The CD34 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted population designed for loss-of-function studies of CD34 in a human haploid background. Supplied as a heterogeneous polyclonal pool, this product provides target-gene disruption without monoclonal isolation, enabling cost-effective functional genomics and pathway analysis.
The HAP1 host line is a near-haploid suspension cell line derived from the KBM-7 chronic myeloid leukemia model. Its largely haploid karyotype simplifies genetic manipulation by eliminating diploid allele complications. Suspension growth supports scalable culture, and the leukemic origin renders it pertinent to myeloid and stem cell biology investigations.
CD34 encodes a sialomucin that acts as a hematopoietic stem cell marker and adhesion molecule. It interacts with L-selectin to recruit the adaptor CrkL, which engages Src family kinases and drives actin cytoskeleton reorganization and cell polarization. Upstream, CD34 expression is transcriptionally regulated by RUNX1 and GATA2, and modulated by KITLG/SCF signaling, positioning CD34 as an integrator of niche-derived signals and cellular adhesion dynamics.
In the HAP1 context, CD34 disruption creates a model to dissect leukemic cell adhesion, migration, and stem cell maintenance. This knockout is relevant to acute myeloid leukemia, myelodysplastic syndromes, and stem cell disorders, and the haploid background facilitates genetic interaction screens and synthetic lethality studies that explore compensatory pathways.
Applications include flow cytometry for CD34 loss, Western blotting and RT-qPCR for knockout confirmation, transwell migration assays, immunofluorescence for cytoskeletal architecture, RNA-seq transcriptomics, and CRISPR viability screens. These support hematopoietic stem cell research, leukemia biology, adhesion studies, and drug target discovery. For further information, please contact Ascent Research.
