This product is a CRISPR/Cas9-edited polyclonal knockout cell population targeting the human KATNA1 gene in A-549 cells. The polyclonal population comprises a heterogeneous mixture of edited cells with loss-of-function mutations in KATNA1, generated via CRISPR/Cas9-mediated gene disruption. As a non-clonal pool, it retains diverse genetic backgrounds and editing outcomes, providing a robust model for studying KATNA1 function without clonal artifacts. This format is ideal for population-level analyses where heterogeneous knockout effects are desired, such as in drug sensitivity or pooled functional screens.
The host cell line, A-549, is a well-characterized human lung adenocarcinoma epithelial cell line isolated from the lung tissue of a 58-year-old Caucasian male. A-549 cells are widely employed as an in vitro model for type II alveolar epithelium and are extensively used in lung cancer research. They exhibit typical epithelial morphology and retain key signaling pathways relevant to non-small-cell lung cancer. Their adherent growth and reliable culture characteristics make them suitable for a broad range of assays investigating oncogenic processes, drug responses, and metastasis-related phenotypes.
KATNA1 encodes the p60 catalytic subunit of katanin, an ATP-dependent microtubule-severing enzyme. It forms a heterodimer with the p80 regulatory subunit KATNB1 to sever microtubules, a process critical for microtubule cytoskeleton remodeling. KATNA1 is regulated by mitotic kinases such as AURKA, CDK1, and PLK1, which phosphorylate and activate its severing activity. It interacts with microtubule-nucleating factors including ??-tubulin and the spindle pole protein ASPM, as well as the spindle organizer NUMA1. Downstream targets include mitotic spindle checkpoint components and the ciliary axoneme. Through these interactions, KATNA1 controls mitotic spindle assembly, chromosome segregation, ciliogenesis, and cell morphology, and its dysregulation contributes to genomic instability and neurodevelopmental disorders.
In the A-549 lung adenocarcinoma background, disruption of KATNA1 provides a powerful model to dissect microtubule-dependent mechanisms underlying cancer cell proliferation and therapy resistance. Loss of katanin function may impair mitotic fidelity, leading to chromosomal instability and aneuploidy??hallmarks of lung cancer. Additionally, KATNA1 knockout can affect ciliogenesis, which is implicated in tumor cell signaling and metastasis. This model enables exploration of how microtubule-severing influences sensitivity to microtubule-targeting chemotherapeutics such as paclitaxel and vincristine, and may reveal synthetic lethal interactions exploitable for novel therapeutic strategies.
This polyclonal knockout cell population is suitable for a range of functional studies. Applications include analyzing KATNA1??s role in mitotic spindle organization and cell-cycle progression by western blotting and flow cytometry; assessing cilia formation and microtubule architecture via immunofluorescence for ??-tubulin, acetylated tubulin, and pericentrin; evaluating migration and invasion in wound-healing and transwell assays; profiling drug sensitivities with microtubule agents; and transcriptomic analyses such as RNA-seq to uncover downstream pathways. The product supports target discovery and validation in lung adenocarcinoma research. For more information, please contact Ascent Research.
