ACE2 Knockout T-47D Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the T-47D human breast cancer cell line. This product consists of a heterogeneous pool of cells with targeted disruption of the ACE2 gene, providing a loss-of-function model to investigate ACE2-dependent processes. The polyclonal format ensures representation of diverse knockout events and facilitates population-level analysis without clonal selection. Cells are supplied as a ready-to-use population for immediate integration into experimental workflows.
The T-47D cell line is a well-characterized model of estrogen receptor-positive breast ductal carcinoma, originally isolated from a pleural effusion. These cells express both estrogen and progesterone receptors and are responsive to hormonal stimuli, making them a standard tool for studying hormone-dependent signaling, endocrine therapy resistance, and breast cancer progression. Their epithelial morphology and adherent growth characteristics support a wide range of cell-based assays.
ACE2 encodes angiotensin-converting enzyme 2, a carboxypeptidase that cleaves angiotensin II to generate angiotensin-(1?C7), a heptapeptide that activates the Mas receptor to counterbalance the classical renin-angiotensin system. ACE2 also serves as the primary receptor for SARS-CoV-2 spike protein, mediating viral entry through interaction with spike and requiring ADAM17-mediated shedding for soluble ACE2 release. In T-47D cells, ACE2 expression is upregulated by estrogen signaling and regulated by cytokines such as interferon gamma and interleukin-1, while transcription factors HNF1?? and FOXA2 control its expression. Downstream, angiotensin-(1?C7) stimulates AKT and ERK pathways, and ACE2 physically interacts with SLC6A19 (B0AT1) and collectrin to facilitate amino acid transport.
Knockout of ACE2 in T-47D cells eliminates the conversion of angiotensin II to angiotensin-(1?C7), disrupting the protective ACE2/Ang-(1?C7)/Mas receptor axis and potentially altering estrogen-responsive signaling. This loss-of-function model allows researchers to dissect ACE2??s contribution to breast cancer cell proliferation, migration, and survival in the context of hormone receptor positivity. By removing the viral receptor, these cells also provide a controlled system to investigate SARS-CoV-2 entry mechanisms and host factor dependencies, highlighting the intersection of viral pathogenesis and cancer biology.
This polyclonal knockout cell pool is designed for a variety of research applications, including enzymatic angiotensin II-to-angiotensin-(1?C7) conversion assays, SARS-CoV-2 pseudovirus entry assays using luciferase or fluorescence reporters, and cell proliferation and migration assays to assess tumorigenic properties. It enables drug screening for ACE2 modulators, investigation of estrogen-ACE2 crosstalk via western blotting, RT-qPCR, and flow cytometry, and analysis of RAS pathway components. Researchers may also employ these cells in co-culture systems or in vivo xenograft models to study tumor microenvironment interactions. For additional information, technical support, or custom solutions, please contact Ascent Research.
