The application notes include recommended starting dilutions; optimal dilutions/concentrations should be determined by the end user.
ELISA: Use at a concentration of 0.25 - 1 µg/ml. Allows the detection of at least 0.2 - 0.4 ng/well of recombinant human sRANKL.
sELISA: Use at a concentration of 0.25 - 1 µg/ml. Allows the detection of at least 0.2 - 0.4 ng/well of recombinant human sRANKL.
WB: Use at a concentration of 0.1 - 0.2 µg/ml. The detection limit for recombinant human sRANKL is 1.5 - 3.0 ng/lane, under either reducing or non-reducing conditions. Predicted molecular weight: 28 kDa.
Not yet tested in other applications.
Optimal dilutions/concentrations should be determined by the end user.
Cytokine that binds to TNFRSF11B/OPG and to TNFRSF11A/RANK. Osteoclast differentiation and activation factor. Augments the ability of dendritic cells to stimulate naive T-cell proliferation. May be an important regulator of interactions between T-cells and dendritic cells and may play a role in the regulation of the T-cell-dependent immune response. May also play an important role in enhanced bone-resorption in humoral hypercalcemia of malignancy.
Highest in the peripheral lymph nodes, weak in spleen, peripheral blood Leukocytes, bone marrow, heart, placenta, skeletal muscle, stomach and thyroid.
Defects in TNFSF11 are the cause of osteopetrosis autosomal recessive type 2 (OPTB2) [MIM:259710]; also known as osteoclast-poor osteopetrosis. Osteopetrosis is a rare genetic disease characterized by abnormally dense bone, due to defective resorption of immature bone. The disorder occurs in two forms: a severe autosomal recessive form occurring in utero, infancy, or childhood, and a benign autosomal dominant form occurring in adolescence or adulthood. Autosomal recessive osteopetrosis is usually associated with normal or elevated amount of non-functional osteoclasts. OPTB2 is characterized by paucity of osteoclasts, suggesting a molecular defect in osteoclast development.
Belongs to the tumor necrosis factor family.
The soluble form of isoform 1 derives from the membrane form by proteolytic processing (By similarity). The cleavage may be catalyzed by ADAM17.