EasySep™ Human PE Positive Selection Kit II

Immunomagnetic positive selection kit

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EasySep™ Human PE Positive Selection Kit II

Immunomagnetic positive selection kit

From: 765 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™ Human PE Positive Selection Kit II (Catalog #17664)
    • EasySep™ PE Selection Cocktail, 1 mL
    • Anti-Human CD32 FcR Blocker, 1 mL
    • EasySep™ Dextran RapidSpheres™, 1 mL
    • RoboSep™ Vial For Primary Conjugated Antibody (not required for manual use), 1 vial
  • EasySep™ Human PE Positive Selection Kit II (Catalog #17694)
    • EasySep™ Human PE Positive Selection Kit II (Catalog #17664) x 5
  • RoboSep™ Human PE Positive Selection Kit II (Catalog #17664RF)
    • EasySep™ PE Selection Cocktail, 1 mL
    • Anti-Human CD32 FcR Blocker, 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

Overview

The EasySep™ Human PE Positive Selection Kit II is designed to isolate cells that are labeled with PE (phycoerythrin)-conjugated antibodies by positive selection. 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 product replaces the EasySep™ Human PE Positive Selection Kit (Catalog #18551).

For highly purified particle-free cells, we recommend the EasySep™ Release Human PE Positive Selection Kit (Catalog #17654)
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
Human
Sample Source
Buffy Coat, Cord Blood, Leukapheresis, Other, PBMC
Selection Method
Positive
Application
Cell Isolation
Brand
EasySep, RoboSep
Area of Interest
Immunology

Data Figures

Starting with human PBMCs, the purities of the start and final isolated fractions in the above example are 59.1% and 98.7%, respectively, using a PE-conjugated anti-human CD3 antibody and EasySep™ Human 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
Catalog #
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Language
Catalog #
17664, 17694
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All
Language
English
Catalog #
17664RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17664
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17664, 17694
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17664, 17694
Lot #
All
Language
English
Document Type
Safety Data Sheet 1
Catalog #
17664RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 2
Catalog #
17664RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 3
Catalog #
17664RF
Lot #
All
Language
English
Document Type
Safety Data Sheet 4
Catalog #
17664RF
Lot #
All
Language
English

Resources and Publications

Publications (2)

Clostridium perfringens $\alpha$-toxin up-regulates plasma membrane CD11b expression on murine neutrophils by changing intracellular localization. M. Takehara et al. Biochimica et biophysica acta. Biomembranes 2022 dec

Abstract

Gas gangrene caused by Clostridium perfringens type A infection is a highly lethal infection of soft tissue characterized by rapid spread of tissue necrosis. This tissue destruction is related to profound attenuation of blood flow accompanied by formation of platelet-leukocyte aggregates in the blood vessels. Several studies have identified $\alpha$-toxin, which has both sphingomyelinase and phospholipase C activities, as a major virulence factor in the aggregate formation via activation of the platelet gpIIbIIIa. Here, we show that $\alpha$-toxin greatly and rapidly increases plasma membrane localization of CD11b, which binds to the platelet gpIIbIIIa via fibrinogen, in mouse neutrophils. Interestingly, short-term treatment of $\alpha$-toxin has little effect on gene expression profiles in neutrophils, and the toxin does not change the total protein expression levels of CD11b in whole cell lysates. The following analysis demonstrated that CD11b localizes to intracellular vesicles in intact cells, but the localization changed to the cytoplasmic membrane in $\alpha$-toxin-treated cells. These results suggest that CD11b is recruited to the cytoplasmic membrane by $\alpha$-toxin. Previously, we reported that $\alpha$-toxin promotes the formation of ceramide by its sphingomyelinase activity in mouse neutrophils. Interestingly, a synthetic cell-permeable ceramide analog, C2-ceramide, increases plasma membrane localization of CD11b, suggesting that ceramide production by $\alpha$-toxin recruits CD11b to the cytoplasmic membrane to promote platelet-leukocyte aggregation. Together, our results illustrate that the increase of cell membrane CD11b expression by $\alpha$-toxin might be crucial for the pathogenesis of C. perfringens to promote formation of platelet-leukocyte aggregates, leading to rapid tissue necrosis due to ischemia.
Endothelin-A Receptor Antagonist Alleviates Allergic Airway Inflammation via the Inhibition of ILC2 Function. X. Zhang et al. Frontiers in immunology 2022

Abstract

Allergic airway inflammation is a universal airway disease that is driven by hyperresponsiveness to inhaled allergens. Group 2 innate lymphoid cells (ILC2s) produce copious amounts of type 2 cytokines, which lead to allergic airway inflammation. Here, we discovered that both peripheral blood of human and mouse lung ILC2s express the endothelin-A receptor (ETAR), and the expression level of ETAR was dramatically induced upon interleukin-33 (IL-33) treatment. Subsequently, both preventive and therapeutic effects of BQ123, an ETAR antagonist, on allergic airway inflammation were observed, which were associated with decreased proliferation and type 2 cytokine productions by ILC2s. Furthermore, ILC2s from BQ123 treatment were found to be functionally impaired in response to an interleukin IL-33 challenged. And BQ123 treatment also affected the phosphorylation level of the extracellular signal-regulated kinase (ERK), as well as the level of GATA binding protein 3 (GATA3) in activated ILC2s. Interestingly, after BQ123 treatment, both mouse and human ILC2s in vitro exhibited decreased function and downregulation of ERK signaling and GATA3 stability. These observations imply that ETAR is an important regulator of ILC2 function and may be involved in ILC2-driven pulmonary inflammation. Therefore, blocking ETAR may be a promising therapeutic strategy for allergic airway inflammation.
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