EasySep™人CD45去除试剂盒II

免疫磁珠法去除人CD45+细胞

产品号 #(选择产品)

产品号 #17898_C

免疫磁珠法去除人CD45+细胞

产品优势

  • 快捷、操作简单,且无需分离柱
  • CD45+细胞的去除效率高达4 log
  • 分选得到的细胞不带标记

产品组分包括

  • EasySep™人CD45去除     试剂盒II(产品号#17898)
    • EasySep™人CD45去除抗体混合物II,1mL
    • EasySep™ Dextran RapidSpheres™ 磁珠,2x1mL
  • RoboSep™人CD45去除试剂盒II  (产品号#17898RF)
    • EasySep™人CD45去除抗体混合物II,1mL
    • EasySep™ Dextran RapidSpheres™  磁珠,2x1mL
    • RoboSep™ 缓冲液(产品号 #20104)
    • RoboSep™过滤吸头(产品号20125)
New look, same high quality and support! You may notice that your instrument or reagent packaging looks slightly different from images displayed on the website, or from previous orders. We are updating our look but rest assured, the products themselves and how you should use them have not changed. Learn more

总览

使用EasySep™人CD45去除试剂盒II,可通过免疫磁珠选择高效去除新鲜或冻存人外周血单个核细胞(PBMC)样本中的CD45+细胞。EasySep™技术结合单克隆抗体的特异性和免分离柱系统的简便性,已在发表的研究中广泛应用超过20年。

此简单优化的EasySep™流程包含用可以识别CD45的抗体复合物和磁珠标记细胞,之后标记的细胞通过EasySep™磁铁分离,最后只需通过简单倾倒去除未标记细胞即可。CD45细胞保留在管中。分选后的细胞可立即用于下游应用,例如流式细胞术、培养或DNA/RNA 提取。CD45抗原在除红细胞和血小板外的所有血源细胞上表达。

该产品可替代EasySep™人CD45去除试剂盒 (产品号 #18259) 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™实现免疫磁珠细胞分选全自动化。探索更多产品优化您的实验流程优化,包括培养基、添加剂、抗体等。

磁体兼容性
• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • RoboSep™-S (Catalog #21000)
 
亚型
细胞分选试剂盒
 
细胞类型
癌细胞及细胞系
 
种属

 
样本来源
PBMC
 
筛选方法
删除
 
应用
细胞分选
 
品牌
EasySep,RoboSep
 
研究领域
癌症,免疫,干细胞生物学
 

Data Figures

Typical EasySep™ Human CD45 Depletion Profile

Figure 1. Typical EasySep™ Human CD45 Depletion Profile

In the example above, CAMA cells were seeded into PBMCs at a starting frequency of 1.1% (98.9% CD45+; gated on DRAQ5™ for nucleated cells). The CAMA cell (EpCAM+) content of the depleted fraction is 98%, which is a 4.0 log depletion of CD45+ cells.
NOTE: EpCAM is an antibody against an epithelial cell surface antigen expressed on CAMA cells.

Protocols and Documentation

Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.

Document Type
Product Name
Catalog #
Lot #
Language
Catalog #
17898RF
Lot #
All
Language
English
Catalog #
17898
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17898RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17898RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17898RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17898
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17898
Lot #
All
Language
English

Resources and Publications

Educational Materials (5)

Publications (5)

Pseudo-mutant P53 is a unique phenotype of DNMT3A-mutated pre-leukemia. A. Tuval et al. Haematologica 2022 nov

Abstract

Pre-leukemic clones carrying DNMT3A mutations have a selective advantage and an inherent chemoresistance, however the basis for this phenotype has not been fully elucidated. Mutations affecting the gene TP53 occur in pre-leukemic hematopoietic stem/progenitor cells (preL-HSPC) and lead to chemoresistance. Many of these mutations cause a conformational change and some of them were shown to enhance self-renewal capacity of preL-HSPC. Intriguingly, a misfolded P53 was described in AML blasts that do not harbor mutations in TP53, emphasizing the dynamic equilibrium between wild-type (WT) and pseudo-mutant" conformations of P53. By combining single cell analyses and P53 conformation-specific monoclonal antibodies we studied preL-HSPC from primary human DNMT3A-mutated AML samples. We found that while leukemic blasts express mainly the WT conformation in preL-HSPC the pseudo-mutant conformation is the dominant. HSPC from non-leukemic samples expressed both conformations to a similar extent. In a mouse model we found a small subset of HSPC with a dominant pseudo-mutant P53. This subpopulation was significantly larger among DNMT3AR882H-mutated HSPC suggesting that while a pre-leukemic mutation can predispose for P53 misfolding additional factors are involved as well. Treatment with a short peptide that can shift the dynamic equilibrium favoring the WT conformation of P53 specifically eliminated preL-HSPC that had dysfunctional canonical P53 pathway activity as reflected by single cell RNA sequencing. Our observations shed light upon a possible targetable P53 dysfunction in human preL-HSPC carrying DNMT3A mutations. This opens new avenues for leukemia prevention."
CD70 as an actionable immunotherapeutic target in recurrent glioblastoma and its microenvironment. M. Seyfrid et al. Journal for immunotherapy of cancer 2022 jan

Abstract

PURPOSE Glioblastoma (GBM) patients suffer from a dismal prognosis, with standard of care therapy inevitably leading to therapy-resistant recurrent tumors. The presence of cancer stem cells (CSCs) drives the extensive heterogeneity seen in GBM, prompting the need for novel therapies specifically targeting this subset of tumor-driving cells. Here, we identify CD70 as a potential therapeutic target for recurrent GBM CSCs. EXPERIMENTAL DESIGN In the current study, we identified the relevance and functional influence of CD70 on primary and recurrent GBM cells, and further define its function using established stem cell assays. We use CD70 knockdown studies, subsequent RNAseq pathway analysis, and in vivo xenotransplantation to validate CD70's role in GBM. Next, we developed and tested an anti-CD70 chimeric antigen receptor (CAR)-T therapy, which we validated in vitro and in vivo using our established preclinical model of human GBM. Lastly, we explored the importance of CD70 in the tumor immune microenvironment (TIME) by assessing the presence of its receptor, CD27, in immune infiltrates derived from freshly resected GBM tumor samples. RESULTS CD70 expression is elevated in recurrent GBM and CD70 knockdown reduces tumorigenicity in vitro and in vivo. CD70 CAR-T therapy significantly improves prognosis in vivo. We also found CD27 to be present on the cell surface of multiple relevant GBM TIME cell populations, notably putative M1 macrophages and CD4 T cells. CONCLUSION CD70 plays a key role in recurrent GBM cell aggressiveness and maintenance. Immunotherapeutic targeting of CD70 significantly improves survival in animal models and the CD70/CD27 axis may be a viable polytherapeutic avenue to co-target both GBM and its TIME.
Association of early changes of circulating cancer stem-like cells with survival among patients with metastatic breast cancer. P.-H. Chang et al. Therapeutic advances in medical oncology 2022

Abstract

BACKGROUND This study aimed to investigate the role of circulating tumor cells (CTCs) and circulating cancer stem-like cells (cCSCs) before and after one cycle of chemotherapy and assessed the effects of early changes in CTCs and cCSCs on the outcomes of patients with metastatic breast cancer. METHODS Patients with stage IV invasive ductal carcinoma of the breast who received first-line chemotherapy between April 2014 and January 2016 were enrolled. CTCs and cCSCs were measured before the first cycle of chemotherapy (baseline) and on day 21, before the second cycle of chemotherapy commenced; a negative selection strategy and flow cytometry protocol were employed. RESULTS CTC and cCSC counts declined in 68.8 and 45.5% of patients, respectively. Declines in CTCs and cCSCs following the first chemotherapy cycle were associated with superior chemotherapy responses, longer progression-free survival (PFS), and longer overall survival (OS). An early decline in cCSCs remained an independent prognostic indicator for OS and PFS in multivariate analysis. CONCLUSIONS A cCSC decline after one cycle of chemotherapy for metastatic breast cancer is predictive of a superior chemotherapy response and longer PFS and OS, implying that cCSC dynamic monitoring may be helpful in early prediction of treatment response and prognosis.

更多信息

更多信息
Species Human
Magnet Compatibility • EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • RoboSep™-S (Catalog #21000)
Sample Source PBMC
Selection Method Depletion
标记抗体
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