The DNAJA2 Knockout 786-O Polyclonal Cells provide a CRISPR/Cas9-edited polyclonal knockout population in the human 786-O renal carcinoma cell line. This product comprises a heterogeneous pool of cells with targeted disruptions in the DNAJA2 gene, generated via CRISPR/Cas9-mediated gene editing. The polyclonal format avoids clonal selection artifacts and offers a flexible loss-of-function model for studying DNAJA2-dependent processes. Cells are supplied as a ready-to-use mixed population for cancer biology and proteostasis research.
The 786-O cell line is derived from a patient with clear cell renal cell carcinoma (ccRCC) and harbors a homozygous VHL mutation, leading to constitutive HIF stabilization. This epithelial line is a widely utilized model for ccRCC, facilitating studies on hypoxia-driven oncogenic signaling. The VHL-deficient background alters proteostasis networks, making it an ideal host for investigating stress-response pathways.
DNAJA2 is a Hsp70 co-chaperone that stimulates ATP hydrolysis, enabling client protein processing. It functions downstream of HSF1 and is activated by heat shock, oxidative stress, and unfolded proteins. DNAJA2 interacts with Hsp70 (HSPA1A/HSPA8), CHIP (STUB1), BAG family co-chaperones, and ubiquitin ligases, linking chaperone activity to the ubiquitin-proteasome system. It directs client proteins??such as steroid hormone receptors and kinases??toward folding, translocation, or degradation. Thus, DNAJA2 participates in protein folding, heat shock response, ER-associated degradation, and apoptosis signaling, regulating the turnover of ubiquitinated proteins and cell cycle regulators.
In 786-O VHL-mutant cells, DNAJA2 knockout is expected to disrupt proteostasis alongside aberrant HIF signaling. The resulting model enables dissection of co-chaperone functions in ccRCC, where heightened chaperone activity may be critical for managing oncogenic stress. Researchers can investigate how DNAJA2 loss affects client protein homeostasis, HIF-mediated pathways, and cellular responses such as migration and drug resistance.
This polyclonal knockout pool supports applications including Western blotting and RT-qPCR for expression profiling, apoptosis and migration assays for phenotypic analysis, co-immunoprecipitation for interaction studies, and immunofluorescence for protein aggregation assessment. Drug sensitivity screens can identify proteostasis modulators effective in VHL-deficient cancers. For additional information, please contact Ascent Research.
