Recombinant Mouse TNFRSF11A/Rank Protein, Active
Beta LifeScience
SKU/CAT #: BLK-00928P-100UG

Mouse TNFRSF11A on Tris-Bis PAGE under reduced condition. The purity is greater than 95%.
Recombinant Mouse TNFRSF11A/Rank Protein, Active
Beta LifeScience
SKU/CAT #: BLK-00928P-100UG
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 TNFRSF11A/Rank Protein is expressed from HEK293 with hFc tag at the C-Terminus.It contains Val31-Ser214. |
Purity | > 95% as determined by Tris-Bis PAGE;> 95% as determined by HPLC |
Accession | O35305 |
Target Symbol | TNFRSF11A/Rank |
Species | Mouse |
Expression System | HEK293 |
Tag | C-hFc |
Expression Range | Val31-Ser214 |
Mol. Weight | The protein has a predicted MW of 47.0 kDa. Due to glycosylation, the protein migrates to 57-67 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. |
Activity | Immobilized Mouse RANKL, His Tag at 0.5ug/ml (100ul/well) on the plate. Dose response curve for Mouse TNFRSF11A, hFc Tag with the EC50 of 8.5ng/ml determined by ELISA. Contact us for detailed testing images. |
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 | TNFRSF11A, also known as receptor activator of NF-κB (RANK), activates several signaling pathways, such as NF-κB, JNK, ERK, p38α, and Akt/PKB. RANK/TNFRSF11A is a novel and frequent target for de novo methylation in gliomas, which affects apoptotic activity and focus formation thereby contributing to the molecular pathogenesis of gliomas. |