The CBR4 Knockout HT29 Polyclonal Cells are a heterogeneous population of CRISPR/Cas9-edited HT29 cells in which the CBR4 gene has been disrupted, providing a robust loss-of-function model for carbonyl reductase 4. This polyclonal knockout product retains the inherent genetic diversity of the edited pool, enabling study of gene disruption effects without clonal selection artifacts.
The HT29 host cell line is a well-characterized human female colorectal adenocarcinoma epithelial model isolated from a primary tumor. It is widely employed as a versatile system for investigating intestinal epithelial biology, colorectal cancer pathobiology, and drug transport mechanisms, and it exhibits an epithelial phenotype with tight junctions and microvilli under appropriate culture conditions.
CBR4 encodes an NADPH-dependent carbonyl reductase that catalyzes the reduction of carbonyl groups in diverse substrates, including xenobiotics and endogenous eicosanoids such as prostaglandin E2 and leukotriene B4. Its expression is regulated upstream by transcription factors NRF2 and PPAR?? in response to oxidative stress and lipid metabolism signals. CBR4 interacts with cytochrome P450 enzymes and requires NADPH as a cofactor, and it acts downstream of xenobiotic-sensing pathways to generate reduced metabolites. Loss of CBR4 disrupts the metabolic detoxification and bioactivation of anthracyclines and alters eicosanoid profiles linked to inflammatory signaling.
In the HT29 colorectal cancer context, CBR4 knockout impairs carbonyl reduction capacity, directly affecting cellular responses to anthracycline chemotherapeutics such as daunorubicin. This makes the model highly relevant for dissecting mechanisms of chemoresistance and for evaluating how eicosanoid metabolism influences colorectal tumor progression and inflammatory conditions. The epithelial origin also permits investigation of intestinal drug metabolism and toxicity.
These polyclonal knockout cells are ideal for applications including western blotting to confirm CBR4 ablation, carbonyl reductase activity assays, drug sensitivity profiling via viability assays, and LC-MS-based eicosanoid quantification. They support research into xenobiotic metabolism, anthracycline resistance, and lipid mediator signaling. For further technical details and ordering information, please contact Ascent Research.
