The BST1 Knockout A-549 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the A-549 human lung adenocarcinoma cell line, targeting the BST1 gene. This heterogeneous pool of cells carries targeted gene disruptions introduced by CRISPR/Cas9-mediated non-homologous end joining, avoiding single-cell cloning and preserving population-level variability. The polyclonal format offers a robust loss-of-function model for studying BST1-dependent phenotypes without clonal bias, making it suitable for functional genomics and drug discovery applications.
The host A-549 cell line is a widely characterized epithelial model derived from a human lung adenocarcinoma, commonly employed in cancer research and respiratory biology. These adherent cells retain alveolar type II pneumocyte features, including expression of surfactant proteins and metabolic pathways relevant to lung physiology. A-549 cells exhibit strong proliferative capacity and are frequently used to investigate tumor cell adhesion, migration, invasion, and calcium signaling, providing a clinically relevant background for BST1 knockout studies.
BST1 encodes CD157, a GPI-anchored ectoenzyme that converts NAD+ into cyclic ADP-ribose (cADPR), a second messenger activating ryanodine receptors on the endoplasmic reticulum to mobilize calcium. Upstream regulators include all-trans retinoic acid and granulocyte colony-stimulating factor; CD157 interacts with integrins, CD38, and extracellular matrix proteins to modulate adhesion and calcium signaling. Thus, BST1 disruption impairs cADPR-dependent calcium release and integrin-mediated adhesion.
In the A-549 background, the knockout disrupts cADPR?Ccalcium signaling, enabling dissection of calcium-driven adhesion, migration, and metastatic potential. The model may also illuminate non-neuronal roles of BST1 in Parkinson??s disease, as genetic associations link BST1 to PD risk, potentially revealing peripheral mechanisms in a lung epithelial context.
Researchers can measure calcium flux, cell adhesion, and migration using standard assays, and validate knockout via western blotting, flow cytometry, or RT-qPCR. NADase activity assays enable evaluation of cADPR production, while the cells support screening of ADP-ribosyl cyclase inhibitors. Co-culture studies can examine immune cell interactions. For inquiries or ordering, contact Ascent Research.
