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J Biol Chem, Vol. 273, Issue 32, 20636-20643, August 7, 1998
From the Department of Biology and Molecular Biology, Institute,
San Diego State University, San Diego, California 92182
In various cell types certain
stresses can stimulate p38 mitogen-activated protein kinase (p38 MAPK),
leading to the transcriptional activation of genes that contribute to
appropriate compensatory responses. In this report the mechanism of
p38-activated transcription was studied in cardiac myocytes where this
MAPK is a key regulator of the cell growth and the cardiac-specific
gene induction that occurs in response to potentially stressful
stimuli. In the cardiac atrial natriuretic factor (ANF) gene, a
promoter-proximal serum response element (SRE), which binds serum
response factor (SRF), was shown to be critical for ANF induction in
primary cardiac myocytes transfected with the selective p38 MAPK
activator, MKK6 (Glu). This ANF SRE does not possess sequences
typically required for the binding of the Ets-related ternary complex
factors (TCFs), such as Elk-1, indicating that p38-mediated induction
through this element may take place independently of such TCFs.
Although p38 did not phosphorylate SRF in vitro, it
efficiently phosphorylated ATF6, a newly discovered SRF-binding protein
that is believed to serve as a co-activator of SRF-inducible
transcription at SREs. Expression of an ATF6 antisense RNA blocked
p38-mediated ANF induction through the ANF SRE. Moreover, when fused to
the Gal4 DNA-binding domain, an N-terminal 273-amino acid fragment of
ATF6 was sufficient to support trans-activation of
Gal4/luciferase expression in response to p38 but not the other stress
kinase, N-terminal Jun kinase (JNK); p38-activating cardiac growth
promoters also stimulated ATF6 trans-activation. These
results indicate that through ATF6, p38 can augment SRE-mediated
transcription independently of Ets-related TCFs, representing a novel
mechanism of SRF-dependent transcription by MAP
kinases.
p38 Mitogen-activated Protein Kinase Mediates the Transcriptional
Induction of the Atrial Natriuretic Factor Gene through a Serum
Response Element
A POTENTIAL ROLE FOR THE TRANSCRIPTION FACTOR ATF6
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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