A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.
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Human Nedd4 interacts with the human epithelial Na+ channel: WW3 but not WW1 binds to Na+-channel subunitsThe Nedd4-like protein KIAA0439 is a potential regulator of the epithelial sodium channelIdentification of Murr1 as a regulator of the human delta epithelial sodium channelThe C2 domain of the ubiquitin protein ligase Nedd4 mediates Ca2+-dependent plasma membrane localizationA mutation causing pseudohypoaldosteronism type 1 identifies a conserved glycine that is involved in the gating of the epithelial sodium channelRegulation of stability and function of the epithelial Na+ channel (ENaC) by ubiquitination.Phosphorylation of Nedd4-2 by Sgk1 regulates epithelial Na(+) channel cell surface expressionLiddle disease caused by a missense mutation of beta subunit of the epithelial sodium channel geneIdentification of a PY motif in the epithelial Na channel subunits as a target sequence for mutations causing channel activation found in Liddle syndromeWW domains of Nedd4 bind to the proline-rich PY motifs in the epithelial Na+ channel deleted in Liddle's syndromeA de novo missense mutation of the beta subunit of the epithelial sodium channel causes hypertension and Liddle syndrome, identifying a proline-rich segment critical for regulation of channel activityCell surface expression of the epithelial Na channel and a mutant causing Liddle syndrome: a quantitative approachAn SGK1 site in WNK4 regulates Na+ channel and K+ channel activity and has implications for aldosterone signaling and K+ homeostasisInteraction of syntaxins with the amiloride-sensitive epithelial sodium channelAll three WW domains of murine Nedd4 are involved in the regulation of epithelial sodium channels by intracellular Na+ENaC subunit-subunit interactions and inhibition by syntaxin 1AA long isoform of the epithelial sodium channel alpha subunit forms a highly active channelRegulation of the epithelial sodium channel by N4WBP5A, a novel Nedd4/Nedd4-2-interacting proteinProgesterone down-regulates the open probability of the amiloride-sensitive epithelial sodium channel via a Nedd4-2-dependent mechanismImmunolocalization of the ubiquitin-protein ligase Nedd4 in tissues expressing the epithelial Na+ channel (ENaC)A human polymorphism affects NEDD4L subcellular targeting by leading to two isoforms that contain or lack a C2 domainEpithelial sodium channel regulated by aldosterone-induced protein sgk.Salt restriction induces pseudohypoaldosteronism type 1 in mice expressing low levels of the beta-subunit of the amiloride-sensitive epithelial sodium channel8-pCPT-cGMP stimulates alphabetagamma-ENaC activity in oocytes as an external ligand requiring specific nucleotide moietiesDefective regulation of the epithelial Na+ channel by Nedd4 in Liddle's syndrome.The heterotetrameric architecture of the epithelial sodium channel (ENaC).Genetic determinants of human hypertension.Hormonal hypertension in children: 11beta-hydroxylase deficiency and apparent mineralocorticoid excess.Gating of amiloride-sensitive Na(+) channels: subunit-subunit interactions and inhibition by the cystic fibrosis transmembrane conductance regulator.Genetics of hypertension: from experimental animals to humans.Purinergic inhibition of ENaC produces aldosterone escapeLiddle's syndrome mutations increase Na+ transport through dual effects on epithelial Na+ channel surface expression and proteolytic cleavage.Overexpression of the epithelial Na+ channel gamma subunit in collecting duct cells: interactions of Liddle's mutations and steroids on expression and function.Concerted action of ENaC, Nedd4-2, and Sgk1 in transepithelial Na(+) transport.Disruption of the beta subunit of the epithelial Na+ channel in mice: hyperkalemia and neonatal death associated with a pseudohypoaldosteronism phenotype.The expanding role of aldosterone in the regulation of body Na content.WNK4 regulates activity of the epithelial Na+ channel in vitro and in vivo.ENaCs and ASICs as therapeutic targets.Feedback inhibition of ENaC: acute and chronic mechanismsAcute downregulation of ENaC by EGF involves the PY motif and putative ERK phosphorylation site.
P2860
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P2860
A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.
description
1995 nî lūn-bûn
@nan
1995 թուականի Յունիսին հրատարակուած գիտական յօդուած
@hyw
1995 թվականի հունիսին հրատարակված գիտական հոդված
@hy
1995年の論文
@ja
1995年論文
@yue
1995年論文
@zh-hant
1995年論文
@zh-hk
1995年論文
@zh-mo
1995年論文
@zh-tw
1995年论文
@wuu
name
A mutation in the epithelial s ...... evis oocyte expression system.
@ast
A mutation in the epithelial s ...... evis oocyte expression system.
@en
A mutation in the epithelial s ...... evis oocyte expression system.
@nl
type
label
A mutation in the epithelial s ...... evis oocyte expression system.
@ast
A mutation in the epithelial s ...... evis oocyte expression system.
@en
A mutation in the epithelial s ...... evis oocyte expression system.
@nl
prefLabel
A mutation in the epithelial s ...... evis oocyte expression system.
@ast
A mutation in the epithelial s ...... evis oocyte expression system.
@en
A mutation in the epithelial s ...... evis oocyte expression system.
@nl
P2093
P2860
P356
P1476
A mutation in the epithelial s ...... evis oocyte expression system.
@en
P2093
P2860
P304
P356
10.1073/PNAS.92.12.5699
P407
P577
1995-06-01T00:00:00Z