The mammalian host defense system is essentially regulated by Toll-like receptor (TLR) family. Toll-like receptors (TLRs) play an important role in recognition of microbial components and induction of innate immunity. At least 10 TLRs have been identified and cloned in mammalian cells which recognize molecular products/signals from all the major classes of pathogens. The Toll signaling to NF-Kb starts form conserved Toll-IL-1-resistance (TIR) domain, which mediated the coupling of TIR adaptor molecules (MyD88, Mal, TICAM and TRAM). Most of the TLRs are dependent on the expression of adapter molecules MyD88 for all their function, the TL3 and TLR 4 are unique in their ability to mediate both MyD88-dependent and independent reposes (1). The MyD88 independent pathway involves induction of a DC maturation and induction of type 1 interferon (IFN-B).
Murine MyD88, an RNA with homology both to the interleukin-1 receptor signaling domain and to ’death-domains’, is rapidly up-regulated during differentiation of the myeloleukemic cell line M1. The murine MyD88 is 53 amino acids larger than human MyD88 and maps to chromosome 3p21.3-p22. The over expression of death region in MyD88 lead to transcriptional activation of IL-8 promoter. The microbial components trigger the activation of two downstream signaling pathways of TLRs; MyD88- and/or TRIF-dependent pathways leading to activation of NF-kappaB. The MyD88 transduces a core set of Toll-like receptor (TLR)-induced signals, microbial-induced host responses are divided broadly into the MyD88-dependent and MyD88-independent pathways. The specific pathogen induced early host responses are generally mediated by MyD88 dependent pathways. Inhaled endotoxins induce an acute inflammatory response in the airways mediated through Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 (MyD88). The endotoxin-induced acute bronchoconstriction, vascular damage resulting in protein leak, Th1 cytokine and chemokine secretion and neutrophil recruitment in the airways are abrogated in mice deficient for either TIRAP or MyD88, but not in TRIF deficient mice (2). The bronchoconstriction and acute inflammatory lung pathology mediated by TLR-4 to inhaled endotoxins critically dependent on the expression and co-operative role of adaptor proteins, TIRAP and MyD88 (3). The MyD88 mediated post-TLR signaling is also involved in a number of allergents ad endotoxins, includding
The MyD88-selective antibodies were generated against peptide form unique region of the MyD88 protein sequence that is not present in other adapter molecules and other proteins listed in the gene-bank. FabGennix Inc. has generated epitope specific rabbit anti-MyD88 polyclonal (epitope-specific) antibodies utilizing linear and cyclic peptide sequences. The MyD88 antibodies are affinity purified over immobilized antigen based chromatography, and the purified immunoglobulins are stabilized in antibody stabilization buffer. Limited quantities of the antigenic blocking peptide for MyD88 antibodies are also available (inquire for availability). FabGennix Inc. will also conjugate antibodies with enzymes or fluorescent probes as custom service upon request at a reasonable cost.
For research use only, not for diagnostic or therapeutic use.
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