IRAK3
Reactivity: Human
WB, ELISA, IHC, IF
Host: Rabbit
Polyclonal
unconjugated
Application Notes
Peptide ELISA: 1/64000. Western Blot: 0.05 - 0.2 μg/mL. Other applications not tested. Optimal dilutions are dependent on conditions and should be determined by the user.
Reduced expression of IRAK-1 and increased expression of IRAK-M after CpG DNA pretreatment resulted in the hyporesponsiveness of macrophages that leads to the protection of mice from hepatic injury and death caused by CpG DNA/D-GalN. Endotoxin tolerance was significantly reduced in macrophages from IRAK-M knockout mice. IRAK-M regulates TLR signaling and innate immune homeostasis. induction of IRAK-M and inhibition of kinase activity of IRAK-1 are crucial to PGN-induced tolerance in macrophages. IRAK-M is a key regulator of the bone loss that is due to osteoclastic resorption of bone. IRAK-M induction negatively regulates Toll-like receptor-dependent interleukin-12 p40 production in macrophages in the presence of Mycobacterium tuberculosis lipoarabinomannan. These findings indicate that IRAK-M selectively attenuates p38 activation and inhibits innate immunity through stabilizing MKP-1. IRAK-M is directly involved in the regulation of both innate and adaptive immune signaling processes, and deletion of IRAK-M enhances host anti-tumor immune response.Synonyms: IL-1 receptor-associated kinase M, IRAK-3, IRAK-M, Interleukin-1 receptor-associated kinase 3