The NUP37 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population designed for loss-of-function studies of the NUP37 gene in B lymphoblastoid models. Generated from the Raji cell line using CRISPR/Cas9-mediated gene disruption, this heterogeneous population provides a robust tool to interrogate nuclear pore complex biology, nucleocytoplasmic transport, and mitotic regulation without the constraints of monoclonal isolation. Researchers can leverage this polyclonal knockout cell model to assess population-level effects of NUP37 deficiency, enabling physiologically relevant analyses of nuclear transport and cell cycle control in a neoplastic lymphocyte background.
Derived from a human Burkitt lymphoma, the Raji host cell line is an EBV-positive, suspension lymphoblastoid line that retains characteristics of mature B lymphocytes. Raji cells are widely utilized as a model system for humoral immune response studies and oncogenic mechanisms, particularly those involving MYC translocation. Their neoplastic origin and active proliferation make them highly suitable for investigating nuclear pore complex dynamics, mitotic fidelity, and transport-dependent signaling pathways in B-cell malignancies. The suspension growth phenotype facilitates high-throughput screening and scalable assay formats.
NUP37 encodes a core scaffold component of the Nup107-160 subcomplex, a structural module essential for nuclear pore complex assembly, bidirectional nucleocytoplasmic transport, and mitotic progression. Functionally, NUP37 is regulated upstream by CDK1, PLK1, and E2F transcription factors, integrating cell cycle signals with nuclear pore biogenesis. It directly interacts with NUP107, NUP133, NUP160, SEC13, SEH1, importin beta, and CRM1 to mediate Ran GTPase-dependent transport and spindle assembly checkpoint signaling. Downstream, NUP37 depletion disrupts mitotic checkpoint complex proteins MAD2 and BUBR1, leading to chromosome missegregation, and impairs nuclear import of key cargoes such as p53 and NF-??B, thereby linking nuclear pore function to genome stability and lymphomagenesis.
In the Raji background, NUP37 knockout profoundly impacts pathways relevant to Burkitt lymphoma. The Nup107-160 subcomplex is critical for maintaining nuclear pore integrity and cell cycle checkpoints; its disruption in this EBV-driven B-cell line illuminates how nuclear transport defects contribute to oncogenic transformation and drug resistance. This model is particularly valuable for dissecting the roles of nucleocytoplasmic trafficking in B-cell neoplasia, including altered localization of the tumor suppressor p53 and the transcription factor NF-??B, both of which are frequently dysregulated in lymphoma. Additionally, the model facilitates studies of mitotic catastrophe mechanisms and synthetic lethal interactions with NPC deficiency.
Typical applications include investigating nuclear transport mechanisms in B-cell lymphoma through nuclear import/export assays and immunofluorescence for NPC components, studying mitotic spindle checkpoint defects via flow cytometry for cell cycle distribution and apoptosis, screening for synthetic lethal partners by drug sensitivity assays with mitotic inhibitors, and performing functional genomics analyses such as RNA-seq to catalog transcriptome changes upon NUP37 loss. Western blotting validates downstream effectors like MAD2 and p53. This polyclonal knockout population supports diverse experimental paradigms in nuclear pore biology and cancer research. For further information, please contact Ascent Research.
