CBX7 Knockout HAP1 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population in which the CBX7 gene has been disrupted via CRISPR/Cas9-mediated gene targeting. CBX7 encodes a chromodomain-containing protein that functions as a critical component of Polycomb repressive complex 1 (PRC1), a key epigenetic regulator of gene silencing. This polyclonal model, generated in the near-haploid human HAP1 cell line, provides a heterogeneous pool of cells with loss-of-function mutations, enabling robust investigation of CBX7-dependent transcriptional control without the constraints of clonal selection. The live cells are ready for downstream functional assays.
HAP1 cells are derived from the KBM-7 chronic myeloid leukemia (CML) blast crisis cell line and exhibit a near-haploid karyotype, with the exception of disomy for chromosome 8. This haploid genetic background simplifies genetic manipulation and phenotypic analysis by eliminating complications from diploid gene redundancy, making HAP1 an ideal host for knockout screens and mechanistic studies of gene function. The CML origin of HAP1 cells additionally provides a disease-relevant context for oncogenic signaling and tumor-suppressor pathways.
CBX7 functions as a transcriptional repressor by binding trimethylated histone H3 lysine 27 (H3K27me3) via its chromodomain and is an integral subunit of canonical PRC1 complexes, interacting with RING1B, BMI1, RYBP, and PHC1 to silence targets such as the INK4a/ARF locus encoding p16INK4a and p15INK4b. It is regulated by upstream factors including E2F1, MYC, and TGF-?? signaling, and its repressive activity influences cellular senescence, epithelial-mesenchymal transition (EMT), and pluripotency through direct transcriptional control of CDKN2A, CDKN2B, CDH1, and HOX genes. CBX7 also cooperates with HDAC2 and CtBP to reinforce chromatin compaction.
In the HAP1 cell context, disruption of CBX7 leads to derepression of its target genes, particularly at the INK4a/ARF locus, resulting in increased expression of p16INK4a and p15INK4b, which in turn activates the p53/Rb tumor suppressor axis and promotes cellular senescence. The loss of CBX7 also modulates TGF-??, Wnt, and Notch signaling pathways, altering proliferation, migration, and invasive properties. This haploid knockout model allows unambiguous genotype-phenotype correlations and facilitates drug screening for compounds that target Polycomb group protein function or restore CBX7-like repressive activity.
This CBX7 knockout product is suited for multiple research areas, such as epigenetic regulation, Polycomb complex function, cancer biology, and haploid genetic screens. Typical assays include Western blotting and RT-qPCR to confirm target gene derepression, ChIP-qPCR to monitor H3K27me3 changes at specific loci, and RNA-seq for transcriptomic profiling. Functional studies often employ cell proliferation, senescence-associated ??-galactosidase staining, wound healing, and transwell invasion assays to assess phenotypic consequences of CBX7 loss. For further details on validation, protocols, or ordering, please contact Ascent Research.
