The NOVA2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblast cell line, engineered to disrupt the NOVA2 gene. This product provides a heterogeneous pool of cells with targeted gene disruption, allowing researchers to investigate NOVA2 loss-of-function effects in a B-cell context without clonal selection artifacts. The polyclonal format avoids bias from single-cell cloning, maintaining genetic diversity while ensuring robust knockout representation across the population.
The parental Raji cell line is a human Burkitt lymphoma-derived B lymphoblast line that is Epstein-Barr virus (EBV)-positive and harbors the characteristic t(8;14) translocation leading to c-MYC overexpression. Widely used in immunology and cancer research, Raji cells serve as a model for B-cell biology, lymphomagenesis, and EBV latency. Their B-lymphocyte identity makes them suitable for studying splicing regulation in lymphoid cells, particularly when coupled with NOVA2 loss.
NOVA2 encodes an RNA-binding protein that regulates alternative splicing by binding YCAY motifs in pre-mRNA, primarily characterized in neuronal tissues but also expressed in other cell types. NOVA2 functions in spliceosome assembly and modulates exon inclusion or skipping of target transcripts such as GRIN1 (encoding NMDA receptor subunit NR1), GABRG2 (GABA-A receptor ??2 subunit), and NRXN1/2 (neurexins). Its activity is influenced by upstream regulators including REST, NeuroD1, and Ca2?/calmodulin-dependent kinase signaling, and it interacts with NOVA1, FMRP, PTBP2, and RBFOX1 to coordinate splicing networks. Knockout of NOVA2 in Raji cells disrupts this regulatory machinery, providing a clean loss-of-function background to dissect post-transcriptional control.
In the Raji B-cell lymphoma background, NOVA2 knockout cells enable the study of splicing dysregulation associated with lymphomagenesis and may shed light on paraneoplastic neurological disorders such as opsoclonus-myoclonus ataxia, where NOVA2 autoantibodies are implicated. The B-cell context is particularly relevant because NOVA2 expression is not restricted to neurons; its roles in hematopoietic cells remain underexplored. Using this model, researchers can examine how NOVA2-dependent splicing events influence B-cell proliferation, apoptosis, and response to therapeutic agents, potentially uncovering splicing vulnerabilities in lymphoma.
This knockout cell pool is ideal for a range of applications including RNA-seq with splicing analysis, RT-qPCR for alternative isoforms, crosslinking immunoprecipitation (CLIP) to map protein-RNA interactions, and functional assays such as B-cell proliferation and apoptosis measurements. It is also suitable for drug screening to identify small-molecule splicing modulators that may rescue or phenocopy NOVA2 loss. For further technical details or custom requests, please contact Ascent Research.
