Equine herpesvirus-2 E10 gene product, but not its cellular homologue, activates NF-kappaB transcription factor and c-Jun N-terminal kinase.
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)-kappaB transcriptional pathways. c- CARMEN or truncated versions thereof do not appear to induce JNK and NF-kappaB activation by themselves, nor do they affect the JNK and NF-kappaB 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-kappaB and JNK. Through activation of NF-kappaB, v- CARMEN may regulate the expression of the cellular and viral genes important for viral replication.[1]References
- Equine herpesvirus-2 E10 gene product, but not its cellular homologue, activates NF-kappaB transcription factor and c-Jun N-terminal kinase. Thome, M., Martinon, F., Hofmann, K., Rubio, V., Steiner, V., Schneider, P., Mattmann, C., Tschopp, J. J. Biol. Chem. (1999) [Pubmed]
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