The CCDC34 Knockout HEK293T Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population designed to ablate expression of the coiled-coil domain-containing 34 (CCDC34) gene. Derived from the widely used HEK293T human embryonic kidney epithelial cell line, this product comprises a heterogeneous pool of cells bearing targeted gene disruptions. The polyclonal format is ideal for pooled loss-of-function studies, enabling robust analysis of CCDC34-dependent phenotypes across a genetically diverse but uniformly edited population.
The HEK293T parental line originates from HEK293 cells transformed with adenovirus 5 DNA, stably expressing the SV40 large T antigen. This feature enhances extrachromosomal replication of plasmids containing the SV40 origin, conferring exceptional transfectability. HEK293T cells are a cornerstone model for recombinant protein expression, viral vector production, and protein quality control research, owing to their high metabolic rate and robust cellular machinery.
CCDC34 functions as a molecular scaffold that coordinates the aggresome-autophagy pathway by bridging the chaperone HSP70 and the co-chaperone BAG3. Under proteotoxic stress, CCDC34 is transcriptionally activated by heat shock factor 1 (HSF1) and NRF2, and it facilitates the sequestration of ubiquitinated misfolded proteins into perinuclear aggresomes. This process promotes autophagic degradation, reflected by changes in LC3 lipidation and p62 turnover. CCDC34 also modulates apoptosis regulators of the Bcl-2 family. Disruption of CCDC34 impairs aggresome formation, blocks autophagic flux, and leads to accumulation of cytotoxic protein aggregates, sensitizing cells to stress-induced cell death.
In HEK293T cells, which sustain high levels of protein synthesis, CCDC34 knockout provides a sensitive system to study proteotoxic stress responses and aggresome biology. This model is particularly relevant for cancer research, where CCDC34 overexpression is linked to chemoresistance, and for neurodegenerative disease studies that involve protein aggregation. The knockout allows dissection of pathways that protect against misfolded protein toxicity and exploration of therapeutic strategies targeting protein quality control.
Recommended applications include Western blotting for autophagy markers (LC3B, p62), aggresome visualization with ProteoStat dye, co-immunoprecipitation of BAG3 and HSP70 complexes, and flow cytometric apoptosis assays under ER stress or chemotherapeutic insult. The polyclonal population is suitable for bulk functional genomics screens, cell viability assays, and RT-qPCR confirmation of knockout efficiency. For further technical details and ordering information, please contact Ascent Research.
