Toll-like Receptor 8 (D3Z6J) Rabbit mAb #11886
- WB
Supporting Data
| REACTIVITY | H |
| SENSITIVITY | Endogenous |
| MW (kDa) | 150 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
Species Cross-Reactivity Key:
- H-Human
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
Storage
Protocol
Specificity / Sensitivity
Toll-like Receptor 8 (D3Z6J) Rabbit mAb recognizes endogenous levels of total TLR8 protein. This antibody cross-reacts with a 30 kDa protein and a 37 kDa protein of unknown origin.
Species Reactivity:
Human
The antigen sequence used to produce this antibody shares 100% sequence homology with the species listed here, but reactivity has not been tested or confirmed to work by CST. Use of this product with these species is not covered under our Product Performance Guarantee.
Species predicted to react based on 100% sequence homology:
Monkey
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Pro141 of human TLR8 protein.
Background
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.
TLR8 is an intracellular TLR localized to the endoplasmic reticulum, endosomes, lysosomes, and endolysosomes (4). It is activated by single-stranded viral RNA, as well as synthetic imidazoquinoline compounds including R-848 (5). TLR8 expression is highest in the lung and in myeloid cells (6,7). In addition, expression is upregulated by IFN-γ in monocyte-like leukemic THP-1 cells that have been differentiated with TPA (7).
Limited Uses
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