The DUS1L Knockout AGS Polyclonal Cells product is a CRISPR/Cas9-edited polyclonal knockout cell population derived from the AGS human gastric adenocarcinoma cell line. This population harbors targeted disruption of the DUS1L gene, resulting in a loss-of-function model for studying dihydrouridine synthase activity in tRNA modification. As a polyclonal knockout pool, these cells represent a heterogeneous collection of edited alleles, providing a robust tool for functional genomics without clonal selection limitations.
The parental AGS cell line originates from a gastric adenocarcinoma patient and serves as a well-characterized epithelial model for gastric cancer biology. These adherent epithelial cells are extensively used in cancer research, including studies on tumor cell proliferation, epithelial barrier integrity, and drug discovery screening. AGS cells exhibit features typical of gastric adenocarcinoma, making them a relevant host for investigating oncogenic signaling and cellular stress responses.
DUS1L encodes a dihydrouridine synthase that catalyzes the NADPH-dependent reduction of uridine to dihydrouridine at conserved positions in the D-loop of tRNAs. This modification influences tRNA folding, stability, and codon recognition, thereby regulating translation of U-rich codons. DUS1L activity is modulated by upstream regulators such as c-Myc, TFIIIB, MAF1, and cellular nutrient or oxidative stress cues. Downstream, DUS1L-dependent dihydrouridine impacts the GCN2 kinase pathway and eIF2?? phosphorylation, linking tRNA modification to translational control and stress adaptation. DUS1L interacts with tRNA substrates, NADPH cofactor, and the Elongator complex, integrating nutrient signals with protein synthesis.
In the context of gastric adenocarcinoma, DUS1L likely contributes to the adaptive translation programs required for tumor cell survival under stress conditions, such as nutrient deprivation. The AGS knockout model enables precise dissection of DUS1L??s role in modifying tRNAs that decode U-rich codons, potentially affecting the expression of stress-responsive proteins. By eliminating DUS1L function, researchers can evaluate changes in cell proliferation, apoptosis, and sensitivity to chemotherapeutic agents, providing insights into the molecular dependencies of gastric cancer.
This product is suitable for a wide range of research applications, including the study of tRNA modification dynamics via RNA sequencing and mass spectrometry-based dihydrouridine detection. Functional assays such as polysome profiling can reveal translation regulation changes, while cell-based assays like proliferation, apoptosis, and drug sensitivity testing help validate DUS1L as a potential therapeutic target. These DUS1L knockout cells are a valuable resource for investigating translation fidelity, mTOR-related stress signaling, and gastric cancer biology. For further details or to discuss your specific experimental needs, please contact Ascent Research.
