The DYNLT3 Knockout HAP1 Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human DYNLT3 gene in the HAP1 near-haploid cell line. This polyclonal pool contains a heterogeneous mixture of edited cells carrying CRISPR/Cas9-mediated disruptions of the DYNLT3 locus, providing a powerful loss-of-function model for studying cytoplasmic dynein-dependent processes.
HAP1 cells are a near-haploid human cell line derived from the KBM-7 chronic myeloid leukemia line. Their haploid karyotype simplifies genetic analysis and knockout validation, making them an ideal platform for functional genomics and genetic screening. HAP1 cells are p53-deficient, which facilitates genome editing but may influence cell cycle and DNA damage responses, an important consideration for phenotypic assays.
DYNLT3 encodes a light chain subunit of the cytoplasmic dynein motor complex, a multisubunit assembly responsible for minus-end-directed transport along microtubules. DYNLT3 directly interacts with dynein intermediate chains DYNC1I1 and DYNC1I2, linking cargo adaptors such as BICD2 and RAB11FIP3 to the dynein heavy chain DYNC1H1 via the dynactin complex subunit DCTN1/p150Glued. This network transports diverse cargoes including signaling receptors, lysosomes, and mitotic spindle proteins. DYNLT3 function is regulated by cell cycle regulators and mitogenic signaling, and is critical in mitotic spindle organization, lysosomal trafficking, and neuronal migration.
In the HAP1 background, DYNLT3 knockout is predicted to compromise dynein-dependent processes, leading to defects in mitotic spindle assembly, organelle positioning, and cargo transport. Such disruptions may result in impaired cell proliferation, altered cell cycle progression, and aberrant intracellular signaling. Because HAP1 cells are p53-deficient, the knockout phenotype may interact with DNA damage checkpoint pathways, offering a unique context to study DYNLT3 in cancer-relevant settings. Researchers can use this polyclonal population to examine the collective impact of DYNLT3 loss on cellular functions without clonal bias.
These DYNLT3 knockout HAP1 polyclonal cells are suitable for a wide range of applications including functional genomics screens, investigation of dynein motor mechanics, cancer research, neurodegenerative disease modeling, and drug target validation. The polyclonal format is particularly advantageous for high-content screening, as it reflects a broad spectrum of editing outcomes. Representative assays include western blotting for target protein expression, immunofluorescence to assess dynein subunits and cargoes, live-cell imaging of organelle transport dynamics, flow cytometry for cell cycle analysis, mitotic index staining, and cell proliferation assays. For further details, please contact Ascent Research.
