Modulation of HCV replication and translation by ErbB3 binding protein1 isoforms.
Modulation of HCV replication and translation by ErbB3 binding protein1 isoforms.
复制标题
DOI：
10.1016/j.virol.2016.10.006
复制
发表时间：
2017-01
期刊：
影响因子：
3.7
通讯作者：
Pandey VN
中科院分区：
文献类型：
--
作者：
Mishra P;Dixit U;Pandey AK;Upadhyay A;Pandey VN
我们最近发现了一种细胞因子，ErbB 3结合蛋白1（Ebp-1），它特异性地与病毒RNA基因组相互作用，并调节HCV的复制和翻译。Ebp 1有两种亚型，p48和p42，由差异剪接产生。我们发现这两种亚型与HCV蛋白NS 5A和NS 5 B以及细胞因子PKR相互作用。定位于细胞质和细胞核中的p48亚型促进HCV复制，而仅存在于细胞质中的较短的p42亚型强烈抑制HCV复制。在Ebp 1敲低的MH 14细胞中瞬时表达单个亚型证实了p48亚型促进HCV复制，而p42亚型抑制HCV复制。我们发现Ebp 1-p42显著增强PKR的自磷酸化，而Ebp 1-我们认为p48亚型对PKR自身磷酸化的调节是HCV逃避先天性感染的重要机制通过规避p42介导的对其复制的抑制来产生抗病毒免疫应答。
We recently identified a cell-factor, ErbB3 binding protein 1 (Ebp-1), which specifically interacts with the viral RNA genome and modulates HCV replication and translation. Ebp1 has two isoforms, p48, and p42, that result from differential splicing. We found that both isoforms interact with HCV proteins NS5A and NS5B, as well as cell-factor PKR. The p48 isoform, which localizes in the cytoplasm and nuclei, promoted HCV replication, whereas the shorter p42 isoform, which resides exclusively in the cytoplasm, strongly inhibited HCV replication. Transient expression of individual isoforms in Ebp1-knockdown MH14 cells confirmed that the p48 isoform promotes HCV replication, while the p42 isoform inhibits it. We found that Ebp1-p42 significantly enhanced autophosphorylation of PKR, while Ebp1-p48 isoform strongly inhibited it. We propose that modulation of autophosphorylation of PKR by p48 isoform is an important mechanism whereby the HCV virus escapes innate antiviral immune responses by circumventing p42-mediated inhibition of its replication.
登录
查看更多内容
影响因子：
64.5
作者：
Dey, M;Cao, C;Dever, TE
通讯作者：
Dever, TE
影响因子：
3.7
作者：
Hong, Z;Cameron, CE;Zhong, WD
通讯作者：
Zhong, WD
DOI：
10.1073/pnas.89.21.10011
发表时间：
1992-11-01
影响因子：
11.1
作者：
CHIEN, DY;CHOO, QL;KUO, G
通讯作者：
KUO, G
影响因子：
5.4
作者：
ALI, N;SIDDIQUI, A
通讯作者：
SIDDIQUI, A
影响因子：
11.2
作者：
Kim, Chung Kwon;Nguyen, Truong L. X.;Ahn, Jee-Yin
通讯作者：
Ahn, Jee-Yin