Sahdev Sudhir, Taneja Tarvinder K, Mohan Manjari, Sah Nand K, Khar Ashok K, Hasnain Seyed E, Athar Mohammad
Laboratory of Molecular and Cellular Biology, CDFD, Hyderabad 500076, India.
Biochem Biophys Res Commun. 2003 Aug 1;307(3):483-90. doi: 10.1016/s0006-291x(03)01224-5.
In this study we report that the baculovirus p35 anti-apoptotic protein prevents cell death by quenching free radicals at a very upstream step in the apoptotic pathway. Mitochondria of activated rat peritoneal macrophages as well as Spodoptera frugiperda (Sf9) insect cells, following treatment with oxidants, H(2)O(2)/UVB irradiation, release cytochrome c followed by activation of caspase-3. Transfection of macrophages/Sf9 cells with a construct carrying the p35 gene under the CMV/HSP promoters resulted in p35 expression and consequent arrest of oxidative stress-induced apoptosis. p35 expression also inhibited cytochrome c release from the mitochondria of oxidant-exposed cells and blocked caspase-3 activation.
在本研究中，我们报告杆状病毒p35抗凋亡蛋白通过在凋亡途径的非常上游步骤淬灭自由基来防止细胞死亡。用氧化剂、H₂O₂/紫外线B照射处理后，活化的大鼠腹膜巨噬细胞以及草地贪夜蛾（Sf9）昆虫细胞的线粒体释放细胞色素c，随后激活caspase-3。用携带在CMV/HSP启动子下的p35基因的构建体转染巨噬细胞/Sf9细胞导致p35表达，并因此阻止氧化应激诱导的凋亡。p35表达还抑制了氧化剂暴露细胞的线粒体中细胞色素c的释放，并阻断了caspase-3的激活。
