The DNPEP Knockout AGS Polyclonal Cells product comprises a population of AGS human gastric adenocarcinoma cells that have undergone CRISPR/Cas9-mediated disruption of the DNPEP gene. This polyclonal knockout model enables loss-of-function studies of aspartyl aminopeptidase in a physiologically relevant gastric epithelial context. The heterogeneous pool of edited cells provides a robust system for investigating gene function without the clonal selection artifacts associated with monoclonal lines.
The AGS cell line was originally derived from a human gastric adenocarcinoma and exhibits epithelial morphology. It is widely employed in gastric cancer biology, drug response screening, and signal transduction research. AGS cells retain key characteristics of gastric epithelium, making them a suitable host for examining DNPEP function in processes such as proliferation, metabolism, and peptide turnover.
DNPEP encodes an aspartyl aminopeptidase, a zinc-dependent metalloprotease that specifically cleaves N-terminal aspartate residues from peptide substrates. This enzymatic activity contributes to the final stages of protein degradation and peptide processing, generating free aspartate and truncated peptides. The enzyme requires zinc as a cofactor and interacts directly with its substrate peptides. In the cellular context, DNPEP participates in the protein catabolic process and peptide metabolic process, linking it to amino acid recycling and intracellular peptide homeostasis. While upstream regulators of DNPEP remain poorly defined, its activity influences the availability of free aspartate and modulates the balance of bioactive peptides.
In the AGS gastric cancer model, disrupting DNPEP may perturb peptide metabolism and alter the intracellular pool of aspartate, which could impact processes such as nucleotide synthesis, energy metabolism, and cell signaling. Given that cancer cells often exhibit altered proteolytic activities, this knockout model provides a valuable tool for dissecting the contribution of aspartyl aminopeptidase to tumor cell behavior and stress responses.
This polyclonal knockout cell population is suitable for a range of functional assays, including Western blotting and immunofluorescence to confirm DNPEP ablation, aminopeptidase activity assays to quantify enzymatic impairment, and RT-qPCR for transcript analysis. Downstream phenotypic analyses such as cell proliferation, migration, or metabolic profiling can reveal the consequences of DNPEP loss in gastric cancer cells. These cells also serve as an appropriate control for peptide processing studies and for screening compounds that may modulate aminopeptidase activity. For further information or custom cell engineering requests, please contact Ascent Research.
