Uncompensated polyuria in a mouse model of Bartter's syndrome - Wikidata - wikimedia - TriplyDB

Uncompensated polyuria in a mouse model of Bartter's syndrome

Uncompensated polyuria in a mouse model of Bartter's syndrome

http://www.wikidata.org/entity/Q30454291

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Molecular regulation of NKCC2 in the thick ascending limb Physiology of SLC12 transporters: lessons from inherited human genetic mutations and genetically engineered mouse knockouts Functional properties of the apical Na+-K+-2Cl- cotransporter isoforms Analysis of double knockout mice lacking aquaporin-1 and urea transporter UT-B. Evidence for UT-B-facilitated water transport in erythrocytes Adenylyl cyclase 6 enhances NKCC2 expression and mediates vasopressin-induced phosphorylation of NKCC2 and NCC Renal effects of Tamm-Horsfall protein (uromodulin) deficiency in mice Thick ascending limb: the Na(+):K (+):2Cl (-) co-transporter, NKCC2, and the calcium-sensing receptor, CaSR Differential regulation of NFAT5 by NKCC2 isoforms in medullary thick ascending limb (mTAL) cells Kidney-targeted Birt-Hogg-Dube gene inactivation in a mouse model: Erk1/2 and Akt-mTOR activation, cell hyperproliferation, and polycystic kidneys Activity of the renal Na+-K+-2Cl- cotransporter is reduced by mutagenesis of N-glycosylation sites: role for protein surface charge in Cl- transport Compensation of proximal tubule malabsorption in AQP1-deficient mice without TGF-mediated reduction of GFR Absence of small conductance K+ channel (SK) activity in apical membranes of thick ascending limb and cortical collecting duct in ROMK (Bartter's) knockout mice Erythrocyte water permeability and renal function in double knockout mice lacking aquaporin-1 and aquaporin-3 Common variants in CLDN14 are associated with differential excretion of magnesium over calcium in urine.Fate of Renin Cells During Development and Disease.Investigation and identification of etiologies involved in the development of acquired hydronephrosis in aged laboratory mice with the use of high-frequency ultrasound imaging.The divergence, actions, roles, and relatives of sodium-coupled bicarbonate transporters Standardized, systemic phenotypic analysis of Slc12a1I299F mutant mice.An in vivo model for gastric physiological and pathophysiological studies in the mouse.A role for VAMP8/endobrevin in surface deployment of the water channel aquaporin 2 mTORC1 maintains renal tubular homeostasis and is essential in response to ischemic stress.Differential regulation of the bumetanide-sensitive cotransporter (NKCC2) by ovarian hormones.Sodium transport deficiency and sodium balance in gene-targeted mice.Molecular mechanisms of cation transport by the renal Na+-K+-Cl- cotransporter: structural insight into the operating characteristics of the ion transport sites.A modest decrease in endothelial NOS in mice comparable to that associated with human NOS3 variants exacerbates diabetic nephropathy Identification of SPRED2 (sprouty-related protein with EVH1 domain 2) as a negative regulator of the hypothalamic-pituitary-adrenal axis.Chloride channels in the kidney: lessons learned from knockout animals.Tumor necrosis factor-alpha is an endogenous inhibitor of Na+-K+-2Cl- cotransporter (NKCC2) isoform A in the thick ascending limb.Impaired phosphorylation of Na(+)-K(+)-2Cl(-) cotransporter by oxidative stress-responsive kinase-1 deficiency manifests hypotension and Bartter-like syndrome Eicosanoids and tumor necrosis factor-alpha in the kidney.The role of cyclooxygenases and prostanoid receptorsin furosemide-like salt losing tubulopathy: the hyperprostaglandin E syndrome.The impact of alternative splicing in vivo: mouse models show the way.Links between dietary salt intake, renal salt handling, blood pressure, and cardiovascular diseases.Salt handling in the distal nephron: lessons learned from inherited human disorders.A missense mutation in solute carrier family 12, member 1 (SLC12A1) causes hydrallantois in Japanese Black cattle Molecular targets that link dioxin exposure to toxicity phenotypes.Hypertension, kidney, and transgenics: a fresh perspective.Novel insights regarding the operational characteristics and teleological purpose of the renal Na+-K+-Cl2 cotransporter (NKCC2s) splice variants.NKCC2A and NFAT5 regulate renal TNF production induced by hypertonic NaCl intake.WNK1 protein kinase regulates embryonic cardiovascular development through the OSR1 signaling cascade.

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P2860

Uncompensated polyuria in a mouse model of Bartter's syndrome

http://www.wikidata.org/entity/Q30454291

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2000 nî lūn-bûn

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2000 թուականի Մայիսին հրատարակուած գիտական յօդուած

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2000 թվականի մայիսին հրատարակված գիտական հոդված

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2000年の論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年論文

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2000年论文

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name

Uncompensated polyuria in a mouse model of Bartter's syndrome

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Uncompensated polyuria in a mouse model of Bartter's syndrome

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type

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Uncompensated polyuria in a mouse model of Bartter's syndrome

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Uncompensated polyuria in a mouse model of Bartter's syndrome

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prefLabel

Uncompensated polyuria in a mouse model of Bartter's syndrome

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Uncompensated polyuria in a mouse model of Bartter's syndrome

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

P1476

Uncompensated polyuria in a mouse model of Bartter's syndrome

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P2093

D R Chernavvsky

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H J Gitelman

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N Takahashi

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R A Gomez

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P2860

Bartter's syndrome, hypokalaemic alkalosis with hypercalciuria, is caused by mutations in the Na-K-2Cl cotransporter NKCC2

Mutations in the chloride channel gene, CLCNKB, cause Bartter's syndrome type III

Fibroblast growth factor receptor 3 is a negative regulator of bone growth

Germ-line transmission of a planned alteration made in a hypoxanthine phosphoribosyltransferase gene by homologous recombination in embryonic stem cells

Hyperplasia of the juxtaglomerular complex with hyperaldosteronism and hypokalemic alkalosis. A new syndrome

A new familial disorder characterized by hypokalemia and hypomagnesemia

Molecular cloning, primary structure, and characterization of two members of the mammalian electroneutral sodium-(potassium)-chloride cotransporter family expressed in kidney

Homeostasis in mice with genetically decreased angiotensinogen is primarily by an increased number of renin-producing cells

Ion transport mechanisms in thick ascending limb of Henle's loop of mammalian nephron

Renin and angiotensinogen gene expression and intrarenal renin distribution during ACE inhibition.

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10

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97

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Oliver Smithies

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12536316

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25846

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