Daxx-mediated transcriptional repression of MMP1 gene is reversed by SPOP

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dc.contributor.authorLa, Mko
dc.contributor.authorKim, Kko
dc.contributor.authorPark, Jko
dc.contributor.authorWon, Jko
dc.contributor.authorLee, JHko
dc.contributor.authorFu, YMko
dc.contributor.authorMeadows, GGko
dc.contributor.authorJoe, Cheol Oko
dc.date.accessioned2013-03-04T14:14:36Z-
dc.date.available2013-03-04T14:14:36Z-
dc.date.created2012-02-06-
dc.date.created2012-02-06-
dc.date.issued2004-07-
dc.identifier.citationBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.320, no.3, pp.760 - 765-
dc.identifier.issn0006-291X-
dc.identifier.urihttp://hdl.handle.net/10203/82911-
dc.description.abstractDaxx-mediated transcriptional repression was modulated by a speckled POZ domain protein SPOP which was first identified as an autoantigen from the serum of a scleroderma patient. This is the first report on the biochemical and functional interactions between Daxx and SPOP. The COOH-terminal region of Daxx interacts with the NH2-terminal region of SPOP. SPOP reversed the transcriptional repression mediated by Daxx which binds with ETS1 transcription factor to repress ETS1-responsive gene expression. Mutagenesis study suggests that the ability of SPOP to self-associate as well as its ability to bind with Daxx was important for the modulation of Daxx-mediated transcriptional repression. (C) 2004 Elsevier Inc. All rights reserved.-
dc.languageEnglish-
dc.publisherACADEMIC PRESS INC ELSEVIER SCIENCE-
dc.subjectPROTEIN DAXX-
dc.subjectPML-
dc.subjectAPOPTOSIS-
dc.subjectDOMAINS-
dc.subjectSEQUESTRATION-
dc.subjectACTIVATION-
dc.subjectINTERACTS-
dc.subjectPATHWAY-
dc.subjectNUCLEUS-
dc.subjectFAMILY-
dc.titleDaxx-mediated transcriptional repression of MMP1 gene is reversed by SPOP-
dc.typeArticle-
dc.identifier.wosid000222723200020-
dc.identifier.scopusid2-s2.0-3042727940-
dc.type.rimsART-
dc.citation.volume320-
dc.citation.issue3-
dc.citation.beginningpage760-
dc.citation.endingpage765-
dc.citation.publicationnameBIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS-
dc.identifier.doi10.1016/j.bbrc.2004.06.022-
dc.contributor.localauthorJoe, Cheol O-
dc.contributor.nonIdAuthorLa, M-
dc.contributor.nonIdAuthorKim, K-
dc.contributor.nonIdAuthorPark, J-
dc.contributor.nonIdAuthorWon, J-
dc.contributor.nonIdAuthorLee, JH-
dc.contributor.nonIdAuthorFu, YM-
dc.contributor.nonIdAuthorMeadows, GG-
dc.type.journalArticleArticle-
dc.subject.keywordAuthorDaxx-
dc.subject.keywordAuthorETS1-
dc.subject.keywordAuthorMMP1-
dc.subject.keywordAuthorscleroderma-
dc.subject.keywordAuthorSPOP-
dc.subject.keywordPlusPROTEIN DAXX-
dc.subject.keywordPlusPML-
dc.subject.keywordPlusAPOPTOSIS-
dc.subject.keywordPlusDOMAINS-
dc.subject.keywordPlusSEQUESTRATION-
dc.subject.keywordPlusACTIVATION-
dc.subject.keywordPlusINTERACTS-
dc.subject.keywordPlusPATHWAY-
dc.subject.keywordPlusNUCLEUS-
dc.subject.keywordPlusFAMILY-
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