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dc.contributor.authorTullai, John W.en_US
dc.contributor.authorTacheva, Silviaen_US
dc.contributor.authorOwens, Laura J.en_US
dc.contributor.authorGraham, Julie R.en_US
dc.contributor.authorCooper, Geoffrey M.en_US
dc.date.accessioned2020-05-06T20:10:12Z
dc.date.available2020-05-06T20:10:12Z
dc.date.issued2011-05-25
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000291006500030&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=6e74115fe3da270499c3d65c9b17d654
dc.identifier.citationJohn W Tullai, Silvia Tacheva, Laura J Owens, Julie R Graham, Geoffrey M Cooper. 2011. "AP-1 Is a Component of the Transcriptional Network Regulated by GSK-3 in Quiescent Cells." PLOS ONE, Volume 6, Issue 5. https://doi.org/10.1371/journal.pone.0020150
dc.identifier.issn1932-6203
dc.identifier.urihttps://hdl.handle.net/2144/40645
dc.description.abstractBACKGROUND: The protein kinase GSK-3 is constitutively active in quiescent cells in the absence of growth factor signaling. Previously, we identified a set of genes that required GSK-3 to maintain their repression during quiescence. Computational analysis of the upstream sequences of these genes predicted transcription factor binding sites for CREB, NFκB and AP-1. In our previous work, contributions of CREB and NFκB were examined. In the current study, the AP-1 component of the signaling network in quiescent cells was explored. METHODOLOGY/PRINCIPAL FINDINGS: Using chromatin immunoprecipitation analysis, two AP-1 family members, c-Jun and JunD, bound to predicted upstream regulatory sequences in 8 of the 12 GSK-3-regulated genes. c-Jun was phosphorylated on threonine 239 by GSK-3 in quiescent cells, consistent with previous studies demonstrating inhibition of c-Jun by GSK-3. Inhibition of GSK-3 attenuated this phosphorylation, resulting in the stabilization of c-Jun. The association of c-Jun with its target sequences was increased by growth factor stimulation as well as by direct GSK-3 inhibition. The physiological role for c-Jun was also confirmed by siRNA inhibition of gene induction. CONCLUSIONS/SIGNIFICANCE: These results indicate that inhibition of c-Jun by GSK-3 contributes to the repression of growth factor-inducible genes in quiescent cells. Together, AP-1, CREB and NFκB form an integrated transcriptional network that is largely responsible for maintaining repression of target genes downstream of GSK-3 signaling.en_US
dc.description.sponsorshipThis work was supported by the National Institutes of Health Grant R01 CA18689 (GMC) and by American Cancer Society Grant IRG-72-001-33-IRG (JWT). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. (R01 CA18689 - National Institutes of Health; IRG-72-001-33-IRG - American Cancer Society)en_US
dc.format.extent9 pagesen_US
dc.languageEnglish
dc.language.isoen_US
dc.publisherPUBLIC LIBRARY SCIENCEen_US
dc.relation.ispartofPLOS ONE
dc.rights© 2011 Tullai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.en_US
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/
dc.subjectScience & technologyen_US
dc.subjectAnimalsen_US
dc.subjectCell line, tumoren_US
dc.subjectCyclic AMP response element-binding proteinen_US
dc.subjectEnzyme stabilityen_US
dc.subjectGene regulatory networksen_US
dc.subjectGlycogen synthase kinase 3en_US
dc.subjectHumansen_US
dc.subjectIndolesen_US
dc.subjectJNK mitogen-activated protein kinasesen_US
dc.subjectMaleimidesen_US
dc.subjectMiceen_US
dc.subjectNF-kappa Ben_US
dc.subjectPhosphorylationen_US
dc.subjectProtein kinase inhibitorsen_US
dc.subjectProto-oncogene proteins c-Junen_US
dc.subjectRNA, small interferingen_US
dc.subjectResting phase, cell cycleen_US
dc.subjectTranscription factor AP-1en_US
dc.subjectTranscriptional activationen_US
dc.titleAP-1 is a component of the transcriptional network regulated by GSK-3 in quiescent cellsen_US
dc.typeArticleen_US
dc.identifier.doi10.1371/journal.pone.0020150
pubs.elements-sourceweb-of-scienceen_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Arts & Sciencesen_US
pubs.organisational-groupBoston University, College of Arts & Sciences, Department of Biologyen_US
pubs.publication-statusPublisheden_US
dc.identifier.mycv94446


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© 2011 Tullai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Except where otherwise noted, this item's license is described as © 2011 Tullai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.