DNAJC25 Knockout HeLa Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, featuring targeted disruption of the DNAJC25 gene. This genetically engineered model provides a robust system for investigating the functional roles of the DNAJC25 co-chaperone in protein homeostasis. The polyclonal knockout population offers a heterogeneous loss-of-function background, enabling bulk analysis of DNAJC25-dependent cellular processes without the confounding effects of clonal selection. As a research tool, it facilitates the study of chaperone-mediated protein quality control, stress response mechanisms, and pathways relevant to cancer biology.
The host HeLa cell line is an immortalized cervical adenocarcinoma cell line of human epithelial origin, characterized by the stable integration of human papillomavirus 18 (HPV-18) sequences. This well-established model is extensively utilized in cancer research, drug discovery, and molecular cell biology. Its epithelial phenotype and transformed nature make it particularly suitable for dissecting the chaperone networks that support malignant cell survival and proliferation. The HeLa background provides a consistent genomic and proteomic context for evaluating the impact of DNAJC25 knockout on cellular fitness and stress adaptation.
DNAJC25 encodes a DnaJ-domain-containing co-chaperone that is proposed to interact with Hsp70 family members, notably HSPA8 (Hsc70) and HSPA14, to regulate protein folding, translocation, and degradation. Functioning as a cofactor in chaperone cycles, DNAJC25 participates in ATP-dependent substrate recognition and processing, contributing to the maintenance of proteome integrity under both basal and stress conditions. Its activity is modulated by upstream cellular stress signals, including heat shock and oxidative stress, and it operates within broader networks that encompass the unfolded protein response and chaperone-mediated protein quality control pathways.
In the HeLa cell context, disruption of DNAJC25 has the potential to impair chaperone-mediated protein quality control, leading to heightened sensitivity to proteotoxic insults and altered stress signaling. This model enables researchers to dissect how co-chaperones influence cancer cell resilience, protein aggregation dynamics, and apoptotic thresholds. Since HeLa cells inherently exhibit dysregulated growth control, the knockout offers a platform for exploring synthetic vulnerabilities that could inform therapeutic strategies targeting the protein-folding machinery in malignancies and other diseases linked to proteostasis dysfunction.
Typical research applications include investigations into protein folding and degradation, cancer biology, and cellular stress responses. The polyclonal knockout population can be employed in a range of experimental assays such as Western blotting to verify target depletion, RT-qPCR for transcriptional profiling, proteasome inhibition sensitivity assays, apoptosis detection, and flow cytometry-based phenotyping. This tool is well-suited for functional genomics screens, interactome studies, and the identification of downstream client proteins. For additional technical specifications or ordering information, please contact Ascent Research.
