The ACE2 Knockout 143B Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal cell population derived from the human 143B osteosarcoma line, featuring targeted disruption of the ACE2 gene. This heterogeneous knockout model encompasses a range of loss-of-function alleles, enabling population-level functional analysis without the constraints of single-cell clonal selection. The polyclonal format supports diverse experimental designs requiring robust ACE2 ablation, such as pooled screening and population-based phenotypic assays.
The host cell line 143B is a well-characterized human osteosarcoma model with osteoblast-like properties, including alkaline phosphatase expression and the capacity for osteoid mineralization. These cells are highly tumorigenic and are widely used to study osteosarcoma pathogenesis, tumor?Cbone microenvironment interactions, and bone cancer therapeutic responses. Their consistent growth kinetics and compatibility with standard gene-editing workflows make them an ideal foundation for generating knockout models.
ACE2 is a zinc metallopeptidase that catalyzes the conversion of angiotensin II to angiotensin-(1-7), counteracting the vasoconstrictive and pro-inflammatory actions of the classical renin-angiotensin system (RAS). It also functions as the primary entry receptor for SARS-CoV-2, engaging the viral spike glycoprotein. ACE2 expression is regulated by upstream signals including angiotensin II, IL-1??, TNF-??, interferon-??, and hypoxia. Its product angiotensin-(1-7) activates the Mas receptor, triggering downstream nitric oxide synthase and anti-inflammatory cytokine pathways. ACE2 interacts with the neutral amino acid transporter SLC6A19 (B0AT1). Core RAS components include renin, angiotensinogen, ACE, angiotensin II, ACE2, angiotensin-(1-7), and the Mas receptor.
In the 143B osteosarcoma background, ACE2 knockout facilitates dissection of the enzyme’s role in osteoblast-like cell differentiation, tumor invasiveness, and paracrine signaling within the bone microenvironment. Given the involvement of the ACE2/Ang-(1-7)/Mas axis in inflammation and fibrosis, this model supports investigation of how ACE2 loss influences osteosarcoma progression and drug resistance. Additionally, the knockout cells offer a relevant system to examine SARS-CoV-2 host?Cvirus interactions in a bone cancer context, potentially uncovering tissue-specific aspects of viral entry.
Detailed research applications include SARS-CoV-2 infection studies, renin-angiotensin system modulation, cardiovascular and lung disease modeling, osteosarcoma bone biology, and host?Cvirus interaction assays. Representative techniques such as ACE2 western blotting, RT-qPCR for ACE2 mRNA, ACE2 enzymatic activity assays, pseudovirus entry tests, angiotensin-(1-7) ELISA, and immunofluorescence staining are applicable to this model. For lot-specific information on knockout efficiency, culture conditions, or ordering, please contact Ascent Research.
