The CD2AP Knockout AGS Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. This product features a targeted disruption of the CD2AP gene, which encodes an adaptor protein critical for cytoskeletal organization and receptor signaling. The polyclonal format provides a heterogeneous population of edited cells, enabling robust loss-of-function studies without clonal selection artifacts. This model is designed for researchers investigating CD2AP-dependent mechanisms in gastric epithelial biology and related pathologies.
The parental AGS cell line is a widely used epithelial model established from a patient with gastric adenocarcinoma. These cells exhibit adherent morphology and retain key characteristics of gastric mucosal epithelium, making them suitable for studies of gastric cancer cell behavior, including proliferation, migration, and invasion. The AGS background provides a relevant human context for exploring the role of CD2AP in gastric carcinogenesis and MET receptor-driven signaling pathways.
CD2AP functions as a scaffold adaptor linking membrane receptors, such as the MET receptor, to the actin cytoskeleton. It interacts with CBL, endophilin, cortactin, and actin to regulate receptor endocytosis and actin polymerization. CD2AP is activated downstream of HGF/MET and TGF-?? receptor stimulation, and it modulates the activity of RAC1 and cortactin, thereby influencing cell adhesion and migration. In the CD2AP knockout AGS cells, disruption of this network impairs MET receptor trafficking and downstream actin reorganization, providing a clean background to dissect these signaling events.
In the context of gastric adenocarcinoma, CD2AP loss is associated with altered cell migration and invasion, processes critical for cancer metastasis. The knockout in AGS cells enables precise interrogation of how CD2AP coordinates MET signaling with cytoskeletal dynamics, offering insights into tumor progression and potential therapeutic resistance mechanisms. This model is particularly valuable for studying focal adhesion turnover and epithelial-to-mesenchymal transition (EMT) in gastric cancer, as well as for identifying biomarkers linked to CD2AP dysfunction.
Typical research applications include Western blotting to confirm CD2AP knockout and assess downstream targets, Transwell migration and invasion assays to evaluate metastatic potential, co-immunoprecipitation to study protein interactions, and immunofluorescence to visualize actin cytoskeleton reorganization. Phospho-MET analysis can further delineate receptor activation states. These polyclonal knockout cells are a versatile tool for MET signaling pathway analysis, gastric cancer invasion studies, and drug resistance research. For additional technical details, please contact Ascent Research.
