Toll-like receptors activate programmed necrosis in macrophages through a receptor-interacting kinase-3–mediated pathway

By Sudan He, Yuqiong Liang, F. Shao, Xiaodong Wang. Proceedings of the National Academy of Sciences of the United States of America, 2011

701 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology, Molecular Biology

View Paper: https://www.semanticscholar.org/paper/e0cbbcb7349bd1fe7b9df865c1a2483d7e6e7f36

How researchers see this paper

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

In Cancer Research

1. D. Ofengeim
2. J. Upton
3. Junying Yuan
4. William J. Kaiser
5. E. Mocarski
6. Peter Vandenabeele

In Immunology

1. D. Ofengeim
2. Junying Yuan
3. Peter Vandenabeele
4. T. Kanneganti
5. R. Malireddi
6. S. Kesavardhana

In Molecular Biology

1. D. Ofengeim
2. D. Sharma
3. Y. K. Dhuriya
4. J. Upton
5. Junying Yuan
6. William J. Kaiser
7. E. Mocarski
8. Peter Vandenabeele

Citations in the corpus

• Apoptosis, autophagy, necroptosis, and cancer metastasis (2015, background): “receptors [113], Toll-like receptors (TLRs) [114], cellular metabolic and genotoxic stresses, or various anti-cancer agents.”
• A guide to cell death pathways (2023, positive): “Activation of ZBP1 by viral Z-RNA or Z-DNA with interferon stimulation can promote necroptosis as part of a host defence response, independent of RIPK1 and TNFR1 88,89 .”
• Necroptosis: the release of damage-associated molecular patterns and its physiological relevance. (2013, background): “In this respect, it has been shown that stimulation of TLR3 by dsRNA (poly[I:C]) or TLR4 by LPS in combination with caspase inhibition leads to RIPK3-mediated necroptosis in murine macrophages (He et al., 2011) and FADD-deficient Jurkat cells (Kalai et al.”
• The RIP1/RIP3 Necrosome Forms a Functional Amyloid Signaling Complex Required for Programmed Necrosis (2012, neutral): “For instance, macrophage necrosis induced through TLR-3/4 requires RHIMmediated interaction between the adaptor TRIF and RIP3 (He et al., 2011).”
• Toll-like Receptor 3-mediated Necrosis via TRIF, RIP3, and MLKL* (2013, background): “TLR3 and TLR4 both activated cell death pathways via TRIF (5).”
• Necroptosis: a regulated inflammatory mode of cell death (2018, background): “TLR3 and TLR4 also initiate the necroptosis mediated by TRIF and RIPK3 [40, 41].”
• DAI complexes with RIP3 to mediate virus-induced programmed necrosis that is targeted by murine cytomegalovirus vIRA (2012, positive): “Whereas DR-induced necroptosis relies on a RHIM-dependent RIP1-RIP3 signaling complex, virus-induced necrosis follows a RIP3 RHIM-dependent pathway that is independent of RIP1 or TRIF (Upton et al., 2008, 2010).”