IRAK-4: A novel member of the IRAK family with the properties of an IRAK-kinase

By Shyun Li, Astrid Strelow, E. Fontana, H. Wesche. Proceedings of the National Academy of Sciences of the United States of America, 2002

763 citations recorded by the source corpus.

Subfields: Cancer Research, Immunology

View Paper: https://www.semanticscholar.org/paper/e3f3a74490d3abc50e1b5c5e433906e81cd672e4

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Citations in the corpus

Recognition of microbial infection by Toll-like receptors. (2003, background): “Several IRAK genes have now been discovered; IRAK-1 and IRAK-4 both have kinase activity [12,13], whereas IRAK-2 and IRAK-M do not [14,15].”
Toll-like receptors. (2003, background): “The IRAK family is comprised of four members that contain a conserved death domain and kinase domain: IRAK-1, IRAK-2, IRAK-M, and IRAK-4 (193).”
The Interleukin-1 Receptor/Toll-Like Receptor Superfamily: Signal Transduction During Inflammation and Host Defense (2000, background): “phate (ATP) binding led to the search for an IRAK-1-activating kinase and the subsequent identification of IRAK-4 (129).”
Pathogen recognition and innate immunity. (2006, neutral): “After IRAK-1 associates with MyD88, it is phosphorylated by the activated IRAK-4 and subsequently associates with TNFR-associated factor 6 (TRAF6), which acts as an ubiquitin protein ligase (E3) (Li et al., 2002).”
TLR signaling pathways. (2004, background): “A biochemical study revealed that IRAK-4 acts upstream of, and phosphorylates, IRAK-1 upon stimulation [22].”
IRAK-M is a negative regulator of Toll-like receptor signaling. (2002, background): “…kinase-inactive mutant of IRAK-4 has a dominantIRAK/IRAK-4 results in reduced affinity for the TLR signaling comnegative effect on IL-1R signaling (Li et al., 2002). plex, and IRAK/IRAK-4 are released to make possible the activation We propose the following model for IRAK-M function. of…”
Pathogen Recognition and Inflammatory Signaling in Innate Immune Defenses (2009, background): “protein ligase (E3) (214) that, together with the ubiquitination”
LPS-TLR4 Signaling to IRF-3/7 and NF-κB Involves the Toll Adapters TRAM and TRIF (2003, background): “The recruitment of MyD88 to proximal TIR domains of activated TLRs allows for the interaction and activation of the IL-1R–associated kinase (IRAK) family members (6, 7) and the subsequent activation of TNF receptor–associated factor (TRAF)-6 (8).”