Cell death by necrosis: towards a molecular definition.
By P. Golstein, Guido Kroemer. TIBS -Trends in Biochemical Sciences. Regular ed, 2007
1,118 citations recorded by the source corpus.
Subfields: Epidemiology, Molecular Biology, Parasitology
View Paper: https://www.semanticscholar.org/paper/6e286d53a811921c012d59d28ee3e02caada4258
How researchers see this paper
The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.
In Epidemiology
- Guido Kroemer
- Beth Levine
- L. Galluzzi
- Douglas R. Green
- P. Boya
- Nektarios Tavernarakis
- M. Maiuri
- Frank Madeo
In Molecular Biology
- Guido Kroemer
- L. Galluzzi
- Beth Levine
- Douglas R. Green
- Simone Fulda
- P. Boya
- M. Maiuri
- Nektarios Tavernarakis
In Parasitology
- Guido Kroemer
- L. Galluzzi
- Douglas R. Green
- Beth Levine
- V. Deretic
- D. Klionsky
- G. Hotamışlıgil
- N. Mizushima
Citations in the corpus
- The hypersensitive response; the centenary is upon us but how much do we know? (2008, background): “However, oncosis need not be a totally unprogrammed event as increased intracellular calcium levels activates enzymes likely to derive signalling molecules, for example, phospolipase A2, as well as proteolytic enzymes (Trump and Berezesky, 1996; Liu et al., 2004; Cummings et al., 2000; Golstein and ”
- Lysosomal membrane permeabilization in cell death (2008, background): “In addition, the inhibition of specific proteins involved in regulating apoptosis or autophagy can change the morphological appearance of cell death to necrosis (Festjens et al., 2006; Golstein and Kroemer, 2007).”
- Induction of autophagy by spermidine promotes longevity (2009, background): “Recent research suggests, however, that the occurrence and course of necrosis can be subject to complex controlled processes and that necrosis can therefore also be 'programmed”
- Classification of cell death (2005, positive): “, calpains and cathepsins).(4,53) In several (but not all) instances of necrotic cell death, a crucial role for the serine/threonine kinase RIP1 has been demonstrated.”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “[59] P.”
- Phosphorylation-Driven Assembly of RIP1-RIP3 Complex Regulates Programmed Necrosis and Virus-Induced Inflammation (2009, neutral): “Cell death by programmed necrosis (also known as caspaseindependent cell death or necroptosis) is characterized by rapid loss of plasma membrane integrity prior to the exposure of phagocytic signal (Golstein and Kroemer, 2007).”
- Self-eating and self-killing: crosstalk between autophagy and apoptosis (2007, background): “It should be noted that inhibition of autophagy does not always induce cell death by apoptosis, and that other types of cell death may also result from autophagy inhibitio”
- Mitochondria, oxidative metabolism and cell death in stroke. (2010, neutral): “Furthermore, these responses can behighly regulated, or even programmed, and are potentially modifiable [26,31,32].”
- Mechanisms underlying acute protection from cardiac ischemia-reperfusion injury. (2008, background): “Until recently, necrosis was thought to be an unregulated process, but recent studies suggest that necrosis can be regulated and that interventions can reduce necrotic cell death (83, 290).”
- Autophagic cell death: the story of a misnomer (2008, background): “Parallel to the consequences of apoptosis inhibition in animal cell deat”
- Targeting mitochondria for cancer therapy (2010, background): “Furthermore, mitochondria play a major part in multiple forms of non-apoptotic cell death and, in particular, in necroptosis (regulated necrosis”