The NAB2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-mediated gene-disrupted population derived from human Raji B lymphocytes. This polyclonal knockout pool contains a heterogeneous collection of NAB2 alleles, collectively resulting in loss of functional protein. Unlike clonal lines, the polyclonal format preserves the genetic diversity of the parental line and is ideal for pooled functional genomics, drug-response profiling, and signaling-pathway interrogation in a lymphoma background. The targeted disruption of NAB2, a critical transcriptional corepressor, permits dissection of its role in negative regulation of growth factor-driven transcription within immune cells.
The parental Raji cell line is an EBV-positive Burkitt lymphoma suspension line that expresses B-cell surface antigens CD19 and CD20. Widely used in immunology and cancer biology, Raji cells provide a physiologically relevant model for studying B-cell receptor signaling, antigen presentation, and viral oncogenesis. The EBV-driven proliferation background renders these cells particularly informative for examining negative-feedback mechanisms controlling growth factor-induced transcription, and the suspension growth format facilitates scalable culture and high-throughput screening.
NAB2 functions as an inducible corepressor that interacts with EGR1, EGR2, and EGR3 zinc-finger transcription factors. In response to ligands such as EGF and PDGF, the RAS-RAF-MEK-ERK1/2 cascade triggers ELK1/SRF-mediated transcription of EGR1. EGR1 then binds to cognate promoters of target genes including TGFB1 and PDGFA, while also inducing NAB2. The NAB2 protein recruits HDAC1- and CHD4-containing NuRD complexes to repress EGR-driven transcription, forming a negative feedback loop. This regulation also influences the expression of apoptosis-related factors like BAX and BCL2, thereby coupling mitogenic signaling to cell fate decisions.
Disruption of NAB2 in the Raji B-cell lymphoma model allows investigators to interrogate how loss of this corepressor shifts the balance between proliferation and apoptosis. Because Burkitt lymphomas often exhibit hyperactive ERK signaling and altered EGR activity, NAB2 knockout cells serve as a platform to dissect gene programs governed by EGR-NAB regulatory circuits. Furthermore, these cells can act as a comparator for studying oncogenic NAB2 fusions, such as the NAB2-STAT6 chimera found in solitary fibrous tumors, within a hematological environment.
Researchers can deploy these cells in chromatin immunoprecipitation, co-immunoprecipitation, RNA-seq, and functional assays for proliferation (CFSE dilution) or apoptosis (Annexin V). These polyclonal knockout cells are suited for mapping NAB2-dependent transcriptional programs and screening inhibitors of MEK/ERK signaling or HDAC activity. For further technical details, please contact Ascent Research.
