Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
50
pubmed:dateCreated
1996-10-22
pubmed:abstractText
The transcription factor Sp1 plays a key role in the activation of many cellular and viral gene promoters, including those that are regulated during the cell cycle. However, recent evidence indicates that Sp1 belongs to a larger family of factors which bind G/C box elements in order to either activate or repress transcription. Sp3, a member of this family, functions to repress transcriptional activation in two viral promoters, most likely by competing with Sp1 for GC box/Sp binding sites. However, the physiological role of Sp3 in the repression of endogenous cellular promoters has not been experimentally addressed. In the present study, we analyze the activity and binding of Sp3 on several eukaryotic promoters that contain G/C boxes and are known to be regulated during cellular proliferation and the cell cycle. Using antibodies specific for Sp1 and Sp3, we observe that both of these factors localize to the cell nucleus and have a similar, dispersed subnuclear distribution. Further, using gel mobility shift assays, we show that both Sp1 and Sp3 interact specifically with the histone H4 promoter. Transient cotransfections of Drosophila cells with Sp1 and Sp3 expression vectors and with the histone H4, thymidine kinase (TK), or dihydrofolate reductase (DHFR) promoters show that only the DHFR promoter, containing multiple functional GC boxes, displays Sp3 repression of Sp1 activation. In contrast, the single G/C boxes within the histone H4 or TK promoters, which confer transcriptional activation via Sp1 binding, are not responsive to repression by Sp3. Therefore, we demonstrate that the endogenous cellular DHFR promoter is selectively responsive to Sp3 repression. The data suggest that Sp3 may contribute to the control of proliferation- and/or cell-regulated promoters depending upon the context and/or number of functional Sp1 binding sites.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0006-2960
pubmed:author
pubmed:issnType
Print
pubmed:day
19
pubmed:volume
34
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
16503-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:8845379-Animals, pubmed-meshheading:8845379-Base Sequence, pubmed-meshheading:8845379-Cell Compartmentation, pubmed-meshheading:8845379-Cell Cycle, pubmed-meshheading:8845379-Cell Nucleus, pubmed-meshheading:8845379-Cricetinae, pubmed-meshheading:8845379-DNA-Binding Proteins, pubmed-meshheading:8845379-Drosophila, pubmed-meshheading:8845379-Gene Expression Regulation, pubmed-meshheading:8845379-HeLa Cells, pubmed-meshheading:8845379-Histones, pubmed-meshheading:8845379-Humans, pubmed-meshheading:8845379-Molecular Sequence Data, pubmed-meshheading:8845379-Promoter Regions, Genetic, pubmed-meshheading:8845379-Protein Binding, pubmed-meshheading:8845379-Recombinant Proteins, pubmed-meshheading:8845379-Sp1 Transcription Factor, pubmed-meshheading:8845379-Sp3 Transcription Factor, pubmed-meshheading:8845379-Tetrahydrofolate Dehydrogenase, pubmed-meshheading:8845379-Thymidine Kinase, pubmed-meshheading:8845379-Transcription Factors, pubmed-meshheading:8845379-Transcriptional Activation, pubmed-meshheading:8845379-Transfection
pubmed:year
1995
pubmed:articleTitle
Sp1 trans-activation of cell cycle regulated promoters is selectively repressed by Sp3.
pubmed:affiliation
Department of Cell Biology, University of Massachusetts Medical School, Worcester 01655, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't