The abstract is read at the publisher; the summary is JClub's.
In hyperglycemic settings, the lysosomal DRAM1–GLUT1 axis coordinates glucose sensing by routing newly made GLUT1 to lysosomes, lowering surface GLUT1 and braking glucose entry reversibly.
- Why it matters: Excess glucose drives metabolic disease and cancer, yet how cells sense and restrain glucose uptake is not fully defined, especially via lysosomal control.
- What they did: The study shows pathophysiological glucose induces DRAM1 through the MLX/ChREBP complex, then DRAM1 binds newly synthesized GLUT1 to promote lysosomal trafficking; NOX inhibition increases complex assembly and NADPH is implicated.
- The result: Sequestering GLUT1 suppresses glucose uptake and glycolysis while shifting metabolism toward glutamine anaplerosis, creating vulnerability to GLS inhibition; Dram1 -/- tumors show a glycolytic metabolite profile consistent with loss of this brake.
The findingWhy it mattersWhat they didThe result
AI summary of the abstract · may contain errors · not medical advice · read the paper.