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dc.contributor.authorGroisman, Irina
dc.contributor.authorIvshina, Maria
dc.contributor.authorMarin, Veronica
dc.contributor.authorKennedy, Norman J.
dc.contributor.authorDavis, Roger J.
dc.contributor.authorRichter, Joel D.
dc.date2022-08-11T08:08:58.000
dc.date.accessioned2022-08-23T16:14:00Z
dc.date.available2022-08-23T16:14:00Z
dc.date.issued2006-10-04
dc.date.submitted2008-09-17
dc.identifier.citationGenes Dev. 2006 Oct 1;20(19):2701-12. <a href="http://dx.doi.org/10.1101/gad.1438906">Link to article on publisher's site</a>
dc.identifier.issn0890-9369 (Print)
dc.identifier.doi10.1101/gad.1438906
dc.identifier.pmid17015432
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33757
dc.description.abstractCytoplasmic polyadenylation element-binding protein (CPEB) is a sequence-specific RNA-binding protein that promotes polyadenylation-induced translation. While a CPEB knockout (KO) mouse is sterile but overtly normal, embryo fibroblasts derived from this mouse (MEFs) do not enter senescence in culture as do wild-type MEFs, but instead are immortal. Exogenous CPEB restores senescence in the KO MEFs and also induces precocious senescence in wild-type MEFs. CPEB cannot stimulate senescence in MEFs lacking the tumor suppressors p53, p19ARF, or p16(INK4A); however, the mRNAs encoding these proteins are unlikely targets of CPEB since their expression is the same in wild-type and KO MEFs. Conversely, Ras cannot induce senescence in MEFs lacking CPEB, suggesting that it may lie upstream of CPEB. One target of CPEB regulation is myc mRNA, whose unregulated translation in the KO MEFs may cause them to bypass senescence. Thus, CPEB appears to act as a translational repressor protein to control myc translation and resulting cellular senescence.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17015432&dopt=Abstract">Link to article in PubMed</a>
dc.relation.urlhttp://dx.doi.org/10.1101/gad.1438906
dc.subjectAnimals; Blotting, Western; Cell Aging; Cell Cycle; Cell Cycle Proteins; Cells, Cultured; Cyclin-Dependent Kinase Inhibitor p16; Fibroblasts; Male; Mice; Mice, Knockout; Phosphorylation; Protein Binding; Protein Biosynthesis; Proto-Oncogene Proteins c-myc; RNA, Messenger; RNA-Binding Proteins; Tumor Suppressor Protein p14ARF; Tumor Suppressor Protein p53; mRNA Cleavage and Polyadenylation Factors
dc.subjectBiochemistry, Biophysics, and Structural Biology
dc.subjectCell and Developmental Biology
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleControl of cellular senescence by CPEB
dc.typeJournal Article
dc.source.journaltitleGenes and development
dc.source.volume20
dc.source.issue19
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/418
dc.identifier.contextkey632028
html.description.abstract<p>Cytoplasmic polyadenylation element-binding protein (CPEB) is a sequence-specific RNA-binding protein that promotes polyadenylation-induced translation. While a CPEB knockout (KO) mouse is sterile but overtly normal, embryo fibroblasts derived from this mouse (MEFs) do not enter senescence in culture as do wild-type MEFs, but instead are immortal. Exogenous CPEB restores senescence in the KO MEFs and also induces precocious senescence in wild-type MEFs. CPEB cannot stimulate senescence in MEFs lacking the tumor suppressors p53, p19ARF, or p16(INK4A); however, the mRNAs encoding these proteins are unlikely targets of CPEB since their expression is the same in wild-type and KO MEFs. Conversely, Ras cannot induce senescence in MEFs lacking CPEB, suggesting that it may lie upstream of CPEB. One target of CPEB regulation is myc mRNA, whose unregulated translation in the KO MEFs may cause them to bypass senescence. Thus, CPEB appears to act as a translational repressor protein to control myc translation and resulting cellular senescence.</p>
dc.identifier.submissionpathgsbs_sp/418
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages2701-12
dc.contributor.studentMaria Ivshina


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