Toll‐like Receptor and RIG‐1‐like Receptor Signaling
By Taro Kawai, Shizuo Akira. Annals of the New York Academy of Sciences, 2008
959 citations recorded by the source corpus.
Subfields: Cancer Research, Immunology
View Paper: https://www.semanticscholar.org/paper/332b00821d4155976c01dc0c9650cf2f13e083ee
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Citations in the corpus
- Type I interferon inhibits interleukin-1 production and inflammasome activation. (2011, background): “…(PRRs) that differ fundamentally with respect to their cellular localization to detect viruses: the transmembrane-localized Toll-like receptors (TLRs) and the cytosolic retinoic acidinducible gene-I (RIG-I) andmelanomadifferentiation-associated gene 5 (MDA5) receptors (Kawai and Akira, 2008).”
- RIG-I dependent sensing of poly(dA-dT) via the induction of an RNA polymerase III transcribed RNA intermediate (2009, neutral): “The innate immune system is the first line of defens”
- Innate immunity and neuroinflammation in the CNS: The role of microglia in Toll‐like receptor‐mediated neuronal injury (2009, background): “To date, at least 13 TLRs have been identified in mammals, which trigger innate and modify adaptive immune responses (Kawai and Akira, 2008).”
- The role of pattern-recognition receptors in innate immunity: update on Toll-like receptors (2010, background): “In addition to recognizing poly(I:C), TLR3 recognizes the genomic RNA of reoviruses, dsRNA produced during the replication of single-stranded RNA (ssRNA), viruses, including respiratory syncytial virus, encephalomyocarditis virus and West Nile virus, and certain small interfering RNA”
- Quantitative proteomics reveals subset-specific viral recognition in dendritic cells. (2010, background): “RIG-I and MDA5 recruit adaptor molecules like Mavs (also called Cardif, VISA, or IPS-1) (Meylan et al., 2005) that are distinct from those that mediate TLR signaling, although both pathways converge on IFN regulatory factors (IRFs) and NF-kB for the production of inflammatory cytokines and IFNs (Kaw”