The NMRK1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblast line, featuring targeted disruption of the NMRK1 gene. This product provides a loss-of-function model for investigating NMRK1-dependent NAD+ salvage metabolism in a heterogeneous cell pool, avoiding clonal selection artifacts and enabling robust studies of nicotinamide riboside kinase 1 function in B cell contexts.
The Raji host cell line originates from a Burkitt lymphoma and is Epstein-Barr virus (EBV)-positive. As B lymphoblasts, Raji cells are widely utilized for research on antibody production, B cell receptor signaling, and lymphomagenesis. Their transformed status permits continuous proliferation and offers a unique platform to examine metabolic reprogramming and oncogenic signaling in a human immune cell model.
NMRK1 encodes nicotinamide riboside kinase 1, which phosphorylates nicotinamide riboside to produce nicotinamide mononucleotide (NMN), a direct precursor of NAD+. Downstream, NMN is converted to NAD+ by NMNAT enzymes, fueling sirtuin deacetylases, PARP polymerases, and CD38 hydrolase. Upstream, NMRK1 is regulated by cellular NAD+ demand, AMPK, and SIRT1. Disruption of NMRK1 impairs NAD+ salvage synthesis, attenuating sirtuin-mediated deacetylation and PARP-dependent DNA repair, thereby altering cellular energy metabolism and stress responses.
In Raji B lymphoblasts, NMRK1 is critical for maintaining NAD+ pools that support rapid proliferation and antibody synthesis. The EBV-positive background may heighten reliance on NAD+ salvage, making this knockout model valuable for probing metabolic vulnerabilities in B cell malignancies. Loss of NMRK1 is expected to impact sirtuin activity, influencing histone deacetylation and gene expression, while compromised PARP1 function could sensitize cells to DNA-damaging agents.
Research applications include NAD+ metabolism profiling, cancer metabolic studies, aging research, and screening of NAD+ modulators. Representative assays comprise NAD+/NADH quantification, ATP luminescence, metabolic flux analysis with Seahorse, western blotting for NMRK1 and sirtuins, RT-qPCR, and immunofluorescence. This model enables dissection of NAD+ salvage in B cell immunobiology and lymphoma. For further information, please contact Ascent Research.
