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10.1111/jcmm.12660 http://scihub22266oqcxt.onion/10.1111/jcmm.12660 C4687697!4687697!26404773     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       J+Cell+Mol+Med 2015 ; 19 (12): 2771-9 Nephropedia Template TP {{tp|p=26404773|t=2015. Inhibition of TRPC6 by protein kinase C isoforms in cultured human podocytes |pdf=|usr=}}{{26404773}} gab.com Text Inhibition of TRPC6 by protein kinase C isoforms in cultured human podocytes JO: J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26404773 #FOAvip Transient receptor potential canonical?6 (TRPC6) ion channels, expressed at high levels in podocytes of the filtration barrier, are recently implicated in the pathogenesis of various forms of proteinuric kidney diseases. Indeed, inherited or acquired up?regulation of TRPC6 activities are suggested to play a role in podocytopathies. Yet, we possess limited information about the regulation of TRPC6 in human podocytes. Therefore, in this study, we aimed at defining how the protein kinase C (PKC) system, one of the key intracellular signalling pathways, regulates TRPC6 function and expression. On human differentiated podocytes, we identified the molecular expressions of both TRPC6 and several PKC isoforms. We also showed that TRPC6 channels are functional since the TRPC6 activator 1?oleoyl?2?acetyl?sn?glycerol (OAG) induced Ca2+?influx to the cells. By assessing the regulatory roles of the PKCs, we found that inhibitors of the endogenous activities of classical and novel PKC isoforms markedly augmented TRPC6 activities. In contrast, activation of the PKC system by phorbol 12?myristate 13?acetate (PMA) exerted inhibitory actions on TRPC6 and suppressed its expression. Importantly, PMA treatment markedly down?regulated the expression levels of PKC?, PKC?, and PKC? reflecting their activation. Taken together, these results indicate that the PKC system exhibits a ?tonic? inhibition on TRPC6 activity in human podocytes suggesting that pathological conditions altering the expression and/or activation patterns of podocyte?expressed PKCs may influence TRPC6 activity and hence podocyte functions. Therefore, it is proposed that targeted manipulation of certain PKC isoforms might be beneficial in certain proteinuric kidney diseases with altered TRPC6 functions. Twit Text FOAVip Inhibition of TRPC6 by protein kinase C isoforms in cultured human podocytes ????J Cell Mol Med http://www.kidney.de/pget.php?&tw=1&pmid=26404773 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26404773 #FOAvip English Wikipedia <ref>{{Cite pmid|26404773}}</ref> Inhibition of TRPC6 by protein kinase C isoforms in cultured human podocytes #MMPMID26404773 Ambrus L; Oláh A; Oláh T; Balla G; Saleem MA; Orosz P; Zsuga J; Bíró K; Csernoch L; Bíró T; Szabó T J Cell Mol Med 2015[Dec]; 19 (12): 2771-9 PMID26404773show ga Transient receptor potential canonical?6 (TRPC6) ion channels, expressed at high levels in podocytes of the filtration barrier, are recently implicated in the pathogenesis of various forms of proteinuric kidney diseases. Indeed, inherited or acquired up?regulation of TRPC6 activities are suggested to play a role in podocytopathies. Yet, we possess limited information about the regulation of TRPC6 in human podocytes. Therefore, in this study, we aimed at defining how the protein kinase C (PKC) system, one of the key intracellular signalling pathways, regulates TRPC6 function and expression. On human differentiated podocytes, we identified the molecular expressions of both TRPC6 and several PKC isoforms. We also showed that TRPC6 channels are functional since the TRPC6 activator 1?oleoyl?2?acetyl?sn?glycerol (OAG) induced Ca2+?influx to the cells. By assessing the regulatory roles of the PKCs, we found that inhibitors of the endogenous activities of classical and novel PKC isoforms markedly augmented TRPC6 activities. In contrast, activation of the PKC system by phorbol 12?myristate 13?acetate (PMA) exerted inhibitory actions on TRPC6 and suppressed its expression. Importantly, PMA treatment markedly down?regulated the expression levels of PKC?, PKC?, and PKC? reflecting their activation. Taken together, these results indicate that the PKC system exhibits a ?tonic? inhibition on TRPC6 activity in human podocytes suggesting that pathological conditions altering the expression and/or activation patterns of podocyte?expressed PKCs may influence TRPC6 activity and hence podocyte functions. Therefore, it is proposed that targeted manipulation of certain PKC isoforms might be beneficial in certain proteinuric kidney diseases with altered TRPC6 functions. äInhibition of TRPC6 by protein kinase C isoforms in cultured human pod(epmc).pdf DeepDyve Pubget Overpricing