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Journal ArticleDOI

The DNA Damage Response: Making It Safe to Play with Knives

TL;DR: This review will focus on how the DDR controls DNA repair and the phenotypic consequences of defects in these critical regulatory functions in mammals.
About: This article is published in Molecular Cell.The article was published on 2010-10-22 and is currently open access. It has received 3678 citations till now. The article focuses on the topics: DNA damage & DNA repair.
Citations
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Journal ArticleDOI
04 Mar 2011-Cell
TL;DR: Recognition of the widespread applicability of these concepts will increasingly affect the development of new means to treat human cancer.

51,099 citations


Cites background from "The DNA Damage Response: Making It ..."

  • ...Notable among the apoptosis-inducing stresses are signaling imbalances resulting from elevated levels of oncogene signaling, as mentioned earlier, and DNA damage associated with hyperproliferation....

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  • ...The telomeres, composed of multiple tandem hexanucleotide repeats, shorten progressively in nonimmortalized cells propagated in culture, eventually losing the ability to protect the ends of chromosomal DNAs from end-to-end fusions; such fusions generate unstable dicentric chromosomes whose resolution results in a scrambling of karyotype that threatens cell viability....

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  • ...Most notable is a DNAdamage sensor that functions via the TP53 tumor suppressor (Junttila and Evan, 2009); TP53 induces apoptosis by upregulating expression of the Noxa and Puma BH3-only proteins, doing so in response to substantial levels of DNA breaks and other chromosomal abnormalities....

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  • ...Because heritable phenotypes, e.g., inactivation of tumor suppressor genes, can also be acquired through epigenetic mechanisms such asDNAmethylation and histonemodifications (Berdasco and Esteller, 2010; Esteller, 2007; Jones and Baylin, 2007), some clonal expansions may well be triggered by nonmutational changes affecting the regulation of gene expression....

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  • ...The eventual immortalization of rare variant cells that proceed to form tumors has been attributed to their ability to maintain telomeric DNA at lengths sufficient to avoid triggering senescence or apoptosis, achieved most commonly by upregulating expression of telomerase or, less frequently, via an alternative recombination-based telomere maintenance mechanism....

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Journal ArticleDOI
TL;DR: In this paper, the kinase ATR (ATM- and Rad3-related) stabilizes and helps to restart stalled replication forks, avoiding the generation of DNA damage and genome instability.
Abstract: Replication stress is a complex phenomenon that has serious implications for genome stability, cell survival and human disease. Generation of aberrant replication fork structures containing single-stranded DNA activates the replication stress response, primarily mediated by the kinase ATR (ATM- and Rad3-related). Along with its downstream effectors, ATR stabilizes and helps to restart stalled replication forks, avoiding the generation of DNA damage and genome instability. Understanding this response may be key to diagnosing and treating human diseases caused by defective responses to replication stress.

1,492 citations

Journal ArticleDOI
19 Jan 2012-Nature
TL;DR: A better understanding of the cellular response to DNA damage will not only inform the knowledge of cancer development but also help to refine the classification as well as the treatment of the disease.
Abstract: Genomic instability is one of the most pervasive characteristics of tumour cells and is probably the combined effect of DNA damage, tumour-specific DNA repair defects, and a failure to stop or stall the cell cycle before the damaged DNA is passed on to daughter cells. Although these processes drive genomic instability and ultimately the disease process, they also provide therapeutic opportunities. A better understanding of the cellular response to DNA damage will not only inform our knowledge of cancer development but also help to refine the classification as well as the treatment of the disease.

1,425 citations

Journal ArticleDOI
TL;DR: This review aims at providing novel insight into the regulatory pathways of autophagy in response to glucose and amino acid deprivation, as well as their tight interconnection with metabolic networks and redox homeostasis.
Abstract: Autophagy is a catabolic process aimed at recycling cellular components and damaged organelles in response to diverse conditions of stress, such as nutrient deprivation, viral infection and genotoxic stress. A growing amount of evidence in recent years argues for oxidative stress acting as the converging point of these stimuli, with reactive oxygen species (ROS) and reactive nitrogen species (RNS) being among the main intracellular signal transducers sustaining autophagy. This review aims at providing novel insight into the regulatory pathways of autophagy in response to glucose and amino acid deprivation, as well as their tight interconnection with metabolic networks and redox homeostasis. The role of oxidative and nitrosative stress in autophagy is also discussed in the light of its being harmful for both cellular biomolecules and signal mediator through reversible posttranslational modifications of thiol-containing proteins. The redox-independent relationship between autophagy and antioxidant response, occurring through the p62/Keap1/Nrf2 pathway, is also addressed in order to provide a wide perspective upon the interconnection between autophagy and oxidative stress. Herein, we also attempt to afford an overview of the complex crosstalk between autophagy and DNA damage response (DDR), focusing on the main pathways activated upon ROS and RNS overproduction. Along these lines, the direct and indirect role of autophagy in DDR is dissected in depth.

1,376 citations


Cites background from "The DNA Damage Response: Making It ..."

  • ...Different classes of proteins are implicated in DDR, among which the sensors specifically recognize the lesions to DNA, whereas the mediators and the effectors transduce the signal from the nucleus to the cytosol where several processes are contextually activated in order to better face up to adverse conditions.(102,103) For instance, cell cycle checkpoints are soon activated to block proliferation until lesions are repaired....

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Journal ArticleDOI
TL;DR: The components of the end resection machinery, the role of end structure, and the cell-cycle phase on resection and the interplay of end processing with NHEJ are reviewed.
Abstract: DNA double-strand breaks (DSBs) are cytotoxic lesions that can result in mutagenic events or cell death if left unrepaired or repaired inappropriately. Cells use two major pathways for DSB repair: nonhomologous end joining (NHEJ) and homologous recombination (HR). The choice between these pathways depends on the phase of the cell cycle and the nature of the DSB ends. A critical determinant of repair pathway choice is the initiation of 5′-3′ resection of DNA ends, which commits cells to homology-dependent repair, and prevents repair by classical NHEJ. Here, we review the components of the end resection machinery, the role of end structure, and the cell-cycle phase on resection and the interplay of end processing with NHEJ.

1,363 citations


Cites background from "The DNA Damage Response: Making It ..."

  • ...The initial recruitment and activation of ATM at sites of damage are followed by modifications of the surrounding chromatin—phosphorylation of H2AX—which in turns facilitates the recruitment of ubiquitin ligases that modify chromatin to assemble multiprotein complexes (33)....

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References
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Journal ArticleDOI
TL;DR: In this paper, a histone H2AX species that has been phosphorylated specifically at serine 139 was found to be a major component of DNA double-stranded break.

5,132 citations


"The DNA Damage Response: Making It ..." refers background in this paper

  • ...A critical aspect of this process involves the phosphorylation of Ser139 on the specialized histone H2AX called gH2AX (Figure 1A) (Rogakou et al., 1998)....

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Journal ArticleDOI
22 Oct 2009-Nature
TL;DR: The authors' improving understanding of DNA-damage responses is providing new avenues for disease management, and these responses are biologically significant because they prevent diverse human diseases.
Abstract: The prime objective for every life form is to deliver its genetic material, intact and unchanged, to the next generation. This must be achieved despite constant assaults by endogenous and environmental agents on the DNA. To counter this threat, life has evolved several systems to detect DNA damage, signal its presence and mediate its repair. Such responses, which have an impact on a wide range of cellular events, are biologically significant because they prevent diverse human diseases. Our improving understanding of DNA-damage responses is providing new avenues for disease management.

4,871 citations


"The DNA Damage Response: Making It ..." refers background in this paper

  • ...Indeed, BRCA2, BACH1, and PALB2 mutations predispose carriers to breast cancer formation when monoallelic and lead to FA syndrome—complementation groups D1, J, and N, respectively—when biallelic....

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  • ...Alternatively, assembly of RAD51 filaments on RPA-coated ssDNA mediated by BRCA2 can lead to HR (Figure 2B) (West, ouble-Strand Breaks 2003)....

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  • ...Depletion of HSCs has been observed in a variety of mouse models defective for DDR components, including ATM, BRCA2, ERCC1, FANCC, Ku80, LIG4, MSH2, XPD, and mouse telomerase RNA (mTR) (Niedernhofer, 2008; Park and Gerson, 2005; Sharpless and DePinho, 2007)....

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  • ...Heterozygous individuals carrying mutations of the BRCA1 or BRCA2 genes have a 40%–80% risk of developing breast cancer (Fackenthal and Olopade, 2007)....

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  • ...Moreover, PARP1 inhibitors have been successfully used to treat tumors that carry mutations in HR genes, such as BRCA1 and BRCA2 (Jackson and Bartek, 2009)....

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Book
01 Jan 1973
TL;DR: Radiobiology for the radiologist, Radiobiology in general, Radiology for radiologists as mentioned in this paper, Radiology in the field of radiology, radiology for radiology.
Abstract: Radiobiology for the radiologist , Radiobiology for the radiologist , کتابخانه دیجیتال جندی شاپور اهواز

4,040 citations

Journal ArticleDOI
23 Nov 2000-Nature
TL;DR: The inability to repair DNA damage properly in mammals leads to various disorders and enhanced rates of tumour development, and this work has shown that direct activation of DNA repair networks is needed to correct this problem.
Abstract: The inability to repair DNA damage properly in mammals leads to various disorders and enhanced rates of tumour development. Organisms respond to chromosomal insults by activating a complex damage response pathway. This pathway regulates known responses such as cell-cycle arrest and apoptosis (programmed cell death), and has recently been shown to control additional processes including direct activation of DNA repair networks.

3,230 citations


"The DNA Damage Response: Making It ..." refers background in this paper

  • ...These include the determination to undergo apoptosis or enter terminal differentiation through senescence, the activation of heightened immune surveillance, DNA damage prophylaxis through tanning, as well as DNA repair itself (Cui et al., 2007; Gasser and Raulet, 2006; Zhou and Elledge, 2000)....

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  • ...Localization of DDR factors to sites of DNAdamage is initiated by sensor proteins that directly recognize specific DNA lesions and activate the DDR (Zhou and Elledge, 2000)....

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  • ...Following the recognition of DNA lesions by sensor proteins, ATM and ATR initially phosphorylate mediator proteins, which can amplify the DDR by acting as recruiters of ATM/ATR substrates (Zhou and Elledge, 2000)....

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  • ...The most extensively studied component of this response is p53, which is regulated by ATM and CHK2 in response to DSBs (Figure 1A) (Zhou and Elledge, 2000). p53 induces cell-cycle arrest, apoptosis, or senescence in response to DNA damage by transcriptionally regulating, among others, the CDK…...

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Journal ArticleDOI
25 May 2007-Science
TL;DR: A large-scale proteomic analysis of proteins phosphorylated in response to DNA damage on consensus sites recognized by ATM and ATR is performed and more than 900 regulated phosphorylation sites encompassing over 700 proteins are identified.
Abstract: Cellular responses to DNA damage are mediated by a number of protein kinases, including ATM (ataxia telangiectasia mutated) and ATR (ATM and Rad3-related). The outlines of the signal transduction portion of this pathway are known, but little is known about the physiological scope of the DNA damage response (DDR). We performed a large-scale proteomic analysis of proteins phosphorylated in response to DNA damage on consensus sites recognized by ATM and ATR and identified more than 900 regulated phosphorylation sites encompassing over 700 proteins. Functional analysis of a subset of this data set indicated that this list is highly enriched for proteins involved in the DDR. This set of proteins is highly interconnected, and we identified a large number of protein modules and networks not previously linked to the DDR. This database paints a much broader landscape for the DDR than was previously appreciated and opens new avenues of investigation into the responses to DNA damage in mammals.

2,967 citations


"The DNA Damage Response: Making It ..." refers background in this paper

  • ...A large number of DDR-deficient mice and various human DDR syndromes, such as A-T, BS, and FA, display aberrant meiotic progression and infertility (Table 2) (Biton et al., 2008; Bohr, 2008; Matzuk and Lamb, 2008)....

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