Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3
Cytochrome c release and apoptosis induced by mitochondrial targeting of nuclear orphan receptor TR3
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DOI：
10.1126/science.289.5482.1159
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发表时间：
2000-08-18
期刊：
影响因子：
56.9
通讯作者：
Zhang, XK
中科院分区：
文献类型：
--
作者：
Li, H;Kolluri, SK;Zhang, XK
TR3是一种即时早期反应基因，是类固醇-甲状腺激素-类视黄醇受体转录因子超家族的孤儿成员，通过一种未知的机制调节细胞凋亡。在凋亡刺激下，TR3从细胞核转位到线粒体，诱导细胞色素c释放和细胞凋亡。线粒体靶向TR3，而不是其DNA结合和反激活，是其促凋亡作用的必要条件。我们的研究结果揭示了核转录因子易位到线粒体启动细胞凋亡的机制。
TR3, an immediate-early response gene and an orphan member of the steroid-thyroid hormone-retinoid receptor superfamily of transcription factors, regulates apoptosis through an unknown mechanism. In response to apoptotic stimuli, TR3 translocates from the nucleus to mitochondria to induce cytochrome c release and apoptosis. Mitochondrial targeting of TR3, but not its DNA binding and transactivation, is essential for its proapoptotic effect. Our results reveal a mechanism by which a nuclear transcription factor translocates to mitochondria to initiate apoptosis.