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J Biol Chem, Vol. 275, Issue 20, 15336-15342, May 19, 2000

TAJ, a Novel Member of the Tumor Necrosis Factor Receptor Family, Activates the c-Jun N-terminal Kinase Pathway and Mediates Caspase-independent Cell Death*

Michael T. EbyDagger , Alan JasminDagger , Arvind KumarDagger , Kiran Sharma§, and Preet M. ChaudharyDagger

From the Dagger  Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, Dallas, Texas 75390-8593 and the § University of Washington, Seattle, Washington 98195

We have isolated a novel member of the TNFR family, designated TAJ, that is highly expressed during embryonic development. TAJ possesses a unique cytoplasmic domain with no sequence homology to the previously characterized members of the TNFR family. TAJ interacts with the TRAF family members and activates the JNK pathway when overexpressed in mammalian cells. Although it lacks a death domain, TAJ is capable of inducing apoptosis by a caspase-independent mechanism. Based on its unique expression profile and signaling properties, TAJ may play an essential role in embryonic development.


* 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.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF167552-AF167555.

To whom correspondence and reprint requests should be addressed: The Hamon Center for Therapeutic Oncology Research, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75390-8593. Tel.: 214-648-1837; Fax: 214-648-4940; E-mail: pchaud@mednet.swmed.edu.


Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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