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dc.contributor.authorTajima, Kenen_US
dc.contributor.authorYae, Toshifumien_US
dc.contributor.authorJavaid, Sarahen_US
dc.contributor.authorTam, Oliveren_US
dc.contributor.authorComaills, Valentineen_US
dc.contributor.authorMorris, Roberten_US
dc.contributor.authorWittner, Ben S.en_US
dc.contributor.authorLiu, Mingzhuen_US
dc.contributor.authorEngstrom, Amandaen_US
dc.contributor.authorTakahashi, Fumiyukien_US
dc.contributor.authorBlack, Joshua C.en_US
dc.contributor.authorRamaswamy, Sridharen_US
dc.contributor.authorShioda, Toshihiroen_US
dc.contributor.authorHammell, Mollyen_US
dc.contributor.authorHaber, Daniel A.en_US
dc.contributor.authorWhetstine, Johnathan R.en_US
dc.contributor.authorMaheswaran, Shyamalaen_US
dc.date.accessioned2016-01-04T19:23:31Z
dc.date.issued2015en_US
dc.identifier.citationTajima, K., T. Yae, S. Javaid, O. Tam, V. Comaills, R. Morris, B. S. Wittner, et al. 2015. “SETD1A modulates cell cycle progression through a miRNA network that regulates p53 target genes.” Nature Communications 6 (1): 8257. doi:10.1038/ncomms9257. http://dx.doi.org/10.1038/ncomms9257.en
dc.identifier.issn2041-1723en
dc.identifier.urihttp://nrs.harvard.edu/urn-3:HUL.InstRepos:23993555
dc.description.abstractExpression of the p53-inducible antiproliferative gene BTG2 is suppressed in many cancers in the absence of inactivating gene mutations, suggesting alternative mechanisms of silencing. Using a shRNA screen targeting 43 histone lysine methyltransferases (KMTs), we show that SETD1A suppresses BTG2 expression through its induction of several BTG2-targeting miRNAs. This indirect but highly specific mechanism, by which a chromatin regulator that mediates transcriptional activating marks can lead to the downregulation of a critical effector gene, is shared with multiple genes in the p53 pathway. Through such miRNA-dependent effects, SETD1A regulates cell cycle progression in vitro and modulates tumorigenesis in mouse xenograft models. Together, these observations help explain the remarkably specific genetic consequences associated with alterations in generic chromatin modulators in cancer.en
dc.language.isoen_USen
dc.publisherNature Pub. Groupen
dc.relation.isversionofdoi:10.1038/ncomms9257en
dc.relation.hasversionhttp://www.ncbi.nlm.nih.gov/pmc/articles/PMC4667427/pdf/en
dash.licenseLAAen_US
dc.titleSETD1A modulates cell cycle progression through a miRNA network that regulates p53 target genesen
dc.typeJournal Articleen_US
dc.description.versionVersion of Recorden
dc.relation.journalNature Communicationsen
dash.depositing.authorYae, Toshifumien_US
dc.date.available2016-01-04T19:23:31Z
dc.identifier.doi10.1038/ncomms9257*
dash.authorsorderedfalse
dash.contributor.affiliatedYae, Toshifumi
dash.contributor.affiliatedComaills, Valentine
dash.contributor.affiliatedMorris, Robert
dash.contributor.affiliatedWittner, Ben
dash.contributor.affiliatedHaber, Daniel
dash.contributor.affiliatedWhetstine, Johnathan
dash.contributor.affiliatedRamaswamy, Sridhar
dash.contributor.affiliatedShioda, Toshihiro
dash.contributor.affiliatedMaheswaran, Shyamala


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