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Pseudorabies virus glycoprotein gE triggers ERK1/2 phosphorylation and degradation of the pro-apoptotic protein Bim in epithelial cells
- Pontes, Maria S., Van Waesberghe, Cliff, Nauwynck, Hans, Verhasselt, Bruno, Favoreel, Herman W.
- Virus research 2016 v.213 pp. 214-218
- Suid herpesvirus 1, T-lymphocytes, apoptosis, cell viability, epithelial cells, glycoproteins, mitogen-activated protein kinase, phosphorylation, pro-apoptotic proteins, signal transduction, virulence, viruses
- ERK1/2 (Extracellular signal Regulated Kinase 1/2) signaling is a key cellular signaling axis controlling many cellular events, including cell survival. Activation of ERK 1/2 may trigger an anti-apoptotic response, and different viruses have been shown to benefit from this process. We have described recently that the viral glycoprotein gE mediates pseudorabies virus (PRV)-induced activation of ERK 1/2 in T lymphocytes. In the present study, we report that PRV gE-mediated ERK 1/2 phosphorylation also occurs in epithelial cells and that in these cells, gE-mediated ERK 1/2 signaling is associated with degradation of the pro-apoptotic protein Bim. Our results for the first time link the viral glycoprotein gE, an important alphaherpesvirus virulence factor, with the apoptotic signaling pathway.