Identification of TRIM23 as a Cofactor Involved in the Regulation of NF-κB by Human Cytomegalovirus

• DOI: 10.1128/jvi.02072-08
• Publication Date: 2009-01-29T01:45:45Z
• Authors: Emma Poole; Ian Groves; Andrew Macdonald; Yin Pang; Antonio Alcami; John Sinclair
• Keywords: TNF Receptor-Associated Factor 6; 0301 basic medicine; Membrane Glycoproteins; NF-kappa B; Cytomegalovirus; Cell Line; 3. Good health; Viral Proteins; 03 medical and health sciences; GTP-Binding Proteins; Humans; Cells, Cultured; Protein Binding

Human cytomegalovirus (HCMV) regulates NF-kappaB during infection by a variety of mechanisms. For example, the HCMV gene product, UL144, is known to activate in tumor necrosis factor receptor (TNFR)-associated 6 (TRAF6)-dependent manner, causing upregulation chemokine CCL22 (MDC). Viral UL144 expressed from UL/b' region genome at early times postinfection and TNFR1-like homologue. Despite this homology TNFR1 superfamily, does not bind members TNF ligand superfamily. We show here that dependent upon cellular tripartite motif 23 (TRIM23) protein. propose mechanism which activates through direct interaction with protein TRIM23 complex containing TRAF6. In contrast, involved conventional double-stranded RNA signaling via NF-kappaB. Therefore, we present novel role for specific UL144-mediated activation course virus infection.