Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1-2
pubmed:dateCreated
2001-4-12
pubmed:abstractText
Upon uracil depletion, the transcriptional activator Ppr1p stimulates expression of the Saccharomyces cerevisiae URA3 gene only four-fold. We performed a split-ubiquitin screen with Tup1p as bait, and we found that the global repressor Tup1p interacts with the transcriptional activator Ppr1p both in vivo and in vitro. The interaction is biologically significant, since the deletion of the TUP1 gene as well as the removal of the Tup1p-binding domain from Ppr1p results in an increased expression of the URA3 gene. Our results suggest that Tup1p blocks Ppr1p directly, and that Ppr1p is a weak activator of transcription because of its interaction with Tup1p. Thus we were able to demonstrate that the global repressor Tup1p can modulate transcription by interacting with an activator.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0014-5793
pubmed:author
pubmed:issnType
Print
pubmed:day
6
pubmed:volume
494
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
64-8
pubmed:dateRevised
2009-7-24
pubmed:meshHeading
pubmed:year
2001
pubmed:articleTitle
Why Ppr1p is a weak activator of transcription.
pubmed:affiliation
Max-Delbrück-Laboratorium in der Max-Planck-Gesellschaft, Carl-von-Linné-Weg 10, 50829, Cologne, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't