The KATNBL1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma epithelial cell line. This product enables loss-of-function studies of the KATNBL1 gene, which encodes the p80 regulatory subunit of the microtubule-severing katanin complex. The polyclonal format provides a heterogeneous pool of gene-disrupted cells, representing a population-level knockout model without clonal isolation. CRISPR/Cas9-mediated disruption of target loci generates a versatile tool for investigating the functional consequences of KATNBL1 ablation in an adenocarcinoma background.
The A-549 cell line was isolated from a 58-year-old Caucasian male with lung adenocarcinoma and displays type II alveolar epithelial characteristics. It serves as a common model for human lung adenocarcinoma research, offering insights into oncogenic signaling and drug sensitivity. A-549 cells possess adherent epithelial morphology and retain relevant genetic features, providing a robust platform for studying cytoskeletal dynamics and mitotic processes.
KATNBL1 encodes the p80 regulatory subunit of the katanin complex, which severs microtubules in an ATP-dependent manner. It interacts with the catalytic KATNA1 subunit and KATNB1 to form a heteromeric complex that binds microtubules. Complex activity is regulated by mitotic phosphorylation, primarily through CDK1/cyclin B, downstream of cell cycle kinases. Katanin-mediated severing promotes microtubule minus-end depolymerization and is essential for mitotic spindle organization and cell migration. KATNBL1 disruption abrogates complex function, leading to impaired microtubule dynamics, mitotic defects, and reduced cellular motility.
In A-549 cells, KATNBL1 knockout creates a model to study how microtubule severing influences lung adenocarcinoma cell behavior. The reliance of these cells on dynamic microtubule networks for proliferation and invasion makes this knockout relevant for investigating mitotic spindle abnormalities and motility defects. Moreover, loss of KATNBL1 may sensitize cells to microtubule-stabilizing or -destabilizing agents, enabling drug sensitivity profiling in a non-small cell lung adenocarcinoma context.
Key applications include investigating katanin subunit function in lung adenocarcinoma through immunofluorescence-based visualization of microtubule and mitotic spindle morphology, western blotting for katanin components, and cell cycle profiling by flow cytometry. The knockout cells are also valuable for assessing cell migration and invasion capabilities using transwell or scratch-wound assays, as well as for profiling drug sensitivity to microtubule-directed agents. These assays enable comprehensive phenotypic characterization of KATNBL1 loss in a disease-relevant cellular context. For further details or technical support, please contact Ascent Research.
