产品号 #70025_C
冻存的人原代细胞
Maximize your savings on high-quality PBMCs! Take advantage of our bulk pricing discounts and price matching offer to get the best value for your purchase. Now available for specific lots, the standard flow cytometry panel provides the exact frequencies of common cell types in each vial of PBMCs. See Figure 1 in the Data Figures section below to view a representative panel. Browse our Frequently Asked Questions for more information.
总览
选择即用型、符合伦理的人原代单个核细胞助您轻松开启实验。我们提供个性化的服务、定制产品、灵活的交付周期，并支持提前测试筛选并预留整个批次，以确保您获得所需的细胞。
通过密度梯度离心法和/或红细胞裂解法从外周血白细胞单采术样本中分离细胞，并冻存于不含动物成分的CryoStor® CS10冻存液（产品号#07930）中。遵循机构审查委员会（IRB）或研究伦理委员会（REC）批准的知情同意书和方案进行收集。如有需要，可提供其他文档、高分辨率HLA分型（I类和II类等位基因）以及CMV状态。采集过程中添加酸-柠檬酸-葡萄糖溶液A （ACDA）作为抗凝剂。选择产品选项后，供体信息（如BMI范围、吸烟状态、种族等）可以在上面的评论框中查询。所有供体均经过HIV-1/2、乙肝和丙肝筛查。
某些产品仅在特定地区出售。请与您当地的销售代表或产品与科学支持联系techsupport@stemcell.com获取更多信息。
欲了解更多信息，请浏览有关原代细胞的常见问题解答（FAQs）。
包含
• CryoStor® CS10
亚型
冻存
细胞类型
单个核细胞
种属
人
细胞和组织来源
外周血
供体状态
Normal
Data Figures
Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (8)
Publications (12)
Eradication of Triple-Negative Breast Cancer Cells by Targeting Glycosylated PD-L1. Cancer cell 2018 FEB
Abstract
Protein glycosylation provides proteomic diversity in regulating protein localization, stability, and activity; it remains largely unknown whether the sugar moiety contributes to immunosuppression. In the study of immune receptor glycosylation, we showed that EGF induces programmed death ligand 1 (PD-L1) and receptor programmed cell death protein 1 (PD-1) interaction, requiring beta$-1,3-N-acetylglucosaminyl transferase (B3GNT3) expression in triple-negative breast cancer. Downregulation of B3GNT3 enhances cytotoxic T cell-mediated anti-tumor immunity. A monoclonal antibody targeting glycosylated PD-L1 (gPD-L1) blocks PD-L1/PD-1 interaction and promotes PD-L1 internalization and degradation. In addition to immune reactivation, drug-conjugated gPD-L1 antibody induces a potent cell-killing effect as well as a bystander-killing effect on adjacent cancer cells lacking PD-L1 expression without any detectable toxicity. Our work suggests targeting protein glycosylation as a potential strategy to enhance immune checkpoint therapy.
Dendritic Cells but Not Macrophages Sense Tumor Mitochondrial DNA for Cross-priming through Signal Regulatory Protein α Signaling. Immunity 2017 AUG
Abstract
Inhibition of cytosolic DNA sensing represents a strategy that tumor cells use for immune evasion, but the underlying mechanisms are unclear. Here we have shown that CD47-signal regulatory protein α (SIRPα) axis dictates the fate of ingested DNA in DCs for immune evasion. Although macrophages were more potent in uptaking tumor DNA, increase of DNA sensing by blocking the interaction of SIRPα with CD47 preferentially occurred in dendritic cells (DCs) but not in macrophages. Mechanistically, CD47 blockade enabled the activation of NADPH oxidase NOX2 in DCs, which in turn inhibited phagosomal acidification and reduced the degradation of tumor mitochondrial DNA (mtDNA) in DCs. mtDNA was recognized by cyclic-GMP-AMP synthase (cGAS) in the DC cytosol, contributing to type I interferon (IFN) production and antitumor adaptive immunity. Thus, our findings have demonstrated how tumor cells inhibit innate sensing in DCs and suggested that the CD47-SIRPα axis is critical for DC-driven antitumor immunity.
Phosphorylation of NEUROG3 Links Endocrine Differentiation to the Cell Cycle in Pancreatic Progenitors. Developmental cell 2017 APR
Abstract
During pancreatic development, proliferating pancreatic progenitors activate the proendocrine transcription factor neurogenin 3 (NEUROG3), exit the cell cycle, and differentiate into islet cells. The mechanisms that direct robust NEUROG3 expression within a subset of progenitor cells control the size of the endocrine population. Here we demonstrate that NEUROG3 is phosphorylated within the nucleus on serine 183, which catalyzes its hyperphosphorylation and proteosomal degradation. During progression through the progenitor cell cycle, NEUROG3 phosphorylation is driven by the actions of cyclin-dependent kinases 2 and 4/6 at G1/S cell-cycle checkpoint. Using models of mouse and human pancreas development, we show that lengthening of the G1 phase of the pancreatic progenitor cell cycle is essential for proper induction of NEUROG3 and initiation of endocrine cell differentiation. In sum, these studies demonstrate that progenitor cell-cycle G1 lengthening, through its actions on stabilization of NEUROG3, is an essential variable in normal endocrine cell genesis.
更多信息
| Species | Human |
|---|---|
| Contains | • CryoStor® CS10 |
| Cell And Tissue Source | Peripheral Blood |
| Donor Status | Normal |
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PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.
