ARID4B Knockout HAP1 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population in which the ARID4B gene is disrupted. This product provides a genetically heterogeneous pool of HAP1 cells that collectively harbor loss-of-function mutations in ARID4B, enabling robust loss-of-function studies without clonal selection. The polyclonal format is particularly suited for pooled CRISPR screening applications, minimizing clonal bias while maintaining target-gene representation across the population. Researchers can employ this model to investigate ARID4B function in a near-haploid background, facilitating efficient knockout screening and downstream phenotypic assays.
HAP1 is a near-haploid human cell line derived from the chronic myeloid leukemia line KBM-7. It carries the Philadelphia chromosome, resulting in BCR-ABL1 fusion-driven oncogenic signaling. The near-haploid karyotype reduces genetic redundancy, making HAP1 cells an ideal host for CRISPR/Cas9-based knockout screens. Their rapid proliferation and stable culture characteristics further support high-throughput functional genomics studies. HAP1 cells have been widely adopted for investigating gene essentiality, drug mechanism of action, and cancer biology due to the simplicity of achieving complete gene disruption in a single allele.
ARID4B encodes a subunit of the SIN3-HDAC transcriptional corepressor complex, which is central to chromatin remodeling and gene silencing. ARID4B directly interacts with the retinoblastoma protein RB1, and together they are recruited to E2F-responsive promoters to repress transcription of cell cycle genes. The complex also includes SIN3A, HDAC1, and HDAC2, which deacetylate histones and promote chromatin compaction. This pathway is regulated upstream by RB1 phosphorylation and by Notch intracellular domain signaling. Downstream targets include CDKN1A and pro-apoptotic factors, thereby linking ARID4B to cell cycle arrest and apoptosis. Disruption of ARID4B can relieve transcriptional repression, altering E2F-dependent gene expression and impacting cellular proliferation and survival.
In the HAP1 leukemia context, ARID4B knockout helps dissect the interplay between epigenetic silencing and oncogenic signaling. The BCR-ABL1-driven proliferation may intersect with ARID4B-mediated transcriptional repression, making this model valuable for exploring how chromatin regulators modulate leukemic cell fitness. Moreover, ARID4B??s role in retinoblastoma protein function and E2F regulation positions these cells as a tool for studying solid tumor biology and responses to CDK inhibitors or HDAC inhibitors. The model enables investigation of synthetic lethal interactions and resistance mechanisms in a genetically tractable system.
These cells are suitable for diverse functional assays including Western blotting, ChIP-qPCR, RT-qPCR, flow cytometry for cell cycle and apoptosis, co-immunoprecipitation, proliferation assays, drug sensitivity testing, and RNA-seq. They support research in acute and chronic myeloid leukemia, retinoblastoma, and solid tumors, as well as HDAC inhibitor development and epigenetic drug screening. The polyclonal knockout pool is ideal for CRISPR knockout screening, pooled library formats, and high-throughput drug?Cgene interaction studies. For further technical details, pricing, and availability, please contact Ascent Research.
