The current evidence for defective repair of oxidatively damaged DNA in Cockayne syndrome

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Abstract

Cockayne syndrome (CS) is a rare recessive disorder characterized by a number of developmental abnormalities and premature aging. Two complementation groups (A and B) have been identified so far in CS cases. Defective transcription-coupled nucleotide excision repair is the hallmark of these patients, but in recent years evidence has been presented for a possible defect in the base excision repair pathway that removes oxidized bases. Recent results indicate that both A and B complementation groups are involved but the phenotypical consequences of this flaw remain undetermined.

Original languageEnglish
Pages (from-to)165-177
Number of pages13
JournalFree Radical Biology and Medicine
Volume43
Issue number2
DOIs
Publication statusPublished - Jul 15 2007

Keywords

  • 8-Oxo-7,8-dihydroguanine
  • Aging
  • Cockayne syndrome
  • DNA base excision repair
  • Free radicals
  • Glycosylase
  • Mutation
  • Neurological deterioration
  • Oxidative DNA damage
  • Transcription-coupled repair

ASJC Scopus subject areas

  • Medicine(all)
  • Toxicology
  • Clinical Biochemistry

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