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10.1073/pnas.1414004111 http://scihub22266oqcxt.onion/10.1073/pnas.1414004111 C4273402!4273402!25453086     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Proc+Natl+Acad+Sci+U+S+A 2014 ; 111 (50): 17809-14 Nephropedia Template TP {{tp|p=25453086|t=2014. Self-assembled FUS binds active chromatin and regulates gene transcription |pdf=|usr=}}{{25453086}} gab.com Text Self-assembled FUS binds active chromatin and regulates gene transcription JO: Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25453086 #FOAvip Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder and mutations in fused in sarcoma (FUS) cause a subset of familial ALS. Mutant FUS forms cytoplasmic inclusions, but it is unclear whether loss of FUS function in the nucleus or toxicity gained in the cytoplasm is more critical in the ALS etiology. The physiological function of FUS is also uncharacterized. We found that a significant portion of FUS was bound to active chromatin and that ALS mutations dramatically reduced FUS chromatin binding. A high order FUS assembly is mediated by the N-terminal QGSY (glutamine-glycine-serine-tyrosine)-rich region and is required for FUS chromatin binding and the transcription activation by FUS. ALS mutations in FUS can cause its loss of function in the nucleus by disrupting this assembly and chromatin binding. Twit Text FOAVip Self-assembled FUS binds active chromatin and regulates gene transcription ????Proc Natl Acad Sci U S A http://www.kidney.de/pget.php?&tw=1&pmid=25453086 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25453086 #FOAvip English Wikipedia <ref>{{Cite pmid|25453086}}</ref> Self-assembled FUS binds active chromatin and regulates gene transcription #MMPMID25453086 Yang L; Gal J; Chen J; Zhu H Proc Natl Acad Sci U S A 2014[Dec]; 111 (50): 17809-14 PMID25453086show ga Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder and mutations in fused in sarcoma (FUS) cause a subset of familial ALS. Mutant FUS forms cytoplasmic inclusions, but it is unclear whether loss of FUS function in the nucleus or toxicity gained in the cytoplasm is more critical in the ALS etiology. The physiological function of FUS is also uncharacterized. We found that a significant portion of FUS was bound to active chromatin and that ALS mutations dramatically reduced FUS chromatin binding. A high order FUS assembly is mediated by the N-terminal QGSY (glutamine-glycine-serine-tyrosine)-rich region and is required for FUS chromatin binding and the transcription activation by FUS. ALS mutations in FUS can cause its loss of function in the nucleus by disrupting this assembly and chromatin binding. äSelf-assembled FUS binds active chromatin and regulates gene transcrip(epmc).pdf DeepDyve Pubget Overpricing