The MPG Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout population derived from the Raji B lymphoblastoid cell line. This heterogeneous pool harbors disrupted alleles of the MPG gene, which encodes N-methylpurine DNA glycosylase, a critical initiator of base excision repair (BER). By using polyclonal cells rather than a single-cell-derived clone, this product minimizes clonal selection artifacts and provides a biologically relevant population-level model of MPG deficiency. Supplied as a ready-to-use resource, these cells are ideal for investigations into DNA repair dynamics, genomic stability, and therapeutic responses.
The Raji cell line is an Epstein-Barr virus (EBV)-positive B lymphoblastoid line derived from a Burkitt lymphoma patient. These suspension-adapted cells exhibit features of mature B lymphocytes and are widely utilized in studies of apoptosis, immunoglobulin regulation, and viral oncogenesis. Their origin in a lymphoid malignancy makes them a pertinent system for exploring DNA repair mechanisms in the context of B-cell biology and lymphomagenesis.
Mechanistically, MPG recognizes and removes alkylated and oxidized DNA bases, including 3-methyladenine, 7-methylguanine, and hypoxanthine, thereby initiating the BER pathway. Its expression is induced by DNA damage, oxidative stress, and the transcription factor NRF2. After base excision, MPG functionally engages the scaffold protein XRCC1, which then coordinates the sequential recruitment and activity of AP endonuclease 1 (APE1), DNA polymerase beta (POLB), and DNA ligase III (LIG3). Proliferating cell nuclear antigen (PCNA) is implicated in long-patch BER and interacts with MPG?CXRCC1 complexes. In this knockout model, the absence of functional MPG blocks efficient lesion excision, leading to an accumulation of abasic sites and single-strand breaks. Unrepaired intermediates may be converted to double-strand breaks during DNA replication, activating the broader DNA damage response mediated in part by poly(ADP-ribose) polymerase 1 (PARP1).
In the Raji lymphoma environment, MPG knockout results in persistent alkylation-induced DNA lesions, elevated mutation rates, and heightened sensitivity to alkylating chemotherapeutics such as temozolomide and methyl methanesulfonate. Combined with the inherent genomic instability and EBV-driven proliferative signals, MPG deficiency may influence lymphomagenesis and therapeutic outcomes. This model thus offers a powerful system for dissecting the contributions of BER to B-cell malignancy, investigating synthetic lethal relationships with inhibitors of PARP or other repair factors, and testing strategies to exploit DNA repair vulnerabilities.
The MPG Knockout Raji Polyclonal Cells support a broad range of assays, including Western blotting and flow cytometry for protein expression analysis, RT-qPCR for transcript quantification, comet assay and ??H2AX immunofluorescence for DNA damage assessment, cell cycle profiling, and dose-response drug sensitivity tests with alkylating agents. Mutagenesis and clonogenic survival assays can further explore genomic instability and long-term cytotoxicity. Together, these polyclonal knockout cells provide a multifaceted and physiologically relevant platform for advancing research in DNA repair, cancer biology, and therapeutic development. For further details, please contact Ascent Research.
