Fig. 8: Working model.

CUL4A, through DTL-specific recognition and ubiquitination of DNA-PKcs, affects the NHEJ repair pathway to increase cell genomic instability and enhance subsequent malignant transformation of normal cells.
CUL4A, through DTL-specific recognition and ubiquitination of DNA-PKcs, affects the NHEJ repair pathway to increase cell genomic instability and enhance subsequent malignant transformation of normal cells.