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Article: A nuclear factor, ASC-2, as a cancer-amplified transcriptional coactivator essential for ligand-dependent transactivation by nuclear receptors in vivo

TitleA nuclear factor, ASC-2, as a cancer-amplified transcriptional coactivator essential for ligand-dependent transactivation by nuclear receptors in vivo
Authors
Issue Date1999
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 1999, v. 274 n. 48, p. 34283-34293 How to Cite?
AbstractMany transcription coactivators interact with nuclear receptors in a ligand- and C-terminal transactivation function (AF2)-dependent manner. We isolated a nuclear factor (designated ASC-2) with such properties by using the ligand-binding domain of retinoid X receptor as a bait in a yeast two- hybrid screening. ASC-2 also interacted with other nuclear receptors, including retinoic acid receptor, thyroid hormone receptor, estrogen receptor α, and glucocorticoid receptor, basal factors TFIIA and TBP, and transcription integrators CBP/p300 and SRC-1. In transient cotransfections, ASC-2, either alone or in conjunction with CBP/p300 and SRC-1, stimulated ligand-dependent transactivation by wild type nuclear receptors but not mutant receptors lacking the AF2 domain. Consistent with an idea that ASC-2 is essential for the nuclear receptor function in vivo, microinjection of anti-ASC-2 antibody abrogated the ligand-dependent transactivation of retinoic acid receptor, and this repression was fully relieved by coinjection of ASC-2-expression vector. Surprisingly, ASC-2 was identical to a gene previously identified during a search for genes amplified and overexpressed in breast and other human cancers. From these results, we concluded that ASC- 2 is a bona fide transcription coactivator molecule of nuclear receptors, and its altered expression may contribute to the development of cancers.
Persistent Identifierhttp://hdl.handle.net/10722/72018
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, SKen_HK
dc.contributor.authorAnzick, SLen_HK
dc.contributor.authorChoi, JEen_HK
dc.contributor.authorBubendorf, Len_HK
dc.contributor.authorGuan, XYen_HK
dc.contributor.authorJung, YKen_HK
dc.contributor.authorKallioniemi, OPen_HK
dc.contributor.authorKononen, Jen_HK
dc.contributor.authorTrent, JMen_HK
dc.contributor.authorAzorsa, Den_HK
dc.contributor.authorJhun, BHen_HK
dc.contributor.authorCheong, JHen_HK
dc.contributor.authorLee, YCen_HK
dc.contributor.authorMeltzer, PSen_HK
dc.contributor.authorLee, JWen_HK
dc.date.accessioned2010-09-06T06:37:32Z-
dc.date.available2010-09-06T06:37:32Z-
dc.date.issued1999en_HK
dc.identifier.citationJournal Of Biological Chemistry, 1999, v. 274 n. 48, p. 34283-34293en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/72018-
dc.description.abstractMany transcription coactivators interact with nuclear receptors in a ligand- and C-terminal transactivation function (AF2)-dependent manner. We isolated a nuclear factor (designated ASC-2) with such properties by using the ligand-binding domain of retinoid X receptor as a bait in a yeast two- hybrid screening. ASC-2 also interacted with other nuclear receptors, including retinoic acid receptor, thyroid hormone receptor, estrogen receptor α, and glucocorticoid receptor, basal factors TFIIA and TBP, and transcription integrators CBP/p300 and SRC-1. In transient cotransfections, ASC-2, either alone or in conjunction with CBP/p300 and SRC-1, stimulated ligand-dependent transactivation by wild type nuclear receptors but not mutant receptors lacking the AF2 domain. Consistent with an idea that ASC-2 is essential for the nuclear receptor function in vivo, microinjection of anti-ASC-2 antibody abrogated the ligand-dependent transactivation of retinoic acid receptor, and this repression was fully relieved by coinjection of ASC-2-expression vector. Surprisingly, ASC-2 was identical to a gene previously identified during a search for genes amplified and overexpressed in breast and other human cancers. From these results, we concluded that ASC- 2 is a bona fide transcription coactivator molecule of nuclear receptors, and its altered expression may contribute to the development of cancers.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.subject.meshAmino Acid Sequenceen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshCloning, Molecularen_HK
dc.subject.meshGene Amplificationen_HK
dc.subject.meshGene Expressionen_HK
dc.subject.meshGene Expression Regulation, Neoplasticen_HK
dc.subject.meshHistone Acetyltransferasesen_HK
dc.subject.meshHumansen_HK
dc.subject.meshIntracellular Signaling Peptides and Proteinsen_HK
dc.subject.meshLigandsen_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshNeoplasms - geneticsen_HK
dc.subject.meshNuclear Proteins - genetics - metabolismen_HK
dc.subject.meshNuclear Receptor Coactivator 1en_HK
dc.subject.meshNuclear Receptor Coactivatorsen_HK
dc.subject.meshOocytes - metabolismen_HK
dc.subject.meshProtein Bindingen_HK
dc.subject.meshReceptors, Cytoplasmic and Nuclear - genetics - metabolism - physiologyen_HK
dc.subject.meshRecombinant Fusion Proteins - genetics - metabolismen_HK
dc.subject.meshSequence Alignmenten_HK
dc.subject.meshTrans-Activators - genetics - metabolism - physiologyen_HK
dc.subject.meshTranscription Factors - genetics - metabolism - physiologyen_HK
dc.subject.meshTranscriptional Activation - geneticsen_HK
dc.subject.meshTumor Cells, Cultureden_HK
dc.subject.meshTwo-Hybrid System Techniquesen_HK
dc.subject.meshXenopusen_HK
dc.titleA nuclear factor, ASC-2, as a cancer-amplified transcriptional coactivator essential for ligand-dependent transactivation by nuclear receptors in vivoen_HK
dc.typeArticleen_HK
dc.identifier.emailGuan, XY:xyguan@hkucc.hku.hken_HK
dc.identifier.authorityGuan, XY=rp00454en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1074/jbc.274.48.34283en_HK
dc.identifier.pmid10567404-
dc.identifier.scopuseid_2-s2.0-0033607672en_HK
dc.identifier.hkuros52963en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-0033607672&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume274en_HK
dc.identifier.issue48en_HK
dc.identifier.spage34283en_HK
dc.identifier.epage34293en_HK
dc.identifier.isiWOS:000083857500069-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLee, SK=35074429000en_HK
dc.identifier.scopusauthoridAnzick, SL=6603376140en_HK
dc.identifier.scopusauthoridChoi, JE=16021161400en_HK
dc.identifier.scopusauthoridBubendorf, L=7004153777en_HK
dc.identifier.scopusauthoridGuan, XY=7201463221en_HK
dc.identifier.scopusauthoridJung, YK=35358575000en_HK
dc.identifier.scopusauthoridKallioniemi, OP=7005031465en_HK
dc.identifier.scopusauthoridKononen, J=7003792216en_HK
dc.identifier.scopusauthoridTrent, JM=7201692482en_HK
dc.identifier.scopusauthoridAzorsa, D=6601989499en_HK
dc.identifier.scopusauthoridJhun, BH=7003967772en_HK
dc.identifier.scopusauthoridCheong, JH=7004933286en_HK
dc.identifier.scopusauthoridLee, YC=26643158700en_HK
dc.identifier.scopusauthoridMeltzer, PS=7102464641en_HK
dc.identifier.scopusauthoridLee, JW=36014826400en_HK

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