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Anti-RANKL Antibody, clone 6A12.1 clone 6A12.1, from mouse

ITEM#: 3042-MABS1696

MFR#: MABS1696

Tumor necrosis factor ligand superfamily member 11 (UniProt: O14788; also known as Osteoclast differentiation factor, ODF, Osteoprotegerin ligand, OPGL, Receptor activator of nuclear factor kappa-B ligand, RANKL, TNF-related activation-induced cytoki

Tumor necrosis factor ligand superfamily member 11 (UniProt: O14788; also known as Osteoclast differentiation factor, ODF, Osteoprotegerin ligand, OPGL, Receptor activator of nuclear factor kappa-B ligand, RANKL, TNF-related activation-induced cytokine, TRANCE, CD254) is encoded by the TNFSF11 (also known as OPGL, RANKL, TRANCE) gene (Gene ID: 8600) in human. RANKL is a single-pass type II membrane protein that is found in high levels in the peripheral lymph nodes and in lower levels in the spleen, peripheral blood Leukocytes, bone marrow, heart, placenta, skeletal muscle, stomach and thyroid. Its levels are shown to be up-regulated by T-cell receptor stimulation. RANKL has a cytoplasmic domain (aa 1-47), a helical domain (aa 48-68) and an extracellular domain (aa 69-317). RANKL has been identified to affect the immune system and control bone regeneration and remodeling. RANKL is a cytokine that binds to TNFRSF11B/OPG and to TNFRSF11A/RANK. It is shown to augment the ability of dendritic cells to stimulate naive T-cell proliferation and is 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. It is shown to induce osteoclastogenesis by activating multiple signaling pathways in osteoclast precursor cells. RANKL is also reported to activate Akt through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which suggests a role of RANKL in the regulation of cell apoptosis. Three isoforms of RANKL have been described that are produced by alternative splicing. Defects in TNFS11 gene can cause osteoporosis, both a severe autosomal recessive form as well a benign autosomal dominant form.