The NMT2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid line, designed to disrupt the NMT2 gene encoding N-myristoyltransferase 2. This polyclonal knockout model provides a heterogeneous pool of edited cells, enabling loss-of-function studies of NMT2-mediated protein myristoylation without the limitations of clonal selection. The product is intended for advanced biomedical research applications requiring abrogation of NMT2 catalytic activity.
The Raji host cell line is an Epstein-Barr virus (EBV)-positive B lymphoblast line originally derived from a Burkitt lymphoma patient, harboring the characteristic t(8;14) translocation that juxtaposes the MYC oncogene to the immunoglobulin heavy chain locus, driving constitutive MYC expression. Raji cells are widely employed in immunology and cancer research, particularly for studying B-cell malignancies, signal transduction pathways, and viral interactions due to their transformed phenotype and EBV latency.
NMT2 catalyzes the N-terminal myristoylation of nascent proteins by covalently attaching a myristate moiety to glycine residues, a co-translational modification essential for membrane targeting and proper subcellular localization of numerous signaling molecules. NMT2 expression is regulated by oncogenic transcription factors such as MYC and nutrient-sensing pathways including mTORC1 and PI3K/AKT signaling. Its downstream substrates include Src family kinases (e.g., Lyn, Fyn, Src), heterotrimeric G protein alpha subunits, and ADP-ribosylation factors (ARFs), all of which require myristoylation for membrane association and signal transmission. Additionally, NMT2 interacts with calmodulin and utilizes myristoyl-CoA as a co-substrate, and it is involved in the myristoylation of viral proteins such as HIV Nef, linking it to viral replication processes.
In the Raji cellular context, NMT2-mediated myristoylation is critical for the oncogenic signaling network driven by MYC and EBV latency programs. Src family kinases myristoylated by NMT2 are key mediators of B-cell receptor signaling, proliferation, and survival. Disruption of NMT2 in Raji polyclonal knockout cells impairs the membrane localization and activity of these kinases, thereby attenuating downstream signal transduction, altering apoptosis regulation, and potentially interfering with viral protein processing. This model is therefore valuable for dissecting the contribution of NMT2 to Burkitt lymphoma pathogenesis and for evaluating the dependency of EBV-positive B-cells on myristoylation-dependent signaling.
This polyclonal knockout cell product is suitable for a range of research applications, including B-cell lymphoma functional genomics, Src kinase activity profiling, apoptosis assays, and NMT inhibitor screening. Users can perform myristoylation assays using click chemistry to monitor protein lipidation, phospho-proteomic analyses to track Src substrate phosphorylation, and flow cytometry to assess apoptotic responses. Furthermore, the model supports viral replication studies in EBV-positive B cells and drug sensitivity testing for NMT-targeted therapies. For further information or to request a quotation, please contact Ascent Research.
