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10.1186/s12860-016-0093-9 http://scihub22266oqcxt.onion/10.1186/s12860-016-0093-9 C4896244!4896244!27229147     free     free     free       BMC+Cell+Biol 2016 ; 17 (Suppl 1): ä Nephropedia Template TP {{tp|p=27229147|t=2016. Connexins: substrates and regulators of autophagy |pdf=|usr=}}{{27229147}} gab.com Text Connexins: substrates and regulators of autophagy JO: BMC Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27229147 #FOAvip Connexins mediate intercellular communication by assembling into hexameric channel complexes that act as hemichannels and gap junction channels. Most connexins are characterized by a very rapid turn-over in a variety of cell systems. The regulation of connexin turn-over by phosphorylation and ubiquitination events has been well documented. Moreover, different pathways have been implicated in connexin degradation, including proteasomal and lysosomal-based pathways. Only recently, autophagy emerged as an important connexin-degradation pathway for different connexin isoforms. As such, conditions well known to induce autophagy have an immediate impact on the connexin-expression levels. This is not only limited to experimental conditions but also several pathophysiological conditions associated with autophagy (dys)function affect connexin levels and their presence at the cell surface as gap junctions. Finally, connexins are not only substrates of autophagy but also emerge as regulators of the autophagy process. In particular, several connexin isoforms appear to recruit pre-autophagosomal autophagy-related proteins, including Atg16 and PI3K-complex components, to the plasma membrane, thereby limiting their availability and capacity for regulating autophagy. Twit Text FOAVip Connexins: substrates and regulators of autophagy ????BMC Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27229147 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27229147 #FOAvip English Wikipedia <ref>{{Cite pmid|27229147}}</ref> Connexins: substrates and regulators of autophagy #MMPMID27229147 Iyyathurai J; Decuypere JP; Leybaert L; D?hondt C; Bultynck G BMC Cell Biol 2016[]; 17 (Suppl 1): ä PMID27229147show ga Connexins mediate intercellular communication by assembling into hexameric channel complexes that act as hemichannels and gap junction channels. Most connexins are characterized by a very rapid turn-over in a variety of cell systems. The regulation of connexin turn-over by phosphorylation and ubiquitination events has been well documented. Moreover, different pathways have been implicated in connexin degradation, including proteasomal and lysosomal-based pathways. Only recently, autophagy emerged as an important connexin-degradation pathway for different connexin isoforms. As such, conditions well known to induce autophagy have an immediate impact on the connexin-expression levels. This is not only limited to experimental conditions but also several pathophysiological conditions associated with autophagy (dys)function affect connexin levels and their presence at the cell surface as gap junctions. Finally, connexins are not only substrates of autophagy but also emerge as regulators of the autophagy process. In particular, several connexin isoforms appear to recruit pre-autophagosomal autophagy-related proteins, including Atg16 and PI3K-complex components, to the plasma membrane, thereby limiting their availability and capacity for regulating autophagy. äConnexins: substrates and regulators of autophagy (epmc).pdf DeepDyve Pubget Overpricing