In the first study, the researchers found that the protein APOBEC3G (A3G) helps repair DNA double-strand breaks and can even rescue mice from lethal doses of radiation. This protein is also involved in nucleotide excision repair and homologous recombination DNA repair pathways. These findings suggest that inhibiting A3G could increase the sensitivity of tumor cells to genotoxic treatments.
To the paper
In the second study, transgenic mice expressing A3G were able to survive lethal doses of radiation, while wild-type mice did not. A3G was also found to promote error-free repair of DNA damage. These findings have important implications for cancer treatment – inhibiting A3G may make genotoxic therapies more effective, while increasing A3G activity may help protect against radiation exposure.
To the paper
Models for participation of A3G in DNA damage repair. (A) (DNA) double-strand break repair pathways. (B) UV-damage repair: (B1) GG-NER; (B2) transcription-coupled UV damage repair; (B3) topoisomerase I-mediated NER-independent UV damage repair.
