DTNA Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DTNA gene in A-549 human lung adenocarcinoma cells. This loss-of-function model is generated by CRISPR/Cas9-mediated gene disruption in a polyclonal format, providing a heterogeneous population of cells with DTNA ablation. The product enables investigation of alpha-dystrobrevin function in a non-muscle epithelial context, supporting studies of dystrophin-glycoprotein complex biology in lung adenocarcinoma-derived cells.
A-549 cells are a widely used human alveolar basal epithelial cell line derived from a lung adenocarcinoma. They serve as a model for type II pneumocytes, displaying epithelial morphology, robust adhesion characteristics, and responsiveness to extracellular matrix signals. This line is commonly employed in cancer biology, drug transport, and mechanotransduction research, making it an ideal host for dissecting the role of dystrobrevin in epithelial pathophysiology.
DTNA encodes alpha-dystrobrevin, a scaffold protein of the dystrophin-glycoprotein complex (DGC). Knockout of DTNA disrupts the linkage between the extracellular matrix and the actin cytoskeleton, impairing signal transduction and membrane stability. Alpha-dystrobrevin interacts with dystrophin, utrophin, syntrophin, sarcoglycans, dystroglycan, Grb2, and nNOS, and functions downstream of extracellular matrix ligands such as laminin via dystroglycan. It anchors neuronal nitric oxide synthase (nNOS) and aquaporin-4 to the membrane and, through syntrophins, contributes to focal adhesion kinase (FAK) signaling and actin cytoskeleton reorganization, mediating cell-matrix adhesion and mechanotransduction pathways.
In A-549 cells, DTNA knockout disrupts the DGC??s role in epithelial cell adhesion and migration, offering a model to study how loss of dystrobrevin affects alveolar epithelial integrity and signal transduction. Given the involvement of dystrobrevin in left ventricular non-compaction, muscular dystrophy, and cardiomyopathy, this non-muscle cell system permits dissection of DGC pathways in a cancer-relevant epithelial background. The knockout may influence cell-matrix interactions, migration, and invasion, providing insight into potential roles of dystrobrevin in lung adenocarcinoma progression.
Researchers can employ these polyclonal knockout cells for western blotting to confirm loss of alpha-dystrobrevin and associated DGC components, co-immunoprecipitation to examine protein interaction networks, and immunofluorescence to visualize cytoskeletal and adhesion structures. Functional assays such as cell adhesion, migration, and invasion assays enable investigation of dystrobrevin??s role in metastatic behavior, while phospho-signaling analysis can assess FAK and downstream targets. This model is suitable for drug target validation in cardiomyopathy and cancer contexts. For further information, please contact Ascent Research.
