MyD88 Antibody #3699
Filter:
- WB
Supporting Data
REACTIVITY | H Mk |
SENSITIVITY | Endogenous |
MW (kDa) | 33 |
SOURCE | Rabbit |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
- Mk-Monkey
Product Information
Product Usage Information
Application | Dilution |
---|---|
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
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 Drosophila, 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 adaptor proteins containing TIR domains, including myeloid differentiation factor 88 (MyD88), MyD88-adaptor-like/TIR-associated protein (MAL/TIRAP), Toll-receptor-associated activator of interferon (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).
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).
- Akira, S. (2003) J Biol Chem 278, 38105-8.
- Beutler, B. (2004) Nature 430, 257-63.
- Dunne, A. and O'Neill, L.A. (2003) Sci STKE 2003, re3.
- Medzhitov, R. et al. (1997) Nature 388, 394-7.
- Schwandner, R. et al. (1999) J Biol Chem 274, 17406-9.
- Takeuchi, O. et al. (1999) Immunity 11, 443-51.
- Alexopoulou, L. et al. (2001) Nature 413, 732-8.
- Zhang, F.X. et al. (1999) J Biol Chem 274, 7611-4.
- Horng, T. et al. (2001) Nat Immunol 2, 835-41.
- Oshiumi, H. et al. (2003) Nat Immunol 4, 161-7.
- Muzio, M. et al. (1997) Science 278, 1612-5.
- Wesche, H. et al. (1997) Immunity 7, 837-47.
- Suzuki, N. et al. (2002) Nature 416, 750-6.
- Irie, T. et al. (2000) FEBS Lett 467, 160-4.
- Harroch, S. et al. (1995) Nucleic Acids Res. 23, 3539-46.
- Hardiman, G. et al. (1996) Oncogene 13, 2467-75.
- Bonnert, T.P. et al. (1997) FEBS Lett. 402, 81-4.
- Medzhitov, R. et al. (1998) Mol. Cell 2, 253-8.
- Wesche, H. et al. (1997) Immunity 7, 837-47.
- Muzio, M. et al. (1997) Science 278, 1612-5.
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For Research Use Only. Not For Use In Diagnostic Procedures.
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