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2219
Toll-like Receptor 4 Antibody (Rodent Specific)

Toll-like Receptor 4 Antibody (Rodent Specific) #2219

This product is discontinued

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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.

Toll-like Receptor 4 Antibody (Rodent Specific) detects transfected levels of total TLR4 protein. Cross reactivity was not detected with other TLR family members.

Species predicted to react based on 100% sequence homology:

Rat

Polyclonal antibodies are produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Cys549 within the extracellular region of mouse and rat TLR4 protein. Antibodies were purified by peptide affinity chromatography.

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.

TLR4 functions in association with MD-2 in the recognition and initiation of immune responses elicited by lipopolysaccharide (LPS) of Gram-negative bacteria (4-8). TLR4 triggers the activation of NF-κB, IRF-3, and MAPK pathways leading to the production of inflammatory cytokines (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. 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. Rock, F.L. et al. (1998) Proc. Natl. Acad. Sci. USA 95, 588-593.
  16. Poltorak, A. et al. (1998) Science 282, 2085-2088.
  17. Chow, J.C. et al. (1999) J. Biol. Chem. 274, 10689-10692.
  18. Hoshino, K. et al. (1999) J. Immunol. 162, 3749-3752.
  19. Shimazu, R. et al. (1999) J. Exp. Med. 189, 1777-1782.
  20. Kawai, T. and Akira, S. (2006) Cell Death Differ. 13, 816-825.
Entrez-Gene Id
7099
Swiss-Prot Acc.
O00206
For Research Use Only. Not For Use In Diagnostic Procedures.

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