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10.1155/2015/362768 http://scihub22266oqcxt.onion/10.1155/2015/362768 C4609835!4609835 !26508816     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26508816 &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 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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\26508816 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mediators+Inflamm 2015 ; 2015 (ä): 362768 Nephropedia Template TP {{tp|p=26508816 |t=2015. Proinflammatory Cytokines and Potassium Channels in the Kidney |pdf=|usr=}}{{26508816 }} gab.com Text Proinflammatory Cytokines and Potassium Channels in the Kidney JO: Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26508816 #FOAvip Proinflammatory cytokines affect several cell functions via receptor-mediated processes. In the kidney, functions of transporters and ion channels along the nephron are also affected by some cytokines. Among these, alteration of activity of potassium ion (K(+)) channels induces changes in transepithelial transport of solutes and water in the kidney, since K(+) channels in tubule cells are indispensable for formation of membrane potential which serves as a driving force for the transepithelial transport. Altered K(+) channel activity may be involved in renal cell dysfunction during inflammation. Although little information was available regarding the effects of proinflammatory cytokines on renal K(+) channels, reports have emerged during the last decade. In human proximal tubule cells, interferon-? showed a time-dependent biphasic effect on a 40?pS K(+) channel, that is, delayed suppression and acute stimulation, and interleukin-1? acutely suppressed the channel activity. Transforming growth factor-?1 activated KCa3.1 K(+) channel in immortalized human proximal tubule cells, which would be involved in the pathogenesis of renal fibrosis. This review discusses the effects of proinflammatory cytokines on renal K(+) channels and the causal relationship between the cytokine-induced changes in K(+) channel activity and renal dysfunction. Twit Text FOAVip Proinflammatory Cytokines and Potassium Channels in the Kidney ????Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26508816 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26508816 #FOAvip English Wikipedia <ref>{{Cite pmid|26508816 }}</ref> Proinflammatory Cytokines and Potassium Channels in the Kidney #MMPMID26508816 Nakamura K ; Hayashi H ; Kubokawa M Mediators Inflamm 2015[]; 2015 (ä): 362768 PMID26508816 show ga Proinflammatory cytokines affect several cell functions via receptor-mediated processes. In the kidney, functions of transporters and ion channels along the nephron are also affected by some cytokines. Among these, alteration of activity of potassium ion (K(+)) channels induces changes in transepithelial transport of solutes and water in the kidney, since K(+) channels in tubule cells are indispensable for formation of membrane potential which serves as a driving force for the transepithelial transport. Altered K(+) channel activity may be involved in renal cell dysfunction during inflammation. Although little information was available regarding the effects of proinflammatory cytokines on renal K(+) channels, reports have emerged during the last decade. In human proximal tubule cells, interferon-? showed a time-dependent biphasic effect on a 40?pS K(+) channel, that is, delayed suppression and acute stimulation, and interleukin-1? acutely suppressed the channel activity. Transforming growth factor-?1 activated KCa3.1 K(+) channel in immortalized human proximal tubule cells, which would be involved in the pathogenesis of renal fibrosis. This review discusses the effects of proinflammatory cytokines on renal K(+) channels and the causal relationship between the cytokine-induced changes in K(+) channel activity and renal dysfunction. |Animals [MESH] |Biological Transport [MESH] |Cytokines/*metabolism [MESH] |Fibrosis/pathology [MESH] |Humans [MESH] |Inflammation/*metabolism [MESH] |Kidney Tubules/metabolism [MESH] |Kidney/*metabolism/pathology [MESH] |Mice [MESH] |Potassium Channels/*metabolism [MESH] |Potassium/chemistry [MESH]Proinflammatory Cytokines and Potassium Channels in the Kidney (epmc).pdf DeepDyve Pubget Overpricing