NF-κB and IRF7 Pathway Activation by Epstein-Barr Virus Latent Membrane Protein 1

Viruses

Ina Ersing¹  Katharina Bernhardt¹ 

关键词: herpesvirus;    apoptosis;    cancer;    innate immunity;    transformation;    integral membrane protein;    signal transduction;    proliferation;    ubiquitin;    lymphoma;    oncogene;   

DOI  :  10.3390/v5061587

来源: mdpi

【 摘 要 】

The 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.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.