BAG5 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line, designed for targeted disruption of the BAG5 gene. This loss-of-function model is generated through CRISPR/Cas9-mediated gene editing, producing a heterogeneous pool of knockout cells suitable for pooled genetic perturbation studies. The polyclonal format avoids clonal selection bias and is appropriate for applications such as viability screens, mitophagy pathway dissection, and functional genomics research where population-level responses are of interest. Researchers can employ this product to interrogate the cellular consequences of BAG5 ablation in a gastric epithelial cancer context.
The AGS cell line is a well-characterized human gastric adenocarcinoma model isolated from a 54-year-old female patient. These adherent epithelial cells retain key features of gastric cancer and are widely used to investigate oncogenic signaling, drug sensitivity, and tumor cell biology. AGS cells are amenable to standard transfection and lentiviral transduction protocols, enabling stable gene modification and downstream functional assays. Their genetic background and culture conditions are well established, making them a reliable platform for studying the role of BAG5 in cancer-relevant processes.
BAG5 encodes a cochaperone that inhibits Hsp70-mediated protein refolding and functions downstream of PINK1 and mitochondrial depolarization to promote parkin recruitment to depolarized mitochondria. It interacts with Hsp70, parkin, PINK1, and Bcl-2, linking protein quality control, mitophagy, and apoptosis regulation. Under oxidative stress, PINK1 accumulates and phosphorylates parkin, and BAG5 facilitates parkin translocation to mitochondria, recruiting autophagic adaptors LC3 and p62 to drive mitophagy. Through these interactions, BAG5 modulates apoptotic signaling and protein homeostasis, influencing cellular outcomes in neurodegeneration and cancer.
In the gastric cancer background, BAG5 knockout disrupts the balance between pro-survival and pro-death signals, potentially affecting drug resistance and apoptotic sensitivity. The loss of BAG5 may impair parkin-dependent mitophagy, leading to accumulation of damaged mitochondria and altered metabolic and apoptotic profiles. This model allows researchers to dissect how mitochondrial quality control contributes to gastric tumor cell survival and to explore vulnerabilities that could be therapeutically exploited.
Typical applications include investigating parkin-dependent mitophagy mechanisms, examining BAG5-Hsp70 interactions, and assessing mitochondrial dysfunction?Cinduced apoptosis. The polyclonal knockout cells support various assays: Western blotting for BAG5, parkin, and LC3; mitochondrial membrane potential measurement with JC-1; mitophagy quantification via mt-mKeima; apoptosis detection with Annexin V; co-immunoprecipitation of BAG5-Hsp70 complexes; immunofluorescence of parkin translocation; and cell viability assays (CCK-8). Applications span gastric cancer biology, neurodegeneration-related mitophagy, and drug resistance research. For further information, contact Ascent Research.
