>> finding that IFNß also induces the expression of un-phosphorylated STAT2 (U-STAT2) and IRF9, which combine with U-STAT1 to form un-phosphorylated ISGF3 (U-ISGF3), a novel transcription factor in which these proteins form a ternary complex without tyrosine phosphorylation. <<
and.....
>> We show that prolonged exposure of cells to a low level of IFNß induces a steady state in which only the U-ISGF3-dependent genes are expressed, suggesting that secretion of IFNß by cancer cells may account for their similar phenotype. <<
IFNß-dependent increases in STAT1, STAT2, and IRF9 mediate resistance to viruses and DNA damage
HyeonJoo Cheon1, Elise G Holvey-Bates1, John W Schoggins2, Samuel Forster3, Paul Hertzog3, Naoko Imanaka2, Charles M Rice2, Mark W Jackson4, Damian J Junk4 and George R Stark1
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