DNA interstrand crosslink repair in mammalian cells

Kevin M. Mccabe, Susan Olson, Robb Moses

Research output: Contribution to journalArticle

38 Citations (Scopus)

Abstract

DNA damage by agents crosslinking the strands presents a formidable challenge to the cell to repair for survival and to repair accurately for maintenance of genetic information. It appears that repair of DNA crosslinks occurs in a path involving double strand breaks (DSBs) in the DNA. Mammalian cells have multiple systems involved in the repair response to such damage, including the Fanconi anemia pathway that appears to be directly involved, although the mechanisms and site of action remain elusive. A particular finding relating to deficiency of the Fanconi anemia pathway is the observation of chromosomal radial formations after ICL damage. The basis of formation of such chromosomal aberrations is unknown although they appear secondarily to DSBs. Here we review the processes involved in response to DNA interstrand crosslinks which might lead to radial formation and the role of the nucleotide excision repair gene, ERCC1, which is required for a normal response, not just to DNA crosslinks, but also for DSBs at collapsed replication forks caused by substrate depletion.

Original languageEnglish (US)
Pages (from-to)569-573
Number of pages5
JournalJournal of Cellular Physiology
Volume220
Issue number3
DOIs
StatePublished - Sep 2009

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Fanconi Anemia
DNA Repair
Repair
Cells
Double-Stranded DNA Breaks
DNA
Chromosome Aberrations
DNA Damage
Observation
Genes
Aberrations
Crosslinking
Nucleotides
Substrates

ASJC Scopus subject areas

  • Clinical Biochemistry
  • Cell Biology
  • Physiology

Cite this

DNA interstrand crosslink repair in mammalian cells. / Mccabe, Kevin M.; Olson, Susan; Moses, Robb.

In: Journal of Cellular Physiology, Vol. 220, No. 3, 09.2009, p. 569-573.

Research output: Contribution to journalArticle

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