RIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis

By Duanwu Zhang, J. Shao, Juan Lin, Na Zhang, B. Lu, Sheng-Cai Lin, M. Dong, Jiahuai Han. Science, 2009

1,919 citations recorded by the source corpus.

Subfields: Immunology, Molecular Biology, Nutrition and Dietetics

View Paper: https://www.semanticscholar.org/paper/b59d6afc1b366eb4e6b3740b97bfca8e3467934d

How researchers see this paper

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

In Immunology

1. Guido Kroemer
2. T. Kanneganti
3. Brent R. Stockwell
4. L. Galluzzi
5. D. Ofengeim
6. D. Tang
7. Junying Yuan
8. R. Kang

In Molecular Biology

1. Guido Kroemer
2. T. Kanneganti
3. L. Galluzzi
4. Douglas R. Green
5. D. Tang
6. R. Kang
7. Simone Fulda
8. Brent R. Stockwell

In Nutrition and Dietetics

1. D. Tang
2. R. Kang
3. Brent R. Stockwell
4. Xuejun Jiang
5. Douglas R. Green
6. Guido Kroemer
7. G. Núñez
8. Scott J. Dixon

Citations in the corpus

• Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway (2011, background): “Similarly, in the presence of z-VAD-fmk, TLR4 ligation triggered mouse peritoneal macrophage death, which was ablated in RIP3-deficient cells (17).”
• Caspase-8 regulates TNF-alpha induced epithelial necroptosis and terminal ileitis (2011, positive): “Indeed, we were able to demonstrate constitutive expression of RIP3, a kinase sensitizing cells to necroptosis 17,18 , in human Paneth cells.”
• DAI complexes with RIP3 to mediate virus-induced programmed necrosis that is targeted by murine cytomegalovirus vIRA (2012, positive): “…drive programmed necrosis whether induced by death receptor (DR) or pattern recognition receptor (PRR) activation (He et al., 2011; He et al., 2009; Zhang et al., 2009), during development (Kaiser et al., 2011; Oberst et al., 2011) or in the course of viral infection (Cho et al., 2009; Upton et…”
• Mixed lineage kinase domain-like protein mediates necrosis signaling downstream of RIP3 kinase. (2012, neutral): “Cells expressing RIP3 are capable of undergoing necrosis in response to the TNF family of cytokines (Cho et al., 2009; He et al., 2009; Zhang et al., 2009).”
• Synchronized renal tubular cell death involves ferroptosis (2014, methodology): “hypothesis and are in contrast to previously published data (33, 34).”
• Mixed lineage kinase domain-like protein MLKL causes necrotic membrane disruption upon phosphorylation by RIP3. (2014, background): “This form of necrosis, also termed necroptosis, requires the activity of receptor-interacting protein kinase 1 (RIP1) and its related kinase, RIP3 (Cho et al., 2009; Degterev et al., 2008; He et al., 2009; Holler et al., 2000; Zhang et al., 2009).”