The KDM1B Knockout HAP1 Polyclonal Cells provide a CRISPR/Cas9-mediated polyclonal knockout population in the HAP1 cell line, targeting the KDM1B gene. This heterogeneous pool of cells carries diverse loss-of-function mutations, enabling robust functional analysis while minimizing clonal artifacts. The polyclonal format ensures broad representation of mutations, facilitating reproducible studies of KDM1B-dependent processes.
HAP1 is an adherent near-haploid human cell line derived from KBM-7 chronic myeloid leukemia cells. Its near-haploid karyotype simplifies genetic analysis by reducing allelic complexity, making it ideal for CRISPR screening and knockout studies. Originating from a male donor, HAP1 cells are widely used for functional genomics due to stable growth and compatibility with diverse downstream assays, offering a clean genetic background for epigenetic investigations.
KDM1B encodes a histone demethylase that removes methyl groups from mono- and dimethylated H3K4 (H3K4me1/2), acting as a transcriptional corepressor. Within the CoREST complex, KDM1B interacts with RCOR1 and associates with HDAC1/2 to coordinate chromatin remodeling and gene silencing. Upstream regulation by the CoREST complex and transcription factors directs KDM1B activity toward target genes enriched in H3K4me1/2, including neurodevelopmental regulators and tumor suppressors, thereby controlling transcriptional programs essential for development and disease.
In the HAP1 near-haploid background, KDM1B knockout provides a simplified model to dissect epigenetic regulation without diploid confounding effects. The polyclonal population mitigates off-target concerns and ensures phenotypes reflect genuine loss of function. This system is particularly informative for studying KDM1B in cancer biology, given the chronic myeloid leukemia origin, and for exploring its role in neurodevelopmental gene expression, linking epigenetic changes to developmental disorders.
This knockout model supports applications in epigenetic regulation, functional genomics, cancer epigenetics, drug target validation, and neurodevelopment research. Researchers can characterize KDM1B disruption using assays such as western blotting for H3K4 methylation, ChIP-qPCR for promoter occupancy, RT-qPCR for target gene expression, immunofluorescence for histone marks, and RNA-seq for transcriptome-wide effects. For further information, contact Ascent Research.
