The KIF13A Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population targeting the KIF13A gene. This product provides a loss-of-function model for studying KIF13A-dependent processes in a human near-haploid cellular context. The polyclonal population contains a heterogeneous mix of cells with targeted disruption of KIF13A, enabling functional genomics analyses without requiring clonal isolation. Researchers can use this model to investigate the role of KIF13A in endosomal trafficking, cell migration, and Wnt signal transduction.
The host HAP1 cell line is a near-haploid human fibroblast-like line derived from the KBM-7 chronic myeloid leukemia cell line. HAP1 cells possess a stable haploid karyotype except for disomy of chromosome 8, making them a powerful tool for genetic knockout studies and haploid genetic screens. Their rapid growth and ease of genetic manipulation allow efficient generation of polyclonal knockout populations, which retain the essential characteristics of the parental line while lacking target gene function.
KIF13A encodes a plus-end directed microtubule motor protein of the kinesin-3 family. It functions as a key regulator of endocytic recycling and melanosome transport by interacting with Rab11 and the adaptor protein (AP)-1 complex. In the Wnt signaling pathway, KIF13A is activated downstream of Wnt ligands and Frizzled receptors, where it binds to Dishevelled (Dvl) and mediates its translocation to the cell periphery along microtubules. This interaction promotes the redistribution of Dvl and facilitates integrin-containing vesicle trafficking, thereby enhancing cell migration and invasion. KIF13A thus connects Wnt signaling to cytoskeletal dynamics, acting upstream of integrin-based adhesion complexes.
In the HAP1 cell context, disruption of KIF13A provides a unique platform to dissect Wnt-driven migration and endosomal trafficking pathways without interference from diploid gene redundancy. The near-haploid genome simplifies interpretation of knockout phenotypes, especially in genetic screens aimed at identifying modifiers of KIF13A function. This model is particularly relevant for investigating mechanisms of cancer metastasis and melanoma progression, where KIF13A-mediated transport of melanosomes and integrins contributes to invasive behavior. Additionally, the polyclonal format allows rapid assessment of gene essentiality and pathway analysis.
Applications of this knockout model include functional assays such as wound healing and Transwell migration/invasion to quantify cell motility, immunofluorescence and live-cell imaging for visualizing Dvl localization and vesicle dynamics, and biochemical analyses via co-immunoprecipitation, RT-qPCR, and western blotting to assess protein interactions and gene expression changes. These cells are suitable for genome-wide CRISPR screens leveraging the haploid background. For further technical details and ordering information, contact Ascent Research.
