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10.1097/MNH.0000000000000253 http://scihub22266oqcxt.onion/10.1097/MNH.0000000000000253 C4975530!4975530!27490784     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27490784&cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27490784.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Curr+Opin+Nephrol+Hypertens 2016 ; 25 (5): 424-8 Nephropedia Template TP {{tp|p=27490784|t=2016. Paracellular transport in the collecting duct |pdf=|usr=}}{{27490784}} gab.com Text Paracellular transport in the collecting duct JO: Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=27490784 #FOAvip Purpose of review: The paracellular pathway through the tight junction provides an important route for chloride reabsorption in the collecting duct of the kidney. This review describes recent findings of how defects in paracellular chloride permeation pathway may cause kidney diseases and how such a pathway may be regulated to maintain normal chloride homeostasis. Recent findings: The tight junction in the collecting duct expresses two important claudin genes ? claudin-4 and claudin-8. Transgenic knockout of either claudin gene causes hypotension, hypochloremia, and metabolic alkalosis in experimental animals. The claudin-4 mediated chloride permeability can be regulated by a protease endogenously expressed by the collecting duct cell ? Cap1. Cap1 regulates the intercellular interaction of claudin-4 and its membrane stability. KLHL3, previously identified as a causal gene for Gordon?s syndrome, also known as pseudohypoaldosteronism II (PHA-II), directly interacts with claudin-8 and regulates its ubiquitination and degradation. The dominant PHA-II mutation (R528H) in KLHL3 abolishes claudin-8 binding, ubiquitination, and degradation. Summary: The paracellular chloride permeation pathway in the kidney is an important but understudied area in nephrology. It plays vital roles in renal salt handling and regulation of extracellular fluid volume and blood pressure. Two claudin proteins ? claudin-4 and claudin-8 contribute to the function of this paracellular pathway. Deletion of either claudin protein from the collecting duct causes renal chloride reabsorption defects and low blood pressure. Claudins can be regulated on post-translational levels by several mechanisms involving protease and ubiquitin ligase. Deregulation of claudins may cause human hypertension as exemplified in the Gordon?s syndrome. Twit Text FOAVip Paracellular transport in the collecting duct ????Curr Opin Nephrol Hypertens http://www.kidney.de/pget.php?&tw=1&pmid=27490784 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27490784 #FOAvip English Wikipedia <ref>{{Cite pmid|27490784}}</ref> Paracellular transport in the collecting duct #MMPMID27490784 Hou J Curr Opin Nephrol Hypertens 2016[Sep]; 25 (5): 424-8 PMID27490784show ga Purpose of review: The paracellular pathway through the tight junction provides an important route for chloride reabsorption in the collecting duct of the kidney. This review describes recent findings of how defects in paracellular chloride permeation pathway may cause kidney diseases and how such a pathway may be regulated to maintain normal chloride homeostasis. Recent findings: The tight junction in the collecting duct expresses two important claudin genes ? claudin-4 and claudin-8. Transgenic knockout of either claudin gene causes hypotension, hypochloremia, and metabolic alkalosis in experimental animals. The claudin-4 mediated chloride permeability can be regulated by a protease endogenously expressed by the collecting duct cell ? Cap1. Cap1 regulates the intercellular interaction of claudin-4 and its membrane stability. KLHL3, previously identified as a causal gene for Gordon?s syndrome, also known as pseudohypoaldosteronism II (PHA-II), directly interacts with claudin-8 and regulates its ubiquitination and degradation. The dominant PHA-II mutation (R528H) in KLHL3 abolishes claudin-8 binding, ubiquitination, and degradation. Summary: The paracellular chloride permeation pathway in the kidney is an important but understudied area in nephrology. It plays vital roles in renal salt handling and regulation of extracellular fluid volume and blood pressure. Two claudin proteins ? claudin-4 and claudin-8 contribute to the function of this paracellular pathway. Deletion of either claudin protein from the collecting duct causes renal chloride reabsorption defects and low blood pressure. Claudins can be regulated on post-translational levels by several mechanisms involving protease and ubiquitin ligase. Deregulation of claudins may cause human hypertension as exemplified in the Gordon?s syndrome. �Paracellular transport in the collecting duct (epmc).pdf DeepDyve Pubget Overpricing