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TLR3 Protein (Primary Amine Labeling), Human, Recombinant (His), Biotinylated is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 78.7 kDa and the accession number is Q6PCD4.
Pack Size | Price | Availability | Quantity |
---|---|---|---|
100 μg | $814 | 7-10 days | |
500 μg | $3,250 | 7-10 days | |
1 mg | $5,440 | 7-10 days |
Biological Activity | Activity has not been tested. It is theoretically active, but we cannot guarantee it. If you require protein activity, we recommend choosing the eukaryotic expression version first. |
Description | TLR3 Protein (Primary Amine Labeling), Human, Recombinant (His), Biotinylated is expressed in HEK293 mammalian cells with C-His tag. The predicted molecular weight is 78.7 kDa and the accession number is Q6PCD4. |
Species | Human |
Expression System | HEK293 Cells |
Tag | C-His |
Accession Number | Q6PCD4 |
Synonyms | TLR3,IIAE2,CD283 |
Construction | Ser23-Glu703 |
Protein Purity | > 95% as determined by Tris-Bis PAGE; > 95% as determined by HPLC |
Molecular Weight | 78.7 kDa (predicted). Due to glycosylation, the protein migrates to 100-120 kDa based on Tris-Bis PAGE result. |
Endotoxin | < 1 EU/μg by the LAL method. |
Formulation | Supplied as 0.22 μm filtered solution in PBS (pH 7.4). |
Stability & Storage | It is recommended to store the product under sterile conditions at -70°C or lower. Samples are stable for up to 12 months at -80°C. Please avoid multiple freeze-thaw cycles and store products in aliquots. |
Shipping | Shipping with blue ice. |
Research Background | TLR3 is expressed in the central nervous system (CNS), where it is required to control HSV-1, which spreads from the epithelium to the CNS via cranial nerves. TLR3 is also expressed in epithelial and dendritic cells, which apparently use TLR3-independent pathways to prevent further dissemination of HSV-1 and to provide resistance to other pathogens in TLR3-deficient patients. Human TLR3 appears to be redundant in host defense to most microbes but is vital for natural immunity to HSV-1 in the CNS, which suggests that neurotropic viruses have contributed to the evolutionary maintenance of TLR3. |
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