Linked Life Data

9343426

Source:http://linkedlifedata.com/resource/pubmed/id/9343426

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
11
pubmed:dateCreated
1997-11-21
pubmed:abstractText
Different mechanisms of transcriptional activation may be required for distinct classes of promoters and cellular conditions. The Epstein-Barr virus (EBV)-encoded transcriptional activator Zta recruits the general transcription factors IID (TFIID) and IIA (TFIIA) to promoter DNA and induces a TATA box-binding protein (TBP)-associated factor-dependent footprint downstream of the transcriptional initiation site. In this study, we investigated the functional significance of TFIID-TFIIA (D-A complex) recruitment by Zta. Alanine substitution mutations in the Zta activation domain which eliminate the ability of Zta to stimulate the D-A complex were examined. These Zta mutants were defective in the ability to activate transcription from an EBV-derived promoter (BHLF1) but activated a highly responsive synthetic promoter (Z7E4T). Both the number of activator binding sites and the core promoter region contribute to the requirement for D-A complex recruitment. These functionally distinct core promoters had significant differences in affinity for TBP and TFIID binding. The D-A complex-recruiting activity of Zta was found to be important for promoter selection in the presence of a competitor template. Conditions which limit TFIID binding to the TATA element or compromise the ability of TFIIA to bind TBP required activator stimulation of the D-A complex. These results indicate that D-A complex recruitment is one of at least two activation pathways utilized by Zta and is the essential pathway for a subset of promoters and conditions which limit TFIID binding to the TATA element.
pubmed:grant
pubmed:commentsCorrections
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pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0270-7306
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
6624-32
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
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