The KIF13B Knockout HAP1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human KIF13B gene in the near-haploid HAP1 background. This pooled knockout model circumvents clonal selection artifacts, offering a heterogeneous loss-of-function system for studying KIF13B-dependent processes.
HAP1 cells originate from the BCR-ABL1-positive KBM-7 chronic myeloid leukemia line and feature a near-haploid karyotype, simplifying genetic analysis. As adherent male cells, they are well suited for adhesion and migration assays, and their haploid nature enhances phenotypic penetrance in knockout studies. This host line retains endocytic trafficking machinery, making it a practical platform for investigating kinesin-mediated transport.
KIF13B is a plus-end-directed kinesin motor that drives the transport of VEGFR2-containing vesicles from recycling endosomes to the plasma membrane. Under the regulation of Rab11 and VEGFR2 activation, KIF13B cooperates with the AP-1 adaptor complex to deliver cargoes essential for angiogenesis and downstream PI3K/Akt-mTORC1 signaling. The motor also mediates insulin-induced GLUT4 translocation and contributes to actin remodeling through its interaction with RhoA. Thus, KIF13B integrates signals from growth factors and metabolic cues to coordinate cell migration, vascular homeostasis, and glucose uptake.
In HAP1 cells, ablation of KIF13B creates a clean phenotype due to the reduced genetic redundancy of the haploid genome. Although these cells are not endothelial, they enable VEGFR2 trafficking assays and surrogate angiogenic readouts such as tube formation and wound healing migration. The polyclonal knockout pool further ensures that observed effects represent consistent population-level responses rather than artifacts from a single clone, making the model reliable for comparing KIF13B-dependent and -independent mechanisms.
These polyclonal knockout cells are optimized for immunofluorescence-based tracking of VEGFR2 localization, western blot validation, and co-immunoprecipitation of KIF13B-interacting partners like Rab11. Functional analyses can include wound closure assays, tube formation, and flow cytometry to quantify surface VEGFR2 levels. Beyond angiogenesis research, the model supports diabetes studies through GLUT4 translocation experiments and neurobiological investigations of kinesin function. For technical support or additional information, please contact Ascent Research.
