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J Biol Chem, Vol. 274, Issue 15, 9962-9968, April 9, 1999
B Transcription Factor and c-Jun
N-terminal Kinase
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From the We have previously reported on the death effector
domain containing E8 gene product from equine
herpesvirus-2, designated FLICE inhibitory protein
(v-FLIP), and on its cellular homologue, c-FLIP, which inhibit the
activation of caspase-8 by death receptors. Here we report on the
structure and function of the E10 gene product of equine herpesvirus-2,
designated v-CARMEN, and on its cellular homologue, c-CARMEN, which
contain a caspase-recruiting domain (CARD) motif. c-CARMEN is highly
homologous to the viral protein in its N-terminal CARD motif but
differs in its C-terminal extension. v-CARMEN and c-CARMEN interact
directly in a CARD-dependent manner yet reveal different
binding specificities toward members of the tumor necrosis factor
receptor-associated factor (TRAF) family. v-CARMEN binds to TRAF6 and
weakly to TRAF3 and, upon overexpression, potently induces the c-Jun
N-terminal kinase (JNK), p38, and nuclear factor (NF)- Institute of Biochemistry,
B
transcriptional pathways. c-CARMEN or truncated versions thereof do not
appear to induce JNK and NF-B activation by themselves, nor do they
affect the JNK and NF-B activating potential of v-CARMEN. Thus, in
contrast to the cellular homologue, v-CARMEN may have additional
properties in its unique C terminus that allow for an autonomous
activator effect on NF-B and JNK. Through activation of NF-B,
v-CARMEN may regulate the expression of the cellular and viral genes
important for viral replication.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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