The NAGK Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population generated by CRISPR/Cas9-mediated disruption of the NAGK gene in the Raji B lymphocyte cell line. This product provides a heterogeneous pool of edited cells with targeted disruption of N-acetylglucosamine kinase (NAGK), enabling loss-of-function studies without clonal isolation. The polyclonal format preserves population-level genetic diversity and avoids single-cell cloning artifacts, making it suitable for investigating NAGK-dependent processes in B cell malignancies.
Raji cells are an Epstein-Barr virus (EBV)-positive Burkitt lymphoma-derived B cell line originally established from a male patient. As neoplastic B lymphocytes, Raji cells are widely used to model B cell malignancies and study immune signaling pathways. Their derivation from an aggressive lymphoma makes them a relevant host for exploring metabolic dependencies and glycosylation alterations in cancerous B cells. The EBV-positive background adds context for investigating viral-oncogene interactions with host metabolic pathways.
NAGK encodes N-acetylglucosamine kinase, which phosphorylates GlcNAc to GlcNAc-6-phosphate in the hexosamine salvage pathway. This reaction is upstream of UDP-GlcNAc biosynthesis, where GlcNAc-6-phosphate is further processed by enzymes such as AMDHD2, GNPDA, and UAP1 to generate UDP-GlcNAc. UDP-GlcNAc serves as a critical substrate for O-GlcNAc transferase (OGT)-mediated protein O-GlcNAcylation and for N- and O-linked glycosylation of glycoconjugates. Thus, NAGK functions as a key node linking hexosamine salvage to cellular glycosylation capacity and energy metabolism. Disruption of NAGK is predicted to reduce intracellular UDP-GlcNAc pools, impair O-GlcNAc modification of proteins including B cell receptor components, and alter glycoconjugate biosynthesis.
In Raji lymphoma cells, the hexosamine salvage pathway is particularly relevant due to the high glycosylation demands of rapidly proliferating B cells and the importance of surface glycans in immune signaling. NAGK knockout in this context may compromise B cell receptor glycosylation, affecting downstream signaling and cell survival. Moreover, cancer cells often upregulate hexosamine pathway flux to support biomass production and redox homeostasis, so targeting NAGK offers a model to study metabolic vulnerabilities in Burkitt lymphoma. This polyclonal population allows researchers to assess the overall impact of NAGK loss without clonal bias, reflecting the heterogeneity of tumor cell populations.
Key applications include probing glycosylation dynamics in B cell lymphoma through lectin blotting and O-GlcNAc modification analysis, evaluating metabolic flux via metabolic tracing with labeled GlcNAc, and assessing cellular proliferation and drug sensitivity in the context of hexosamine pathway disruption. Flow cytometry can be used to monitor surface glycan profiles and apoptosis markers. This model also supports studies on the interplay between oncogenic signaling and nutrient-sensing pathways. For further details or to request a quote, please contact Ascent Research.
