KIF2C Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HEK293T human embryonic kidney epithelial cell line. This product features a targeted disruption of the KIF2C gene, resulting in a loss-of-function model for investigating the roles of the encoded mitotic centromere-associated kinesin (MCAK). The polyclonal nature of these knockout cells provides a heterogeneous population with varied gene editing events, offering a robust tool for functional genomics studies without the clonal bias often associated with single-cell-derived lines. This knockout product is particularly suited for experiments requiring genetic ablation of KIF2C function in a widely used host cell background.
HEK293T cells are a human embryonic kidney epithelial cell line stably expressing SV40 large T antigen, which enhances replication of plasmids with SV40 origin, enabling high-level protein expression and efficient viral production. Their robust transfection efficiency and rapid growth make them ideal for transient transfection, lentiviral packaging, and biochemical assays. This well-characterized background is extensively employed in mitosis research and drug discovery.
KIF2C encodes MCAK, a kinesin-13 microtubule depolymerase that corrects erroneous kinetochore-microtubule attachments during mitosis. Its activity is regulated by Aurora B phosphorylation at centromeres, which activates depolymerization to promote microtubule turnover. Additional regulators include PLK1 and CDK1/cyclin B, and MCAK functions in concert with the Ska complex, Ndc80 complex, CENP-C, EB1, and TIP150 to ensure proper chromosome segregation. Downstream, KIF2C-mediated depolymerization facilitates the correction of misattachments, safeguarding genomic stability.
In HEK293T cells, KIF2C knockout serves as a model for studying mitotic spindle dynamics and aneuploidy. The flat epithelial morphology supports high-resolution microscopy, and the polyclonal population captures diverse editing outcomes. Loss of KIF2C is predicted to cause chromosome misalignment and segregation errors, leading to aneuploidy. This system enables analysis of how heterogeneous KIF2C disruption influences mitotic fidelity and genomic integrity.
Applications include immunofluorescence and live-cell imaging to visualize spindle defects, flow cytometry for cell cycle perturbations, colony formation assays for long-term genomic instability, and drug sensitivity screens with microtubule poisons. These polyclonal knockout cells also facilitate functional genomics screens to identify mitotic regulators. For technical assistance, contact Ascent Research.
