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Selective repression of c- fos gene transcription in rat embryo fibroblasts transformed by oncogenes E1A and cHa-ras

Transformation of REF cells by oncogenes E1A and c Ha-ras leads to activation of AP-1 factor concomitantly with down-regulation of c- fos gene transcription. Here we addressed two issues: (i) how does transcription of Fos/Jun-regulated genes change in the cells lacking Fos-Jun heterodimers; (ii) to...

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Published in:Biochemical and biophysical research communications 2003-06, Vol.306 (2), p.483-487
Main Authors: Abramova, M.V, Kukushkin, A.N, Svetlikova, S.B, Pospelova, T.V, Pospelov, V.A
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cited_by cdi_FETCH-LOGICAL-c392t-95eecac5556d6ec1166805602825dde4e69892d490afc518b730af3264cad4a53
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description Transformation of REF cells by oncogenes E1A and c Ha-ras leads to activation of AP-1 factor concomitantly with down-regulation of c- fos gene transcription. Here we addressed two issues: (i) how does transcription of Fos/Jun-regulated genes change in the cells lacking Fos-Jun heterodimers; (ii) to which extent HDAC-mediated chromatin reorganization does affect, apart from c- fos, transcription of some other early and late-response genes. To this end, we studied the kinetics of serum-stimulated transcription of c- fos, c- jun, fra-1, egr-1, and cyclinD1 genes, as well as the effects of sodium butyrate, an inhibitor of histone deacetylase activity, on transcription of these genes in normal REF cells and transformants E1A + ras.
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subjects Adenovirus E1A Proteins - metabolism
Animals
Blotting, Western
c- fos Repression
Cell Line, Transformed
Cells, Cultured
Chromatin - metabolism
Chromatin remodeling
Dimerization
E1A and ras oncogenes
Fibroblasts - metabolism
Histone deacetylase
Histone Deacetylases - metabolism
Kinetics
Proto-Oncogene Proteins c-fos - metabolism
ras Proteins - metabolism
Rats
Reverse Transcriptase Polymerase Chain Reaction
RNA, Messenger - metabolism
Sodium butyrate
Sodium Oxybate - pharmacology
Transcription, Genetic
title Selective repression of c- fos gene transcription in rat embryo fibroblasts transformed by oncogenes E1A and cHa-ras
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