The DLGAP4 Knockout NCI-H1299 Polyclonal Cells comprise a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population, derived from the NCI-H1299 human non-small cell lung carcinoma line. Unlike clonal isolates, this polyclonal knockout format incorporates a spectrum of editing events across the cell pool, minimizing clonal artifacts and providing a physiologically relevant loss-of-function model. The product enables dissection of DLGAP4-dependent signaling without presupposing a single genetic lesion, making it well-suited for pooled functional genomics and comparative analyses with isogenic controls.
The NCI-H1299 cell line was established from a metastatic lymph node of a patient with non-small cell lung carcinoma and is characterized by its null p53 status. This genetic background eliminates p53-mediated checkpoint responses, facilitating studies of oncogenic signaling and tumor progression independent of p53-dependent apoptosis or senescence. As a widely used model for lung adenocarcinoma, NCI-H1299 provides a relevant host for examining the role of neuronal scaffold proteins in epithelial cancer contexts, where aberrant expression of synaptic genes has been increasingly recognized.
DLGAP4 encodes a key scaffolding protein that bridges membrane-associated guanylate kinases (MAGUKs), such as DLG4 (PSD-95) and DLG1 (SAP97), to the actin cytoskeleton through interactions with SHANK family proteins and other GKAP family members. Within the postsynaptic density, DLGAP4 organizes macromolecular complexes containing NMDA receptors, HOMER, and SHANK3, thereby coordinating synaptic plasticity and cell adhesion. Upstream regulators include neuronal activity and Wnt signaling pathways, while downstream effectors encompass DLG4, SHANK proteins, and the actin cytoskeleton. In non-neuronal cells, DLGAP4 may anchor analogous complexes at cell?Ccell and cell?Cmatrix adhesions, modulating actin dynamics and signaling.
Disruption of DLGAP4 in NCI-H1299 cells is predicted to uncouple MAGUK-dependent adhesion complexes from the actin cytoskeleton, potentially altering cell morphology, motility, and proliferation. Given the p53-null background, this model permits investigation of DLGAP4??s contribution to tumorigenic behaviors without interference from canonical p53-mediated pathways. Recent evidence linking synaptic scaffold proteins to cancer cell invasion and metastasis underscores the importance of this knockout model for uncovering non-canonical roles of neuronal genes in lung carcinoma.
This polyclonal DLGAP4 knockout product is optimized for a range of experimental approaches, including western blotting, immunofluorescence, transwell migration assays, proliferation analyses, co-immunoprecipitation, and RNA-seq. Researchers can employ it to study lung cancer biology, cell adhesion dynamics, synaptic protein function in non-neuronal settings, drug response profiling, and signal transduction networks. Loss-of-function phenotypes can be reliably compared to parental NCI-H1299 or wild-type controls, facilitating robust data interpretation. For further information or to inquire about availability, please contact Ascent Research.
