Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.5.1.18 (glutathione S-transferase)
 22,582 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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.
 ...
PMID:Prevention of apoptosis by the interaction between FIH1 and Bax. 2106 36