Cytochrome c release from mitochondria proceeds by a two-step process
By M. Ott, J. Robertson, V. Gogvadze, B. Zhivotovsky, S. Orrenius. Proceedings of the National Academy of Sciences of the United States of America, 2002
984 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/8428e1b9f813c635367987adbc1932613a34b5d7
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Molecular Biology
- S. Orrenius
- V. Gogvadze
- B. Zhivotovsky
- Douglas R. Green
- S. Tait
- Peter Vandenabeele
- K. Mihara
- S. Reddy
Citations in the corpus
- REACTIVE OXYGEN SPECIES, CELLULAR REDOX SYSTEMS AND APOPTOSIS (2010, positive): “Mitochondria-to-cytosol release of cytochrome c sequentially occurs via detachment from cardiolipin and translocation through the mitochondrial outer membrane [191].”
- Calcium, ATP, and ROS: a mitochondrial love-hate triangle. (2004, background): “There are also binding sites on respiratory complexes III and IV, and it has been shown that cytochrome c release is a two-step process (143), involving release of the protein from its inner membrane binding sites followed by outer membrane translocation.”
- Mitochondria, oxidative stress and cell death (2007, background): “Apparently, simple permeabilization of the outer mitochondrial membrane (OMM) by oligomeric Bax in a low-ionic strength medium is insufficient for cytochrome c release from mitochondria [37].”
- Molecular Mechanisms of Ischemia-Reperfusion Injury in Brain: Pivotal Role of the Mitochondrial Membrane Potential in Reactive Oxygen Species Generation (2012, background): “However, there is evidence that release of Cytc is a two-step process, involving (1) the release of proteins usually tethered to inner membrane by cardiolipin, combined with (2) pore formation [123].”
- The role of mitochondrial factors in apoptosis: a Russian roulette with more than one bullet (2002, background): “Lipid peroxidation may mediate the transition from the tightly to the loosely bound pool of cytochrome c, which is then released by a Bax-dependent mechanism.(10) Further studies will be required to evaluate whether or not a hierarchical model exists of mitochondrial protein release and whether diff”
- Mitochondria-Ros Crosstalk in the Control of Cell Death and Aging (2011, background): “In 2002, the group of Orrenius elegantly showed how oxidative modification of mitochondrial lipids, specifically cardiolipin, is fundamental for tightly bound pool of cytochrome c mobilization, that is so detached because of disturbances in membrane structure [118].”
- Mitochondrial Glutathione, a Key Survival Antioxidant (2009, background): “Cytochrome c is normally bound to the MIM by association with cardiolipin, and it has been postulated that cardiolipin loss or peroxidation lessens the binding of cytochrome c to the MIM, favoring the permeabilization of isolated liver mitochondria and release of cytochrome c (66, 111).”
- Mitochondrial fission factor Drp1 is essential for embryonic development and synapse formation in mice (2009, background): “Alternatively, because cytochrome c is associated with cardiolipi”
- Mitochondria and cell death: outer membrane permeabilization and beyond (2010, background): “Electrostatic interactions between cytochrome c and the mitochondrial lipid cardiolipin have been proposed to regulate its releas”
- Cytochrome c acts as a cardiolipin oxygenase required for release of proapoptotic factors (2005, background): “, and a growing body of evidence implicates CL peroxidation products over nonoxidized CL as the real players in mitochondrial cyt c releas”