HOOK3 Knockout HAP1 Polyclonal Cells are a heterogeneous population of CRISPR/Cas9-edited HAP1 cells carrying targeted disruptions in the HOOK3 gene. This polyclonal knockout cell product provides a loss-of-function model for studying HOOK3-dependent processes without requiring single-cell clone isolation, preserving the diversity of editing outcomes across the population.
The HAP1 cell line is a near-haploid human cell line derived from the chronic myeloid leukemia line KBM-7. Its haploid karyotype facilitates unambiguous genetic manipulations, making it an ideal host for knockout and screening applications. HAP1 cells retain key characteristics of the parental cancer line while allowing efficient generation of knockout populations.
HOOK3 is a member of the hook protein family and functions as an adaptor that links organelles to the dynein-dynactin motor complex for minus-end-directed transport along microtubules. It is regulated by phosphorylation through CDK1 and CDK5 and by upstream Rab GTPases, and it interacts directly with dynein intermediate chain, dynactin subunits, HOOK1, HOOK2, FTS, and AKTIP. HOOK3 is essential for endosomal trafficking, retrograde transport, autophagy, and ciliogenesis, coordinating the movement of late endosomes and lysosomes. Disruption of HOOK3 impairs dynein-mediated motility, leading to defects in cargo delivery and organelle positioning.
In the HAP1 background, HOOK3 knockout polyclonal cells offer a simplified genetic system to dissect the role of this adaptor in intracellular transport and cancer cell biology. The near-haploid nature reduces genetic redundancy, allowing clear phenotypic readouts of HOOK3 loss. This model is particularly valuable for investigating how HOOK3-dependent trafficking influences cancer cell migration, invasion, and proliferation, given the oncogenic context of the host line.
Researchers can employ these cells in a variety of functional assays, including immunofluorescence staining of endosomal markers to assess organelle distribution, live-cell imaging of vesicle motility, western blotting for HOOK3 expression validation, and co-immunoprecipitation to probe dynein binding interactions. Additionally, migration and invasion assays can be used to explore the role of HOOK3 in cancer cell behavior. This knockout model is suitable for genetic screens, pathway analysis, and drug target validation in the context of intracellular trafficking and cancer. For further technical details and ordering information, please contact Ascent Research.
