Department of Microbiology & Molecular Biology, College of Biological Science and Biotechnology, Chungnam National University, Daejeon 34134, Korea.
BMB Rep. 2017 May;50(5):257-262. doi: 10.5483/bmbrep.2017.50.5.023.
The subcellular localization of Bax plays a crucial role during apoptosis. In response to apoptotic stimuli, Bax translocates from the cytoplasm to the mitochondria, where it promotes the release of cytochrome c to the cytoplasm. In cells infected with HSV-1, apoptosis is triggered or blocked by diverse mechanisms. In this study, we demonstrate how HSV-1 ICP27 induces apoptosis and modulates mitochondrial membrane potential in HEK 293T cells. We found that ICP27 interacts with 14-3-3θ which sequesters Bax to the cytoplasm. In addition, ICP27 promotes the translocation of Bax to the mitochondria by inhibiting the interaction between 14-3-3θ and Bax. Our findings may provide a novel apoptotic regulatory pathway induced by ICP27 during HSV-1 infection. [BMB Reports 2017; 50(5): 257-262].
Bax 的亚细胞定位在细胞凋亡过程中起着至关重要的作用。在凋亡刺激下,Bax 从细胞质转位到线粒体,在那里它促进细胞色素 c 释放到细胞质中。在感染 HSV-1 的细胞中,凋亡是通过多种机制触发或阻断的。在这项研究中,我们展示了 HSV-1 ICP27 如何诱导凋亡并调节 HEK 293T 细胞中的线粒体膜电位。我们发现 ICP27 与 14-3-3θ 相互作用,将 Bax 隔离在细胞质中。此外,ICP27 通过抑制 14-3-3θ 和 Bax 之间的相互作用,促进 Bax 向线粒体的易位。我们的发现可能为 HSV-1 感染期间 ICP27 诱导的新的凋亡调节途径提供了依据。[BMB 报告 2017;50(5):257-262]。