ArticleMolecular and cellular biochemistry2011
Prevention of apoptosis by the interaction between FIH1 and Bax.
Article in Molecular and cellular biochemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- eIF4E3 forms an active eIF4F complex during stresses (eIF4FS) targeting mTOR and re-programs the translatome.Nucleic acids research · 2021Article
- Article
- FIH-1-Mint3 axis does not control HIF-1 transcriptional activity in nucleus pulposus cells.The Journal of biological chemistry · 2014Article
- Escherichia coli induces apoptosis in human monocytic U937 cells through the Fas/FasL signaling pathway.Molecular and cellular biochemistry · 2011Article
- Expression of myogenes in longissimus dorsi muscle during prenatal development in commercial and local Piau pigs.Genetics and molecular biologyArticle
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
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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Registered trials
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