Recombinant Mouse Tumor necrosis factor ligand superfamily member 11 (Tnfsf11), partial

Code CSB-YP023986MO
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Source Yeast
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Code CSB-EP023986MO-B
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Source E.coli
Conjugate Avi-tag Biotinylated
E. coli biotin ligase (BirA) is highly specific in covalently attaching biotin to the 15 amino acid AviTag peptide. This recombinant protein was biotinylated in vivo by AviTag-BirA technology, which method is BriA catalyzes amide linkage between the biotin and the specific lysine of the AviTag.
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Code CSB-BP023986MO
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Source Baculovirus
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Code CSB-MP023986MO
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Source Mammalian cell
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Product Details

>85% (SDS-PAGE)
Target Names
Uniprot No.
Alternative Names
Tnfsf11; Opgl; Rankl; Trance; Tumor necrosis factor ligand superfamily member 11; Osteoclast differentiation factor; ODF; Osteoprotegerin ligand; OPGL; Receptor activator of nuclear factor kappa-B ligand; RANKL; TNF-related activation-induced cytokine; TRANCE; CD antigen CD254) [Cleaved into: Tumor necrosis factor ligand superfamily member 11; membrane form; Tumor necrosis factor ligand superfamily member 11; soluble form]
Mus musculus (Mouse)
Protein Length
Tag Info
Tag type will be determined during the manufacturing process.
The tag type will be determined during production process. If you have specified tag type, please tell us and we will develop the specified tag preferentially.
Lyophilized powder
Note: We will preferentially ship the format that we have in stock, however, if you have any special requirement for the format, please remark your requirement when placing the order, we will prepare according to your demand.
Buffer before Lyophilization
Tris/PBS-based buffer, 6% Trehalose, pH 8.0
We recommend that this vial be briefly centrifuged prior to opening to bring the contents to the bottom. Please reconstitute protein in deionized sterile water to a concentration of 0.1-1.0 mg/mL.We recommend to add 5-50% of glycerol (final concentration) and aliquot for long-term storage at -20℃/-80℃. Our default final concentration of glycerol is 50%. Customers could use it as reference.
Troubleshooting and FAQs
Storage Condition
Store at -20°C/-80°C upon receipt, aliquoting is necessary for mutiple use. Avoid repeated freeze-thaw cycles.
Shelf Life
The shelf life is related to many factors, storage state, buffer ingredients, storage temperature and the stability of the protein itself.
Generally, the shelf life of liquid form is 6 months at -20°C/-80°C. The shelf life of lyophilized form is 12 months at -20°C/-80°C.
Lead Time
Delivery time may differ from different purchasing way or location, please kindly consult your local distributors for specific delivery time.
Note: All of our proteins are default shipped with normal blue ice packs, if you request to ship with dry ice, please communicate with us in advance and extra fees will be charged.
Repeated freezing and thawing is not recommended. Store working aliquots at 4°C for up to one week.
Please contact us to get it.

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Target Background

Cytokine that binds to TNFRSF11B/OPG and to TNFRSF11A/RANK. Osteoclast differentiation and activation factor. Augments the ability of dendritic cells to stimulate naive T-cell proliferation. May be an important regulator of interactions between T-cells and dendritic cells and may play a role in the regulation of the T-cell-dependent immune response. May also play an important role in enhanced bone-resorption in humoral hypercalcemia of malignancy. Induces osteoclastogenesis by activating multiple signaling pathways in osteoclast precursor cells, chief among which is induction of long lasting oscillations in the intracellular concentration of Ca (2+) resulting in the activation of NFATC1, which translocates to the nucleus and induces osteoclast-specific gene transcription to allow differentiation of osteoclasts. During osteoclast differentiation, in a TMEM64 and ATP2A2-dependent manner induces activation of CREB1 and mitochondrial ROS generation necessary for proper osteoclast generation.
Gene References into Functions
  1. The results demonstrate that the membrane-bound form of RANKL is sufficient for most functions of this protein but that the soluble form does contribute to physiological bone remodeling in adult mice. PMID: 30046091
  2. the molecular level, we confirmed, for the first time, that RES upregulated FoxO1 transcriptional activity by inhibiting the PI3K/AKT signaling pathway, and hence promoted resistance to oxidative damage and restrained osteoclastogenesis. Inhibition of the PI3K/AKT signaling pathway may be induced by RANKL. PMID: 29115382
  3. Deletion of the RANKL D5 enhancer delays the progression of atherosclerotic plaque development and plaque calcification in hypercholesterolemic mice. PMID: 28419519
  4. these results suggest that A2BAR stimulation inhibits the activation of ERK1/2, p38 and NF-kappaB by RANKL, which suppresses the induction of osteoclast marker genes, thus contributing to the decrease in osteoclast cell-cell fusion and bone resorption activity. PMID: 29047264
  5. compressive force induced the differentiation of RAW264.7 from increase in RANK and decrease in LGR4 expression. PMID: 29572179
  6. miR-145 expression was inhibited in RANKL-induced osteoclastogenesis PMID: 29577879
  7. LPS increased mRNA and protein expressions of IL-6 and RANKL on day 14 PMID: 28637991
  8. hBD-1 potentiates the induction of in vitro osteoclastogenesis by RANKL via enhanced phosphorylation of the p44/42 MAPKs PMID: 28709835
  9. In conclusion, the results suggest that linarin has anti-osteoclastic effects and may serve as potential modulatory agents for the prevention and treatment of bone loss-associated diseases. PMID: 29269297
  10. Rankl(-/-) bone marrow-mesenchymal stromal cell displayed reduced clonogenicity and osteogenic capacity. PMID: 28100034
  11. In this study, the authors identified by gene expression profiling that microgravity induces high levels of TRAIL expression in murine preosteoclast cells in the absence of RANKL stimulation compared to ground based cultures. PMID: 27142480
  12. These results suggest that LOX has the ability to induce RANKL expression on stromal cells; however, it fails to substitute for RANKL in osteoclastogenesis. PMID: 27606829
  13. Results demonstrated picroside II strongly inhibited RANKL-induced osteoclast formation when added during the early stage of BMMs cultures, suggesting that it acts on osteoclast precursors to inhibit RANKL/RANK signaling. PMID: 28464271
  14. loss of BMP signaling specifically in osteocytes dramatically increases bone mass presumably through simultaneous inhibition of RANKL and SOST, leading to osteoclast inhibition and Wnt activation together. PMID: 27402532
  15. The potentiation of RANKL induced CTX release by dexamethasone was significantly less in bone marrow macrophage cells from mice with conditional knockout of the osteoclastic glucocorticoid receptor and completely absent in cells from GR(dim) mice, which carry a point mutation in one dimerizing interface of the GC receptor. PMID: 27596806
  16. findings demonstrate that mTORC1 activation-stimulated RANKL expression in B cells is sufficient to induce bone loss and osteoporosis. The study also established a link between mTORC1 and the RANKL/OPG axis via negative regulation of beta-catenin. PMID: 26825871
  17. dihydroartemisinin inhibited RANKL-induced NF-kappaB and NFAT activity. PMID: 26684711
  18. Cyanidin chloride is capable of inhibiting osteoclast formation, hydroxyapatite resorption and RANKL-induced signal pathways in vitro and ovariectomy-induced bone loss in vivo. PMID: 28771720
  19. Together these data indicate that osteocyte apoptosis plays a central and controlling role in triggering osteocyte RANKL production and the activation of new resorption leading to bone loss in disuse. PMID: 26852281
  20. data suggest that, particularly with combination treatment of zoledronic acid (ZA) and glucocorticoids, surviving lymphocytes might be the source of inflammation-induced sRANKL. Thus, circulating sRANKL levels might be modulated by ZA. PMID: 26999703
  21. matrine abrogated RANKL-induced activation of NF-kappaB, AKT, and MAPK pathways and suppressed osteoclastogenesis-related marker expression, including matrix metalloproteinase 9, NFATc1, TRAP, C-Src, and cathepsin K PMID: 28739641
  22. The anti-osteoclastic and anti-resorptive actions of Luteoloside are mediated via blocking NFATc1 activity and the attenuation of RANKL-mediated Ca(2+) signaling as well as NF-kappaB and MAPK pathways. PMID: 28681916
  23. Osteoprotegerin facilitates pulmonary arterial hypertension pathogenesis by regulating pulmonary arterial smooth muscle cell proliferation via integrin alphavbeta3/FAK/AKT signaling pathway. PMID: 28077433
  24. results demonstrate that IL-15 and RANKL induce osteoclastogenesis synergistically, and IL-15 might play a novel and major role in destructive inflammatory bone diseases PMID: 27608420
  25. Absence of Musashi2 in osteoclast precursors promotes apoptosis and inhibits RANKL-induced NF-kappaB activation, which is essential for osteoclast survival. PMID: 27441652
  26. This study demonstrates that Col6a1-Cre driver mice are as useful as Twist2-Cre driver mice for functional analyses of GALT-resident mesenchymal cells, including MCi cells. PMID: 28882590
  27. Estrogens and androgens inhibit osteoblast-driven osteoclastogenesis through non-genomic mechanism(s) that entail, MMP-mediated RANKL dissociation from the cell membrane. PMID: 28213978
  28. sRANKL increased macrophage glucose uptake at normal glucose concentrations, which was impaired by hyperglycemia pretreatment through the inhibition of Glut1 membrane translocation and the insulin receptor and IRS-1 gene transcription. PMID: 28624040
  29. Our findings show that anti-RANKL antibody administration during pregnancy results in not only an undesirable increase in bone mass, but also has harmful effects on newborn survival. PMID: 28760341
  30. RANKL represses the transcription of the E3 ubiquitin ligase RNF146 through an NF-kappaB-related inhibitory element in the RNF146 promoter. PMID: 28287403
  31. This study showed that RANKL favors osteoclastogenesis via attenuation of Nrf2-mediated antioxidant enzyme expression by competing with Bach1 nuclear accumulation. PMID: 27836987
  32. Membrane-bound RANKL induces M cell differentiation and CCL20 expression in the follicle associated epithelium of gut-associated lymphoid tissues. PMID: 28436956
  33. The data show that S. aureus enhances bone resorption and periosteal osteoclast formation by increasing osteoblast RANKL production through TLR2. PMID: 27311019
  34. Data (including data from studies using knockout mice) suggest that RANKL enhances TNF-induced osteoclast formation from precursor spleen cells and enhances bone resorption independently of Traf6 by degrading Traf3, a known inhibitor of osteoclastogenesis. (RANKL = osteoclast differentiation factor; TNF = tumor necrosis factor; Traf = TNF receptor-associated factor) PMID: 28438834
  35. Results suggest that MAPK signaling pathway is necessary for receptor activator of nuclear factor kappa-B ligand (RANKL) expression in bone marrow stromal cell. PMID: 28161637
  36. endocortical resorption is driven by reduced osteoprotegerin rather than elevated RANKL expression PMID: 27460899
  37. The results showed that AG490 inhibited (p)-JAK2 and RANKL expression. PMID: 28278513
  38. Play a supportive role in the RANKL-dependent differentiation. PMID: 27413168
  39. increased expression of RANKL in heterogeneous bone marrow cells provoked bone destruction during Group A Streptococcus infection. PMID: 26894505
  40. beta-lapachone inhibits RANKL-induced osteoclastogenesis and could be considered a potent inhibitor of RANKL-mediated bone diseases PMID: 27913299
  41. differentiation by suppressing the Ca(2+)-calcineurin-NFATc1 signaling pathway. Although many questions remain unresolved, to our knowledge, this is the first report demonstrating that PEMF is beneficial against RANKL-dependent osteoclastic differentiation in RAW264.7 cells in vitro via inhibiting the Ca(2+)-calcineurin-NFATc1 signaling pathway. PMID: 27856256
  42. these results demonstrate that RANKL expressed by osteocytes is required for the bone loss as well as the increase in B cell number caused by estrogen deficiency. PMID: 27733688
  43. In conclusion, the present study demonstrated that EA can suppress osteoclastogenesis in vitro. Moreover, we clarified that these inhibitory effects of EA occur through suppression of NF-kappaB and ERK activation. Therefore, EA may be a potential agent in the treatment of osteoclast-related diseases such as osteoporosis. PMID: 27349866
  44. MDH1 expression was induced by receptor activator of nuclear factor kappa-B ligand (RANKL) treatment. PMID: 27179783
  45. miR-338-3p may play a significant role in glucocorticoid-induced osteoclast differentiation and function by targeting RANKL in osteoclasts. PMID: 27706599
  46. the protein and RNA levels of RANKLinduced cFos and nuclear factor of activated T-cell cytoplasmic 1 were suppressed by centipedegrass extract (CGE). These results indicated that CGE may serve as a useful drug in the prevention of bone loss. PMID: 27035226
  47. Lipopolysaccharides significantly up-regulated RANKL expression and activated the ERK1/2 pathway to induce IL-6 mRNA expression and protein synthesis in MLO-Y4 cells. PMID: 27778412
  48. this study shows that OPG constitutes an early biomarker with in experimental model od severe malaria PMID: 26766771
  49. Osteoprotegerin plays a role in preserving myocardial structure and function with ageing through a reduction in apoptosis and preservation of the matrix structure PMID: 26825553
  50. These results indicate that activation of Panx1 and P2X7 R are required for apoptotic osteocytes in fatigued bone to trigger RANKL production in neighboring bystander osteocytes and implicate ATP as an essential signal mediating this process. PMID: 26553756

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Involvement in disease
Deficiency in Tnfsf11 results in failure to form lobulo-alveolar mammary structures during pregnancy, resulting in death of newborns. Trance-deficient mice show severe osteopetrosis, with no osteoclasts, marrow spaces, or tooth eruption, and exhibit profound growth retardation at several skeletal sites, including the limbs, skull, and vertebrae and have marked chondrodysplasia, with thick, irregular growth plates and a relative increase in hypertrophic chondrocytes.
Subcellular Location
[Isoform 1]: Cell membrane; Single-pass type II membrane protein.; [Isoform 2]: Cell membrane; Single-pass type II membrane protein.; [Isoform 3]: Cytoplasm.; [Tumor necrosis factor ligand superfamily member 11, soluble form]: Secreted.
Protein Families
Tumor necrosis factor family
Tissue Specificity
Highly expressed in thymus and lymph nodes, but not in non-lymphoid tissues and is abundantly expressed in T-cells but not in B-cells. A high level expression is also seen in the trabecular bone and lung.
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