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Virology. 2002 Feb 15;293(2):205-9.

Dephosphorylation failure of tyrosine-phosphorylated STAT1 in IFN-stimulated Sendai virus C protein-expressing cells.

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Department of Viral Diseases and Vaccine Control, National Institute of Infectious Diseases, 4-7-1 Gakuen, Musashimurayama, Tokyo 208-0011, Japan.


Sendai virus C protein (SeV C) has been reported to counteract the antiviral activities of interferons (IFNs) by inhibiting the expression of IFN-stimulated gene products. In SeV C-expressing cells, formation of an active ISGF3 complex and translocation of STAT1 into the nucleus were not observed. STAT1 was continuously phosphorylated at tyrosine 701 by IFN signaling; however, its serine phosphorylation was suppressed. In addition, tyrosine-phosphorylated STAT1 grew to form abnormally huge complexes. These findings suggest that the counteraction of IFN in SeV C-expressing cells is caused by disordered phosphorylation and dephosphorylation of STAT1.

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