DNAJA2 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population for studying DNAJA2 (Hdj2) function in a hepatic adenocarcinoma background. The product contains a heterogeneous pool of SK-HEP-1 cells bearing targeted gene disruptions introduced by non-homologous end joining, enabling loss-of-function experiments without clonal isolation. The polyclonal format retains parental genetic diversity while disrupting the target gene across the population, suitable for pooled knockout studies or enrichment-based workflows.
The parental SK-HEP-1 cell line is a human liver adenocarcinoma epithelial line isolated from ascitic fluid of a metastatic liver cancer patient. SK-HEP-1 cells display epithelial morphology and aggressive metastatic traits, widely used as a model for hepatocellular carcinoma and tumor dissemination. Their reproducible growth and extensive characterization make them a reliable platform for liver cancer biology, signaling, and drug response studies.
DNAJA2 (Hdj2) belongs to the HSP40 (J-domain protein) family and functions as an essential co-chaperone that regulates the ATPase cycle of HSP70. By stimulating HSP70 ATP hydrolysis, DNAJA2 promotes substrate binding and release, coordinating folding, trafficking, and degradation of client proteins. This chaperone cycle is critical for proteostasis and is integrated with stress-responsive signaling networks. DNAJA2 is transcriptionally upregulated by heat shock factor 1 (HSF1) upon cellular stress and it directly interacts with HSP70, HSP90, and co-chaperones including BAG family proteins and CHIP. Through these interactions, DNAJA2 modulates the stability of key signaling molecules such as p53, Akt, and JNK pathway components, thereby influencing apoptosis, proliferation, and stress adaptation.
In the SK-HEP-1 liver adenocarcinoma context, loss of DNAJA2 likely impairs HSP70 chaperone function, leading to misfolded protein accumulation, altered JNK signaling, and apoptosis sensitization. Given HSP70’s role in cancer cell survival and its overexpression in hepatocellular carcinoma, this knockout model provides a relevant system for studying co-chaperone dependency in tumor cells. The epithelial and metastatic nature of SK-HEP-1 also enables investigation of DNAJA2’s contribution to migration, invasion, and signal transduction.
These cells support diverse functional studies, including HSP70 ATPase activity assays, protein aggregation analyses under stress, and co-immunoprecipitation to map chaperone-client interactions. They are well-suited for apoptosis and proliferation assays to assess cell fate, as well as migration and invasion assays to evaluate metastatic behavior. Additionally, the model facilitates drug target validation for liver cancer by examining DNAJA2’s influence on client protein stability and therapeutic response. Standard techniques such as Western blotting and RT-qPCR can verify knockout efficiency. For further details, please contact Ascent Research.
