Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
By Alexei Degterev, Zhihong Huang, M. Boyce, Yaqiao Li, P. Jagtap, N. Mizushima, G. Cuny, T. Mitchison, M. Moskowitz, Junying Yuan. Nature Chemical Biology, 2005
2,945 citations recorded by the source corpus.
Subfields: Endocrinology, Epidemiology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/604173c8250d2c44163341ff99d45adf630dc995
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In Endocrinology
- Guido Kroemer
- L. Galluzzi
- Herbert W. Virgin
- P. Boya
- G. Núñez
- Beth Levine
- Eric H. Baehrecke
- D. Klionsky
In Epidemiology
In Molecular Biology
- Guido Kroemer
- Douglas R. Green
- L. Galluzzi
- Simone Fulda
- Beth Levine
- Junying Yuan
- T. Kanneganti
- D. Tang
Citations in the corpus
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- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “[69] A.”
- Ischemia/Reperfusion (2016, positive): “activated by ligation of receptors in the TNF family (240) but are also critical for the progression of regulated necrotic death in response to stressful stimuli (141,175,176,234,349).”
- Pattern Recognition Receptors and the Host Cell Death Molecular Machinery (2018, background): “The first molecule to be identified in the necroptotic pathway was RIPK1 as its kinase activity inhibitor, necrostatin-1 (Nec-1), was shown to suppress cell death triggered by caspase inhibition during TNFR1/Fas stimulation (39).”
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- Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018 (2018, background): “, Nec-1s) robustly inhibit TNFR1-driven necroptosis, in vitro and in vivo [425, 427].”