The DPF3 Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the DPF3 gene. This product provides a heterogeneous pool of loss-of-function cells, avoiding clonal selection while enabling robust functional studies. The knockout model serves as a powerful tool for investigating DPF3-dependent processes without the bias of single-cell cloning, preserving population diversity for assays where phenotypic heterogeneity is relevant.
HAP1 is a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line. Its haploid karyotype simplifies genetic modification and mutagenesis screens, making it a preferred system for functional genomics and drug target discovery. HAP1 cells exhibit mesenchymal-like morphology and express a single copy of most genes, facilitating complete gene knockout without compensatory alleles.
DPF3 functions as a core subunit of the SWI/SNF (BAF) ATP-dependent chromatin remodeling complex. It contains tandem PHD fingers that specifically recognize methylated histone H3 tails, anchoring the complex to chromatin. DPF3 interacts directly with the ATPase BRG1 (SMARCA4) and the scaffolding subunits ARID1A and BAF155/BAF170. Through these interactions, DPF3 modulates nucleosome positioning and chromatin accessibility, thereby governing transcriptional programs. Its activity is regulated by upstream cardiogenic transcription factors such as GATA4 and NKX2-5, and it directly promotes expression of downstream cardiac targets including NPPA and MYH6, while also influencing tumor suppressor genes and cell cycle regulators.
In the HAP1 background, knockout of DPF3 is expected to disrupt BAF complex targeting and function, leading to altered chromatin landscapes and dysregulated gene expression. Given the involvement of DPF3 in congenital heart defects and lung adenocarcinoma, this model provides a relevant system to dissect its role in both developmental and oncogenic contexts. The near-haploid state ensures that even single-allele disruption results in complete loss of protein function, offering a clean genetic background for mechanistic studies.
This DPF3 knockout cell pool is suitable for a wide range of applications including chromatin accessibility profiling by ATAC-seq, transcription factor binding analysis via ChIP-qPCR, gene expression quantification by RT-qPCR, protein interaction studies by co-immunoprecipitation, and functional assays such as cell cycle analysis and proliferation measurements. It supports investigations into SWI/SNF complex biology, epigenetic regulation in cancer, and developmental signaling pathways. For additional information or ordering, please contact Ascent Research.
