Cytochrome c Release and Apoptosis Induced by Mitochondrial Targeting of Nuclear Orphan Receptor TR3
Hui Li(Sanford Burnham Prebys Medical Discovery Institute), Siva K. Kolluri(Sanford Burnham Prebys Medical Discovery Institute), Jian Gu(Sanford Burnham Prebys Medical Discovery Institute), Marcia I. Dawson(Molecular Medicine Research Institute), Xihua Cao(Sanford Burnham Prebys Medical Discovery Institute), Peter D. Hobbs(SRI International), Bingzhen Lin(Sanford Burnham Prebys Medical Discovery Institute), Guo-quen Chen(Sanford Burnham Prebys Medical Discovery Institute), Jiang-song Lu(John D. Dingell VA Medical Center), Feng Lin(Sanford Burnham Prebys Medical Discovery Institute), Zhihua Xie(Sanford Burnham Prebys Medical Discovery Institute), Joseph A. Fontana(John D. Dingell VA Medical Center), John C. Reed(Sanford Burnham Prebys Medical Discovery Institute), Xiao-kun Zhang(Sanford Burnham Prebys Medical Discovery Institute)
Cited by 670
Abstract
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.
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