The CBX6 Knockout K-562 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the K-562 human chronic myelogenous leukemia (CML) cell line, providing a heterogeneous loss-of-function model for CBX6 gene studies. This polyclonal format ensures broad representation of knockout events, enabling robust functional assays without clonal selection biases. The product is designed for advanced epigenetic and leukemia research, offering a versatile platform to explore CBX6-dependent mechanisms.
The host K-562 cell line was established from a pleural effusion of a 53-year-old female with CML in blast crisis and carries the BCR-ABL fusion oncogene. Widely used as a model for CML pathology and erythroid differentiation, K-562 cells exhibit progenitor-like features that facilitate investigations into leukemogenic signaling, epigenetic regulation, and therapeutic responses.
CBX6 is a canonical component of Polycomb Repressive Complex 1 (PRC1) that specifically binds H3K27me3 marks deposited by PRC2 (EZH2/SUZ12). It mediates transcriptional silencing through chromatin compaction and RING1B-dependent H2A ubiquitination, directly repressing downstream targets including HOX clusters, p16INK4a/p14ARF, p21, and p53. CBX6 interacts with RING1A/B, PCGF, and PHC proteins within PRC1 and is regulated upstream by developmental signals and H3K27me3 placement, thereby integrating epigenetic cues to maintain cellular identity and control proliferation.
In the CML background, CBX6 knockout likely impairs PRC1 function, leading to derepression of Polycomb target genes and potential perturbation of leukemic cell growth, survival, or differentiation. This enables precise dissection of CBX6??s contribution to chromatin remodeling and transcriptional repression in BCR-ABL-driven leukemia, offering insights into epigenetic vulnerabilities in blast crisis CML and other cancers where CBX6 is dysregulated.
The cells are suitable for validation by Western blotting of CBX6 and PRC1 components, RT-qPCR for Polycomb target transcripts, ChIP-qPCR for H3K27me3 and CBX6 localization, and RNA-seq for transcriptome profiling. Functional assays include cell proliferation measurements, flow cytometric cell cycle analysis, and drug sensitivity testing for epigenetic inhibitors. This knockout model supports research on Polycomb function in leukemia, epigenetic regulation in CML, chromatin remodeling in cancer, and validation of epigenetic therapeutic targets. For further details, please contact Ascent Research.
