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Article: Specific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complex

TitleSpecific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complex
Authors
Issue Date2004
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.retrovirology.com/home/
Citation
Retrovirology, 2004, v. 1 How to Cite?
AbstractBackground: Human T-cell leukemia virus type I (HTLV-I) Tax protein is a transcriptional regulator of viral and cellular genes. In this study we have examined in detail the determinants for Tax-mediated transcriptional activation. Results: Whereas previously the LTR enhancer elements were thought to be the sole Tax-targets, herein, we find that the core HTLV-I TATAA motif also provides specific responsiveness not seen with either the SV40 or the E1b TATAA boxes. When enhancer elements which can mediate Tax-responsiveness were compared, the authentic HTLV-I 21-bp repeats were found to be the most effective. Related bZIP factors such as CREB, ATF4, c-Jun and LZIP are often thought to recognize the 21-bp repeats equivalently. However, amongst bZIP factors, we found that CREB, by far, is preferred by Tax for activation. When LTR transcription was reconstituted by substituting either κB or serum response elements in place of the 21-bp repeats, Tax activated these surrogate motifs using surfaces which are different from that utilized for CREB interaction. Finally, we employed artificial recruitment of TATA-binding protein to the HTLV-I promoter in "bypass" experiments to show for the first time that Tax has transcriptional activity subsequent to the assembly of an initiation complex at the promoter. Conclusions: Optimal activation of the HTLV-I LTR by Tax specifically requires the core HTLV-I TATAA promoter, CREB and the 21-bp repeats. In addition, we also provide the first evidence for transcriptional activity of Tax after the recruitment of TATA-binding protein to the promoter. © 2004 Ching et al; licensee BioMed Central Ltd.
Persistent Identifierhttp://hdl.handle.net/10722/42620
ISSN
2023 Impact Factor: 2.7
2023 SCImago Journal Rankings: 0.845
PubMed Central ID
References

 

DC FieldValueLanguage
dc.contributor.authorChing, YPen_HK
dc.contributor.authorChun, ACSen_HK
dc.contributor.authorChin, KTen_HK
dc.contributor.authorZhang, ZQen_HK
dc.contributor.authorJeang, KTen_HK
dc.contributor.authorJin, DYen_HK
dc.date.accessioned2007-03-23T04:28:01Z-
dc.date.available2007-03-23T04:28:01Z-
dc.date.issued2004en_HK
dc.identifier.citationRetrovirology, 2004, v. 1en_HK
dc.identifier.issn1742-4690en_HK
dc.identifier.urihttp://hdl.handle.net/10722/42620-
dc.description.abstractBackground: Human T-cell leukemia virus type I (HTLV-I) Tax protein is a transcriptional regulator of viral and cellular genes. In this study we have examined in detail the determinants for Tax-mediated transcriptional activation. Results: Whereas previously the LTR enhancer elements were thought to be the sole Tax-targets, herein, we find that the core HTLV-I TATAA motif also provides specific responsiveness not seen with either the SV40 or the E1b TATAA boxes. When enhancer elements which can mediate Tax-responsiveness were compared, the authentic HTLV-I 21-bp repeats were found to be the most effective. Related bZIP factors such as CREB, ATF4, c-Jun and LZIP are often thought to recognize the 21-bp repeats equivalently. However, amongst bZIP factors, we found that CREB, by far, is preferred by Tax for activation. When LTR transcription was reconstituted by substituting either κB or serum response elements in place of the 21-bp repeats, Tax activated these surrogate motifs using surfaces which are different from that utilized for CREB interaction. Finally, we employed artificial recruitment of TATA-binding protein to the HTLV-I promoter in "bypass" experiments to show for the first time that Tax has transcriptional activity subsequent to the assembly of an initiation complex at the promoter. Conclusions: Optimal activation of the HTLV-I LTR by Tax specifically requires the core HTLV-I TATAA promoter, CREB and the 21-bp repeats. In addition, we also provide the first evidence for transcriptional activity of Tax after the recruitment of TATA-binding protein to the promoter. © 2004 Ching et al; licensee BioMed Central Ltd.en_HK
dc.format.extent1175820 bytes-
dc.format.extent25088 bytes-
dc.format.mimetypeapplication/pdf-
dc.format.mimetypeapplication/msword-
dc.languageengen_HK
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.retrovirology.com/home/en_HK
dc.relation.ispartofRetrovirologyen_HK
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subject.meshAntigens, neoplasm - geneticsen_HK
dc.subject.meshGene products, tax - metabolismen_HK
dc.subject.meshHistocompatibility antigens - geneticsen_HK
dc.subject.meshHuman t-lymphotropic virus 1 - geneticsen_HK
dc.subject.meshPeptide chain initiation, translationalen_HK
dc.titleSpecific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complexen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1742-4690&volume=1&issue=18&spage=1&epage=12&date=2004&atitle=Specific+TATAA+and+bZIP+requirements+suggest+that+HTLV-I+Tax+has+transcriptional+activity+subsequent+to+the+assembly+of+an+initiation+complexen_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.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1186/1742-4690-1-18en_HK
dc.identifier.pmid15285791en_HK
dc.identifier.pmcidPMC509288-
dc.identifier.scopuseid_2-s2.0-17744377229en_HK
dc.identifier.hkuros94878-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-17744377229&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume1en_HK
dc.publisher.placeUnited Kingdomen_HK
dc.identifier.scopusauthoridChing, YP=7005431277en_HK
dc.identifier.scopusauthoridChun, ACS=7003650706en_HK
dc.identifier.scopusauthoridChin, KT=7202995491en_HK
dc.identifier.scopusauthoridZhang, ZQ=8606786700en_HK
dc.identifier.scopusauthoridJeang, KT=7004824803en_HK
dc.identifier.scopusauthoridJin, DY=7201973614en_HK
dc.identifier.issnl1742-4690-

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