IFN alpha-IFNAR-IN-1 hydrochloride
目录号 : GC60927An inhibitor of the IFN-α-IFNAR protein-protein interaction
Cas No.:2070014-98-9
Sample solution is provided at 25 µL, 10mM.
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IFN-α-IFNAR-IN-1 is an inhibitor of the protein-protein interaction between the cytokine IFN-α and the IFN-α/β receptor (IFNAR; Kd = 4 ?M for binding to IFN-α).1 It inhibits virus-induced increases in the production of IFN-α and IL-12 in bone marrow-derived plasmacytoid dendritic cells (BM-pDCs) infected with modified Vaccinia virus Ankara (MVA) or vesicular stomatitis virus (VSV) when used at a concentration of 18 ?M. IFN-α-IFNAR-IN-1 also reduces increases in IL-12 production induced by stimulation with the toll-like receptor 9 (TLR9) agonist CpG 2216 or the TLR3 agonist poly(I:C) in the same cells.
1.Geppert, T., Bauer, S., Hiss, J.A., et al.Immunosuppressive small molecule discovered by structure-based virtual screening for inhibitors of protein-protein interactionsAgnew. Chem. Int. Ed. Engl.51(1)258-261(2012)
Cas No. | 2070014-98-9 | SDF | |
Canonical SMILES | CNCC1=CC=CC=C1SC2=C(C=CC=C3)C3=CC=C2.[H]Cl | ||
分子式 | C18H18ClNS | 分子量 | 315.86 |
溶解度 | DMSO: 125 mg/mL (395.74 mM) | 储存条件 | Store at -20°C |
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1 mg | 5 mg | 10 mg | |
1 mM | 3.166 mL | 15.8298 mL | 31.6596 mL |
5 mM | 0.6332 mL | 3.166 mL | 6.3319 mL |
10 mM | 0.3166 mL | 1.583 mL | 3.166 mL |
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% DMSO % % Tween 80 % saline | ||||||||||
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1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
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Stimulation of Mononuclear Cells Through Toll-Like Receptor 9 Induces Release of Microvesicles Expressing Double-Stranded DNA and Galectin 3-Binding Protein in an Interferon-α-Dependent Manner
Front Immunol 2019 Oct 11;10:2391.PMID:31681284DOI:10.3389/fimmu.2019.02391.
Background: Microvesicles (MVs) expressing the type 1 interferon (IFN)-inducible protein galectin-3 binding protein (G3BP) may play a pathogenic role in systemic lupus erythematosus (SLE). Co-expression of double-stranded DNA (dsDNA) on such MVs may render them immunogenic and targets for anti-dsDNA antibodies. Little is known about the mechanisms underlying generation of this MV population. In this study, we investigated how Toll-like receptors (TLRs), IFN-α, and T cells are involved in this process in healthy subjects. Methods: Peripheral blood mononuclear cells (PBMCs) isolated from 12 healthy donors were stimulated in-vitro for 24 h with a series of TLR-agonists or the T cell activating antibody OKT3 or were subjected to apoptosis by incubation with staurosporine. MVs in the supernatants were subsequently isolated by differential centrifugation and were quantified and characterized with respect to expression of G3BP and dsDNA by flow cytometry. Results: Stimulation of PBMCs with the TLR9-agonist and strong IFN-α inducer ODN2395 significantly increased the release of MVs expressing G3BP. The production of MVs with this phenotype was markedly enhanced by co-stimulation of T cells. Furthermore, dependency on IFN-α in the generation of G3BP-expressing MVs was indicated by a marked reduction following addition of the IFN-α inhibitor IFN alpha-IFNAR-IN-1 hydrochloride. Conclusion: Release of G3BP-expressing MVs from healthy donor PBMCs is induced by stimulation of TLR9 in an IFN-α-dependent manner and is enhanced by co-stimulation of T cells.