Biotinylated Human TNFSF11 / RANKL / CD254 Protein, His,Avitag™, active trimer (MALS verified)

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RAL-H82Q5-25ug
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RAL-H82Q5
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Synonyms

RANKL, CD254, TRANCE, OPGL, ODF

Source

Biotinylated Human TNFSF11 Protein, His,Avitag (RAL-H82Q5) is expressed from human 293 cells (HEK293). It contains AA Gly 64 - Asp 245 (Accession # AAC51762.1) trimer Design.

Predicted N-terminus: His

Molecular Characterization

This protein carries a polyhistidine tag at the N-terminus, followed by an Avi tag (Avitag™).

The protein has a calculated MW of 24.1 kDa. The protein migrates as 30-35 kDa when calibrated against Star Ribbon Pre-stained Protein Marker under reducing (R) condition (SDS-PAGE) due to glycosylation.

Labeling

Biotinylation of this product is performed using Avitag™ technology. Briefly, the single lysine residue in the Avitag is enzymatically labeled with biotin.

Protein Ratio

Passed as determined by the SABA assay / HABA assay / binding ELISA.

Purity

>90% as determined by SDS-PAGE.

Formulation

Lyophilized from 0.22 μm filtered solution in PBS, pH7.4 with trehalose as protectant.

Contact us for customized product form or formulation.

Reconstitution

Please see Certificate of Analysis for specific instructions.

For best performance, we strongly recommend you to follow the reconstitution protocol provided in the CoA.

Shipping and Storage

This product is shipped at ambient temperature.

For long term storage, the product should be stored at lyophilized state at -20°C or lower.

Please avoid repeated freeze-thaw cycles.

This product is stable after storage at:
  • -20°C to -70°C for 12 months in lyophilized state;
  • -70°C for 3 months under sterile conditions after reconstitution.

Background

Receptor activator of nuclear factor kappa-B ligand (RANKL), also known as tumor necrosis factor ligand superfamily member 11 (TNFSF11), TNF-related activation-induced cytokine (TRANCE), osteoprotegerin ligand (OPGL), and osteoclast differentiation factor (ODF), is known as a type II membrane protein and is a member of the tumor necrosis factor (TNF) superfamily. RANKL, through its ability to stimulate osteoclast formation and activity, is a critical mediator of bone resorption and overall bone density. Some findings also suggestion some cancer cells, particularly prostate cancer cells, can activate an increase in bone remodeling and ultimately increase overall bone production.[17] This increase in bone remodeling and bone production increases the overall growth of bone metastasizes. The overall control of bone remodeling is regulated by the binding of RANKL with its receptor or its decoy receptor, respectively, RANK and OPG.