BLVRB Knockout HAP1 Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal cell population designed for loss-of-function studies of the BLVRB gene in a haploid human cell background. The engineered disruption of BLVRB in HAP1 cells abolishes biliverdin reductase B function, providing a defined genetic model to dissect heme catabolism and antioxidant defense pathways. This product is supplied as a heterogeneous pool of edited cells, ensuring population-level representation of knockout effects and facilitating robust functional genomics applications without the constraints of single-cell clonal selection.
HAP1 cells are derived from the KBM-7 chronic myeloid leukemia cell line and maintain a near-haploid karyotype, which simplifies genetic manipulation and phenotypic interpretation. Originating from a male donor, this cell line has been optimized for high-throughput genetic knockout screening due to its haploid genome, allowing efficient gene disruption by CRISPR/Cas9. The HAP1 background is well-characterized for studies involving signaling networks, drug response, and disease modeling, offering a reproducible platform for investigating gene function in a leukemic context.
BLVRB encodes biliverdin reductase B, a cytoplasmic enzyme that catalyzes the NADPH-dependent reduction of biliverdin IX?? to bilirubin, the terminal step in heme degradation. Bilirubin functions as a potent endogenous antioxidant, protecting cells from oxidative stress. BLVRB is regulated upstream by HMOX1-mediated heme cleavage, which generates biliverdin as its substrate, and interacts with cofactors FMN and NADPH. The enzyme acts downstream of heme oxygenase 1 (HMOX1) to produce bilirubin, which subsequently undergoes conjugation by UGT1A1 for excretion. Through these interactions, BLVRB contributes to cellular antioxidant capacity and redox homeostasis.
In the HAP1 haploid model, disruption of BLVRB is particularly informative for interrogating the heme degradation pathway and its role in diseases associated with bilirubin metabolism, such as hyperbilirubinemia, cancer, and neurodegenerative disorders. The loss of BLVRB-mediated bilirubin production sensitizes cells to oxidative stress, enabling researchers to delineate the contribution of this enzyme to cytoprotection in leukemic cells and other oxidative stress-related pathologies.
Key applications include high-throughput screening for modulators of heme catabolism, mechanistic studies of antioxidant defense, and assessment of BLVRB in cancer cell viability. Researchers can employ western blotting for BLVRB expression analysis, bilirubin quantification by ELISA or HPLC, ROS detection with DCFDA, cell viability MTT assays, NADPH consumption measurements, and RT-qPCR for heme degradation genes. This knockout model is essential for drug discovery targeting redox pathways and bilirubin metabolism. For further details, please contact Ascent Research.
