Recombinant Mouse TLR3 Protein
Beta LifeScience
SKU/CAT #: BLK-01272P-100UG

Mouse TLR3 on Tris-Bis PAGE under reduced condition. The purity is greater than 95%.
Recombinant Mouse TLR3 Protein
Beta LifeScience
SKU/CAT #: BLK-01272P-100UG
Collections: All products, High-quality recombinant proteins
Our products are highly customizable to meet your specific needs. You can choose options such as endotoxin removal, liquid or lyophilized forms, preferred tags, and the desired functional sequence range for proteins. Submitting a written inquiry expedites the quoting process.
Product Overview
Description | Recombinant Mouse TLR3 Protein is expressed from HEK293 with His tag at the C-Terminus.It contains Thr25-Leu705. |
Purity | > 95% as determined by Tris-Bis PAGE;> 95% as determined by HPLC |
Accession | Q99MB1 |
Target Symbol | TLR3 |
Synonyms | TLR3; CD283; IIAE2 |
Species | Mouse |
Expression System | HEK293 |
Tag | C-His |
Expression Range | Thr25-Leu705 |
Mol. Weight | The protein has a predicted MW of 78.6 kDa. Due to glycosylation, the protein migrates to 85-110 kDa based on Tris-Bis PAGE result. |
Form | Lyophilized |
Formulation | Lyophilized from 0.22um filtered solution in PBS (pH 7.4). Normally 8% trehalose is added as protectant before lyophilization. |
Endotoxin | Less than 1EU per ug by the LAL method. |
Storage | Reconstituted protein stable at -80°C for 12 months, 4°C for 1 week. Use a manual defrost freezer and avoid repeated freeze-thaw cycles. |
Shipping | Shipped at ambient temperature. |
Gene 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. |