The DNAJC1 Knockout A2780 Polyclonal Cells consist of a polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the DNAJC1 gene in the A2780 human ovarian carcinoma cell line. This product provides a mixed-background knockout model suitable for unbiased functional genomics and drug response analyses.
The A2780 parental cell line was originally derived from an untreated human female with ovarian endometrioid adenocarcinoma and serves as a widely used epithelial model for ovarian cancer research. These cells are estrogen receptor-positive and retain key oncogenic signaling features, making them valuable for investigating drug sensitivity, resistance mechanisms, and tumor xenograft studies. A2780 cells exhibit relatively rapid proliferation and are amenable to genetic manipulation and high-throughput screening.
DNAJC1 encodes a DnaJ/Hsp40 homolog that functions as a co-chaperone for Hsp70 family members, including HSPA1A and HSPA1B, stimulating their ATPase activity to drive protein folding, translocation, and endoplasmic reticulum-associated degradation (ERAD). DNAJC1 sits at the interface of proteostasis and stress responses, with its expression upregulated by heat shock, ER stress, and transcription factors such as HSF1, XBP1, and ATF6. Downstream, DNAJC1 modulates the activity of the unfolded protein response (UPR) via effectors like ATF4, CHOP, and XBP1 spliced isoform, and influences apoptosis through Bcl-2 family members. Key interaction partners include HSPA8, BAG3, STUB1, and HSP90, positioning DNAJC1 within a network regulating protein quality control and cell fate decisions.
In the A2780 ovarian cancer model, disruption of DNAJC1 is expected to compromise cellular proteostasis, leading to accumulation of misfolded proteins and heightened sensitivity to proteotoxic stress. This sensitization may affect ER stress responses and the UPR, thereby altering cell survival and apoptosis thresholds. DNAJC1 knockout A2780 cells thus constitute a relevant platform for studying how co-chaperone dysfunction influences ovarian cancer progression, chemoresistance, and adaptation to microenvironmental stressors. The polyclonal format avoids biases associated with single-cell clones and better reflects population-level heterogeneity.
Researchers can employ this knockout model to dissect DNAJC1 functions in proteostasis and stress signaling using Western blotting for Hsp70 activation, RT-qPCR for UPR gene expression, immunofluorescence for protein aggregation, and flow cytometry for apoptosis. Cell viability assays under ER stress or drug treatment reveal altered chemosensitivity. Co-immunoprecipitation with Hsp70, RNA-seq, and proteomics further map the DNAJC1 signaling network. For technical support, please contact Ascent Research.
