DNA damage responses to oxidative stress

Ari Barzilai, Ken-ichi Yamamoto

Research output: Contribution to journalArticle

422 Citations (Scopus)

Abstract

The DNA damage response is a hierarchical process. DNA damage is detected by sensor proteins such as the MRN complex that transmit the information to transducer proteins such as ATM and ATR, which control the damage response through the phosphorylation of effector proteins. The extent of the DNA damage determines cell fate: cell cycle arrest and DNA repair or the activation of apoptotic pathways. In aerobic cells, reactive oxygen species (ROS) are generated as a by-product of normal mitochondrial activity. If not properly controlled, ROS can cause severe damage to cellular macromolecules, especially the DNA. We describe here some of the cellular responses to alterations in the cellular redox state during hypoxia or oxidative stress. Oxidative damage in DNA is repaired primarily via the base excision repair (BER) pathway which appears to be the simplest of the three excision repair pathways. To allow time for DNA repair, the cells activate their cell cycle checkpoints, leading to cell cycle arrest and preventing the replication of damage and defective DNA.

Original languageEnglish
Pages (from-to)1109-1115
Number of pages7
JournalDNA Repair
Volume3
Issue number8-9
DOIs
Publication statusPublished - Aug 2004
Externally publishedYes

Fingerprint

Oxidative stress
DNA Damage
Oxidative Stress
DNA Repair
Cell Cycle Checkpoints
DNA
Repair
Reactive Oxygen Species
Cells
Proteins
Transducers
Oxidation-Reduction
Phosphorylation
Automatic teller machines
Macromolecules
Byproducts
Chemical activation
Sensors

Keywords

  • Damage
  • DNA
  • Oxidative stress

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology

Cite this

DNA damage responses to oxidative stress. / Barzilai, Ari; Yamamoto, Ken-ichi.

In: DNA Repair, Vol. 3, No. 8-9, 08.2004, p. 1109-1115.

Research output: Contribution to journalArticle

Barzilai, Ari ; Yamamoto, Ken-ichi. / DNA damage responses to oxidative stress. In: DNA Repair. 2004 ; Vol. 3, No. 8-9. pp. 1109-1115.
@article{f0ad87dab8054b5ab1e25fa656dcc809,
title = "DNA damage responses to oxidative stress",
abstract = "The DNA damage response is a hierarchical process. DNA damage is detected by sensor proteins such as the MRN complex that transmit the information to transducer proteins such as ATM and ATR, which control the damage response through the phosphorylation of effector proteins. The extent of the DNA damage determines cell fate: cell cycle arrest and DNA repair or the activation of apoptotic pathways. In aerobic cells, reactive oxygen species (ROS) are generated as a by-product of normal mitochondrial activity. If not properly controlled, ROS can cause severe damage to cellular macromolecules, especially the DNA. We describe here some of the cellular responses to alterations in the cellular redox state during hypoxia or oxidative stress. Oxidative damage in DNA is repaired primarily via the base excision repair (BER) pathway which appears to be the simplest of the three excision repair pathways. To allow time for DNA repair, the cells activate their cell cycle checkpoints, leading to cell cycle arrest and preventing the replication of damage and defective DNA.",
keywords = "Damage, DNA, Oxidative stress",
author = "Ari Barzilai and Ken-ichi Yamamoto",
year = "2004",
month = "8",
doi = "10.1016/j.dnarep.2004.03.002",
language = "English",
volume = "3",
pages = "1109--1115",
journal = "DNA Repair",
issn = "1568-7864",
publisher = "Elsevier",
number = "8-9",

}

TY - JOUR

T1 - DNA damage responses to oxidative stress

AU - Barzilai, Ari

AU - Yamamoto, Ken-ichi

PY - 2004/8

Y1 - 2004/8

N2 - The DNA damage response is a hierarchical process. DNA damage is detected by sensor proteins such as the MRN complex that transmit the information to transducer proteins such as ATM and ATR, which control the damage response through the phosphorylation of effector proteins. The extent of the DNA damage determines cell fate: cell cycle arrest and DNA repair or the activation of apoptotic pathways. In aerobic cells, reactive oxygen species (ROS) are generated as a by-product of normal mitochondrial activity. If not properly controlled, ROS can cause severe damage to cellular macromolecules, especially the DNA. We describe here some of the cellular responses to alterations in the cellular redox state during hypoxia or oxidative stress. Oxidative damage in DNA is repaired primarily via the base excision repair (BER) pathway which appears to be the simplest of the three excision repair pathways. To allow time for DNA repair, the cells activate their cell cycle checkpoints, leading to cell cycle arrest and preventing the replication of damage and defective DNA.

AB - The DNA damage response is a hierarchical process. DNA damage is detected by sensor proteins such as the MRN complex that transmit the information to transducer proteins such as ATM and ATR, which control the damage response through the phosphorylation of effector proteins. The extent of the DNA damage determines cell fate: cell cycle arrest and DNA repair or the activation of apoptotic pathways. In aerobic cells, reactive oxygen species (ROS) are generated as a by-product of normal mitochondrial activity. If not properly controlled, ROS can cause severe damage to cellular macromolecules, especially the DNA. We describe here some of the cellular responses to alterations in the cellular redox state during hypoxia or oxidative stress. Oxidative damage in DNA is repaired primarily via the base excision repair (BER) pathway which appears to be the simplest of the three excision repair pathways. To allow time for DNA repair, the cells activate their cell cycle checkpoints, leading to cell cycle arrest and preventing the replication of damage and defective DNA.

KW - Damage

KW - DNA

KW - Oxidative stress

UR - http://www.scopus.com/inward/record.url?scp=3242886115&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=3242886115&partnerID=8YFLogxK

U2 - 10.1016/j.dnarep.2004.03.002

DO - 10.1016/j.dnarep.2004.03.002

M3 - Article

C2 - 15279799

AN - SCOPUS:3242886115

VL - 3

SP - 1109

EP - 1115

JO - DNA Repair

JF - DNA Repair

SN - 1568-7864

IS - 8-9

ER -