NF-κB and IRF7 Pathway Activation by Epstein-Barr Virus Latent Membrane Protein 1
MetadataShow full item record
CitationErsing, Ina, Katharina Bernhardt, and Benjamin E. Gewurz. 2013. “NF-κB and IRF7 Pathway Activation by Epstein-Barr Virus Latent Membrane Protein 1.” Viruses 5 (6): 1587-1606. doi:10.3390/v5061587. http://dx.doi.org/10.3390/v5061587.
AbstractThe principal Epstein-Barr virus (EBV) oncoprotein, Latent Membrane Protein 1 (LMP1), is expressed in most EBV-associated human malignancies. LMP1 mimics CD40 receptor signaling to provide infected cells with constitutive NF-κB, MAP kinase, IRF7, and PI3 kinase pathway stimulation. EBV-transformed B-cells are particularly dependent on constitutive NF-κB activity, and rapidly undergo apoptosis upon NF-κB blockade. Here, we review LMP1 function, with special attention to current understanding of the molecular mechanisms of LMP1-mediated NF-κB and IRF7 pathway activation. Recent advances include the elucidation of transmembrane motifs important for LMP1 trafficking and ligand-independent signaling, analysis of genome-wide LMP1 gene targets, and the identification of novel cell proteins that mediate LMP1 NF-κB and IRF7 pathway activation.
Citable link to this pagehttp://nrs.harvard.edu/urn-3:HUL.InstRepos:11717491
- FAS Scholarly Articles 
- HMS Scholarly Articles 
Contact administrator regarding this item (to report mistakes or request changes)