2013
DOI: 10.1089/ars.2012.4938
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New Insights into the Link Between DNA Damage and Apoptosis

Abstract: Significance: When lesions are unrepaired or there are defects in the DNA repair system, DNA damage is often correlated to apoptosis. However, different kinds of lesions and different degrees of lesion severity can trigger numerous signaling responses. Recent Advances: DNA repair proteins involved in specific DNA repair pathways can modulate the function or activity of some apoptotic factors, further emphasizing the crosstalk between DNA damage and cell death. Critical Issues: Here, we discuss the signaling ne… Show more

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Cited by 107 publications
(80 citation statements)
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“…[Colour figure can be viewed at wileyonlinelibrary.com] mitochondria dysfunction and DNA damage. [31][32][33] Therefore, combination should include some active ingredients that each of them targets deficient pathways. One of the synthetic anticancer drugs that widely used in different type of cancers is CPF, as a fluoroquinolone derivate.…”
Section: Discussionmentioning
confidence: 99%
“…[Colour figure can be viewed at wileyonlinelibrary.com] mitochondria dysfunction and DNA damage. [31][32][33] Therefore, combination should include some active ingredients that each of them targets deficient pathways. One of the synthetic anticancer drugs that widely used in different type of cancers is CPF, as a fluoroquinolone derivate.…”
Section: Discussionmentioning
confidence: 99%
“…Increase in reactive oxygen molecules production; decrease in anti-oxidant enzyme levels, and/or defect DNA repair mechanisms increase the oxidative DNA damage (22)(23)(24). In a healthy body, DNA damage can be repaired because the oxidative and anti-oxidative balance is maintained (25). If the oxidative DNA damage reaches a level where it doesn't comply with life anymore, cell death (apoptosis) or genotoxic damages occur (25,26).…”
Section: Discussionmentioning
confidence: 99%
“…2/15 1 Although the functional purpose of p53 within a cell has been widely studied, its 2 dynamics have yet to be fully characterized. The p53 tumor suppressor protein, 3 mutated in 50% of all cancers, is responsible for activating cell cycle arrest or apoptosis 4 programs following cellular stress [1][2][3][4]. To guide these decisions, p53 must integrate 5 information about stress from multiple sources-including DNA damage, hypoxia, 6 transcriptional stress, and telomere erosion-that each affect its total level and 7 activation dynamics differently.…”
Section: Plosmentioning
confidence: 99%