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dc.contributor.authorDas, Madhumita
dc.contributor.authorJiang, Feng
dc.contributor.authorSluss, Hayla Karen
dc.contributor.authorZhang, Chao
dc.contributor.authorShokat, Kevan M.
dc.contributor.authorFlavell, Richard A.
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:09:33.000
dc.date.accessioned2022-08-23T16:35:06Z
dc.date.available2022-08-23T16:35:06Z
dc.date.issued2007-10-02
dc.date.submitted2009-03-16
dc.identifier.citationProc Natl Acad Sci U S A. 2007 Oct 2;104(40):15759-64. Epub 2007 Sep 24. <a href="http://dx.doi.org/10.1073/pnas.0707782104">Link to article on publisher's site</a>
dc.identifier.issn0027-8424 (Print)
dc.identifier.doi10.1073/pnas.0707782104
dc.identifier.pmid17893331
dc.identifier.urihttp://hdl.handle.net/20.500.14038/38481
dc.description.abstractThe JNK signaling pathway is implicated in the regulation of the AP1 transcription factor and cell proliferation. Here, we examine the role of JNK by using conditional and chemical genetic alleles of the ubiquitously expressed murine genes that encode the isoforms JNK1 and JNK2. Our analysis demonstrates that JNK is not essential for proliferation. However, JNK is required for expression of the cJun and JunD components of the AP1 transcription factor, and JNK-deficient cells exhibit early p53-dependent senescence. These data demonstrate that JNK can act as a negative regulator of the p53 tumor suppressor.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=17893331&dopt=Abstract">Link to Article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1073/pnas.0707782104
dc.rights<p>Publisher PDF posted as allowed by the publisher's author rights policy at http://www.pnas.org/site/aboutpnas/authorfaq.xhtml.</p>
dc.subjectAP1
dc.subjectcJun
dc.subjectcell cycle
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titleSuppression of p53-dependent senescence by the JNK signal transduction pathway
dc.typeJournal Article
dc.source.journaltitleProceedings of the National Academy of Sciences of the United States of America
dc.source.volume104
dc.source.issue40
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=2353&amp;context=oapubs&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/oapubs/1354
dc.identifier.contextkey783036
refterms.dateFOA2022-08-23T16:35:06Z
html.description.abstract<p>The JNK signaling pathway is implicated in the regulation of the AP1 transcription factor and cell proliferation. Here, we examine the role of JNK by using conditional and chemical genetic alleles of the ubiquitously expressed murine genes that encode the isoforms JNK1 and JNK2. Our analysis demonstrates that JNK is not essential for proliferation. However, JNK is required for expression of the cJun and JunD components of the AP1 transcription factor, and JNK-deficient cells exhibit early p53-dependent senescence. These data demonstrate that JNK can act as a negative regulator of the p53 tumor suppressor.</p>
dc.identifier.submissionpathoapubs/1354
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages15759-64


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