Transcriptional repression mediated by the serum response factor.
The serum response element (SRE) contributes to transcriptional repression of the c-fos proto-oncogene. We show that the transcription factor SRF is able to repress SRE-dependent transcription, apparently by sequestering a co-activator. Only the DNA-binding core region is required for this SRE-dependent repression. Furthermore the phosphorylation status at potential casein kinase II sites within an N-terminal repression domain affects SRE-independent transcription. SRF may thus pleiotropically influence cellular transcription, representing a novel aspect of SRF function.
Ernst
W H
WH
Institut für Molekularbiologie, Medizinische Hochschule Hannover, Germany.
Janknecht
R
R
Cahill
M A
MA
Nordheim
A
A
D016475:3T3 Cells; D000595:Amino Acid Sequence; D000818:Animals; D004268:DNA-Binding Proteins / Q000502:physiology*; D015536:Down-Regulation; D005786:Gene Expression Regulation; D016762:Genes, fos; D051379:Mice; D008969:Molecular Sequence Data; D009687:Nuclear Proteins / Q000502:physiology*; D010766:Phosphorylation; D026362:Serum Response Factor; D016385:TATA Box; D035362:Transcription Factor TFIID; D014157:Transcription Factors / Q000378:metabolism / Q000502:physiology*; D014158:Transcription, Genetic
D004268:DNA-Binding Proteins; D009687:Nuclear Proteins; D026362:Serum Response Factor; D035362:Transcription Factor TFIID; D014157:Transcription Factors