Recombinant Mouse TNFSF11/RANKL/CD254 Protein
Sizes: 10ug, 20g, 50ug, 100ug
Catalogue Numbers: RP02134-10, RP02134-20, RP02134-50, RP02134-100
Citations, Manuals and MSDS Available upon request.
Description: Recombinant Mouse TNFSF11/RANKL/CD254 Protein is produced by HEK293 cells expression system. The target protein is expressed with sequence (Arg72-Asp316) of mouse TNFSF11/RANKL/CD254 (Accession #AAC40113.1) fused with a His and hFc tag at the N-terminus.
Alternate Names: ODF, OPGL, RANKL, Ly109l, Trance, TNFSF11
SWISS: O35235-1
GeneID: 21943
Species: Mouse
Purity: ≥ 95 % as determined by SDS-PAGE; ≥ 95 % as determined by HPLC.
Storage: Store at -20 ℃. Store the lyophilized protein at -20℃ to -80 ℃ up to 1 year from the date of receipt. After reconstitution, the protein solution is stable at -20℃ for 3 months, at 2-8℃ for up to 1 week.
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.
Bio-Activity: M-CSF (50 ng/mL) and RANKL (100 ng/mL) can induced differentiation of osteoclasts from primary mouse bone marrow cells for 3 days; RANKL (100 ng/mL) can induced differentiation of osteoclasts from RAW264.7 cells for 5 days.
Source: HEK293 cells
Tag: N-His＆N-hFC
Formulation: Lyophilized from a 0.22 μm filtered solution of PBS, pH 7.4.
Antigen Sequence: RAQMDPNRISEDSTHCFYRILRLHENADLQDSTLESEDTLPDSCRRMKQAFQGAVQKELQHIVGPQRFSGAPAMMEGSWLDVAQRGKPEAQPFAHLTINAASIPSGSHKVTLSSWYHDRGWAKISNMTLSNGKLRVNQDGFYYLYANICFRHHETSGSVPTDYLQLMVYVVKTSIKIPSSHNLMKGGSTKNWSGNSEFHFYSINVGGFFKLRAGEEISIQVSNPSLLDPDQDATYFGAFKVQDID
Endotoxin: < 0.01 EU/μg of the protein by LAL method
Research Use Only