The NUDT2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B lymphocyte cell line, engineered to disrupt the NUDT2 gene. This polyclonal model provides a heterogeneous loss-of-function system suitable for studying NUDT2-dependent purine metabolism and signaling without assuming clonal uniformity. The knockout was generated using CRISPR/Cas9-mediated gene disruption, creating a mixed population of edited cells that collectively lack functional NUDT2 expression, enabling robust assessment of biological consequences in a B-cell context.
The Raji cell line is an Epstein-Barr virus (EBV)-positive B lymphoblast line originally established from a Burkitt’s lymphoma patient. These cells retain key features of B lymphocytes, including active immunoglobulin production and responses to immune stimuli, making them a standard model for B-cell malignancies, lymphomagenesis, and immune function. Their EBV-transformed status confers continuous proliferation while preserving many native signaling pathways, offering a tractable background to interrogate gene function in B-cell lymphoma and stress adaptation.
NUDT2 encodes a diadenosine polyphosphate hydrolase that asymmetrically cleaves diadenosine tetraphosphate (Ap4A) into ATP and AMP, thereby regulating intracellular purine nucleotide pools and purinergic receptor signaling. Its activity is positioned downstream of oxidative stress, p53 signaling, and the NF-??B pathway, and upstream of AMPK activation and apoptosis regulators through modulation of the ATP/AMP ratio. Representative pathway partners include adenylate kinase, AMP deaminase, and purine nucleoside phosphorylase, with Ap4A serving as the direct substrate and purinergic receptors acting as indirect interactors. Disruption of NUDT2 thus reconfigures purine metabolism, energetics, and related cellular stress responses.
In the Raji B-cell context, NUDT2 knockout is expected to perturb purinergic-mediated immune functions, energy homeostasis, and apoptotic thresholds. Since Raji cells originate from a B-cell lymphoma, this model is particularly relevant for dissecting how altered nucleotide hydrolysis impacts malignant B-cell survival, proliferation, and sensitivity to metabolic or genotoxic stress. It provides a unique platform to explore connections between NUDT2-dependent purine turnover and pathways driving lymphomagenesis, potentially revealing vulnerabilities related to NF-??B or AMPK signaling.
This NUDT2 knockout model supports a wide range of research applications, including fundamental studies of purine metabolism, B-cell lymphoma biology, and apoptosis regulation, as well as drug target validation for NUDT2-associated diseases. Researchers can employ assays such as western blotting for pathway markers, RT-qPCR and RNA-seq for transcriptional profiling, flow cytometry to quantify apoptosis, cellular ATP measurements, proliferation assays, and drug sensitivity testing. Combined with metabolomics, these analyses enable comprehensive interrogation of NUDT2’s role in cellular metabolism and immune cell function. For further information, please contact Ascent Research.
