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Cat. No. ARG36198

ACE2 Knockout KYSE150 Polyclonal Cells

  • Product Type:

    Polyclonal Cell Population

  • Species:

    Homo sapiens (Human)

  • Tissue Source:

    Esophagus

  • Disease:

    Squamous cell carcinoma

ACE2 Knockout KYSE-150 Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the KYSE-150 human esophageal squamous cell carcinoma line. The ACE2 gene product is a transmembrane carboxypeptidase that hydrolyzes angiotensin II to angiotensin 1?C7 and acts as the cellular receptor for SARS-CoV-2, interacting with TMPRSS2 and ADAM17. Loss of ACE2 allows detailed investigation of the renin?Cangiotensin system, Mas receptor activation, bradykinin signaling, and SARS-CoV-2 viral entry mechanisms. Key applications include pseudovirus entry assays, angiotensin metabolism profiling, drug screening for ACE2 modulators, and esophageal cancer migration and invasion studies.

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Shipping Info:

Cryopreserved in vials and shipped on dry ice


Disclaimer:

For Research Use Only

  • Characteristics

    Host Cell

    KYSE-150

    Sex of Donor

    Female

    Age

    49 years

    Gene Name

    ACE2

    Gene Identifier

    NCBI Gene ID 59272

    Morphology

    Epithelial-like

    Growth Mode

    Adherent

    Storage

    Liquid nitrogen (LN2)

  • Culture Conditions

    Growth medium

    RPMI 1640:Ham's F-12(1:1)

    Supplement(s)

    10% Fetal Bovine Serum, 1% Penicillin-Streptomycin Solution

    Temperature

    37°C

    Atmosphere

    5% CO₂

  • Quality Control

    Sterility testing

    The bacterial, yeast, and fungi are not detected in these cells by daily monitor.

    Mycoplasma testing

    Negative for mycoplasma through PCR analysis

  • Disclaimer

    Intended Use

    This product is intended for laboratory in vitro use only. lt is not intended for diagnostic, therapeutic, or clinical applications.

    Disclaimer

    Ascent Research endeavors to provide accurate and up-to-date product information. However, no warranties or representations are made regarding its completeness or reliability. References to scientific literature and patents are for informational purposes only, and the customer assumes sole responsibility for verifying their accuracy.

    By accepting this product, the customer acknowledges and agrees to assume all risks associated with its receipt, handling, storage, disposal, and use, including compliance with all applicable safety and environmental regulations and precautions. Relevant laws, regulations, and ethical guidelines must be followed in conducting any research, modifications, or derivatives derived from this product.

    This product is provided "AS IS", and except as expressly stated herein, Ascent Research disclaims all other warranties, express or implied. Under no circumstances shall Ascent Research, its affiliates, or representatives be liable for indirect, incidental, consequential, or punitive damages arising from the use of this material. While Ascent Research employs rigorous quality control measures, we shall not be held responsible for damages resulting from misidentification or misinterpretation of the provided materials.

Description

ACE2 Knockout KYSE-150 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout cell population enabling loss-of-function investigation of the ACE2 gene in a human esophageal squamous cell carcinoma model. The heterogeneous pool of gene-disrupted cells provides a powerful system for studying ACE2-dependent signaling, viral entry mechanisms, and tumor biology without the clonal artifacts associated with monoclonal lines.

The parental KYSE-150 cell line originates from a poorly differentiated esophageal squamous cell carcinoma resected from a 49-year-old Japanese female. This line is extensively characterized for esophageal cancer studies, offering a clinically relevant context for examining ACE2 function in carcinogenesis and host?Cpathogen interactions.

ACE2 encodes a transmembrane carboxypeptidase that converts the vasoconstrictor angiotensin II to the vasodilatory angiotensin 1?C7, which activates the Mas receptor to counteract the renin?Cangiotensin system. ACE2 also serves as the cellular receptor for SARS-CoV and SARS-CoV-2 spike proteins, requiring TMPRSS2-mediated priming and ADAM17 sheddase activity. The protein interacts with CALM and is regulated by angiotensin II, angiotensin 1?C7, and viral spike protein. Downstream, angiotensin 1?C7 signals through Mas and AT2 receptors, and ACE2 activity influences the bradykinin B1/B2 receptor and apelin pathways. In esophageal cancer, ACE2 may modulate proliferation and the tumor microenvironment.

Within the KYSE-150 esophageal cancer background, ACE2 knockout allows dissection of the enzyme’s impact on angiotensin/bradykinin-mediated signaling, cell growth, and susceptibility to viral infection. The model is pertinent for exploring how ACE2 loss alters cancer cell behavior and for evaluating the esophageal epithelium’s response to SARS-CoV-2 entry, given the reported ACE2 expression in esophageal tissues.

Key research applications encompass SARS-CoV-2 pseudovirus entry assays, angiotensin metabolism profiling through enzymatic activity measurements, and protein interaction analyses via co-immunoprecipitation with spike protein. Additional applications include drug screening for ACE2 modulators, migration/invasion studies, immunofluorescence, Western blotting, RT-qPCR, and flow cytometry for surface ACE2. These polyclonal knockout cells offer a versatile tool for both cancer biology and virology. For technical consultations, contact Ascent Research.

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