Description
Key facts
Purity:undefined HPLC,
Endotoxin level:<0.005 EU/µg,
Expression system:HEK 293 cells,
Tags:Tag free,
Applications:FuncS, SDS-PAGE, Mass SpecSee reactivity dataSee the reactivity data table below for information on validated species and application combinations.,
Biologically active:Yes,
Biological activity:Fully biologically active determined by dose-dependent inhibition of RANKL-mediated NF-kb activation in mouse RAW264.7 NF-kb luciferase reporter cell line.ED50 is ≤ 56.66, corresponding to a specific activity of 1.8 X 104 units/mg.,
Accession:O00300,
Animal free:Yes,
Carrier free:No,
Species:Human,
Reconstitution:Reconstitute in PBS,
Storage buffer:pH: 7.4Constituents: 10.26% Trehalose, 0.727% Dibasic monohydrogen potassium phosphate, 0.248% Potassium phosphate monobasic
Properties and Storage Information:
Shipped at conditions-Ambient - Can Ship with Ice, Appropriate short-term storage conditions-Ambient, Appropriate long-term storage conditions-Ambient
Supplementary Information:
This supplementary information is collated from multiple sources and compiled automatically.
Osteoprotegerin (OPG) also known as osteoclastogenesis inhibitory factor is a glycoprotein with a mass of approximately 60 kDa. It acts as a soluble decoy receptor for receptor activator of nuclear factor kappa-Β ligand (RANKL) and is encoded by the TNFRSF11B gene. OPG is mainly expressed in osteoblasts fibroblasts and endothelial cells. Its expression can be found in diverse tissues throughout the body including the liver and lungs.
Biological function summary
OPG inhibits the differentiation and activation of osteoclasts by binding to RANKL preventing its interaction with the receptor RANK on the surface of osteoclast progenitor cells. As part of a non-classical signaling pathway OPG plays a significant role in the regulation of bone remodeling and maintenance by controlling bone resorption. This activity preserves bone density and structure by limiting excessive osteoclastic activity.
Pathways
OPG operates within the RANK/RANKL/OPG signaling axis which is important for bone metabolism. It counteracts the bone-resorption pathway driven by the RANKL-RANK interaction inhibiting osteoclastogenesis. This axis involves interactions with other proteins such as RANK RANKL and TRAIL where TRAIL’s involvement hints towards a broader immune regulation role for OPG.
OPG has a significant association with conditions such as osteoporosis and vascular calcification. In osteoporosis an imbalance in the RANKL/OPG ratio can lead to excessive bone loss due to increased osteoclast activity. In vascular calcification OPG appears to play a protective role likely linked with regulatory mechanisms involving RANKL and TRAIL. Understanding these interactions opens potential therapeutic avenues particularly in managing bone-related and cardiovascular conditions.
