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10.1074/jbc.M115.707877 http://scihub22266oqcxt.onion/10.1074/jbc.M115.707877 C4777858!4777858!26728465     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 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       J+Biol+Chem 2016 ; 291 (10): 5259-69 Nephropedia Template TP {{tp|p=26728465|t=2016. Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion* |pdf=|usr=}}{{26728465}} gab.com Text Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion* JO: J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=26728465 #FOAvip Romk knock-out mice show a similar phenotype to Bartter syndrome of salt wasting and dehydration due to reduced Na-K-2Cl-cotransporter activity. At least three ROMK isoforms have been identified in the kidney; however, unique functions of any of the isoforms in nephron segments are still poorly understood. We have generated a mouse deficient only in Romk1 by selective deletion of the Romk1-specific first exon using an ES cell Cre-LoxP strategy and examined the renal phenotypes, ion transporter expression, ROMK channel activity, and localization under normal and high K intake. Unlike Romk?/? mice, there was no Bartter phenotype with reduced NKCC2 activity and increased NCC expression in Romk1?/? mice. The small conductance K channel (SK) activity showed no difference of channel properties or gating in the collecting tubule between Romk1+/+ and Romk1?/? mice. High K intake increased SK channel number per patch and increased the ROMK channel intensity in the apical membrane of the collecting tubule in Romk1+/+, but such regulation by high K intake was diminished with significant hyperkalemia in Romk1?/? mice. We conclude that 1) animal knockouts of ROMK1 do not produce Bartter phenotype. 2) There is no functional linking of ROMK1 and NKCC2 in the TAL. 3) ROMK1 is critical in response to high K intake-stimulated K+ secretion in the collecting tubule. Twit Text FOAVip Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion* ????J Biol Chem http://www.kidney.de/pget.php?&tw=1&pmid=26728465 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26728465 #FOAvip English Wikipedia <ref>{{Cite pmid|26728465}}</ref> Romk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impaired K Excretion* #MMPMID26728465 Dong K; Yan Q; Lu M; Wan L; Hu H; Guo J; Boulpaep E; Wang W; Giebisch G; Hebert SC; Wang T J Biol Chem 2016[Mar]; 291 (10): 5259-69 PMID26728465show ga Romk knock-out mice show a similar phenotype to Bartter syndrome of salt wasting and dehydration due to reduced Na-K-2Cl-cotransporter activity. At least three ROMK isoforms have been identified in the kidney; however, unique functions of any of the isoforms in nephron segments are still poorly understood. We have generated a mouse deficient only in Romk1 by selective deletion of the Romk1-specific first exon using an ES cell Cre-LoxP strategy and examined the renal phenotypes, ion transporter expression, ROMK channel activity, and localization under normal and high K intake. Unlike Romk?/? mice, there was no Bartter phenotype with reduced NKCC2 activity and increased NCC expression in Romk1?/? mice. The small conductance K channel (SK) activity showed no difference of channel properties or gating in the collecting tubule between Romk1+/+ and Romk1?/? mice. High K intake increased SK channel number per patch and increased the ROMK channel intensity in the apical membrane of the collecting tubule in Romk1+/+, but such regulation by high K intake was diminished with significant hyperkalemia in Romk1?/? mice. We conclude that 1) animal knockouts of ROMK1 do not produce Bartter phenotype. 2) There is no functional linking of ROMK1 and NKCC2 in the TAL. 3) ROMK1 is critical in response to high K intake-stimulated K+ secretion in the collecting tubule. äRomk1 Knockout Mice Do Not Produce Bartter Phenotype but Exhibit Impai(epmc).pdf DeepDyve Pubget Overpricing