The DNAJC5 Knockout 786-O Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population generated from the human 786-O renal cell adenocarcinoma line. This product delivers targeted disruption of the DNAJC5 gene, yielding a heterogeneous pool of loss-of-function cells that avoids clonal selection biases. The polyclonal format enables robust functional genomics studies across a diverse mutational spectrum.
The 786-O parental line, derived from a primary clear cell renal cell carcinoma, is a widely utilized model of renal epithelial cell biology. Its well-documented signaling networks and tumorigenic properties make it an ideal host for examining gene function in oncogenic contexts. Introducing a DNAJC5 knockout into this background facilitates investigation of the gene??s potential roles in renal carcinoma and epithelial physiology.
DNAJC5 encodes cysteine string protein ?? (CSP??), a co-chaperone that facilitates SNARE complex assembly during regulated exocytosis. CSP?? interacts with Hsc70 and SGT to maintain the functional conformation of SNARE proteins syntaxin, SNAP-25, and VAMP, and is regulated by heat shock factor 1 and neuronal activity. The chaperone cycle also involves representative pathway components synaptotagmin and complexin. Loss of DNAJC5 function disrupts SNARE-mediated vesicle fusion and triggers protein aggregation, mechanisms central to neuronal ceroid lipofuscinosis.
Within 786-O renal epithelial cells, DNAJC5 knockout allows exploration of CSP????s non-neuronal functions, particularly in chaperone-mediated secretion and proteostasis. Renal carcinoma cells may depend on exocytic pathways for growth factor release or stress adaptation, making this model valuable for uncovering disease-relevant vulnerabilities. It also provides a comparative system to study how protein misfolding and aggregation, typical of neurodegeneration, manifest in epithelial cancer cells.
Applications include dissecting DNAJC5??s role in renal cell carcinoma, analyzing chaperone-driven exocytosis, and modeling aspects of neuronal ceroid lipofuscinosis. Researchers can perform Western blotting to confirm knockout, RT-qPCR for transcriptional analysis, co-immunoprecipitation to assess SNARE complex formation, and immunofluorescence for CSP?? localization. Functional assays such as secretion measurements and cell viability tests further characterize the knockout phenotype. For further information, please contact Ascent Research.
