The NFIA Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-mediated loss-of-function model in which the NFIA gene has been disrupted in the Raji B lymphocyte cell line. As a polyclonal knockout population, this product contains a heterogeneous mixture of edited alleles, reflecting the stochastic nature of CRISPR/Cas9 editing and providing a broad representation of NFIA inactivation across the cell pool. This format is well-suited for pooled functional assays and population-level studies without clonal selection.
The Raji cell line is an Epstein-Barr virus (EBV)-positive B lymphoblastoid line derived from a Burkitt lymphoma patient. It exhibits characteristics of mature B cells, including expression of surface immunoglobulins and CD markers, and serves as a widely used model for B cell biology, lymphomagenesis, and immune signaling. The EBV-positive status allows investigation of viral oncoprotein interactions with host regulatory networks, making Raji cells particularly relevant for studies of B cell malignancies and oncogenic signaling pathways.
NFIA encodes a member of the nuclear factor I (NFI) family of transcription factors that plays essential roles in glial differentiation, brain development, and hematopoietic stem cell maintenance. Upon activation by Notch and TGF-?? signaling, NFIA translocates to the nucleus where it cooperates with co-regulators such as STAT3 and SMAD proteins to modulate transcription of target genes including GFAP and HES1. Upstream regulators include NOTCH1, RBPJ, and the TGFBR1?CSMAD2/3 axis, while Wnt and SOX2 provide additional input. NFIA also physically interacts with NFIB and NFIC, integrating multiple developmental cues.
In Raji B lymphocytes, NFIA knockout disrupts transcriptional programs that may influence cell differentiation, proliferation, and survival. Although NFIA is best characterized in neural lineages, its expression in hematopoietic cells and the presence of Notch and TGF-?? pathways in B cells suggest a functional role in modulating B cell identity and oncogenic potential. Loss of NFIA in this EBV-driven lymphoma context can help elucidate the interplay between viral latency programs and host transcription factor networks, potentially revealing dependencies that contribute to lymphomagenesis.
This knockout cell model supports a wide range of experimental applications. Western blotting and RT-qPCR can confirm NFIA disruption and quantify downstream target expression. RNA-seq enables transcriptome-wide profiling to identify NFIA-dependent gene networks. Flow cytometry is suitable for assessing surface marker changes, cell cycle, and apoptosis. Functional assays such as proliferation and drug sensitivity screens benefit from the polyclonal format by capturing population-level responses. ChIP-qPCR allows mapping of NFIA genomic occupancy and histone modifications. For inquiries or technical support, please contact Ascent Research.
