The DNPEP Knockout Huh-7 Polyclonal Cells represent a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the Huh-7 human hepatocellular carcinoma cell line. This product is designed for researchers aiming to investigate the functional roles of DNPEP, the gene encoding aspartyl aminopeptidase, in hepatic biology. The polyclonal nature of the knockout population provides a heterogeneous pool of edited cells, each carrying distinct CRISPR/Cas9-induced disruptions in the DNPEP locus, enabling robust loss-of-function studies without the need for single-cell cloning. This model serves as a versatile tool for exploring DNPEP-dependent mechanisms in a liver-derived cellular context.
The parental Huh-7 cell line is a well-differentiated hepatocellular carcinoma line originally derived from a 57-year-old Japanese male. Huh-7 cells are extensively used as an epithelial model for liver biology, hepatotropic virus infection (such as hepatitis C virus), and drug metabolism research. Their hepatic origin and retention of many liver-specific functions make them a suitable platform for studying the molecular pathways that govern hepatocyte physiology and pathology. This cellular background provides a clinically relevant system for probing the role of DNPEP in hepatocellular carcinoma and liver-associated diseases.
DNPEP encodes a cytosolic zinc-dependent metallopeptidase that selectively cleaves N-terminal aspartate residues from oligopeptides, positioning it as a critical modulator of peptide hormone processing. Within the renin-angiotensin system (RAS), DNPEP acts downstream of Angiotensin II and is regulated by upstream signals such as inflammatory cytokines and hypoxia. The enzyme converts Angiotensin I to des-Asp1-Angiotensin I and directly generates Angiotensin III from Angiotensin II, thereby influencing the balance of vasoactive peptides. DNPEP functions in concert with other RAS components, including Renin, Angiotensinogen, ACE, AT1R, Aminopeptidase A, and Aminopeptidase N, and relies on a zinc cofactor for its catalytic activity. Through these interactions, DNPEP helps regulate blood pressure, cardiac remodeling, and local tissue signaling.
In the Huh-7 hepatic context, the disruption of DNPEP expression enables the dissection of aspartyl aminopeptidase function in liver-specific RAS pathways and peptide turnover. The liver is a central site for angiotensinogen production and harbors a local RAS that contributes to hepatic fibrosis, inflammation, and tumorigenesis. By ablating DNPEP in this hepatocellular carcinoma model, researchers can assess how altered Angiotensin peptide metabolism affects cell proliferation, migration, and fibrogenic responses. This knockout model is particularly valuable for studying the interplay between RAS signaling and hepatocellular carcinoma progression, as well as for exploring DNPEP as a potential therapeutic target in hypertension and liver disease.
Key research applications include the investigation of hepatic renin-angiotensin system dynamics, functional analysis of aspartyl aminopeptidase in hepatocellular carcinoma, and drug screening for RAS modulators. This polyclonal knockout cell population is compatible with a range of experimental techniques, including Western blotting and RT-qPCR for expression analysis, ELISA or Luminex-based quantification of angiotensin peptides, ACE activity assays, and phenotypic assays such as flow cytometry, immunofluorescence, cell viability, and migration assays. These cells provide a robust platform for probing DNPEP-dependent mechanisms in liver fibrosis models and peptide hormone processing. For further technical details or to request a quote, please contact Ascent Research.
