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10.1038/s41467-017-00689-z http://scihub22266oqcxt.onion/10.1038/s41467-017-00689-z C5662736!5662736!29084947     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 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 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Commun 2017 ; 8 (ä): ä Nephropedia Template TP {{tp|p=29084947|t=2017. Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease |pdf=|usr=}}{{29084947}} gab.com Text Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease JO: Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29084947 #FOAvip Autophagy-mediated degradation of synaptic components maintains synaptic homeostasis but also constitutes a mechanism of neurodegeneration. It is unclear how autophagy of synaptic vesicles and components of presynaptic active zones is regulated. Here, we show that Pleckstrin homology containing family member 5 (Plekhg5) modulates autophagy of synaptic vesicles in axon terminals of motoneurons via its function as a guanine exchange factor for Rab26, a small GTPase that specifically directs synaptic vesicles to preautophagosomal structures. Plekhg5 gene inactivation in mice results in a late-onset motoneuron disease, characterized by degeneration of axon terminals. Plekhg5-depleted cultured motoneurons show defective axon growth and impaired autophagy of synaptic vesicles, which can be rescued by constitutively active Rab26. These findings define a mechanism for regulating autophagy in neurons that specifically targets synaptic vesicles. Disruption of this mechanism may contribute to the pathophysiology of several forms of motoneuron disease. Twit Text FOAVip Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease ????Nat Commun http://www.kidney.de/pget.php?&tw=1&pmid=29084947 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=29084947 #FOAvip English Wikipedia <ref>{{Cite pmid|29084947}}</ref> Plekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic mechanism in motoneuron disease #MMPMID29084947 Lüningschrör P; Binotti B; Dombert B; Heimann P; Perez-Lara A; Slotta C; Thau-Habermann N; R. von Collenberg C; Karl F; Damme M; Horowitz A; Maystadt I; Füchtbauer A; Füchtbauer EM; Jablonka S; Blum R; Üçeyler N; Petri S; Kaltschmidt B; Jahn R; Kaltschmidt C; Sendtner M Nat Commun 2017[]; 8 (ä): ä PMID29084947show ga Autophagy-mediated degradation of synaptic components maintains synaptic homeostasis but also constitutes a mechanism of neurodegeneration. It is unclear how autophagy of synaptic vesicles and components of presynaptic active zones is regulated. Here, we show that Pleckstrin homology containing family member 5 (Plekhg5) modulates autophagy of synaptic vesicles in axon terminals of motoneurons via its function as a guanine exchange factor for Rab26, a small GTPase that specifically directs synaptic vesicles to preautophagosomal structures. Plekhg5 gene inactivation in mice results in a late-onset motoneuron disease, characterized by degeneration of axon terminals. Plekhg5-depleted cultured motoneurons show defective axon growth and impaired autophagy of synaptic vesicles, which can be rescued by constitutively active Rab26. These findings define a mechanism for regulating autophagy in neurons that specifically targets synaptic vesicles. Disruption of this mechanism may contribute to the pathophysiology of several forms of motoneuron disease. äPlekhg5-regulated autophagy of synaptic vesicles reveals a pathogenic (epmc).pdf DeepDyve Pubget Overpricing