Cleavage of BID during cytotoxic drug and UV radiation-induced apoptosis occurs downstream of the point of Bcl-2 action and is catalysed by caspase-3: a potential feedback loop for amplification of apoptosis-associated mitochondrial cytochrome c release
- 10 May 2000
- journal article
- Published by Springer Nature in Cell Death & Differentiation
- Vol. 7 (6), 556-565
- https://doi.org/10.1038/sj.cdd.4400689
Abstract
Cell death and differentiation is a monthly research journal focused on the exciting field of programmed cell death and apoptosis. It provides a single accessible source of information for both scientists and clinicians, keeping them up-to-date with advances in the field. It encompasses programmed cell death, cell death induced by toxic agents, differentiation and the interrelation of these with cell proliferation.Keywords
This publication has 46 references indexed in Scilit:
- Molecular characterization of mitochondrial apoptosis-inducing factorNature, 1999
- THE MITOCHONDRIAL DEATH/LIFE REGULATOR IN APOPTOSIS AND NECROSISAnnual Review of Physiology, 1998
- Apoptotic PathwaysCell, 1998
- Caspases: Enemies WithinScience, 1998
- Mitochondria and ApoptosisScience, 1998
- Caspases: Intracellular Signaling by ProteolysisCell, 1997
- Prevention of Apoptosis by Bcl-2: Release of Cytochrome c from Mitochondria BlockedScience, 1997
- The Release of Cytochrome c from Mitochondria: A Primary Site for Bcl-2 Regulation of ApoptosisScience, 1997
- Programmed Cell Death in Animal DevelopmentCell, 1997
- Protease activation during apoptosis: Death by a thousand cuts?Cell, 1995