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dc.contributor.author Lee, Jiwon -
dc.contributor.author Park, Eonyoung -
dc.contributor.author Kim, Ga Hye -
dc.contributor.author Kwon, Ilmin -
dc.contributor.author Kim, Kyungjin -
dc.date.accessioned 2019-01-16T15:00:06Z -
dc.date.available 2019-01-16T15:00:06Z -
dc.date.created 2018-12-20 -
dc.date.issued 2018-12 -
dc.identifier.citation Experimental and Molecular Medicine, v.50, no.12, pp.159 - 10 -
dc.identifier.issn 1226-3613 -
dc.identifier.uri http://hdl.handle.net/20.500.11750/9511 -
dc.description.abstract Bmal1 is one of the key molecules that controls the mammalian molecular clock. In humans, two isoforms of Bmal1 are generated by alternative RNA splicing. Unlike the extensively studied hBmal1b, the canonical form of Bmal1 in most species, the expression and/or function of another human-specific isoform, hBmal1a, are poorly understood. Due to the lack of the N-terminal nuclear localization signal (NLS), hBMAL1a does not enter the nucleus as hBMAL1b does. However, despite the lack of the NLS, hBMAL1a still dimerizes with either hCLOCK or hBMAL1b and thereby promotes cytoplasmic retention or protein degradation, respectively. Consequently, hBMAL1a interferes with hCLOCK: hBMAL1-binduced transcriptional activation and the circadian oscillation of Period2. Moreover, when the expression of endogenous hBmal1a is aborted by CRISPR/Cas9-mediated knockout, the rhythmic expression of hPer2 and hBmal1b is restored in cultured HeLa cells. Together, these results suggest a role for hBMAL1a as a negative regulator of the mammalian molecular clock. © The Author(s) 2018 -
dc.language English -
dc.publisher 생화학분자생물학회 -
dc.title A splice variant of human Bmal1 acts as a negative regulator of the molecular circadian clock -
dc.type Article -
dc.identifier.doi 10.1038/s12276-018-0187-x -
dc.identifier.wosid 000452306600001 -
dc.identifier.scopusid 2-s2.0-85058602094 -
dc.type.local Article(Overseas) -
dc.type.rims ART -
dc.description.journalClass 1 -
dc.citation.publicationname Experimental and Molecular Medicine -
dc.identifier.kciid ART002415128 -
dc.contributor.nonIdAuthor Lee, Jiwon -
dc.contributor.nonIdAuthor Park, Eonyoung -
dc.contributor.nonIdAuthor Kim, Ga Hye -
dc.contributor.nonIdAuthor Kwon, Ilmin -
dc.contributor.nonIdAuthor Kim, Kyungjin -
dc.identifier.citationVolume 50 -
dc.identifier.citationNumber 12 -
dc.identifier.citationStartPage 159 -
dc.identifier.citationEndPage 10 -
dc.identifier.citationTitle Experimental and Molecular Medicine -
dc.type.journalArticle Article -
dc.description.isOpenAccess Y -
dc.subject.keywordPlus TRANSCRIPTION FACTOR -
dc.subject.keywordPlus PROTEIN -
dc.subject.keywordPlus TEMPERATURE -
dc.subject.keywordPlus EXPRESSION -
dc.subject.keywordPlus CELLS -
dc.subject.keywordPlus PHOSPHORYLATION -
dc.subject.keywordPlus VISUALIZATION -
dc.subject.keywordPlus DEGRADATION -
dc.subject.keywordPlus ACTIVATION -
dc.subject.keywordPlus MECHANISMS -
dc.contributor.affiliatedAuthor Lee, Jiwon -
dc.contributor.affiliatedAuthor Park, Eonyoung -
dc.contributor.affiliatedAuthor Kim, Ga Hye -
dc.contributor.affiliatedAuthor Kwon, Ilmin -
dc.contributor.affiliatedAuthor Kim, Kyungjin -
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