The DNAJB14 Knockout MES-OV Polyclonal Cells are a genetically modified polyclonal population derived from the human ovarian clear cell carcinoma line MES-OV, engineered using CRISPR/Cas9 to disrupt the DNAJB14 gene. This knockout model abolishes expression of the DNAJB14 co-chaperone, enabling functional studies of its role in protein quality control and associated cellular pathways. As a heterogeneous cell pool, the product offers a robust loss-of-function system for investigating the consequences of DNAJB14 deficiency without clonal selection artifacts.
MES-OV is an established human ovarian epithelial cell line originating from an ovarian clear cell carcinoma, a histologically distinct and chemoresistant subtype of epithelial ovarian cancer. These cells retain key features of ovarian cancer biology, including aberrant signaling networks and stress response pathways. The MES-OV line is widely used in cancer research to model tumor cell behavior, drug response, and mechanisms of oncogenesis, making it a relevant platform for interrogating DNAJB14 function in ovarian clear cell carcinoma.
DNAJB14 encodes a J-domain co-chaperone that partners with HSP70 family members, such as HSPA1A and HSPA8, to facilitate protein folding and direct misfolded substrates to the ubiquitin-proteasome system for degradation. Under endoplasmic reticulum (ER) stress, DNAJB14 is transcriptionally regulated by HSF1, ATF6, and XBP1, key mediators of the unfolded protein response. It interacts with BAG3 and the E3 ubiquitin ligase STUB1 to triage client proteins, linking chaperone-mediated refolding with ER-associated degradation (ERAD). Disruption of DNAJB14 impairs these quality control mechanisms, leading to proteotoxic stress and altered proteostasis.
In MES-OV cells, which exhibit heightened ER stress due to oncogenic signaling and metabolic demands, DNAJB14 knockout provides a critical tool for dissecting proteostasis networks in ovarian clear cell carcinoma. Loss of DNAJB14 function may exacerbate accumulation of misfolded proteins, activate compensatory stress pathways, and influence cancer cell survival, migration, or drug sensitivity. This model allows investigation of how co-chaperone deficiency impacts tumor biology, offering insights into potential therapeutic vulnerabilities associated with proteotoxic stress in ovarian cancer.
Researchers can employ these polyclonal knockout cells in a variety of assays including western blotting and RT-qPCR for gene expression analysis, proteasome activity and ubiquitination assays to monitor protein degradation, and immunofluorescence to visualize protein aggregation. The model is suited for studying ER stress responses, identifying DNAJB14-dependent substrates, and validating drug targets for ovarian cancer or protein aggregation diseases. Additional applications include cell viability, migration, and drug sensitivity testing. For further information, please contact Ascent Research.
