DNA repair in mammalian cells: Transcription-coupled DNA repair: directing your effort where it's most needed.
Arrest of transcription at sites of DNA damage represents a strong signal for apoptosis. To overcome the impasse represented by transcription complexes arrested at sites of damage, cells have evolved a specialized nucleotide excision repair (NER) pathway called transcription-coupled DNA repair (TCR), dedicated to removal of transcription-blocking lesions from the genome. This repair pathway was discovered in Phil Hanawalt's laboratory 20 years ago, but the mechanistic details are still subject of intense research. This article will review the recent literature on the subject with emphasis on how lesions affect the elongation step of transcription and how the initial steps of TCR occur in human cells. (Part of a Multi-author Review).
Tornaletti
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Department of Anatomy and Cell Biology, University of Florida, Gainesville, Florida 32610, USA. silviat@ufl.edu
D000970:Antineoplastic Agents / Q000494:pharmacology; D017209:Apoptosis / Q000187:drug effects / Q000502:physiology / Q000528:radiation effects; D002945:Cisplatin / Q000494:pharmacology; D003057:Cockayne Syndrome / Q000378:metabolism; D004249:DNA Damage / Q000502:physiology*; D004260:DNA Repair / Q000502:physiology*; D045643:DNA Repair Enzymes / Q000378:metabolism*; D006801:Humans; D010084:Oxidation-Reduction; D011740:Pyrimidine Dimers / Q000378:metabolism; D012319:RNA Polymerase II / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D014158:Transcription, Genetic
D000970:Antineoplastic Agents; D011740:Pyrimidine Dimers; D012319:RNA Polymerase II; D045643:DNA Repair Enzymes; D002945:Cisplatin