The FAM98A Knockout Raji Polyclonal Cells consist of a heterogeneous population of human Raji Burkitt lymphoma B lymphocytes engineered with CRISPR/Cas9-mediated disruption of the FAM98A gene. This polyclonal knockout cell pool is intended for loss-of-function studies in a B-cell context. The editing strategy generates diverse genomic modifications without clonal selection, yielding a population that reflects the spectrum of functional effects of target-gene disruption. Compared to clonal lines, this polyclonal format reduces clonal bias and provides a more robust model for initial phenotypic screening and mechanistic investigations.
The Raji host cell line originates from an EBV-positive Burkitt lymphoma patient and retains latent EBV infection. They display characteristic B lymphocyte features including surface immunoglobulin expression and the capacity for antibody production, antigen presentation, and immune memory functions. Raji cells are a widely used model in lymphoma research, immunology, and virology, offering a robust platform for studying B-cell malignancies and EBV-driven oncogenesis. Their suspension growth and well-characterized molecular background support standardized culture and reproducibility, facilitating diverse downstream applications.
FAM98A encodes a conserved subunit of the heteromeric tRNA-splicing ligase complex, which ligates tRNA exon halves following intron excision. Within this complex, FAM98A interacts directly with RTCB ligase, DDX1 helicase, and cofactors CGI-99 and HSPC117 to generate mature tRNAs. Consequently, FAM98A is essential for efficient protein translation and cell proliferation. Disruption of FAM98A causes accumulation of unspliced pre-tRNA introns, defects in tRNA maturation, and impaired translation, linking the gene to ribosome biogenesis and growth control. The complex also interfaces with the spliceosome, suggesting additional roles in RNA processing.
In Raji B lymphocytes, FAM98A loss-of-function is particularly relevant for lymphomagenesis and sustained malignant growth, as Burkitt lymphoma cells depend on robust protein synthesis and tRNA processing. Disabling FAM98A permits investigation of how tRNA maturation defects affect B-cell viability, antigen presentation, and responses to microenvironmental signals. The latent EBV status further allows exploration of virally modulated host RNA processing. Moreover, the polyclonal knockout population mirrors tumor heterogeneity, providing a physiologically relevant system for dissecting FAM98A??s contributions to B-cell malignancy and its therapeutic potential.
Researchers can use this knockout pool for functional studies of tRNA processing, assembly and substrate specificity of the RNA ligase complex, and mechanisms of FAM98A in lymphomagenesis. Assays include Western blotting, RT-qPCR, RNA-seq, Northern blotting, MTT viability, apoptosis flow cytometry, co-immunoprecipitation, and drug sensitivity testing. The model is suitable for drug screening in B-cell lymphoma and target validation in RNA biology. For further technical information, contact Ascent Research.
