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  4. Rat soluble receptor activator of nuclear factor-kB ligand,sRANKL ELISA Kit

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

  • 中文名称：
    大鼠可溶性核因子κB受体活化因子配基(sRANKL)酶联免疫试剂盒
  • 货号：
    CSB-E05126r
  • 规格：
    96T/48T
  • 价格：
    ￥3200/￥2500
  • 其他：

产品详情

  • 产品描述：

    The Rat soluble receptor activator of nuclear factor-kB ligand (sRANKL) ELISA Kit is a powerful tool for quantitative analysis of the Receptor activator of nuclear factor-kB ligand (Tumor necrosis factor ligand superfamily member 11 protein) in rat samples.

    This ELISA kit is specifically designed for the measurement of sRANKL protein levels in a variety of sample types, including serum, plasma, and cell culture supernates from Rattus norvegicus (Rat) species. With a detection range of 62.5 pg/mL to 4000 pg/mL and a sensitivity of 15.6 pg/mL, this ELISA kit can accurately detect even low levels of sRANKL protein.

    The assay principle is based on a sandwich immunoassay, which involves the use of two specific antibodies that bind to different epitopes of the target protein. This approach ensures high specificity and sensitivity in the measurement of sRANKL levels. The assay can be completed in just 1-5 hours, with a sample volume of 50-100ul, making it a fast and convenient option for research. This ELISA kit has been cited in over 14 research articles, demonstrating its reliability and accuracy.

  • 别名：
    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
  • 缩写：
  • Uniprot No.：
  • 种属：
    Rattus norvegicus (Rat)
  • 样本类型：
    serum, plasma, cell culture supernates
  • 检测范围：
    62.5 pg/mL-4000 pg/mL
  • 灵敏度：
    15.6 pg/mL
  • 反应时间：
    1-5h
  • 样本体积：
    50-100ul
  • 检测波长：
    450 nm
  • 研究领域：
    Cardiovascular
  • 测定原理：
    quantitative
  • 测定方法：
    Sandwich
  • 精密度：
    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.
  • 线性度：
    To assess the linearity of the assay, samples were spiked with high concentrations of rat sRANKL in various matrices and diluted with the Sample Diluent to produce samples with values within the dynamic range of the assay.
    　SampleSerum(n=4)
    1:1Average %95
    Range %89-101
    1:2Average %96
    Range %91-105
    1:4Average %97
    Range %93-102
    1:8Average %94
    Range %90-99
  • 回收率：
    The recovery of rat 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) 9489-100
    EDTA plasma (n=4)10096-103
  • 标准曲线：
    These standard curves are provided for demonstration only. A standard curve should be generated for each set of samples assayed.
    pg/mlOD1OD2AverageCorrected
    40001.934 1.829 1.882 1.719
    20001.194 1.139 1.167 1.004
    10000.753 0.733 0.743 0.580
    5000.548 0.538 0.543 0.380
    2500.385 0.375 0.380 0.217
    1250.304 0.294 0.299 0.136
    62.50.241 0.237 0.239 0.076
    00.163 0.162 0.163 　
  • 数据处理：
  • 货期：
    3-5 working days

引用文献

产品评价

靶点详情

  • 功能：
    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.
  • 基因功能参考文献：
    1. results of this study concluded that the RANK, RANK-L and OPG system participates in bone remodeling after RME PMID: 29297549
    2. in this animal model the increase of RANK/RANKL and HGF markers is related to a specific immune response, and probably contributed to the evolution of periodontal disease PMID: 29211121
    3. In the supplemented and nonsupplemented rats groups, RANKL was upregulated compared with the control group. PMID: 28473060
    4. the canonical Wnt pathway inhibitor DKK1 blocked the osteogenesis effect and rescued the ratio of RANKL/OPG in periodontal ligament stem cells under force treatment for 1h PMID: 27154288
    5. study identified a number of differentially expressed bone-related mRNAs of potential significance and confirmed the osteoprotegerin/receptor activator of nuclear factor kappa-B (RANK)/RANK ligand (RANKL) pathway PMID: 25406873
    6. High-dose diosgenin treatment down-regulated expression of RANKL significantly in tibia from OVX rats compared to control. PMID: 25257532
    7. Data indicate that after loading jump (JL) for 6 weeks, the expressions of of interleukin 6 (IL-6), and ligand of receptor activator of NF-kappaB (RANKL) genes were markedly elevated in tibia. PMID: 25200151
    8. mechanical stimulation inhibits the activity of RANKL in rats PMID: 23553492
    9. Our findings indicate that the expression of RANKL in the occlusal portion of the bony crypt is unrelated to osteoclast recruitment and differentiation but is crucial to their activation during the creation of the eruption pathway. PMID: 23636419
    10. RANK and RANKL were expressed by T lymphocytes and macrophages in acute cellular kidney rejection after transplantation in rats PMID: 23769040
    11. In rheumatoid arthritis methotrexate/leflunomide combination therapy would relive the synovium hypertrophy through depressing cell viability and osteoclasia through decreasing RANKL and Il-17. PMID: 23334376
    12. There was no change in OPN expression after orthodontic retention and bone remodeling. PMID: 22353912
    13. the increase in RANK-RANKL expression is a response to podocyte injury, and RANK-RANKL may be a novel receptor-ligand complex for the survival response during podocyte injury. PMID: 22848465
    14. Insulin could promote osteoblastic differentiation of calcifying vascular smooth muscle cells by increased RANKL expression through ERK1/2 activation, but not PI3K/Akt activation. PMID: 22194983
    15. TRANCE/RANKL is constituively expressed by rat plasmacytoid dendritic cells. PMID: 22428075
    16. Pressure-overloaded myocardium generates RANKL, which induces inflammation mediators and myocardial inflammation. PMID: 22298642
    17. Bone loss and recovery in a receptor activator for nuclear factor kappa B ligand (RANKL)-administered rat model was assessed PMID: 20480144
    18. RANKL/OPG are key factors linking bone formation to resorption during bone remodeling. PMID: 21771583
    19. Vitamin C deficiency increased osteoclastogenesis by increasing RANK expression. PMID: 20444587
    20. These results suggest that antibody to RANKL can inhibit A. actinomycetemcomitans-specific T cell-induced periodontal bone resorption by blockade and reduction of tissue sRANKL. PMID: 21078845
    21. RANKL contributes to vascular calcification by regulating bone morphogenetic protein-2 and calcification inhibitor matrix Gla protein (MGP) expression, as well as bone-related proteins, and is counteracted by estrogen in a receptor-dependent manner. PMID: 20595654
    22. the toothless (tl) osteopetrotic rat mutation is not in the TNFSF11 locus PMID: 11804028
    23. accelerates nuclear translocation of nuclear factor kappa B in osteoclasts by elevaing cytosolic Ca2+ PMID: 12496256
    24. Effects of 12-O-tetradecanoylphorbol-13-acetate on osteoclastogenesis and its role in RANKL-induced signaling. PMID: 14672351
    25. RANK ligand is strongly up-regulated during acute heart allograft rejection; its blockade prolongs rat heart allograft survival. PMID: 14734743
    26. Detection of RANKL mRNA and protein in bone cells. PMID: 15704000
    27. Results suggest that the RANKL expressed in thymic epithelial cells plays a role in the development of T cells during thymic regeneration. PMID: 15844004
    28. Portasystemic shunting caused low turnover osteoporosis that was RANKL independent. PMID: 16874862
    29. Prolactin decreased RANKL mrna in cultured osteoblasts. PMID: 18432284
    30. These data indicate that serum 25-hydroxyvitamin D levels are a major determinant of osteoclastogenesis and bone mineral volume. PMID: 18597628
    31. Recombinant RANKL (rRANKL) mutants within the TNF-like core domain exhibited diminished osteoclastogenic potential as compared with wild-type rRANKL1 encoding the full TNF-like core domain [amino acids (aa) 160-318]. PMID: 19008464
    32. Orchiectomy increases the concentration of free sRANKL in bone marrow of aged rats. PMID: 19501680
    33. Bony spur formation can thus be considered a process that occurs independent of TNFalpha and RANKL and is triggered by destructive arthritis. PMID: 19714640

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  • 亚细胞定位：
    Cell membrane; Single-pass type II membrane protein.; [Tumor necrosis factor ligand superfamily member 11, soluble form]: Secreted.
  • 蛋白家族：
    Tumor necrosis factor family
  • 组织特异性：
    Highly expressed in thymus and bone tissues.
  • 数据库链接：