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J Biol Chem, Vol. 273, Issue 43, 28355-28359, October 23, 1998
From the Tumor necrosis factor (TNF)-related
activation-induced cytokine (TRANCE), a member of the TNF family
expressed on activated T-cells, bone marrow stromal cells, and
osteoblasts, regulates the function of dendritic cells (DC) and
osteoclasts. The TRANCE receptor (TRANCE-R), recently identified as
receptor activator of NF-
The TRAF Family of Signal Transducers Mediates NF-
B Activation
by the TRANCE Receptor
,,
Howard Hughes Medical Institute,
Laboratory of Immunology, and § Laboratory of
Cellular Physiology and Immunology, The Rockefeller University, New
York, New York 10021 and ¶ Department of Pathology, Hallym
University, Chunchon, Kangwon-Do 200-702, Korea
(RANK), activates NF-B, a
transcription factor critical in the differentiation and activation of
those cells. In this report we identify the TNF
receptor-associated factor (TRAF) family of signal transducers as
important components of TRANCE-R-mediated NF-B activation.
Coimmunoprecipitation experiments suggested potential interactions
between the cytoplasmic tail of TRANCE-R with TRAF1, TRAF2, TRAF3,
TRAF5, and TRAF6. Dominant negative forms of TRAF2, TRAF5, and TRAF6
and an endogenous inhibitor of TRAF2, TRAF-interacting protein (TRIP),
substantially inhibited TRANCE-R-mediated NF-B activation,
suggesting a role of TRAFs in regulating DC and osteoclast function.
Overexpression of combinations of TRAF dominant negative proteins
revealed competition between TRAF proteins for the TRANCE-R and
the possibility of a TRAF-independent NF-B pathway. Analysis
of TRANCE-R deletion mutants suggested that the TRAF2 and TRAF5
interaction sites were restricted to the C-terminal 93 amino acids
(C-region). TRAF6 also complexed to the C-region in addition to several
regions N-terminal to the TRAF2 and TRAF5 association sites.
Furthermore, transfection experiments with TRANCE-R deletion mutants
revealed that multiple regions of the TRANCE-R can mediate NF-B
activation.
Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.
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