EasySep™ Release Human CD19 Positive Selection Kit

总览

使用EasySep™ Release人CD19正选试剂盒，通过免疫磁珠正选可从新鲜、冻存的外周血单个核细胞或白细胞单采样品中分离出高纯度、无磁珠颗粒的人CD19+细胞。该过程使用抗体复合物和可解离磁珠RapidSpheres™标记目标细胞。标记细胞经EasySep™磁极分选后，未标记细胞被去除，目标细胞保留在管中，再经解离试剂处理去除磁珠。整个过程最快仅需30分钟。CD19抗原在成熟B细胞和B细胞前体上表达，但在分化为浆细胞后丧失表达，也存在于滤泡树突状细胞上。所得CD19+细胞可直接用于流式细胞术、培养或分子实验。

了解更多EasySep™免疫磁性技术或RoboSep™系统。

磁极兼容性
• EasySep™磁极（产品号 #18000）
• “The Big Easy” EasySep™磁极（产品号 #18001）
• EasyPlate™ EasySep™磁极（产品号 #18102）
• EasyEights™ EasySep™磁极（产品号 #18103）

分类
细胞分选试剂盒

细胞类型
B 细胞

种属
人

样本来源
白细胞单采术样本、PBMC

分选方法
正选

品牌
EasySep

研究领域
免疫

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实验数据

Starting with a single-cell suspension of human PBMCs, the CD19+ cell content of the isolated fraction is typically 97.7 ± 2.3% (mean ± SD using the purple EasySep™ Magnet). In the above example, the purities of the start and final isolated fractions are 6.2% and 98.0%, respectively.

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

Product Information Sheet

Product Name

EasySep™ Release Human CD19 Positive Selection Kit

Catalog #

17754

Lot #

All

Language

English

Document Type

Safety Data Sheet 1

Product Name

EasySep™ Release Human CD19 Positive Selection Kit

Catalog #

17754

Lot #

All

Language

English

Document Type

Safety Data Sheet 2

Product Name

EasySep™ Release Human CD19 Positive Selection Kit

Catalog #

17754

Lot #

All

Language

English

Document Type

Safety Data Sheet 3

Product Name

EasySep™ Release Human CD19 Positive Selection Kit

Catalog #

17754

Lot #

All

Language

English

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。

Research Area

Workflow Stages

Workflow Stages for B Cell Research

Cell Sourcing

Cell Isolation

Cell Expansion

Cell Characterization

相关材料与文献

Leukemia-on-a-chip: Dissecting the chemoresistance mechanisms in B cell acute lymphoblastic leukemia bone marrow niche. C. Ma et al. Science advances 2020 oct

Abstract

B cell acute lymphoblastic leukemia (B-ALL) blasts hijack the bone marrow (BM) microenvironment to form chemoprotective leukemic BM niches facilitating chemoresistance and, ultimately, disease relapse. However, the ability to dissect these evolving, heterogeneous interactions among distinct B-ALL subtypes and their varying BM niches is limited with current in vivo methods. Here, we demonstrated an in vitro organotypic leukemia-on-a-chip" model to emulate the in vivo B-ALL BM pathology and comparatively studied the spatial and genetic heterogeneity of the BM niche in regulating B-ALL chemotherapy resistance. We revealed the heterogeneous chemoresistance mechanisms across various B-ALL cell lines and patient-derived samples. We showed that the leukemic perivascular endosteal and hematopoietic niche-derived factors maintain B-ALL survival and quiescence (e.g. CXCL12 cytokine signal VCAM-1/OPN adhesive signals and enhanced downstream leukemia-intrinsic NF-$\kappa$B pathway). Furthermore we demonstrated the preclinical use of our model to test niche-cotargeting regimens which may translate to patient-specific therapy screening and response prediction."

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Fli1 Downregulation in Scleroderma Myeloid Cells Has Profibrotic and Proinflammatory Effects. A. M. Bujor et al. Frontiers in immunology 2020

Abstract

Scleroderma (SSc) is an autoimmune connective tissue disease characterized by immune dysregulation, vasculopathy, and fibrosis. We have previously demonstrated that low Fli1 expression in SSc fibroblasts and endothelial cells plays an important role in SSc pathogenesis. Cells of myeloid and lymphoid origin also express Fli1 and are dysregulated in patients with SSc, playing key roles in disease pathogenesis. However, the role for immune Fli1 in SSc is not yet clear. Our aim was to elucidate whether Fli1 contributes to the immune dysregulation seen in SSc. Comparison of the expression of Fli1 in monocytes, B- and T-cell fractions of PBMCs isolated from SSc patients and healthy controls (HC), showed an increase in Fli1 levels in monocytes. We used siRNA transfected human myeloid cells and mouse peritoneal macrophages obtained from Fli1 flox/flox LysMCre+/+ mice, and found that markers of alternative macrophage activation were increased with Fli1 deletion. Coculture of Fli1-deficient myeloid cells and primary human or mouse fibroblasts resulted in a potent induction of collagen type I, independent of TGF$\beta$ upregulation. We next analyzed global gene expression profile in response to Fli1 downregulation, to gain further insight into the molecular mechanisms of this process and to identify differentially expressed genes in myeloid cells. Of relevance to SSc, the top most upregulated pathways were hallmark IFN-$\gamma$ and IFN-$\alpha$ response. Additionally, several genes previously linked to SSc pathogenesis and fibrosis in general were also induced, including CCL2, CCL7, MMP12, and CXCL10. ANKRD1, a profibrotic transcription co-regulator was the top upregulated gene in our array. Our results show that Fli1-deficient myeloid cells share key features with cells from SSc patients, with higher expression of profibrotic markers and activation of interferon responsive genes, thus suggesting that dysregulation of Fli1 in myeloid cells may contribute to SSc pathogenesis.

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CRISPR/Cas9-Correctable mutation-related molecular and physiological phenotypes in iPSC-derived Alzheimer's PSEN2 N141I neurons. M. Ortiz-Virumbrales et al. Acta neuropathologica communications 2017 dec

Abstract

Basal forebrain cholinergic neurons (BFCNs) are believed to be one of the first cell types to be affected in all forms of AD, and their dysfunction is clinically correlated with impaired short-term memory formation and retrieval. We present an optimized in vitro protocol to generate human BFCNs from iPSCs, using cell lines from presenilin 2 (PSEN2) mutation carriers and controls. As expected, cell lines harboring the PSEN2 N141I mutation displayed an increase in the A$\beta$42/40 in iPSC-derived BFCNs. Neurons derived from PSEN2 N141I lines generated fewer maximum number of spikes in response to a square depolarizing current injection. The height of the first action potential at rheobase current injection was also significantly decreased in PSEN2 N141I BFCNs. CRISPR/Cas9 correction of the PSEN2 point mutation abolished the electrophysiological deficit, restoring both the maximal number of spikes and spike height to the levels recorded in controls. Increased A$\beta$42/40 was also normalized following CRISPR/Cas-mediated correction of the PSEN2 N141I mutation. The genome editing data confirms the robust consistency of mutation-related changes in A$\beta$42/40 ratio while also showing a PSEN2-mutation-related alteration in electrophysiology.

View publication

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物种	人类
Magnet Compatibility	• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyPlate™ Magnet (Catalog #18102) • EasyEights™ Magnet (Catalog #18103)
样本来源	PBMC, 白细胞单采术样本
Selection Method	Positive

EasySep™ Release人CD19 正选试剂盒

产品号 #17754

产品号 #（选择产品）

产品号 #17754_C

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EasySep™ Release人CD19 正选试剂盒

产品号 #17754

产品号 #（选择产品）

产品号 #17754_C

产品优势

产品组分包括

总览

实验数据

产品说明书及文档

应用领域

相关材料与文献

技术资料 (9)

文献 (3)

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