The DUS1L Knockout Raji Polyclonal Cells comprise a CRISPR/Cas9-edited polyclonal population derived from Raji B lymphocytes, engineered to disrupt the endogenous DUS1L gene. This heterogeneous knockout pool serves as a loss-of-function model for studying the collective effects of abolished dihydrouridine synthase activity without introducing biases from single-cell cloning. The cells are supplied as a ready-to-use research tool for downstream functional analyses.
Raji is a widely utilized EBV-positive Burkitt lymphoma B cell line characterized by the t(8;14) chromosomal translocation that juxtaposes c-MYC with the immunoglobulin heavy chain locus, leading to constitutive c-MYC overexpression. This oncogenic driver promotes high proliferative rates and renders Raji cells a standard model for investigating B-cell lymphoma biology, immunoglobulin production, and immune cell signaling. The line also retains features of germinal center B cells, making it relevant for studying lymphomagenesis and translational control.
DUS1L encodes a flavin mononucleotide (FMN)-dependent dihydrouridine synthase that utilizes NADPH to reduce specific uridine residues in tRNAs to dihydrouridine. Its validated substrates include tRNA-Leu(UUR), tRNA-Phe(GAA), and tRNA-Gly(GCC). This modification enhances tRNA structural flexibility, which in turn modulates codon?Canticodon pairing stability and translation elongation. DUS1L activity thereby influences global protein synthesis dynamics and cellular responses to oxidative stress. Although direct upstream regulators remain undefined, the enzyme may be linked to mTOR signaling and the RNA polymerase III transcriptional machinery that governs tRNA production. DUS1L is thought to interact with other DUS family tRNA-modifying enzymes, methyltransferases, and ribosome-associated proteins, positioning it at a hub connecting tRNA modifications to translation fidelity.
When introduced into MYC-hyperactive Raji cells, DUS1L knockout provides a powerful system to dissect the interplay between oncogenic translation and tRNA modification. MYC-driven lymphomas often depend on elevated protein synthesis, and impairments in tRNA modification can selectively compromise translation of certain mRNAs. Hence, DUS1L-deficient Raji cells may uncover synthetic lethal interactions with c-MYC overexpression, offering insights into therapeutic vulnerabilities. The model further enables examination of how dihydrouridine modification affects B-cell receptor signaling, immunoglobulin synthesis, and sensitivity to oxidative or proteotoxic stress.
This polyclonal knockout product is suited for diverse quantitative assays, including LC-MS/MS-based tRNA modification profiling, polysome fractionation, ribosome footprinting, and puromycin incorporation to measure translation. Stress pathway activation can be monitored by Western blotting for phospho-eIF2??, while cell viability and apoptosis assays assess growth phenotypes. Drug sensitivity screens can identify compounds that exploit DUS1L loss in B-cell malignancies. For additional details or technical support, please contact AscentResearch.
