Do inducers of apoptosis trigger caspase-independent cell death?

By J. Chipuk, Douglas R. Green. Nature reviews. Molecular cell biology, 2005

341 citations recorded by the source corpus.

Subfields: Epidemiology, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/823eeb5e63d6f6be6b9f0a585554d8835d0cbf77

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. Guido Kroemer
2. L. Galluzzi
3. Douglas R. Green
4. Beth Levine
5. Oliver Kepp
6. Simone Fulda
7. D. Rubinsztein
8. Peter Vandenabeele

In Immunology

1. Guido Kroemer
2. L. Galluzzi
3. Simone Fulda
4. Oliver Kepp
5. Douglas R. Green
6. W. El-Deiry
7. G. Shadel
8. Junying Yuan

In Molecular Biology

1. Guido Kroemer
2. L. Galluzzi
3. Douglas R. Green
4. Simone Fulda
5. C. Brenner
6. Oliver Kepp
7. J. Chipuk
8. Seamus J. Martin

Citations in the corpus

• Caspase-independent cell death (2005, background): “When inhibition of caspases does not inhibit cell death, this often leads to a shift in the morphology of cell deat”
• Classification of cell death (2005, neutral): “appearance of some morphological signs of apoptosis (such as chromatin condensation and DNA fragmentation), yet only retards cell death.(32) In many instances, caspase inhibition”
• Mitochondrial membrane permeabilization in cell death. (2007, background): “This “caspase-independent death” (129, 407) can occur because of an irreversible loss of mitochondrial function as well as because of the mitochondrial release of caspaseindependent death effectors including apoptosis-inducing factor (AIF) (742), endonuclease G (EndoG) (448), and others (Fig.”
• Mitochondrial outer membrane permeabilization during apoptosis: the innocent bystander scenario (2006, background): “tractable mechanisms, such as ROS (reactive oxygen species), loss of mitochondrial function or released mitochondrial intermembrane space proteins such as apoptosisinducing factor or endonuclease G to catalyze death.(4) In both situations, caspase-dependent and -independent cell death, MOMP occurs.”
• Apoptotic caspases prevent the induction of type I interferons by mitochondrial DNA (2014, background): “Although caspases are key mediators of apoptotic cell death (Kumar, 2007), multiple mechanisms of caspase-independent cell death exist (Chipuk and Green, 2005; Tait et al., 2014; Vanden Berghe et al., 2014).”
• Molecular definitions of cell death subroutines: recommendations of the Nomenclature Committee on Cell Death 2012 (2011, background): “Thus, at least in vitro, caspase activation is not a strict requirement for multiple cases of apoptosis (see below).(16,17) Similarly, phosphatidylserine (PS) exposure, which is widely considered as an early marker of apoptotic cell death,(18) reportedly does not occur in autophagy-deficient cells s”
• IMMUNE TOLERANCE INDUCTION BY APOPTOTIC CELLS REQUIRES CASPASE-DEPENDENT OXIDATION OF HMGB1 (2008, background): “Although often not required for cell death per se (Chipuk and Green, 2005), they are important for many of the cellular events associated with apoptosis; such events include DNA fragmentation, membrane blebbing, and fragmentation of the cell into membrane-bound apoptotic bodies (Taylor et al.,…”