The NFIB Knockout Raji Polyclonal Cells product provides a CRISPR/Cas9-edited polyclonal cell population derived from the Raji B-lymphocyte cell line, with targeted disruption of the NFIB gene. This heterogeneous knockout pool contains a mixture of loss-of-function alleles generated by Cas9-mediated DNA cleavage, enabling robust assessment of NFIB-dependent phenotypes without clonal artifacts. The polyclonal format preserves cellular diversity and minimizes the risk of off-target clonal effects, making it suitable for high-throughput screening and bulk functional genomics analyses. Researchers can use this model to interrogate the roles of NFIB in B-cell biology and lymphoma pathology.
The parental Raji cell line originates from a Burkitt??s lymphoma patient and is Epstein-Barr virus (EBV) positive, displaying lymphoblastoid morphology and expressing characteristic B-cell surface markers. Raji cells are widely employed as a model for studying EBV-driven lymphomagenesis, B-cell receptor signaling, and immune surveillance escape mechanisms. Their rapid proliferation and genetic tractability facilitate experimental manipulation, while the EBV-positive status provides a unique context for examining interactions between viral proteins and host transcriptional machinery.
NFIB encodes Nuclear Factor I B, a transcription factor that binds with high affinity to the palindromic sequence TTGGC(N5)GCCAA and regulates the expression of genes involved in cell proliferation, differentiation, and migration. NFIB can act as both a transcriptional activator and repressor, depending on promoter context and association with cofactors such as the histone acetyltransferases CBP/p300 or histone deacetylases (HDACs). It physically interacts with other NFI family members (NFIA, NFIC, NFIX) and is modulated by upstream mitogenic signals, developmental cues, and key transcription factors including MYC and TP53. Among its downstream targets are genes encoding integrin ??1 (ITGB1), N-cadherin (CDH2), and aromatase (CYP19A1), linking NFIB function to cell adhesion and hormone metabolism.
In the context of Raji lymphoma cells, NFIB knockout disrupts transcriptional programs that govern cell cycle progression, apoptosis, and migratory capacity. The dual role of NFIB as a potential tumor suppressor or oncogene??depending on cellular environment and complement of co-regulators??makes this model particularly valuable for dissecting context-specific effects in EBV-positive B-cell lymphomas. Loss of NFIB may alter the expression of downstream effectors such as ITGB1 and CDH2, impacting cell adhesion and metastatic potential, while crosstalk with MYC and TP53 pathways could modulate responses to genotoxic stress and therapeutic agents.
This knockout pool is ideally suited for functional investigations into transcriptional regulation in lymphomagenesis. Representative applications include western blotting and RT-qPCR for confirming gene and protein expression changes, flow cytometry for proliferation and apoptosis profiling, RNA-seq for global transcriptome analysis, and colony formation assays for clonogenic survival. The model also supports drug sensitivity screening, migration/invasion assays, and oncogene/tumor suppressor functional studies. For additional information, please contact Ascent Research.
