目录产品 » PD-L1/B7-H1 hFc Chimera, Mouse

PD-L1/B7-H1 hFc Chimera, Mouse

B7-H1, also known as PD-L1 and CD274, is an approximately 65 kDa transmembrane glycoprotein in the B7 family of immune regulatory molecules. PD-L1 has been identified as the ligand for the immunoinhibitory receptor programmed death-1(PD1/PDCD1) and has been demonstrated to play a role in the regulation of immune responses and peripheral tolerance.
Z06301
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Species Mouse
Protein Construction
PD-L1/B7-H1 (Phe19-Arg237)_x000D_
Accession # NP_068693
hFc
N-term C-term
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 Human PD­1, His Tag captured on CM5 Chip via anti­his antibody can bind PD-L1/B7-H1 hFc Chimera, Mouse in SPR assay (Biacore T200). Test result was comparable to standard batch.
Expression System HEK293
Theoretical Molecular Weight 51.5 kDa
Apparent Molecular Weight Due to glycosylation, the protein migrates to 70-80 kDa based on Bis-Tris PAGE result.
Formulation Lyophilized from 0.22μm 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.

Target Background B7-H1, also known as PD-L1 and CD274, is an approximately 65 kDa transmembrane glycoprotein in the B7 family of immune regulatory molecules. PD-L1 has been identified as the ligand for the immunoinhibitory receptor programmed death-1(PD1/PDCD1) and has been demonstrated to play a role in the regulation of immune responses and peripheral tolerance.
Synonyms CD274; PDL1; PD-L1; PD-L1B7 homolog 1;B7-H; B7H1; B7-H1; PDCD1L1; PDCD1LG1

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


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