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The Mitochondrial Pathways of Apoptosis
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Apoptosis is a process of programmed cell death that serves as a major mechanism for the precise regulation of cell numbers, and as a defense mechanism to remove unwanted and potentially dangerous cells. Studies in nematode, Drosophila and mammals have shown that, although regulation of the cell death machinery is somehow different from one species to another, it is controlled by homologous proteins and involves mitochondria. In mammals, activation of caspases (cysteine proteases that are the main executioners of apoptosis) is under the tight control of the Bcl-2 family proteins, named in reference to the first discovered mammalian cell death regulator. These proteins mainly act by regulating the release of caspases activators from mitochondria. Although for a long time the absence of mitochondrial changes was considered as a hallmark of apoptosis, mitochondria appear today as the central executioner of apoptosis. In this chapter, we present the current view on the mitochondrial pathway of apoptosis with a particular attention to new aspects of the regulation of the Bcl-2 proteins family control of mitochondrial membrane permeabilization: the mechanisms implicated in their mitochondrial targeting and activation during apoptosis, the function(s) of the oncosuppressive protein p53 at the mitochondria and the role of the processes of mitochondrial fusion and fission.
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“The details of the apoptotic pathway differ between mammals and the model organisms Drosophila and C. elegans, however the major players are largely conserved (Figure 1).”
From Programmed cell death in aging (2015) · cites this paper as Estaquier et al., 2012
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Self-citation
Metadata
- Authors
- Estaquier, J., Vallette, F., Vayssiere, J.-L., & Mignotte, B.
- Affiliations
- Centre National de la Recherche Scientifique (FR)
- École Pratique des Hautes Études (FR)
- Corresponding author
- Mignotte, Bernard
- Venue
- Advances in experimental medicine and biology
- Publisher
- Springer Netherlands
- Published
- 2011-12-22
- Volume
- 942
- Pages
- 157-183
- ISSN
- 0065-2598 (ISSN-L)
- OpenAlex
- W116732461
- Cited by
- 637
- References
- 263
- Citations by year
- 2026: 15 · 2025: 42 · 2024: 41 · 2023: 75 · 2022: 75 · 2021: 57 · 2020: 52 · 2019: 37 · 2018: 42 · 2017: 23 · 2016: 36 · 2015: 49 · 2014: 35 · 2013: 42 · 2012: 15
- FWCI
- 38.19
- Type
- book chapter
- Language
- en
- Open access
- green
- uvsq.hal.science
- Licence
- Locations
- Advances in experimental medicine and biology (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion, other-oa)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- mitochondrial apoptosis, Bcl-2 family proteins, caspase activation, mitochondrial membrane permeabilization, p53, mitochondrial fusion, mitochondrial fission, programmed cell death
- MeSH terms
- Animals, Enzyme Activation, Mitochondria, Apoptosis, Caspases
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