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J. Biol. Chem., Vol. 278, Issue 18, 15794-15799, May 2, 2003
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From the Laboratory of Molecular Cell Biology, The Rockefeller
University, New York, New York 10021
The c-fos gene was one of the
earliest vertebrate genes shown to be transcriptionally induced by
growth factors. Intensive study of the promoter of c-fos
(
Independent and Cooperative Activation of Chromosomal
c-fos Promoter by STAT3*
325 to 80) by transient or permanent transfections of synthetic
DNA constructs has repeatedly shown the importance of several sequence
elements and the resident nuclear proteins that bind them
(e.g. ternary complex factor/ELK1; serum response factor,
cAMP response element-binding protein/amino-terminal fragment/AP-1). However these studies have left unanswered
numerous questions about the role of these proteins in the regulation
of the native chromosomal gene. In particular, the role of a site in
this enhancer that binds STATs has been controversial. We present evidence here that STAT3 and not STAT1 accumulates on the chromosomal c-fos promoter and provides a boost to transcription
without the activation of resident nuclear proteins through serine
kinases. Also, when resident nuclear proteins such as ELK1 are
activated to varying extents by mitogen-activated protein kinase
pathways, STAT3 activation provides a 2-fold boost regardless of the
final level of activated transcription. Thus the several proteins that interact with the c-fos enhancer apparently can act either
in a cooperative or independent manner to achieve very different levels
of transcription.
*
This work was supported by National Institutes of Health
(NIH) Grants AI34420 and AI32489 (to J. E. D.), Medical Scientist Training Program Grant GM07739 (to E. Y.), and NIH Training
Grant CA09673 (to E. Y. and D. B.)The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.:
212-327-8796; Fax: 212-327-8801; E-mail:
darnell@mail.rockefeller.edu.
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