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. 2011 Feb;348(1-2):1-9.
doi: 10.1007/s11010-010-0631-2. Epub 2010 Nov 11.

Prevention of apoptosis by the interaction between FIH1 and Bax

Biao Yan  1 , Men Kong, Yi-han Chen
Affiliations

Prevention of apoptosis by the interaction between FIH1 and Bax

Biao Yan et al. Mol Cell Biochem. 2011 Feb.

Abstract

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.

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