The NME3 Knockout Raji Polyclonal Cells product consists of a CRISPR/Cas9-mediated gene-disrupted polyclonal cell population derived from the human Raji B lymphocyte line, targeting the NME3 locus. This loss-of-function model is supplied as a mixed population, allowing pooled analysis without clonal biases, and is suitable for studying NME3-dependent pathways in a Burkitt lymphoma cellular context. The CRISPR/Cas9 approach ensures targeted disruption of NME3, providing a robust tool for research on nucleoside diphosphate kinase function and its role in cancer biology.
The Raji host cell line is an EBV-positive B lymphocyte derived from a Burkitt lymphoma patient. These suspension cells are extensively utilized for immunology and cancer research, particularly for studying B-cell malignancies, NF-??B signaling, and apoptosis. Raji cells exhibit constitutive NF-??B activation, making them an ideal system for investigating pathways that intersect with NF-??B-mediated survival and proliferation. Their lymphoma origin offers a clinically relevant model for therapeutic development and mechanistic studies in hematological cancers.
NME3 encodes nucleoside diphosphate kinase 3, which catalyzes phosphate transfer to nucleoside diphosphates, maintaining GTP pools critical for signaling and cytoskeletal organization. It functions downstream of p53 and NF-??B, is regulated by steroid hormones and oxidative stress, and interacts with NME1, NME2, mitochondrial D-loop DNA, and OPA1. NME3 activity influences mitochondrial dynamics through DRP1 and OPA1 modulation and impacts apoptosis via Bcl-2 family proteins and caspase activation. Loss of NME3 disrupts mitochondrial homeostasis and cell death regulation, potentially contributing to lymphomagenesis and metastasis.
In Raji B lymphoma cells, NME3 knockout enables dissection of the interplay between nucleoside diphosphate kinase activity, mitochondrial dynamics, and NF-??B survival signaling. Because NME3 is a putative metastasis suppressor, its deletion may reveal how GTP homeostasis loss and mitochondrial dysfunction promote aggressive behavior. The polyclonal population reflects tumor heterogeneity, allowing evaluation of NF-??B target gene expression, apoptotic threshold, and metabolic reprogramming. Researchers can use this system to explore mechanisms underlying lymphomagenesis and to identify vulnerabilities in NME3-deficient lymphomas.
This NME3 knockout product supports applications such as functional B-cell lymphoma studies, apoptosis and differentiation research, and metastasis mechanism investigation. Representative assays include Western blotting, RT-qPCR, GTP activity assays, Annexin V apoptosis assays, mitochondrial membrane potential measurements, proliferation assays, and RNA-seq transcriptomics. By enabling analysis of NME3 function in a lymphoma context, the polyclonal cells help elucidate mechanisms of drug resistance and identify novel therapeutic strategies. For further information, please contact Ascent Research.
