DNAJC10 Knockout MES-OV Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population in which the DNAJC10 gene (ERdj5) has been disrupted via targeted gene editing. This heterogeneous pool of MES-OV cells carries loss-of-function mutations, enabling robust investigation of ER protein quality control and stress signaling without clonal bias. The polyclonal format is ideal for population-level phenotypic analyses, including drug response profiling and pathway interrogation.
The MES-OV cell line, originally derived from a primary human ovarian endometrioid carcinoma, retains molecular features pertinent to this malignancy subtype. It is extensively used to study ovarian cancer biology, particularly mechanisms of chemoresistance and adaptation to microenvironmental stress. This background provides a clinically relevant platform for examining ER stress pathways that influence tumor cell survival.
DNAJC10 (ERdj5) is an ER co-chaperone and disulfide reductase that partners with BiP to recognize misfolded proteins and facilitates their ER-associated degradation (ERAD). It interacts with EDEM, SEL1L, and the DERL1 translocon to promote retrotranslocation of substrates to the cytosol for proteasomal degradation. ER stress sensed by IRE1, PERK, and ATF6 upregulates DNAJC10, linking the UPR branches??IRE1-XBP1, PERK-eIF2??-ATF4, and ATF6??to ERAD. Knockout of DNAJC10 impairs retrotranslocation, causing accumulation of misfolded proteins, persistent UPR activation, and increased apoptosis sensitivity.
In ovarian cancer, DNAJC10 disruption serves as a tool to dissect ER proteostasis in tumor fitness and therapy response. Endometrioid ovarian carcinoma cells exploit the UPR for growth under hypoxia and chemotherapy; loss of DNAJC10 compromises clearance of misfolded proteins, raising ER stress and lowering apoptotic threshold. This sensitization is relevant for studying drug resistance and identifying synthetic lethal vulnerabilities.
Applications include mechanistic studies of ERAD and UPR, screening of ER stress modulators, and chemoresistance research. Standard assays encompass western blot for BiP and CHOP, RT-qPCR for XBP1 splicing, apoptosis detection via TUNEL or caspase-3 activation, and cell viability assays under tunicamycin treatment. Co-immunoprecipitation defines DNAJC10??s interactome, and immunofluorescence visualizes ER morphology. These cells are also suitable for functional genomics screens. For further information, please contact Ascent Research.
