This protein carries a mouse IgG2a Fc tag at the C-terminus.
The protein has a calculated MW of 80.4 kDa. The protein migrates as 110-130 kDa under reducing (R) condition (SDS-PAGE) due to glycosylation.
Less than 0.1 EU per μg by the LAL method.
>90% as determined by reduced SDS-PAGE.
Lyophilized from 0.22 μm filtered solution in Tris with Glycine, Arginine and NaCl, pH7.5. Normally trehalose is added as protectant before lyophilization.
Contact us for customized product form or formulation.
Please see Certificate of Analysis for specific instructions.
For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.
For long term storage, the product should be stored at lyophilized state at -20°C or lower.
Please avoid repeated freeze-thaw cycles.
No activity loss was observed after storage at:
4-8°C for 12 months in lyophilized state;
-70°C for 3 months under sterile conditions after reconstitution.
Human CD96, Mouse IgG2a Fc Tag, low endotoxin on SDS-PAGE under reducing (R) condition. The gel was stained overnight with Coomassie Blue. The purity of the protein is greater than 90%.
Immobilized Human CD96, Mouse IgG2a Fc Tag, low endotoxin (Cat. No. TAE-H5252) at 2 μg/mL (100 μL/well) can bind Human CD155, Fc Tag (Cat. No. CD5-H5251) with a linear range of 0.078-1.25 μg/mL (QC tested).
The progression of pancreatic cancer (PC) is significantly associated with tumor immune escape, which may be associated with nature killer (NK) cell dysfunction. CD226, CD96, and TIGIT, which share the ligand CD155, play important roles in the regulation of NK cell function. The present study was conducted to investigate the roles of these molecules in NK cells from PC patients.
TIGIT and CD96 together with the co-stimulatory receptor CD226 form a pathway that is analogous to the CD28/CTLA-4 pathway, in which shared ligands and differential receptor:ligand affinities fine-tune the immune response. Although the roles of TIGIT and CD96 as immune checkpoint receptors in T cell and natural killer cell biology are just beginning to be uncovered, accumulating data support the targeting of these receptors for improving anti-tumor immune responses. A clear understanding of the immune cell populations regulated by TIGIT and CD96 is key to the design of immunotherapies that target these receptors in combination with other existing immune checkpoint blockade therapies.
The dysfunction of CD96 may trigger C syndrome: A syndrome characterized by trigonocephaly, severe mental retardation, hypotonia, variable cardiac defects, redundant skin, and dysmorphic facial features, including upslanted palpebral fissures, epicanthal folds, depressed nasal bridge, and low-set, posteriorly rotated ears.