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Article: Ets1 is required for p53 transcriptional activity in UV-induced apoptosis in embryonic stem cells

TitleEts1 is required for p53 transcriptional activity in UV-induced apoptosis in embryonic stem cells
Authors
KeywordsApoptosis
CBP
Ets1
p53
UV
Issue Date2002
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/emboj/index.html
Citation
EMBO Journal, 2002, v. 21 n. 15, p. 4081-4093 How to Cite?
AbstractEmbryonic stem (ES) cells contain a p53-dependent apoptosis mechanism to avoid the continued proliferation and differentiation of damaged cells. We show that mouse ES cells lacking Ets1 are deficient in their ability to undergo UV-induced apoptosis, similar to p53 null ES cells. In Ets1-/- ES cells, UV induction of the p53 regulated genes mdm2, perp, cyclin G and bax was decreased both at mRNA and protein levels. While p53 protein levels were unaltered in Ets1-/- cells, its ability to transactivate genes such as mdm2 and cyclin G was reduced. Furthermore, electrophoretic mobility shift assays and immunoprecipitations demonstrated that the presence of Ets1 was necessary for a CBP/p53 complex to be formed. Chromatin immunoprecipitations demonstrated that Ets1 was required for the formation of a stable p53-DNA complex under physiological conditions and activation of histone acetyltransferase activity. These data demonstrate that Ets1 is an essential component of a UV-responsive p53 transcriptional activation complex in ES cells and suggests that Ets1 may contribute to the specificity of p53-dependent gene transactivation in distinct cellular compartments.
Persistent Identifierhttp://hdl.handle.net/10722/49390
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 5.489
PubMed Central ID
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorXu, Den_HK
dc.contributor.authorWilson, TJen_HK
dc.contributor.authorChan, Den_HK
dc.contributor.authorDe Luca, Een_HK
dc.contributor.authorZhou, Jen_HK
dc.contributor.authorHertzog, PJen_HK
dc.contributor.authorKola, Ien_HK
dc.date.accessioned2008-06-12T06:41:10Z-
dc.date.available2008-06-12T06:41:10Z-
dc.date.issued2002en_HK
dc.identifier.citationEMBO Journal, 2002, v. 21 n. 15, p. 4081-4093en_HK
dc.identifier.issn0261-4189en_HK
dc.identifier.urihttp://hdl.handle.net/10722/49390-
dc.description.abstractEmbryonic stem (ES) cells contain a p53-dependent apoptosis mechanism to avoid the continued proliferation and differentiation of damaged cells. We show that mouse ES cells lacking Ets1 are deficient in their ability to undergo UV-induced apoptosis, similar to p53 null ES cells. In Ets1-/- ES cells, UV induction of the p53 regulated genes mdm2, perp, cyclin G and bax was decreased both at mRNA and protein levels. While p53 protein levels were unaltered in Ets1-/- cells, its ability to transactivate genes such as mdm2 and cyclin G was reduced. Furthermore, electrophoretic mobility shift assays and immunoprecipitations demonstrated that the presence of Ets1 was necessary for a CBP/p53 complex to be formed. Chromatin immunoprecipitations demonstrated that Ets1 was required for the formation of a stable p53-DNA complex under physiological conditions and activation of histone acetyltransferase activity. These data demonstrate that Ets1 is an essential component of a UV-responsive p53 transcriptional activation complex in ES cells and suggests that Ets1 may contribute to the specificity of p53-dependent gene transactivation in distinct cellular compartments.en_HK
dc.format.extent386 bytes-
dc.format.mimetypetext/html-
dc.languageengen_HK
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/emboj/index.htmlen_HK
dc.relation.ispartofEMBO Journalen_HK
dc.subjectApoptosisen_HK
dc.subjectCBPen_HK
dc.subjectEts1en_HK
dc.subjectp53en_HK
dc.subjectUVen_HK
dc.titleEts1 is required for p53 transcriptional activity in UV-induced apoptosis in embryonic stem cellsen_HK
dc.typeArticleen_HK
dc.identifier.emailChan, D:dwchan@hkucc.hku.hken_HK
dc.identifier.authorityChan, D=rp00543en_HK
dc.description.naturelink_to_OA_fulltexten_HK
dc.identifier.doi10.1093/emboj/cdf413en_HK
dc.identifier.pmid12145208-
dc.identifier.pmcidPMC126157en_HK
dc.identifier.scopuseid_2-s2.0-0036683054en_HK
dc.identifier.hkuros81103-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0036683054&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume21en_HK
dc.identifier.issue15en_HK
dc.identifier.spage4081en_HK
dc.identifier.epage4093en_HK
dc.identifier.isiWOS:000177470700016-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridXu, D=7404073425en_HK
dc.identifier.scopusauthoridWilson, TJ=7403495583en_HK
dc.identifier.scopusauthoridChan, D=26533900600en_HK
dc.identifier.scopusauthoridDe Luca, E=6701490916en_HK
dc.identifier.scopusauthoridZhou, J=38061795700en_HK
dc.identifier.scopusauthoridHertzog, PJ=7005991492en_HK
dc.identifier.scopusauthoridKola, I=7006455084en_HK
dc.identifier.issnl0261-4189-

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