The DNAJB14 Knockout AGS Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal population of AGS human gastric adenocarcinoma epithelial cells carrying a targeted disruption of the DNAJB14 gene. This heterogeneous knockout pool is designed for loss-of-function studies without clonal isolation, enabling researchers to examine collective gene knockout effects across a mixed cell population. The polyclonal format retains genetic diversity, reducing the confounding influence of single-cell-derived artifacts and offering a robust model for interrogating DNAJB14-dependent processes.
AGS cells are a well-established human gastric cancer-derived epithelial line, extensively used as a model system to investigate gastric adenocarcinoma biology, including proliferation, invasion, and response to therapeutic stress. These cells exhibit characteristic epithelial morphology and express key signaling components of the unfolded protein response (UPR) and proteostasis machinery, making them particularly suitable for examining ER stress-related pathways and chaperone networks in a cancer-relevant context.
DNAJB14 functions as a J-domain co-chaperone that directly recruits Hsp70 family chaperones, principally HSPA8 and HSPA1A, to misfolded or aggregation-prone client proteins, thereby coupling substrate recognition to ATP-dependent refolding or ubiquitin-mediated degradation. Its activity is integrated into the broader proteostasis network through interactions with the co-chaperone STUB1 (CHIP) and members of the BAG protein family, such as BAG3, which dictate client fate toward refolding or proteasomal/autophagic clearance. Upstream, DNAJB14 expression and function are regulated by ER stress sensors including IRE1, PERK, and ATF6, as well as by the heat shock transcription factor HSF1, linking it to both acute stress response and chronic adaptation pathways.
In the AGS gastric cancer background, disruption of DNAJB14 compromises the efficiency of Hsp70-mediated protein quality control, sensitizing cells to proteotoxic insults such as tunicamycin-induced ER stress or heat shock. This loss of function likely perturbs the balance between client protein refolding and degradation, potentially altering autophagy flux and cell survival signaling. Consequently, the polyclonal knockout model serves as a valuable tool to dissect the chokepoints where chaperone dependency intersects with oncogenic signaling and stress adaptation in gastric adenocarcinoma.
Researchers can employ this knockout model in a variety of experimental workflows, including western blotting to confirm DNAJB14 ablation and monitor Hsp70 levels, RT-qPCR quantification of ER stress markers such as CHOP and BiP, cell viability assays under tunicamycin or heat shock challenge, co-immunoprecipitation to probe interactions with HSPA8/HSPA1A, and cycloheximide chase experiments to evaluate protein stability. These applications support investigations into cancer biology, ER stress response mechanisms, chaperone network analysis, proteostasis research, and drug target validation. For additional product information or technical support, please contact Ascent Research.
