Center for AIDS Health Disparities Research, School of Medicine, Meharry Medical College, Nashville, Tennessee 37208, USA.
J Virol. 2010 May;84(9):4840-4. doi: 10.1128/JVI.01911-09. Epub 2010 Feb 10.
Proteasomal degradation of APOBEC3G is a critical step for human immunodeficiency virus type 1 (HIV-1) replication. However, the necessity for polyubiquitination of APOBEC3G in this process is still controversial. In this study, we showed that although macaque simian immunodeficiency virus (SIVmac) Vif is more stable than HIV-1 Vif in human cells, SIVmac Vif induces degradation of APBOEC3G as efficiently as HIV-1 Vif. Overexpression of APOBEC3G or lysine-free APOBEC3G stabilized HIV-1 Vif, indicating that APOBEC3G degradation is independent of the degradation of Vif. Furthermore, an in vivo polyubiquitination assay showed that lysine-free APOBEC3G was also polyubiquitinated. These data suggest that polyubiquitination of APOBEC3G, not that of HIV-1 Vif, is crucial for APOBEC3G degradation.
APOBEC3G 的蛋白酶体降解是人类免疫缺陷病毒 1 型（HIV-1）复制的关键步骤。然而，在这个过程中 APOBEC3G 多泛素化的必要性仍存在争议。在本研究中，我们表明，尽管猕猴猴免疫缺陷病毒（SIVmac）Vif 在人细胞中的稳定性高于 HIV-1 Vif，但 SIVmac Vif 诱导 APOBEC3G 的降解效率与 HIV-1 Vif 相当。APOBEC3G 或缺乏赖氨酸的 APOBEC3G 的过表达稳定了 HIV-1 Vif，表明 APOBEC3G 的降解不依赖于 Vif 的降解。此外，体内多泛素化测定表明，缺乏赖氨酸的 APOBEC3G 也被多泛素化。这些数据表明，APOBEC3G 的多泛素化，而不是 HIV-1 Vif 的多泛素化，对 APOBEC3G 的降解至关重要。
