Laboratory of Human Retrovirology, Institut de Recherches Cliniques de Montréal (IRCM) and Department of Microbiology, Infectiology and Immunology, Université de Montréal, Montreal, QC H2W 1R7, Canada.
Cell Host Microbe. 2014 Feb 12;15(2):125-7. doi: 10.1016/j.chom.2014.01.012.
HIV Vpr induces a cell-cycle arrest at the G2-to-M transition through a poorly understood mechanism. In a recent issue of Cell, Laguette et al. (2014) demonstrate that untimely activation of the structure-specific endonuclease regulator SLX4 complex by Vpr promotes G2/M arrest and escape from innate immune sensing.
HIV Vpr 通过一种尚未完全阐明的机制诱导细胞周期在 G2 到 M 期过渡时停滞。在最近一期的《Cell》杂志上，Laguette 等人（2014）证明，Vpr 会过早激活结构特异性内切酶调控因子 SLX4 复合物，从而促进 G2/M 期停滞并逃避先天免疫感应。
