Cell Signaling Technology

Product Pathways - NF-kB Signaling

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

Applications Reactivity Sensitivity MW (kDa) Source
W M (R) Transfected Only 110 Rabbit

Applications Key:  W=Western Blotting
Reactivity Key:  M=Mouse  R=Rat
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 4 Antibody (Rodent Specific) detects transfected levels of total TLR4 protein. Cross reactivity was not detected with other TLR family members.

Source / Purification

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.

Western Blotting

Western Blotting

Western blot analysis of extracts from HeLa cells, mock transfected or transfected with mouse TLR4, using Toll-like Receptor 4 Antibody (Rodent Specific).

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.

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).

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  2. Beutler, B. (2004) Nature 430, 257-63.
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  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.

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