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10.1152/ajprenal.00577.2015 http://scihub22266oqcxt.onion/10.1152/ajprenal.00577.2015 26792067!5002062!26792067     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Physiol+Renal+Physiol 2016 ; 310 (10): F923-30 Nephropedia Template TP {{tp|p=26792067|t=2016. New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule |pdf=|usr=}}{{26792067}} gab.com Text New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26792067 #FOAvip Since its identification as the underlying molecular cause of Bartter's syndrome type 3, ClC-Kb (ClC-K2 in rodents, henceforth it will be referred as ClC-Kb/2) is proposed to play an important role in systemic electrolyte balance and blood pressure regulation by controlling basolateral Cl(-) exit in the distal renal tubular segments from the cortical thick ascending limb to the outer medullary collecting duct. Considerable experimental and clinical effort has been devoted to the identification and characterization of disease-causing mutations as well as control of the channel by its cofactor, barttin. However, we have only begun to unravel the role of ClC-Kb/2 in different tubular segments and to reveal the regulators of its expression and function, e.g., insulin and IGF-1. In this review we discuss recent experimental evidence in this regard and highlight unexplored questions critical to understanding ClC-Kb/2 physiology in the kidney. Twit Text FOAVip New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=26792067 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26792067 #FOAvip English Wikipedia <ref>{{Cite pmid|26792067}}</ref> New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal tubule #MMPMID26792067 Zaika O; Tomilin V; Mamenko M; Bhalla V; Pochynyuk O Am J Physiol Renal Physiol 2016[May]; 310 (10): F923-30 PMID26792067show ga Since its identification as the underlying molecular cause of Bartter's syndrome type 3, ClC-Kb (ClC-K2 in rodents, henceforth it will be referred as ClC-Kb/2) is proposed to play an important role in systemic electrolyte balance and blood pressure regulation by controlling basolateral Cl(-) exit in the distal renal tubular segments from the cortical thick ascending limb to the outer medullary collecting duct. Considerable experimental and clinical effort has been devoted to the identification and characterization of disease-causing mutations as well as control of the channel by its cofactor, barttin. However, we have only begun to unravel the role of ClC-Kb/2 in different tubular segments and to reveal the regulators of its expression and function, e.g., insulin and IGF-1. In this review we discuss recent experimental evidence in this regard and highlight unexplored questions critical to understanding ClC-Kb/2 physiology in the kidney. |Animals[MESH] |Bartter Syndrome/genetics[MESH] |Chloride Channels/genetics/*metabolism[MESH] |Humans[MESH] |Insulin-Like Growth Factor I/metabolism[MESH] |Insulin/metabolism[MESH] |Kidney Tubules, Collecting/metabolism[MESH]New perspective of ClC-Kb/2 Cl- channel physiology in the distal renal(epmc).pdf DeepDyve Pubget Overpricing