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Molecular and Cellular Biology, March 1999, p. 1841-1852, Vol. 19, No. 3
Department of Human
Genetics,1 Huntsman Cancer
Institute,2 Program in Human Molecular Biology
and Genetics, Departments of Oncological Sciences, Human Genetics, and
Internal Medicine, University of Utah, Salt Lake City, Utah 84112
Received 3 September 1998/Returned for modification 22 October
1998/Accepted 10 December 1998
Hypertrophic growth of cardiac muscle cells is induced by a variety
of physiological and pathological stimuli and is associated with a
number of changes, including activation of genes such as atrial
natriuretic factor. We found that two serum response element (SRE)-like
DNA elements, one of which does not meet the consensus sequence and
binds serum response factor (SRF) with low affinity, regulate the
activity of this promoter. Surprisingly, the ability to induce the
promoter by two different physiologic stimuli, as well as various
activated transcription factors, including SRF-VP16, was primarily
dependent upon the nonconsensus rather than the consensus SRE. This SRE
controls the induction of gene expression via an unusual mechanism in
that it is required to allow some, but not all, active transcription
factors at unrelated sites on the promoter to stimulate gene
expression. Thus, in addition to regulation of SRF activity by growth
stimuli, regulation of a low-affinity SRE element controls inducible
gene expression by modulating the ability of other transcription
factors to stimulate the transcription machinery.
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
A Low-Affinity Serum Response Element Allows Other
Transcription Factors To Activate Inducible Gene Expression in
Cardiac Myocytes
*
Corresponding author. Mailing address: Huntsman Cancer
Institute, Department of Oncological Sciences, 15 N 2030 E, Rm. 4160b, University of Utah, Salt Lake City, UT 84112. Phone: (801) 585 6332. Fax: (801) 585 3501. E-mail:
andrew.thorburn{at}hci.utah.edu.
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