EasySep™小鼠TIL（CD45）正选试剂盒
产品号 #15622_C
免疫密度梯度离心法去除CD4+细胞
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专为您的实验方案打造的产品
要查看实验方案所需的所有配套产品，请参阅《实验方案与技术文档》。
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Lymphoprep™Density gradient medium for the isolation of mononuclear cells
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Dulbecco's Phosphate Buffered Saline with 2% ...Cell culture buffer
总览
RosetteSep™人CD8去除混合物从全血中去除CD8+细胞。四聚体抗体复合物可识别CD8以及红细胞（RBC）上的糖蛋白A，从而靶向去除非目的细胞。当在密度梯度介质如Lymphoprep™（产品号#18060）上离心后），非目的细胞会与红细胞一起沉淀。去除CD8+细胞后的目的细胞为血浆和密度梯度离心液的交界界面中高度富集的细胞。
亚型
细胞分选试剂盒
细胞类型
T 细胞，T 细胞，CD4+
种属
人
样本来源
Buffy Coat，Whole Blood
筛选方法
删除
应用
细胞分选
品牌
RosetteSep
研究领域
免疫
实验数据
产品说明书及文档
请在《产品说明书》中查找相关支持信息和使用说明，或浏览下方更多实验方案。
应用领域
本产品专为以下研究领域设计，适用于工作流程中的高亮阶段。探索这些工作流程，了解更多我们为各研究领域提供的其他配套产品。
相关材料与文献
技术资料 (4)
常见问题
文献 (2)
Metformin Inhibits the Type 1 IFN Response in Human CD4+ T Cells. Journal of immunology (Baltimore, Md. : 1950) 2019 jul
Abstract
In systemic lupus erythematosus, defective clearance of apoptotic debris and activation of innate cells result in a chronically activated type 1 IFN response, which can be measured in PBMCs of most patients. Metformin, a widely used prescription drug for Type 2 diabetes, has a therapeutic effect in several mouse models of lupus through mechanisms involving inhibition of oxidative phosphorylation and a decrease in CD4+ T cell activation. In this study, we report that in CD4+ T cells from human healthy controls and human systemic lupus erythematosus patients, metformin inhibits the transcription of IFN-stimulated genes (ISGs) after IFN-alpha treatment. Accordingly, metformin inhibited the phosphorylation of pSTAT1 (Y701) and its binding to IFN-stimulated response elements that control ISG expression. These effects were independent of AMPK activation or mTORC1 inhibition but were replicated using inhibitors of the electron transport chain respiratory complexes I, III, and IV. This indicates that mitochondrial respiration is required for ISG expression in CD4+ T cells and provides a novel mechanism by which metformin may exert a therapeutic effect in autoimmune diseases.
Developmental regulation of Wnt signaling by Nagk and the UDP-GlcNAc salvage pathway. Mechanisms of development 2019
Abstract
In a screen for human kinases that regulate Xenopus laevis embryogenesis, we identified Nagk and other components of the UDP-GlcNAc glycosylation salvage pathway as regulators of anteroposterior patterning and Wnt signaling. We find that the salvage pathway does not affect other major embryonic signaling pathways (Fgf, TGF$\beta$, Notch, or Shh), thereby demonstrating specificity for Wnt signaling. We show that the role of the salvage pathway in Wnt signaling is evolutionarily conserved in zebrafish and Drosophila. Finally, we show that GlcNAc is essential for the growth of intestinal enteroids, which are highly dependent on Wnt signaling for growth and maintenance. We propose that the Wnt pathway is sensitive to alterations in the glycosylation state of a cell and acts as a nutritional sensor in order to couple growth/proliferation with its metabolic status. We also propose that the clinical manifestations observed in congenital disorders of glycosylation (CDG) in humans may be due, in part, to their effects on Wnt signaling during development.
更多信息
| 种属 | Human |
|---|---|
| 样本来源 | Buffy Coat, Whole Blood |
| Selection Method | Depletion |
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