DNAJC7 Knockout Huh-7 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Huh-7 human hepatocellular carcinoma cell line. This product provides a loss-of-function model for the DNAJC7 gene, which encodes a co-chaperone critical for Hsp70/Hsp90-mediated protein quality control. The polyclonal population contains a heterogeneous mix of cells with gene disruptions at the targeted locus, enabling studies of DNAJC7 function without clonal selection biases. This knockout model is suitable for investigating proteostasis, stress responses, and chaperone biology in a hepatic cellular context.
The Huh-7 cell line is a well-characterized model of hepatocellular carcinoma, originally established from a liver tumor in a 57-year-old Japanese male. These adherent epithelial cells retain many hepatocyte-specific functions, including metabolic activity and the ability to support replication of hepatitis C virus (HCV) and other pathogens. As a widely used host for viral replication studies and hepatic metabolism research, Huh-7 cells provide a physiologically relevant platform for examining gene function in liver-derived cancer cells. Their robust growth and transfectability make them amenable to CRISPR-based genome editing and downstream functional assays.
DNAJC7 acts as a co-chaperone that regulates the ATPase cycle of Hsc70 (HSPA8) and facilitates substrate transfer to Hsp90 (HSP90AA1) or to the ubiquitin ligase CHIP (STUB1) for proteasomal degradation. It is involved in the cellular response to proteotoxic stress and is transcriptionally regulated by HSF1, the master regulator of the heat shock response. Under stress conditions, DNAJC7 participates in stress granule dynamics by interacting with RNA-binding proteins such as G3BP1 and TDP-43. Upstream regulators include HIF1A under hypoxia and ER stress sensors (IRE1, PERK, ATF6), linking DNAJC7 to multiple stress signaling pathways. Its interactions with client proteins like steroid hormone receptors and kinases position it as a key node in proteostasis networks.
In Huh-7 cells, DNAJC7 knockout can disrupt the balance of chaperone-assisted folding and degradation, potentially sensitizing the cells to proteotoxic agents and impairing their ability to cope with misfolded proteins. Given the liver’s central role in metabolism and protein secretion, this model is particularly relevant for studying hepatic protein quality control and its link to diseases such as cancer and viral infection. For instance, HCV replication relies on host chaperone machinery, and DNAJC7 deficiency may alter viral propagation. Moreover, the model enables investigation of how compromised proteostasis influences hepatocellular carcinoma cell growth and stress adaptation.
Researchers can employ this polyclonal knockout population to dissect DNAJC7’s role in proteostasis and stress granule biology using techniques such as western blotting for Hsp70/Hsp90, immunofluorescence for stress granule markers, and ubiquitination assays. The model is applicable to cancer biology studies examining chaperone-dependent oncogenic pathways, viral replication assays for HCV or influenza, and neurodegenerative disease research exploring TDP-43 aggregation. Transcriptomic analysis via RNA-seq can reveal global changes in stress-responsive genes. For further information on this product and its validation, please contact Ascent Research.
