Impaired KLHL3-mediated ubiquitination of WNK4 causes human hypertension (Q24321928)

Kelch like family member 3

inferred from title

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Cullin 3

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WNK lysine deficient protein kinase 4

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distal tubule morphogenesis

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protein ubiquitination

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Mai Wakabayashi

1

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Takayasu Mori

2

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Kiyoshi Isobe

3

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Eisei Sohara

4

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Koichiro Susa

5

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Yuya Araki

6

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Motoko Chiga

7

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Eriko Kikuchi

8

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Naohiro Nomura

9

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Yutaro Mori

10

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Hiroshi Matsuo

11

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Tomohiro Murata

12

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Shinsuke Nomura

13

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Takako Asano

14

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Hiroyuki Kawaguchi

15

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Shigeaki Nonoyama

16

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Tatemitsu Rai

17

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Sei Sasaki

18

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Shinichi Uchida

Immunolocalization of WNK4 in mouse kidney.

19

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language of work or name

English

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publication date

28 March 2013

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published in

Cell Reports

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volume

3

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issue

3

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page(s)

858-68

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cites work

1 reference

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7 January 2021

Effect of heterozygous deletion of WNK1 on the WNK-OSR1/ SPAK-NCC/NKCC1/NKCC2 signal cascade in the kidney and blood vessels.

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Liddle's syndrome: heritable human hypertension caused by mutations in the beta subunit of the epithelial sodium channel

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Molecular pathogenesis of pseudohypoaldosteronism type II: generation and analysis of a Wnk4(D561A/+) knockin mouse model

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The Cullin 3 substrate adaptor KLHL20 mediates DAPK ubiquitination to control interferon responses

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Dietary salt regulates the phosphorylation of OSR1/SPAK kinases and the sodium chloride cotransporter through aldosterone

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Mutations in kelch-like 3 and cullin 3 cause hypertension and electrolyte abnormalities

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Wnk4 controls blood pressure and potassium homeostasis via regulation of mass and activity of the distal convoluted tubule

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

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The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hypertension

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Enhanced phosphorylation of Na(+)-Cl- co-transporter in experimental metabolic syndrome: role of insulin

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Phenotypic and genetic heterogeneity of familial hyperkalaemic hypertension (Gordon syndrome).

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Disease-causing mutant WNK4 increases paracellular chloride permeability and phosphorylates claudins

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

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Activation of the renal Na+:Cl- cotransporter by angiotensin II is a WNK4-dependent process

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

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Ubiquitin ligase activity of Cul3-KLHL7 protein is attenuated by autosomal dominant retinitis pigmentosa causative mutation

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WNK1 regulates phosphorylation of cation-chloride-coupled cotransporters via the STE20-related kinases, SPAK and OSR1.

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PDZ-RhoGEF ubiquitination by Cullin3-KLHL20 controls neurotrophin-induced neurite outgrowth

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Kelch-like homologue 9 mutation is associated with an early onset autosomal dominant distal myopathy

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Targeted disruption of the Wnk4 gene decreases phosphorylation of Na-Cl cotransporter, increases Na excretion and lowers blood pressure

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Downregulation of NCC and NKCC2 cotransporters by kidney-specific WNK1 revealed by gene disruption and transgenic mouse models

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Simple and highly efficient BAC recombineering using galK selection

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Vasopressin-stimulated chloride transport in transimmortalized mouse cell lines derived from the distal convoluted tubule and cortical and inner medullary collecting ducts.

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Human hypertension caused by mutations in WNK kinases

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Constitutive turnover of cyclin E by Cul3 maintains quiescence

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Characterization of the kinase activity of a WNK4 protein complex

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Regulation of the renal Na+-Cl- cotransporter by phosphorylation and ubiquitylation

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A new method for measurement of blood pressure, heart rate, and activity in the mouse by radiotelemetry

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The WNKs: atypical protein kinases with pleiotropic actions.

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Syndrome of hypertension and hyperkalemia with normal glomerular filtration rate

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Epithelial sodium channel: mendelian versus essential hypertension

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WNK1 regulates vasoconstriction and blood pressure response to α 1-adrenergic stimulation in mice

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WNK kinases regulate thiazide-sensitive Na-Cl cotransport

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Mechanisms of WNK1 and WNK4 interaction in the regulation of thiazide-sensitive NaCl cotransport

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A minor role of WNK3 in regulating phosphorylation of renal NKCC2 and NCC co-transporters in vivo

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Phenotypes of pseudohypoaldosteronism type II caused by the WNK4 D561A missense mutation are dependent on the WNK-OSR1/SPAK kinase cascade.

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Acute insulin stimulation induces phosphorylation of the Na-Cl cotransporter in cultured distal mpkDCT cells and mouse kidney

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Dietary electrolyte-driven responses in the renal WNK kinase pathway in vivo.

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SPAK-knockout mice manifest Gitelman syndrome and impaired vasoconstriction

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