NFIL3 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from Raji B lymphocytes, designed to disrupt the NFIL3 (E4BP4) gene. This loss-of-function model captures a spectrum of editing outcomes, providing a heterogeneous system to study NFIL3-dependent processes without clonal bias. The polyclonal format is suited for bulk population analyses where diverse genotypes reflect the complexity of CRISPR-mediated gene targeting.
The Raji cell line, derived from an EBV-positive African Burkitt??s lymphoma, maintains a mature B-lymphoblastoid phenotype with capacity for antigen presentation and antibody production. Widely employed in immunology and oncology, these suspension-grown cells are standard models for B-cell activation, apoptosis, and EBV-mediated transformation. They provide a robust and well-characterized platform for genetic modification and diverse functional analyses.
NFIL3 is a basic leucine zipper transcription factor that represses or activates gene expression by integrating circadian and immune inputs. It is regulated by the CLOCK/BMAL1 complex, IL-3 and IL-4 via JAK/STAT and PI3K/AKT pathways, and cAMP/PKA signaling. NFIL3 directly represses IL-3 and IL-4 transcription and modulates apoptosis through Bim and Bcl-2 family members. It forms complexes with PAR-bZIP factors (DBP, TEF, HLF) and REV-ERB??, and can homodimerize or recruit co-repressors to control rhythmic gene networks.
In the Raji B-cell context, NFIL3 knockout enables dissection of its contributions to lymphomagenesis and B-cell survival. Disruption alters the balance of pro- and anti-apoptotic signals, potentially affecting EBV-related oncogenic processes. The polyclonal population reveals heterogeneous responses in apoptosis, activation marker expression, and cytokine secretion, making it valuable for examining NFIL3??s interplay with circadian and immune pathways in a relevant lymphoma background.
This polyclonal knockout model supports applications ranging from therapeutic screening for B-cell malignancies to mechanistic studies of circadian-dependent cytokine regulation. Representative assays include RT-qPCR for IL-3 and Bim, Western blotting for NFIL3 and apoptotic markers, flow cytometry for annexin V and activation markers, ELISA for cytokine secretion, and circadian bioluminescence reporter assays. Transcriptome profiling via RNA-seq and cell proliferation assays (MTS) further extend its utility. For additional information or custom cell services, please contact Ascent Research.
