HSV-1 ICP27 suppresses NF-kappaB activity by stabilizing IkappaBalpha.
Nuclear factor kappaB (NF-kappaB) is associated with the transcriptional activation of genes encoding chemokines, adhesion molecules, cytokines, and anti-apoptotic proteins, which are key components in immune responses and viral infection. Many viruses modulate NF-kappaB through numerous viral gene products to allow productive infections and immune escape. Here we report that ... herpes simplex virus-1 infected cell protein 27 (HSV-1 ICP27), an immediate early protein of HSV-1, represses NF-kappaB activity through binding to inhibitor of kappaB (IkappaBalpha), blocking phosphorylation and ubiquitination of IkappaBalpha, and stabilizing IkappaBalpha. These data may explain how NF-kappaB activity is regulated by ICP27 to escape immune responses during the very early period of HSV-1 infection.
Mesh Terms:
Animals, Cell Line, Cercopithecus aethiops, I-kappa B Proteins, Immediate-Early Proteins, NF-kappa B, Phosphorylation, Ubiquitination, Vero Cells
Animals, Cell Line, Cercopithecus aethiops, I-kappa B Proteins, Immediate-Early Proteins, NF-kappa B, Phosphorylation, Ubiquitination, Vero Cells
FEBS Lett.
Date: Jul. 09, 2008
PubMed ID: 18539148
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