| 產(chǎn)品詳情 |
| Edit |   |
| Antigenic Specificity | TLR2, Mouse |
| Clone | mT2.7 |
| Host Species | Mouse |
| Reactive Species | mouse |
| Isotype | IgG2a |
| Format | biotin conjugate |
| Size | 50 μg |
| Concentration | 100 μg/ml |
| Applications | frozen sections, FC |
| Reviews / Ratings | If you have used this antibody, please help fellow researchers by submitting reviews to pAbmAbs and antYbuddY. |
| Description | Monoclonal antibody mT2.7 reacts with mouse Toll-like receptor 2 (TLR2, CD282). Toll-like receptors (TLR) are highly conserved throughout evolution and have been implicated in the innate defense to many pathogens. In Drosophila toll is required for the anti-fungal response, while the related 18-wheeler is involved in antibacterial defenses. In mammals, TLR identified as type I transmembrane signaling receptors with pattern recognition capabilities, have been implicated in the innate host defense to pathogens. TLR2 has been identified as a receptor that is central to the innate immune response to lipoproteins of Gram-negative bacteria, several whole Gram-positive bacteria, as well as a receptor for peptidoglycan and lipoteichoic acid and other bacterial cell membrane products. A functional interaction between TLR2 and TLR6 in the cellular response to various bacterial products has been discovered. The currently accepted paradigm regards TLR2 as an essential receptor for many eubacterial cell wall components, including lipoproteins and peptidoglycan. Bacterial species as diverse as mycobacteria, spirochetes, mycoplasma, Staphylococcus aureus, and Streptococcus pneumoniae have all been shown to mediate cellular activation via TLR2. The monoclonal antibody mT2.7 stained overexpressed, as well as endogenous cell surface- and intracellular TLR2. The antibody does not affect cell activation through TLR2. |
| Immunogen | n/a |
| Other Names | n/a |
| Gene, Accession # | n/a |
| Catalog # | HM1059 |
| Price | |
| Order / More Info | TLR2, Mouse Antibody from HYCULT BIOTECH |
| Product Specific References | n/a |
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