The DNAJB5 Knockout SK-HEP-1 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the SK-HEP-1 human hepatic adenocarcinoma cell line. This product features a targeted disruption of the DNAJB5 gene, generated using CRISPR/Cas9 technology, resulting in a heterogeneous pool of gene-edited cells. The polyclonal format provides a versatile loss-of-function model for studying DNAJB5 biology without the clonal selection bottleneck, preserving cellular heterogeneity and facilitating robust functional analyses.
The SK-HEP-1 cell line was originally established from the ascites of a male patient with liver adenocarcinoma. As a widely used hepatic cancer epithelial model, SK-HEP-1 cells exhibit characteristic features of hepatocellular carcinoma including aberrant growth signaling, metastatic potential, and altered stress responses. This genetic background is well-suited for investigating the role of molecular chaperones in liver cancer progression and therapy resistance.
DNAJB5 encodes a J-domain-containing co-chaperone that regulates protein quality control by recruiting the HSP70 chaperone (encoded by HSPA1A) to misfolded or damaged client proteins. Through its interaction with HSP70, DNAJB5 facilitates the triage of substrates toward either folding or degradation, collaborating with cofactors such as the E3 ubiquitin ligase STUB1 (CHIP) and the co-chaperone BAG3. DNAJB5 is transcriptionally activated by HSF1 in response to heat shock and oxidative stress, and is also regulated by MAPK signaling pathways. Key client proteins influenced by DNAJB5 activity include the tumor suppressor p53, the survival kinase AKT, and the ER stress sensor IRE1. Disruption of DNAJB5 perturbs proteostasis networks, leading to altered ubiquitin-proteasome function and potential changes in autophagy and apoptosis.
In the SK-HEP-1 hepatic adenocarcinoma context, DNAJB5 knockout disrupts the delicate balance between protein folding, degradation, and cellular stress responses. Given that hepatocellular carcinoma cells often rely on enhanced chaperone activity to survive proteotoxic stress and maintain oncogenic signaling, loss of DNAJB5 function may sensitize cells to apoptosis, impair proliferation, and modulate pathways critical for tumor progression. This model enables dissection of how co-chaperone dysfunction influences liver cancer cell fate, including interactions with critical client proteins such as p53 and AKT.
Researchers can employ this polyclonal knockout model to study DNAJB5-dependent processes in liver cancer biology, including chaperone-assisted protein folding, stress-induced signaling, and therapeutic resistance mechanisms. Representative experimental approaches include western blotting to assess DNAJB5 and HSP70 levels, cell viability and apoptosis assays (e.g., Annexin V staining) to measure cytotoxic responses, immunoprecipitation to probe protein?Cprotein interactions, and HSF1 transcriptional activity reporter assays. Additional applications encompass cell migration and invasion studies, enabling exploration of DNAJB5??s role in metastatic behavior. For further technical information or ordering inquiries, please contact Ascent Research.
