StemSep™ Human CD34 Positive Selection Cocktail

Immunomagnetic column-based positive selection kit

More Views

StemSep™ Human CD34 Positive Selection Cocktail

Contact for availability

2 x 109 cells
Catalog #14756

StemSep™ Human CD34 Positive Selection Cocktail

Contact for availability

1 x 1010 cells
Catalog #14766

Required Products

Overview

The StemSep™ Human CD34 Positive Selection Cocktail is designed to isolate CD34+ cells from fresh or previously frozen bone marrow, cord blood, or mobilized peripheral blood mononuclear cells by positive selection. Desired cells are targeted with Tetrameric Antibody Complexes recognizing CD34 and dextran-coated magnetic particles. The cocktail also contains an antibody to human Fc receptor to minimize nonspecific binding. Labeled cells are then separated using StemSep™ Columns and Magnets. The CD34 antigen is expressed on hematopoietic stem and progenitor cells.
Components:
  • StemSep™ Human CD34 Positive Selection Cocktail (Catalog #14756)
    • StemSep™ Human CD34 Selection Cocktail, 1 mL
    • StemSep™ Magnetic Colloid, 1.5 mL
  • StemSep™ Human CD34 Positive Selection Cocktail (Catalog #14766)
    • StemSep™ Human CD34 Selection Cocktail, 5 x 1 mL
    • StemSep™ Magnetic Colloid, 4 x 1.5 mL
Magnet Compatibility:
• StemSep™ Magnet (Catalog #11030, 11050, 11060 11070) or a magnet with the strength of at least 0.6 Tesla
• Commercially available positive selection columns
Subtype:
Cell Isolation Kits
Cell Type:
Hematopoietic Stem and Progenitor Cells
Species:
Human
Sample Source:
Bone Marrow; Cord Blood; PBMC
Selection Method:
Positive
Application:
Cell Isolation
Brand:
StemSep
Area of Interest:
Immunology; Stem Cell Biology

Scientific Resources

Educational Materials

(2)

Product 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.

Data and Publications

Publications

(1)
Cancer research 2011 FEB

BCR/ABL stimulates WRN to promote survival and genomic instability.

Slupianek A et al.

Abstract

BCR/ABL-transformed chronic myeloid leukemia (CML) cells accumulate numerous DNA double-strand breaks (DSB) induced by reactive oxygen species (ROS) and genotoxic agents. To repair these lesions BCR/ABL stimulate unfaithful DSB repair pathways, homologous recombination repair (HRR), nonhomologous end-joining (NHEJ), and single-strand annealing (SSA). Here, we show that BCR/ABL enhances the expression and increase nuclear localization of WRN (mutated in Werner syndrome), which is required for processing DSB ends during the repair. Other fusion tyrosine kinases (FTK), such as TEL/ABL, TEL/JAK2, TEL/PDGFβR, and NPM/ALK also elevate WRN. BCR/ABL induces WRN mRNA and protein expression in part by c-MYC-mediated activation of transcription and Bcl-xL-dependent inhibition of caspase-dependent cleavage, respectively. WRN is in complex with BCR/ABL resulting in WRN tyrosine phosphorylation and stimulation of its helicase and exonuclease activities. Activated WRN protects BCR/ABL-positive cells from the lethal effect of oxidative and genotoxic stresses, which causes DSBs. In addition, WRN promotes unfaithful recombination-dependent repair mechanisms HRR and SSA, and enhances the loss of DNA bases during NHEJ in leukemia cells. In summary, we postulate that BCR/ABL-mediated stimulation of WRN modulates the efficiency and fidelity of major DSB repair mechanisms to protect leukemia cells from apoptosis and to facilitate genomic instability.
STEMCELL TECHNOLOGIES INC.’S QUALITY MANAGEMENT SYSTEM IS CERTIFIED TO ISO 13485. PRODUCTS ARE FOR RESEARCH USE ONLY AND NOT INTENDED FOR HUMAN OR ANIMAL DIAGNOSTIC OR THERAPEUTIC USES UNLESS OTHERWISE STATED.