The role of Cockayne syndrome group A (CSA) protein in transcription-coupled nucleotide excision repair.

Nucleotide excision repair (NER) removes a variety of DNA lesions, including ultraviolet-induced cyclobutane pyrimidine dimers. NER comprises two subpathways: transcription-coupled NER (TC-NER) and global genome NER. TC-NER efficiently removes lesions from the transcribed strands of active genes. Mutations in Cockayne syndrome groups A and B genes (CSA and CSB) result in defective TC-NER. In mammalian cells, TC-NER is presumably initiated by the arrest of RNA polymerase II at a lesion on the transcribed strand of an active gene, but the molecular mechanism underlying TC-NER remains unclear. The CSA protein has seven WD40 repeat motifs and beta-propeller architecture. A protein complex consisting of CSA, DDB1, cullin 4A, and Roc1 exhibits ubiquitin ligase activity. The role of CSA protein in TC-NER is described in this review. Copyright © 2013 Elsevier Ireland Ltd. All rights reserved.

Citation

Masafumi Saijo. The role of Cockayne syndrome group A (CSA) protein in transcription-coupled nucleotide excision repair. Mechanisms of ageing and development. 2013 May-Jun;134(5-6):196-201

PMID: 23571135

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