In Stock Cell Lines
Homo sapiens (Human)
Lung
Adherent
The NQO1 Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited knockout model in immortalized human bronchial epithelial cells. It targets NQO1, an Nrf2-regulated oxidoreductase that detoxifies quinones, reduces oxidative stress, and bioactivates prodrugs like ??-lapachone. NQO1 functions downstream of KEAP1/Nrf2/ARE signaling and interacts with p53 and HIF-1??. Applications include studying chemoresistance, oxidative stress response, and Nrf2 pathway dynamics using assays such as menadione reduction, ARE-luciferase reporters, and ROS flow cytometry. This cell line is well-suited for lung cancer and toxicology research.
FMC1 Knockout Hela Polyclonal Cells
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CAMKK2 Knockout HCT116 Polyclonal Cells
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LY96 Knockout 786O Polyclonal Cells
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CHST3 Knockout AGS Polyclonal Cells
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The NQO1 Knockout BEAS-2B Cell Line is a CRISPR/Cas9-edited knockout cell line targeting the NQO1 gene in BEAS-2B human bronchial epithelial cells. This loss-of-function model enables dissection of NQO1-mediated quinone detoxification, antioxidant defense, and prodrug bioactivation in a physiologically relevant airway system. The stable gene disruption eliminates enzymatic activity, providing a clean platform for Nrf2-dependent oxidative stress and xenobiotic metabolism studies.
BEAS-2B cells are SV40 large T-antigen immortalized normal human bronchial epithelial cells, widely used as a non-tumorigenic model for airway biology and toxicology. They retain key epithelial features and exhibit robust ARE-driven transcription upon Nrf2 activation, making them ideal for investigating NQO1??s role in defending against environmental quinones and oxidative damage.
NQO1 is an NAD(P)H-dependent flavoprotein that catalyzes obligatory two-electron reduction of quinones to hydroquinones, avoiding semiquinone-mediated redox cycling. Its transcription is primarily governed by the KEAP1-Nrf2-ARE axis: under stress, Nrf2 escapes KEAP1, translocates to the nucleus, and heterodimerizes with small MAF proteins to activate AREs, inducing NQO1 together with HO-1 and GSTs. AhR also contributes. The hydroquinone products act as antioxidants, while for prodrugs like ??-lapachone, bioactivation triggers futile cycling and ROS overproduction. NQO1 additionally interacts with p53, HIF-1??, and the 20S proteasome, influencing p53 stability and proteasomal function.
In bronchial epithelial cells, NQO1 is critical for detoxifying inhaled quinones and electrophiles. Knockout of NQO1 in BEAS-2B abrogates this defense, increasing sensitivity to oxidative and electrophilic stress. This model is thus valuable for studying early lung carcinogenic events, airway toxicology, and Nrf2 pathway dysfunction. The non-tumorigenic background permits examination of NQO1??s role prior to transformation, including its crosstalk with p53.
The cell line supports menadione-based activity assays, RT-qPCR and western blotting for NQO1 and downstream targets, ROS flow cytometry, ARE-luciferase reporter assays, and ??-lapachone cytotoxicity tests. Co-immunoprecipitation can explore NQO1 protein interactions. Applications include chemoresistance mechanisms, oxidative stress signaling, Nrf2 pathway modulation, and environmental toxicology screening. For additional information, contact Ascent Research.
