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Anti-TLR2 Antibody EPNCIR133
Also for TLR2 (NM_003264)
|A recombinant protein corresponding to human TLR-2 extracellular domain was used as an immunogen.|
|Mouse, Rat, Human
||Lot dependent; please refer to CoA along with shipment
||WB: 1:1000 - 1:10000; IP: 1:10 - 1:100; ICC: 1:250 - 1:500
|PBS 49%,Sodium azide 0.01%,Glycerol 50%,BSA 0.05%|
|Tissue culture supernatant
|Is unsuitable for Flow Cyt or IHC-P.
|Homo sapiens toll-like receptor 2 (TLR2)|
|Toll-like receptor 2 (TLR2) is a signalling receptor that is activated by LPS in a response that depends on LPS-binding protein and is enhanced by CD14. A region in the intracellular domain of TLR2 with homology to a portion of the interleukin (IL)-1 receptor that is implicated in the activation of the IL-1-receptor-associated kinase is required for this response. Results indicate that TLR2 is a direct mediator of signalling by LPS (1). All bacterial pathogens produce lipoproteins (BLPs), which trigger the innate immune response. BLPs were found to induce apoptosis in THP-1 monocytic cells through human TLR2. BLPs also initiated apoptosis in an epithelial cell line transfected with TLR2. BLPs stimulated nuclear factor-kappaB, a transcriptional activator of multiple host defense genes, and activated the respiratory burst through TLR2. Thus, TLR2 is a molecular link between microbial products, apoptosis, and host defense mechanisms (2). It has been found that in TLR2 extracellular domain (C-term) all four predicted glycosylation sites are substituted, although one site is inefficiently core-glycosylated and its removal drastically affects secretion. The remaining TLR2 glycosylation sites also contribute to efficient protein secretion, albeit to a lesser degree (3).|
Toll-like receptor signaling pathway
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Western blot - TLR2 antibody [EPNCIR133]; All lanes : Anti-TLR2 antibody [EPNCIR133] at 1/1000 dilution.Lane 1 : THP1 cell lysate.Lane 2 : A549 cell lysate.Lane 3 : Ramos cell lysate.Lane 4 : SW480 cell lysate.Lysates/proteins at 10 ug per lane.Predicted band size : 90 kDa.