ABfinity™ Recombinant Rabbit Monoclonal Antibody validated to Human and expected reactivity with human, mouse, rat, primates, sheep, equine, swine, bovine, canine, Xenopus. This antibody is validated for use in Immunofluorescence and Flow Cytometry. IRAK4 is encoded by the 51135 gene, also known as Interleukin-1 receptor-associated kinase 4, IPD1, REN64, NY-REN-64.
Interleukin-1 receptor-associated kinases (IRAKs) are important mediators in the signal transduction of the Toll⁄IL-1 receptor (TIR) family. Members of the TIL family play a role in innate immune responses by coordinating host defense mechanisms. IRAK4 has been shown to interact with IRAK1 and TRAF6 in an IL-1-dependent manner, and overexpression of IRAK4 has been shown to activate NFκB as well as mitogen-activated protein (MAP) kinase pathways (1). Studies demonstrate that mice lacking IRAK4 are severely impaired in their IL-1, Toll-like receptor (TLR) signaling and response to viral and bacterial challenges; this indicates that IRAK4 has an important role in innate immunity (2). Humans lacking IRAK4 exhibit pyogenic bacterial infections, while their blood and fibroblast cells fail to activate NF-κB (3). IRAK4 is believed to be required for the LPS-induced activation of antigen-presenting cells (4). IRAK4 activity is required for both adaptive and innate immune responses and is essential for removal of self-reactive B cells (5,6)
Cao Z, et al. (1996) TRAF6 is a signal transducer for interleukin-1. Nature 383: 443-6.
Suzuki N, et al. (2002) Severe impairment of interleukin-1 and Toll-like receptor signalling in mice lacking IRAK-4. Nature 416: 750-6.
Picard C. et al., (2003) Pyogenic Bacterial Infections in Humans with IRAK-4 Deficiency. Science 299: 2076-2079.
Suzuki, N. et al. (2003) IL-1R-Associated Kinase 4 Is Required for Lipopolysaccharide- Induced Activation of APC. J. Immunol. 171: 6065-6071.
Lye E, et al. (2008) IRAK-4 kinase activity is required for IRAK-4-dependent innate and adaptive immune responses. Eur J Immunol. 38(3):870-6.
Isnardi I, et al. (2008) IRAK-4- and MyD88-dependent pathways are essential for the removal of developing autoreactive B cells in humans. Immunity 29(5):746-57.