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RANKL/OPGL/TNFSF11/CD254  Protein, Antibody, ELISA Kit, cDNA Clone

Expression host: Human Cells  
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11682-H01H-5
11682-H01H-20
11682-H01H-100
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20 µg 
100 µg 
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Description:   
Expression host: Human Cells  
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11682-HNCH-5
11682-HNCH-20
11682-HNCH-100
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20 µg 
100 µg 
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Expression host: Human Cells  
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11682-H15H-5
11682-H15H-20
11682-H15H-100
5 µg 
20 µg 
100 µg 
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Expression host: Human Cells  
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11682-H04H-5
11682-H04H-20
11682-H04H-100
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20 µg 
100 µg 
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Expression host: Human Cells  
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50343-M01H-20
50343-M01H-10
20 µg 
10 µg 
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Expression host: Human Cells  
  • Slide 1
90301-C01H-5
90301-C01H-20
90301-C01H-100
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20 µg 
100 µg 
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RANKL/OPGL/TNFSF11/CD254 Related Area

RANKL/OPGL/TNFSF11/CD254 Related Pathways

RANKL/OPGL/TNFSF11/CD254 Related Protein, Antibody, cDNA Gene, and ELISA Kits

RANKL/OPGL/TNFSF11/CD254 Summary & Protein Information

RANKL/OPGL/TNFSF11/CD254 Background

Gene Summary: This TNFSF11 gene encodes a member of the tumor necrosis factor (TNF) cytokine family which is a ligand for osteoprotegerin and functions as a key factor for osteoclast differentiation and activation. TNFSF11 was shown to be a dentritic cell survival factor and is involved in the regulation of T cell-dependent immune response. T cell activation was reported to induce expression of this TNFSF11 gene and lead to an increase of osteoclastogenesis and bone loss. This protein was shown to activate antiapoptotic kinase AKT/PKB through a signaling complex involving SRC kinase and tumor necrosis factor receptor-associated factor (TRAF) 6, which indicated TNFSF11 may have a role in the regulation of cell apoptosis. Targeted disruption of the related gene in mice led to severe osteopetrosis and a lack of osteoclasts. The deficient mice exhibited defects in early differentiation of T and B lymphocytes, and failed to form lobulo-alveolar mammary structures during pregnancy. Two alternatively spliced transcript variants have been found.
General information above from NCBI
Subunit structure: Homotrimer (Probable). Interacts with TNFRSF11B.
Subcellular location: Isoform 1: Cell membrane; Single-pass type II membrane protein.
Isoform 3: Cell membrane; Single-pass type II membrane protein.
Isoform 2: Cytoplasm (By similarity).
Tumor necrosis factor ligand superfamily member 11, soluble form: Secreted (By similarity).
Tissue specificity: Highest in the peripheral lymph nodes, weak in spleen, peripheral blood Leukocytes, bone marrow, heart, placenta, skeletal muscle, stomach and thyroid.
Induction: Up-regulated by T-cell receptor stimulation.
Post-translational: The soluble form of isoform 1 derives from the membrane form by proteolytic processing (By similarity). The cleavage may be catalyzed by ADAM17.
Involvement in disease: Osteopetrosis, autosomal recessive 2 (OPTB2) [MIM:259710]: A rare genetic disease characterized by abnormally dense bone, due to defective resorption of immature bone. Osteopetrosis occurs in two forms: a severe autosomal recessive form occurring in utero, infancy, or childhood, and a benign autosomal dominant form occurring in adolescence or adulthood. Recessive osteopetrosis commonly manifests in early infancy with macrocephaly, feeding difficulties, evolving blindness and deafness, bone marrow failure, severe anemia, and hepatosplenomegaly. Deafness and blindness are generally thought to represent effects of pressure on nerves. OPTB2 is characterized by paucity of osteoclasts, suggesting a molecular defect in osteoclast development. Note=The disease is caused by mutations affecting the gene represented in this entry.
Sequence similarity: Belongs to the tumor necrosis factor family.C
General information above from UniProt

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/CD254 Alternative Name

ODF,OPGL,sOdf,CD254,OPTB2,RANKL,TRANCE,hRANKL2, [homo-sapiens]
CD254,hRANKL2,ODF,OPGL,OPTB2,RANKL,RP11-86N24.2,sOdf,TNFSF11,TRANCE, [human]
Ly109l,ODF,OPG,OPGL,RANKL,Tnfsf11,Trance, [mouse]
ODF,OPG,OPGL,RANKL,Ly109l,Trance, [mus-musculus]

RANKL/OPGL/TNFSF11/CD254 Related Studies

  • 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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