The DTNA Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal HeLa cell population with targeted disruption of the DTNA gene. This gene encodes ??-dystrobrevin, a scaffold protein of the dystrophin-glycoprotein complex (DGC). The polyclonal format provides a heterogeneous knockout cell pool, minimizing clonal bias and enabling robust loss-of-function studies. The cells are produced using CRISPR/Cas9-mediated gene disruption, ensuring efficient ablation of ??-dystrobrevin expression across the population.
HeLa cells are a transformed human cervical epithelial cell line derived from the adenocarcinoma of Henrietta Lacks. They are extensively characterized and routinely employed in studies of cell signaling, adhesion, migration, and cancer biology, providing a well-suited host for CRISPR knockout models of non-muscle DGC function.
DTNA encodes ??-dystrobrevin, a cytoplasmic scaffold that organizes the dystrophin-glycoprotein complex (DGC) by binding dystrophin, utrophin, and syntrophins. It recruits signaling molecules such as nNOS and calcium/calmodulin-dependent kinase. The DGC links the actin cytoskeleton to the extracellular matrix via dystroglycans and sarcoglycans, mediating mechanical stability and signal transduction. DTNA transcription is regulated by MEF2 factors, SRF, and mechanical stretch, while its disruption impairs nNOS signaling, calcium/calmodulin-dependent kinase cascades, and actin cytoskeleton remodeling.
In HeLa epithelial cells, DTNA knockout removes ??-dystrobrevin scaffolding, potentially disrupting DGC-mediated cell-extracellular matrix adhesion and downstream signaling. Although DGC is primarily studied in muscle, its components are present in epithelial cells where they influence adhesion, migration, and polarity. Loss of ??-dystrobrevin in this cervical cancer line may impair integrin-mediated adhesion and mislocalize nNOS and calcium/calmodulin-dependent kinase, thereby providing a model to explore non-muscle DGC functions relevant to cancer cell behavior.
This knockout cell product supports investigations into non-muscle DGC function, cell adhesion and migration, cancer biology, and protein-protein interaction mapping. Representative assays include western blotting, immunofluorescence, adhesion and migration assays, co-immunoprecipitation, and phospho-signaling analysis. The polyclonal population enables consistent loss-of-function phenotypes in bulk experiments. For more information, please contact Ascent Research.
