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Anti-hTLR4-IgG

Anti-hTLR4-IgG Unit size Cat. code Docs Qty Price
Neutralization - monoclonal mouse IgG1
100 µg
mabg-htlr4
+-
$336.00

Neutralization - monoclonal mouse IgG1

Anti-hTLR4-IgG (W7C11) is a monoclonal antibody specific for human Toll-like receptor 4 (hTLR4, CD284).

TLR4 is the receptor for bacterial lipopolysaccharide (LPS) and lipid A, its toxic moiety [1]. However, TLR4 alone is not sufficient to confer LPS responsiveness. This receptor requires both MD-2 and CD14 to functionally interact with LPS [2, 3]. Ultimately, this leads to the activation of NF-κB and the production of proinflammatory cytokines [3].

Anti-hTLR4-IgG is a neutralizing antibody, it blocks LPS-induced cellular activation.  Anti-hTLR4-IgG has been selected for its ability to efficiently neutralize the biological activity of hTLR4. The neutralizing activity of this IgG1 antibody was determined using InvivoGen’s HEK-Blue™ hTLR4 cells.

 

References

1. Chow J. et al., 1999. Toll-like receptor-4 mediates lipopolysaccharide-induced signal transduction. J Biol Chem 274: 10689-92.
2. Shimazu R. et al., 1999. MD-2, a molecule that confers lipopolysaccharide responsiveness on Toll-like receptor 4. J Exp Med, 189(11): 1777-82.
3. Shuto T. et al., 2005. Membrane-anchored CD14 is required for LPS-induced TLR4 endocytosis in TLR4/MD-2/CD14 overexpressing CHO cells. Biochem Biophys Res Commun 338: 1402-9.

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Specifications

Clonality: Monoclonal antibody

Applications: Neutralizing human TLR4-induced cellular activation

Specificity: Human TLR4

Clone: W7C11

Isotype: Mouse IgG1, kappa

Formulation: phosphate buffered saline (PBS; pH 7.4), 5% saccharose

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Contents

  • 100 μg purified monoclonal anti-hTLR4 IgG antibody (anti-hTLR4-IgG) provided lyophilized.

room temperature Product is shipped at room temperature.

store Store lyophilized anti-hTLR4-IgG at -20°C.

stability Lyophilized anti-hTLR4-IgG is stable for 1 year at -20°C. Resuspended anti-hTLR4-IgG is stable up to 3 months when stored at -20°C.

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Description

Toll-like receptors (TLRs) play a critical role in early innate immunity to invading pathogens by sensing microorganisms. These evolutionary conserved receptors recognize highly conserved structural motifs only expressed by microbial pathogens, called pathogen-associated microbial patterns (PAMPs). Stimulation of TLRs by PAMPs initiates a signaling cascade leading to the secretion of proinflammatory cytokines following NF-κB activation. To date ten human and twelve murine TLRs have been characterized, TLR1 to TLR10 in humans, and TLR1 to TLR9, TLR11, TLR12 and TLR13 in mice, the homolog of TLR10 being a pseudogene.

TLR4, the first human TLR identified, is the receptor for Gram-negative lipopolysaccharide (LPS). The TLR4 gene was shown to be mutated in C3H/HeJ and C57BL/10ScCr mice, both of which are low responders to LPS [1]. However, TLR4 alone is not sufficient to confer LPS responsiveness. TLR4 requires MD-2, a secreted molecule, to functionally interact with LPS [2]. Furthermore, a third protein, called CD14, was shown to participate in LPS signaling, leading to NF-κB translocation. This signaling is mediated through several adaptor proteins: MyD88 TIRAP/Mal [3] , TRIF/TICAM1 and TRAM/TICAM2 [4].

 

1. Poltorak A. et al., 1998. Defective LPS signaling in C3H/HeJ and C57BL/10ScCr mice: mutations in Tlr4 gene. Science, 282(5396):2085-8.
2. Shimazu R. et al., 1999. MD-2, a molecule that confers lipopolysaccharide responsiveness on Toll-like receptor 4. J Exp Med, 189(11):1777-82.
3. Horng T. GM. Barton, and R. Medzhitov, 2001. TIRAP: an adapter molecule in the Toll signaling pathway. Nat Immunol, 2(9):835-41.
4. Fitzgerald KA. et al., 2003. LPS-TLR4 Signaling to IRF-3/7 and NF-{kappa}B Involves the Toll Adapters TRAM and TRIF. J Exp Med. 198(7):1043-1055.
 

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Citations

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