Prevention of apoptosis by the interaction between FIH1 and Bax
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Bax induces mitochondrial-dependent cell apoptosis signals in mammalian cells. However, the mechanism of how Bax is kept inactive is not fully elucidated. Here, we identify FIH1 as a potential interactor of Bax through mass spectrometry analysis. Coimmunoprecipitation and GST pull-down experiments show that FIH1 can directly interact with Bax. Bax-mediated apoptosis is suppressed by FIH1 overexpression, but accelerated by FIH1 deficiency. FIH1 functions as a cytosol retention factor of Bax, blocking Bax translocation from cytosol to mitochondria in response to apoptotic stimuli. Overall, there results unveil a novel role of FIH1 in the regulation of Bax-mediated apoptosis.
KeywordsFIH1 Apoptosis Bax Translocation
We thank the Harvard medical school to provide the technical platform, and the joint PhD student Education Program between Harvard University (USA) and Tongji University (China). This study was supported by State Scholarship Fund of China (NO: 2009626129) from China Scholarship Council (CSC). This work was also supported by the ‘973’ Program Fund of China (2007CB512100) and the ‘863’ Program Fund of China (2007AA02Z438).
Conflict of interest
The authors declare that they have no conflict of interest.
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