The KATNAL1 Knouckout A-549 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of A-549 cells with targeted disruption of the KATNAL1 gene. This knockout model serves as a versatile tool for investigating microtubule dynamics and cell cycle regulation in a lung carcinoma background. The polyclonal format provides a heterogeneous knockout pool, enabling functional studies without clonal selection bottlenecks. The gene editing was performed using CRISPR/Cas9 to introduce loss-of-function mutations, creating a reliable platform for dissecting KATNAL1-dependent pathways.
The host cell line, A-549, is a well-characterized human lung adenocarcinoma epithelial line derived from a male patient. As a model for non-small cell lung cancer (NSCLC), A-549 cells recapitulate key features of lung tumor biology, including aberrant proliferation and signaling. Their adherent growth and robust culture characteristics make them suitable for high-content imaging, biochemical assays, and drug sensitivity screens. This cell line provides a physiologically relevant context for examining the role of microtubule-severing enzymes in cancer cell behavior.
KATNAL1 encodes a microtubule-severing ATPase that functions as part of the katanin complex alongside KATNA1 and KATNB1. The enzyme is regulated by mitotic kinases including CDK1, AURKA, and PLK1, which phosphorylate KATNAL1 to control its activity. KATNAL1 localizes to centrosomes, spindle microtubules, and cilia, where it interacts with tubulin, SPAG6, and other katanin subunits. Through its severing activity, KATNAL1 modulates microtubule mass and dynamics during mitotic spindle organization and ciliary disassembly, thereby influencing cell division and cilia-dependent signaling.
In A-549 cells, loss of KATNAL1 is expected to impair microtubule severing, leading to defective mitotic spindle formation and chromosome segregation errors. This may result in reduced proliferation, altered cell cycle profiles, and compromised ciliogenesis. Given that microtubule-targeting agents are a mainstay of lung cancer therapy, the KATNAL1 knockout A-549 polyclonal population provides a powerful model to explore resistance mechanisms and identify synthetic lethal interactions. Moreover, disruptions in ciliary function can affect key cancer pathways such as Hedgehog and Wnt signaling, adding to the model’s utility.
Researchers can employ this knockout product in a broad range of applications, including investigating microtubule dynamics via immunofluorescence for acetylated tubulin, assessing cell proliferation by MTT or BrdU assays, and performing cell cycle analysis by flow cytometry. Cilia formation assays and RNA-sequencing can reveal downstream transcriptional changes. Western blotting enables confirmation of KATNAL1 loss. This polyclonal knockout population is also suitable for drug target validation and functional genomics screens. For further information or technical support, please contact Ascent Research.
