Product Pathways - NF-kappaB 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 enclosed in parentheses are predicted to react based on 100% sequence homology. Species cross-reactivity is determined by Western blot.
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 rabbits with a synthetic peptide (KLH-coupled) corresponding to residues surrounding Cys549 within the extracellular region of mouse and rat TLR4. Antibodies were purified by peptide affinity chromatography.
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 (1-3). 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.
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).
- 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.
- Rock, F.L. et al. (1998) Proc. Natl. Acad. Sci. USA 95, 588-593.
- Poltorak, A. et al. (1998) Science 282, 2085-2088.
- Chow, J.C. et al. (1999) J. Biol. Chem. 274, 10689-10692.
- Hoshino, K. et al. (1999) J. Immunol. 162, 3749-3752.
- Shimazu, R. et al. (1999) J. Exp. Med. 189, 1777-1782.
- Kawai, T. and Akira, S. (2006) Cell Death Differ. 13, 816-825.
Application References
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This product is for in vitro research use only and is not intended for use in humans or animals. This product is not intended for use as therapeutic or in diagnostic procedures.
