CST, 3699S, MyD88 Antibody

Polyclonal Antibody for studying MyD88. Validated for Western Blotting. Highly specific and rigorously validated in-house, MyD88 Antibody (CST #3699) is ready to ship. Product Usage Information Western Blotting: 1:1000 Storage Supplied in 10 mM sodium HEPES (pH 7.5), 150 mM NaCl, 100 µg/ml BSA and 50% glycerol. Store at -20°C. Do not aliquot the antibody. Protocol Available protocols: Western Blotting Specificity / Sensitivity MyD88 Antibody detects endogenous levels of total MyD88 protein. Species Reactivity: Human, Monkey Source / Purification Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding lysine 119 of human MyD88. Antibodies were purified by protein A and peptide affinity chromatography. Background Members of the Toll-like receptor (TLR) family, named for the closely related Toll receptor in , play a pivotal role in innate immune responses (1-4). TLRs recognize conserved motifs found in various pathogens and mediate defense responses (5-7). Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes (4). The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the Toll/Interleukin-1 receptor (TIR) domain (1). Upon activation, TLRs associate with a number of cytoplasmic adapter proteins containing TIR domains, including myeloid differentiation factor 88 (MyD88), MyD88-adapter-like/TIR-associated protein (MAL/TIRAP), TIR domain-containing adapter-inducing IFN-β (TRIF), and Toll-receptor-associated molecule (TRAM) (8-10). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK (8,11-14). Activation of IKK leads to the degradation of IκB, which normally maintains NF-κB in an inactive state by sequestering it in the cytoplasm. MyD88 was originally isolated as a myeloid differentiation primary response gene that is rapidly induced upon IL-6 stimulated differentiation of M1 myeloleukemic cells into macrophages (15-17). It contains an amino-terminal death domain separated from a carboxyl-terminal TIR domain and functions as an adaptor in TLR/IL-1 receptor signaling (18). The death domain of MyD88 mediates interactions with the IRAK complex triggering a signaling cascade that includes the activation of NF-κB (19,20). Alternate Names IMD68; mutant myeloid differentiation primary response 88; MYD88; MYD88 innate immune signal transduction adaptor; MYD88D; myeloid differentiation primary response 88; myeloid differentiation primary response gene (88); Myeloid differentiation primary response protein MyD88 Specification REACTIVITY: H Mk SENSITIVITY: Endogenous MW (kDa): 33 SOURCE: Rabbit