The EasySep™ Human Basophil Isolation Kit is designed to isolate basophils from a polymorphonuclear cell-rich fraction by negative selection. Unwanted cells are targeted for removal with Tetrameric Antibody Complexes recognizing non-basophils and dextran-coated magnetic particles. Labeled cells are separated using an EasySep™ magnet without the use of columns. Desired cells are poured off into a new tube.
The isolation kit is compatible with cells prepared using HetaSep™ (Catalog #07906) sedimentation of fresh peripheral blood.
This product replaces the EasySep™ Human Basophil Enrichment Kit (Catalog #19069) for even faster cell isolations.
The isolation kit is compatible with cells prepared using HetaSep™ (Catalog #07906) sedimentation of fresh peripheral blood.
This product replaces the EasySep™ Human Basophil Enrichment Kit (Catalog #19069) for even faster cell isolations.
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Protocols and Documentation
Find supporting information and directions for use in the Product Information Sheet or explore additional protocols below.
Applications
This product is designed for use in the following research area(s) as part of the highlighted workflow stage(s). Explore these workflows to learn more about the other products we offer to support each research area.
Resources and Publications
Educational Materials (8)
Publications (1)
miR-3934 regulates the apoptosis and secretion of inflammatory cytokines of basophils via targeting RAGE in asthma. Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology 2022 aug
Abstract
BACKGROUND Several miRNAs are now known to have clear connections to the pathogenesis of asthma. The present study focused on the potential role of miR-3934 during asthma development. METHODS miR-3934 was detected as a down-regulated miRNA in basophils by sequencing analysis. Next, the expression levels of miR-3934 in peripheral blood mononuclear cells of 50 asthma patients and 50 healthy volunteers were examined by RT-qPCR methods. The basophils were then treated with AGEs and transfected with miR-3934 mimics. The apoptosis levels were examined by flow cytometry assay; and the expression levels of cytokines were detected using the ELISA kits. Finally, the Western blot was performed to examined the expression of key molecules in the TGF-$\beta$/Smad signaling pathway. RESULTS miR-3934 was down-regulated in the basophils of asthmatic patients. The expression of the pro-inflammatory cytokines IL-6, IL-8 and IL-33 was enhanced in basophils from asthmatic patients, and this effect was partially reversed by transfection of miR-3934 mimics. Furthermore, receiver operating characteristics analysis showed that miR-3934 levels can be used to distinguish asthma patients from healthy individuals. miR-3934 partially inhibited advanced glycation end products-induced increases in basophil apoptosis by suppressing expression of RAGE. CONCLUSION Our results indicate that miR-3934 acts to mitigate the pathogenesis of asthma by targeting RAGE and suppressing TGF-$\beta$/Smad signaling.
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