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Irradiation of mammalian cells with short wavelength ultraviolet
light (UVC) evokes a cascade of phosphorylation events leading to
altered gene expression. Both the classic mitogen-activated protein
(MAP) kinases and the distantly related c-Jun N-terminal kinases (JNK)
contribute to the response via phosphorylation of transcription factors
including AP-1. These kinases are themselves regulated via reversible
phosphorylation, and several recently identified specific MAP kinase
phosphatases (MKP) have been implicated in down-regulating MAP
kinase-dependent gene expression in response to mitogens. Here, we
provide evidence that MKP-1 plays a role in regulating transcriptional
activation in response to UVC as well as another genotoxic agent,
methyl methanesulfonate (MMS). We further demonstrate that JNK is a
likely target for MKP-1. JNK is shown to be activated by UVC and MMS
treatment, while MAP kinase activation occurs only with UVC. Like JNK
activation, MKP-1 mRNA is induced by both treatments, and elevated
MKP-1 expression coincides with a decline in JNK activity. Constitutive
expression of MKP-1 in vivo inhibits JNK activity and reduces
UVC- and MMS-induced activation of AP-1-dependent reporter genes.
Volume 270,
Number 15,
Issue of April 14, pp. 8377-8380, 1995
©1995 by The American Society for Biochemistry and Molecular Biology, Inc.
INHIBITION OF c-Jun N-TERMINAL KINASE ACTIVITY AND AP-1-DEPENDENT
GENE ACTIVATION
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