The ACE2 Knockout 786-O Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the 786-O human renal cell adenocarcinoma line. This product provides a genetically modified model in which the ACE2 gene has been disrupted, resulting in loss of functional angiotensin-converting enzyme 2 protein expression. The polyclonal nature of the knockout pool offers a heterogeneous population suitable for experiments requiring pooled knockouts, enabling studies on ACE2-dependent signaling and receptor functions without clonal variation limitations.
The host cell line 786-O originates from a primary human renal cell adenocarcinoma and is widely employed as a tumorigenic model in cancer biology research. These cells exhibit characteristic features of renal carcinoma, including VHL gene inactivation, and provide a relevant epithelial background for exploring the roles of ACE2 in both physiological and pathological contexts. Their renal origin makes them particularly suitable for investigating ACE2-mediated processes within the kidney, a key organ in renin-angiotensin system regulation and SARS-CoV-2 tropism.
ACE2 functions as a carboxypeptidase that catalyzes the conversion of the vasoconstrictor angiotensin II to the vasodilatory peptide angiotensin-(1-7), thereby counterbalancing the classical renin-angiotensin system axis driven by ACE. As the primary receptor for SARS-CoV-2 entry, ACE2 directly interacts with the viral spike protein, a process facilitated by the protease TMPRSS2 and the trafficking chaperone B0AT1 (SLC6A19). Downstream, angiotensin-(1-7) signals through the Mas receptor to promote anti-inflammatory and protective effects. Representative pathway components include AGT, renin, ACE, angiotensin II, ACE2, and the Mas receptor, all converging on blood pressure regulation and tissue protection.
In the 786-O renal adenocarcinoma cell line, ACE2 knockout provides a loss-of-function model to dissect its dual roles in tumor biology and viral infection. By disrupting ACE2 expression, researchers can evaluate the impact on angiotensin II/angiotensin-(1-7) balance and downstream signaling pathways in a cancer cell context, which may influence cell proliferation, migration, or sensitivity to therapeutics. Additionally, ablation of ACE2 renders these cells resistant to SARS-CoV-2 entry, enabling studies of viral tropism and host factors required for infection in kidney-derived cells.
This polyclonal knockout cell population supports a broad range of research applications. In COVID-19 research, it facilitates host-virus interaction assays, viral entry inhibitor screening, and pseudovirus neutralization tests. For hypertension and cardiovascular studies, it enables angiotensin-converting activity assays and signaling pathway analysis via RT-qPCR, Western blotting, and immunofluorescence. ACE2’s role in acute respiratory distress syndrome can be explored through co-culture models or cytokine profiling. The knockout cells are also valuable for validating antibodies and studying interactions with partners like TMPRSS2 or B0AT1 using co-immunoprecipitation. For further information or custom orders, please contact Ascent Research.
