Yedavalli V.S.R.K.Shih H.-M.Chiang Y.-P.CHUN-YI LULUAN-YIN CHANGChen M.-Y.Chuang C.-Y.Dayton A.I.Jeang K.-T.LI-MIN HUANG2020-12-152020-12-1520050022-538Xhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-27144529047&doi=10.1128%2fJVI.79.21.13735-13746.2005&partnerID=40&md5=3ce7572b5c209cbaa339e177ed9170c5https://scholars.lib.ntu.edu.tw/handle/123456789/525661Human immunodeficiency virus type 1 viral protein R (Vpr) is required for viral pathogenesis and has been implicated in T-cell apoptosis through its activation of caspase 3 and caspase 9 and perturbation of mitochondrial membrane potential. To understand better Vpr-mitochondria interaction, we report here the identification of antiapoptotic mitochondrial protein HAX-1 as a novel Vpr target. We show that Vpr and HAX-1 physically associate with each other. Overexpression of Vpr in cells dislocates HAX-1 from its normal residence in mitochondria and creates mitochondrion instability and cell death. Conversely, overexpression of HAX-1 suppressed the proapoptotic activity of Vpr. Copyright ? 2005, American Society for Microbiology. All Rights Reserved.[SDGs]SDG3caspase 3; caspase 9; inhibitor of apoptosis protein; mitochondrial protein; protein HAX 1; unclassified drug; Vpr protein; apoptosis; article; controlled study; enzyme activation; human; human cell; Human immunodeficiency virus 1; membrane potential; mitochondrial membrane; nonhuman; priority journal; protein expression; protein protein interaction; protein targeting; T lymphocyte; virus pathogenesis; Apoptosis; Down-Regulation; Gene Products, vpr; Hela Cells; HIV Infections; HIV-1; Humans; Mitochondria; Protein Binding; Proteins; Human immunodeficiency virus 1journal article10.1128/JVI.79.21.13735-13746.2005162272932-s2.0-27144529047