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J Biol Chem, Vol. 274, Issue 42, 29595-29598, October 15, 1999
From the Laboratory of Gene Regulation and Signal
Transduction, Department of Pharmacology, School of Medicine,
University of California, San Diego, La
Jolla, California 92093-0636.
DNA damage and environmental stress activate
signaling and induce genes involved in cell cycle and cell death.
Expression of the Gadd45 protein is induced following DNA damage and
other stress. Gadd45 is believed to play a role in growth arrest and possibly in cell death. The JNK signaling pathway is also activated by
some DNA-damaging agents. This activation leads to phosphorylation and
activation of transcription factors, such as c-Jun/AP-1 and ATF2, which
mediate immediate early gene induction. Recently Gadd45 was suggested
to be involved in JNK activation. However, as this suggestion relied on
in vitro experiments and ectopic overexpression of Gadd45
protein, we examined whether physiological levels of Gadd45 that are
induced following exposure to DNA damaging agents and stress can lead
to JNK induction. We found that JNK activation by UV irradiation and
anisomycin treatment precedes the induction of gadd45
mRNA by these agents. Gadd45 protein induction by methyl methanesulfonate also lagged behind JNK activation. The use of protein
synthesis inhibitors suggested that newly synthesized proteins,
including the stress-induced Gadd45, make only a marginal contribution
to JNK activation. We also found that stresses such as 
irradiation
induce Gadd45 and do not activate JNK in mouse fibroblasts. Therefore,
stress-induced JNK does not depend on Gadd45 induction.
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