ACE2 Knockout AGS Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human AGS gastric epithelial cell line. The ACE2 gene, encoding angiotensin-converting enzyme 2, has been targeted for disruption using CRISPR/Cas9-mediated genome editing, yielding a heterogeneous pool of knockout cells. This polyclonal format avoids clonal selection bias and provides a population-level gene disruption model for functional studies.
The AGS cell line is a widely used model of gastric epithelium, originally established from a human gastric adenocarcinoma. These adherent epithelial cells are instrumental in studying gastric cancer biology, mucosal homeostasis, and host-pathogen interactions. Their gastric origin makes them particularly valuable for modeling gastrointestinal manifestations of systemic diseases and tissue-specific gene functions.
ACE2 is a carboxypeptidase that critically regulates the renin-angiotensin system by converting angiotensin II into angiotensin-(1-7), which activates the Mas receptor to promote vasodilation and anti-inflammatory responses. Its expression is modulated by angiotensin II, inflammatory cytokines IL-1?? and TNF, type I interferons, HNF1??, and glucocorticoids. Downstream, angiotensin-(1-7) stimulates the PI3K/Akt pathway and nitric oxide synthase. ACE2 also serves as the cellular receptor for SARS-CoV-2, interacting directly with viral spike protein, with entry facilitated by TMPRSS2 and the amino acid transporter B0AT1.
In AGS gastric epithelial cells, ACE2 plays a crucial role in regulating local angiotensin II to angiotensin-(1-7) conversion, influencing pathways downstream of the Mas receptor, including PI3K/Akt and nitric oxide synthase. Loss of ACE2 disrupts this protective axis and may affect gastric mucosal integrity, inflammation, and carcinogenic processes. The knockout model enables researchers to examine ACE2-dependent contributions to gastric cancer biology and to study how SARS-CoV-2 exploits epithelial entry factors in a relevant cellular context.
These polyclonal knockout cells are well-suited for investigating SARS-CoV-2 entry mechanisms in gastric epithelium using pseudovirus neutralization assays, spike protein binding studies, and TMPRSS2 co-expression analysis. They enable detailed analysis of ACE2-dependent regulation of the renin-angiotensin system in gastric cells, including quantification of angiotensin peptides by mass spectrometry or ELISA and assessment of downstream signaling via Western blotting, RT-qPCR, and flow cytometry. In addition, the cells can be employed in functional studies of gastrointestinal inflammation and epithelial homeostasis, as well as for high-throughput screening of small molecules modulating ACE2 enzymatic activity or expression. For further information and technical support, please contact Ascent Research.
