The DNMBP Knockout AGS Polyclonal Cells comprise a heterogeneous population of AGS gastric adenocarcinoma epithelial cells carrying CRISPR/Cas9-mediated disruption of the DNMBP gene. This polyclonal loss-of-function model is designed to investigate the role of the scaffold protein DNMBP (also known as Tuba) without the limitations of clonal selection, enabling the study of gene disruption effects across a diverse genetic background. The knockout cell population provides a reliable tool for examining DNMBP-dependent cellular processes in a widely used gastric cancer cell line.
The AGS cell line was originally derived from a 54-year-old female patient with gastric adenocarcinoma and serves as a well-characterized model of gastric epithelial biology. These cells exhibit typical epithelial morphology and express markers relevant to gastric mucosal barrier function. Their widespread use in cancer research makes AGS cells particularly suitable for studying molecular mechanisms underlying gastric adenocarcinoma progression, metastasis, and epithelial homeostasis.
DNMBP encodes a multidomain scaffold protein that integrates upstream Cdc42-GTP and growth factor receptor signals to regulate the actin cytoskeleton, tight junction formation, and endocytosis. Mechanistically, activated Cdc42 binds to DNMBP, which in turn recruits N-WASP and dynamin-2, leading to Arp2/3 complex activation and actin polymerization. This pathway is critical for maintaining epithelial barrier integrity through the assembly of tight junction proteins such as ZO-1. DNMBP also interfaces with other Rho family GTPases and participates in endocytic trafficking, underscoring its role as a central node in coordinating actin dynamics and membrane remodeling.
In the context of gastric adenocarcinoma, disruption of DNMBP is expected to compromise tight junction architecture and actin-mediated processes, potentially contributing to epithelial barrier dysfunction, increased cell motility, and metastatic behavior. The AGS knockout model therefore offers a physiologically relevant system to dissect how loss of DNMBP impacts epithelial-to-mesenchymal transition (EMT), cell-cell adhesion, and tumor cell invasion. By employing these polyclonal knockout cells, researchers can interrogate the contribution of DNMBP to gastric cancer pathogenesis without the confounding factors of clonal variation.
These knockout cells are suitable for a broad range of experimental applications, including immunofluorescence and phalloidin staining to visualize actin cytoskeletal rearrangements, co-immunoprecipitation to study protein?Cprotein interactions, TEER measurements to assess barrier function, and migration/invasion assays to evaluate metastatic potential. Additionally, they can be employed in RT-qPCR and western blotting to quantify changes in gene and protein expression, as well as in small molecule screening for modulators of cell-cell adhesion. For further details or technical support, please contact Ascent Research.
