Cell Signaling Technology

Product Pathways - NF-kB Signaling

MyD88 (D80F5) XP™ Rabbit mAb #4283

Applications Reactivity Sensitivity MW (kDa) Isotype
W IP H M R (Mk) Endogenous 33 Rabbit IgG

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  M=Mouse  R=Rat  Mk=Monkey
Species cross-reactivity is determined by Western blot.

Protocols

Specificity / Sensitivity

MyD88 (D80F5) XP™ Rabbit mAb detects endogenous levels of total MyD88 protein.

Source / Purification

Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Cys233 of human MyD88 protein.

Western Blotting

Western Blotting

Western blot analysis of extracts from Raji, A549, and THP-1 cells using MyD88 (D80F5) XP™ Rabbit mAb.

Western Blotting

Western Blotting

Western blot analysis of extracts from A549 cells, untransfected (-) or transfected with a MyD88 siRNA (+), using MyD88 (D80F5) XP™ Rabbit mAb.

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 (1-3). TLRs recognize conserved motifs found in various pathogens and mediate defense responses. Triggering of the TLR pathway leads to the activation of NF-κB and subsequent regulation of immune and inflammatory genes. The TLRs and members of the IL-1 receptor family share a conserved stretch of approximately 200 amino acids known as the TIR domain. Upon activation, TLRs associate with a number of cytoplasmic adaptor proteins containing TIR domains including MyD88 (myeloid differentiation factor), MAL/TIRAP (MyD88-adaptor-like/TIR-associated protein), TRIF (Toll-receptor-associated activator of interferon) and TRAM (Toll-receptor-associated molecule). This association leads to the recruitment and activation of IRAK1 and IRAK4, which form a complex with TRAF6 to activate TAK1 and IKK. Activation of IKK leads to the degradation of IκB that normally maintains NF-κB inactivity 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 (4-6). 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 (7). The death domain of MyD88 mediates interactions with the IRAK complex triggering a signaling cascade that includes the activation of NF-κB (8,9).

  1. Akira, S. (2003) J Biol Chem 278, 38105-8.
  2. Beutler, B. (2004) Nature 430, 257-63.
  3. Dunne, A. and O'Neill, L.A. (2003) Sci STKE 2003, re3.
  4. Harroch, S. et al. (1995) Nucleic Acids Res 23, 3539-46.
  5. Hardiman, G. et al. (1996) Oncogene 13, 2467-75.
  6. Bonnert, T.P. et al. (1997) FEBS Lett 402, 81-4.
  7. Medzhitov, R. et al. (1998) Mol Cell 2, 253-8.
  8. Wesche, H. et al. (1997) Immunity 7, 837-47.
  9. Muzio, M. et al. (1997) Science 278, 1612-5.

Application References

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Companion Products

This product is intended for research purposes only. The product is not intended to be used for therapeutic or diagnostic purposes in humans or animals.

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