The NUP210 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population of the human B lymphocyte Raji cell line, engineered to disrupt the NUP210 gene encoding the nuclear pore complex glycoprotein NUP210. This pooled knockout model provides a biologically relevant system for studying nucleocytoplasmic transport and innate immune regulation without clonal effects, offering a polyclonal representation of NUP210 loss-of-function.
The Raji cell line, originally established from a Burkitt lymphoma patient, is an Epstein-Barr virus (EBV)-positive, immortalized B lymphocyte model that retains key features of lymphoblastoid cells, including active B cell receptor signaling and robust endocytic activity. These cells are extensively employed in studies of lymphomagenesis, viral latency, and immune cell biology.
NUP210 is a critical component of the nuclear pore complex, where it mediates the nucleocytoplasmic shuttling of macromolecules and contributes to nuclear envelope integrity. The glycoprotein interacts with core nucleoporins, including NUP62 and NUP153, as well as transport receptors such as importin-?? and exportin-1, and the small GTPase RAN. NUP210 expression is upregulated by interferon-?? and interferon-??, and its function is essential for the nuclear translocation of immune transcription factors IRF3 and NF-??B, a process activated by upstream kinases TBK1 and the mitochondrial adaptor MAVS during antiviral responses. Consequently, NUP210 knockout impairs the induction of interferon-?? and downstream interferon-stimulated genes, altering cellular innate immune competence.
In the Raji B lymphocyte context, NUP210 knockout compromises the nuclear import of IRF3 and NF-??B, thereby attenuating the innate antiviral transcriptional program that restricts viral replication. Since Raji cells harbor latent EBV, the loss of NUP210 provides a unique opportunity to dissect how nuclear transport gateways influence herpesvirus latency and reactivation, and how B cell malignancy-associated pathways intersect with nucleoporin function. This model also enables investigation of cell cycle kinase-dependent regulation of nuclear pore complexes in highly proliferative lymphoma cells.
Researchers can employ these NUP210 knockout polyclonal Raji cells in a wide range of experimental settings, including high-content imaging of nuclear pore complex integrity, quantitative analysis of transcription factor nuclear translocation by flow cytometry, and RNA-seq profiling of interferon-stimulated gene networks. The cells are ideally suited for antiviral innate immunity studies, where viral infection and replication assays can be combined with RT-qPCR readouts of interferon-?? and ISG induction. In cancer biology, the knockout model facilitates nucleoporin-targeted drug screening and co-immunoprecipitation studies of transport factor interactions. Additionally, the model supports autoimmune disease research relevant to primary biliary cirrhosis. For technical specifications and validation data, please contact Ascent Research.
