The DNAJB9 Knockout AGS Polyclonal Cells are a heterogeneous population of AGS gastric adenocarcinoma cells with CRISPR/Cas9-mediated disruption of the DNAJB9 gene. This polyclonal knockout model offers a flexible system for loss-of-function studies of DNAJB9, an ER-resident co-chaperone. The CRISPR-based editing generates a mixture of cells with gene-inactivating mutations, enabling functional analysis without clonal bias.
The AGS cell line is derived from a human gastric adenocarcinoma and exhibits epithelial morphology. It is widely used as a model for gastric cancer, retaining characteristics relevant to tumor cell signaling, invasion, and drug response. AGS cells are amenable to genetic modification and phenotypic characterization, making them an appropriate host for targeted gene knockout.
DNAJB9 (ERdj4) is a stress-inducible ER co-chaperone that collaborates with HSPA5/BiP to recognize misfolded proteins and promote their disposal via ER-associated degradation (ERAD). It functions downstream of the unfolded protein response (UPR) sensors IRE1?? and PERK, and is transcriptionally regulated by ATF6 and XBP1 in response to ER stress. By facilitating degradation of ERAD substrates, DNAJB9 reduces proteotoxic burden and maintains ER homeostasis, supporting cell survival under stress.
In AGS gastric cancer cells, DNAJB9 knockout provides a valuable tool to explore ER stress contributions to malignancy. Gastric tumors often experience elevated ER stress; thus, loss of DNAJB9 permits investigation of how ERAD deficiency affects tumor cell viability, apoptosis, and drug sensitivity. This model is particularly useful for dissecting ATF6- and XBP1-driven adaptive pathways and for probing synthetic lethal relationships in the context of gastric adenocarcinoma.
Researchers can employ this polyclonal knockout cell population in a variety of applications. Typical assays include western blotting for ER stress markers, RT-qPCR of UPR target genes, cell viability assays under ER stress induction, co-immunoprecipitation with BiP, and immunofluorescence for ER localization. Additional studies may involve apoptosis, migration/invasion, colony formation, and drug sensitivity testing. The model is instrumental for investigating protein folding disorders and ERAD mechanisms. For further information, please contact Ascent Research.
