The KIF2C Knockout HeLa Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the microtubule depolymerizing kinesin MCAK, encoded by the KIF2C gene. This polyclonal knockout model is generated in the widely used HeLa cell line, providing a genetically disrupted pool of cells for investigating mitotic regulation and chromosomal stability without clonal selection. The product is supplied as a ready-to-use polyclonal knockout population, enabling robust functional genomics, drug target validation, and mechanistic studies of mitosis.
The host HeLa cell line is an HPV18-positive cervical adenocarcinoma model with p53 and Rb tumor suppressor proteins inactivated by the viral oncoproteins E6 and E7. This genetic background drives continuous proliferation and aneuploidy, making HeLa cells a classic system for studying cancer biology, chromosomal instability, and mitotic progression. The line??s well-characterized karyotype and rapid growth facilitate a wide range of experimental assays.
KIF2C encodes the kinesin-13 family member MCAK, a potent microtubule depolymerase that localizes to kinetochores, spindle poles, and microtubule plus-ends to correct erroneous attachments and ensure faithful chromosome segregation. MCAK activity is tightly regulated by mitotic kinases, including AURKA, AURKB, PLK1, and CDK1, which phosphorylate distinct residues to modulate its localization and catalytic activity. MCAK interacts with Aurora B, CENPE, EB1/MAPRE1, CLASP1, and tubulin to coordinate microtubule dynamics. It functions downstream of the spindle assembly checkpoint components BUB1, BUBR1, MAD2, and the APC/C?CCDC20 complex, ultimately controlling Cyclin B degradation and mitotic exit.
In the HeLa cellular context, KIF2C knockout profoundly disrupts chromosome congression and segregation, leading to lagging chromosomes, anaphase bridges, and mitotic arrest. These defects arise from failure to resolve syntelic and merotelic attachments, increasing chromosomal instability??a hallmark of many aggressive cancers. The polyclonal knockout population recapitulates these mitotic phenotypes, providing a physiologically relevant model to study the consequences of MCAK loss in a p53/Rb-deficient background. This model is particularly valuable for exploring synthetic lethality relationships and assessing antimitotic drug responses in cells with pre-existing genomic instability.
This product is ideally suited for a broad spectrum of applications, including live-cell imaging of microtubule and chromosome dynamics, immunofluorescence analysis of mitotic spindle abnormalities, flow cytometric cell cycle profiling, and western blotting for checkpoint protein activation. Researchers can employ it in RNAi or drug combination screens to identify novel mitotic regulators or to validate KIF2C as a therapeutic target in cancers characterized by chromosomal instability. For detailed technical specifications or to request a quote, please contact Ascent Research.
