The DNAJB4 Knockout A2780 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the A2780 human ovarian carcinoma cell line, with targeted disruption of the DNAJB4 gene. This product provides a loss-of-function model for investigating DNAJB4, which encodes an Hsp40 co-chaperone critical for regulating Hsp70 ATPase activity and protein quality control. The polyclonal population captures heterogeneity of CRISPR-mediated gene disruption, offering a relevant tool for studying DNAJB4-dependent proteostasis without selecting single clones.
The parental A2780 cell line is an adherent, epithelial human ovarian carcinoma model widely utilized in cancer research, including studies of tumor biology, metastasis, and therapeutic response. Originating from an untreated patient, A2780 cells retain key characteristics of ovarian cancer and are particularly valuable for examining signal transduction pathways and drug resistance mechanisms. The A2780 background provides a well-characterized platform for dissecting the contribution of DNAJB4 to cancer cell behavior under standardized culture conditions.
DNAJB4 functions as an Hsp40 co-chaperone binding Hsp70 family members, including HSPA1A and HSPA8, to stimulate ATPase activity and direct client protein folding, translocation, or degradation. It interacts with BAG3 and the ubiquitin ligase STUB1 (CHIP), linking the Hsp70 cycle to the ubiquitin-proteasome system. DNAJB4 expression is regulated by HSF1, the estrogen receptor, and cellular stress. Downstream, DNAJB4 modulates the stability of client proteins such as p53, AKT, and apoptotic regulators, integrating stress signals with cell survival.
In A2780 cells, DNAJB4 disruption impairs proteostasis, potentially sensitizing cells to apoptosis and disrupting oncogenic signaling. Loss of DNAJB4 co-chaperone activity impairs Hsp70-mediated quality control, causing misfolded protein accumulation and altered client degradation. This is highly relevant for ovarian cancer research, where chaperone networks influence tumor progression, metastasis, and drug resistance. The knockout model enables studies of how proteostasis disruption impacts pathways involving p53 and AKT.
These polyclonal knockout cells suit protein homeostasis research, stress response studies, and cancer cell biology applications. Representative assays include western blotting and RT-qPCR for target validation, cell viability and apoptosis assays for functional impact, co-immunoprecipitation for complex analysis, heat shock protein aggregation assays for proteostasis, and migration assays for metastatic behavior. For details, contact Ascent Research.
