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(Received for publication, June 27, 1996, and in revised form, August 7, 1996)
From ONYX Pharmaceuticals, 3031 Research Drive, Richmond,
California 94806
The role of protein kinase C (PKC) in
inflammation, mitogenesis, and differentiation has been deduced in part
through the use of a variety of PKC inhibitors. Two widely used
inhibitors are the structurally related compounds GF109203X and
Ro-31-8220, both of which potently inhibit PKC activity and are
believed to be highly selective. While using GF109203X and Ro-31-8220
to address the role of PKC in immediate early gene expression, we
observed striking differential effects by each of these two compounds.
Growth factors induce the expression of the immediate early gene
products MAP kinase phosphatase-1 (MKP-1), c-Fos and c-Jun. Ro-31-8220
inhibits growth factor-stimulated expression of MKP-1 and c-Fos but
strongly stimulated c-Jun expression, even in the absence of growth
factors. GF109203X displays none of these properties.
These data suggest that Ro-31-8220 may have other pharmacological
actions in addition to PKC inhibition. Indeed, Ro-31-8220 strongly
stimulates the stress-activated protein kinase, JNK1. Furthermore,
Ro-31-8220 apparently activates JNK in a PKC-independent manner.
Neither the down-regulation of PKC by phorbol esters nor the inhibition
of PKC by GF109203X affected the ability of Ro-31-8220 to activate
JNK1. These data suggest that, in addition to potently inhibiting PKC,
Ro-31-8220 exhibits novel pharmacological properties which are
independent of its ability to inhibit PKC.
Volume 271, Number 43,
Issue of October 25, 1996
pp. 27018-27024
©1996 by The American Society for Biochemistry and Molecular Biology, Inc.
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