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10.1016/j.febslet.2014.01.049 http://scihub22266oqcxt.onion/10.1016/j.febslet.2014.01.049 C3989505!3989505!24508467     free     free     free 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 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       FEBS+Lett 2014 ; 588 (8): 1423-9 Nephropedia Template TP {{tp|p=24508467|t=2014. Specific Cx43 phosphorylation events regulate gap junction turnover in vivo |pdf=|usr=}}{{24508467}} gab.com Text Specific Cx43 phosphorylation events regulate gap junction turnover in vivo JO: FEBS Lett http://www.kidney.de/pget.php?&tw=1&pmid=24508467 #FOAvip Gap junctions, composed of proteins from the connexin gene family, are highly dynamic structures that are regulated by kinase-mediated signaling pathways and interactions with other proteins. Phosphorylation of Connexin43 (Cx43) at different sites controls gap junction assembly, gap junction size and gap junction turnover. Here we present a model describing how Akt, mitogen activated protein kinase (MAPK) and src kinase coordinate to regulate rapid turnover of gap junctions. Specifically, Akt phosphorylates Cx43 at S373 eliminating interaction with zona occludens-1 (ZO-1) allowing gap junctions to enlarge. Then MAPK and src phosphorylate Cx43 to initiate turnover. We integrate published data with new data to test and refine this model. Finally, we propose that differential coordination of kinase activation and Cx43 phosphorylation controls the specific routes of disassembly, e.g., annular junction formation or gap junctions can potentially ?unzip? and be internalized/endocytosed into the cell that produced each connexin. Twit Text FOAVip Specific Cx43 phosphorylation events regulate gap junction turnover in vivo ????FEBS Lett http://www.kidney.de/pget.php?&tw=1&pmid=24508467 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24508467 #FOAvip English Wikipedia <ref>{{Cite pmid|24508467}}</ref> Specific Cx43 phosphorylation events regulate gap junction turnover in vivo #MMPMID24508467 Solan JL; Lampe PD FEBS Lett 2014[Apr]; 588 (8): 1423-9 PMID24508467show ga Gap junctions, composed of proteins from the connexin gene family, are highly dynamic structures that are regulated by kinase-mediated signaling pathways and interactions with other proteins. Phosphorylation of Connexin43 (Cx43) at different sites controls gap junction assembly, gap junction size and gap junction turnover. Here we present a model describing how Akt, mitogen activated protein kinase (MAPK) and src kinase coordinate to regulate rapid turnover of gap junctions. Specifically, Akt phosphorylates Cx43 at S373 eliminating interaction with zona occludens-1 (ZO-1) allowing gap junctions to enlarge. Then MAPK and src phosphorylate Cx43 to initiate turnover. We integrate published data with new data to test and refine this model. Finally, we propose that differential coordination of kinase activation and Cx43 phosphorylation controls the specific routes of disassembly, e.g., annular junction formation or gap junctions can potentially ?unzip? and be internalized/endocytosed into the cell that produced each connexin. äSpecific Cx43 phosphorylation events regulate gap junction turnover in(epmc).pdf DeepDyve Pubget Overpricing