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副粘病毒猴病毒5的V蛋白会减缓细胞周期进程。

The paramyxovirus simian virus 5 V protein slows progression of the cell cycle.

作者信息

Lin G Y, Lamb R A

机构信息

Department of Biochemistry, Molecular Biology, and Cell Biology, Northwestern University, Evanston, Illinois 60208, USA.

出版信息

J Virol. 2000 Oct;74(19):9152-66. doi: 10.1128/jvi.74.19.9152-9166.2000.

Abstract

Infection of cells by many viruses affects the cell division cycle of the host cell to favor viral replication. We examined the ability of the paramyxovirus simian parainfluenza virus 5 (SV5) to affect cell cycle progression, and we found that SV5 slows the rate of proliferation of HeLa T4 cells. The SV5-infected cells had a delayed transition from G(1) to S phase and prolonged progression through S phase, and some of the infected cells were arrested in G(2) or M phase. The levels of p53 and p21(CIP1) were not increased in SV5-infected cells compared to mock-infected cells, suggesting that the changes in the cell cycle occur through a p53-independent mechanism. However, the phosphorylation of the retinoblastoma protein (pRB) was delayed and prolonged in SV5-infected cells. The changes in the cell cycle were also observed in cells expressing the SV5 V protein but not in the cells expressing the SV5 P protein or the V protein lacking its unique C terminus (VDeltaC). The unique C terminus of the V protein of SV5 was shown previously to interact with DDB1, which is the 127-kDa subunit of the multifunctional damage-specific DNA-binding protein (DDB) heterodimer. The coexpression of DDB1 with V can partially restore the changes in the cell cycle caused by expression of the V protein.

摘要

许多病毒感染细胞会影响宿主细胞的分裂周期,以利于病毒复制。我们研究了副粘病毒猴副流感病毒5型(SV5)影响细胞周期进程的能力,发现SV5减缓了HeLa T4细胞的增殖速率。被SV5感染的细胞从G1期到S期的转变延迟,且S期进程延长,一些被感染的细胞停滞在G2期或M期。与模拟感染的细胞相比,被SV5感染的细胞中p53和p21(CIP1)的水平并未升高,这表明细胞周期的变化是通过一种不依赖p53的机制发生的。然而,在被SV5感染的细胞中,视网膜母细胞瘤蛋白(pRB)的磷酸化延迟且持续时间延长。在表达SV5 V蛋白的细胞中也观察到了细胞周期的变化,但在表达SV5 P蛋白或缺乏其独特C末端(VDeltaC)的V蛋白的细胞中未观察到。SV5 V蛋白的独特C末端先前已被证明与DDB1相互作用,DDB1是多功能损伤特异性DNA结合蛋白(DDB)异二聚体的127 kDa亚基。DDB1与V的共表达可部分恢复由V蛋白表达引起的细胞周期变化。

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