Mechanisms of cytochrome c release by proapoptotic BCL-2 family members.

By L. Scorrano, S. Korsmeyer. Biochemical and Biophysical Research Communications - BBRC, 2003

734 citations recorded by the source corpus.

Subfields: Molecular Biology

View Paper: https://www.semanticscholar.org/paper/113f64198922ef435efeb645b6ce70c2b3d4176d

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

1. L. Scorrano
2. D. Sinclair
3. S. Cipolat
4. C. Frezza
5. Hidde L. Ploegh
6. Roy A. Frye
7. D. C. Chan
8. Lígia C. Gomes

Citations in the corpus

• Organelle isolation: functional mitochondria from mouse liver, muscle and cultured filroblasts (2007, background): “Although it appears clear that mitochondria play a crucial role in apoptosis, the precise mechanism by which cytochrome c is released remains a matter of intense debate and researc”
• Targeting Apoptosis Pathways in Cancer Therapy (2005, background): “Following a death signal, proapoptotic proteins undergo posttranslational modifications that include dephosphorylation and cleavage resulting in their activation and translocation to the mitochondria leading to apoptosis.(19) All BH3-only molecules require multidomain BH3 proteins (Bax, Bak) to exer”
• Electron transfer between cytochrome c and p66Shc generates reactive oxygen species that trigger mitochondrial apoptosis. (2005, neutral): “…leading to alterations of the mitochondrial membrane integrity is the translocation of proapoptotic proteins such as Bax and Bid from the cytosol to the outer mitochondrial membrane, where they form channels and/or regulate the function of preexisting channels (Scorrano and Korsmeyer, 2003).”
• Acetylation of the C terminus of Ku70 by CBP and PCAF controls Bax-mediated apoptosis. (2004, background): “We demonstrate that increased acetylation tochrome c (Scorrano and Korsmeyer, 2003).of Ku70 disrupts the Ku70-Bax interaction and coinA recent study has shed light on a mechanism bycides with cytoplasmic accumulation of CBP.”
• OPA1 controls apoptotic cristae remodeling independently from mitochondrial fusion. (2006, neutral): “Asterisks: BAK multimers.”