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Originally published In Press as doi:10.1074/jbc.M010681200 on January 30, 2001

J. Biol. Chem., Vol. 276, Issue 20, 17252-17260, May 18, 2001
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Phosphorylation of the Tumor Necrosis Factor Receptor CD120a (p55) Recruits Bcl-2 and Protects against Apoptosis*

Vincent CottinDagger §, Annemie A. Van LindenDagger , and David W. H. RichesDagger ||**Dagger Dagger §§

From the Dagger  Program in Cell Biology, Department of Pediatrics, National Jewish Medical and Research Center, Denver, Colorado, 80206 and the || Department of Biochemistry and Molecular Genetics, ** Division of Pulmonary and Critical Care Medicine, Department of Medicine, Dagger Dagger  Department of Pharmacology and  Department of Immunology, University of Colorado Health Sciences Center, Denver, Colorado 80262

Ligation of the tumor necrosis factor alpha  receptor CD120a initiates responses as diverse as apoptosis and the expression of NF-kappa B-dependent pro-survival genes. How these opposing responses are controlled remains poorly understood. Here we demonstrate that phosphorylation by p42mapk/erk2 inhibits the apoptotic activity of CD120a while preserving its ability to activate NF-kappa B. Phosphorylated CD120a is re-localized from the Golgi complex to tubular structures of the endoplasmic reticulum wherein it recruits Bcl-2. Antisense-mediated down-regulation of Bcl-2 antagonized the localization of CD120a to tubular structures and reversed the protection from apoptosis conferred by receptor phosphorylation. We propose that phosphorylation of CD120a represents a novel, Bcl-2-dependent mechanism by which the apoptotic activity of the receptor may be regulated. Thus, oncogenic activation of p42mapk/erk2 may serve to inhibit the apoptotic activity of this death receptor while preserving NF-kappa B-dependent responses and may thus indirectly contribute to a failure to eliminate cells bearing oncogenes of the Ras-Raf-MEK-p42mapk/erk2 pathway.

* This work was supported in part by United States Public Health Services Grants HL55549 and SCOR HL 56556 from the National Institutes of Health.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 Traveling Fellowship grants from the Société de Pneumologie de Langue Française, the Association pour la Recherche contre le Cancer, Fondation Alain Philippe, Fondation Lavoisier du Ministère des Affaires Etrangères, and a Michael and Eleanore Stobin 1999 Pediatric Fellowship from National Jewish Medical and Research Center, Denver, CO.

§§ To whom correspondence should be addressed: Dept. of Pediatrics, National Jewish Medical and Research Center, Neustadt Rm. D405, 1400 Jackson St., Denver, CO 80206. Tel.: 303-398-1188; Fax: 303-398-1381; E-mail: richesd@njc.org.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
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