The DLGAP4 Knockout AGS Polyclonal Cells product offers a CRISPR/Cas9-mediated gene-disrupted polyclonal population of AGS cells, providing a loss-of-function model for the DLGAP4 scaffold protein. This heterogeneous pool ensures broad representation of editing events and is suited for studying DLGAP4-dependent processes without the constraints of clonal selection. The knockout abrogates DLGAP4 expression, enabling investigation of its roles in cell adhesion, actin cytoskeleton regulation, and signal transduction.
The AGS cell line originates from a human gastric adenocarcinoma and is a well-characterized epithelial model for gastric biology and cancer research. These adherent cells retain key properties of gastric mucosal epithelium, including robust cell?Ccell adhesion, migratory capacity, and sensitivity to growth factor signaling. They are extensively employed to examine gastric cancer progression, drug responses, and epithelial?Cmesenchymal transition mechanisms, offering a relevant host for evaluating non-neuronal functions of synaptic scaffold proteins.
DLGAP4 functions as a crucial scaffold that links DLG family membrane-associated guanylate kinases (DLG4/PSD95, DLG2, DLG3) to the actin cytoskeleton. It directly binds Shank1, Shank3, NMDA receptor subunits GRIN1 and GRIN2B, actin, and cortactin, forming complexes such as the PSD95?CDLGAP4?CShank network. Upstream regulators include CAMK2 and Src kinases, which phosphorylate DLGAP4 to modulate interactions, while downstream effects involve NMDA receptor clustering, actin remodeling, and adhesion signaling. Although primarily characterized in synapses, these molecular interfaces suggest broader functions in cell adhesion and cytoskeletal dynamics.
In AGS cells, loss of DLGAP4 disrupts scaffolding at adhesion sites, potentially impairing actin organization, intercellular junctions, and signaling pathways downstream of DLG proteins. This provides a unique model to interrogate how synaptic scaffold proteins contribute to gastric epithelial homeostasis and carcinoma pathophysiology. Alterations in migration, proliferation, and adhesion following knockout can reveal non-canonical roles and identify novel therapeutic vulnerabilities in gastric cancer.
This polyclonal knockout product is suitable for a range of functional assays, including western blotting, co-immunoprecipitation, immunofluorescence, cell adhesion assays, migration assays, proliferation assays, and drug sensitivity testing. Researchers can apply it to study synaptic gene functions in epithelial contexts, model neuropsychiatric disorder mechanisms (autism spectrum disorder, schizophrenia, intellectual disability), investigate DLGAP4??s role in gastric cancer cell adhesion, or validate drug targets. For further information and ordering details, please contact Ascent Research.
