RANKL / OPGL / TNFSF11 Protein (CD254 Protein)

Receptor Activator of Nuclear Factor Kappa B Ligand / Osteoprotegerin Ligand / Tumor Necrosis Factor (ligand) Superfamily, member 11 (Cluster of Differentiation 254)

RANKL / OPGL / TNFSF11 Products

RANKL / OPGL / TNFSF11 Protein, Recombinant

Molecule	Species	Description //For Detailed Info. and Price------CLICK!	Cat No
RANKL/OPGL/TNFSF11	Human	RANKL/OPGL/TNFSF11/Fc Protein, Recombinant	11682-H01H

RANKL / OPGL / TNFSF11 cDNA Clone

Molecule	Species	Description //For Detailed Info. and Price------CLICK!	Cat No
RANKL/OPGL/TNFSF11	Human	Homo sapiens RANKL/OPGL/TNFSF11 cDNA Clone	HG11682-G

RANKL / OPGL / TNFSF11 Related Areas

Immunology>>Cytokine & Receptor>>TNF Superfamily>>RANKL/OPGL/TNFSF11

Immunology>>Adaptive Immunity>>T Cell>>Regulatory T Cell>>RANKL/OPGL/TNFSF11

Immunology>>Cluster of Differentiation>>T Cell CD Antigen>>Regulatory T Cells>>RANKL/OPGL/TNFSF11/CD254

RANKL / OPGL / TNFSF11 Alternative Names

RANKL, OPGL, TNFSF11, TRANCE, CD254, RP11-86N24.2, ODF, OPTB2, hRANKL2, sOdf [Homo sapiens]

RANKL, OPGL, Tnfsf11, Trance, Ly109l, ODF, OPG [Mus musculus]

RANKL / OPGL / TNFSF11 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 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.

RANKL / OPGL / TNFSF11 Related Studies

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