A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism - Wikidata - awgldk - TriplyDB

A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

http://www.wikidata.org/entity/Q36611582

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Role of the UPS in Liddle syndrome Modulation of epithelial sodium channel (ENaC) expression in mouse lung infected with Pseudomonas aeruginosa Embryonic epithelial membrane transporters Ethanol alters alveolar fluid balance via Nadph oxidase (NOX) signaling to epithelial sodium channels (ENaC) in the lung Compensation of proximal tubule malabsorption in AQP1-deficient mice without TGF-mediated reduction of GFR Af17 deficiency increases sodium excretion and decreases blood pressure Salt restriction induces pseudohypoaldosteronism type 1 in mice expressing low levels of the beta-subunit of the amiloride-sensitive epithelial sodium channel Mice heterozygous for beta-ENaC deletion have defective potassium excretion.Functional expression of a pseudohypoaldosteronism type I mutated epithelial Na+ channel lacking the pore-forming region of its alpha subunit.Amiloride-sensitive sodium channels contribute to the woes of the flu.Impaired renal Na(+) retention in the sgk1-knockout mouse.ERp29 regulates epithelial sodium channel functional expression by promoting channel cleavage.Sodium transport deficiency and sodium balance in gene-targeted mice.Expression and role of serum and glucocorticoid-regulated kinase 2 in the regulation of Na+/H+ exchanger 3 in the mammalian kidney.UT-A urea transporter promoter, UT-Aalpha, targets principal cells of the renal inner medullary collecting duct.Voltage-dependent gating underlies loss of ENaC function in Pseudohypoaldosteronism type 1.Disruption of the beta subunit of the epithelial Na+ channel in mice: hyperkalemia and neonatal death associated with a pseudohypoaldosteronism phenotype.H-Ras mediates the inhibitory effect of epidermal growth factor on the epithelial Na+ channel Collecting duct-specific gene inactivation of alphaENaC in the mouse kidney does not impair sodium and potassium balance.A nonconventional look at ionic fluxes in the skin: lessons from genetically modified mice.GPR48 increases mineralocorticoid receptor gene expression.Nadph oxidase regulates alveolar epithelial sodium channel activity and lung fluid balance in vivo via O⁻₂ signaling Role of Sgk1 in salt and potassium homeostasis.SGK1: a rapid aldosterone-induced regulator of renal sodium reabsorption.Ion channels in renal disease.Hypertension, kidney, and transgenics: a fresh perspective.RNA interference for CFTR attenuates lung fluid absorption at birth in rats.Role of gammaENaC subunit in lung liquid clearance and electrolyte balance in newborn mice. Insights into perinatal adaptation and pseudohypoaldosteronism.The kinase Grk2 regulates Nedd4/Nedd4-2-dependent control of epithelial Na+ channels.Activation of the epithelial Na+ channel in the collecting duct by vasopressin contributes to water reabsorption.Renal acid-base regulation: new insights from animal models.The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.Development and Diseases of the Collecting Duct System.Tetracycline-inducible gene expression in cultured rat renal CD cells and in intact CD from transgenic mice.Pseudohypoaldosteronism type 1 and Liddle's syndrome mutations that affect the single-channel properties of the epithelial Na+ channel.Restoration of Epithelial Sodium Channel Function by Synthetic Peptides in Pseudohypoaldosteronism Type 1B Mutants.Selected contribution: limiting Na(+) transport rate in airway epithelia from alpha-ENaC transgenic mice: a model for pulmonary edema.Pseudohypoaldosteronism type 1 and respiratory distress syndrome.Chronic hyperaldosteronism in a transgenic mouse model fails to induce cardiac remodeling and fibrosis under a normal-salt diet.Defective respiratory amiloride-sensitive sodium transport predisposes to pulmonary oedema and delays its resolution in mice.

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P2860

A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

http://www.wikidata.org/entity/Q36611582

description

1997 nî lūn-bûn

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年論文

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1997年论文

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1997年论文

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1997年论文

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name

A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

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A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

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type

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A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

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A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

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prefLabel

A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

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A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

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Proceedings of the National Academy of Sciences of the United States of America

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A mouse model for the renal salt-wasting syndrome pseudohypoaldosteronism

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B C Rossier

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B Grubb

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C Talbot

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C Verdumo

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E Hummler

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F Beermann

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J D Horisberger

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J Gatzy

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M Burnier

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P Barker

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P2860

A mutation causing pseudohypoaldosteronism type 1 identifies a conserved glycine that is involved in the gating of the epithelial sodium channel

A salt wasting syndrome in infancy

Amiloride-sensitive epithelial Na+ channel is made of three homologous subunits

Epithelial sodium channel related to proteins involved in neurodegeneration

Mutations in subunits of the epithelial sodium channel cause salt wasting with hyperkalaemic acidosis, pseudohypoaldosteronism type 1

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

Targeted disruption of the glucocorticoid receptor gene blocks adrenergic chromaffin cell development and severely retards lung maturation

A mutation in the epithelial sodium channel causing Liddle disease increases channel activity in the Xenopus laevis oocyte expression system.

Regulation of Na channels of the rat cortical collecting tubule by aldosterone.

Regulation of expression of the lung amiloride-sensitive Na+ channel by steroid hormones.

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