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dc.contributor.author Kim, Yoon Ha ko
dc.contributor.author Kim, EunSeon ko
dc.contributor.author Chung, Chang Geon ko
dc.contributor.author Lee, Sung-Bae ko
dc.date.accessioned 2021-08-26T05:55:31Z -
dc.date.available 2021-08-26T05:55:31Z -
dc.date.created 2019-06-10 -
dc.date.issued 2019-06-03 -
dc.identifier.citation 2019 생화학분자생물학회 정기학술대회 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/14437 -
dc.description.abstract G4C2 repeat expansion mutation of C9orf72 is the most common cause of familial amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). RNA G4C2 repeats produce 5 dipeptide repeat (DPR) proteins via repeat-associated non-ATG translation. Arginine-rich DPR proteins such as polyGly-Arg (GR) and polyPro-Arg (PR) are highly toxic and can perturb the dynamics and functions of various RNA binding proteins (RBPs). Recently, Staufen, a double-stranded RNA binding protein, was identified as one of the top interactors of poly (GR) and poly (PR), but the way in which Staufen mediates toxicity is currently unknown. Here, we show that poly (GR) and poly (PR) cause RNA-dependent nuclear accumulation of Staufen. Taken together, these data suggest that nuclear accumulation of Staufen may contribute to C9ALS/FTD pathogenesis. -
dc.language English -
dc.publisher 생화학분자생물학회 -
dc.title Increased accumulation of Staufen in nucleus contributes to C9ALS/FTD pathology -
dc.type Conference -
dc.type.local Article(Overseas) -
dc.type.rims CONF -
dc.description.journalClass 1 -
dc.contributor.localauthor Lee, Sung-Bae -
dc.identifier.citationTitle 2019 생화학분자생물학회 정기학술대회 -
dc.identifier.conferencecountry KO -
dc.identifier.conferencelocation 제주 국제컨벤션센터 -

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