EasySep™ Mouse PE Positive Selection Kit II

Immunomagnetic positive selection kit

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EasySep™ Mouse PE Positive Selection Kit II

Immunomagnetic positive selection kit

From: 624 USD
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Immunomagnetic positive selection kit
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Product Advantages


  • Fast and easy-to-use

  • No columns required

What's Included

  • EasySep™ Mouse PE Positive Selection Kit II (Catalog #17666)
    • EasySep™ PE Selection Cocktail, 1 mL
    • Mouse FcR Blocker, 0.1 mL
    • EasySep™ Dextran RapidSpheres™, 1 mL
    • RoboSep™ Vial For Primary Conjugated Antibody (not required for manual use), 1 vial
  • RoboSep™ Mouse PE Positive Selection Kit II (Catalog #17666RF)
    • EasySep™ PE Selection Cocktail, 1 mL
    • Mouse FcR Blocker, 0.1 mL
    • EasySep™ Dextran RapidSpheres™, 1 mL
    • RoboSep™ Vial For Primary Conjugated Antibody (not required for manual use), 1 vial
    • RoboSep™ Buffer (Catalog #20104)
    • RoboSep™ Filter Tips (Catalog #20125) x 2
  • EasySep™ Mouse PE Positive Selection Kit II (Catalog #17696)
    • EasySep™ Mouse PE Positive Selection Kit (Catalog #17666) x 5
  • RoboSep™ Mouse PE Positive Selection Kit II (Catalog #17696RF)
    • EasySep™ Mouse PE Positive Selection Kit (Catalog #17666) x 5
    • RoboSep™ Buffer (Catalog #20104) x 5
    • RoboSep™ Filter Tips (Catalog #20125) x 10

Overview

The EasySep™ Mouse PE Positive Selection Kit II is designed to isolate cells that are labeled with PE-conjugated antibodies. Desired cells are targeted with antibody complexes recognizing PE and dextran-coated magnetic particles. Labeled cells are separated using an EasySep™ magnet without the use of columns. Cells of interest remain in the tube while unwanted cells are poured off.

This kit replaces the EasySep™ Mouse PE Positive Selection Kit (Catalog #18554).

For highly purified particle-free cells, we recommend the EasySep™ Release Mouse PE Positive Selection Kit (Catalog #17656).
Magnet Compatibility
• EasySep™ Magnet (Catalog #18000)
• “The Big Easy” EasySep™ Magnet (Catalog #18001)
• EasyEights™ EasySep™ Magnet (Catalog #18103)
• RoboSep™-S (Catalog #21000)
Subtype
Cell Isolation Kits
Cell Type
B Cells, Dendritic Cells, Granulocytes and Subsets, Hematopoietic Stem and Progenitor Cells, Macrophages, Marrow Stromal Cells, Mesenchymal Stem and Progenitor Cells, Monocytes, Mononuclear Cells, Myeloid Cells, NK Cells, Other, Plasma, T Cells
Species
Mouse
Sample Source
Bone Marrow, Other, Spleen
Selection Method
Positive
Application
Cell Isolation
Brand
EasySep, RoboSep
Area of Interest
Immunology

Data Figures

Starting with mouse splenocytes, the purities of the start and final isolated fractions in the above example are 20.5% and 91.6%, respectively, using a PEconjugated anti-mouse CD4 antibody and EasySep™ Mouse PE 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
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Catalog #
17666, 17696
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All
Language
English
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17666RF, 17696RF
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All
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English
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Safety Data Sheet 1
Catalog #
17666, 17696
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All
Language
English
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Safety Data Sheet 2
Catalog #
17666, 17696
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17666, 17696
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17666RF, 17696RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17666RF, 17696RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17666RF, 17696RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 4
Catalog #
17666RF, 17696RF
Lot #
All
Language
English

Resources and Publications

Publications (6)

B7-H3 Suppresses Antitumor Immunity via the CCL2-CCR2-M2 Macrophage Axis and Contributes to Ovarian Cancer Progression. T. Miyamoto et al. Cancer immunology research 2022 jan

Abstract

New approaches beyond PD-1/PD-L1 inhibition are required to target the immunologically diverse tumor microenvironment (TME) in high-grade serous ovarian cancer (HGSOC). In this study, we explored the immunosuppressive effect of B7-H3 (CD276) via the CCL2-CCR2-M2 macrophage axis and its potential as a therapeutic target. Transcriptome analysis revealed that B7-H3 is highly expressed in PD-L1-low, nonimmunoreactive HGSOC tumors, and its expression negatively correlated with an IFN$\gamma$ signature, which reflects the tumor immune reactivity. In syngeneic mouse models, B7-H3 (Cd276) knockout (KO) in tumor cells, but not in stromal cells, suppressed tumor progression, with a reduced number of M2 macrophages and an increased number of IFN$\gamma$+CD8+ T cells. CCL2 expression was downregulated in the B7-H3 KO tumor cell lines. Inhibition of the CCL2-CCR2 axis partly negated the effects of B7-H3 suppression on M2 macrophage migration and differentiation, and tumor progression. In patients with HGSOC, B7-H3 expression positively correlated with CCL2 expression and M2 macrophage abundance, and patients with B7-H3-high tumors had fewer tumoral IFN$\gamma$+CD8+ T cells and poorer prognosis than patients with B7-H3-low tumors. Thus, B7-H3 expression in tumor cells contributes to CCL2-CCR2-M2 macrophage axis-mediated immunosuppression and tumor progression. These findings provide new insights into the immunologic TME and could aid the development of new therapeutic approaches against the unfavorable HGSOC phenotype.
Activated NK cells reprogram MDSCs via NKG2D-NKG2DL and IFN-$\gamma$ to modulate antitumor T-cell response after cryo-thermal therapy. P. Peng et al. Journal for immunotherapy of cancer 2022 dec

Abstract

BACKGROUND Myeloid-derived suppressor cells (MDSCs) can potently inhibit T-cell activity, promote growth and metastasis of tumor and contribute to resistance to immunotherapy. Targeting MDSCs to alleviate their protumor functions and immunosuppressive activities is intimately associated with cancer immunotherapy. Natural killer (NK) cells can engage in crosstalk with multiple myeloid cells to alter adaptive immune responses, triggering T-cell immunity. However, whether the NK-cell-MDSC interaction can modulate the T-cell immune response requires further study. Cryo-thermal therapy could induce the maturation of MDSCs by creating an acute inflammatory environment to elicit a CD4+ Th1-dominant immune response, but the mechanism regulating this process remains unclear. METHODS NK cells were depleted and NKG2D was blocked with monoclonal antibodies in vivo. MDSCs, NK cells and T cells were assessed by flow cytometry and isolated by magnetic-activated cell sorting (MACS). MDSCs and NK cells were cocultured with T cells to determine their immunological function. The transcriptional profiles of MDSCs were measured by qRT-PCR and RNA-sequencing. Isolated NK cells and MDSCs by MACS were cocultured to study the viability and maturation of MDSCs regulated by NK cells. TIMER was used to comprehensively examine the immunological, clinical, and genomic features of tumors. RESULTS NK-cell activation after cryo-thermal therapy decreased MDSC accumulation and reprogrammed immunosuppressive MDSCs toward a mature phenotype to promote T cell antitumor immunity. Furthermore, we discovered that NK cells could kill MDSCs via the NKG2D-NKG2DL axis and promote MDSC maturation by interferon gamma (IFN-$\gamma$) in response to NKG2D. In addition, CD4+ Th1-dominant antitumor immune response was dependent on NKG2D, which promoted the major histocompatibility complex …¡ pathway of MDSCs. High activated NK-cell infiltration and NKG2D level in tumors were positively correlated with better clinical outcomes. CONCLUSIONS Cryo-thermal therapy induces effective CD4+ Th1-dominant antitumor immunity by activating NK cells to reprogram MDSCs, providing a promising therapeutic strategy for cancer immunotherapy.
Multiple metabolic pathways fuel the truncated tricarboxylic acid cycle of the prostate to sustain constant citrate production and secretion. L. Fr\'egeau-Proulx et al. Molecular metabolism 2022 aug

Abstract

OBJECTIVE The prostate is metabolically unique: it produces high levels of citrate for secretion via a truncated tricarboxylic acid (TCA) cycle to maintain male fertility. In prostate cancer (PCa), this phenotype is reprogrammed, making it an interesting therapeutic target. However, how the truncated prostate TCA cycle works is still not completely understood. METHODS We optimized targeted metabolomics in mouse and human organoid models in ex vivo primary culture. We then used stable isotope tracer analyses to identify the pathways that fuel citrate synthesis. RESULTS First, mouse and human organoids were shown to recapitulate the unique citrate-secretory program of the prostate, thus representing a novel model that reproduces this unusual metabolic profile. Using stable isotope tracer analysis, several key nutrients were shown to allow the completion of the prostate TCA cycle, revealing a much more complex metabolic profile than originally anticipated. Indeed, along with the known pathway of aspartate replenishing oxaloacetate, glutamine was shown to fuel citrate synthesis through both glutaminolysis and reductive carboxylation in a GLS1-dependent manner. In human organoids, aspartate entered the TCA cycle at the malate entry point, upstream of oxaloacetate. Our results demonstrate that the citrate-secretory phenotype of prostate organoids is supported by the known aspartate-oxaloacetate-citrate pathway, but also by at least three additional pathways: glutaminolysis, reductive carboxylation, and aspartate-malate conversion. CONCLUSIONS Our results add a significant new dimension to the prostate citrate-secretory phenotype, with at least four distinct pathways being involved in citrate synthesis. Better understanding this distinctive citrate metabolic program will have applications in both male fertility as well as in the development of novel targeted anti-metabolic therapies for PCa.
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