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J. Biol. Chem., Vol. 279, Issue 16, 16050-16056, April 16, 2004

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Positive Regulation of Apoptosis Signal-regulating Kinase 1 by hD53L1^*

Sayeon Cho¶, Hyung-Mun Ko, Jeong-Min Kim||, Jung-A Lee, Jae-Eun Park, Mi-Sun Jang, Sung Goo Park, Do Hee Lee, Seong-Eon Ryu||, and Byoung-Chul Park**

From the Research Center for Systemic Proteomics and ^||Center for Cellular Switch Protein Structure, Korea Research Institute of Bioscience and Biotechnology, P.O. Box 115, Yusong, Taejon 305-600, South Korea

Apoptosis signal-regulating kinase 1 (ASK1) is a mitogen-activated protein kinase kinase kinase family member that plays a central role in cytokine- and stress-induced apoptosis by activating c-Jun N-terminal kinase and p38 signaling cascades. ASK1-induced apoptotic activity is up-regulated by two cellular factors, Daxx and TRAF2, through direct protein-protein interactions. Daxx and TRAF2 are death receptor-associated proteins in Fas and tumor necrosis factor- pathways, respectively. Recent studies suggest that calcium signaling may regulate ASK1 pathway. Here we report that human D53L1, a member of the tumor protein D52 family involved in cell proliferation and calcium signaling, up-regulates the ASK1-induced apoptosis. The human D53L1 physically interacts with the C-terminal regulatory domain of ASK1 and promotes ASK1-induced apoptotic activity by activating caspase signaling in mammalian cells. In luciferase reporter assays, hD53L1 activates c-Jun N-terminal kinase-mediated transactivation in the presence of ASK1. Expression of hD53L1 enhances autophosphorylation and kinase activity of ASK1 but has no effect on ASK1 oligomerization that is necessary for kinase activity and on binding of ASK1 to MKK6, a downstream factor of ASK1. Taken together, these results suggest that activation of ASK1 by hD53L1 may provide a novel mechanism for ASK1 regulation.

Received for publication, June 2, 2003 , and in revised form, January 29, 2004.

^* This work was supported by a Korea Health 21 R&D Project, Ministry of Health & Welfare, Republic of Korea Grant 01-PJ10-PG6-01GN16-0005. 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.

Both authors contributed equally to this work.

¶ To whom correspondence should be addressed. Tel.: 82-42-860-4263; Fax: 82-42-860-4593; E-mail: scho{at}kribb.re.kr. ** To whom correspondence should be addressed. Tel.: 82-42-860-4260; Fax: 82-42-860-4593; E-mail: parkbc{at}kribb.re.kr.

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