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Inhibition of the gamma interferon response by a Sendai virus C protein mutant with no STAT1‐binding ability
Author(s) -
Gotoh Bin,
Takeuchi Kenji,
Komatsu Takayuki
Publication year - 2004
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2004.05.001
Subject(s) - sendai virus , stat1 , stat protein , mutant , microbiology and biotechnology , interferon , activator (genetics) , interferon gamma , phosphorylation , biology , transcription factor , dna binding protein , chemistry , virology , virus , biochemistry , stat3 , receptor , gene , in vitro
Sendai virus C protein interacts with the signal transducer and activator of transcription (STAT) 1. This interaction is believed to be essential for the Sendai virus inhibition of the interferon (IFN) response. We here analyzed C F170S (a C protein mutant with the F170S mutation) with no STAT1‐binding ability. C F170S lacked the ability to inhibit the IFN‐α response, but retained the ability to inhibit the IFN‐γ response. IFN‐γ stimulation caused STAT1 phosphorylation, formation of the gamma‐activated factor capable of binding to a gamma‐activated sequence DNA probe, and STAT1 nuclear translocation, even in the presence of C F170S . These results suggest that C protein has the STAT1‐binding‐independent anti‐IFN‐γ mechanism, which targets processes after the STAT1 nuclear translocation event.