Anti-mTLR5-IgG2a
Anti-mTLR5-IgG | Unit size | Cat. code | Docs | Qty | Price |
---|---|---|---|---|---|
Mouse TLR5 Neutralizing antibody - Monoclonal Rat IgG2a (Q23D11) |
100 µg |
mabg-mtlr5 |
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Mouse TLR5 Neutralizing antibody - Monoclonal Rat IgG2a (Q23D11)
Anti-mTLR5-IgG2a (Q23D11) is a monoclonal antibody specific for mouse Toll-like receptor 5.
This monoclonal antibody was produced in hybridoma cells and purified by affinity chromatography.
Back to the topSpecifications
Clonality: Monoclonal antibody
Specificity: Mouse TLR5, kappa
Clone: Q23D11
Isotype: Rat IgG2a
Control: Rat Control IgG2a
Source: Hybridoma cells
Formulation: 0.2 µm filtered solution in PBS with 5% saccharose
Applications: Neutralization of mouse TLR5-induced cellular activation. It can also be used fordetection using flow cytometry
Back to the topContents
- 100 μg purified monoclonal anti-mTLR5 IgG antibody (anti-mTLR5-IgG), provided lyophilized.
Product is shipped at room temperature.
Store lyophilized anti-mTLR5-IgG at -20°C.
Lyophilized anti-mTLR5-IgG is stable for 1 year at -20°C. Resuspended anti-mTLR5-IgG is stable up to 3 months when stored at -20°C.
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.
TLR5 recognizes flagellin from both Gram-positive and Gram-negative bacteria. Activation of the receptor stimulates the production of proinflammatory cytokines, such as TNF-α, through signaling via the adaptor protein MyD88 and the serine kinase IRAK [1, 2]. TLR5 can generate a proinflammatory signal as a homodimer suggesting that it might be the only TLR participating in flagellin recognition [2]. However, TLR5 may require the presence of a co-receptor or adaptor molecule for efficient ligand recognition and/or signaling [3].
1. Gewirtz AT. et al., 2001. Cutting edge: bacterial flagellin activates basolaterally expressed TLR5 to induce epithelial proinflammatory gene expression. J Immunol, 167(4):1882-5.
2. Hayashi F. et al., 2001. The innate immune response to bacterial flagellin is mediated by Toll-like receptor 5. Nature, 410(6832):1099-103.
3. Tallant T. et al., 2004. Flagellin acting via TLR5 is the major activator of key signaling pathways leading to NF-kappa B and proinflammatory gene program activation in intestinal epithelial cells. BMC Microbiol. 4(1):33.