Recombinant Human sRANKR protein (His tag) is a Human Fragment protein, in the 1 to 212 aa range, expressed in HEK 293, with >95% purity, < 1 EU/µg endotoxin level and suitable for SDS-PAGE.
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Receptor for TNFSF11/RANKL/TRANCE/OPGL; essential for RANKL-mediated osteoclastogenesis (PubMed:9878548). Its interaction with EEIG1 promotes osteoclastogenesis via facilitating the transcription of NFATC1 and activation of PLCG2 (By similarity). Involved in the regulation of interactions between T-cells and dendritic cells (By similarity).
CD265, RANK, TNFRSF11A, Tumor necrosis factor receptor superfamily member 11A, Osteoclast differentiation factor receptor, Receptor activator of NF-KB, ODFR
Recombinant Human sRANKR protein (His tag) is a Human Fragment protein, in the 1 to 212 aa range, expressed in HEK 293, with >95% purity, < 1 EU/µg endotoxin level and suitable for SDS-PAGE.
pH: 7.4
Constituents: 100% PBS
Receptor for TNFSF11/RANKL/TRANCE/OPGL; essential for RANKL-mediated osteoclastogenesis (PubMed:9878548). Its interaction with EEIG1 promotes osteoclastogenesis via facilitating the transcription of NFATC1 and activation of PLCG2 (By similarity). Involved in the regulation of interactions between T-cells and dendritic cells (By similarity).
SRANKR also known as soluble receptor activator of nuclear factor kappa B receptor is a protein involved in important signaling within cells. It is expressed mainly in bone tissue and immune cells. sRANKR consists of approximately 38 kDa mass. It acts by binding the ligands that usually interact with the RANK receptor which is found on the cell surface modulating the effects of these interactions by acting as a decoy receptor.
SRANKR plays a role in regulating bone metabolism and immune function. It serves as a part of a complex with RANKL (RANK Ligand) and OPG (Osteoprotegerin) mediating critical interactions within this system. sRANKR acts by inhibiting the binding of RANKL to RANK thereby influencing the process of bone resorption and immune cell activation. This modulation suggests it has a negative regulatory role in these biological processes.
SRANKR's function integrates tightly within the RANK/RANKL/OPG signaling pathway which is important for the regulation of bone remodeling and immune response. The RANK/RANKL/OPG axis involves intricate interactions with RANKL binding to RANK to promote osteoclast differentiation while sRANKR and OPG inhibit this interaction. These pathways highlight a balance necessary for maintaining bone homeostasis and immune cell functions in normal physiological conditions.
SRANKR is relevant in osteoporosis and rheumatoid arthritis. Its role in intercepting the RANKL and RANK interaction involves the regulation of bone density by preventing excessive osteoclast activity which can lead to bone degradation in osteoporosis. In rheumatoid arthritis sRANKR modulates immune responses and inflammation through its interaction with proteins like RANK and RANKL contributing to the pathological bone erosion observed in this autoimmune condition.
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SDS-PAGE analysis of ab276718
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