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J Biol Chem, Vol. 274, Issue 40, 28697-28707, October 1, 1999
From the Interleukin (IL)-6 plays an important role in a
wide range of biological activities, including differentiation of
murine M1 myeloid leukemic cells into mature macrophages. At the onset
of M1 differentiation, a set of myeloid differentiation primary
response (MyD) genes are induced, including the proto-oncogene for
JunB. In order to examine the molecular nature of the mechanisms by which IL-6 activates the immediate early expression of MyD genes, JunB
was used as a paradigm. A novel IL-6 response element,
Interleukin-6 and Leukemia Inhibitory Factor Induction of JunB Is
Regulated by Distinct Cell Type-specific Cis-acting Elements
§,, and
Fels Institute for Cancer Research and
Molecular Biology and Department of Biochemistry, Temple University
School of Medicine, Philadelphia, Pennsylvania 19140 and the
§ Department of Biochemistry and Molecular Biophysics,
University of Pennsylvania School of Medicine,
Philadelphia, Pennsylvania 19104
65/52 IL-6RE, to which a 100-kDa protein complex is bound, has been identified on the JunB promoter. Leukemia inhibitory factor
(LIF)-induced activation of JunB in M1 cells was also mediated via the
65/52 IL-6RE. The STAT3 and CRE-like binding sites of the JunB
promoter, identified as IL-6-responsive elements in HepG2 liver cells
were found, however, to play no role in JunB inducibility by IL-6 in M1
myeloid cells. Conversely, the 65/52 IL-6RE is shown not to be
necessary for JunB inducibility by IL-6 or LIF in liver cells. It
appears, therefore, that immediate early activation of JunB is
regulated differently in M1 myeloid cells than in HepG2 liver cells.
This indicates that distinct cis-acting control elements participate in
cell type-specific induction of JunB by members of the IL-6 cytokine superfamily.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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