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HSV-1 ICP27 induces apoptosis by promoting Bax translocation to mitochondria through interacting with 14-3-3ヨ
Ji Ae Kim1,#, Jin Chul Kim1,2,#, Jung Sun Min1, Inho Kang1, Jeongho Oh1, Jeong Keun Ahn1,*
1Department of Microbiology & Molecular Biology, College of Biological Science and Biotechnology, Chungnam National University,
2Division of Biological Sciences, University of California
The subcellular localization of Bax plays crucial role for 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. Here, we show that HSV-1 ICP27 induces apoptosis and modulates mitochondrial membrane potential in HEK 293T cells. We found that ICP27 interacts with 14-3-3ヨ which sequesters Bax to the cytoplasm. Moreover, ICP27 promotes the translocation of Bax to the mitochondria by inhibiting the interaction between 14-3-3ヨ and Bax. Our findings may provide a novel apoptotic regulatory pathway induced by ICP27 during HSV-1 infection.
Abstract, Accepted Manuscript(in press) [Submitted on February 9, 2017, Accepted on March 3, 2017]
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