NEIL2 Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes with targeted disruption of the NEIL2 gene, generating a loss-of-function model for investigating the biological roles of this DNA glycosylase. This product provides a genetically heterogeneous pool of knockout cells, reflecting a range of editing outcomes without clonal isolation, and is designed to facilitate robust functional studies while avoiding the limitations of single-clone selection. The polyclonal format enables researchers to evaluate NEIL2-dependent phenotypes in a population context that more closely mimics physiological diversity, making it particularly suited for assays that require bulk cell analysis such as biochemical fractionation, transcriptional profiling, and drug response screens.
Raji cells are an EBV-positive B lymphocyte line established from a patient with Burkitt lymphoma, a highly aggressive non-Hodgkin lymphoma. This cell line retains characteristics of germinal center B cells and serves as a widely used in vitro model for studying lymphomagenesis, B cell receptor signaling, and immunoglobulin diversification processes. Due to their rapid proliferation and well-defined genetic background, Raji cells enable reproducible investigation of DNA damage responses in a malignant lymphoid environment, providing a relevant cellular context for dissecting pathways that maintain genomic integrity during antibody maturation and in the pathogenesis of B cell malignancies.
NEIL2 encodes a bifunctional DNA glycosylase/lyase that initiates base excision repair primarily at oxidized pyrimidines within transcriptionally active regions, thereby protecting the transcribed genome from oxidative stress-induced lesions. NEIL2 expression is transcriptionally activated by NRF2 under oxidative conditions and is functionally regulated by ATM-mediated phosphorylation, establishing its role in the orchestrated cellular response to reactive oxygen species. During repair, NEIL2 interacts with PCNA at replication forks, cooperates with APE1 for downstream processing, and forms complexes with scaffold proteins XRCC1 and LIG3 to complete lesion removal, while its association with RNA polymerase II couples repair directly to transcription. This molecular network, which also includes POLB and ATM, underscores NEIL2??s critical role in preserving transcriptional fidelity and genomic stability.
In the context of B lymphocytes, NEIL2 is indispensable for somatic hypermutation and class switch recombination during antibody affinity maturation, processes that require the introduction and subsequent resolution of DNA lesions. Disruption of NEIL2 function leads to the accumulation of oxidative DNA damage, which can compromise B cell viability, impair immune responses, and promote genomic instability??features that are particularly relevant in Burkitt lymphoma models characterized by heightened replicative stress and MYC-driven proliferation. The Raji polyclonal knockout system therefore provides a valuable tool to dissect how base excision repair defects contribute to lymphomagenesis, aberrant hypermutation, and altered drug sensitivities in malignant B cells.
This NEIL2 knockout model is well-suited for a broad range of research applications, including mechanistic studies of DNA repair in B cell biology, the assessment of oxidative DNA damage responses using comet assays and ??-H2AX immunofluorescence, and the evaluation of somatic hypermutation through immunoglobulin gene sequencing. It also supports RNA-seq-based transcriptomic analyses to map NEIL2-dependent gene expression changes and drug sensitivity assays to identify potential therapeutic vulnerabilities. By enabling manipulation of the base excision repair pathway in a lymphoma-relevant cell context, this product facilitates functional genomics and drug discovery efforts targeting DNA repair inhibitors. For further information, please contact Ascent Research.
