Identification of RIP1 kinase as a specific cellular target of necrostatins.
By Alexei Degterev, J. Hitomi, Megan Germscheid, Irene L. Ch’en, O. Korkina, Xin-Chen Teng, Derek W. Abbott, G. Cuny, C. Yuan*, G. Wagner and 4 more. Nature Chemical Biology, 2008
2,015 citations recorded by the source corpus.
Subfields: Cell Biology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/38e5e4b5f2052e7949d8c7ea7309317f8326df37
How researchers see this paper
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In Cell Biology
- Guido Kroemer
- Beth Levine
- D. Klionsky
- L. Galluzzi
- Douglas R. Green
- J. Cubillos-Ruiz
- Junying Yuan
- Y. Tsujimoto
In Molecular Biology
- Guido Kroemer
- Douglas R. Green
- L. Galluzzi
- Brent R. Stockwell
- Simone Fulda
- T. Kanneganti
- Beth Levine
- D. Tang
Citations in the corpus
- Molecular mechanisms of necroptosis: an ordered cellular explosion (2010, background): “In 2005, Yuan and colleagues identified necrostatin 1 and necrostatin 3, small molecules that allosterically block the kinase activity of RIP1, thereby inhibiting necroptosis but leaving RIP1-mediated activation of NF-κB, mitogen-activated protein kinase p38 and JUN N-terminal kinase 1 (JNK1) unaf”
- Caspase-8 regulates TNF-alpha induced epithelial necroptosis and terminal ileitis (2011, positive): “RIP-mediated necroptosis can be blocked in vitro and in vivo by using necrostatin-1 (nec-1), an allosteric small-molecule inhibitor of the RIP1 kinase 21 .”
- Catalytic activity of the caspase-8-FLIPL complex inhibits RIPK3-dependent necrosis (2011, neutral): “Necrosis induced by TNF in the presence of caspase inhibitors is dependent on the kinase activity of Receptor-Interacting Protein Kinase-1 (RIPK1)4,8 and RIPK39–11, although the mechanisms remain obscure.”
- Receptor interacting protein kinase-3 determines cellular necrotic response to TNF-alpha. (2009, background): “This is consistent with the notion that Necrostatin-1 inhibits RIPK1 kinase activity, which is required for the formation of RIPK1/FADD/caspase-8 complex (Degterev et al., 2008; Wang et al., 2008).”
- Cellular Stress Responses: Cell Survival and Cell Death (2010, background): “[70] A.”
- The Ripoptosome, a signaling platform that assembles in response to genotoxic stress and loss of IAPs. (2011, methodology): “To this end we used Necrostatin-1 (Nec-1), an inhibitor of RIP1 kinase that blocks RIP1mediated necroptosis (Degterev et al., 2008).”
- 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].”