CBR4 Knockout HEK293T Polyclonal Cells provide a genetically disrupted model of the carbonyl reductase 4 (CBR4) gene in a human embryonic kidney cell background. This product consists of a polyclonal population of HEK293T cells that have undergone CRISPR/Cas9-mediated gene disruption at the CBR4 locus, generating a heterogeneous knockout model suitable for studying loss-of-function effects without clonal selection. The polyclonal format captures diverse editing outcomes across the cell pool, enabling robust and reproducible functional analyses in a widely used host system.
The HEK293T host cell line is an extensively characterized derivative of human embryonic kidney 293 cells, constitutively expressing the SV40 large T antigen to enhance episomal replication and protein production. These epithelial-derived cells are a mainstay in biomedical research for recombinant protein expression, viral packaging, and signal transduction studies. Their rapid growth, high transfection efficiency, and well-documented genetic background make them an ideal platform for generating knockout models to investigate gene function in a renal epithelial context.
CBR4 encodes an NADPH-dependent carbonyl reductase belonging to the short-chain dehydrogenase/reductase family, which catalyzes the reduction of endogenous and exogenous carbonyl compounds. This enzyme plays a critical role in prostaglandin metabolism by converting 15-keto prostaglandin F2?? to less active metabolites, thereby modulating inflammatory and proliferative signaling. Its activity is regulated upstream by transcription factors such as Nrf2 and PPAR??, as well as ERK signaling cascades, and operates within a pathway involving PTGS2 (cyclooxygenase-2) and HPGD (15-hydroxyprostaglandin dehydrogenase). Disruption of CBR4 function through knockout abrogates this metabolic step, potentially leading to altered prostaglandin levels and impaired xenobiotic detoxification capacity.
In the HEK293T background, CBR4 knockout disrupts the enzymatic machinery responsible for carbonyl reduction, providing a physiologically relevant model to dissect its role in renal epithelial biology and beyond. This cell system is particularly valuable for investigating the intersection of prostaglandin signaling and detoxification pathways, which are implicated in cancer cell survival, drug resistance, and metabolic reprogramming. By eliminating CBR4 activity, researchers can examine how accumulation of unreduced carbonyl substrates affects cellular redox balance, gene expression programs governed by Nrf2 and PPAR??, and sensitivity to chemotherapeutic agents or environmental toxins. The model thus bridges fundamental biochemistry with translational applications in oncology and toxicology.
This polyclonal knockout cell population is designed for a wide array of experimental applications, including quantitative assessment of CBR4 transcript and protein levels via RT-qPCR and western blotting, functional enzyme activity measurements monitoring NADPH oxidation, and LC-MS-based profiling of prostaglandin metabolites and xenobiotic conjugates. It is ideally suited for cellular detoxification assays with model carbonyl substrates, cell viability studies under oxidative stress conditions, and mechanistic investigations into CBR4-dependent modulation of Nrf2/ERK/PPAR?? signaling nodes. For further technical specifications and ordering assistance, please contact Ascent Research.
