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10.3389/fnins.2017.00145 http://scihub22266oqcxt.onion/10.3389/fnins.2017.00145 C5362620!5362620 !28386214     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 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28386214 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Front+Neurosci 2017 ; 11 (ä): 145 Nephropedia Template TP {{tp|p=28386214 |t=2017. Chaperones in Polyglutamine Aggregation: Beyond the Q-Stretch |pdf=|usr=}}{{28386214 }} gab.com Text Chaperones in Polyglutamine Aggregation: Beyond the Q-Stretch JO: Front Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=28386214 #FOAvip Expanded polyglutamine (polyQ) stretches in at least nine unrelated proteins lead to inherited neuronal dysfunction and degeneration. The expansion size in all diseases correlates with age at onset (AO) of disease and with polyQ protein aggregation, indicating that the expanded polyQ stretch is the main driving force for the disease onset. Interestingly, there is marked interpatient variability in expansion thresholds for a given disease. Between different polyQ diseases the repeat length vs. AO also indicates the existence of modulatory effects on aggregation of the upstream and downstream amino acid sequences flanking the Q expansion. This can be either due to intrinsic modulation of aggregation by the flanking regions, or due to differential interaction with other proteins, such as the components of the cellular protein quality control network. Indeed, several lines of evidence suggest that molecular chaperones have impact on the handling of different polyQ proteins. Here, we review factors differentially influencing polyQ aggregation: the Q-stretch itself, modulatory flanking sequences, interaction partners, cleavage of polyQ-containing proteins, and post-translational modifications, with a special focus on the role of molecular chaperones. By discussing typical examples of how these factors influence aggregation, we provide more insight on the variability of AO between different diseases as well as within the same polyQ disorder, on the molecular level. Twit Text FOAVip Chaperones in Polyglutamine Aggregation: Beyond the Q-Stretch ????Front Neurosci http://www.kidney.de/pget.php?&tw=1&pmid=28386214 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28386214 #FOAvip English Wikipedia <ref>{{Cite pmid|28386214 }}</ref> Chaperones in Polyglutamine Aggregation: Beyond the Q-Stretch #MMPMID28386214 Kuiper EF ; de Mattos EP ; Jardim LB ; Kampinga HH ; Bergink S Front Neurosci 2017[]; 11 (ä): 145 PMID28386214 show ga Expanded polyglutamine (polyQ) stretches in at least nine unrelated proteins lead to inherited neuronal dysfunction and degeneration. The expansion size in all diseases correlates with age at onset (AO) of disease and with polyQ protein aggregation, indicating that the expanded polyQ stretch is the main driving force for the disease onset. Interestingly, there is marked interpatient variability in expansion thresholds for a given disease. Between different polyQ diseases the repeat length vs. AO also indicates the existence of modulatory effects on aggregation of the upstream and downstream amino acid sequences flanking the Q expansion. This can be either due to intrinsic modulation of aggregation by the flanking regions, or due to differential interaction with other proteins, such as the components of the cellular protein quality control network. Indeed, several lines of evidence suggest that molecular chaperones have impact on the handling of different polyQ proteins. Here, we review factors differentially influencing polyQ aggregation: the Q-stretch itself, modulatory flanking sequences, interaction partners, cleavage of polyQ-containing proteins, and post-translational modifications, with a special focus on the role of molecular chaperones. By discussing typical examples of how these factors influence aggregation, we provide more insight on the variability of AO between different diseases as well as within the same polyQ disorder, on the molecular level. äChaperones in Polyglutamine Aggregation: Beyond the Q-Stretch (epmc).pdf DeepDyve Pubget Overpricing