The ART1 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the A2780 human ovarian carcinoma cell line. This product comprises a heterogeneously edited cell pool in which the ART1 gene has been disrupted via CRISPR/Cas9-mediated gene editing, creating a loss-of-function model without clonal selection. The polyclonal format retains broader genetic representation compared to monoclonal lines, reducing the impact of clonal variation and providing a robust system for functional genomics studies.
The A2780 cell line is a well-characterized epithelial ovarian adenocarcinoma model originally established from an untreated patient. These adherent, epithelial-like cells are extensively employed in cancer research, particularly for studying drug sensitivity and resistance mechanisms. A2780 cells are known to be responsive to standard chemotherapeutics such as cisplatin and paclitaxel, making them a relevant platform for evaluating how genetic perturbations affect therapeutic outcomes.
ART1 encodes a glycosylphosphatidylinositol (GPI)-anchored ectoenzyme that catalyzes mono-ADP-ribosylation, transferring ADP-ribose from NAD+ to arginine residues on extracellular domains of target proteins. Its activity is regulated by upstream inflammatory cytokines, including TNF?? and IFN??, and by integrin activation. Among its substrates, integrin ??7 and the stimulatory G protein alpha subunit (Gs??) are key downstream targets. ADP-ribosylation of integrin ??7 modulates cell adhesion and migration, while modification of Gs?? influences cAMP signaling. ART1 also intersects with focal adhesion kinase signaling and other cell surface receptor systems.
In the ovarian cancer setting, ART1-mediated ADP-ribosylation is hypothesized to contribute to tumor cell adhesion, invasive capacity, and potentially chemoresistance. A2780 cells endogenously express the ADP-ribosylation machinery and relevant integrins, making them an ideal host for ART1 knockout studies. Disruption of ART1 in these cells enables precise interrogation of how loss of mono-ADP-ribosylation affects integrin-dependent cell adhesion, migration, and downstream signaling events. Moreover, the model facilitates investigation into whether ART1 influences sensitivity to chemotherapeutic agents commonly used in ovarian cancer treatment, such as cisplatin and paclitaxel, thereby linking post-translational modifications to drug response phenotypes.
This polyclonal ART1 knockout population enables functional studies of ADP-ribosylation in cancer. Key applications include ADP-ribosylation assays, cell adhesion and migration assays, western blotting, flow cytometry, and drug sensitivity testing with cisplatin or paclitaxel. It is ideal for target validation of ART1. For further technical information and support, please contact Ascent Research.
