Human immunodeficiency virus type 1 cell cycle control: Vpr is cytostatic and mediates G(2) accumulation by a mechanism which differs from DNA damage checkpoint control
Human immunodeficiency virus type 1 cell cycle control: Vpr is cytostatic and mediates G(2) accumulation by a mechanism which differs from DNA damage checkpoint control
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DOI：
10.1128/jvi.70.4.2324-2331.1996
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发表时间：
1996-04-01
影响因子：
5.4
通讯作者：
Emerman, M
中科院分区：
文献类型：
--
作者：
Bartz, SR;Rogel, ME;Emerman, M
Vpr 是一种由 1 型人类免疫缺陷病毒 (HIV-1) 编码的 96 个氨基酸蛋白质，可防止受感染细胞的增殖。我们建立了一个 100% HIV 感染 T 细胞群的系统，并使用该系统表明，在 HIV-1 感染的情况下，Vpr 主要具有细胞抑制作用，而不是细胞毒性。 Vpr 在有丝分裂细胞周期蛋白依赖性激酶去磷酸化的上游发挥作用，并导致受感染的细胞在细胞周期的 G(2) 阶段积累。然而，一些 HIV-1 感染细胞的倍性和大小增加，将 DNA 积累到 8N 水平。此外，Vpr 有丝分裂阻断的机制与 G(2) DNA 损伤检查点控制的机制有本质上的不同。
Vpr is a 96-amino-acid protein encoded by human immunodeficiency virus type 1 (HIV-1) that prevents proliferation of infected cells. We have established a system for infection of 100% of a T-cell population with HIV and use this system to show that within the context of HIV-1 infection, Vpr is primarily cytostatic rather than cytotoxic. Vpr acts upstream of dephosphorylation of the mitotic cyclin-dependent kinase, and causes infected cells to accumulate in the G(2) stage of the cell cycle. However, some HIV-1 infected cells increase in ploidy and size, accumulating DNA to an 8N level. Furthermore, the mechanism of the Vpr mitotic block is qualitatively different from that of G(2) DNA damage checkpoint control.