CBX3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from Jurkat cells, designed for functional loss-of-function studies of the CBX3 gene. This gene-edited pool provides a heterogeneous population of cells with targeted disruption of CBX3, enabling robust investigation of its biological roles without clonal selection bias. The polyclonal format maintains genetic diversity, reducing artifacts from single-cell bottlenecks, and is suitable for pooled phenotypic screens and bulk assays.
Jurkat cells are a widely used human T lymphocyte cell line established from a 14-year-old male with acute T cell leukemia. These suspension cells serve as a fundamental model for T cell signaling, acute lymphoblastic leukemia (ALL) pathogenesis, and T cell biology. The Jurkat background offers a defined genetic context for studying chromatin-mediated gene regulation in T cell malignancies, with well-characterized signaling pathways including TCR and IL-2 cascades.
CBX3 (HP1??) functions as a key reader of H3K9me3 marks, binding via its chromodomain to recruit chromatin-modifying complexes and enforce transcriptional silencing. It is regulated by upstream factors such as SUV39H1-mediated methylation, Aurora B and CDK-dependent phosphorylation, and SUMOylation. CBX3 interacts with HP1?? (CBX5), HP1?? (CBX1), SUV39H1, Lamin B receptor, CAF-1, and DNMT3A, mediating heterochromatin assembly and gene repression. Downstream, it targets CDKN1A (p21) expression and centromere function. CBX3 operates within a network involving H3K9me3, SETDB1, HDACs, and KRAB-ZNFs, integrating epigenetic and cell cycle control.
In Jurkat T-ALL cells, CBX3 dysregulation contributes to leukemogenesis by altering chromatin states and silencing tumor suppressor genes. Disrupting CBX3 in this context allows dissection of its role in T cell leukemia progression, heterochromatin dynamics, and transcriptional reprogramming. The knockout polyclonal cells provide a physiologically relevant platform to study how CBX3 loss impacts proliferation, apoptosis, and chemotherapeutic response in a lymphoid malignancy setting.
These cells are suited for a range of experimental workflows, including chromatin immunoprecipitation (ChIP-qPCR), RNA-seq transcriptome profiling, and Western blotting for protein expression changes. Functional assays such as flow cytometry-based cell cycle and apoptosis analysis, colony formation, and proliferation assays can assess phenotypic consequences. Additionally, xenograft tumor models and drug sensitivity screens can evaluate the therapeutic potential of targeting CBX3 pathways. For customized inquiries or bulk orders, please contact Ascent Research.
