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Article: Human T-cell leukemia virus oncoprotein Tax represses nuclear receptor-dependent transcription by targeting coactivator TAX1BP1

TitleHuman T-cell leukemia virus oncoprotein Tax represses nuclear receptor-dependent transcription by targeting coactivator TAX1BP1
Authors
Issue Date2007
PublisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/
Citation
Cancer Research, 2007, v. 67 n. 3, p. 1072-1081 How to Cite?
AbstractHuman T-cell leukemia virus type 1 oncoprotein Tax is a transcriptional regulator that interacts with a large number of host cell factors. Here, we report the novel characterization of the interaction of Tax with a human cell protein named Tax1-binding protein 1 (TAX1BP1). We show that TAX1BP1 is a nuclear receptor coactivator that forms a complex with the glucocorticoid receptor. TAX1BP1 and Tax colocalize into intranuclear speckles that partially overlap with but are not identical to the PML oncogenic domains. Tax binds TAX1BP1 directly, induces the dissociation of TAX1BP1 from the glucocorticoid receptor-containing protein complex, and represses the coactivator function of TAX1BP1. Genetic knockout of Tax1bp1 in mice abrogates the influence of Tax on the activation of nuclear receptors. We propose that Tax-TAX1BP1 interaction mechanistically explains the previously reported repression of nuclear receptor activity by Tax. ©2007 American Association for Cancer Research.
Persistent Identifierhttp://hdl.handle.net/10722/54241
ISSN
2023 Impact Factor: 12.5
2023 SCImago Journal Rankings: 3.468
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChin, KTen_HK
dc.contributor.authorChun, ACSen_HK
dc.contributor.authorChing, YPen_HK
dc.contributor.authorJeang, KTen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2009-04-03T07:40:49Z-
dc.date.available2009-04-03T07:40:49Z-
dc.date.issued2007en_HK
dc.identifier.citationCancer Research, 2007, v. 67 n. 3, p. 1072-1081en_HK
dc.identifier.issn0008-5472en_HK
dc.identifier.urihttp://hdl.handle.net/10722/54241-
dc.description.abstractHuman T-cell leukemia virus type 1 oncoprotein Tax is a transcriptional regulator that interacts with a large number of host cell factors. Here, we report the novel characterization of the interaction of Tax with a human cell protein named Tax1-binding protein 1 (TAX1BP1). We show that TAX1BP1 is a nuclear receptor coactivator that forms a complex with the glucocorticoid receptor. TAX1BP1 and Tax colocalize into intranuclear speckles that partially overlap with but are not identical to the PML oncogenic domains. Tax binds TAX1BP1 directly, induces the dissociation of TAX1BP1 from the glucocorticoid receptor-containing protein complex, and represses the coactivator function of TAX1BP1. Genetic knockout of Tax1bp1 in mice abrogates the influence of Tax on the activation of nuclear receptors. We propose that Tax-TAX1BP1 interaction mechanistically explains the previously reported repression of nuclear receptor activity by Tax. ©2007 American Association for Cancer Research.en_HK
dc.languageengen_HK
dc.publisherAmerican Association for Cancer Research. The Journal's web site is located at http://cancerres.aacrjournals.org/en_HK
dc.relation.ispartofCancer Researchen_HK
dc.subject.meshNeoplasm Proteins - antagonists & inhibitors - metabolismen_HK
dc.subject.meshCell Nucleus - metabolismen_HK
dc.subject.meshNeoplasm Proteins - antagonists & inhibitors - metabolismen_HK
dc.subject.meshReceptors, Cytoplasmic and Nuclear - antagonists & inhibitors - metabolismen_HK
dc.subject.meshSignal Transductionen_HK
dc.titleHuman T-cell leukemia virus oncoprotein Tax represses nuclear receptor-dependent transcription by targeting coactivator TAX1BP1en_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0008-5472&volume=67&issue=3&spage=1072&epage=1081&date=2007&atitle=Human+T-cell+leukemia+virus+oncoprotein+tax+represses+nuclear+receptor-dependent+transcription+by+targeting+coactivator+TAX1BP1en_HK
dc.identifier.emailChing, YP:ypching@hku.hken_HK
dc.identifier.emailJin, DY:dyjin@hkucc.hku.hken_HK
dc.identifier.authorityChing, YP=rp00469en_HK
dc.identifier.authorityJin, DY=rp00452en_HK
dc.description.naturepostprinten_HK
dc.identifier.doi10.1158/0008-5472.CAN-06-3053en_HK
dc.identifier.pmid17283140-
dc.identifier.scopuseid_2-s2.0-33847010696en_HK
dc.identifier.hkuros126752-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33847010696&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume67en_HK
dc.identifier.issue3en_HK
dc.identifier.spage1072en_HK
dc.identifier.epage1081en_HK
dc.identifier.isiWOS:000244137300031-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridChin, KT=7202995491en_HK
dc.identifier.scopusauthoridChun, ACS=7003650706en_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridJeang, KT=7004824803en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.issnl0008-5472-

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