This product comprises a CRISPR/Cas9-edited polyclonal knockout cell population targeting the DNAJA2 gene in the human HGC-27 gastric carcinoma epithelial cell line. The polyclonal knockout cells are produced by CRISPR/Cas9-mediated disruption of DNAJA2, yielding a heterogeneous pool of cells with loss-of-function mutations. This model enables the investigation of DNAJA2-dependent processes without clonal selection, preserving population-level variability.
The cells are derived from Homo sapiens and are suitable for a wide range of applications in molecular and cellular biology, including the study of chaperone-mediated pathways and proteostasis in a gastric cancer context. The host HGC-27 cell line was originally established from a metastatic lymph node of a patient with gastric adenocarcinoma. HGC-27 cells are widely utilized as a model system for gastric cancer research, including studies of tumor cell signaling, migration, invasion, and drug sensitivity.
These cells retain key characteristics of gastric carcinoma, such as epithelial morphology and dysregulated growth pathways, making them a relevant platform for exploring the molecular mechanisms underlying gastric cancer progression and for evaluating potential therapeutic interventions targeting proteostasis networks. DNAJA2 functions as an Hsp40 co-chaperone that stimulates the ATPase activity of Hsp70, a central component of protein folding, translocation, and quality control. Under normal conditions, DNAJA2 is regulated upstream by heat shock factor 1 (HSF1) in response to heat shock, oxidative stress, and the unfolded protein response.
It interacts directly with Hsp70/Hsc70 and collaborates with other DnaJ homologs and ubiquitin ligases such as CHIP to facilitate the processing of client proteins. DNAJA2 is implicated in multiple pathways, including protein processing in the endoplasmic reticulum, endocytosis, and ubiquitin-mediated proteolysis, and it acts downstream of HSF1 while upstream of Hsp70 client protein triage, thereby influencing proteostasis and stress adaptation. Disruption of DNAJA2 in HGC-27 gastric cancer cells is expected to perturb proteostasis, sensitizing the cells to proteotoxic stress and impairing protein trafficking and degradation.
Given the dysregulated stress responses and heightened proteostatic demand characteristic of gastric carcinoma, this knockout model provides a powerful tool to dissect how co-chaperone dysfunction affects cancer cell survival, proliferation, and metastatic behavior. The polyclonal nature of the knockout pool allows for the assessment of heterogeneous cellular responses, which may reveal vulnerabilities that are not apparent in clonal populations, facilitating the study of chaperone network dependencies and the identification of synthetic lethal interactions in gastric cancer. This DNAJA2 knockout polyclonal cell product is specifically designed for advanced research applications, including the study of protein misfolding and stress responses, chaperone-mediated pathways in cancer cell survival, and the assessment of therapeutic strategies targeting heat shock proteins. Representative experimental techniques that can be employed with these cells include Western blotting for DNAJA2 and Hsp70, immunofluorescence to detect protein aggregation, cell viability assays under stress conditions, proteasomal activity measurements, co-immunoprecipitation of Hsp70 complexes, migration and invasion assays, and RT-qPCR analysis of heat shock response genes. For further technical inquiries, please contact Ascent Research.
