Journal
CELLULAR & MOLECULAR IMMUNOLOGY
Volume 8, Issue 1, Pages 67-74Publisher
CHIN SOCIETY IMMUNOLOGY
DOI: 10.1038/cmi.2010.55
Keywords
interferon regulatory factor 3; negative regulation; splicing variant
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Funding
- China National Human Liver Proteomics Project [2004BA711A19]
- China National High-Tech 863 Program [2006AA 02A310]
- Natural Science Foundation of Hubei Province of China [2009CDB012]
- Educational Commission of Hubei Province of China [D20091004]
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Interferon regulatory factor 3 (IRF3), one member of the IRF family, plays a central role in induction of type I interferon (IFN) and regulation of apoptosis. Controlled activity of IRF3 is essential for its functions. During reverse transcription (RT)-PCR to clone the full-length open reading frame (ORF) of IRF3, we cloned a full-length ORF encoding an isoform of IRF3, termed as IRF3-CL, and has a unique carboxyl-terminus of 125 amino acids. IRF3-CL is ubiquitously expressed in distinct cell lines. Overexpression of IRF3-CL inhibits Sendai virus (SeV)-triggered induction of IFN-beta and SeV-induced and inhibitor of NF-kappa B kinase-epsilon (IKK epsilon)-mediated nuclear translocation of IRF3. When IKK epsilon is overexpressed, IRF3-CL is associated with IRF3. These results suggest that IRF3-CL, the alternative splicing isoform of IRF-3, may function as a negative regulator of IRF3. Cellular & Molecular Immunology (2011) 8, 67-74; doi:10.1038/cmi.2010.55; published online 6 December 2010
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