The EFCAB14 Knockout AGS Polyclonal Cells are a pooled population of CRISPR/Cas9-edited gastric epithelial cells in which the EFCAB14 gene has been disrupted. This polyclonal knockout model preserves the genetic heterogeneity of the targeted cell pool, providing a robust system for studying loss-of-function effects without the clonal selection bias of single-cell-derived lines. The use of CRISPR/Cas9-mediated gene disruption enables efficient ablation of EFCAB14 expression, allowing researchers to interrogate the functional consequences of EFCAB14 deficiency within a representative gastric epithelial background.
AGS is a human gastric adenocarcinoma cell line derived from a poorly differentiated tumor of a 54-year-old Caucasian female. These epithelial cells maintain characteristics relevant to gastric mucosal barrier function, including the ability to secrete mucins and acid. As a widely used model in gastric cancer research, AGS cells exhibit unregulated proliferation and are amenable to manipulation for functional genomics studies. The AGS background provides a pathologically relevant context in which to examine the role of calcium-binding proteins in gastric carcinogenesis.
EFCAB14 encodes an EF-hand calcium-binding protein that is predicted to participate in calcium-mediated intracellular signaling. It contains EF-hand motifs that facilitate direct calcium ion binding, and it interacts with calmodulin and other EF-hand proteins. Within the calcium signaling cascade, EFCAB14 is regulated by dynamic intracellular calcium levels and may function downstream of calmodulin to influence calmodulin-dependent kinases (e.g., CaMKII) and downstream transcription factors. In the AGS cellular environment, EFCAB14 likely intersects with the MAPK/ERK pathway, as calcium signaling is known to modulate ERK1/2 phosphorylation, thereby affecting proliferation and survival signals. Thus, the knockout of EFCAB14 perturbs this network, potentially disrupting calcium-dependent activation of proliferative and migratory programs.
In gastric adenocarcinoma, aberrant calcium signaling contributes to tumor progression, metastasis, and resistance to apoptosis. By eliminating EFCAB14 in AGS cells, this knockout model enables dissection of EFCAB14-specific roles in cancer cell phenotypes. Given the protein??s involvement in calcium-modulated proliferation and migration, the EFCAB14 knockout AGS polyclonal cells serve as a powerful tool for investigating mechanisms of gastric cancer progression. Moreover, the model can be used to assess how loss of EFCAB14 affects downstream effectors such as CaMKII and ERK1/2, providing insights into pathway dependencies that may be exploited therapeutically.
Typical applications of these cells include functional genomics studies, calcium signaling investigations, and cancer cell biology assays. Researchers can employ western blotting and RT-qPCR to confirm EFCAB14 knockout and monitor gene expression changes, calcium imaging to assess alterations in intracellular calcium dynamics, and cell-based assays such as MTT, migration/invasion, and apoptosis assays to evaluate functional outcomes. This product is suitable for drug target validation and pathway analysis in the context of gastric adenocarcinoma. For further details, please contact Ascent Research.
