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10.1038/ncomms14577 http://scihub22266oqcxt.onion/10.1038/ncomms14577 C5333130!5333130!28233855     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=28233855|t=2017. Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus |pdf=|usr=}}{{28233855}} gab.com Text Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28233855 #FOAvip NF-E2-related factor-2 (Nrf2) regulates cellular responses to oxidative and electrophilic stress. Loss of Keap1 increases Nrf2 protein levels, and Keap1-null mice die of oesophageal hyperkeratosis because of Nrf2 hyperactivation. Here we show that deletion of oesophageal Nrf2 in Keap1-null mice allows survival until adulthood, but the animals develop polyuria with low osmolality and bilateral hydronephrosis. This phenotype is caused by defects in water reabsorption that are the result of reduced aquaporin 2 levels in the kidney. Renal tubular deletion of Keap1 promotes nephrogenic diabetes insipidus features, confirming that Nrf2 activation in developing tubular cells causes a water reabsorption defect. These findings suggest that Nrf2 activity should be tightly controlled during development in order to maintain renal homeostasis. In addition, tissue-specific ablation of Nrf2 in Keap1-null mice might create useful animal models to uncover novel physiological functions of Nrf2. Twit Text FOAVip Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=28233855 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28233855 #FOAvip English Wikipedia <ref>{{Cite pmid|28233855}}</ref> Hyperactivation of Nrf2 in early tubular development induces nephrogenic diabetes insipidus #MMPMID28233855 Suzuki T; Seki S; Hiramoto K; Naganuma E; Kobayashi EH; Yamaoka A; Baird L; Takahashi N; Sato H; Yamamoto M Nat Commun 2017[]; 8 (ä): ä PMID28233855show ga NF-E2-related factor-2 (Nrf2) regulates cellular responses to oxidative and electrophilic stress. Loss of Keap1 increases Nrf2 protein levels, and Keap1-null mice die of oesophageal hyperkeratosis because of Nrf2 hyperactivation. Here we show that deletion of oesophageal Nrf2 in Keap1-null mice allows survival until adulthood, but the animals develop polyuria with low osmolality and bilateral hydronephrosis. This phenotype is caused by defects in water reabsorption that are the result of reduced aquaporin 2 levels in the kidney. Renal tubular deletion of Keap1 promotes nephrogenic diabetes insipidus features, confirming that Nrf2 activation in developing tubular cells causes a water reabsorption defect. These findings suggest that Nrf2 activity should be tightly controlled during development in order to maintain renal homeostasis. In addition, tissue-specific ablation of Nrf2 in Keap1-null mice might create useful animal models to uncover novel physiological functions of Nrf2. äHyperactivation of Nrf2 in early tubular development induces nephrogen(epmc).pdf DeepDyve Pubget Overpricing