Pathogenesis and treatment of autosomal-dominant nephrogenic diabetes insipidus caused by an aquaporin 2 mutation. - Wikidata - awgldk - TriplyDB

Pathogenesis and treatment of autosomal-dominant nephrogenic diabetes insipidus caused by an aquaporin 2 mutation.

Pathogenesis and treatment of autosomal-dominant nephrogenic diabetes insipidus caused by an aquaporin 2 mutation.

http://www.wikidata.org/entity/Q35080543

about

The Trafficking of the Water Channel Aquaporin-2 in Renal Principal Cells-a Potential Target for Pharmacological Intervention in Cardiovascular Diseases The renal channelopathies A novel therapeutic effect of statins on nephrogenic diabetes insipidus Protein trafficking defects in inherited kidney diseases Nephrogenic diabetes insipidus in mice caused by deleting COOH-terminal tail of aquaporin-2.KLF4-dependent epigenetic remodeling modulates podocyte phenotypes and attenuates proteinuria Acute insulin stimulation induces phosphorylation of the Na-Cl cotransporter in cultured distal mpkDCT cells and mouse kidney.High-throughput chemical screening identifies AG-490 as a stimulator of aquaporin 2 membrane expression and urine concentration WNK4 is the major WNK positively regulating NCC in the mouse kidney Adenylate cyclase 6 determines cAMP formation and aquaporin-2 phosphorylation and trafficking in inner medulla.Aberrant glycosylation and localization of polycystin-1 cause polycystic kidney in an AQP11 knockout model.Aquaporin-2: new mutations responsible for autosomal-recessive nephrogenic diabetes insipidus-update and epidemiology.A minor role of WNK3 in regulating phosphorylation of renal NKCC2 and NCC co-transporters in vivo Regulation of transport in the connecting tubule and cortical collecting duct Generation and analysis of knock-in mice carrying pseudohypoaldosteronism type II-causing mutations in the cullin 3 gene.Nephrogenic diabetes insipidus: essential insights into the molecular background and potential therapies for treatment.Mouse models and the urinary concentrating mechanism in the new millennium.Hsp90 inhibitor partially corrects nephrogenic diabetes insipidus in a conditional knock-in mouse model of aquaporin-2 mutation.Physiology and pathophysiology of the vasopressin-regulated renal water reabsorption.Dissecting the roles of aquaporins in renal pathophysiology using transgenic mice.Congenital nephrogenic diabetes insipidus: what can we learn from mouse models?A selective EP4 PGE2 receptor agonist alleviates disease in a new mouse model of X-linked nephrogenic diabetes insipidus.Roflumilast and aquaporin-2 regulation in rat renal inner medullary collecting duct.Cell culture models and animal models for studying the patho-physiological role of renal aquaporins.Congenital nephrogenic diabetes insipidus: the current state of affairs.Urinary concentration: different ways to open and close the tap.Dynamic regulation and dysregulation of the water channel aquaporin-2: a common cause of and promising therapeutic target for water balance disorders.FAPP2 is required for aquaporin-2 apical sorting at trans-Golgi network in polarized MDCK cells.Function of the membrane water channel aquaporin-5 in the salivary gland KLHL3 Knockout Mice Reveal the Physiological Role of KLHL3 and the Pathophysiology of Pseudohypoaldosteronism Type II Caused by Mutant KLHL3.Pancreas-specific aquaporin 12 null mice showed increased susceptibility to caerulein-induced acute pancreatitis.Targeted disruption of the Wnk4 gene decreases phosphorylation of Na-Cl cotransporter, increases Na excretion and lowers blood pressure.Aquaporin Protein-Protein Interactions.Hereditary Nephrogenic Diabetes Insipidus: Pathophysiology and Possible Treatment. An Update.Dominant-negative suppression of big brain ion channel activity by mutation of a conserved glutamate in the first transmembrane domain.Plant and Mammal Aquaporins: Same but Different.Activation of AQP2 water channels without vasopressin: therapeutic strategies for congenital nephrogenic diabetes insipidus.Impaired degradation of WNK1 and WNK4 kinases causes PHAII in mutant KLHL3 knock-in mice.Generation and analyses of R8L barttin knockin mouse Progranulin Deficient Mice Develop Nephrogenic Diabetes Insipidus

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Pathogenesis and treatment of autosomal-dominant nephrogenic diabetes insipidus caused by an aquaporin 2 mutation.

http://www.wikidata.org/entity/Q35080543

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2006 nî lūn-bûn

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2006 թուականի Սեպտեմբերին հրատարակուած գիտական յօդուած

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

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Pathogenesis and treatment of ...... ed by an aquaporin 2 mutation.

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Akihiro Harada

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Eisei Sohara

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Keiko Uchida

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Kosaku Nitta

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Mayuko Ohno

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Sei Sasaki

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Shigeru Horita

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Shinichi Uchida

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Sung-Sen Yang

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Tatemitsu Rai

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P2860

Non-polarized targeting of AE1 causes autosomal dominant distal renal tubular acidosis

Vasopressin increases water permeability of kidney collecting duct by inducing translocation of aquaporin-CD water channels to plasma membrane

An aquaporin-2 water channel mutant which causes autosomal dominant nephrogenic diabetes insipidus is retained in the Golgi complex

Requirement of human renal water channel aquaporin-2 for vasopressin-dependent concentration of urine

A comparison of plasma vasopressin measurements with a standard indirect test in the differential diagnosis of polyuria

Heteroligomerization of an Aquaporin-2 mutant with wild-type Aquaporin-2 and their misrouting to late endosomes/lysosomes explains dominant nephrogenic diabetes insipidus.

Nephrogenic diabetes insipidus.

Three families with autosomal dominant nephrogenic diabetes insipidus caused by aquaporin-2 mutations in the C-terminus.

Severe urinary concentrating defect in renal collecting duct-selective AQP2 conditional-knockout mice.

Quantitative phosphoproteomics of vasopressin-sensitive renal cells: regulation of aquaporin-2 phosphorylation at two sites

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