The NME6 Knockout Raji Polyclonal Cells product provides a heterogeneous population of Homo sapiens B lymphocytes engineered via CRISPR/Cas9-mediated disruption of the NME6 gene. These polyclonal knockout cells, derived from the Raji lymphoblastoid cell line, offer a powerful loss-of-function model to investigate the mitochondrial functions of NME6 in a B-cell lymphoma background. The polyclonal nature ensures representation of diverse editing events, enabling robust assessment of gene function without clonal bias.
Raji is an EBV-positive, suspension cell line isolated from a Burkitt lymphoma patient. As a widely used model for B-cell lymphomas, Raji cells exhibit characteristics of mature B lymphocytes and retain key oncogenic drivers, including MYC translocations. This EBV-transformed lymphoblastoid line serves as a robust platform for studying lymphomagenesis and apoptosis regulation, with relevance to both basic and translational cancer research.
NME6 encodes a mitochondrial nucleoside diphosphate kinase that maintains nucleotide homeostasis and regulates mitochondrial dynamics. Within the intrinsic apoptosis pathway, NME6 functions downstream of p53 and MYC, and its activity influences ATP synthesis, mitochondrial membrane potential, and the activation of BAX/BAK. The kinase interacts with OPA1, BCL2 family proteins, and nucleotide diphosphates, positioning it at the intersection of purine metabolism and mitochondrial respiratory chain function. Disruption of NME6 is predicted to impair mitochondrial respiration and sensitize cells to apoptosis by facilitating BAX/BAK activation and cytochrome c release, thus altering the balance between pro-survival and pro-apoptotic signals.
In the Raji Burkitt lymphoma background, where MYC overexpression and p53 dysregulation drive proliferation and survival, NME6 knockout exacerbates mitochondrial vulnerability and apoptotic priming. This model enables dissection of how nucleotide metabolism interfaces with mitochondrial stress responses and BCL2-regulated apoptosis, providing insights into mechanisms that could be exploited for therapeutic intervention in B-cell malignancies. The availability of a polyclonal population allows for the examination of NME6-dependent phenotypes without the confounding effects of single-cell clonal selection.
Researchers can employ these NME6 polyclonal knockout cells in a variety of functional assays, including Seahorse-based mitochondrial respiration analysis, Annexin V staining for apoptosis quantification, and co-immunoprecipitation to assess interactions with BCL2 proteins. The cells are suitable for drug sensitivity screens targeting mitochondrial function, as well as for RT-qPCR and Western blot analyses to validate NME6 disruption and its downstream effects on cytochrome c release and ATP levels. For detailed technical specifications and ordering information, please contact Ascent Research.
