Komatsu Takayuki, Takeuchi Kenji, Yokoo Junko, Gotoh Bin
Department of Microbiology, Fukui Medical University School of Medicine, Fukui 910-1193, Japan.
FEBS Lett. 2002 Jan 30;511(1-3):139-44. doi: 10.1016/s0014-5793(01)03301-4.
Sendai virus expresses C protein that blocks interferon (IFN) signaling. We previously reported suppression of IFN-stimulated tyrosine phosphorylation of signal transducers and activators of transcription (Stats) in infected cells. However this conclusion has remained controversial. To settle it, we re-examined the effect of C protein expression on phosphorylation of Stat1 in detail. IFN-stimulated tyrosine phosphorylation of Stat1 was doubtlessly suppressed early in infection, but the suppression was incomplete, suggesting the importance of the unknown blocking mechanism that inactivates the tyrosine-phosphorylated (pY)-Stat1 generated as the signaling leak. Interestingly, the dephosphorylation process of pY-Stat1 was also impaired. These effects on both phosphorylation and dephosphorylation processes were attributable to the function of the C protein.
仙台病毒表达的C蛋白可阻断干扰素(IFN)信号传导。我们之前报道过,在受感染细胞中,干扰素刺激的信号转导和转录激活因子(Stats)的酪氨酸磷酸化受到抑制。然而,这一结论一直存在争议。为了解决这个问题,我们详细重新研究了C蛋白表达对Stat1磷酸化的影响。在感染早期,干扰素刺激的Stat1酪氨酸磷酸化无疑受到抑制,但这种抑制并不完全,这表明存在未知的阻断机制,该机制可使作为信号泄漏产生的酪氨酸磷酸化(pY)-Stat1失活,这一点很重要。有趣的是,pY-Stat1的去磷酸化过程也受到损害。对磷酸化和去磷酸化过程的这些影响都归因于C蛋白的功能。