The BLVRB Knockout HT29 Polyclonal Cells product offers a CRISPR/Cas9-edited polyclonal knockout population in the HT29 human colorectal adenocarcinoma line, with targeted disruption of the BLVRB gene. This ready-to-use loss-of-function model eliminates biliverdin reductase B activity, facilitating research into heme degradation and oxidative stress without requiring in-house genome editing. The polyclonal format retains the genetic heterogeneity of an edited cell pool, making it well-suited for comparative assays against wild-type HT29 controls in population-based experiments.
HT29 is a human colon adenocarcinoma cell line with epithelial morphology, widely employed as an intestinal epithelial model. It harbors well-characterized mutations in the tumor suppressor genes APC and TP53, resulting in dysregulated Wnt signaling and impaired p53-mediated stress responses. These genetic features make HT29 particularly valuable for studies of colorectal cancer pathogenesis, drug metabolism, and cellular redox balance. Its adherent growth and tumorigenic properties support diverse functional assays, including migration and invasion experiments.
BLVRB catalyzes the NADPH-dependent reduction of biliverdin IX?? to the antioxidant bilirubin IX??, functioning downstream of heme oxygenase-1 (HO-1) in the heme catabolic pathway. This reaction requires the cofactor FAD and is integrated with the activity of biliverdin reductase A (BLVRA), which reduces biliverdin IX??. BLVRB expression is regulated by upstream factors such as Nrf2 and hypoxia-inducible factors, and its product bilirubin IX?? modulates antioxidant response elements, the NADPH/NADP+ ratio, and anti-inflammatory cytokine production. Through these interactions, BLVRB contributes to cellular redox homeostasis and defense against oxidative stress.
In HT29 colorectal cancer cells, where metabolic reprogramming and oncogenic mutations elevate oxidative stress, BLVRB-mediated bilirubin IX?? production may serve as a critical endogenous antioxidant mechanism. Disrupting BLVRB allows researchers to dissect this protective pathway and investigate potential synthetic vulnerabilities or altered sensitivity to ROS-inducing chemotherapeutics in a cancer-relevant context. This knockout model thus provides a platform to examine the intersection of heme metabolism, redox signaling, and colorectal cancer biology.
This polyclonal knockout population is applicable to antioxidant response studies, heme metabolism research, oxidative stress modeling, and colorectal cancer investigations. Representative experimental approaches include biliverdin reductase activity assays, western blotting, RT-qPCR, HPLC-based quantification of bilirubin species, reactive oxygen species measurement, NADPH/NADP+ ratio determination, and cell viability assessment under oxidative conditions. Immunofluorescence and cell migration or invasion assays further enable phenotypic characterization in the HT29 background. For technical inquiries or to discuss custom requirements, please contact Ascent Research.
