The NAMPT Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population derived from human Raji B lymphocytes. This loss-of-function model is designed to study the biological consequences of NAMPT disruption in NAD+ metabolism and associated signaling networks. The polyclonal nature ensures a heterogeneous knockout pool, minimizing clonal selection artifacts while providing a robust platform for functional genomics and drug target validation in B-cell lymphoma contexts.
Raji cells are an Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma-derived B-lymphoblastoid cell line that retains key characteristics of antibody-producing immune cells. These cells exhibit rapid proliferation, express B-cell surface markers, and serve as a widely used model for B-cell malignancies. The EBV-transformed status confers unique metabolic and signaling dependencies, including heightened NAD+ turnover, which makes Raji cells particularly relevant for investigating NAMPT function in lymphoma biology.
NAMPT encodes the rate-limiting enzyme of the NAD+ salvage pathway, catalyzing the conversion of nicotinamide to nicotinamide mononucleotide (NMN), which is subsequently converted to NAD+ by NMNAT1. NAD+ serves as a critical cofactor for sirtuin-mediated deacetylation (e.g., SIRT1) and PARP-catalyzed DNA repair (e.g., PARP1). NAMPT expression is transcriptionally regulated by AMPK, HIF-1??, and the circadian CLOCK/BMAL1 complex, and can be induced by inflammatory cytokines TNF?? and IL-1??. The protein also functions extracellularly as visfatin, interacting with the insulin receptor to modulate glucose metabolism and inflammation. Thus, NAMPT sits at the nexus of energy sensing, circadian rhythm, inflammation, and genomic stability.
In Raji B-lymphoma cells, NAMPT knockout disrupts NAD+ biosynthesis, leading to impaired SIRT1 deacetylase activity and reduced PARP1-dependent DNA repair, which can trigger metabolic stress and apoptosis. Given the high proliferative rate of Raji cells and their reliance on aerobic glycolysis, the loss of NAMPT-mediated NAD+ salvage is expected to severely compromise mitochondrial complex I function and sirtuin signaling, potentially enhancing sensitivity to chemotherapeutic agents or NAMPT inhibitors. This model is therefore instrumental for dissecting the molecular mechanisms linking NAD+ metabolism to B-cell lymphoma survival and for evaluating therapeutic strategies targeting the NAD+ salvage pathway.
The NAMPT Knockout Raji Polyclonal Cells are suitable for a broad spectrum of research applications, including NAD+ metabolism studies, investigation of sirtuin signaling, and validation of NAMPT as a therapeutic target in B-cell lymphomas. Experimentally, researchers can assess NAMPT protein levels by Western blotting, quantify intracellular NAD+ and NMN concentrations, measure cell viability and apoptosis via Annexin V and colony formation assays, and evaluate downstream transcriptional effects on SIRT1 targets by RT-qPCR. Drug sensitivity assays with NAMPT inhibitors (e.g., FK866) can further explore synergistic effects with standard chemotherapy. For further information, please contact Ascent Research.
