The DLGAP4 Knockout 786-O Polyclonal Cells represent a heterogeneous population of 786-O human clear cell renal carcinoma cells engineered via CRISPR/Cas9-mediated gene disruption to abolish expression of the DLGAP4 scaffold protein. This polyclonal knockout cell population, generated through electroporation of Cas9-sgRNA ribonucleoprotein complexes, is supplied as a mixed pool containing diverse loss-of-function alleles, enabling robust assessment of DLGAP4-dependent phenotypes without clonal selection biases. The product serves as a ready-to-use tool for investigating the non-neuronal functions of DLGAP4 in epithelial tumor biology.
The parental 786-O cell line was originally established from a primary clear cell renal cell carcinoma of a 58-year-old male patient and is widely used as a model for VHL wild-type renal cancer. These adherent epithelial cells exhibit tumorigenic properties, including anchorage-independent growth and tumor formation in xenograft models. The 786-O line retains expression of epithelial markers and key signaling pathways relevant to renal cell carcinoma progression, providing a physiologically relevant background for studying DLGAP4-mediated scaffolding interactions in cancer.
DLGAP4 encodes a critical postsynaptic density scaffold protein that bridges ionotropic glutamate receptors to the actin cytoskeleton through interactions with PSD-95 (DLG4), SHANK1/SHANK2/SHANK3, and neuroligin family proteins. In neurons, DLGAP4 is activated downstream of NMDA receptor-mediated calcium influx and CaMKII or PKA phosphorylation, facilitating the clustering of AMPA receptors and organizing the SHANK-PSD-95 complex to regulate synaptic plasticity and dendritic spine morphogenesis. Additionally, DLGAP4 binds ??-catenin and actin filaments, suggesting roles in cell adhesion and cytoskeletal dynamics that may extend to non-neuronal contexts.
In 786-O renal carcinoma cells, DLGAP4 knockout disrupts these scaffolding interactions, potentially impairing cell adhesion, polarity, and migration. Given the protein??s capacity to link surface receptors to the cytoskeleton and its interaction with ??-catenin, loss of DLGAP4 may alter Wnt/??-catenin signaling output, actin remodeling, and tumor cell invasiveness. Thus, this polyclonal knockout model offers a unique opportunity to dissect the scaffolding functions of DLGAP4 in renal cancer biology and uncouple its synaptic roles from oncogenic processes.
This polyclonal knockout cell product is ideally suited for a wide range of biomedical research applications, including functional studies of scaffold-protein contributions to tumor growth, migration, and invasion using proliferation, wound-healing, and transwell assays. Researchers can employ co-immunoprecipitation and immunofluorescence to characterize altered protein-protein interactions and subcellular localization of PSD-95, SHANK, and ??-catenin complexes. Further applications include phospho-signaling analysis by Western blot, RNA-seq transcriptomic profiling, and apoptosis assays to evaluate therapeutic vulnerabilities. Representative assays such as RT-qPCR and phospho-kinase arrays enable systematic dissection of signaling pathways rewired upon DLGAP4 loss. For additional information or custom inquiries, please contact Ascent Research.
