Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
35
pubmed:dateCreated
1996-10-10
pubmed:abstractText
Previous studies revealed that sequences surrounding the initiation sites in many mammalian and viral gene promoters, called initiator (Inr) elements, may be essential for promoter strength and for determining the actual transcription start sites. DNA sequences in the vicinity of the human metallothionein IIA (hMTIIA) gene transcription start site share homology with some of the previously identified Inr elements. However, in the present study we have found by in vitro transcription assays that the hMTIIA promoter does not contain a typical Inr. Electrophoretic mobility shift assays identified several DNA-protein complexes at the hMTIIA gene transcription start site. A partially purified protein fraction containing replication protein A (RPA) binds to the hMTIIA gene transcription start site and represses transcription from the hMTIIA promoter in vitro. In addition, overexpression of the human 70-kDa RPA-1 protein represses transcription of a reporter gene controlled by the hMTIIA promoter in vivo. These findings suggest that hMTIIA transcription initiation is controlled by a mechanism different from most mammalian and viral promoters and that the previously identified RPA may also be involved in transcription regulation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0021-9258
pubmed:author
pubmed:issnType
Print
pubmed:day
30
pubmed:volume
271
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
21637-44
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Replication protein A is a component of a complex that binds the human metallothionein IIA gene transcription start site.
pubmed:affiliation
Moffitt Cancer Center & Research Institute, University of South Florida, Tampa, Florida, 33612, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.