All RANKL reagents are produced in house and quality controlled, including 7 RANKL Antibody, 1 RANKL ELISA, 52 RANKL Gene, 1 RANKL IPKit, 6 RANKL Lysate, 6 RANKL Protein, 3 RANKL qPCR. All RANKL reagents are ready to use.
Recombinant RANKL proteins are expressed by HEK293 Cells with fusion tags as N-mouse IgG1-Fc, N-rabbit IgG-Fc, N-human IgG1-Fc, N-cleavage.
RANKLantibodies are validated with different applications, which are ELISA, Neutralization, ELISA(Cap), WB, ELISA(Det), IP.
RANKLcDNA clones are full length sequence confirmed and expression validated. There are 13 kinds of tags for each RANKL of different species, especially GFP tag, OFP tag, FLAG tag and so on. There are three kinds of vectors for choice, cloning vector, expression vector and lentivrial expression vector.
RANKLELISA Kit are quality controlled by 8 internation QC standard which guarantee every ELISA Kit with high quality.
Tumor necrosis factor ligand superfamily member 11, also known as Receptor activator of nuclear factor kappa-B ligand, Osteoprotegerin ligand, TNFSF11, RANKL, TRANCE, OPGL and CD254, is a single-pass type II membrane protein which belongs to the tumor necrosis factor family. The receptor activator of nuclear factor-kappaB ligand (RANKL), its cognate receptor RANK, and its natural decoy receptor osteoprotegerin have been identified as the final effector molecules of osteoclastic bone resorption. RANK and RANKL are key regulators of bone remodeling and regulate T cell/dendritic cell communications, and lymph node formation. Moreover, RANKL and RANK are expressed in mammary gland epithelial cells and control the development of a lactating mammary gland during pregnancy. Genetically, RANKL and RANK are essential for the development and activation of osteoclasts and bone loss in response to virtually all triggers tested. Inhibition of RANKL function via the natural decoy receptor osteoprotegerin (OPG, TNFRSF11B) prevents bone loss in postmenopausal osteoporosis and cancer metastases. Importantly, RANKL appears to be the pathogenetic principle that causes bone and cartilage destruction in arthritis. RANK-RANKL signaling not only activates a variety of downstream signaling pathways required for osteoclast development, but crosstalk with other signaling pathways also fine-tunes bone homeostasis both in normal physiology and disease. In addition, RANKL and RANK have essential roles in lymph node formation, establishment of the thymic microenvironment, and development of a lactating mammary gland during pregnancy.