Linked Life Data

1922364

Source:http://linkedlifedata.com/resource/pubmed/id/1922364

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6344
pubmed:dateCreated
1991-11-7
pubmed:abstractText
A central issue in eukaryotic transcriptional regulation is the mechanism by which promoter-specific transcription factors (activators) stimulate transcription. Two lines of evidence indicate that the general transcription factor TFIIB is a pivotal component in the mechanism by which an acidic activator functions. First, during assembly of the preinitiation complex TFIIB binding is a rate-limiting step enhanced by an acidic activator. Second, the TFIIB activity in a HeLa cell nuclear extract is specifically retained on a column containing an acidic activating region. But because our previous study monitored only TFIIB activity, it remains possible that the interaction between TFIIB and the acidic activating region is mediated through additional proteins, for example, those designated as adaptors, coactivators or mediators. A complementary clone encoding TFIIB has recently been isolated and shown to encode a polypeptide of relative molecular mass 35,000. Here we report that TFIIB expressed in and purified from Escherichia coli (recombinant TFIIB) binds directly to the potent acidic activating region of the herpes simplex virus-1 VP16 protein.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0028-0836
pubmed:author
pubmed:issnType
Print
pubmed:day
10
pubmed:volume
353
pubmed:geneSymbol
TFIIB, TFIID
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
569-71
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Binding of general transcription factor TFIIB to an acidic activating region.
pubmed:affiliation
Program in Molecular Medicine, University of Massachusetts Medical Center, Worcester 01605.
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, P.H.S.