The DNMBP Knockout NCI-H1975 Polyclonal Cells product comprises a CRISPR/Cas9-edited polyclonal population of NCI-H1975 human lung adenocarcinoma cells harboring a targeted disruption of the DNMBP gene. This loss-of-function model provides researchers with a tool to investigate the cellular roles of DNMBP, a scaffold protein that coordinates actin dynamics and membrane trafficking. The polyclonal format enables population-level studies while preserving the heterogeneity typical of edited cell pools. As a genetic knockout, this product facilitates the dissection of DNMBP-dependent pathways in a disease-relevant cellular context.
The NCI-H1975 cell line was derived from a non-small cell lung adenocarcinoma and is widely employed as a model for EGFR-driven lung cancer. These cells harbor activating L858R and resistance-associated T790M mutations in the epidermal growth factor receptor (EGFR), making them particularly valuable for studies of tyrosine kinase inhibitor sensitivity and acquired resistance. The epithelial origin of NCI-H1975 cells supports investigations of cell polarity, junctional integrity, and metastatic behavior. Their genetic background renders them a suitable host for examining how DNMBP disruption impacts signaling downstream of oncogenic EGFR.
DNMBP (dynamin binding protein) is a multidomain scaffold that bridges membrane scission by dynamin with actin filament assembly via N-WASP, thereby coupling endocytosis to cytoskeletal reorganization. This function positions DNMBP at the intersection of receptor internalization, actin remodeling, and cell junction maintenance. Upstream signals from Wnt ligands, EGFR, and Rho GTPases converge on DNMBP, while downstream it promotes actin nucleation through the Arp2/3 complex. DNMBP interacts directly with dynamin 2, N-WASP, cortactin, and F-actin, and participates in the Wnt planar cell polarity pathway, where it links Dishevelled to RhoA-ROCK signaling and localized actin polymerization.
In the NCI-H1975 cell line, DNMBP knockout is expected to perturb EGFR endocytosis and trafficking, potentially altering receptor degradation and signaling output. Given the role of DNMBP in actin dynamics and cell polarity, its disruption may affect migration, invasion, and junctional integrity??processes frequently dysregulated in lung adenocarcinoma progression. This polyclonal knockout model therefore enables the study of how DNMBP-dependent actin remodeling contributes to malignant phenotypes and drug resistance in the context of EGFR-mutant lung cancer, offering a platform for functional validation of DNMBP as a therapeutic target.
Researchers can employ this knockout cell population in a variety of assays, including western blotting and immunofluorescence to confirm protein loss, endocytosis assays to measure EGFR internalization, and migration or invasion assays to assess metastatic potential. Co-immunoprecipitation and RT-qPCR can further probe DNMBP??s interaction partners and transcriptional responses. These cells are suited for investigating EGFR signaling, actin dynamics, and cell polarity mechanisms in lung adenocarcinoma. For additional information or to request ordering details, please contact Ascent Research.
