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(Received for publication, January 14, 1997)
From the Molecular Neurobiology Laboratory, Massachusetts General
Hospital, Department of Neurology, Harvard Medical School, Boston,
Massachusetts 02114
Ciliary neurotrophic factor
(CNTF)-dependent induction of expression of the
neuropeptide vasoactive intestinal peptide (VIP) gene is mediated by a
180-base pair cytokine response element (CyRE) in the VIP promoter. To
elucidate the molecular mechanisms mediating the transcriptional
activation by CNTF, intracellular signaling to the CyRE has been
studied in a neuroblastoma cell line. It has been shown previously that
CNTF induces Stat proteins to bind to a site within the CyRE. CNTF also
induces a second protein to bind to a C/EBP-like site within the CyRE.
In this report, we show that this inducible CyRE binding protein is
composed of the AP-1 proteins c-Fos, JunB, and JunD. These proteins
bind to a non-canonical AP-1 site located near the previously
characterized C/EBP site. The serine/threonine kinase inhibitor H7
prevents CNTF-dependent induction of AP-1 binding and
CyRE-mediated transcription, suggesting that an H7-sensitive kinase is
important to mediating CNTF effects on VIP transcription. The
integration at the VIP CyRE of the Jak-Stat and AP-1 signaling pathways
with other pre-existing proteins provides a cellular mechanism for
cell- and cytokine-specific signaling.
Volume 272, Number 15,
Issue of April 11, 1997
pp. 9648-9654
©1997 by The American Society for Biochemistry and Molecular Biology, Inc.
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