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DNA Repair (Amst). 2019 Apr;76:60-69. doi: 10.1016/j.dnarep.2019.02.006. Epub 2019 Feb 18.

A new perspective on oxidation of DNA repair proteins and cancer.

Author information

1
Department of Therapeutic Radiology and Department of Genetics, Yale University School of Medicine, New Haven, CT, 06520, United States. Electronic address: khadijeh.alnajjar@yale.edu.
2
Department of Therapeutic Radiology and Department of Genetics, Yale University School of Medicine, New Haven, CT, 06520, United States.

Abstract

Reactive oxygen and nitrogen species (RONS) are formed as byproducts of many endogenous cellular processes, in response to infections, and upon exposure to various environmental factors. An increase in RONS can saturate the antioxidation system and leads to oxidative stress. Consequently, macromolecules are targeted for oxidative modifications, including DNA and protein. The oxidation of DNA, which leads to base modification and formation of abasic sites along with single and double strand breaks, has been extensively investigated. Protein oxidation is often neglected and is only recently being recognized as an important regulatory mechanism of various DNA repair proteins. This is a review of the current state of research on the regulation of DNA repair by protein oxidation with emphasis on the correlation between inflammation and cancer.

KEYWORDS:

Base excision repair; DNA damage; Double strand break repair; Oxidation of DNA repair proteins; Oxidative stress

PMID:
30818170
PMCID:
PMC6419097
[Available on 2020-04-01]
DOI:
10.1016/j.dnarep.2019.02.006

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