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PMID: 2511007 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Repression of c-fos transcription is mediated through p67SRF bound to the SRE.

The EMBO journal ·Vol. 8 ·No. 9 ·1989-09-00 ·Pages 2567-74

Shaw PE, Frasch S, Nordheim A

Abstract

Human c-fos expression is subject to tight transcriptional control. The gene is expressed at a high, constitutive level in some cell types and at a very low, but rapidly inducible level in many others. Induction of transcription by serum growth factors is mediated by the serum response element (SRE) to which at least two transcription factors, p67SRF and p62, bind. In this paper it is demonstrated that the low basal level of transcription is mediated through p67SRF bound to the SRE and that high, constitutive expression is observed when binding is prohibited. In this situation, an AP-1 consensus binding site adjacent to the SRE permits transactivation of the gene. Thus three levels of c-fos expression, induced, repressed and constitutive, appear to be determined by occupation of the SRE by p67SRF and its interaction with other proteins.

MeSH Terms
Base Sequence Blood Physiological Phenomena DNA Mutational Analysis DNA-Binding Proteins/physiology Enhancer Elements, Genetic HeLa Cells Humans Promoter Regions, Genetic Proto-Oncogene Proteins/genetics Proto-Oncogene Proteins c-fos Proto-Oncogene Proteins c-jun/physiology Regulatory Sequences, Nucleic Acid Repressor Proteins/physiology Transcription Factors/metabolism,physiology Transcription, Genetic
Chemicals
DNA-Binding Proteins Proto-Oncogene Proteins Proto-Oncogene Proteins c-fos Proto-Oncogene Proteins c-jun Repressor Proteins Transcription Factors
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Shaw P E
Zentrum für Molekulare Biologie Heidelberg, Universität Heidelberg, FRG.
Frasch S
Nordheim A
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Article Info
Journal
The EMBO journal
Abbr.
EMBO J
ISSN
0261-4189
Published
1989-09-00
Pages
2567-74
Language
English
Region
England
NLM ID
8208664
PMCID
PMC401258
Subset
IM
External Links
PubMed source PMC Full Text View journal details
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