The CBX6 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for studying CBX6 loss-of-function. This pool of HAP1 cells contains diverse CBX6 gene disruptions introduced by CRISPR/Cas9, avoiding clonal selection and enabling robust functional genomics analysis without clone-specific artifacts. The polyclonal format preserves heterogeneity for pooled screening applications and comparative expression studies.
HAP1 cells are a near-haploid human myeloid line derived from KBM-7 chronic myeloid leukemia, expressing BCR-ABL1. Their stable haploidy makes them ideal for genetic screens, particularly loss-of-function screens, and their myeloid origin supports investigation of leukemia biology and epigenetic regulation. This background provides a unique platform for dissecting gene function in a simplified genomic context.
CBX6 is a chromodomain-containing subunit of PRC1 that binds H3K27me3, the repressive mark laid down by PRC2 (EZH2, SUZ12, EED). It collaborates with PRC1 partners RING1A/B, PHC proteins, and PCGF factors to compact chromatin and silence target genes. CBX6 functions downstream of EZH2 and BMI1, and its activity represses HOX clusters, developmental genes, and tumor suppressors. Aberrant CBX6 expression contributes to oncogenic silencing, linking PRC2 activity to transcriptional repression.
In the HAP1 model, CBX6 knockout relieves PRC1-mediated repression, enabling interrogation of polycomb target derepression in a haploid background suitable for high-throughput screens. This system is particularly valuable for cancer epigenetics, as CBX6 is implicated in breast cancer, hepatocellular carcinoma, and AML, allowing dissection of oncogenic mechanisms and evaluation of therapeutic agents targeting polycomb repression.
Applications include ChIP-qPCR for H3K27me3, RT-qPCR for HOX gene expression, western blot analysis of PRC1/2 complexes, and RNA-seq transcriptomics. Functional assays such as clonogenic survival and drug sensitivity screening can assess epigenetic vulnerabilities. These cells support synthetic lethal screens and PRC1 complex characterization in leukemia. For further information, please contact Ascent Research.
