Abstract

The BCL-2 protein family determines the commitment of cells to apoptosis, an ancient cell suicide programme that is essential for development, tissue homeostasis and immunity. Too little apoptosis can promote cancer and autoimmune diseases; too much apoptosis can augment ischaemic conditions and drive neurodegeneration. We discuss the biochemical, structural and genetic studies that have clarified how the interplay between members of the BCL-2 family on mitochondria sets the apoptotic threshold. These mechanistic insights into the functions of the BCL-2 family are illuminating the physiological control of apoptosis, the pathological consequences of its dysregulation and the promising search for novel cancer therapies that target the BCL-2 family.

Keywords

ApoptosisBcl-2 familyMitochondrionNeurodegenerationBiologyProtein familyCell biologyCancerProgrammed cell deathImmunologyGeneticsGeneMedicineDiseaseInternal medicine

MeSH Terms

Amino Acid SequenceAnimalsApoptosisApoptosis Regulatory ProteinsHumansModelsMolecularMolecular Sequence DataMolecular Targeted TherapyNeoplasmsProtein MultimerizationProtein StructureSecondaryProto-Oncogene Proteins c-bcl-2Signal Transduction

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Publication Info

Year
2013
Type
review
Volume
15
Issue
1
Pages
49-63
Citations
3083
Access
Closed

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Cite This

Peter E. Czabotar, Guillaume Lessène, Andreas Strasser et al. (2013). Control of apoptosis by the BCL-2 protein family: implications for physiology and therapy. Nature Reviews Molecular Cell Biology , 15 (1) , 49-63. https://doi.org/10.1038/nrm3722

Identifiers

DOI
10.1038/nrm3722
PMID
24355989

Data Quality

Data completeness: 81%