The DNAJB11 Knockout MES-OV Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population derived from the MES-OV human epithelial ovarian carcinoma cell line, providing a loss-of-function model for the DNAJB11 gene. DNAJB11 encodes the endoplasmic reticulum (ER) co-chaperone ERdj3, a critical regulator of protein folding and ER proteostasis. This polyclonal format offers a heterogeneous pool of edited cells, enabling functional studies of DNAJB11 without the biases introduced by clonal isolation, and is suitable for investigating ER stress biology, chaperone networks, and cancer cell vulnerability.
The MES-OV cell line is a well-characterized model of human ovarian carcinoma, an epithelial cancer type with high secretory demand and frequent reliance on ER quality control mechanisms for survival. As an adherent ovarian cancer cell line, MES-OV provides a physiologically relevant context for examining how disruption of ER chaperone function impacts tumor cell fitness, particularly under conditions of pharmacological ER stress or increased protein load.
Molecularly, DNAJB11 (ERdj3) functions as an Hsp40 co-chaperone that interacts directly with the Hsp70 chaperone BiP/GRP78 (HSPA5) to stimulate its ATPase activity, promoting efficient folding of nascent polypeptides and preventing aggregation of unfolded protein substrates. DNAJB11 expression is up-regulated by ER stress stimuli such as thapsigargin and tunicamycin, and is transcriptionally regulated by the UPR transducers ATF6 and XBP1. By activating BiP, DNAJB11 attenuates signaling through the UPR sensors IRE1??, PERK, and ATF6, thereby maintaining ER homeostasis. Additionally, DNAJB11 contributes to ER-associated degradation (ERAD) via interactions with VCP/p97 and Derlin-1, facilitating retrotranslocation and proteasomal clearance of terminally misfolded proteins. CRISPR/Cas9-mediated disruption of DNAJB11 therefore impairs BiP chaperone activity, leading to unresolved ER stress, accumulation of misfolded substrates, and potential activation of UPR-mediated apoptosis or autophagy.
In the context of MES-OV ovarian carcinoma cells, DNAJB11 knockout abrogates a key ER proteostasis factor that supports the enhanced protein secretion and survival of cancer cells under stress. Ovarian tumors often upregulate chaperone networks to cope with oncogenic proteotoxicity; thus, this knockout model allows researchers to probe the dependency of ovarian cancer cells on ERdj3-mediated quality control and to evaluate therapeutic strategies that target the UPR or ERAD pathways.
This polyclonal knockout population is well-suited for multiple experimental applications, including Western blotting for knockout validation, RT-qPCR measurement of UPR target genes (e.g., BiP, CHOP), and cell viability assays in response to ER stressors. Further functional studies may include apoptosis detection by annexin V staining, co-immunoprecipitation to assess BiP?CDNAJB11 interaction, immunofluorescence to visualize ER morphology, and transcriptomic analysis by RNA-seq to define downstream UPR networks. The cells also support chemical screening for modulators of ER stress in an ovarian cancer background. For additional details, please contact Ascent Research.
