The DNAJC7 Knockout A-549 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A-549 human lung adenocarcinoma cell line, designed to disrupt the DNAJC7 gene. This gene-edited pool provides a heterogeneous loss-of-function model to study DNAJC7-dependent cellular processes without clonal selection biases, enabling robust analysis of population-level responses following target-gene disruption.
The parental A-549 cell line is an epithelial-like lung adenocarcinoma model originally established from a 58-year-old Caucasian male, widely utilized in cancer biology, drug testing, and virology research. Its well-characterized signaling landscape and responsiveness to therapeutic agents make it an ideal host for investigating molecular mechanisms underlying lung adenocarcinoma progression and treatment resistance.
DNAJC7 encodes a co-chaperone that cooperates with HSP70 and HSP90 to regulate the folding, assembly, and maturation of steroid hormone receptors, including the glucocorticoid receptor and androgen receptor. Through interactions with BAG1 and STUB1/CHIP, DNAJC7 modulates receptor transcriptional activity and influences downstream apoptotic regulators. This co-chaperone network is activated by cellular stress, such as heat shock, linking protein quality control to hormone signaling and cell fate decisions.
In the A-549 lung adenocarcinoma context, loss of DNAJC7 may disrupt glucocorticoid receptor signaling and associated gene expression programs, impacting cell proliferation, apoptosis, and stress responses. This polyclonal knockout model therefore facilitates dissection of DNAJC7??s role in tumorigenic signaling and drug sensitivity, particularly to agents targeting the HSP90 chaperone machinery, which is often exploited in lung cancer therapy.
Researchers can employ this polyclonal knockout cell population in diverse functional assays, including western blotting and RT-qPCR to confirm gene disruption, co-immunoprecipitation to map altered protein interactions, and steroid hormone receptor reporter assays to quantify transcriptional changes. Apoptosis and cell proliferation assays further enable investigation of DNAJC7??s impact on survival pathways and chemotherapeutic drug resistance. These cells are suitable for genome-wide CRISPR screens and targeted functional genomics studies in lung adenocarcinoma. For additional technical details and ordering information, please contact Ascent Research.
