RANKL (蛋白 | 抗体 | cDNA 克隆 | ELISA 试剂盒)

All RANKL reagents are produced in house and quality controlled, including 8 RANKL Antibody, 1 RANKL ELISA, 51 RANKL Gene, 1 RANKL IP Kit, 6 RANKL Lysate, 6 RANKL Protein, 3 RANKL qPCR. All RANKL reagents are ready to use.

RANKL Protein (6)

RANKL Antibody (8)

RANKL ELISA 试剂盒(即用型)& ELISA 抗体对套装(非即用型)(1)

RANKL cDNA Clone (51)

NM_011613.3

克隆载体 cDNA 产品

In lentiviral vector

NM_057149.1

克隆载体 cDNA 产品

In lentiviral vector

XM_001092669.2

克隆载体 cDNA 产品

In lentiviral vector

RANKL Lysate (6)

RANKL 分子背景

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 参考文献

  • 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.