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Invivo Anti-Mouse RANKL (CD254) Recombinant mAb

Invivo Anti-Mouse RANKL (CD254) Recombinant mAb

Catalog Number: S0B7218 Application: in vivo blocking Reactivity: Ms Conjugation: Unconjugated Brand: Starter
Price:
Regular price $175 USD
Regular price Sale price $175 USD
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Product Details

Product Specification


Host Rat
Antigen RANKL (CD254)
Location Cell membrane
Accession O35235
Clone Number S-5539
Antibody Type Rat mAb
Isotype Rat IgG2a, κ
Isotype Control S0B0932
Application in vivo blocking
Reactivity Ms
Purification Protein G
Concentration 5 mg/ml
Purity >95% (Determined by SDS-PAGE)
Endotoxin <1EU/mg
Conjugation Unconjugated
Physical Appearance Liquid
Storage Buffer

PBS pH7.4, containing no preservative

Stability & Storage

2 to 8 °C for 2 weeks under sterile conditions;
-20 °C for 3 months under sterile conditions;
-80 °C for 24 months under sterile conditions.
Please avoid repeated freeze-thaw cycles.

Background

RANKL (receptor activator of nuclear factor-κB ligand), also known as TNFSF11, OPG ligand, or TRANCE, is a type II transmembrane protein of the tumor necrosis factor (TNF) superfamily whose extracellular domain can be cleaved by proteases to form a soluble form, functioning biologically as a trimer. RANKL is mainly expressed on osteoblasts, bone marrow stromal cells, activated T cells, and synovial fibroblasts. Its core function is to bind the receptor RANK on the surface of osteoclast precursors and mature osteoclasts, recruiting adaptor proteins such as TRAF6 and activating signaling pathways including NF-κB, MAPK, and NFATc1, thereby driving osteoclast differentiation, maturation, and bone-resorbing activity. This action is naturally regulated by the soluble decoy receptor osteoprotegerin (OPG), which blocks RANK signaling by competitively binding RANKL; therefore, the RANKL/OPG ratio is regarded as a key indicator of bone resorption activity. Beyond bone metabolism, RANKL also participates in immune system regulation, influencing B cell development, dendritic cell function, and T cell differentiation, and in the tumor microenvironment it promotes immune tolerance by suppressing antigen-presenting cell function, thereby supporting tumor progression. Given its dual role in bone destruction and immune suppression, RANKL has become an important therapeutic target.