The mitochondrial permeability transition pore and its role in cell death.
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Summary
Current evidence that the pore complex is involved in outer-membrane rupture and release of these proteins during programmed cell death is reviewed, along with indications that transient pore opening may provoke 'accidental' apoptosis.
- Type
- article
- Published
- 1999-07-15
- Cited by
- 2,517
- References
- 21
- Access
- Open access
- OpenAlex
- https://openalex.org/W1968112618
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:21123711
Keywords
Mitochondrial permeability transition pore, Voltage-dependent anion channel, Cell biology, Intermembrane space, Programmed cell death
References
Cited by
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- Ischaemic Preconditioning Inhibits Opening of Mitochondrial Permeability Transition Pores in the Reperfused Rat Heart
- Radiation protection of HepG2 cells by Podophyllum hexandrum Royale
- Improving cardioprotection during cardiac bypass surgery
- Induction of the mitochondrial permeability transition by selenium compounds mediated by oxidation of the protein thiol groups and generation of the superoxide.
- Calcineurin‐independent inhibition of mitochondrial Ca2+ uptake by cyclosporin A
- Natural human polyreactive IgM induce apoptosis of lymphoid cell lines and human peripheral blood mononuclear cells.
- Astrocyte apoptosis: implications for neuroprotection.
- Bax Does Not Directly Participate in the Ca2+-induced Permeability Transition of Isolated Mitochondria*
- Mechanisms of B cell receptor induced apoptosis
- Mitochondrial DNA Mutations, Apoptosis, and the Misfolded Protein Response
- Clinical treatments for mitochondrial dysfunctions after brain injury
- Calcium-mediated activation of PI3K and p53 leads to apoptosis in thyroid carcinoma cells
- Regulation und Funktion lymphozytärer Ionenkanäle – CRAC und ORCC – in Proliferation und Apoptose
- The mitochondrial death pathway.
- Mechanisms of berberine (natural yellow 18)-induced mitochondrial dysfunction: interaction with the adenine nucleotide translocator.
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