JNK acts as a molecular brake of the CDC73 positive feedback loop to modulate osteosarcoma malignant progression via UBR5.
A novel JNK-dependent UBR5-CDC73 axis is defined that acts as a molecular brake of the CDC73 positive feedback loop to orchestrate transcriptional programs, providing new mechanistic insights into CDC73 post-translational regulation in tumorigenesis and promising therapeutic targets for CDC73-dysregulated diseases.