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Prevention of apoptosis by the interaction between FIH1 and Bax.

Biao B Yan, Men M Kong, and Yi-han YH Chen

Mol Cell Biochem 348(1-2):1-9 (2011) PMID 21069436

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.

DOI: 10.1007/s11010-010-0631-2
Version: za2963e q8zad q8zb5 q8zc9 q8zd2 q8ze9 q8zfa q8zgb

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