KIF20B Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cervical adenocarcinoma cell line. These cells feature CRISPR/Cas9-mediated disruption of the KIF20B gene, providing a loss-of-function model to study KIF20B-dependent processes in a human epithelial cancer background. The polyclonal nature of this knockout pool reflects a heterogeneous mixture of gene-edited alleles, enabling robust analysis of KIF20B deficiency without the clonal selection artifacts inherent in single-cell-derived lines. This product is particularly suited for detecting population-level phenotypes in mitotic progression and cytokinesis studies.
The parental HeLa cell line is an immortalized human epithelial line from cervical adenocarcinoma. It is a widely used cancer research model with rapid proliferation and well-characterized mitotic behavior, ideal for studying mitotic kinesins. Its aneuploid karyotype and extensive history in functional genomics provide a robust reference for interpreting KIF20B knockout phenotypes in chromosomal instability and oncogenic signaling.
KIF20B is a kinesin-6 motor protein that localizes to the central spindle and midbody during mitosis. It is activated by CDK1/cyclin B and regulated by Aurora B and PLK1. KIF20B interacts directly with the chromosomal passenger complex components Aurora B, INCENP, and Survivin, as well as with tubulin, to organize microtubule dynamics and promote cytokinesis completion. Downstream, KIF20B drives midbody formation and abscission; its loss disrupts these processes, leading to multinucleation and mitotic catastrophe. This positions KIF20B as a critical effector at the intersection of the Aurora B signaling hub and the cell cycle machinery.
In the HeLa background, KIF20B knockout recapitulates key mitotic defects observed in cancer cells with deficient cytokinesis. These cells become multinucleated and undergo apoptotic cell death or senescence-like arrest, mirroring phenotypes associated with chromosomal instability and tumor suppressor loss. Given that KIF20B is implicated in cervical adenocarcinoma, lung, breast, and bladder cancers, this model allows direct interrogation of KIF20B??s role in promoting aberrant cell division in a cancer-relevant epithelium. The polyclonal format maintains the heterogeneous nature of tumor cell populations, enhancing physiological relevance for cancer biology studies.
This knockout cell population supports functional genomic screens, mitotic progression studies, and anti-mitotic drug screening. Typical assays include immunofluorescence for tubulin and midbody markers, live-cell imaging of mitosis, Western blotting for KIF20B, flow cytometry for DNA content, and apoptosis or colony formation assays to assess cell fate after division failure. These approaches enable detailed studies of KIF20B function within the Aurora B?CPLK1?CCDK1 axis and microtubule regulation. For further information, please contact Ascent Research.
