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J Biol Chem, Vol. 273, Issue 38, 24285-24288, September 18, 1998
From the Department of Biophysics, Graduate School of Science,
Kyoto University, Sakyo-ku, Kyoto 606-8502, Japan
Nerve growth factor (NGF) induces sustained
activation of classical MAP kinase (MAPK, also known as ERK) and
neuronal differentiation in PC12 cells, whereas epidermal growth factor
(EGF) induces transient activation of ERK/MAPK and stimulates
proliferation of the cells. Although previous studies showed that
sustained activation of ERK/MAPK is important for neuronal
differentiation of the cells, a recent report revealed that inhibition
of the sustained phase of ERK/MAPK activation alone does not block
neurite outgrowth caused by NGF. These results suggest requirement for
an additional signaling pathway(s) triggered by NGF in neuronal
differentiation. Here we show that NGF induces sustained activation of
p38, a subfamily member of the MAPK superfamily, and that inhibition of
the p38 pathway blocks neurite outgrowth in PC12 cells. Surprisingly, expression of constitutively active MAPK/ERK kinase (MAPKK, also known
as MEK) results in p38 activation as well as ERK/MAPK activation, and a
p38 inhibitor blocks neurite outgrowth caused by the constitutively active MAPKK/MEK. Moreover, constitutive activation of p38 is able to
induce neurite outgrowth when combined with EGF treatment. These
results reveal an essential role of p38 in neuronal differentiation in
PC12 cells.
COMMUNICATION
Requirement of p38 Mitogen-activated Protein Kinase for
Neuronal Differentiation in PC12 Cells
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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