The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway
Open accessAbstract
We report here that mouse macrophages undergo receptor-interacting kinase-3 (RIP3)-dependent but TNF-α–independent necrosis when Toll-like receptors (TLR) 3 and 4 are activated by poly(I:C) and LPS, respectively. An adaptor protein, Toll/IL-1 receptor domain-containing adapter inducing IFN-β (TRIF/TICAM-1), which is dispensable for TNF-α–induced necrosis, forms a complex with RIP3 upon TLR3/TLR4 activation and is essential for TLR3/TLR4-induced necrosis. Mice without RIP3 or functional TRIF did not show macrophage loss and elevation of inflammatory cytokines when they were exposed to LPS. Necrosis in mouse macrophages induced by either TNFR or TLR3/TLR4 is executed by reactive oxygen species. Taken together, these data indicate that there are multiple upstream necrosis-initiating signaling pathways converging on the RIP3 during an innate immune response to viral and bacterial infections in mammals.
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Cites
Recognition of double-stranded RNA and activation of NF-κB by Toll-like receptor 3
Alexopoulou, L., Holt, A. C., Medzhitov, R., & Flavell, R. A. (2001) · Nature · doi:10.1038/35099560 · Cited by 6,129
Chemical inhibitor of nonapoptotic cell death with therapeutic potential for ischemic brain injury
Degterev, A., Huang, Z., Boyce, M., Li, Y., Jagtap, P., Mizushima, N., Cuny, G. D., Mitchison, T. J., Moskowitz, M. A., & Yuan, J. (2005) · Nature Chemical Biology · doi:10.1038/nchembio711 · Cited by 3,068
Cho, Y., Challa, S., Moquin, D., Genga, R., Ray, T. D., Guildford, M., & Chan, F. K.-M. (2009) · Cell · doi:10.1016/j.cell.2009.05.037 · Cited by 2,435
Molecular mechanisms of necroptosis: an ordered cellular explosion
Vandenabeele, P., Galluzzi, L., Vanden Berghe, T., & Kroemer, G. (2010) · Nature Reviews Molecular Cell Biology · doi:10.1038/nrm2970 · Cited by 2,382
Receptor Interacting Protein Kinase-3 Determines Cellular Necrotic Response to TNF-α
He, S., Wang, L., Miao, L., Wang, T., Du, F., Zhao, L., & Wang, X. (2009) · Cell · doi:10.1016/j.cell.2009.05.021 · Cited by 2,214
Self-citationRIP3, an Energy Metabolism Regulator That Switches TNF-Induced Cell Death from Apoptosis to Necrosis
Zhang, D.-W., Shao, J., Lin, J., Zhang, N., Lu, B.-J., Lin, S.-C., Dong, M.-Q., & Han, J. (2009) · Science · doi:10.1126/science.1172308 · Cited by 1,931
Catalytic activity of the caspase-8–FLIPL complex inhibits RIPK3-dependent necrosis
Oberst, A., Dillon, C. P., Weinlich, R., McCormick, L. L., Fitzgerald, P., Pop, C., Hakem, R., Salvesen, G. S., & Green, D. R. (2011) · Nature · doi:10.1038/nature09852 · Cited by 1,278 · cited 1×
“One possible explanation for this apparent paradox is that the RIP1-mediated signal, and possibly the induction of cFLIP [cellular FLICE (FADD-like IL-1β–converting enzyme)inhibitory protein], is particularly important for macrophage survival (25).”
Background
Research works printed but not linked: 24
- 10.1016/j.chom.2010.03.006 · DOI · Paper page
- 10.1073/pnas.1009179107 · DOI · Paper page
- 10.1038/ni914 · DOI
- 10.1074/jbc.M511276200 · DOI · Paper page
- 10.1038/ni.1863 · DOI · Paper page
- 10.1159/000315469 · DOI
- 10.1126/science.282.5396.2085 · DOI · Paper page
- K Hoshino, et al., Cutting edge: Toll-like receptor 4 (TLR4)-deficient mice are hyporesponsive to lipopolysaccharide: Evidence for TLR4 as the Lps gene product. J Immunol 162, 3749–3752 (1999). · DOI · Paper page
- 10.1016/S1074-7613(00)80086-2 · DOI · Paper page
- 10.1038/nature01889 · DOI · Paper page
- 10.1126/science.1087262 · DOI · Paper page
- 10.1074/jbc.M510849200 · DOI
- 10.1038/sj.cdd.4401051 · DOI
- 10.1016/j.ejphar.2008.01.026 · DOI · Paper page
- 10.1016/j.crvi.2004.04.002 · DOI
- 10.1038/ni1061 · DOI · Paper page
- 10.1016/j.molcel.2007.04.021 · DOI · Paper page
- 10.1016/S1074-7613(00)80535-X · DOI · Paper page
- 10.1016/j.molcel.2011.06.011 · DOI · Paper page
- 10.1016/j.molcel.2011.06.006 · DOI · Paper page
- 10.1074/jbc.M305633200 · DOI · Paper page
- 10.1016/j.cellsig.2007.05.016 · DOI · Paper page
- 10.1128/MCB.26.6.2215-2225.2006 · DOI
- Li et al. A small molecule Smac mimic potentiates TRAIL- and TNFalpha-mediated cell death Science. 305 1471–1474 (2004). · DOI · Paper page
Cited by
Necroptosis and its role in inflammation
Pasparakis, M., & Vandenabeele, P. (2015) · Nature · doi:10.1038/nature14191 · Cited by 2,148
TLR4 and CD14 trafficking and its influence on LPS-induced pro-inflammatory signaling
Ciesielska, A., Matyjek, M., & Kwiatkowska, K. (2021) · Cellular and Molecular Life Sciences · doi:10.1007/s00018-020-03656-y · Cited by 1,420
Necroptosis: The Release of Damage-Associated Molecular Patterns and Its Physiological Relevance
Kaczmarek, A., Vandenabeele, P., & Krysko, D. V. (2013) · Immunity · doi:10.1016/j.immuni.2013.02.003 · Cited by 1,411
Li, J., McQuade, T., Siemer, A. B., Napetschnig, J., Moriwaki, K., Hsiao, Y.-S., Damko, E., Moquin, D., Walz, T., McDermott, A., et al. (2012) · Cell · doi:10.1016/j.cell.2012.06.019 · Cited by 1,222
Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL
Kaiser, W. J., Sridharan, H., Huang, C., Mandal, P., Upton, J. W., Gough, P. J., Sehon, C. A., Marquis, R. W., Bertin, J., & Mocarski, E. S. (2013) · Journal of Biological Chemistry · doi:10.1074/jbc.m113.462341 · Cited by 959
Metadata
- Authors
- He, S., Liang, Y., Shao, F., & Wang, X.
- Venue
- Proceedings of the National Academy of Sciences
- Published
- 2011-11-28
- Volume
- 108
- Issue
- 50
- Pages
- 20054-20059
- ISSN
- 0027-8424 (ISSN-L)
- 1091-6490
- OpenAlex
- W2141738274
- Cited by
- 729
- References
- 7
- FWCI
- 11.78
- Type
- journal article
- Language
- en
- Open access
- bronze
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- He, S., Liang, Y., Shao, F., & Wang, X. (2011). Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway. Proceedings of the National Academy of Sciences. https://doi.org/10.1073/pnas.1116302108
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