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.
FGF18 Knockout HT29 Polyclonal Cells
Cat. No. ARG14257
HEATR9 Knockout HAP1 Polyclonal Cells
Cat. No. ARG22479
APMAP Knockout jurkat Polyclonal Cells
Cat. No. ARG33866
AP5S1 Knockout jurkat Polyclonal Cells
Cat. No. ARG33858
DNAJC6 Knockout NCI-H1975 Polyclonal Cells
Cat. No. ARG39331
GBE1 Knockout 786-O Polyclonal Cells
Cat. No. ARG5422
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.
