Transcription-coupled nucleotide excision repair: New insights revealed by genomic approaches.

摘要: Elongation of RNA polymerase II (Pol II) is affected by many factors including DNA damage. Bulky damage, such as lesions caused ultraviolet (UV) radiation, arrests Pol and inhibits gene transcription, may lead to genome instability cell death. Cells activate transcription-coupled nucleotide excision repair (TC-NER) remove II-impeding damage allow transcription resumption. TC-NER initiation in humans mediated Cockayne syndrome group B (CSB) protein, which binds the stalled promotes assembly machinery. Given complex nature pathway its unique function at interface between repair, new approaches are required gain in-depth understanding mechanism. Advances genomic provide an important opportunity investigate how initiated upon damage-induced stalling what involved this process. In Review, we discuss mechanisms revealed genome-wide mapping identified high-throughput screening. As conducts strand-specific mutagenic also causes mutational strand asymmetry cancer genome.