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dc.contributor.authorXu, Ping
dc.contributor.authorDavis, Roger J.
dc.date2022-08-11T08:08:17.000
dc.date.accessioned2022-08-23T15:49:07Z
dc.date.available2022-08-23T15:49:07Z
dc.date.issued2010-03-01
dc.date.submitted2016-05-25
dc.identifier.citationMol Cell Biol. 2010 Mar;30(6):1329-40. doi: 10.1128/MCB.00795-09. Epub 2010 Jan 11. <a href="http://dx.doi.org/10.1128/MCB.00795-09">Link to article on publisher's site</a>
dc.identifier.issn0270-7306 (Linking)
dc.identifier.doi10.1128/MCB.00795-09
dc.identifier.pmid20065035
dc.identifier.urihttp://hdl.handle.net/20.500.14038/28357
dc.description.abstractThe c-Jun NH(2)-terminal kinase (JNK) is implicated in proliferation. Mice with a deficiency of either the Jnk1 or the Jnk2 genes are viable, but a compound deficiency of both Jnk1 and Jnk2 causes early embryonic lethality. Studies using conditional gene ablation and chemical genetic approaches demonstrate that the combined loss of JNK1 and JNK2 protein kinase function results in rapid senescence. To test whether this role of JNK was required for stem cell proliferation, we isolated embryonic stem (ES) cells from wild-type and JNK-deficient mice. We found that Jnk1(-/-) Jnk2(-/-) ES cells underwent self-renewal, but these cells proliferated more rapidly than wild-type ES cells and exhibited major defects in lineage-specific differentiation. Together, these data demonstrate that JNK is not required for proliferation or self-renewal of ES cells, but JNK plays a key role in the differentiation of ES cells.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&list_uids=20065035&dopt=Abstract">Link to Article in PubMed</a>
dc.rightsPublisher PDF posted as allowed by the publisher's author rights policy at http://journals.asm.org/site/misc/ASM_Author_Statement.xhtml.
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectMolecular Biology
dc.titlec-Jun NH2-terminal kinase is required for lineage-specific differentiation but not stem cell self-renewal
dc.typeJournal Article
dc.source.journaltitleMolecular and cellular biology
dc.source.volume30
dc.source.issue6
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1081&amp;context=davis&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/davis/82
dc.identifier.contextkey8646726
refterms.dateFOA2022-08-23T15:49:07Z
html.description.abstract<p>The c-Jun NH(2)-terminal kinase (JNK) is implicated in proliferation. Mice with a deficiency of either the Jnk1 or the Jnk2 genes are viable, but a compound deficiency of both Jnk1 and Jnk2 causes early embryonic lethality. Studies using conditional gene ablation and chemical genetic approaches demonstrate that the combined loss of JNK1 and JNK2 protein kinase function results in rapid senescence. To test whether this role of JNK was required for stem cell proliferation, we isolated embryonic stem (ES) cells from wild-type and JNK-deficient mice. We found that Jnk1(-/-) Jnk2(-/-) ES cells underwent self-renewal, but these cells proliferated more rapidly than wild-type ES cells and exhibited major defects in lineage-specific differentiation. Together, these data demonstrate that JNK is not required for proliferation or self-renewal of ES cells, but JNK plays a key role in the differentiation of ES cells.</p>
dc.identifier.submissionpathdavis/82
dc.contributor.departmentProgram in Molecular Medicine
dc.source.pages1329-40


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