The AKAP9 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed to disrupt the AKAP9 gene in the HeLa host cell line. This product provides a heterogeneous pool of gene-edited cells, enabling robust functional studies of AKAP9-dependent processes without clonal selection. The polyclonal format preserves population-level variability, making it suitable for pooled screening applications and broader phenotypic characterization of AKAP9 loss-of-function effects.
The host cell line, HeLa, is an HPV18-positive cervical adenocarcinoma epithelial cell line in which the viral oncoprotein E6 inhibits p53 tumor suppressor function. This genetic background renders HeLa cells highly proliferative and widely utilized in cancer biology, cell cycle analysis, and signal transduction research. The epithelial origin and transformed phenotype make HeLa cells a relevant model for studying centrosome biology, microtubule dynamics, and oncogenic signaling pathways.
AKAP9 encodes A-kinase anchoring protein 9, a large scaffold protein that tethers protein kinase A (PKA) regulatory subunits (RI/RII) to the centrosome and Golgi apparatus, where it coordinates spatial cAMP/PKA signaling. Through interactions with phosphodiesterase 4D, PKN, NMDA receptors, and pericentrin, AKAP9 integrates upstream signals from CDK1 phosphorylation and cAMP fluctuations to regulate phosphorylation of PKA substrates, microtubule-associated proteins, and Golgi matrix proteins. Consequently, AKAP9 is essential for mitotic spindle formation, microtubule organization, Golgi integrity, and ion channel modulation, linking cAMP/PKA signaling to cell cycle progression and cytoskeletal dynamics.
In the HeLa cell context, AKAP9 disruption provides a powerful model for dissecting the roles of centrosomal PKA signaling in cell division and cancer biology. The HPV18-driven p53 inhibition in HeLa cells may accentuate mitotic defects upon AKAP9 loss, offering a sensitive system to study spindle abnormalities and chromosomal instability. This knockout cell population is thus invaluable for investigating how AKAP9-dependent PKA localization impacts centrosome duplication, microtubule nucleation, and Golgi organization in a transformed epithelial background.
Researchers can employ these AKAP9 knockout polyclonal HeLa cells in a variety of assays, including immunofluorescence microscopy to assess centrosome and Golgi marker distribution, western blotting to evaluate PKA substrate phosphorylation, flow cytometry for cell cycle perturbations, and mitotic index quantification. The product is also suitable for phospho-signaling analysis, migration and invasion assays, and long QT syndrome-related ion channel studies. For technical details and ordering information, please contact Ascent Research.
