Cell Signaling Technology

Product Pathways - NF-kB Signaling

Toll-like Receptor 1 Antibody #2209

Applications Reactivity Sensitivity MW (kDa) Source
W IP H (Mk) Endogenous 86 Rabbit

Applications Key:  W=Western Blotting  IP=Immunoprecipitation
Reactivity Key:  H=Human  Mk=Monkey
Species cross-reactivity is determined by western blot. Species enclosed in parentheses are predicted to react based on 100% sequence homology.

Protocols

Specificity / Sensitivity

Toll-like Receptor 1 Antibody detects endogenous levels of total TLR1 protein.

Source / Purification

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues at the amino terminus of human TLR1 protein. Antibodies were purified by peptide affinity chromatography.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, mock transfected or transfected with human TLR1, using Toll-like Receptor 1 Antibody.

Western Blotting

Western Blotting

Western blot analysis of extracts from SR cells using Toll-like Receptor 1 Antibody.

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.

Toll-like receptor expression is highest in peripheral blood leukocytes, monocytes, macrophages, though TLR1 expression may be less restricted than other family members (4,5). TLR1 associates with TLR2 to cooperatively mediate immune responses to bacterial lipoproteins and lead to NF-κB activation (6,7). TLR1 shows highest homology to TLR6, which shares 69% sequence identity (8).

  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. Medzhitov, R. et al. (1997) Nature 388, 394-7.
  5. Schwandner, R. et al. (1999) J Biol Chem 274, 17406-9.
  6. Takeuchi, O. et al. (1999) Immunity 11, 443-51.
  7. Alexopoulou, L. et al. (2001) Nature 413, 732-8.
  8. Zhang, F.X. et al. (1999) J Biol Chem 274, 7611-4.
  9. Horng, T. et al. (2001) Nat Immunol 2, 835-41.
  10. Oshiumi, H. et al. (2003) Nat Immunol 4, 161-7.
  11. Muzio, M. et al. (1997) Science 278, 1612-5.
  12. Wesche, H. et al. (1997) Immunity 7, 837-47.
  13. Suzuki, N. et al. (2002) Nature 416, 750-6.
  14. Irie, T. et al. (2000) FEBS Lett 467, 160-4.
  15. Muzio, M. et al. (2000) J Leukoc Biol 67, 450-6.
  16. Ochoa, M.T. et al. (2003) Immunology 108, 10-5.
  17. Takeuchi, O. et al. (2002) J Immunol 169, 10-4.
  18. Sandor, F. et al. (2003) J Cell Biol 162, 1099-110.
  19. Takeuchi, O. et al. (1999) Gene 231, 59-65.

Application References

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For Research Use Only. Not For Use In Diagnostic Procedures.

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