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10.1016/j.mcn.2015.03.010 http://scihub22266oqcxt.onion/10.1016/j.mcn.2015.03.010 C4449833!4449833!25771431     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mol+Cell+Neurosci 2015 ; 66 (0 0): 53-61 Nephropedia Template TP {{tp|p=25771431|t=2015. Autophagy in Polyglutamine Disease: Imposing Order on Disorder or Contributing to the Chaos?|pdf=|usr=}}{{25771431}} gab.com Text Autophagy in Polyglutamine Disease: Imposing Order on Disorder or Contributing to the Chaos JO: Mol Cell Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25771431 #FOAvip Autophagy is an essential, fundamentally important catabolic pathway in which double membrane-bound vesicles form in the cytosol and encircle macromolecules and organelles to permit their degradation after fusion with lysosomes. More than a decade of research has revealed that autophagy is required for normal central nervous system (CNS) function and plays a central role in maintaining protein and organelle quality controls in neurons. Neurodegenerative diseases occur when misfolded proteins accumulate and disrupt normal cellular processes, and autophagy has emerged as a key arbiter of the cell?s homeostatic response to this threat. One class of inherited neurodegenerative disease is known as the CAG / polyglutamine repeat disorders, and these diseases all result from the expansion of a CAG repeat tract in the coding regions of distinct genes. Polyglutamine (polyQ) repeat diseases result in the production polyQ-expanded proteins that misfold to form inclusions or aggregates that challenge the main cellular proteostasis system of the cell, the ubiquitin proteasome system (UPS). The UPS cannot efficiently degrade polyQ-expanded disease proteins, and components of the UPS are enriched in polyQ disease aggregate bodies found in degenerating neurons. In addition to components of the UPS, polyQ protein cytosolic aggregates co-localize with key autophagy proteins, even in autophagy deficient cells, suggesting that they probably do not reflect the formation of autophagosomes but rather the sequestration of key autophagy components. Furthermore, recent evidence now implicates polyQ proteins in the regulation of the autophagy pathway itself. Thus, a complex model emerges where polyQ proteins play a dual role as both autophagy substrates and autophagy offenders. In this review, we consider the role of autophagy in polyQ disorders and the therapeutic potential for autophagy modulation in these diseases. Twit Text FOAVip Autophagy in Polyglutamine Disease: Imposing Order on Disorder or Contributing to the Chaos ????Mol Cell Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=25771431 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25771431 #FOAvip English Wikipedia <ref>{{Cite pmid|25771431}}</ref> Autophagy in Polyglutamine Disease: Imposing Order on Disorder or Contributing to the Chaos? #MMPMID25771431 Cortes CJ; La Spada AR Mol Cell Neurosci 2015[May]; 66 (0 0): 53-61 PMID25771431show ga Autophagy is an essential, fundamentally important catabolic pathway in which double membrane-bound vesicles form in the cytosol and encircle macromolecules and organelles to permit their degradation after fusion with lysosomes. More than a decade of research has revealed that autophagy is required for normal central nervous system (CNS) function and plays a central role in maintaining protein and organelle quality controls in neurons. Neurodegenerative diseases occur when misfolded proteins accumulate and disrupt normal cellular processes, and autophagy has emerged as a key arbiter of the cell?s homeostatic response to this threat. One class of inherited neurodegenerative disease is known as the CAG / polyglutamine repeat disorders, and these diseases all result from the expansion of a CAG repeat tract in the coding regions of distinct genes. Polyglutamine (polyQ) repeat diseases result in the production polyQ-expanded proteins that misfold to form inclusions or aggregates that challenge the main cellular proteostasis system of the cell, the ubiquitin proteasome system (UPS). The UPS cannot efficiently degrade polyQ-expanded disease proteins, and components of the UPS are enriched in polyQ disease aggregate bodies found in degenerating neurons. In addition to components of the UPS, polyQ protein cytosolic aggregates co-localize with key autophagy proteins, even in autophagy deficient cells, suggesting that they probably do not reflect the formation of autophagosomes but rather the sequestration of key autophagy components. Furthermore, recent evidence now implicates polyQ proteins in the regulation of the autophagy pathway itself. Thus, a complex model emerges where polyQ proteins play a dual role as both autophagy substrates and autophagy offenders. In this review, we consider the role of autophagy in polyQ disorders and the therapeutic potential for autophagy modulation in these diseases. äAutophagy in Polyglutamine Disease: Imposing Order on Disorder or Cont(epmc).pdf DeepDyve Pubget Overpricing