Journal
BIOLOGY OF THE CELL
Volume 108, Issue 10, Pages 279-293Publisher
WILEY
DOI: 10.1111/boc.201600019
Keywords
Apoptosis; Mitochondrial dynamics; Bcl-2; Mcl-1; Drp1; Cancer
Categories
Funding
- Italian Association for Cancer Research [IG-14442, MFAG-13521]
- Italian Ministry of Health
- University of Ferrara
- Telethon [GGP11139B]
- Italian Ministry of Education, University and Research [COFIN 20129JLHSY_002, FIRB RBAP11FXBC_002, Futuro in Ricerca RBFR10EGVP_001]
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Mitochondria actively contribute to apoptotic cell death through mechanisms including the loss of integrity of the outer mitochondrial membrane, the release of intermembrane space proteins, such as cytochrome c, in the cytosol and the caspase cascade activation. This process is the result of careful cooperation not only among members of the Bcl-2 family but also dynamin-related proteins. These events are often accompanied by fission of the organelle, thus linking mitochondrial dynamics to apoptosis. Emerging evidences are suggesting a fine regulation of mitochondrial morphology by Bcl-2 family members and active participation of fission-fusion proteins in apoptosis. The debate whether in mitochondrial morphogenesis the role of Bcl-2 family members is functionally distinct from their role in apoptosis is still open and, above all, which morphological changes are associated with cell death sensitisation. This review will cover the findings on how the mitochondrial fission and fusion machinery may intersect apoptotic pathways focusing on recent advances on the key role played by Mcl-1.
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