DALLAS, TX, June 22 -- Researchers at the University of Texas Southwestern Medical Center have found that a large protein complex, previously thought to mainly regulate protein degradation, plays a significant role in sensitivity to cancer-causing ultraviolet light. The scientists reached their conclusion when they combined the results of their studies of a biological machine called the proteasome and the protein Rad23, which is involved in repair of DNA damaged by ultraviolet light. If the repair machine fails to work, as in the disease xeroderma pigmentosum, DNA mutations occur that lead to skin cancer, according to Steven Russell and Dr. Simon Reed, two of the paper's authors. The team of investigators discovered that by deleting a part of the protein Rad23, a component of the nucleotide excision repair machinery, they could increase sensitivity to UV radiation. The results demonstrate that in order for DNA repair to work properly, that particular domain of Rad23, which binds to the proteasome, must be present. The scientists also showed that inhibiting an ATPase, one of the proteasome's energy sources, impairs the repair machinery, further increasing UV sensitivity.