Résumé
The interaction between Beclin 1, an autophagic protein, and BCL-2, an antiapoptotic protein, is central in the regulation of autophagy, a catabolic process that ends in the lysosome. These last 10 years, much research has been focused on the Beclin 1 and BCL-2 interaction, its regulation and its importance in physiopathology. Many cellular mechanisms have been identified as regulators of this interaction. Among them, extracellular conditions that impact autophagy directly affect both partners through posttranslational modifications. Numerous studies also revealed that Beclin 1- and BCL-2-dependent autophagy is crucial in physiopathology by influencing cell death, metabolism, immunity, neurodegeneration, and cancer.