EFNA5 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population generated from the human AGS gastric adenocarcinoma cell line, featuring targeted disruption of the EFNA5 gene. The polyclonal cell pool contains a heterogeneous mixture of EFNA5-null cells, enabling functional loss-of-function studies without clonal selection. This product is supplied as a ready-to-use knockout cell pool, suitable for a broad range of in vitro assays in gastric cancer biology, cell signaling, and drug discovery.
The parental AGS cell line, derived from a human gastric adenocarcinoma, is a widely utilized epithelial model for investigating gastric carcinogenesis, cell migration, and tumorigenesis. These cells exhibit characteristic epithelial morphology and retain key signaling pathways relevant to gastric cancer progression, making them an appropriate host for genetic manipulation studies. AGS cells are commonly used to examine receptor tyrosine kinase signaling, cytoskeletal dynamics, and epithelial-mesenchymal transition in a gastric context.
EFNA5 encodes ephrin-A5, a glycosylphosphatidylinositol-anchored ephrin ligand that binds EphA2 and EphA4 receptors, initiating bidirectional signaling. Reverse signaling via ephrin-A5 recruits Src family kinases (Fyn, Yes) and focal adhesion kinase (FAK) to membrane microdomains, leading to RhoA/ROCK-mediated actin cytoskeleton reorganization. Ephrin-A5 expression is regulated by p53, Wnt/??-catenin, TGF-??, and hypoxia, and its downstream effectors include ERK1/2, c-Fos, c-Jun, and PI3K/Akt, collectively governing cell adhesion, repulsion, migration, and proliferation.
In AGS gastric cancer cells, EFNA5 knockout disrupts Eph/ephrin bidirectional signaling, altering tumor cell behavior. Ephrin-A5 is implicated in invasive growth and metastasis; its loss in this epithelial model allows dissection of its role in gastric adenocarcinoma progression. Knockout cells may exhibit changes in cell-cell adhesion, collective migration, and extracellular matrix sensing, impacting MAPK/ERK and PI3K/Akt pathways. This model facilitates investigation of actin dynamics, integrin adhesion, and transcriptional responses.
This EFNA5 knockout polyclonal cell product suits studies of Eph/ephrin signaling in epithelial cells, gastric cancer migration and invasion, epithelial-mesenchymal transition, and drug target validation. Compatible assays include wound healing, transwell migration, proliferation, western blotting for phospho-ERK1/2 and FAK, and RT-qPCR for gene disruption confirmation. The polyclonal pool reduces clonal artifacts, ideal for pooled functional screens. For further information, contact Ascent Research.
