Molecular and Cellular Biochemistry

, Volume 348, Issue 1–2, pp 1–9 | Cite as

Prevention of apoptosis by the interaction between FIH1 and Bax

  • Biao Yan
  • Men Kong
  • Yi-han Chen


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.


FIH1 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.

Supplementary material

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Supplementary material 4 (DOC 48 kb)


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Copyright information

© Springer Science+Business Media, LLC. 2010

Authors and Affiliations

  1. 1.Department of Biochemistry and Molecular Biology, College of Life Science and TechnologyTongji UniversityShanghaiChina
  2. 2.Department of Cell Biology, Harvard Medical SchoolBostonUSA
  3. 3.Key Laboratory of Arrhythmias, Ministry of Education, East HospitalTongji University School of MedicineShanghaiChina
  4. 4.Department of Cardiology, East HospitalTongji University School of MedicineShanghaiChina
  5. 5.Institute of Medical GeneticsTongji UniversityShanghaiChina

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