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Article: Transcriptional activation of immediate-early gene ETR101 by human T-cell leukaemia virus type I Tax

TitleTranscriptional activation of immediate-early gene ETR101 by human T-cell leukaemia virus type I Tax
Authors
Issue Date2003
PublisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.org
Citation
Journal Of General Virology, 2003, v. 84 n. 12, p. 3203-3214 How to Cite?
AbstractHuman T-cell leukaemia virus type I (HTLV-I) Tax regulates viral and cellular gene expression through interactions with multiple cellular transcription pathways. This study describes the finding of immediate-early gene ETR101 expression in HTLV-I-infected cells and its regulation by Tax. ETR101 was persistently expressed in HTLV-I-infected cells but not in HTLV-I uninfected cells. Expression of ETR101 was dependent upon Tax expression in the inducible Tax-expressing cell line JPX-9 and also in Jurkat cells transiently transfected with Tax-expressing vectors. Tax transactivated the ETR101 gene promoter in a transient transfection assay. A series of deletion and mutation analyses of the ETR101 gene promoter indicated that a 35 bp region immediately upstream of the TATA-box sequence, which contains a consensus cAMP response element (CRE) and a G+C-rich sequence, is the critical responsive element for Tax activation. Site-directed mutagenesis analysis of the 35 bp region suggested that both the consensus CRE motif and its upstream G+C-rich sequence were critical for Tax transactivation. Electrophoretic mobility shift analysis (EMSA) using the 35 bp sequence as probe showed the formation of a specific protein-DNA complex in HTLV-I-infected cell lines. EMSA with specific antibodies confirmed that the CREB transcription factor was responsible for formation of this specific protein-DNA complex. These results suggested that Tax directly transactivated ETR101 gene expression, mainly through a CRE sequence via the CREB transcription pathway.
Persistent Identifierhttp://hdl.handle.net/10722/42310
ISSN
2015 Impact Factor: 3.192
2015 SCImago Journal Rankings: 1.741
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChen, Len_HK
dc.contributor.authorMa, Sen_HK
dc.contributor.authorLi, Ben_HK
dc.contributor.authorFink, Ten_HK
dc.contributor.authorZachar, Ven_HK
dc.contributor.authorTakahashi, Men_HK
dc.contributor.authorCuttichia, Jen_HK
dc.contributor.authorTsui, LCen_HK
dc.contributor.authorEbbesen, Pen_HK
dc.contributor.authorLiu, Xen_HK
dc.date.accessioned2007-01-08T02:34:15Z-
dc.date.available2007-01-08T02:34:15Z-
dc.date.issued2003en_HK
dc.identifier.citationJournal Of General Virology, 2003, v. 84 n. 12, p. 3203-3214en_HK
dc.identifier.issn0022-1317en_HK
dc.identifier.urihttp://hdl.handle.net/10722/42310-
dc.description.abstractHuman T-cell leukaemia virus type I (HTLV-I) Tax regulates viral and cellular gene expression through interactions with multiple cellular transcription pathways. This study describes the finding of immediate-early gene ETR101 expression in HTLV-I-infected cells and its regulation by Tax. ETR101 was persistently expressed in HTLV-I-infected cells but not in HTLV-I uninfected cells. Expression of ETR101 was dependent upon Tax expression in the inducible Tax-expressing cell line JPX-9 and also in Jurkat cells transiently transfected with Tax-expressing vectors. Tax transactivated the ETR101 gene promoter in a transient transfection assay. A series of deletion and mutation analyses of the ETR101 gene promoter indicated that a 35 bp region immediately upstream of the TATA-box sequence, which contains a consensus cAMP response element (CRE) and a G+C-rich sequence, is the critical responsive element for Tax activation. Site-directed mutagenesis analysis of the 35 bp region suggested that both the consensus CRE motif and its upstream G+C-rich sequence were critical for Tax transactivation. Electrophoretic mobility shift analysis (EMSA) using the 35 bp sequence as probe showed the formation of a specific protein-DNA complex in HTLV-I-infected cell lines. EMSA with specific antibodies confirmed that the CREB transcription factor was responsible for formation of this specific protein-DNA complex. These results suggested that Tax directly transactivated ETR101 gene expression, mainly through a CRE sequence via the CREB transcription pathway.en_HK
dc.format.extent566603 bytes-
dc.format.extent30208 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.languageengen_HK
dc.publisherSociety for General Microbiology. The Journal's web site is located at http://vir.sgmjournals.orgen_HK
dc.relation.ispartofJournal of General Virologyen_HK
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License-
dc.subject.meshCyclic amp response element-binding protein - physiologyen_HK
dc.subject.meshEndopeptidasesen_HK
dc.subject.meshGene expression regulationen_HK
dc.subject.meshGene products, tax - genetics - metabolism - physiologyen_HK
dc.subject.meshGenes, immediate-earlyen_HK
dc.titleTranscriptional activation of immediate-early gene ETR101 by human T-cell leukaemia virus type I Taxen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0022-1317&volume=84&issue=12&spage=3203&epage=3214&date=2003&atitle=Transcriptional+activation+of+immediate–early+gene+ETR101+by+human+T-cell+leukaemia+virus+type+I+Taxen_HK
dc.identifier.emailTsui, LC: tsuilc@hkucc.hku.hken_HK
dc.identifier.authorityTsui, LC=rp00058en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1099/vir.0.19283-0en_HK
dc.identifier.pmid14645902-
dc.identifier.scopuseid_2-s2.0-10744222284en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-10744222284&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume84en_HK
dc.identifier.issue12en_HK
dc.identifier.spage3203en_HK
dc.identifier.epage3214en_HK
dc.identifier.isiWOS:000220465300003-
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChen, L=7409437435en_HK
dc.identifier.scopusauthoridMa, S=55245330800en_HK
dc.identifier.scopusauthoridLi, B=36071197200en_HK
dc.identifier.scopusauthoridFink, T=7005090673en_HK
dc.identifier.scopusauthoridZachar, V=7004220745en_HK
dc.identifier.scopusauthoridTakahashi, M=7406843237en_HK
dc.identifier.scopusauthoridCuttichia, J=6503868742en_HK
dc.identifier.scopusauthoridTsui, LC=7102754167en_HK
dc.identifier.scopusauthoridEbbesen, P=7102907232en_HK
dc.identifier.scopusauthoridLiu, X=36076945600en_HK

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