P50

David H. Ellison

P577

2014-09-24T00:00:00Z

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25250572

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P932

4347254

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