Product Pathways - NF-kB Signaling
Toll-like Receptor 4 Antibody (Rodent Specific) #2219
|W||M (R)||Transfected Only||110||Rabbit|
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.
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.
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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- Rock, F.L. et al. (1998) Proc. Natl. Acad. Sci. USA 95, 588-593.
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- Shimazu, R. et al. (1999) J. Exp. Med. 189, 1777-1782.
- Kawai, T. and Akira, S. (2006) Cell Death Differ. 13, 816-825.
- Kim, J.K. et al. (2011) J Biol Chem 286, 41296-311. Applications: Western Blotting
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For Research Use Only. Not For Use In Diagnostic Procedures.