The DNAJC10 Knockout Huh-7 Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal knockout cell population for loss-of-function analysis of the DNAJC10 gene in a human hepatic carcinoma background. This polyclonal pool, generated through CRISPR/Cas9-mediated gene disruption, provides a genetically diverse knockout model that avoids clonal selection artifacts, enabling robust functional studies of the ER co-chaperone DNAJC10. The population is derived from Huh-7 hepatocellular carcinoma epithelial cells and is intended for use in advanced biomedical research applications requiring a non-clonal knockout system.
Huh-7 is a well-differentiated hepatocellular carcinoma epithelial cell line originally isolated from a 57-year-old male patient. As a model system, Huh-7 cells retain key hepatic functions and are widely employed for investigating hepatocyte biology, drug metabolism, and the replication of hepatotropic viruses such as hepatitis C. Their epithelial nature and stable growth in culture make them an ideal host for studying endoplasmic reticulum (ER) stress responses, protein secretion, and quality control mechanisms relevant to liver pathophysiology.
DNAJC10 (ERdj5) is a critical ER co-chaperone with thioredoxin-like reductase activity that reduces disulfide bonds in misfolded glycoproteins, preparing them for retrotranslocation and proteasomal degradation. Its expression is upregulated by ER stress via the ATF6 and IRE1-XBP1 branches of the unfolded protein response (UPR). Within the ER-associated degradation (ERAD) pathway, DNAJC10 cooperates with BiP/HSPA5, EDEM1, SEL1L, and HRD1/SYVN1, and interacts with calnexin and calreticulin. By facilitating clearance of aberrant proteins, DNAJC10 mitigates ER stress-induced apoptosis mediated by the PERK-eIF2??-CHOP axis, maintaining ER homeostasis.
Knockout of DNAJC10 in Huh-7 cells creates a powerful platform for examining the intersection of ER quality control and hepatocellular carcinoma. The liver’s high secretory load and its exposure to viral pathogens make it particularly vulnerable to ER stress. In this model, loss of DNAJC10 disrupts ERAD efficiency, potentially sensitizing cells to proteotoxic insults and revealing the contribution of unresolved ER stress to liver cancer progression. This knockout thus enables dissection of how ER stress signaling intersects with hepatocarcinogenic processes.
Researchers can utilize this polyclonal knockout population in a variety of assays, including western blotting for UPR markers such as BiP and CHOP, RT-qPCR to quantify XBP1 splicing, and tunicamycin-induced ER stress viability experiments. Co-immunoprecipitation with BiP or EDEM facilitates protein interaction studies, and immunofluorescence using PDI or calnexin enables visualization of ER morphology changes. Applications extend to drug screening for ER stress modulators, proteasome activity assessments, and hepatitis C virus replication studies in a genetically perturbed background. For additional product information or technical consultation, please contact Ascent Research.
