RICK/Rip2/CARDIAK mediates signalling for receptors of the innate and adaptive immune systems
By Koichi S. Kobayashi, N. Inohara, L. Hernandez, J. Galán, G. Núñez, C. Janeway, R. Medzhitov, R. Flavell. Nature, 2002
938 citations recorded by the source corpus.
Subfields: Immunology, Molecular Biology
View Paper: https://www.semanticscholar.org/paper/542fed5b12a5428146566f72b27bec79f039fde9
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In Molecular Biology
Citations in the corpus
- Nod2 is required for the regulation of commensal microbiota in the intestine (2009, background): “The Rip2 kinase is required for downstream signaling of Nod2 (11).”
- Toll-like receptors and innate immunity (2006, background): “Recognition of ligands through the LRR domains activates NOD proteins, which then recruit the serine–threonine kinase RICK (also known as RIP2 or CARDIACK) through a CARD–CARD interaction [80].”
- Toll-like receptors in innate immunity. (2004, neutral): “Introduction of NOD1 or NOD2 into Rip2/ RICK-deficient embryonic fibroblast cells does not induce NF-j B activation (66).”
- Macrophage activation by endogenous danger signals (2008, background): “It is noteworthy that RICK may also be a downstream molecule for TLR2 and TLR4, since RICK-deficient macrophages have reduced production of cytokines following TLR2 or TLR4 activation by extracellular agonists [36].”
- Regulating Intracellular Antiviral Defense and Permissiveness to Hepatitis C Virus RNA Replication through a Cellular RNA Helicase, RIG-I (2005, methodology): “5 cells were subjected to complementation analysis with cotransfected plasmids encoding the IRF3-dependent F3-EGFP reporter construct and the constitutively expressed dsRed protein with a vector control plasmid or a plasmid from a panel of constructs encoding proteins implicated in antiviral signali”
- Function of Nod‐like receptors in microbial recognition and host defense (2009, background): “The inability of RICK null cells or mice to activate NF-jB signaling downstream of Nod1 ⁄2 ligand stimulation indicates that RICK is required in vivo for signaling (40, 42).”
- Toll-like receptors. (2003, background): “Mice deficient in RIP2 exhibit partial impairment in their response to LPS, peptidoglycan, and dsRNA (209, 210).”
- Differential activation of the inflammasome by caspase-1 adaptors ASC and Ipaf (2004, background): “Although overexpression studies suggest that RIP2 induces caspase-1 activation, no defects were reported for RIP2-deficient mice with respect to TLR-induced IL-1β processing and releas”