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Originally published In Press as doi:10.1074/jbc.M208672200 on February 5, 2003

J. Biol. Chem., Vol. 278, Issue 16, 14363-14369, April 18, 2003
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Endogenous Association of TRAF2, TRAF3, cIAP1, and Smac with Lymphotoxin beta  Receptor Reveals a Novel Mechanism of Apoptosis*

Jun KuaiDagger , Elliott Nickbarg§, Joe Wooters§, Yongchang Qiu§, Jack Wang§, and Lih-Ling LinDagger ||

From the Dagger  Musculoskeletal Science and § Protein Chemistry and Proteomics, Wyeth Research, Cambridge, Massachusetts 02140

Lymphotoxin-beta receptor (LTbeta R) is a member of tumor necrosis factor receptor family and plays essential roles in the embryonic development and organization of secondary lymphoid tissues. It binds two types of tumor necrosis factor family cytokines, heterotrimer LTalpha 1beta 2 and homotrimer LIGHT, and activates multiple signaling pathways including transcriptional factor NFkappa B, c-Jun N-terminal kinase, and cell death. However, the molecular mechanism of the activation of these signaling pathways by LTbeta R is not clear. Because there is no enzymatic activity associated with the receptor itself, the signal transduction of LTbeta R is mediated by cytoplasmic proteins recruited to receptors. To identify these proteins, we took a proteomic approach. The endogenous LIGHT·LTbeta R complex was affinity-purified from U937 cells, and proteins associated with the complex were identified by mass spectrometry. Four of five proteins identified, TRAF2, TRAF3, cIAP1, and Smac, are reported here. Their association with LTbeta R was further confirmed by coimmunoprecipitation in U937 cells and HEK293 cells. The presence of cIAP1 and Smac in LIGHT·LTbeta R complex revealed a novel mechanism of LIGHT·LTbeta R-induced apoptosis.

* 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.

Present address: Neogenesis Pharmaceuticals, Inc., 840 Memorial Dr., Cambridge, MA 02139.

|| To whom correspondence should be addressed: Musculoskeletal Science, Wyeth Research, 200 Cambridge Park Dr., Cambridge, MA 02140. Tel.: 617-665-5476; Fax: 617-665-5499; E-mail: llin@wyeth.com.

Copyright © 2003 by The American Society for Biochemistry and Molecular Biology, Inc.
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