The FAM111A Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population from the Raji B lymphocyte line, with targeted disruption of the FAM111A gene. This heterogeneous pool of loss?of?function cells avoids clonal selection bias, providing a robust population?level model for studying FAM111A?dependent DNA replication, repair, and antiviral responses.
Raji cells originate from a Burkitt lymphoma patient and maintain Epstein?CBarr virus (EBV) positivity, typical B cell surface markers, and active proliferation. As a widely used model in immunology and oncology, this line faithfully represents B cell malignancies and virus?Chost interactions, enabling investigations of oncogenic stress and viral latency on genome stability.
FAM111A encodes a serine protease that associates directly with proliferating cell nuclear antigen (PCNA). It functions downstream of cell cycle regulators and E2F transcription factors, and its expression is induced by interferon, linking it to antiviral innate immunity. FAM111A interacts with PCNA, DNA polymerase delta, replication factor C, DNA ligase I, and FEN1 at replication forks, and also binds SV40 large T antigen. Through these associations, FAM111A modulates DNA replication fidelity and repair, and its loss impairs genomic integrity and weakens antiviral defense.
In the Raji background, FAM111A knockout creates a pertinent model of B cell lymphoma-associated genome instability. The EBV?positive environment may intersect with FAM111A pathways, as its interaction with viral replication proteins suggests a role in viral genome processing. Disruption of FAM111A is anticipated to exacerbate replication stress and DNA damage, mirroring aggressive lymphoma phenotypes and offering insight into B cell transformation and immune escape.
These polyclonal knockout cells are applicable to assays including western blotting and immunofluorescence for PCNA and phospho-PCNA, DNA fiber analysis, cell cycle profiling by flow cytometry, and apoptosis quantification. Comet assays for DNA damage and co?immunoprecipitation with PCNA validate disrupted interactions, while RT?qPCR for interferon?stimulated genes probes antiviral responses. This model supports mechanistic studies in oncology and virology. For further details, contact Ascent Research.
