File Download
 
Links for fulltext
(May Require Subscription)
 
Supplementary

Article: Specific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complex
  • Basic View
  • Metadata View
  • XML View
TitleSpecific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complex
 
AuthorsChing, YP2 2
Chun, ACS2
Chin, KT2
Zhang, ZQ1
Jeang, KT
Jin, DY3
 
Issue Date2004
 
PublisherBioMed Central Ltd. The Journal's web site is located at http://www.retrovirology.com/home/
 
CitationRetrovirology, 2004, v. 1 [How to Cite?]
DOI: http://dx.doi.org/10.1186/1742-4690-1-18
 
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.
 
ISSN1742-4690
2012 Impact Factor: 5.657
2012 SCImago Journal Rankings: 1.881
 
DOIhttp://dx.doi.org/10.1186/1742-4690-1-18
 
PubMed Central IDPMC509288
 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorChing, YP
 
dc.contributor.authorChun, ACS
 
dc.contributor.authorChin, KT
 
dc.contributor.authorZhang, ZQ
 
dc.contributor.authorJeang, KT
 
dc.contributor.authorJin, DY
 
dc.date.accessioned2007-03-23T04:28:01Z
 
dc.date.available2007-03-23T04:28:01Z
 
dc.date.issued2004
 
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.
 
dc.description.naturepublished_or_final_version
 
dc.format.extent1175820 bytes
 
dc.format.extent25088 bytes
 
dc.format.mimetypeapplication/pdf
 
dc.format.mimetypeapplication/msword
 
dc.identifier.citationRetrovirology, 2004, v. 1 [How to Cite?]
DOI: http://dx.doi.org/10.1186/1742-4690-1-18
 
dc.identifier.doihttp://dx.doi.org/10.1186/1742-4690-1-18
 
dc.identifier.hkuros94878
 
dc.identifier.issn1742-4690
2012 Impact Factor: 5.657
2012 SCImago Journal Rankings: 1.881
 
dc.identifier.openurl
 
dc.identifier.pmcidPMC509288
 
dc.identifier.pmid15285791
 
dc.identifier.scopuseid_2-s2.0-17744377229
 
dc.identifier.urihttp://hdl.handle.net/10722/42620
 
dc.identifier.volume1
 
dc.languageeng
 
dc.publisherBioMed Central Ltd. The Journal's web site is located at http://www.retrovirology.com/home/
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofRetrovirology
 
dc.relation.referencesReferences in Scopus
 
dc.rightsCreative Commons: Attribution 3.0 Hong Kong License
 
dc.subject.meshAntigens, neoplasm - genetics
 
dc.subject.meshGene products, tax - metabolism
 
dc.subject.meshHistocompatibility antigens - genetics
 
dc.subject.meshHuman t-lymphotropic virus 1 - genetics
 
dc.subject.meshPeptide chain initiation, translational
 
dc.titleSpecific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complex
 
dc.typeArticle
 
<?xml encoding="utf-8" version="1.0"?>
<item><contributor.author>Ching, YP</contributor.author>
<contributor.author>Chun, ACS</contributor.author>
<contributor.author>Chin, KT</contributor.author>
<contributor.author>Zhang, ZQ</contributor.author>
<contributor.author>Jeang, KT</contributor.author>
<contributor.author>Jin, DY</contributor.author>
<date.accessioned>2007-03-23T04:28:01Z</date.accessioned>
<date.available>2007-03-23T04:28:01Z</date.available>
<date.issued>2004</date.issued>
<identifier.citation>Retrovirology, 2004, v. 1</identifier.citation>
<identifier.issn>1742-4690</identifier.issn>
<identifier.uri>http://hdl.handle.net/10722/42620</identifier.uri>
<description.abstract>Background: 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 &#954;B 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 &quot;bypass&quot; 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. &#169; 2004 Ching et al; licensee BioMed Central Ltd.</description.abstract>
<format.extent>1175820 bytes</format.extent>
<format.extent>25088 bytes</format.extent>
<format.mimetype>application/pdf</format.mimetype>
<format.mimetype>application/msword</format.mimetype>
<language>eng</language>
<publisher>BioMed Central Ltd. The Journal&apos;s web site is located at http://www.retrovirology.com/home/</publisher>
<relation.ispartof>Retrovirology</relation.ispartof>
<rights>Creative Commons: Attribution 3.0 Hong Kong License</rights>
<subject.mesh>Antigens, neoplasm - genetics</subject.mesh>
<subject.mesh>Gene products, tax - metabolism</subject.mesh>
<subject.mesh>Histocompatibility antigens - genetics</subject.mesh>
<subject.mesh>Human t-lymphotropic virus 1 - genetics</subject.mesh>
<subject.mesh>Peptide chain initiation, translational</subject.mesh>
<title>Specific TATAA and bZIP requirements suggest that HTLV-I Tax has transcriptional activity subsequent to the assembly of an initiation complex</title>
<type>Article</type>
<identifier.openurl>http://library.hku.hk:4550/resserv?sid=HKU:IR&amp;issn=1742-4690&amp;volume=1&amp;issue=18&amp;spage=1&amp;epage=12&amp;date=2004&amp;atitle=Specific+TATAA+and+bZIP+requirements+suggest+that+HTLV-I+Tax+has+transcriptional+activity+subsequent+to+the+assembly+of+an+initiation+complex</identifier.openurl>
<description.nature>published_or_final_version</description.nature>
<identifier.doi>10.1186/1742-4690-1-18</identifier.doi>
<identifier.pmid>15285791</identifier.pmid>
<identifier.pmcid>PMC509288</identifier.pmcid>
<identifier.scopus>eid_2-s2.0-17744377229</identifier.scopus>
<identifier.hkuros>94878</identifier.hkuros>
<relation.references>http://www.scopus.com/mlt/select.url?eid=2-s2.0-17744377229&amp;selection=ref&amp;src=s&amp;origin=recordpage</relation.references>
<identifier.volume>1</identifier.volume>
<publisher.place>United Kingdom</publisher.place>
<bitstream.url>http://hub.hku.hk/bitstream/10722/42620/3/1742-4690-1-18.pdf</bitstream.url>
</item>
Author Affiliations
  1. National Laboratory of Medical Molecular Biology Beijing
  2. The University of Hong Kong
  3. National Institutes of Health, Bethesda