TNFRSF11B Specific Neutra™ Antibody Products

TNFRSF11B, commonly referred to as Osteoprotegerin (OPG), is a soluble secreted glycoprotein and a member of the TNF receptor superfamily. Structurally, TNFRSF11B consists of four cysteine-rich domains and functions as a homodimer. It is primarily expressed in bone marrow stromal cells, epithelial cells of the gastrointestinal tract, lung, breast, and skin vascular endothelial cells, in addition to B-cells and dendritic cells of the immune system. TNFRSF11B plays a crucial role in bone remodeling by inhibiting osteoclast differentiation and bone resorption, thus maintaining bone homeostasis. Additionally, TNFRSF11B has been implicated in immune system development and signaling, tumor growth, and metastasis.

Its Gene ID: 4982, UniProtKB ID: O00300, and OMIM ID: 602643.

Ligands and Signaling Pathways of TNFRSF11B

TNFRSF11B primarily interacts with two ligands: the receptor activator of nuclear factor kappa-Β ligand (RANKL) and TNF-related apoptosis-inducing ligand (TRAIL). The binding of TNFRSF11B to RANKL prevents RANKL from interacting with its receptor RANK, thereby inhibiting osteoclast differentiation and activation. This interaction is crucial for regulating bone remodeling and maintaining bone density. Additionally, TNFRSF11B can also modulate TRAIL-induced apoptosis by acting as a decoy receptor for TRAIL, thus influencing cell survival and death pathways in various tissues. The specific signaling pathways involved in TNFRSF11B function include the NF-κB pathway, which is central to osteoclast differentiation and activation, as well as the TRAIL-mediated apoptotic signaling pathways, impacting cell survival and death mechanisms. These interactions highlight the diverse roles of TNFRSF11B in bone metabolism, immune regulation, and cancer biology.

Fig.1 Role of RANKL/RANK/OPG(TNFRSF11B) axis on bone homeostasis and immune system.¹

Pathogenic Roles of TNFRSF11B

TNFRSF11B has been implicated in various pathogenic roles in bone, vascular, and tumor diseases. In bone diseases, dysregulation of TNFRSF11B can lead to increased bone resorption, contributing to osteoporosis and bone metastasis in cancer. In vascular diseases, TNFRSF11B has been associated with vascular calcification and atherosclerosis, promoting cardiovascular complications. Moreover, in tumor diseases, TNFRSF11B can influence tumor growth, invasion, and metastasis by modulating the balance between bone remodeling and tumor progression. These pathogenic roles make it a potential target for therapeutic interventions.

Antibodies Targeting TNFRSF11B

Antibodies targeting TNFRSF11B have shown promise in neutralizing its role as a decoy receptor for RANKL, thereby inhibiting osteoclast activation and bone resorption. TNFRSF11B-targeted neutralizing antibodies may have applications in treating osteoporosis, bone metastasis, and other bone-related disorders by modulating bone remodeling processes. Research has revealed the potential of TNFRSF11B blockade in preventing skeletal-related events in cancer patients and improving bone density in postmenopausal women. One human antibody targeting TNFRSF11B has been demonstrated to attenuate pulmonary vascular remodeling associated with pulmonary arterial hypertension. Therefore, due to the multiple pathogenic effects of TNFRSF11B, anti-TNFRSF11 B antibody products have good market prospects.

Creative Biolabs offers high specificity and sensitivity anti-TNFRSF11B antibody products to assist your research projects.

REFERENCE

1. Ming, Jie, Shane JF Cronin, and Josef M. Penninger. "Targeting the RANKL/RANK/OPG axis for cancer therapy." Frontiers in Oncology 10 (2020): 1283. Distributed under Open Access license CC BY 4.0, without modification.