Human Recombinant TNFRSF11B - Fc Tagged
Reference ID:KB-3958
Migration assay
Gene of Interest
Gene Synonyms:TNFRSF11B;OCIF;OPG
Protein Names:Tumor necrosis factor receptor superfamily member 11B (Osteoclastogenesis inhibitory factor) (Osteoprotegerin)
Accession Data
Organism:Homo sapiens (Human)
Mass (kDa):460.26
Length (aa):401
Proteomics (Proteome ID):UP000005640
Proteomics (Chromosome): Chromosome 8
Function [CC]:Acts as decoy receptor for TNFSF11/RANKL and thereby neutralizes its function in osteoclastogenesis. Inhibits the activation of osteoclasts and promotes osteoclast apoptosis in vitro. Bone homeostasis seems to depend on the local ratio between TNFSF11 and TNFRSF11B. May also play a role in preventing arterial calcification. May act as decoy receptor for TNFSF10/TRAIL and protect against apoptosis. TNFSF10/TRAIL binding blocks the inhibition of osteoclastogenesis. {ECO:0000269|PubMed:22664871, ECO:0000269|PubMed:9168977}.
Site:SITE 400 400 Involved in dimerization.
Induction:Up-regulated by increasing calcium-concentration in the medium and estrogens. Down-regulated by glucocorticoids.
Tissue Specificity:Highly expressed in adult lung, heart, kidney, liver, spleen, thymus, prostate, ovary, small intestine, thyroid, lymph node, trachea, adrenal gland, testis, and bone marrow. Detected at very low levels in brain, placenta and skeletal muscle. Highly expressed in fetal kidney, liver and lung.
Disease:Paget disease of bone 5, juvenile-onset (PDB5) [MIM:239000]: An autosomal recessive, juvenile-onset form of Paget disease, a disorder of bone remodeling characterized by increased bone turnover affecting one or more sites throughout the skeleton, primarily the axial skeleton. Osteoclastic overactivity followed by compensatory osteoblastic activity leads to a structurally disorganized mosaic of bone (woven bone), which is mechanically weaker, larger, less compact, more vascular, and more susceptible to fracture than normal adult lamellar bone. PDB5 clinical manifestations include short stature, progressive long bone deformities, fractures, vertebral collapse, skull enlargement, and hyperostosis with progressive deafness. {ECO:0000269|PubMed:12189164}. Note=The disease is caused by mutations affecting the gene represented in this entry.
Mutagenesis:MUTAGEN 78 79 DE->AA: Decreases inhibition of osteoclast differentiation. {ECO:0000269|PubMed:22664871}.; MUTAGEN 116 116 E->A: Reduces affinity for TNFSF11. Decreases inhibition of osteoclast differentiation. {ECO:0000269|PubMed:22664871}.; MUTAGEN 400 401 Missing: Abolishes dimerization.; MUTAGEN 400 400 C->S: Abolishes dimerization. {ECO:0000269|PubMed:9478964}.
Reagent Data
Region:Glu 22 - Leu 401
Molecular Weight:70.2
Purification System:Chromatography
Formulation:Sterile-filtered colorless solution
Formulation Concentration:1 mg/ml
Buffer Volume:Standard
Buffer Solution:PBS
Endotoxin Level:< 1%
Aggregate Tested By:SDS-PAGE
Endotoxin Screened:< 0.1 ng/ug
Purity:> 98%
Determined: SDS-PAGE
Validated: RP-HPLC
Sample Handling
Stability:This bioreagent is stable at 4°C (short-term) and -70°C(long-term). After reconstitution, sample may be stored at 4°C for 2-7 days and below -18°C for future use.
Preparation:Reconstitute in sterile distilled H2O to no less than 100 ug/ml; dilute reconstituted stock further in other aqueous solutions if needed. Please review COA for lot-specific instructions. Final measurements should be determined by the end-user for optimal performance.