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FEBS Lett. 2008 Jul 9;582(16):2371-6. doi: 10.1016/j.febslet.2008.05.044. Epub 2008 Jun 6.

HSV-1 ICP27 suppresses NF-kappaB activity by stabilizing IkappaBalpha.

Author information

1
Department of Microbiology, School of Bioscience and Biotechnology, Chungnam National University, Daejeon 305-764, Republic of Korea.

Abstract

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.

PMID:
18539148
DOI:
10.1016/j.febslet.2008.05.044
[Indexed for MEDLINE]
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