NFIX Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblast line. This heterogeneous pool harbors targeted disruptions in the NFIX gene, enabling loss-of-function studies in a B-cell lymphoma background. The polyclonal format maintains genetic diversity, making it suitable for pooled screening and bulk assays without clonal selection biases.
The host Raji cell line is an Epstein?CBarr virus (EBV)-positive Burkitt’s lymphoma-derived B lymphocyte that grows in suspension and expresses CD19 and CD20 surface markers. Originally isolated from a Burkitt’s lymphoma patient, these cells carry MYC oncogene rearrangements characteristic of this malignancy and retain EBV genomes, which contribute to their transformed phenotype. Raji cells serve as a robust model for studying B-cell malignancies, oncogenic signaling networks, and therapeutic responses.
NFIX belongs to the nuclear factor I family of transcription factors that recognize TTGGC(N5)GCCAA motifs to activate or repress transcription. It is regulated by upstream inputs including SOX9, MYC, NF-??B, Notch, TGF-??, and Wnt signaling, and it interacts with cofactors such as CBP/p300, HDAC1/2, and other NFI members (NFIA, NFIB, NFIC). NFIX controls genes like CDKN1A (p21), GFAP, MBP, BCL2, and MYC, linking it to cell cycle control, apoptosis, and differentiation. In the Raji context, NFIX knockout disrupts these transcriptional networks, potentially altering the balance between proliferation and death signals that sustain lymphoma cells.
In Raji cells, NFIX knockout offers a model to dissect transcription factor contributions to Burkitt lymphomagenesis. NFIX intersects with pathways crucial for B-cell biology, such as Notch, TGF-??, and Wnt/??-catenin. Since MYC is overexpressed in these cells, loss of NFIX-mediated regulation of MYC and CDKN1A may unveil vulnerabilities in proliferation control. This model also permits exploration of interactions between EBV-driven signaling and host transcriptional programs.
The polyclonal knockout cells support functional genomics, drug target validation, and mechanistic studies in lymphoma. Typical applications include RNA-seq for transcriptome profiling, RT-qPCR and Western blotting for expression verification, ChIP-qPCR to assess NFI family binding at target loci, and flow cytometry for apoptosis (Annexin V) and proliferation (Ki-67) analysis. Viability assays (e.g., CellTiter-Glo) and drug sensitivity screens can be performed to identify compounds exploiting NFIX loss. For additional information, contact Ascent Research.
