The MUTYH Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population in which the MUTYH gene has been disrupted to create a loss-of-function model. This product utilizes the Raji B lymphocyte cell line, offering a genetically defined system for investigating the role of MUTYH in DNA damage repair and genome maintenance.
The Raji cell line is an EBV-positive B lymphocyte model derived from a Burkitt’s lymphoma patient. These suspension cells are widely used in immunology and cancer biology due to their rapid proliferation, well-characterized signaling pathways, and relevance to B cell malignancies. The line??s EBV status also makes it valuable for studying viral oncogenesis and immune evasion mechanisms.
MUTYH encodes a DNA glycosylase that specifically excises adenine misincorporated opposite 8-oxoguanine, a critical step in the base excision repair (BER) pathway. Its activity is regulated by Sp1 transcription factor, oxidative stress via the NRF2 pathway, and cell cycle cues. The MUTYH protein interacts with PCNA and the 9-1-1 complex during lesion recognition, and cooperates with downstream factors including APE1 endonuclease and DNA polymerase beta to complete repair. Deficiency of MUTYH disrupts the BER cascade, leading to accumulation of abasic sites and unrepaired oxidative lesions.
In the context of Raji B cells, MUTYH knockout impairs the repair of oxidative DNA damage, causing an increase in G:C to T:A transversions and elevated genomic instability. This mirrors the mutator phenotype observed in MUTYH-associated polyposis and hereditary colorectal cancer predisposition. The model enables dissection of how defective BER contributes to lymphomagenesis and may reveal synthetic lethal vulnerabilities exploitable in B cell malignancies.
These polyclonal knockout cells are suitable for a broad range of applications including DNA repair pathway analysis, oxidative stress response studies, and cancer biology research. They can be used in synthetic lethality screens to identify dependencies created by MUTYH loss, and for validating drugs targeting DNA damage checkpoints or BER enzymes. Representative assays include Western blotting for key repair proteins, RT-qPCR for pathway gene expression, DNA glycosylase activity measurements, alkaline comet assays to detect DNA strand breaks, immunofluorescence visualization of 8-oxoguanine lesions, and mutation frequency analysis. For additional technical specifications, please contact Ascent Research.
