TLR3[Biotin], His & Avi, Human

TLR3[Biotin], His & Avi, Human

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.
Z04624
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Product Introduction
Species Human
Protein Construction
TLR3 (Ser23-Glu703)
Accession # Q6PCD4		 His Avi
N-term C-term
Conjugate Biotin
Purity > 95% as determined by Bis­Tris PAGE 
> 95% as determined by HPLC
Endotoxin Level Less than 1EU per μg by the LAL method.
Biological Activity Measured by its binding ability in a functional ELISA. Immobilized TLR3[Biotin], His & Avi, Human at 0.5μg/ml (100μl/Well) on streptavidin (5μg/ml) precoated plate can bind Anti­TLR3 Antibody, hFc Tag. Test result was comparable to standard batch.
Expression System HEK293
Theoretical Molecular Weight 80.25 kDa
Apparent Molecular Weight Due to glycosylation, the protein migrates to 100-120 kDa based on Bis-Tris PAGE result.
Formulation Lyophilized from 0.22 μm filtered solution in PBS (pH 7.4).
Reconstitution Centrifuge the tube before opening. Reconstituting to a concentration more than 100 μg/ml is recommended. Dissolve the lyophilized protein in distilled water.
Storage & Stability Upon receiving, the product remains stable up to 6 months at -20 °C or below. Upon reconstitution, the product should be stable for 3 months at -80 °C. Avoid repeated freeze-thaw cycles.

Background
Target 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.
Synonyms TLR3; CD283; IIAE2

For research use only. Not intended for human or animal clinical trials, therapeutic or diagnostic use.