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EasySep™ PE正选试剂盒 II

PE 偶联抗体标记细胞的免疫磁珠正选
只有 %1
¥6,834.00

产品号 #(选择产品)

产品号 #17684_C

PE 偶联抗体标记细胞的免疫磁珠正选

产品优势

  • 快捷、操作简单          
  • 无需分离柱

产品组分包括

  • EasySep™ PE 正选试剂盒 II(产品号 #17684)
    • EasySep™ PE分选抗体混合物,1 mL
    • EasySep™ Dextran RapidSpheres™磁珠,1 mL
    • RoboSep™ 偶联一抗专用管(手动操作无需使用),1支
  • RoboSep™ PE正选 试剂盒 II (产品号 #17684RF)
    • EasySep™ PE分选抗体混合物,1 mL
    • EasySep™ Dextran RapidSpheres™磁珠,1 mL
    • RoboSep™ 偶联一抗专用管(手动操作无需使用),1支
    • RoboSep™ 缓冲液(产品号 #20104)
    • RoboSep™ 过滤吸头(产品号 #20125)x 2
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》

总览

使用EasySep™ PE正选 试剂盒 II,通过免疫磁珠正选,可从任何单细胞悬液样本中分离高纯度的藻红蛋白(PE)偶联抗体标记的细胞。EasySep™结合了单克隆抗体的特异性和无柱磁性系统的简便性,迄今已广泛应用于发表的研究中超过20年。    

在此EasySep™正选过程中,目的细胞被识别PE的抗体复合物和磁珠结合标记,使用EasySep™进行无柱分选,只需倾倒或吸弃非目的 细胞,目标细胞则保留在管中。磁珠分选获得的PE阳性细胞即可用于下游应用。

该产品可替代EasySep™PE 正选试剂盒 (产品号 #18557) 以进行更快的细胞分选。

了解更多关于免疫磁珠EasySep™技术的工作原理,或如何通过RoboSep™实现全自动化免疫磁珠细胞分选。探索更多优化您实验流程的产品,包括培养基、添加剂、抗体等。

磁极兼容性
• EasySep™磁极(产品号 #18000)
• “The Big Easy” EasySep™磁极(产品号 #18001)
• EasyEights™ EasySep™磁极(产品号 #18103)
• RoboSep™-S(产品号 #21000)
 
分类
细胞分选试剂盒
 
细胞类型
B 细胞,树突状细胞(DCs),粒细胞及其亚群,造血干/祖细胞,巨噬细胞,骨髓基质细胞,间充质干/祖细胞,单核细胞,单个核细胞,髓系细胞,NK 细胞,其他组织,血浆,T 细胞
 
种属
非人灵长类,其他组织,大鼠
 
样本来源
骨髓,白膜层,脐带血,白细胞单采术样本,其他组织,PBMC,外周血,脾脏
 
分选方法
正选
 
应用
细胞分选
 
品牌
EasySep,RoboSep
 
研究领域
免疫
 

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。

Document Type
Product Name
Catalog #
Lot #
Language
Document Type
产品说明书
Catalog #
17684RF
Lot #
All
Language
中文
Document Type
产品说明书
Catalog #
17684
Lot #
All
Language
中文
Catalog #
17684
Lot #
All
Language
English
Catalog #
17684RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17684
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17684
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17684RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17684RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17684RF
Lot #
All
Language
English

相关材料与文献

技术资料 (6)

文献 (10)

HIV-1 reservoirs in urethral macrophages of patients under suppressive antiretroviral therapy. Y. Ganor et al. Nature microbiology 2019 feb

Abstract

Human immunodeficiency virus type 1 (HIV-1) eradication is prevented by the establishment on infection of cellular HIV-1 reservoirs that are not fully characterized,especially in genital mucosal tissues (the main HIV-1 entry portal on sexual transmission). Here,we show,using penile tissues from HIV-1-infected individuals under suppressive combination antiretroviral therapy,that urethral macrophages contain integrated HIV-1 DNA,RNA,proteins and intact virions in virus-containing compartment-like structures,whereas viral components remain undetectable in urethral T cells. Moreover,urethral cells specifically release replication-competent infectious HIV-1 following reactivation with the macrophage activator lipopolysaccharide,while the T-cell activator phytohaemagglutinin is ineffective. HIV-1 urethral reservoirs localize preferentially in a subset of polarized macrophages that highly expresses the interleukin-1 receptor,CD206 and interleukin-4 receptor,but not CD163. To our knowledge,these results are the first evidence that human urethral tissue macrophages constitute a principal HIV-1 reservoir. Such findings are determinant for therapeutic strategies aimed at HIV-1 eradication.
Myeloid cell-targeted miR-146a mimic inhibits NF-$\kappa$B-driven inflammation and leukemia progression in vivo. Y.-L. Su et al. Blood 2020 jan

Abstract

NF-$\kappa$B is a key regulator of inflammation and cancer progression,with an important role in leukemogenesis. Despite its therapeutic potential,targeting NF-$\kappa$B using pharmacologic inhibitors has proven challenging. Here,we describe a myeloid cell-selective NF-$\kappa$B inhibitor using an miR-146a mimic oligonucleotide conjugated to a scavenger receptor/Toll-like receptor 9 agonist (C-miR146a). Unlike an unconjugated miR146a,C-miR146a was rapidly internalized and delivered to the cytoplasm of target myeloid cells and leukemic cells. C-miR146a reduced expression of classic miR-146a targets (IRAK1 and TRAF6),thereby blocking activation of NF-$\kappa$B in target cells. IV injections of C-miR146a mimic to miR-146a-deficient mice prevented excessive NF-$\kappa$B activation in myeloid cells,and thus alleviated myeloproliferation and mice hypersensitivity to bacterial challenge. Importantly,C-miR146a showed efficacy in dampening severe inflammation in clinically relevant models of chimeric antigen receptor (CAR) T-cell-induced cytokine release syndrome. Systemic administration of C-miR146a oligonucleotide alleviated human monocyte-dependent release of IL-1 and IL-6 in a xenotransplanted B-cell lymphoma model without affecting CD19-specific CAR T-cell antitumor activity. Beyond anti-inflammatory functions,miR-146a is a known tumor suppressor commonly deleted or expressed at reduced levels in human myeloid leukemia. Using The Cancer Genome Atlas acute myeloid leukemia data set,we found an inverse correlation of miR-146a levels with NF-$\kappa$B-related genes and with patient survival. Correspondingly,C-miR146a induced cytotoxic effects in human MDSL,HL-60,and MV4-11 leukemia cells in vitro. The repeated IV administration of C-miR146a inhibited expression of NF-$\kappa$B target genes and thereby thwarted progression of disseminated HL-60 leukemia. Our results show the potential of using myeloid cell-targeted miR-146a mimics for the treatment of inflammatory and myeloproliferative disorders.
Intestinal Macrophages Balance Inflammatory Expression Profiles via Vitamin A and Dectin-1-Mediated Signaling. M. N. Erkelens et al. Frontiers in immunology 2020

Abstract

Tissue resident intestinal macrophages are known to exhibit an anti-inflammatory phenotype and produce little pro-inflammatory cytokines upon TLR ligation,allowing symbiotic co-existence with the intestinal microbiota. However,upon acute events such as epithelial damage and concomitant influx of microbes,these macrophages must be able to quickly mount a pro-inflammatory response while more inflammatory macrophages are recruited from the blood stream simultaneously. Here,we show that dietary intake of vitamin A is required for the maintenance of the anti-inflammatory state of tissue resident intestinal macrophages. Interestingly,these anti-inflammatory macrophages were characterized by high levels of Dectin-1 expression. We show that Dectin-1 expression is enhanced by the vitamin A metabolite retinoic acid and our data suggests that Dectin-1 triggering might provide a switch to induce a rapid production of pro-inflammatory cytokines. In addition,Dectin-1 stimulation resulted in an altered metabolic profile which is linked to a pro-inflammatory response. Together,our data suggests that presence of vitamin A in the small intestine enhances an anti-inflammatory phenotype as well as Dectin-1 expression by macrophages and that this anti-inflammatory phenotype can rapidly convert toward a pro-inflammatory state upon Dectin-1 signaling.

更多信息

更多信息
物种 其它物种, 大鼠, 非人灵长类
Magnet Compatibility • EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyEights™ EasySep™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
样本来源 PBMC, 其它细胞系, 外周血, 白细胞单采术样本, 白膜层, 脐带血, 脾脏, 骨髓
Selection Method Positive
法律声明:

Users of this kit should ensure that they are entitled to use the antibody of interest. STEMCELL Technologies Inc. is not responsible for patent infringements or violations that may occur when using this product. 质量保证:

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