RIP1 is an essential mediator of Toll-like receptor 3–induced NF-κB activation

By E. Meylan, K. Burns, Kay Hofmann, V. Blancheteau, Fabio Martinon, M. Kelliher, J. Tschopp. Nature Immunology, 2004

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NF-κB and the immune response (2006, background): “TRIF interacts with receptor interacting protein (RIP)1 and RIP3 through their RIP homotypic interaction motif (RHIM), and rip1 / embryonic fibroblasts have decreased NF-kB activation following TLR3poly(I:C) signaling (Meylan et al., 2004).”
The family of five: TIR-domain-containing adaptors in Toll-like receptor signalling (2007, background): “TRIF was found to recruit both RIP1 and RIP3 through this domain, and in MEFs deficient in RIP1, polyI:C-induced NF-κB activation was completely blocke”
Pathophysiology of Myocardial Infarction (2015, positive): “(219), receptor interacting protein 3 (RIP3), a kinase that inhibits RIP1-induced NF-κB signaling (252), activating transcription factor 3, the autophagy-related molecule Atg16L1,”