The OSGEPL1 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the Raji B lymphoblastoid cell line, featuring disruption of the OSGEPL1 gene. This polyclonal format offers a heterogeneous pool of cells with targeted OSGEPL1 loss-of-function, enabling functional studies of this critical tRNA modification enzyme without the bias of clonal selection. As part of Ascent Research??s knockout cell portfolio, this product provides a reliable tool for dissecting OSGEPL1-dependent processes in a disease-relevant B-cell context.
The Raji cell line is an Epstein-Barr virus (EBV)-positive Burkitt’s lymphoma-derived B lymphoblastoid cell line established from a human patient. These cells retain key features of B lymphocytes, including expression of surface immunoglobulin and receptors involved in immune signaling, and are widely used to study B cell receptor (BCR) signaling, antibody production, and lymphomagenesis. Raji cells serve as a robust model for exploring oncogenic signaling networks, particularly those driven by MYC and mTOR, making them an ideal host for investigating the intersection of tRNA modification and B-cell proliferation.
OSGEPL1 encodes a subunit of the KEOPS complex, a conserved multiprotein assembly that includes OSGEP, LAGE3, TP53RK, and TPRKB. This complex catalyzes the universal N6-threonylcarbamoyladenosine (t6A) modification at position 37 of tRNAs decoding ANN codons, a modification essential for translational fidelity and ribosome reading-frame maintenance. OSGEPL1 function is regulated upstream by the MYC oncoprotein and mTORC1 signaling, linking nutrient-sensing and growth pathways to protein synthesis. Downstream, OSGEPL1-mediated t6A modification controls the efficient translation of proteins enriched in lysine and asparagine codons, thereby governing cell cycle progression and proliferation. Disruption of OSGEPL1 impairs the KEOPS complex, leading to mistranslation and reduced growth.
In the Raji B lymphoblastoid background, OSGEPL1 knockout is particularly relevant for dissecting how tRNA modification impacts lymphocyte proliferation and immune function. Given Raji cells?? dependence on MYC-driven transcription and mTORC1 activity, loss of OSGEPL1 likely sensitizes these cells to translational stress and perturbed codon-specific protein output. This model facilitates investigation of the KEOPS complex??s role in sustaining high protein synthesis in malignant B cells and may reveal vulnerabilities in B-cell lymphomas or Galloway-Mowat syndrome. The polyclonal nature of this product also mirrors tumor heterogeneity, providing a physiologically relevant system for studying OSGEPL1??s role in cancer.
Researchers can employ these polyclonal knockout cells in a variety of functional assays, including western blotting and RT-qPCR to confirm OSGEPL1 loss, cell proliferation assays and flow cytometric cell cycle analysis to evaluate growth defects, and apoptosis assays to assess stress sensitivity. For specialized tRNA modification studies, mass spectrometry-based approaches can quantify t6A levels in total tRNA or specific tRNA isoacceptors, while polysome profiling and RNA-seq provide insights into translation efficiency and transcriptome-wide effects. This model suits drug target validation screens for the KEOPS complex or mTORC1. For further assistance or to discuss custom applications, please contact Ascent Research.
