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J. Biol. Chem., Vol. 277, Issue 34, 30792-30797, August 23, 2002
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From the Centre de recherche en cancérologie de
l'Université Laval, L'Hôtel-Dieu de Québec,
Centre hospitalier universitaire de Québec, Quebec
G1R 2J6, Canada
Despite the importance of the stress-activated
protein kinase pathways in cell death and survival, it is
unclear how stressful stimuli lead to their activation. In the case of
heat shock, the existence of a specific mechanism of activation has
been evidenced, but the molecular nature of this pathway is undefined.
Here, we found that Ask1 (apoptosis signal-regulating kinase 1), an
upstream activator of the stress-activated protein kinase p38 during
exposure to oxidative stress and other stressful stimuli, was also
activated by heat shock. Ask1 activity was required for p38 activation
since overexpression of a kinase dead mutant of Ask1, Ask1(K709M),
inhibited heat shock-induced p38 activation. The activation of Ask1 by
oxidative stress involves the oxidation of thioredoxin, an endogenous
inhibitor of Ask1. A different activation mechanism takes place during
heat shock. In contrast to p38 induction by
H2O2, induction by heat shock was not
antagonized by pretreatment with the antioxidant N-acetyl-L-cysteine or by overexpressing
thioredoxin and was not accompanied by the dissociation of thioredoxin
from Ask1. Instead, heat shock caused the dissociation of glutathione
S-transferase Mu1-1 (GSTM1-1) from Ask1 and overexpression
of GSTM1-1-inhibited induction of p38 by heat shock. We concluded that
because of an alternative regulation by the two distinct repressors
thioredoxin and GSTM1-1, Ask1 constitutes the converging point of the
heat shock and oxidative stress-sensing pathways that lead to p38 activation.
Activation of the p38 Signaling Pathway by Heat Shock Involves
the Dissociation of Glutathione S-Transferase Mu from
Ask1*
,
*
This work was supported by the Canadian Institutes of Health
Research Grant MT-7088.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by a studentship from the Canadian Institutes of Health Research.
§
To whom correspondence should be addressed. Tel.: 418-525-4444 (ext. 5155); Fax: 418-691-5439; E-mail:
jacques.landry@med.ulaval.ca.
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