Differential damage and repair of anti-cancer drug cisplatin induced DNA-adducts across mouse organs
Journal: Nature Communications
- Comparative analyses of two primate species diverged by more than 60 million years show different rates but similar distribution of genome-wide UV repair events
- Nucleotide excision repair capacity increases during differentiation of human embryonic carcinoma cells into neurons and muscle cells
- Genome-wide mapping of nucleotide excision repair with XR-seq.
- Cisplatin-DNA adduct repair of transcribed genes is controlled by two circadian programs in mouse tissues.
- Genome-wide Excision Repair in Arabidopsis is coupled to transcription and reflects circadian gene expression patterns.
- Single-nucleotide resolution dynamic repair maps of UV damage in Saccharomyces cerevisiae genome.
- Mfd translocase is necessary and sufficient for transcription-coupled repair in Escherichia coli.
- Molecular mechanism of DNA excision repair and excision repair maps of the human and E. coli genomes.
- Dynamic maps of UV damage formation and repair.
- Human genome-wide repair map of DNA damage caused by the cigarette smoke carcinogen benzo[a]pyrene.
- Genome-wide transcription-coupled repair in Escherichia coli is mediated by the Mfd translocase.