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Cited 177 time in webofscience Cited 189 time in scopus
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dc.contributor.authorLee, Y-
dc.contributor.authorSamaco, RC-
dc.contributor.authorGatchel, JR-
dc.contributor.authorThaller, C-
dc.contributor.authorOrr, HT-
dc.contributor.authorZoghbi, HY-
dc.date.accessioned2016-03-31T09:15:44Z-
dc.date.available2016-03-31T09:15:44Z-
dc.date.created2012-02-06-
dc.date.issued2008-10-
dc.identifier.issn1097-6256-
dc.identifier.other2008-OAK-0000024642-
dc.identifier.urihttps://oasis.postech.ac.kr/handle/2014.oak/16909-
dc.description.abstractSpinocerebellar ataxia type 1 is caused by expansion of a translated CAG repeat in ataxin1 (ATXN1). The level of the polyglutamine-expanded protein is one of the factors that contributes to disease severity. Here we found that miR-19, miR-101 and miR-130 co-regulate ataxin1 levels and that their inhibition enhanced the cytotoxicity of polyglutamine-expanded ATXN1 in human cells. We provide a new candidate mechanism for modulating the pathogenesis of neurodegenerative diseases sensitive to protein dosage.-
dc.description.statementofresponsibilityX-
dc.languageEnglish-
dc.publishernature publishing group-
dc.relation.isPartOfNature Neuroscience-
dc.subjectSPINOCEREBELLAR ATAXIA TYPE-1-
dc.subjectTRANSGENIC MICE-
dc.subjectTRINUCLEOTIDE REPEAT-
dc.subjectNEURODEGENERATION-
dc.subjectEXPANSION-
dc.subjectMICRORNAS-
dc.subjectMODEL-
dc.titlemiR-19, miR-101 and miR-130 co-regulate ATXN1 levels to potentially modulate SCA1 pathogenesis-
dc.typeArticle-
dc.contributor.college생명과학과-
dc.identifier.doi10.1038/NN.2183-
dc.author.googleLee, Y-
dc.author.googleSamaco, RC-
dc.author.googleGatchel, JR-
dc.author.googleThaller, C-
dc.author.googleOrr, HT-
dc.author.googleZoghbi, HY-
dc.relation.volume11-
dc.relation.issue10-
dc.relation.startpage1137-
dc.relation.lastpage1139-
dc.contributor.id10143380-
dc.relation.journalNature Neuroscience-
dc.relation.indexSCI급, SCOPUS 등재논문-
dc.relation.sciSCI-
dc.collections.nameJournal Papers-
dc.type.rimsART-
dc.identifier.bibliographicCitationNature Neuroscience, v.11, no.10, pp.1137 - 1139-
dc.identifier.wosid000259528500007-
dc.date.tcdate2019-01-01-
dc.citation.endPage1139-
dc.citation.number10-
dc.citation.startPage1137-
dc.citation.titleNature Neuroscience-
dc.citation.volume11-
dc.contributor.affiliatedAuthorLee, Y-
dc.identifier.scopusid2-s2.0-52949137369-
dc.description.journalClass1-
dc.description.journalClass1-
dc.description.wostc145-
dc.description.scptc147*
dc.date.scptcdate2018-05-121*
dc.type.docTypeArticle-
dc.subject.keywordPlusSPINOCEREBELLAR ATAXIA TYPE-1-
dc.subject.keywordPlusTRANSGENIC MICE-
dc.subject.keywordPlusTRINUCLEOTIDE REPEAT-
dc.subject.keywordPlusNEURODEGENERATION-
dc.subject.keywordPlusEXPANSION-
dc.subject.keywordPlusMICRORNAS-
dc.subject.keywordPlusMODEL-
dc.relation.journalWebOfScienceCategoryNeurosciences-
dc.description.journalRegisteredClassscie-
dc.description.journalRegisteredClassscopus-
dc.relation.journalResearchAreaNeurosciences & Neurology-

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이윤태LEE, YOON TAE
Dept of Life Sciences
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