The CD19 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal cell population derived from the A2780 human ovarian carcinoma line, with targeted disruption of the CD19 gene. This polyclonal pool contains diverse loss-of-function mutations, enabling robust functional studies without clonal isolation artifacts. It is designed for advanced investigation of CD19-dependent signaling, cellular processes, and therapeutic targeting.
The parental A2780 line is an adherent epithelial ovarian carcinoma model from an untreated patient. Widely used in ovarian cancer research, it serves in drug sensitivity assays, chemoresistance profiling, and xenografts. Its consistent growth and epithelial character make it a reliable host for gene editing. In the CD19 knockout context, this line provides a system to assess CD19-mediated signaling outside the B-cell lineage, supporting studies of CD19-targeted therapies.
CD19 is a transmembrane co-receptor that lowers the threshold for B cell activation via BCR signaling. Upon BCR engagement, Lyn kinase phosphorylates CD19, recruiting PI3K and activating the PI3K-Akt axis. CD19 complexes with CD21, CD81, and Leu-13, and links to effectors including Vav, PLC??2, and the MAPK pathway, which regulate NF-??B, c-Myc, and Bcl-xL. These interactions are essential for B cell proliferation and humoral immunity. Knockout of CD19 in A2780 cells disrupts this signaling network, providing a loss-of-function model for mechanistic dissection.
In the A2780 ovarian cancer background, CD19 knockout creates a platform for studying CD19 co-receptor function outside B cells, useful for validating CD19-directed immunotherapies like CAR-T therapy. A2780 CD19 knockout cells serve as negative controls to confirm target specificity. This model also permits investigation of BCR-like signaling modules in epithelial cells, revealing potential crosstalk or off-target effects. The polyclonal nature avoids clonal artifacts, improving translational relevance.
Applications include flow cytometry for CD19 loss verification, western blotting for signaling protein changes, RT-qPCR for transcriptional profiles, co-immunoprecipitation for complex disruption, and phospho-signaling analysis of Akt/MAPK pathways. This knockout model supports B cell development studies, immunodeficiency modeling, B cell malignancy research, and CAR-T target validation, bridging signal transduction research and preclinical drug evaluation. For further information, contact Ascent Research.
