The KIF13B Knockout HT29 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the KIF13B gene in human colorectal adenocarcinoma HT29 cells. This loss-of-function model is designed for investigating KIF13B’s role as a plus-end-directed microtubule motor in endosomal recycling, cell migration, and intracellular transport. The polyclonal format preserves population-level heterogeneity, avoiding clonal selection biases while enabling robust study of gene disruption effects, confirmed by Western blotting.
HT29 cells are a well-characterized epithelial line derived from a colorectal adenocarcinoma, widely employed to model intestinal epithelial biology and colorectal cancer. They form polarized monolayers and are instrumental for studying integrin-dependent adhesion, migration, and drug response. As a tumor cell background, HT29 cells provide a relevant context for examining how microtubule-based transport influences cancer metastasis mechanisms.
KIF13B is a kinesin-3 motor that transports vesicles along microtubules, crucially mediating ??1-integrin recycling from endosomes to the plasma membrane. Its activity is regulated by integrin activation, receptor tyrosine kinases (EGFR, PDGFR), and Rho GTPases. KIF13B interacts with the AP-1 adaptor complex, Centaurin-??1 (ADAP1), and DISC1 for cargo selection. Downstream, KIF13B-driven ??1-integrin delivery activates FAK signaling and actin remodeling, essential for cell-matrix adhesion and motility. This pathway links microtubule-based transport to migration, with KIF13B at the intersection of vesicle trafficking and cytoskeletal reorganization.
In HT29 cells, KIF13B knockout impairs ??1-integrin surface expression and FAK phosphorylation, weakening cell attachment and attenuating migration and invasion??key steps in colorectal cancer metastasis. This disruption allows researchers to dissect how defective endosomal recycling alters epithelial cancer cell behavior, potentially identifying therapeutic targets. The polyclonal model offers a physiologically relevant system for studying population-level migration deficits without clonal artifacts.
Applications include wound healing and Transwell invasion assays to quantify migration and invasion defects, immunofluorescence and co-immunoprecipitation of ??1-integrin and AP-1 complex for trafficking studies, and flow cytometry or phospho-FAK analysis for signaling readouts. The cells are also suitable for drug screening to identify compounds that restore integrin trafficking or inhibit cancer cell motility. For further technical inquiries, please contact Ascent Research.
