The AKAP11 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line. This product is generated through CRISPR/Cas9-mediated disruption of the AKAP11 gene, resulting in a heterogeneous pool of cells with targeted gene knockout. The polyclonal format provides a loss-of-function model suitable for studying AKAP11-dependent processes without requiring single-cell clone isolation. Each lot is quality-controlled to confirm gene disruption at the population level.
The A-549 cell line is a well-established human lung adenocarcinoma model with epithelial morphology. Originally isolated from the lung carcinoma of a 58-year-old male, A-549 cells are widely used in cancer biology, drug development, and respiratory disease research. They retain key characteristics of alveolar type II pneumocytes, including surfactant production and activation of oncogenic signaling pathways. This adherent cell line provides a reproducible and physiologically relevant background for interrogating AKAP11 function in lung adenocarcinoma.
AKAP11 (A-kinase anchoring protein 11) functions as a multivalent scaffold that compartmentalizes protein kinase A (PKA) and protein phosphatase 1 (PP1) to distinct subcellular locales, enabling spatiotemporal control of phosphorylation events. It is regulated by cAMP signaling and the FOXM1 transcription factor, and its scaffolding activity coordinates downstream effectors including PKA substrates, PP1 targets, ??-catenin, and Aurora B kinase. AKAP11 directly interacts with PKA subunits, PP1 catalytic subunit, GSK3??, 14-3-3 proteins, and Beclin-1, forming complexes that regulate cAMP/PKA signal propagation, cell cycle progression, and autophagy. Through these interactions, AKAP11 integrates signals from the cAMP/PKA pathway, Wnt signaling via ??-catenin, and autophagic machinery via Beclin-1.
In A-549 lung adenocarcinoma cells, AKAP11 knockout disrupts the precise compartmentalization of PKA and PP1, leading to aberrant phosphorylation dynamics and dysregulation of mitotic progression and autophagy. This loss-of-function model mimics the disruption of AKAP11-mediated signaling observed in various cancers and neuropsychiatric conditions. The knockout promotes abnormal cell proliferation and survival, making it a valuable tool for dissecting AKAP11-dependent oncogenic mechanisms and identifying therapeutic vulnerabilities specific to lung adenocarcinoma.
This polyclonal knockout cell population is ideally suited for functional studies of AKAP11 in lung adenocarcinoma, including cAMP/PKA signal transduction research, autophagy mechanism investigation, and cell cycle regulation analysis. Researchers can employ a range of downstream assays such as western blotting, RT-qPCR, Sanger sequencing of the target locus, immunofluorescence, flow cytometry, cell cycle analysis, autophagy flux assays, and phospho-PKA substrate western blotting to characterize knockout phenotypes. The cells also provide a platform for cancer drug sensitivity testing and screening of compounds targeting AKAP11-related pathways. For further details on validation, culture conditions, and technical support, please contact Ascent Research.
