IL-23 p19 Monoclonal Antibody (HNU2319), Functional Grade, eBioscience™/IL-23 p19单克隆 (HNU2319), 功能抗体, eBioscience™
货号:16-5236-82,16-5236-85,16-5236-38,16-5236-025,16-5236-050
规格:100 µg,500 µg,5 mg,25 mg,50 mg
价格:1283,3274,24089,72266,120443
产品类型:流式抗体
品牌:eBioscience
抗原:IL-23 p19
物种:人
宿主:小鼠
抗体亚型:IgG1, kappa
克隆号:HNU2319
荧光染料:其它
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类型: | 一抗(功能抗体) | 同型对照: | Mouse IgG1 kappa Isotype Control (P3.6.2.8.1), Functional Grade, eBioscience™ |
浓度: | 1 mg/mL | 用法: | Assay-Dependent(中和);Assay-Dependent(功能检测) |
产品详细信息Description: The HNU2319 monoclonal antibody is specific to the p19 subunit of human IL-23, a heterodimeric cytokine made up of two covalently linked subunits, p40 and p19. It is closely related to IL-12, with which it shares the p40 subunit. Dendritic cells and macrophages produce IL-23 in response to TLR2, TLR4, and TLR8 ligands, as well as the beta-glucan receptor Dectin-1.Human IL-23 induces proliferation of memory T cells and induces moderate levels of IFN-gamma production by naiveand memory T cells, as compared to IL-12. In contrast, the mouse IL-23 biological activities are more distinctly different than those of mouse IL-12 suggesting the signaling or response elements (receptors) differ between species. The IL-23 receptor is also heterodimeric and shares the IL-12Rbeta1 chain with IL-12, while the IL-23R chain is unique to IL-23. Signaling occurs through the Jak/STAT pathway and results in RORgammat expression, which drives the differentiation of CD4^+ T-cells towards the Th17 phenotype.The monoclonal antibody HNU2319 neutralizes the bioactivity of IL-23 without affecting IL-12.Applications Reported: The monoclonal antibody HNU2319 reacts with the p19 subunit of human IL-23 and inhibits its bioactivity.Applications Tested: The ND50 of HNU2319, as determined by the neutralization of mouse IL-17A induction in balb/c splenocytes by recombinant human IL-23, is 0.2-0.4 µg/mL in the presence of 2 ng/mL IL-23. This antibody is specific to the p19 subunit of IL-23, and will not affect the bioactivity of IL-12. The neutralization dose of this antibody will vary depending on cell type, assay method, and concentration of cytokine.Storage and handling: Use in a sterile environment.Filtration: 0.2 µm post-manufacturing filtered.Purity: Greater than 90%, as determined by SDS-PAGE.Endotoxin Level: Less than 0.001 ng/µg antibody, as determined by LAL assay.Aggregation: Less than 10%, as determined by HPLC.靶标信息IL-23 is a heterodimeric cytokine composed of the p40 subunit of IL-12 disulfide-linked with a protein p19. p19, like p35 of IL-12, is biologically inactive by itself. IL-23 interacts with IL-12Rbeta1 and an additional, novel beta2-like receptor subunit with STAT4 binding domain, termed IL-23R. IL-23 is secreted by activated mouse and human dendritic cells. Biological activities of mouse IL-23 are distinct from those of mouse IL-12. Mouse IL-23 was found not to induce significant amounts of IFN-γ. Mouse IL-23 does induce strong proliferation of memory T cells (but not naive T cells), whereas IL-12 has no effect on memory cells. Additionally, mouse IL-23 (but not IL-12) can activate mouse memory T cells to produce the proinflammatory cytokine IL-17. Human IL-23 has biological properties which are less distinct from human IL-12; human IL-23 induces proliferation of memory T cells and induces moderate levels of IFN-γ production by naive and memory T cells, as compared to IL-12.仅用于科研。不用于诊断过程。
数据 |
IL-23 p19 Antibody (16-5236-82) in FNNeutralization of Human IL-23 Recombinant Protein activity as measured by IL-17A induction in BALB/c splenocytes. |
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参考文献: |
中和1.European journal of immunologyPeriodontitis-associated pathogens P. gingivalis and A. actinomycetemcomitans activate human CD14(+) monocytes leading to enhanced Th17/IL-17 responses."16-5236 was used in Neutralization experiments to investigate the mechanism by which the periodontal pathogens promote a Th17/IL-17 response in vitro, showing that they activate human CD14(+) monocytes leading to enhanced Th17/IL-17 responses."AuthorsCheng WC,van Asten SD,Burns LA,Evans HG,Walter GJ,Hashim A,Hughes FJ,Taams LS |
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