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Originally published In Press as doi:10.1074/jbc.M308737200 on February 11, 2004

J. Biol. Chem., Vol. 279, Issue 17, 17148-17157, April 23, 2004
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Translational Induction of the Inhibitor of Apoptosis Protein HIAP2 during Endoplasmic Reticulum Stress Attenuates Cell Death and Is Mediated via an Inducible Internal Ribosome Entry Site Element*

Dinesh Warnakulasuriyarachchi, Sonia Cerquozzi, Herman H. Cheung, and Martin Holcík{ddagger}

From the Apoptosis Research Center, Children's Hospital of Eastern Ontario, Department of Pediatrics, University of Ottawa, Ottawa, Ontario K1H 8L1, Canada

Prolonged endoplasmic reticulum (ER) stress leads to activation of caspases and cell death. The inhibitor of apoptosis (IAP) proteins are intrinsic inhibitors of apoptosis by virtue of inhibiting distinct caspases and are, therefore, critical regulators of cell death. Here we demonstrate that the expression of one member of the IAP family, HIAP2, is induced in response to ER stress and attenuates ER stress-induced cell death. The induction of HIAP2 is executed at the level of protein synthesis and is mediated by an inducible internal ribosome entry site (IRES) element. The triggering of ER stress results in caspase-mediated proteolytic processing of eukaryotic initiation factor p97/DAP5/NAT1, producing a fragment that specifically activates HIAP2 IRES. These data suggest an existence of a novel mechanism that regulates apoptotic response in ER stress.

Received for publication, August 7, 2003 , and in revised form, January 8, 2004.

* This work was supported in part by Canadian Institutes of Health Research Operating Grant 43984. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

{ddagger} A Canadian Institutes of Health Research New Investigator. To whom correspondence should be addressed: Apoptosis Research Center, Children's Hospital of Eastern Ontario Research Institute, Rm. R310, 401 Smyth Rd., Ottawa, ON K1H 8L1, Canada. Tel.: 613-738-3207; Fax: 613-738-4833; E-mail: martin{at}mgcheo.med.uottawa.ca.


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