ACE2 Knockout UM-UC-3 Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the UM-UC-3 human bladder transitional cell carcinoma line. This product provides a heterogeneous pool of cells carrying targeted disruption of the ACE2 gene, enabling loss-of-function studies without clonal selection bias. The polyclonal format is well-suited for applications requiring physiological heterogeneity and rapid functional screening.
UM-UC-3 is a well-established epithelial cell line originally isolated from a 56-year-old male with grade II transitional cell carcinoma of the urinary bladder. These cells exhibit characteristic features of tumorigenic transitional epithelium, including sustained proliferation, invasive potential, and relevant oncogenic signaling pathways. The UM-UC-3 model is widely used to investigate bladder cancer pathobiology, drug responses, and metastatic mechanisms, providing a robust platform for functional genomics.
ACE2 encodes a carboxypeptidase that critically governs the renin-angiotensin system (RAS) by converting angiotensin II to the vasoprotective peptide angiotensin (1?C7), which signals via the Mas receptor to counteract AT1R- and AT2R-mediated effects. ACE2 also serves as the primary cellular entry receptor for SARS-CoV and SARS-CoV-2, interacting directly with viral spike proteins. Its activity is regulated by upstream factors including TNF-??, IL-1, IFN-??, and ADAM17-mediated shedding, while downstream effects involve nitric oxide production, bradykinin metabolite modulation, and amino acid transport through its association with B0AT1 and collectrin. Disruption of ACE2 abolishes this protective axis and viral receptor function.
In the context of bladder cancer, ACE2 expression and its role in RAS signaling have been implicated in tumor proliferation, angiogenesis, and microenvironmental interactions. The UM-UC-3 background represents an aggressive carcinoma model; knockout of ACE2 allows dissection of its contributions to malignant phenotypes such as migration, invasion, and response to RAS-targeted therapeutics. Additionally, this polyclonal knockout model eliminates SARS-CoV-2 susceptibility, enabling biosafe investigation of viral tropism or RAS-dependent bladder cancer mechanisms without confounding viral entry.
This product is designed for advanced research applications including mechanistic studies of RAS signaling in bladder carcinoma, screening for ACE2-modulating small molecules or biologics, and evaluating SARS-CoV-2 pseudovirus entry in relevant epithelial contexts. Representative assays encompass western blotting, RT-qPCR, ACE2 enzymatic activity measurements, angiotensin peptide quantification, and cell-based functional assays such as proliferation, migration, and invasion. The polyclonal nature facilitates population-level analyses and pharmacological testing. For further details or custom project inquiries, please contact Ascent Research.
