期刊
JOURNAL OF BIOLOGICAL CHEMISTRY
卷 280, 期 25, 页码 24153-24158出版社
AMER SOC BIOCHEMISTRY MOLECULAR BIOLOGY INC
DOI: 10.1074/jbc.M502303200
关键词
-
资金
- NCI NIH HHS [CA88071, CA60730] Funding Source: Medline
Activation of NF-kappa B during viral infection is one of the critical elements in innate immune response. Several virus-specific factors, such as double-stranded RNA, can trigger host defense mechanisms by inducing NF-kappa B-mediated expression of cytokines and interferons. Early stages of poliovirus infection are also associated with degradation of I kappa B alpha and translocation of NF-kappa B into the nucleus. However, at later stages of poliovirus replication the p65-RelA component of the NF-kappa B complex undergoes a specific cleavage that coincides with the onset of intensive poliovirus protein synthesis and the appearance of the activity of poliovirus protease 3C. Indeed, the p65-RelA amino acid sequence contains the recognition site for 3C, and recombinant protein 3C was shown to be capable of proteolytic cleavage of p65-RelA, generating truncated product similar to that observed during poliovirus infection. Cleavage of p65-RelA occurs during replication of ECHO-1 and rhinovirus 14, suggesting that inactivation of NF-kappa B function by proteolytic cleavage of p65-RelA is the common mechanism by which picornaviruses suppress the innate immune response.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据