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10.1083/jcb.201512016 http://scihub22266oqcxt.onion/10.1083/jcb.201512016 C5021092!5021092!27597756     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 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+Biol 2016 ; 214 (6): 705-18 Nephropedia Template TP {{tp|p=27597756|t=2016. Munc18-1 is a molecular chaperone for ?-synuclein, controlling its self-replicating aggregation |pdf=|usr=}}{{27597756}} gab.com Text Munc18-1 is a molecular chaperone for -synuclein, controlling its self-replicating aggregation JO: J Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27597756 #FOAvip Munc18-1 heterozygous mutations are associated with developmental diseases, including early infantile epileptic encephalopathy (EIEE). Chai et al. report that Munc18-1 acts as a chaperone for ?-synuclein and controls its aggregative propensity. Munc18-1 EIEE-associated mutations promote the aggregation of endogenous ?-synuclein in neurons, leading to a neurodegenerative phenotype. Twit Text FOAVip Munc18-1 is a molecular chaperone for -synuclein, controlling its self-replicating aggregation ????J Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=27597756 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27597756 #FOAvip English Wikipedia <ref>{{Cite pmid|27597756}}</ref> Munc18-1 is a molecular chaperone for ?-synuclein, controlling its self-replicating aggregation #MMPMID27597756 Chai YJ; Sierecki E; Tomatis VM; Gormal RS; Giles N; Morrow IC; Xia D; Götz J; Parton RG; Collins BM; Gambin Y; Meunier FA J Cell Biol 2016[Sep]; 214 (6): 705-18 PMID27597756show ga Munc18-1 heterozygous mutations are associated with developmental diseases, including early infantile epileptic encephalopathy (EIEE). Chai et al. report that Munc18-1 acts as a chaperone for ?-synuclein and controls its aggregative propensity. Munc18-1 EIEE-associated mutations promote the aggregation of endogenous ?-synuclein in neurons, leading to a neurodegenerative phenotype. äMunc18-1 is a molecular chaperone for ?-synuclein, controlling its sel(epmc).pdf DeepDyve Pubget Overpricing