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10.4161/19336950.2014.949190 http://scihub22266oqcxt.onion/10.4161/19336950.2014.949190 C4594590!4594590 !25483587     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25483587 &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 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25483587 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Channels+(Austin) 2014 ; 8 (5 ): 444-51 Nephropedia Template TP {{tp|p=25483587 |t=2014. Feedback inhibition of ENaC: acute and chronic mechanisms |pdf=|usr=}}{{25483587 }} gab.com Text Feedback inhibition of ENaC: acute and chronic mechanisms JO: Channels (Austin) http://www.kidney.de/pget.php?&tw=1&pmid=25483587 #FOAvip Intracellular [Na(+)] ([Na(+)]i) modulates the activity of the epithelial Na channel (ENaC) to help prevent cell swelling and regulate epithelial Na(+) transport, but the underlying mechanisms remain unclear. We show here that short-term (60-80 min) incubation of ENaC-expressing oocytes in high Na(+) results in a 75% decrease in channel activity. When the ? subunit was truncated, corresponding to a gain-of-function mutation found in Liddle's syndrome, the same maneuver reduced activity by 45% despite a larger increase in [Na(+)]i. In both cases the inhibition occurred with little to no change in cell-surface expression of ?ENaC. Long-term incubation (18 hours) in high Na(+) reduced activity by 92% and 75% in wild-type channels and Liddle's mutant, respectively, with concomitant 70% and 52% decreases in cell-surface ?ENaC. In the presence of Brefeldin A to inhibit forward protein trafficking, high-Na(+) incubation decreased wt ENaC activity by 52% and 88% after 4 and 8 hour incubations, respectively. Cleaved ?ENaC at the cell surface had lifetimes at the surface of 6 hrs in low Na(+) and 4 hrs in high Na(+), suggesting that [Na(+)]i increased the rate of retrieval of cleaved ? ENaC by 50%. This implies that enhanced retrieval of ENaC channels at the cell surface accounts for part, but not all, of the downregulation of ENaC activity shown with chronic increases in [Na(+)]i. Twit Text FOAVip Feedback inhibition of ENaC: acute and chronic mechanisms ????Channels (Austin) http://www.kidney.de/pget.php?&tw=1&pmid=25483587 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25483587 #FOAvip English Wikipedia <ref>{{Cite pmid|25483587 }}</ref> Feedback inhibition of ENaC: acute and chronic mechanisms #MMPMID25483587 Patel AB ; Yang L ; Deng S ; Palmer LG Channels (Austin) 2014[]; 8 (5 ): 444-51 PMID25483587 show ga Intracellular [Na(+)] ([Na(+)]i) modulates the activity of the epithelial Na channel (ENaC) to help prevent cell swelling and regulate epithelial Na(+) transport, but the underlying mechanisms remain unclear. We show here that short-term (60-80 min) incubation of ENaC-expressing oocytes in high Na(+) results in a 75% decrease in channel activity. When the ? subunit was truncated, corresponding to a gain-of-function mutation found in Liddle's syndrome, the same maneuver reduced activity by 45% despite a larger increase in [Na(+)]i. In both cases the inhibition occurred with little to no change in cell-surface expression of ?ENaC. Long-term incubation (18 hours) in high Na(+) reduced activity by 92% and 75% in wild-type channels and Liddle's mutant, respectively, with concomitant 70% and 52% decreases in cell-surface ?ENaC. In the presence of Brefeldin A to inhibit forward protein trafficking, high-Na(+) incubation decreased wt ENaC activity by 52% and 88% after 4 and 8 hour incubations, respectively. Cleaved ?ENaC at the cell surface had lifetimes at the surface of 6 hrs in low Na(+) and 4 hrs in high Na(+), suggesting that [Na(+)]i increased the rate of retrieval of cleaved ? ENaC by 50%. This implies that enhanced retrieval of ENaC channels at the cell surface accounts for part, but not all, of the downregulation of ENaC activity shown with chronic increases in [Na(+)]i. |Animals [MESH] |Dose-Response Relationship, Drug [MESH] |Epithelial Sodium Channel Blockers/pharmacology [MESH] |Epithelial Sodium Channels/genetics/*metabolism [MESH] |Feedback, Physiological/*drug effects [MESH] |Oocytes/drug effects/metabolism [MESH] |Sodium/*pharmacology [MESH] |Structure-Activity Relationship [MESH]Feedback inhibition of ENaC: acute and chronic mechanisms (epmc).pdf DeepDyve Pubget Overpricing