The DPP10 Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population with targeted disruption of the human DPP10 gene in the HAP1 near-haploid cell line. This loss-of-function model enables investigation of DPP10-dependent regulatory mechanisms without diploid genetic complexity. The polyclonal pool reflects a heterogeneous edited population, valuable for functional genomics and drug discovery where monoclonal bias is minimized.
HAP1 cells are a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia (CML) line. Their haploid karyotype simplifies genetic manipulation, avoiding biallelic targeting, and is widely used for haploid genetic screens and CRISPR-based functional genomics. The DPP10 knockout in this background combines the advantages of haploid genetics with targeted loss of an ion channel auxiliary subunit.
DPP10 encodes a transmembrane auxiliary subunit of Kv4 potassium channels, interacting with pore-forming subunits KCND2 (Kv4.2) and KCND3 (Kv4.3). Along with KChIP1, KChIP2, KChIP3, and DPP6, it modulates channel surface expression, trafficking, and gating kinetics of A-type potassium currents. These currents regulate neuronal action potential repolarization and firing patterns. Upstream regulators include neuronal activity, BDNF, and calcium signaling, while downstream targets comprise KCND2/3 channels, A-type currents, and neuronal firing patterns.
DPP10 knockout in HAP1 cells provides a unique model to study Kv4 channel regulation in a human haploid background, facilitating analysis of channel trafficking, surface expression, and electrophysiology without wild-type allele interference. DPP10 is associated with asthma, bipolar disorder, schizophrenia, autism spectrum disorder, and epilepsy, making this model relevant for disease mechanism studies. Additionally, haploid drug screening for Kv4 modulators benefits from consistent gene disruption, enabling identification of compounds acting through DPP10-dependent pathways.
Typical applications include CRISPR knockout validation, patch-clamp electrophysiology to record A-type currents, immunofluorescence and co-immunoprecipitation for channel complex analysis, and calcium imaging to monitor signaling. The model supports flow cytometry-based phenotyping and cell surface protein isolation to quantify trafficking. It is also suited for haploid genetic modifier screens to identify synthetic lethal interactions or resistance mechanisms related to Kv4 channelopathies. For further details or custom projects, please contact Ascent Research.
