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J Biol Chem, Vol. 274, Issue 43, 30603-30610, October 22, 1999
From the National Jewish Medical and Research Center, Division of
Basic Immunology and University of Colorado Health Sciences Center,
Department of Immunology, Denver, Colorado 80206
Tumor necrosis factor (TNF)-related
apoptosis-inducing ligand (TRAIL) is a member of the TNF family that
interacts with several receptors, including TRAIL-R1, TRAIL-R2, and
TRAIL-R4. TRAIL-R1 and TRAIL-R2 can induce apoptosis of cancer cells
and activate the transcription factor NF-
Tumor Necrosis Factor-related Apoptosis-inducing Ligand Receptors
Signal NF-
B and JNK Activation and Apoptosis through Distinct
Pathways
B. TRAIL-R4 can activate
NF-B and protect cells from TRAIL-induced apoptosis. Here we show
that TRAIL-R1-, TRAIL-R2-, and TRAIL-R4-induced NF-B activation are mediated by a TRAF2-NIK-IB kinase 
/
signaling cascade but is MEKK1 independent. TRAIL receptors also activate the protein kinase JNK. JNK activation by TRAIL-R1 is mediated by a TRAF2-MEKK1-MKK4 but
not the TRAF2-NIK/IB kinase / signaling pathway. We also show
that activation of NF-B or overexpression of TRAIL-R4 does not
protect TRAIL-R1-induced apoptosis. Moreover, inhibition of NF-B by
IB sensitizes cells to tumor necrosis factor- but not TRAIL-induced apoptosis. These findings suggest that TRAIL receptors induce apoptosis, NF-B and JNK activation through distinct signaling pathways, and activation of NF-B is not sufficient for protecting cells from TRAIL-induced apoptosis.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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