CD254 (RANK Ligand) Monoclonal Antibody (MIH24), Biotin, eBioscience™

Product Specific Information

Description: The MIH24 monoclonal antibody reacts with human TRANCE (TNF-related activation-induced cytokine receptor) also known as RANKL (receptor activator of NF-kappaB ligand) and OPGL (Osteoprotegerin Ligand). TRANCE is a type II membrane protein with predicted molecular weight of 35 kDa. Its extracellular domain is most closely related to TRAIL, FasL and TNF. TRANCE mRNA is upregulated by TCR stimulation. TRANCE-deficient mouse lacks osteoclasts. In addition, TRANCE has been shown to be involved in the interactions between T-dendritic and T-B cells. It was also found to be critical in osteoclast differentiation. The TRANCE-RANK interaction regulates the expression of the anti-apoptotic molecule Bcl-xL.

Applications Reported: The MIH24 antibody has been reported for use in flow cytometric analysis, and ELISA.

Applications Tested: The MIH24 antibody has been tested by ELISA. It is recommended that the antibody be carefully titrated for optimal performance in the assay of interest.

Filtration: 0.2 µm post-manufacturing filtered.

Target Information

This gene encodes 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. This protein was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. T cell activation was reported to induce expression of this gene and lead to an increase of osteoclastogenesis and bone loss. This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated this protein may have a role in the regulation of cell apoptosis. Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. The deficient mice exhibited defects in early differentiation of T and B lymphocytes, and failed to form lobulo-alveolar mammary structures during pregnancy. Two alternatively spliced transcript variants have been found.