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(Received for publication, April 9, 1996, and in revised form, August 26, 1996)
From the Section on Molecular and Cellular Physiology, Diabetes
Branch, NIDDK, National Institutes of Health, Bethesda, Maryland
20892-1770 and the § Department of Pediatrics, University of
California, San Francisco, California 94143
Insulin-like growth factor-I receptor (IGF-IR)
gene expression is regulated by various stimuli, including hormones,
growth factors, and nutritional status. We have investigated the
molecular mechanism by which two growth factors, insulin-like growth
factor-I (IGF-I) and basic fibroblast growth factor (bFGF) regulate
IGF-IR gene expression. bFGF increases the endogenous IGF-IR mRNA
levels and IGF-IR promoter activity. This effect is mediated by a
region of the IGF-IR promoter located between nucleotides
Volume 272, Number 8,
Issue of February 21, 1997
pp. 4663-4670
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
476 and
188 in the 5
-flanking region. In contrast, IGF-I decreases the
IGF-IR mRNA levels. IGF-I down-regulates IGF-IR transcriptional
activity as deduced from experiments in which the levels of
pre-mRNA and mRNA were measured. IGF-I reduced pre-mRNA and
mRNA levels in parallel, while the mRNA stability was found to
be unchanged by IGF-I treatment. While these results strongly suggest
an effect of IGF-I on IGF-IR transcriptional activity, no specific
IGF-I response element was demonstrated in the 5-untranslated region or 5-flanking region studied. Thus, bFGF and IGF-I have differential effects on IGF-IR gene transcription, with the IGF-I response region as
yet unidentified.
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