The DPF1 Knockout HAP1 Polyclonal Cells product consists of a CRISPR/Cas9-edited polyclonal knockout cell population engineered for targeted disruption of the DPF1 gene in the HAP1 cell line. This loss-of-function model provides a powerful tool to investigate DPF1-dependent biological mechanisms using a heterogeneous pool of edited cells that reflect diverse editing outcomes. The polyclonal format is particularly advantageous for pooled functional genomics screening and high-throughput applications where clonal variation is minimized.
HAP1 cells are a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line, characterized by a stable and simplified chromosomal background that facilitates gene editing and functional assays. Originating from a male donor, these cells retain hematopoietic cancer features and are widely used as a model for leukemia biology, drug sensitivity profiling, and large-scale genetic interaction studies. The haploid nature enhances the penetrance of CRISPR/Cas9-mediated knockouts, as disruption of the single allele typically abolishes gene function.
The DPF1 gene encodes a neuron-specific subunit of the BAF (SWI/SNF) ATP-dependent chromatin remodeling complex, where it interacts with core components SMARCA4, SMARCC1, SMARCC2, ACTL6A, and histone H3. Its expression is regulated by upstream factors including NEUROG2, ASCL1, and retinoic acid signaling, and it transcriptionally activates downstream targets DCX, SYN1, and NEFM, which are critical for neuronal differentiation. Mechanistically, DPF1 facilitates chromatin remodeling to promote dendrite outgrowth and synapse formation, thereby governing neurogenesis and neuronal maturation.
Despite the neural lineage specificity of DPF1, its knockout in the HAP1 CML background provides a unique opportunity to dissect BAF complex functions in hematological malignancies. Since BAF complex components are frequently altered in cancer, this polyclonal knockout pool allows researchers to assess how loss of a tissue-specific subunit influences complex assembly, chromatin accessibility, and gene expression programs. The model enables exploration of downstream effects on cell proliferation, apoptosis, and drug sensitivity, shedding light on epigenetic dependencies in leukemia.
Typical applications include functional dissection of the BAF complex through RNA-seq and ChIP-qPCR, genetic interaction screens, and drug sensitivity testing evaluated via cell proliferation and apoptosis assays. Protein expression changes can be validated by western blotting and immunofluorescence, while transcriptional effects are measured by RT-qPCR. These polyclonal cells also support cancer epigenetics research and chromatin remodeling studies. For further technical information or to discuss customized experimental solutions, please contact Ascent Research.
