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

Code CSB-E05125h
Size 96T,5×96T,10×96T
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Product Details

Target Name
tumor necrosis factor (ligand) superfamily, member 11
Alternative Names
TNFSF11; OPGL; RANKL; TRANCE; Tumor necrosis factor ligand superfamily member 11; Osteoclast differentiation factor; ODF; Osteoprotegerin ligand; Receptor activator of nuclear factor kappa-B ligand; TNF-related activation-induced cytokine; CD antigen CD254
Uniprot No.
Homo sapiens (Human)
Sample Types
serum, plasma, cell culture supeernates, tissue homogenates
Detection Range
7.8 pg/mL-500 pg/mL
1.95 pg/mL
Assay Time
Sample Volume
Detection Wavelength
450 nm
Research Area
Assay Principle
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 human sRANKL in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
1:5Average %94
Range %90-99
1:10Average %87
Range %82-92
1:20Average %92
Range %88-97
1:40Average %90
Range %85-94
The recovery of human 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) 9086-94
EDTA plasma (n=4)9590-99
Typical Data
These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
5002.803 2.752 2.778 2.608
2502.243 2.176 2.210 2.040
1251.465 1.404 1.435 1.265
62.50.891 0.839 0.865 0.695
31.20.472 0.451 0.462 0.292
15.60.364 0.359 0.362 0.192
7.80.295 0.278 0.287 0.117
00.173 0.167 0.170  
and FAQs
Store at 2-8°C. Please refer to protocol.
Lead Time
3-5 working days after you place the order, and it takes another 3-5 days for delivery via DHL or FedEx

The product CSB-E05125h is a ready-to-use microwell, strip plate ELISA kit for quantitatively analyzing the presence of TNFSF11 in different biological samples, including serum, plasma, and tissue homogenates. This TNFSF11 ELISA kit specifically recognizes the human TNFSF11 in the sample. It adopts the Sandwich ELISA technique in conjunction with antibody-antigen specific binding and an enzyme colorimetric reaction to indicate the presence of human TNFSF11 and quantitatively measure the concentration of TNFSF11 in the samples.

TNFSF11, also known as RANKL, is an osteoclastogenic cytokine that combines bone with the immune system. RANKL/RANK signaling regulates osteoclast development, bone metabolism, lymph node development, and T cell/dendritic cell communication. In addition to modulating bone resorption and remodeling, the RANKL/RANK axis is also involved in many other cellular processes, including immunity, proliferation and division of mammary epithelial cells, and mammary gland formation during lactation. Studies have shown that RANKL/RANK is involved in each stage of cancer development, from pre-cancerous lesions to the establishment of metastases.


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Target Background

(From Uniprot)
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. RANK/RANKL were identified as crucial regulators for BRCA1 mutation-driven breast cancer. Current prevention strategies for BRCA1 mutation carriers are associated with wide-ranging risks; therefore, the search for alternative, non-invasive strategies is of paramount importance PMID: 29241686
  2. High RANKL expression is associated with gastric cancer cell migration. PMID: 30015970
  3. A high level of sRANKL in bronchoalveolar lavage fluid of non-small cell lung cancer patients may predict worse survival. PMID: 29052177
  4. RANKL/OPG ratio was significantly higher in the prolactinoma group than in the control group. PMID: 29895074
  5. RANKL mRNA expression was higher in tumour tissue from patients with metastatic prostate cancer compared to local disease. The RANKL/OPG ratio was low in normal prostate tissue and high in tumours with bone metastases. Expression was high in BPH tissue but did not exceed as much as in the tumour tissue. PMID: 29204705
  6. In cardiovascular risks, OPG serum level might increase as a preventive compensatory mechanism to neutralize the RANKL level increment. The determination of the OPG-RANKL system is a diagnostic indicator for the intensity of vascular calcification and atherosclerosis in SSc patients. PMID: 29336616
  7. sRANKL and OPG may play a role in the pathogenesis of diabetes as well as metabolic disturbance PMID: 28146138
  8. regulation of OSCAR by TNF-alpha and receptor activator of NF kappa beta ligand (RANKL) in pre-osteoclasts/osteoclasts PMID: 28555364
  9. The -643C>T RANKL polymorphism, through its significant influence on body weight and BMI value, may contribute to the development of Osteoporosis in Postmenopausal women. PMID: 27304650
  10. In the present study, we measured expression of RANKL in human periosteum-derived cells(hPDCs) undergoing osteoblastic differentiation and found that expression of RANKL mRNA was markedly increased in these cells in a time-dependent manner.RANKL protein expression was also significantly enhanced in osteogenic-conditioned media from hPDCs undergoing osteoblastic differentiation PMID: 29200953
  11. MiR-217 is a useful diagnostic biomarker and is involved in human podocyte cells apoptosis via targeting TNFSF11 in membranous nephropathy. PMID: 29214160
  12. rs9525641 might contribute to bone mineral density PMID: 28488893
  13. Vascular smooth cells are a significant source of osteoprotegerin within the vasculature but that RANKL, once present, downregulates this production and appears capable of preventing the "protective" upregulation of OPG seen with VSMCs exposed to physiological levels of cyclic strain. PMID: 29635231
  14. receptor activator for nuclear factor-kappa B ligand (RANKL), secreted by human embryonic trophoblasts and maternal decidual stromal cells, polarizes decidual macrophages toward a M2 phenotype. PMID: 29022922
  15. There were no significant associations involving the RANKL gene. Thus, it is suggested that alterations in the OPG and RANK genes are primarily responsible for altering the function and expression of the RANKL ligand, resulting in a predisposition to chronic arthralgia and comorbid temporomandibular OA. PMID: 28464982
  16. Vitamin D, tumor necrosis factor (TNF)-alpha, receptor activator of nuclear factor-KB ligand (RANKL), and OPG levels were determined in GCF and serum. Baseline clinical parameters were similar in all periodontitis groups (P > 0.05) but were higher than that in controls PMID: 28904316
  17. study demonstrated the association of the -643C > T polymorphism with bone mineral density variation and osteoporosis risk in postmenopausal Tunisian women PMID: 28453307
  18. down-regulated miR-143-5p promotes the differentiation of DPSCs into odontoblasts by enhancing Runx2 expression via the OPG/RANKL signaling pathway. PMID: 28608628
  19. OPG and OPG/TRAIL ratio expression were significantly increased in rheumatoid arthritis patients compared to controls (fold change = 1.79, p = 0.013 and 2.07, p = 0.030, respectively), RANKL/OPG ratio was significantly decreased (fold change = 0.50, p = 0.020). No significant differences were found between patients and controls in RANKL and TRAIL expression. PMID: 27403809
  20. Results show that pro-inflammatory cytokines upregulated SOX5 and RANKL expression in both synovial fibroblasts of patients with primary rheumatoid arthritis and cell line. IL-6 facilitates the binding of SOX5 to RANKL promoter. PMID: 27550416
  21. Higher concentrations of serum sRANKL were positively associated with risk of estrogen receptor positive breast cancer. PMID: 28701332
  22. RANKL is overexpressed in invariant NKT cells in bone marrow of patients with multiple myeloma. PMID: 27834938
  23. triple-negative breast cancer (TNBC) patients that expressed both RANK and RANKL proteins had significantly worse RFS and OS than patients with RANK-positive, RANKL-negative tumors. RANKL was an independent, poor prognostic factor for RFS and OS in multivariate analysis in samples that expressed both RANK and RANKL. PMID: 28417335
  24. Findings suggest that cell-autonomous activation of the RANKL/RANK signaling axis is a convergently shared, non-oncogenic addiction underlying the generation and maintenance of CSC-like states in response to diverse molecular events such as BRCA1 haploinsufficiency and EMT phenomena. PMID: 28388533
  25. Data suggest that, in children with type I diabetes, serum levels of osteoprotegerin are up-regulated, serum levels of RANKL are unchanged, and serum levels of fetuin-A are down-regulated. (RANKL = receptor activator of nuclear factor kappa B ligand) PMID: 27028343
  26. There was no significant difference in GCF RANKL values among groups (P > 0.05) or during the observation period (P > 0.008). The use of BP may be effective in preventing periodontal breakdown by controlling the levels of these markers in osteoporosis as an adjunct to periodontal treatment PMID: 28367895
  27. Data report that in postmenopausal women without known genetic predisposition, high RANKL serum levels stratify a subpopulation of women at high risk of developing breast cancer 12-24 months before diagnosis. PMID: 28002811
  28. Data suggest that STAT6 and RANKL are involved in regulation of apoptosis, gene expression, and cell proliferation in hepatocellular carcinoma cell lines; depletion of STAT6 using RNA interference increases apoptosis; this mechanism involves down-regulation of expression of RANKL. (STAT6 = signal transducer and activator of transcription 6; RANKL = receptor activator of nuclear factor kappa B ligand) PMID: 28525794
  29. Positivity of RANKL and anti-CCP2 yielded significant risk for progression with negativity for both as reference. No single nucleotide polymorphism encoding TNFSF11 or SOST was associated with increased concentrations of the factors. PMID: 28190118
  30. The compound with greatest potential is E05657 with high activity and low effective concentration in the HTS system. It increases the OPG/RANKL ratio and OPG secretion, decreases the NFATc1 expression, and reduces osteoclastogenesis in vitro PMID: 27301430
  31. Our study suggests that the RANKL/RANK pathway contributes to the development and maintenance of the immunosuppressive tumor microenvironment and denosumab may be a promising adjuvant therapy targeting TAMs in cancer of apocrine origin PMID: 29277763
  32. RANKL/Osteoprotegerin have roles in bone turnover in Hashimoto Thyroiditis PMID: 27328677
  33. present clear evidence that TRAIL can block several key signalling actions of RANKL in vascular cells, providing further evidence of its vasoprotective potential PMID: 29145460
  34. main finding is that OPG levels decreased significantly during 8 weeks of alcohol abstinence. PMID: 27061293
  35. Studies showed that the central hypothalamic-pituitary regulatory system, via it's relative hormones, seems to control OPG/RANKL/RANK system function, and the pulsatility and circadian rhythmicity of these hormones may induce an oscillatory fluctuation of the OPG/ RANKL ratio. Also, psycological characteristics may provoke a shift of the OPG/ RANKL ratio towards an unbalanced or a balanced status. [review] PMID: 27862210
  36. Studies strongly implicates RANK and RANKL as key molecules involved in the initiation of BRCA1-associated breast cancer. [review] PMID: 27881737
  37. RANK is frequently expressed by cancer cells in contrast with RANKL which is frequently detected in the tumor microenvironment, and together they participate in every step in cancer development. (Review) PMID: 27279652
  38. Proinsulin C-peptide prevents a reduction of type I collagen expression and decreases, in combination with insulin, receptor activator of nuclear factor-kappaB (RANKL) levels. PMID: 28007656
  39. The RANKL/OPG ratio significantly increased in the presence of bone metastasis with appropriate sensitivity and specificity (73% and 72%, respectively) at a cutoff of >/=0.14 for the detection of bone metastasis. Serum OPG and RANKL/OPG ratios are promising biomarkers for detecting bone metastasis in breast cancer patients. PMID: 27983911
  40. Correlations between sRANKL and IL-18 in BALF. PMID: 27826889
  41. RANK/RANKL signaling is involved in the androgen deprivation therapy-induced acceleration of bone metastasis in castration-insensitive prostate cancer and is inhibited by osteoprotegerin to prevent bone metastasis. PMID: 28373003
  42. This study suggested that RANKL could be a marker to differentiate between pagetoid squamous cell carcinoma in situ and extramammary Paget disease . PMID: 27251225
  43. TNF-alpha-converting enzyme -mediated cleavage of soluble RANKL from activated lymphocytes, especially B cells, can promote osteoclastogenesis in periodontitis. PMID: 27815441
  44. RANKL is required for progesterone-mediated cell proliferation in BRCA1mut/+ breast tissue. PMID: 27322743
  45. Results show that RANK-L are overexpressed in human chronic periodontitis which subsequently increase alveolar bone loss. PMID: 27992569
  46. MAOA provides tumor cell growth advantages in the bone microenvironment by stimulating interleukin-6 (IL6) release from osteoblasts, and triggers skeletal colonization by activating osteoclastogenesis through osteoblast production of RANKL and IL6. PMID: 28292438
  47. In this review, we will provide a summary of the biological functions of RANK signaling pathway (receptor activator of nuclear factor kappaB ligand RANKL and its receptor RANK ) and downstream pathways in bone remodeling, immunity and epithelial homeostasis, with a particular emphasis on cancer PMID: 26749530
  48. The results showed that AG490 inhibited (p)-JAK2 and RANKL expression. PMID: 28278513
  49. Review: OPG, RANKL and TRAIL are involved in vascular calcification. PMID: 26924459
  50. Our results suggest that the polymorphism of the RANKL, RANK, and OPG genes does not make a significant genetic contribution to heel ultrasound measurements in a population of young Caucasian adults. Further studies replicating the results in independent populations are needed to support these initial findings. PMID: 28252575

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Involvement in disease
Osteopetrosis, autosomal recessive 2 (OPTB2)
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.; [Tumor necrosis factor ligand superfamily member 11, soluble form]: Secreted.
Protein Families
Tumor necrosis factor family
Tissue Specificity
Highest in the peripheral lymph nodes, weak in spleen, peripheral blood Leukocytes, bone marrow, heart, placenta, skeletal muscle, stomach and thyroid.
Database Links

HGNC: 11926

OMIM: 259710

KEGG: hsa:8600

STRING: 9606.ENSP00000239849

UniGene: Hs.333791

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