EasySep™小鼠FITC正选试剂盒II

免疫磁珠正选细胞试剂盒

产品号 #(选择产品)

产品号 #17668_C

免疫磁珠正选细胞试剂盒

产品优势

  • 快速、简单
  • 无需分离柱

产品组分包括

  • EasySep™小鼠FITC正选试剂盒II(产品号 #17668)
    • EasySep™ FITC分选抗体混合物,1 mL
    • 小鼠FcR阻断剂,0.1 mL    
    • EasySep™ Dextran RapidSpheres™磁珠,1 mL
    • RoboSep™ 一抗偶联物专用管(手动操作无需使用),1支
  • EasySep™小鼠FITC     正选试剂盒II(产品号 #17668)
    • EasySep™ FITC分选抗体混合物,1 mL
    • 小鼠FcR阻断剂,0.1 mL    
    • EasySep™ Dextran RapidSpheres™磁珠,1 mL
    • RoboSep™ 一抗偶联物专用管(手动操作无需使用),1支
    • RoboSep™ 缓冲液(产品号 #20104)x 2
    • RoboSep™过滤枪头(目录号20125)x 2
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总览

EasySep™小鼠FITC阳性分选试剂盒II专为分选经FITC偶联抗体标记的小鼠细胞而设计。目的细胞被FITC抗体复合物和磁珠标记,使用EasySep™磁极分选被标记的细胞,无需使用分离柱。目的细胞被保留在试管中,而非目的细胞被倾倒出。

本产品替代EasySep™小鼠FITC阳性分选试剂盒(产品号 #18555)。

磁体兼容性
• EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyEights™ EasySep™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
 
亚型
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,其它细胞系,血浆,T 细胞
 
种属
小鼠
 
样本来源
Bone Marrow,其它细胞系,Spleen
 
筛选方法
Positive
 
应用
细胞分选
 
品牌
EasySep,RoboSep
 
研究领域
免疫
 

Data Figures

Starting with mouse splenocytes, the purities of the start and final isolated fractions in the above example are 24.3% and 95.3%, respectively, using a FITCconjugated anti-mouse CD4 antibody and EasySep™ Mouse FITC Positive Selection Kit II.

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 #
17668
Lot #
All
Language
English
Catalog #
17668RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17668
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17668
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17668
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17668RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17668RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17668RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 4
Catalog #
17668RF
Lot #
All
Language
English

Resources and Publications

Educational Materials (6)

Publications (2)

Accumulation of ?? T cells in visceral fat with aging promotes chronic inflammation. M. E. C. Bruno et al. GeroScience 2022 jun

Abstract

Adipose tissue dysfunction is strongly linked to the development of chronic inflammation and cardiometabolic disorders in aging. While much attention has been given to the role of resident adipose tissue immune cells in the disruption of homeostasis in obesity, age-specific effects remain understudied. Here, we identified and characterized a population of ?? T cells, which show unique age-dependent accumulation in the visceral adipose tissue (VAT) of both mice and humans. Diet-induced obesity likewise increased ?? T cell numbers; however, the effect was greater in the aged where the increase was independent of fat mass. ?? T cells in VAT express a tissue-resident memory T cell phenotype (CD44hiCD62LlowCD69+) and are predominantly IL-17A-producing cells. Transcriptome analyses of immunomagnetically purified ?? T cells identified significant age-associated differences in expression of genes related to inflammation, immune cell composition, and adipocyte differentiation, suggesting age-dependent qualitative changes in addition to the quantitative increase. Genetic deficiency of ?? T cells in old age improved the metabolic phenotype, characterized by increased respiratory exchange ratio, and lowered levels of IL-6 both systemically and locally in VAT. Decreased IL-6 was predominantly due to reduced production by non-immune stromal cells, primarily preadipocytes, and adipose-derived stem cells. Collectively, these findings suggest that an age-dependent increase of tissue-resident ?? T cells in VAT contributes to local and systemic chronic inflammation and metabolic dysfunction in aging.
Combinatorial depletions of G-protein coupled receptor kinases in immune cells identify pleiotropic and cell type-specific functions. K. M. Glaser et al. Frontiers in immunology 2022

Abstract

G-protein coupled receptor kinases (GRKs) participate in the regulation of chemokine receptors by mediating receptor desensitization. They can be recruited to agonist-activated G-protein coupled receptors (GPCRs) and phosphorylate their intracellular parts, which eventually blocks signal propagation and often induces receptor internalization. However, there is growing evidence that GRKs can also control cellular functions beyond GPCR regulation. Immune cells commonly express two to four members of the GRK family (GRK2, GRK3, GRK5, GRK6) simultaneously, but we have very limited knowledge about their interplay in primary immune cells. In particular, we are missing comprehensive studies comparing the role of this GRK interplay for (a) multiple GPCRs within one leukocyte type, and (b) one specific GPCR between several immune cell subsets. To address this issue, we generated mouse models of single, combinatorial and complete GRK knockouts in four primary immune cell types (neutrophils, T cells, B cells and dendritic cells) and systematically addressed the functional consequences on GPCR-controlled cell migration and tissue localization. Our study shows that combinatorial depletions of GRKs have pleiotropic and cell-type specific effects in leukocytes, many of which could not be predicted. Neutrophils lacking all four GRK family members show increased chemotactic migration responses to a wide range of GPCR ligands, whereas combinatorial GRK depletions in other immune cell types lead to pro- and anti-migratory responses. Combined depletion of GRK2 and GRK6 in T cells and B cells shows distinct functional outcomes for (a) one GPCR type in different cell types, and (b) different GPCRs in one cell type. These GPCR-type and cell-type specific effects reflect in altered lymphocyte chemotaxis in vitro and localization in vivo. Lastly, we provide evidence that complete GRK deficiency impairs dendritic cell homeostasis, which unexpectedly results from defective dendritic cell differentiation and maturation in vitro and in vivo. Together, our findings demonstrate the complexity of GRK functions in immune cells, which go beyond GPCR desensitization in specific leukocyte types. Furthermore, they highlight the need for studying GRK functions in primary immune cells to address their specific roles in each leukocyte subset.

更多信息

更多信息
Species Mouse
Magnet Compatibility • EasySep™ Magnet (Catalog #18000) • “The Big Easy” EasySep™ Magnet (Catalog #18001) • EasyEights™ EasySep™ Magnet (Catalog #18103) • RoboSep™-S (Catalog #21000)
Sample Source Bone Marrow, Other, Spleen
Selection Method Positive
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