Human immunodeficiency virus type 1 vif induces cell cycle delay via recruitment of the same E3 ubiquitin ligase complex that targets APOBEC3 proteins for degradation
Human immunodeficiency virus type 1 vif induces cell cycle delay via recruitment of the same E3 ubiquitin ligase complex that targets APOBEC3 proteins for degradation
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DOI：
10.1128/jvi.00377-08
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发表时间：
2008-09-01
影响因子：
5.4
通讯作者：
Planelles, Vicente
中科院分区：
文献类型：
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作者：
DeHart, Jason L.;Bosque, Alberto;Planelles, Vicente
人类免疫缺陷病毒1型(HIV-1)Vif招募了一种以APOBEC3蛋白为目标的Cullin 5泛素连接酶来降解。最近，Vif也被证明在G(2)中诱导细胞周期紊乱。我们发现，与VPR的表达相反，Vif的表达并不排除细胞分裂，因此，Vif在G2中导致延迟而不是停滞。我们还证明了Vif与泛素连接酶的相互作用是细胞周期中断所必需的，就像之前在HIV-1 VPR中所显示的那样。APOBEC3 D/E、F和G的存在对Vif诱导的细胞周期改变没有影响。我们得出结论，VIF导致的细胞周期延迟是一种不同于已知的APOBEC3家族成员的细胞蛋白质泛素化和降解的结果。
Human immunodeficiency virus type 1 (HIV-1) Vif recruits a Cullin 5 ubiquitin ligase that targets APOBEC3 proteins for degradation. Recently, Vif has also been shown to induce cell cycle disturbance in G(2). We show that in contrast to the expression of Vpr, the expression of Vif does not preclude cell division, and therefore, Vif causes delay and not arrest in G2. We also demonstrate that the interaction of Vif with the ubiquitin ligase is required for cell cycle disruption, as was previously shown for HIV-1 Vpr. The presence of APOBEC3 D/E, F, and G had no influence on Vif-induced alteration of the cell cycle. We conclude that cell cycle delay by Vif is a result of ubiquitination and degradation of a cellular protein that is different from the known APOBEC3 family members.