NME7 Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal knockout cell population derived from the human Raji B-lymphocyte line, engineered for targeted disruption of the NME7 gene. This polyclonal pool provides a heterogeneous loss-of-function model suitable for studying NME7-dependent processes in B-cell lymphoma biology. As a non-clonal population, these cells offer a representative genetic background for functional genomics screening, drug sensitivity profiling, and mechanistic interrogation of NME7??s role in oncogenic signaling and cytoskeletal regulation. The knockout is achieved through CRISPR/Cas9-mediated gene disruption, generating a mixed population that captures diverse mutational events while maintaining the core cellular context of an EBV-positive Burkitt lymphoma model.
The Raji cell line was established from a Burkitt lymphoma patient and is a widely employed model of aggressive B-cell malignancy. These lymphoblastoid cells are Epstein-Barr virus-positive and retain features of germinal center-derived B cells, including constitutive expression of immunoglobulin and key B-cell surface markers. Raji cells are extensively utilized for dissecting B-cell receptor signaling, lymphomagenesis, and mechanisms of chemoresistance. Their robust proliferation in suspension culture and compatibility with standard transfection and genome-editing protocols make them a practical system for generating knockout models such as this NME7-targeted polyclonal population, enabling high-throughput analyses of gene function in hematological cancer.
NME7 encodes a nucleoside diphosphate kinase (NDPK) that uniquely localizes to centrosomes and cilia, where it regulates microtubule organization and participates in canonical Wnt/??-catenin signaling. Through direct interaction with ??-catenin, NME7 promotes ??-catenin stabilization and TCF/LEF-dependent transcriptional activity, impacting cell proliferation and survival. In microtubule biology, NME7 interacts with ??- and ??-tubulin, facilitates GTP provision for microtubule polymerization, and contributes to centrosome duplication and mitotic spindle integrity. Its expression is controlled by RFX family transcription factors and FOXJ1, linking NME7 to ciliogenesis programs. Representative pathway components affected by NME7 loss include the ??-catenin destruction complex (GSK3??, Axin), Wnt target genes, and structural proteins governing microtubule dynamics and central pair assembly.
In the Raji B-lymphoma context, NME7 knockout offers a valuable model to explore its contribution to malignant B-cell behavior. Genomic amplification at 1q24.2, where NME7 is located, has been reported in B-cell lymphomas, suggesting a potential oncogenic role. Disruption of NME7 impairs microtubule-dependent mitotic progression and attenuates Wnt/??-catenin signaling, which are often dysregulated in lymphoma. Consequently, these polyclonal knockout cells enable investigation of how NME7 loss influences cell cycle progression, apoptosis susceptibility, and sensitivity to microtubule-targeting agents. The model aids in deciphering the integration of NME7??s dual functions in cytoskeletal dynamics and ??-catenin/TCF-mediated transcription within the context of EBV-driven lymphoproliferation.
Research applications for NME7 Knockout Raji Polyclonal Cells are diverse. They are suited for functional genomics screens to identify synthetic lethal partners in B-cell lymphoma, as well as for evaluating drug sensitivity to tubulin inhibitors such as vincristine and taxol. Typical assays include Western blotting and RT-qPCR to assess NME7, ??-catenin, and Wnt target gene expression; immunofluorescence to visualize microtubule and centrosome organization; flow cytometry for cell cycle and apoptosis analysis; co-immunoprecipitation to confirm NME7-??-catenin interaction; and proliferation/viability assays. Additionally, these cells can be employed in signaling studies of Wnt pathway modulation and in characterization of centrosomal abnormalities. For further technical details or to discuss customized applications, please contact Ascent Research.
