The DUS3L Knockout Raji Polyclonal Cells represent a CRISPR/Cas9-edited polyclonal knockout cell population originating from the human Raji B lymphocyte line, featuring targeted disruption of the DUS3L gene. As a heterogeneous pool of edited cells, this product bypasses single-cell cloning and preserves genetic diversity, offering a practical loss-of-function model for investigating DUS3L-dependent phenotypes in population-based assays.
The Raji cell line is a suspension-adapted B lymphoblastoid model established from a Burkitt lymphoma patient. These cells maintain mature B cell characteristics and are Epstein-Barr virus (EBV)-positive, making them a robust platform for studying B cell signaling, apoptosis regulation, NF-??B pathway dynamics, and EBV latency mechanisms. Their rapid proliferation and well-documented oncogenic background enable high-throughput functional genomics and drug screening applications.
DUS3L encodes a dihydrouridine synthase responsible for post-transcriptional reduction of uridine to dihydrouridine in tRNA substrates. This modification critically influences tRNA folding, stability, and codon?Canticodon recognition, thereby regulating translation elongation rates and fidelity. Functionally, DUS3L operates upstream of the ribosome, with dihydrouridine-modified tRNAs acting as direct effectors in translation control. Although its upstream regulators and interacting partners remain unidentified, the enzyme is a key node connecting RNA metabolism to protein synthesis, with its catalytic product impacting the translation landscape of potentially oncogenic transcripts.
In the context of Raji B lymphoma, DUS3L knockout provides a unique tool to examine how tRNA modification deficits alter malignant phenotypes. Given the elevated translational demand of Burkitt lymphoma cells, loss of dihydrouridine modification may selectively affect the synthesis of proteins involved in proliferation or survival, potentially altering NF-??B-mediated signaling or apoptotic set points. This model thus bridges fundamental RNA biology with translational cancer research, enabling dissection of tRNA modification??s role in lymphomagenesis and drug response.
Key applications include HPLC-based quantification of tRNA dihydrouridine levels, puromycin incorporation or polysome profiling to assess global translation efficiency, and cell viability or apoptosis assays following chemotherapeutic challenge. The polyclonal knockout population is particularly suited for synthetic lethal screens and drug sensitivity profiling to identify therapeutic vulnerabilities associated with tRNA modification disruptions. For further technical information or custom requests, please contact Ascent Research.
