The NF-κB luciferase reporter lentivirus is a versatile, ready-to-use vector system designed to convert NF-κB pathway activity into a robust and quantifiable luminescent signal. Built on a modern self-inactivating lentiviral backbone, this system couples a minimal promoter with tandem NF-κB response elements upstream of the luciferase gene, resulting in low basal expression, high inducibility, and an excellent signal-to-noise ratio. Because lentiviral vectors stably integrate into the host genome, this reporter gene supports long-term studies, the generation of clonal cell lines, and stable data acquisition across generations. Its broad host cell tropism allows for efficient transduction of a wide variety of cell types, including many primary cells and difficult-to-transfect cells, while the minimal promoter structure reduces background signal, revealing subtle differences in pathway activation.
This reporter gene is ideally suited for basic research, translational research, and drug discovery, particularly in applications where NF-κB is a key node. In cell biology and immunology, it enables quantitative monitoring of inflammatory signal transduction and feedback control, supporting studies on receptor binding, adaptor protein function, and downstream transcriptional regulation. In disease modeling, it helps elucidate the role of NF-κB in chronic inflammation, autoimmunity, metabolic dysfunction, neuroinflammation, and tumor-associated signaling in the tumor microenvironment. Drug discovery teams can utilize this reporter gene to analyze small molecules or biologics that modulate pathway components, build high-throughput screening platforms for identifying inhibitors or activators, and generate precise dose-response curves and kinetic profiles for hit compound screening and mechanism of action assessment.
BAP1, a deubiquitinating enzyme, has been implicated in the initiation and progression of pancreatic ductal adenocarcinoma (PDAC), particularly in the context of chronic pancreatitis. The researchers investigated the role of BAP1 in regulating NF-κB signaling in PDAC models. Using dual-luciferase reporter assays with Creative Biogene's NF-κB reporter plasmids, along with shRNA-mediated knockdown and expression of wild-type or mutant BAP1, they demonstrated that BAP1 deletion promotes NF-κB overactivation, enhancing PDAC cell proliferation, migration, and invasion. Mechanistically, BAP1 binds to IRAK1 and prevents IRAK4-mediated IRAK1 phosphorylation and dissociation from the Myddosome complex, thereby inhibiting sequential NF-κB activation. These findings provide mechanistic insights into BAP1-mediated suppression of PDAC progression and suggest therapeutic potential for targeting IRAK1/4 in BAP1-deficient tumors.
Figure 1.Dual-luciferase reporter assays and immunocytochemistry revealed that BAP1 loss enhances NF-κB nuclear translocation and reporter activity in PDAC cells, while re-expression of BAP1 suppresses these effects. (Zhao Y, et al., 2025)
Customer Reviews
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The NF-κB reporter lentivirus from Creative Biogene works flawlessly in our lab. We’ve used it in multiple cell lines, and the luciferase signal is strong and reproducible. Highly recommended!
United Kingdom
12/13/2021
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