The BLVRB knockout Jurkat polyclonal cell product comprises a heterogeneous population of Jurkat T lymphocytes engineered via CRISPR/Cas9-mediated gene disruption to abrogate biliverdin reductase B (BLVRB) expression. This polyclonal knockout cell pool provides researchers with a loss-of-function model that reflects a broad spectrum of editing events across the cell population, enabling robust functional studies without the clonal selection artifacts associated with single-cell-derived lines. The targeted disruption of the BLVRB locus eliminates the enzymatic conversion of biliverdin IX?? to bilirubin IX??, thereby perturbing cellular heme catabolic flux and redox homeostasis.
The host cell line, Jurkat, is an immortalized human CD4+ T-lymphocyte line originally established from the peripheral blood of a 14-year-old male with acute T-cell leukemia. Jurkat cells are a widely adopted model system in immunology and cancer research, extensively utilized to dissect T-cell receptor (TCR) signal transduction, apoptosis mechanisms, and HIV-1 infection dynamics. Their leukemic origin and sustained in vitro growth provide a relevant background for investigating the intersection of oxidative stress and malignant T-cell biology.
BLVRB encodes a dual-function enzyme that catalyzes the NADPH-dependent reduction of biliverdin IX?? to bilirubin IX??, a critical step in heme degradation, and also exhibits flavin reductase and dual-specificity kinase activities. The enzyme operates downstream of heme oxygenase-1 (HO-1), which generates biliverdin IX?? from heme, and is transcriptionally regulated by the NFE2L2/KEAP1 oxidative stress response pathway. BLVRB directly interacts with NADPH and biliverdin IX??, and its product bilirubin IX?? acts as an endogenous antioxidant. Additionally, BLVRB??s kinase function may impinge on insulin signaling via phosphorylation of IRS1, linking heme metabolism to metabolic pathways. The knockout model disrupts these interactions, providing a clean background to study BLVRB??s multifaceted roles.
In the Jurkat T-cell context, loss of BLVRB is expected to accumulate biliverdin IX?? and diminish bilirubin IX?? levels, thereby altering the intracellular redox environment and potentially sensitizing cells to oxidative damage. Given the sensitivity of T-cell receptor signaling to reactive oxygen species, BLVRB knockout may influence downstream events such as proliferation, cytokine production, and apoptosis. This model is particularly pertinent for exploring how heme metabolite flux modulates leukemic T-cell survival and immune functions, offering insights into therapeutic vulnerabilities in acute leukemia.
This polyclonal knockout cell pool is suited for a wide range of experimental applications, including investigation of bilirubin-dependent antioxidant defense, signaling through the NFE2L2/HO-1 axis, and the role of BLVRB in T-cell malignancies. Researchers can perform biliverdin reductase activity assays, intracellular ROS detection, viability screens under oxidative challenge, and flow cytometry-based apoptosis profiling. Transcriptomic analysis via RNA-seq can uncover global gene expression changes linked to BLVRB loss. Standard validation methods such as Western blotting and RT-qPCR enable confirmation of target knockdown. For technical specifications or ordering details, please contact Ascent Research.
