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KMID : 0624620170500050257
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BMB Reports
2017 Volume.50 No. 5 p.257 ~ p.262
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HSV-1 ICP27 induces apoptosis by promoting Bax translocation to mitochondria through interacting with 14-3-3θ
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Kim Ji-Ae
Kim Jin-Chul
Min Jung-Sun
Kang In-Ho
Oh Jeong-Ho
Ahn Jeong-Keun
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Abstract
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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.
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KEYWORD
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Apoptosis, Bax, ICP27, 14-3-3θ
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