The DNAJC5 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line. This product comprises a heterogeneous pool of cells with targeted disruption of the DNAJC5 gene (encoding cysteine string protein ??, CSP??), providing a loss-of-function model for investigating CSP??-dependent processes. The polyclonal format preserves biological variability and is suitable for population-level functional assays without requiring single-cell cloning, offering a robust tool for pathway analysis and phenotypic screening.
The parental A2780 cell line was established from an untreated patient with ovarian endometrioid adenocarcinoma and is characteristically cisplatin-sensitive, widely used for ovarian cancer research and drug sensitivity studies. A2780 cells retain oncogenic signaling features and are employed in cytotoxicity, migration, and invasion assays. In this background, DNAJC5 knockout enables dissection of CSP????s role in cancer cell communication, chemoresponse, and exosome-mediated signaling.
DNAJC5 encodes CSP??, a co-chaperone that partners with Hsc70 to facilitate ATP-dependent disassembly of SNARE complexes composed of SNAP-25, syntaxin, and VAMP2, thereby sustaining vesicle exocytosis. CSP?? is palmitoylated by DHHC palmitoyltransferases for membrane anchoring and interacts with SGT and synaptotagmin. Through its chaperone activity, CSP?? regulates proteostasis and exosome secretion, positioning it at the interface of membrane trafficking and protein quality control.
In the A2780 ovarian carcinoma context, DNAJC5 knockout provides a model to explore how CSP??-mediated exosome secretion affects tumor microenvironment communication and drug sensitivity. Given its role in proteostasis, loss of CSP?? may alter protein aggregation handling and modulate chemosensitivity, including cisplatin response. Moreover, as CSP?? mutations cause neuronal ceroid lipofuscinosis (CLN4) and link to Parkinson disease, this system enables investigation of neurodegeneration-related pathways in an epithelial cancer framework, potentially revealing convergence between neuronal maintenance and tumor biology.
This polyclonal knockout pool is suited for exosome secretion quantification, SNARE complex dynamics analysis, proteostasis evaluation, and drug sensitivity profiling. Researchers can use Western blotting, RT-qPCR, immunofluorescence, flow cytometry, exosome isolation, and migration/invasion assays to characterize CSP??-dependent phenotypes. The model also supports co-culture systems and high-throughput modifier screens. For further information or customization, contact Ascent Research.
