Apaf1 inhibition promotes cell recovery from apoptosis.
10.1007/s13238-015-0200-2
- Author:
Anna GORTAT
1
;
Mónica SANCHO
1
;
Laura MONDRAGÓN
1
;
Àngel MESSEGUER
2
;
Enrique PÉREZ-PAYÁ
1
;
Mar ORZÁEZ
3
Author Information
1. Laboratory of Peptide and Protein Chemistry, Centro de Investigación Príncipe Felipe, 46012, Valencia, Spain.
2. Department of Chemical and Biomolecular Nanotechnology, Instituto Química Avanzada de Cataluña (CSIC), 08034, Barcelona, Spain.
3. Laboratory of Peptide and Protein Chemistry, Centro de Investigación Príncipe Felipe, 46012, Valencia, Spain. morzaez@cipf.es.
- Publication Type:Journal Article
- Keywords:
Apaf1;
Apaf1 inhibitors;
apoptosis;
apoptosome;
autophagy;
cell recovery
- MeSH:
Adenosine Triphosphate;
metabolism;
Apoptosis;
drug effects;
Apoptotic Protease-Activating Factor 1;
genetics;
metabolism;
Cell Hypoxia;
drug effects;
Cell Line, Tumor;
Doxorubicin;
pharmacology;
HeLa Cells;
Humans;
Microscopy, Electron, Transmission
- From:
Protein & Cell
2015;6(11):833-843
- CountryChina
- Language:English
-
Abstract:
The protein apoptotic protease activating factor 1 (Apaf1) is the central component of the apoptosome, a multiprotein complex that activates procaspase-9 after cytochrome c release from the mitochondria in the intrinsic pathway of apoptosis. We have developed a vital method that allows fluorescence-activated cell sorting of cells at different stages of the apoptotic pathway and demonstrated that upon pharmacological inhibition of Apaf1, cells recover from doxorubicin- or hypoxia-induced early apoptosis to normal healthy cell. Inhibiting Apaf1 not only prevents procaspase-9 activation but delays massive mitochondrial damage allowing cell recovery.
