Mouse soluble receptor activator of nuclear factor-kB ligand,sRANKL ELISA Kit

Code CSB-E05127m
Size 96T,5×96T,10×96T
See More Details 24T ELISA kits trial application
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Product Details

Target Name tumor necrosis factor (ligand) superfamily, member 11
Alternative Names Tnfsf11 ELISA Kit; Opgl ELISA Kit; Rankl ELISA Kit; Trance ELISA Kit; Tumor necrosis factor ligand superfamily member 11 ELISA Kit; Osteoclast differentiation factor ELISA Kit; ODF ELISA Kit; Osteoprotegerin ligand ELISA Kit; OPGL ELISA Kit; Receptor activator of nuclear factor kappa-B ligand ELISA Kit; RANKL ELISA Kit; TNF-related activation-induced cytokine ELISA Kit; TRANCE ELISA Kit; CD antigen CD254) [Cleaved into: Tumor necrosis factor ligand superfamily member 11 ELISA Kit; membrane form; Tumor necrosis factor ligand superfamily member 11 ELISA Kit; soluble form] ELISA Kit
Abbreviation TNFSF11
Uniprot No. O35235
Species Mus musculus (Mouse)
Sample Types serum, plasma, cell culture supernates, tissue homogenates
Detection Range 15.6 pg/mL-1000 pg/mL
Sensitivity 3.9 pg/mL
Assay Time 1-5h
Sample Volume 50-100ul
Detection Wavelength 450 nm
Research Area Cardiovascular
Assay Principle quantitative
Measurement Sandwich
Intra-assay Precision (Precision within an assay): CV%<8%
Three samples of known concentration were tested twenty times on one plate to assess.
Inter-assay Precision (Precision between assays): CV%<10%
Three samples of known concentration were tested in twenty assays to assess.
To assess the linearity of the assay, samples were spiked with high concentrations of mouse sRANKL in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
1:100Average %90
Range %86-93
1:200Average %103
Range %99-105
1:400Average %94
Range %88-97
1:800Average %97
Range %92-100
The recovery of mouse sRANKL spiked to levels throughout the range of the assay in various matrices was evaluated. Samples were diluted prior to assay as directed in the Sample Preparation section.
Sample TypeAverage % RecoveryRange
Serum (n=5) 9589-97
EDTA plasma (n=4)9591-98
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
10002.284 2.262 2.273 2.120
5001.665 1.646 1.656 1.503
2501.137 1.122 1.130 0.977
1250.712 0.700 0.706 0.553
62.50.417 0.422 0.420 0.267
31.20.295 0.282 0.289 0.136
15.60.212 0.222 0.217 0.064
00.156 0.150 0.153  
and FAQs
Storage Store at 2-8°C. Please refer to protocol.
Lead Time 3-5 working days

Target Data

Function 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 (By similarity). 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
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
  51. These results suggest that GP2(+)Tnfaip2(+) cells in NALT are equivalent to intestinal M cells, and that RANKL-RANK signaling induces their differentiation. PMID: 26553655
  52. These results highlight the role of distal enhancers in the regulation of RANKL expression by PTH and perhaps 1,25(OH)2D3 and suggest that the RL-D2 and RL-D5 enhancers contribute in either an additive or synergistic manner to regulate bone remodeling. PMID: 26332516
  53. NMP4 deficiency suppressed the arthritis-induced increase in bone resorption, expression of RANKL and MMP-3 mRNA. PMID: 26378628
  54. the results of the present study strongly suggest that mimosine, a normoxic inducer of HIF, inhibits the PGF2ainduced osteoprotegerin synthesis without affecting the IL-6 synthesis in osteoblasts PMID: 26744072
  55. Adiponectin exerts novel effects to limit the production and action of mono-MPs, underscoring yet another pleiotropic effect of this adipokine. PMID: 26687997
  56. NF-kappaB regulates RANKL-induced osteoclast differentiation and mitochondrial biogenesis via independent mechanisms PMID: 26094846
  57. RANKL has a role in proliferation-coupled osteoclast differentiation PMID: 26265539
  58. Whole-body Rankl deletion completely abrogates tumorigenesis. PMID: 26659571
  59. a dual action of HDFCs in osteoclastogenesis; moreover, parathyroid hormone-related protein, CSF-1 and BMP-2 might influence osteoclastogenesis by regulating the expression of RANKL and OPG in HDFCs PMID: 26149648
  60. The ligand of the RANKLinduced osteoclastogenesis. PMID: 26324422
  61. OPG inhibits osteoclast differentiation via the MAPK signaling pathway. PMID: 26329402
  62. Stromal reticular cells activate lymphatic endothelial cells via RANKL and support the action of hematopoietic cell-derived lymphotoxin. PMID: 27010197
  63. SAA inhibits osteoclast formation from mouse macrophages. SAA blocks RANKL-induced osteoclastogenesis. PMID: 26563612
  64. Adseverin knockdown also suppressed the RANKL-mediated induction of nuclear factor of activated T-cell c1 (NFATc1), which is a key transcription factor in osteoclastogenesis. PMID: 26642432
  65. Expression of RANKL is related to sex differences in collagen-induced arthritis PMID: 25863233
  66. Study reports that loss of the Opg gene results in deterioration of abdominal aortic aneurysms (AAA), possibly through involvement of TRAIL in smooth muscle actin (SMA)-positive cells and myofibroblasts. PMID: 26783750
  67. Data (including data from studies in transgenic mice) suggest RANKL induces incomplete cytokinesis (as well as cell fusion) as myeloid precursors commit to becoming polyploid osteoclasts; Akt activation via phosphorylation appears to be involved. PMID: 26670608
  68. OPG induces osteoclasts and osteoclast progenitor cells apoptosis partly by the Fas/FasL signaling pathway. PMID: 26571489
  69. Taken together, our results show that niclosamide is effective in suppressing osteoclastogenesis and may be considered as a new and safe therapeutic candidate for the clinical treatment of osteoclast-related diseases such as osteoporosis. PMID: 26792726
  70. Although RL-D5 (enhancer) mediates RANKL expression in multiple lineages, other cell type- or factor-specific enhancers are required for its appropriate control, demonstrating the cell type-specific and complex regulation of RANKL expression. PMID: 26646205
  71. These findings indicated that AMPK regulated RANKL and sclerostin expression through the mevalonate pathway in osteocytes. PMID: 26713363
  72. these findings suggest a possible mechanism underlying the RANKL expression induced by wear particles in fibroblasts, and downregulating ER stress and the XBP1s expression of fibroblasts PMID: 26112372
  73. results demonstrate that osteocytes, not osteoblasts or lining cells, are the main source of the RANKL required for osteoclast formation in remodeling cancellous bone PMID: 26393791
  74. Data show that receptor activator of nuclear factor-kappa B ligand (RANKL)-binding peptide OP3-4 prevented the collagen-induced arthritis (CIA)-induced bone loss at the periarticular sites of joints, promoting bone formation. PMID: 26373710
  75. RANKL directly stimulates osteoclasts to resorb bone, it also controls the osteoclasts' ability to induce regulatory T cells PMID: 25656537
  76. Taken together, these results suggested that the expression of RANKL induced by TiPs was mediated by ER stress in fibroblasts. PMID: 26366858
  77. resveratrol markedly amplifies BMP4induced OPG mRNA expression. PMID: 26044505
  78. These findings indicated that Arl6ip5 was an anti-catabolic factor by binding with RANKL and disturbing its subcellular trafficking in osteoblast. PMID: 26220341
  79. we performed proteomics analysis and bioinformatics analysis to comprehensively compare the differential expression of proteins in receptor activator of nuclear factor-kappaB ligand RANKL-induced osteoclasts in the presence and absence of estrogen. PMID: 26120583
  80. mouse Tnfsf11 gene locus contains the necessary genetic information to direct appropriate tissue-specific and factor-regulated RANKL expression in vivo. PMID: 25431114
  81. These findings suggest that RACK1 specifies the RANKL-stimulated activation of p38 MAPK by facilitating the association of MKK6 with TAK1 PMID: 26038599
  82. Galectin-8 induces RANKL expression, osteoclastogenesis, and bone mass reduction in mice. PMID: 25955862
  83. we show that estrogen signaling in osteoblasts abrogates RUNX2-mediated RANKL membrane association and differentiation of co-cultured splenocytes into mature osteoclasts. PMID: 25701138
  84. results strongly suggest that resveratrol inhibits PGE1-stimulated OPG synthesis via suppressing SAPK/JNK but not p38 MAP kinase in osteoblasts. PMID: 25677506
  85. demonstrate that LPS P. gingivalis stimulates periosteal osteoclast formation and bone resorption by stimulating RANKL in osteoblasts via TLR2 PMID: 26085099
  86. These data identify osteoprotegerin as a novel protector of muscle integrity. PMID: 25708645
  87. Study examined the role of miR-26a in RANKL-induced osteoclastogenesis. The expression of miR-26a was up-regulated by RANKL at the late stage of osteoclastogenesis. PMID: 25518928
  88. TR deficiency inhibits osteoclastogenesis by decreasing RANKL/OPG ratio, resulting in a high bone mass phenotype PMID: 25460576
  89. triptolide inhibited osteoclastogenesis and bone resorption, as well as RANKL-induced NF-B activities as monitored by luciferase reporter gene assays and the nuclear translocation of p65. PMID: 25448849
  90. Blockade of Cav2.2 in inflammatory arthritis leads to up-regulation of the osteoclast activator RANKL and concomitant joint and bone destruction. PMID: 25733371
  91. Advanced glycation end products, but not glucose, significantly decreased the expression of RANKL protein and mRNA. PMID: 25721666
  92. results suggest that IL-33-ST2 interactions down-regulate both RANKL-induced NFATc1 activation and osteoclast differentiation via the regulation of Blimp-1 and IRF-8 expressio PMID: 25795135
  93. The data point to a novel role of the RANKL-RANK axis in the regulation of B cell homeostasis and highlight an unexpected link between IL-10 CD40 signaling and the RANKL pathway. PMID: 25825446
  94. Carboxypeptidase E is an important modulator of RANKL-induced osteoclast differentiation. PMID: 25220258
  95. In collagen-antibody-induced arthritis there was increased expression of RANKL on immune cells. PMID: 22830570
  96. microRNA-17/20a may play a significant role in glucocorticoid-induced osteoclast differentiation and function by targeting the RANKL expression in osteoblast cells. PMID: 25138550
  97. RANKL, an essential cytokine for osteoclastogenesis, induces a metabolic shift towards oxidative metabolism, which is accompanied by an increase in S-adenosylmethionine (SAM) production. PMID: 25706873
  98. These results suggested that, at least in part, RANKL expression by osteoblasts in an acidic environment was mediated by cAMP/PKA signaling resulting. PMID: 25668130
  99. megakaryocyte secreted factors cannot access cortical bone sufficiently to inhibit osteoclastogenesis or that OPG itself is required to inhibit osteoclastogenesis in cortical bone PMID: 25205203
  100. Homozygous deletion of Opg in apo E-deficient mice (ApoE(-/-)Opg(-/-)) inhibited angiotensin II-induced aortic dilatation. Survival free from aortic rupture was increased from 67% in ApoE(-/-)Opg(+/+) controls to 94% in ApoE(-/-)Opg(-/-) (P=0.040). PMID: 25301844

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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, SUBCELLULAR LOCATION: Isoform 2: Cell membrane, Single-pass type II membrane protein, SUBCELLULAR LOCATION: Isoform 3: Cytoplasm, SUBCELLULAR LOCATION: 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.
Database Links

KEGG: mmu:21943

STRING: 10090.ENSMUSP00000022592

UniGene: Mm.249221

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