Name :
Recombinant Human RANKL/TNFSF11 Protein (ECD, hFc Tag)
Biological Activity :
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. Cancer Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy
Biological Activity :
1. Immobilized Recombinant Human Osteoprotegerin / TNFRSF11B Protein (His Tag) (Cat: 10271-H08H) at 2 μg/ml (100 μl/well) can bind Recombinant Human RANKL / OPGL / TNFSF11 / CD254 Protein (ECD, Fc Tag) (Cat:11682-H01H), the EC50 is 22-68 ng/mL.2. The bioactivity of hRANKL was determined by measuring the ability of hRANKL to induce TRAP activity in Raw 264.7 cells. The ED50 for this effect is typically 7-35 ng/mL.
Expression Host :
Human
Source :
HEK293 Cells
Tag :
Protein Accession No. :
AAC51762.1
NCBI Gene ID :
Synonyms :
Synonyms :
tumor necrosis factor (ligand) superfamily, member 11
Amino Acid Sequence :
Molecular Weight :
The recombinant human TNFSF11/Fc chimera is a disulfide-linked homodimeric protein. The reduced monomer consists of 443 amino acids and has a calculated molecular mass of 48.9 kDa. In SDS-PAGE under reducing conditions, the apparent molecular mass of rh TNFSF11/Fc monomer is approximately 52 kDa due to the glycosylation.
Purity :
≥ 90 % as determined by SDS-PAGE.
State of Matter :
Product Concentration :
Storage and Stability :
Samples are stable for up to twelve months from date of receipt at -20℃ to -80℃. Store it under sterile conditions at -20℃ to -80℃. It is recommended that the protein be aliquoted for optimal storage. Avoid repeated freeze-thaw cycles.
Endotoxin Level :
< 1.0 EU per μg of the protein as determined by the LAL method
Protein Construction :
A DNA sequence encoding the human TNFSF11 (AAC51762.1) (Gly64-Asp245) was fused with the Fc region of human IgG1 at the N-terminus.
Buffer Solution :
Lyophilized from sterile PBS, pH 7.4.Please contact us for any concerns or special requirements. Normally 5 % – 8 % trehalose, mannitol and 0.01% Tween80 are added as protectants before lyophilization. Please refer to the specific buffer information in the hardcopy of datasheet.
Shipping :
In general, recombinant proteins are provided as lyophilized powder which are shipped at ambient temperature.Bulk packages of recombinant proteins are provided as frozen liquid. They are shipped out with blue ice unless customers require otherwise.
Redissolution :
A hardcopy of datasheet with reconstitution instructions is sent along with the products. Please refer to it for detailed information.
Synonyms :
CD254 Protein, Human; hRANKL2 Protein, Human; ODF Protein, Human; OPGL Protein, Human; OPTB2 Protein, Human; RANKL Protein, Human; sOdf Protein, Human; TNFSF11 Protein, Human; TRANCE Protein, Human RANKL/TNFSF11 背景信息 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. Cancer Immunotherapy Immune Checkpoint Immunotherapy Targeted Therapy
References & Citations :
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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