The CBR3 Knockout HEK293T Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for functional studies of carbonyl reductase 3 (CBR3) in a human embryonic kidney background. This polyclonal product format captures a heterogeneous loss-of-function population, enabling robust gene disruption analyses without clonal selection. The CBR3 gene has been disrupted via CRISPR/Cas9-mediated gene editing, creating a versatile model for investigating the enzyme’s roles in carbonyl metabolism and cellular stress responses.
The HEK293T host cell line is a widely utilized human embryonic kidney epithelial derivative that stably expresses the SV40 large T antigen. This genetic modification confers high transfection efficiency and supports robust recombinant protein expression and viral vector production. Its well-characterized proteome, rapid growth, and ease of genetic manipulation make HEK293T an ideal chassis for knockout studies, particularly for genes involved in metabolic and stress-related pathways.
CBR3 encodes an NADPH-dependent short-chain dehydrogenase/reductase that catalyzes the reduction of carbonyl groups on diverse endogenous and exogenous substrates. It acts downstream of oxidative stress and electrophilic xenobiotics, regulated by transcription factors such as NFE2L2 (Nrf2) and AHR. Upon activation, CBR3 converts prostaglandin E2 to 15-keto-prostaglandins and reduces xenobiotic carbonyls to hydroquinone conjugates, facilitating detoxification. These activities place CBR3 within critical nodes of arachidonic acid metabolism, steroid hormone biosynthesis, and xenobiotic metabolism. The enzyme interacts with NADPH as a cofactor and belongs to a superfamily whose members govern cellular redox balance and metabolic clearance.
Disruption of CBR3 in HEK293T cells yields a physiologically relevant loss-of-function model that bypasses the need for pharmacological inhibition. Because HEK293T cells possess an active prostaglandin catabolic pathway and respond robustly to oxidative cues, CBR3 knockout enables dissection of how carbonyl reduction integrates with stress signaling. The model is particularly suited to explore how Nrf2-mediated antioxidant responses and AHR-driven xenobiotic metabolism converge on CBR3 activity. Researchers can directly assess the enzyme’s contribution to maintaining prostaglandin homeostasis and to modulating cellular sensitivity toward electrophilic chemotherapeutics.
This knockout cell pool is ideally suited for xenobiotic metabolism studies, prostaglandin signaling research, drug resistance assays, and oxidative stress pathway analysis. Standard validation and functional readouts include Western blotting and RT-qPCR to confirm CBR3 disruption, carbonyl reductase activity assays, prostaglandin E2 metabolite profiling via LC-MS/MS, and ROS detection under induced oxidative stress. Cell viability assays in the presence of chemotherapeutic agents further support translational investigations into cancer susceptibility and chemotherapy resistance. For further information or to discuss custom applications, please contact Ascent Research.
