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10.1152/ajprenal.00112.2016 http://scihub22266oqcxt.onion/10.1152/ajprenal.00112.2016 C4967162!4967162!27122539     free     free     free Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 213.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 311 (1): F12-5 Nephropedia Template TP {{tp|p=27122539|t=2016. The expression, regulation, and function of Kir4 1 (Kcnj10) in the mammalian kidney |pdf=|usr=}}{{27122539}} gab.com Text The expression, regulation, and function of Kir4 1 (Kcnj10) in the mammalian kidney JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27122539 #FOAvip Kir4.1 is an inwardly rectifying potassium (K+) channel and is expressed in the brain, inner ear, and kidney. In the kidney, Kir4.1 is expressed in the basolateral membrane of the late thick ascending limb (TAL), the distal convoluted tubule (DCT), and the connecting tubule (CNT)/cortical collecting duct (CCD). It plays a role in K+ recycling across the basolateral membrane in corresponding nephron segments and in generating negative membrane potential. The renal phenotypes of the loss-function mutations of Kir4.1 include mild salt wasting, hypomagnesemia, hypokalemia, and metabolic alkalosis, suggesting that the disruption of Kir4.1 mainly impairs the transport in the DCT. Patch-clamp experiments and immunostaining demonstrate that Kir4.1 plays a predominant role in determining the basolateral K+ conductance in the DCT. However, the function of Kir4.1 in the TAL and CNT/CCD is not essential, because K+ channels other than Kir4.1 are also expressed. The downregulation of Kir4.1 in the DCT reduced basolateral chloride (Cl?) conductance, suppressed the expression of ste20 proline-alanine-rich kinase (SPAK), and decreased Na-Cl cotransporter (NCC) expression and activity. This suggests that Kir4.1 regulates NCC expression by the modulation of the Cl?-sensitive with-no-lysine kinase?SPAK pathway. Twit Text FOAVip The expression, regulation, and function of Kir4 1 (Kcnj10) in the mammalian kidney ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=27122539 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27122539 #FOAvip English Wikipedia <ref>{{Cite pmid|27122539}}</ref> The expression, regulation, and function of Kir4 1 (Kcnj10) in the mammalian kidney #MMPMID27122539 Su XT; Wang WH Am J Physiol Renal Physiol 2016[Jul]; 311 (1): F12-5 PMID27122539show ga Kir4.1 is an inwardly rectifying potassium (K+) channel and is expressed in the brain, inner ear, and kidney. In the kidney, Kir4.1 is expressed in the basolateral membrane of the late thick ascending limb (TAL), the distal convoluted tubule (DCT), and the connecting tubule (CNT)/cortical collecting duct (CCD). It plays a role in K+ recycling across the basolateral membrane in corresponding nephron segments and in generating negative membrane potential. The renal phenotypes of the loss-function mutations of Kir4.1 include mild salt wasting, hypomagnesemia, hypokalemia, and metabolic alkalosis, suggesting that the disruption of Kir4.1 mainly impairs the transport in the DCT. Patch-clamp experiments and immunostaining demonstrate that Kir4.1 plays a predominant role in determining the basolateral K+ conductance in the DCT. However, the function of Kir4.1 in the TAL and CNT/CCD is not essential, because K+ channels other than Kir4.1 are also expressed. The downregulation of Kir4.1 in the DCT reduced basolateral chloride (Cl?) conductance, suppressed the expression of ste20 proline-alanine-rich kinase (SPAK), and decreased Na-Cl cotransporter (NCC) expression and activity. This suggests that Kir4.1 regulates NCC expression by the modulation of the Cl?-sensitive with-no-lysine kinase?SPAK pathway. äThe expression, regulation, and function of Kir4 1 (Kcnj10) in the mam(epmc).pdf DeepDyve Pubget Overpricing