The CBR3 Knockout Jurkat Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Jurkat T-lymphocyte line, designed for loss-of-function studies of the CBR3 gene. This product comprises a heterogeneous mixture of cells harboring diverse CRISPR/Cas9-mediated disruptions in the CBR3 locus, enabling robust assessment of gene function without clonal selection bias. It provides a physiologically relevant model to investigate the role of CBR3 in carbonyl metabolism and redox regulation.
Jurkat is a well-characterized human acute T-cell leukemia cell line established from a 14-year-old male, widely employed to study T-cell receptor (TCR) signaling, cytokine production, and apoptotic pathways. As a model of immune surveillance, Jurkat cells express key signaling components downstream of TCR engagement, including LCK, ZAP70, and NFAT, and they secrete IL-2 upon activation. Their leukemic origin also makes them a relevant platform for oncogenic signaling and drug resistance research.
CBR3 encodes an NADPH-dependent carbonyl reductase that catalyzes the reduction of endogenous and xenobiotic carbonyl substrates, including prostaglandin E2 (PGE2), steroid hormones, and quinones, thereby regulating signaling lipid levels and detoxifying electrophilic compounds. Its expression is transcriptionally activated by NFE2L2 (NRF2) in response to oxidative stress and is also regulated by PI3K/AKT signaling. CBR3 functions in concert with other short-chain dehydrogenase/reductase family members, such as AKR1C3, and interacts with NADPH as an essential cofactor. The enzyme contributes to the metabolic network involving PTGS2 (COX-2)-generated PGE2, CYP3A4-mediated steroid metabolism, HPGDS-dependent prostaglandin D2 synthesis, and NQO1-driven quinone detoxification. Consequently, CBR3 modulates cellular redox balance, inflammatory signaling, and chemosensitivity.
Disruption of CBR3 in Jurkat T-cells is expected to impair NADPH-dependent carbonyl reduction, leading to accumulation of reactive carbonyl species and altered PGE2 catabolism. This metabolic perturbation may disturb redox homeostasis, amplify oxidative stress-induced apoptosis, and affect prosurvival signals downstream of PI3K/AKT. Given the importance of prostaglandin signaling in T-cell function and the role of redox balance in leukemic cell fitness, this knockout model offers a unique tool to dissect how carbonyl metabolism intersects with T-cell biology, leukemogenesis, and acquired drug resistance.
The CBR3 Knockout Jurkat Polyclonal Cells are suited for a broad range of investigations, including drug metabolism and chemoresistance studies using MTT-based viability assays, functional genomics screens, and transcriptomic profiling via RNA-seq. Researchers can validate CBR3 knockout by western blotting and RT-qPCR, assess alterations in reactive oxygen species (ROS) and apoptosis by flow cytometry, and quantify PGE2 levels by ELISA. The model also facilitates the study of NADPH/NADP+ dynamics and high-throughput screening of carbonyl-reducing enzyme inhibitors. For further information, please contact Ascent Research.
