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http://dx.doi.org/10.5483/BMBRep.2017.50.5.023

HSV-1 ICP27 induces apoptosis by promoting Bax translocation to mitochondria through interacting with 14-3-3θ  

Kim, Ji Ae (Department of Microbiology & Molecular Biology, College of Biological Science and Biotechnology, Chungnam National University)
Kim, Jin Chul (Division of Biological Sciences, University of California)
Min, Jung Sun (Department of Microbiology & Molecular Biology, College of Biological Science and Biotechnology, Chungnam National University)
Kang, Inho (Department of Microbiology & Molecular Biology, College of Biological Science and Biotechnology, Chungnam National University)
Oh, Jeongho (Department of Microbiology & Molecular Biology, College of Biological Science and Biotechnology, Chungnam National University)
Ahn, Jeong Keun (Department of Microbiology & Molecular Biology, College of Biological Science and Biotechnology, Chungnam National University)
Publication Information
BMB Reports / v.50, no.5, 2017 , pp. 257-262 More about this Journal
Abstract
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 $14-3-3{\theta}$ which sequesters Bax to the cytoplasm. In addition, ICP27 promotes the translocation of Bax to the mitochondria by inhibiting the interaction between $14-3-3{\theta}$ and Bax. Our findings may provide a novel apoptotic regulatory pathway induced by ICP27 during HSV-1 infection.
Keywords
Apoptosis; Bax; ICP27; $14-3-3{\theta}$;
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