RANKL Proteins, Antibodies, cDNA Clones, ELISA Kits Research Reagents

TNFSF11 (TNF Superfamily Member 11) is a protein coding gene located on human chromosome 13q14.11. TNFSF11 is also known as ODF, OPGL, sOdf, CD254, OPTB2, RANKL, TNLG6B, TRANCE and hRANKL2. The human TNFSF11 gene encodes a 35478 Da protein containing 317 amino acids. The TNFSF11 protein is biasedly expressed in lymph node, appendix and other tissues. Among its related pathways are Development_Hedgehog and PTH signaling pathways in bone and cartilage development and PEDF Induced Signaling. TNFSF11 is related to cytokine activity and tumor necrosis factor receptor superfamily binding. TNFSF10 is an important paralog of TNFSF11 gene. TNFSF11 is associated with some diseases, including Osteopetrosis, Autosomal Recessive 2 and Autosomal Recessive Malignant Osteopetrosis.

RANKL Protein (6)

    RANKL Antibody (8)

      RANKL ELISA Kit & Match Antibody ELISA Pair Set (1)

      RANKL cDNA Clone (51)

      NM_011613.3
      NM_057149.1
      XM_001092669.2

      RANKL Lysate (6)

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        RANKL Background

        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 that 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.

        RANKL References

        • Takayanagi H, et al. (2002) Signaling crosstalk between RANKL and interferons in osteoclast differentiation. Arthritis Res. 4 Suppl 3: S227-32.
        • Nakashima T, et al. (2003) RANKL and RANK as novel therapeutic targets for arthritis. Curr Opin Rheumatol. 15(3): 280-7.
        • Schwarz EM, et al. (2007) Clinical development of anti-RANKL therapy. Arthritis Res Ther. 9 Suppl 1: S7.
        • Leibbrandt A, et al. (2008) RANK/RANKL: regulators of immune responses and bone physiology. Ann N Y Acad Sci. 1143: 123-50.

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