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Recombinant Mouse TNFSF11/RANKL protein (rFc Tag)

Species

Mouse

Purity

>90 %, SDS-PAGE

Tag

rFc Tag

Activity

not tested

Cat no : Eg1956

Validation Data Gallery

  • Purity of Recombinant Mouse TNFSF11 was determined by SDS-PAGE. The protein was resolved in an SDS-PAGE in reducing (R) and non-reducing (NR) conditions and stained using Coomassie blue.

    Purity of Recombinant Mouse TNFSF11 was determined by SDS-PAGE. The protein was resolved in an SDS-PAGE in reducing (R) and non-reducing (NR) conditions and stained using Coomassie blue.

Product Information

Purity >90 %, SDS-PAGE
Endotoxin <0.1 EU/μg protein, LAL method
Activity 
Not tested
Expression HEK293-derived Mouse TNFSF11 protein Arg72-Asp316 (Accession# O35235-1) with a rabbit IgG Fc tag at the N-terminus.
GeneID 21943
Accession O35235-1
PredictedSize 54.8 kDa
SDS-PAGE 52-65 kDa, reducing (R) conditions
Formulation Lyophilized from 0.22 μm filtered solution in PBS, pH 7.4. Normally 5% trehalose and 5% mannitol are added as protectants before lyophilization.
Reconstitution Briefly centrifuge the tube before opening. Reconstitute at 0.1-0.5 mg/mL in sterile water.
Storage Conditions
It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
  • Until expiry date, -20℃ to -80℃ as lyophilized proteins.
  • 3 months, -20℃ to -80℃ under sterile conditions after reconstitution.
Shipping The product is shipped at ambient temperature. Upon receipt, store it immediately at the recommended temperature.

Background

TNFSF11 also known as RANKL, is a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. RANKL is produced by a diverse set of lineage-specific cells and is involved in a wide variety of physiological processes that include skeletal remodeling, lymph node organogenesis, mammary gland development, and thermal regulation. RANKL was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. The deficient mice exhibited defects in early differentiation of T and B lymphocytes, and failed to form lobulo-alveolar mammary structures during pregnancy.

References:

1. Giuliani N. et al. (2004) Exp Hematol. 32(8):685-91.
2. Hanada R. et al. (2011) J Mol Med (Berl). 89(7):647-56.
3. Onal M.et al. (2015) J Bone Miner Res. 30(5):855-68.
4. Danks L. et al. (2016) Ann Rheum Dis. 75(6):1187-95.