The ACE2 Knockout HeLa Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa human cervical epithelial line, featuring targeted disruption of the angiotensin-converting enzyme 2 (ACE2) gene. This heterogeneous loss-of-function model avoids clonal artifacts and is suitable for investigating ACE2-mediated signaling and viral entry mechanisms in a reproducible human epithelial context.
HeLa cells, originally established from cervical adenocarcinoma, are a widely characterized epithelial model for studying barrier function, host?Cpathogen interactions, and signal transduction. They endogenously express renin-angiotensin system components and, upon ACE2 expression, support SARS-CoV-2 entry, making them a relevant platform for COVID-19 research and cardiovascular studies.
ACE2 operates as a carboxypeptidase that converts angiotensin II to angiotensin 1-7, counterbalancing the vasoconstrictive RAS through Mas receptor and Akt-eNOS signaling. As the receptor for SARS-CoV-2, it binds the spike protein, with TMPRSS2 facilitating membrane fusion. Its expression is regulated by interferon signaling and transcription factors (HNF1A, HNF1B, GATA6), and it interacts with integrins and angiotensinogen within the RAS. Representative pathway elements transmitting signals downstream include renin, angiotensinogen, angiotensin I, ACE, angiotensin II, angiotensin 1-7, and Mas receptor.
Disruption of ACE2 in HeLa cells removes its catalytic and receptor functions, enabling dissection of ACE2-dependent phenotypes in an epithelial context. This model allows researchers to quantify angiotensin peptide shifts, assess viral entry requirements, and investigate epithelial barrier and inflammatory responses under ACE2-null conditions. By providing a clean loss-of-function background, the knockout cells help validate specific roles of ACE2 in SARS-CoV-2 infection and RAS-mediated cardiovascular signaling.
Applications include pseudovirus and live virus entry assays, RAS signaling studies via angiotensin peptide quantification, and antiviral drug screening. Downstream analyses using Western blotting, RT-qPCR, immunofluorescence, and flow cytometry characterize ACE2 depletion and target modulation. The polyclonal format reduces clone-specific biases, making it ideal for large-scale functional genomics and pharmacological profiling. For further inquiries, contact Ascent Research.
