The EFNB1 Knockout AGS Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout pool targeting the EFNB1 gene in AGS human gastric adenocarcinoma epithelial cells. This loss-of-function model is generated without single-cell clone isolation, preserving genetic diversity within the engineered population. CRISPR/Cas9-mediated gene disruption eliminates ephrin-B1 ligand expression, enabling study of its functions.
AGS cells are a widely used gastric epithelial line derived from a human adenocarcinoma, serving as a robust model for gastric cancer biology, Helicobacter pylori pathogenesis, and mucosal research. Their adherent epithelial phenotype supports investigation of cell adhesion, migration, and signal transduction relevant to gastric tumor progression.
EFNB1 encodes ephrin-B1, a transmembrane ligand for EphB receptors (EphB1?CEphB3) that initiates juxtacrine bidirectional signaling. Forward signaling is transduced through EphB kinases, while reverse signaling propagates via ephrin-B1??s cytoplasmic domain, which recruits adaptors Grb4, PICK1, PDZ proteins, and Src kinases. Upstream regulators include the MSX1 transcription factor, ADAM10-mediated ectodomain shedding, and mechanical stress. Key downstream effectors encompass EphB4 phosphorylation, Rac1, RhoA, FAK, and activation of MAPK/ERK and PI3K/Akt cascades. Disruption of EFNB1 in this polyclonal AGS population ablates both forward and reverse ephrin-B1 signaling, decoupling the ligand from its cytoskeletal and adhesive outputs.
Loss of ephrin-B1 in gastric epithelial cells is anticipated to impair cell repulsion, enhance adhesion, and alter migration, processes critical to cancer cell dissemination. By eliminating ephrin-B1 reverse signaling, this model illuminates its specific contributions to gastric cancer cell behavior and may reveal vulnerabilities linked to Eph/ephrin dysregulation.
This polyclonal knockout cell reagent is designed for experiments exploring ephrin-B1??s role in gastric cancer invasion and metastasis, dissecting Eph/ephrin signaling networks, screening pharmacological inhibitors, and modeling craniofrontonasal syndrome in vitro. Compatible applications include western blotting, RT-qPCR, scratch wound and transwell migration/invasion assays, adhesion assays, immunofluorescence, and co-immunoprecipitation. For additional information or tailored applications, please reach out to Ascent Research.
