人类免疫缺陷病毒1型病毒蛋白R：G2期细胞周期停滞、巨噬细胞与核转运

HIV-1 Vpr: G2 cell cycle arrest, macrophages and nuclear transport.

作者信息

Re F, Luban J

机构信息

Department of Microbiology, Columbia University, College of Physicians and Surgeons, New York, NY 10032, USA.

出版信息

Prog Cell Cycle Res. 1997;3:21-7. doi: 10.1007/978-1-4615-5371-7_2.

DOI:10.1007/978-1-4615-5371-7_2

PMID:9552403

Abstract

HIV-1 possesses six open reading frames in addition to the gag, pol, and env shared by all retroviruses. One of these accessory genes, vpr, is required for maximal viral replication in macrophages. The molecular mechanism underlying this effect may be related to one of the unusual properties of the encoded protein: some believe Vpr promotes nuclear translocation of preintegration complexes in non-dividing cells; also, Vpr arrests the cell cycle in G2 by inhibiting an upstream activator of p34cdc2-cyclin B. Elucidation of Vpr-cell cycle interactions may provide insight into both HIV-1 and basic cell biology.

摘要

除了所有逆转录病毒共有的gag、pol和env基因外，HIV-1还拥有六个开放阅读框。这些辅助基因之一vpr，是巨噬细胞中病毒最大程度复制所必需的。这种作用背后的分子机制可能与编码蛋白的一种特殊性质有关：一些人认为Vpr促进非分裂细胞中前整合复合物的核转位；此外，Vpr通过抑制p34cdc2-细胞周期蛋白B的上游激活剂，使细胞周期停滞在G2期。对Vpr与细胞周期相互作用的阐明可能为HIV-1和基础细胞生物学提供深入了解。