The DOI matches its Crossref record; 246 of the 246 references it cites were found in a registry or an index.
The DNA Damage Response: Making It Safe to Play with Knives
Open accessAbstract
Damage to our genetic material is an ongoing threat to both our ability to faithfully transmit genetic information to our offspring as well as our own survival. To respond to these threats, eukaryotes have evolved the DNA damage response (DDR). The DDR is a complex signal transduction pathway that has the ability to sense DNA damage and transduce this information to the cell to influence cellular responses to DNA damage. Cells possess an arsenal of enzymatic tools capable of remodeling and repairing DNA; however, their activities must be tightly regulated in a temporal, spatial, and DNA lesion-appropriate fashion to optimize repair and prevent unnecessary and potentially deleterious alterations in the structure of DNA during normal cellular processes. This review will focus on how the DDR controls DNA repair and the phenotypic consequences of defects in these critical regulatory functions in mammals.
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In the citing paper
“Poly-ADP-ribose chains act as a scaffold for repair proteins, ensuring effective recruitment of single-strand break repair (SSBR) and double-strand break repair (DSBR) machinery.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“PARP1 and PARP2 are the main enzymes with a function in damage signaling.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“Poly-ADP-ribose (PAR) chains are rapidly disassembled by poly (ADP-ribose) glycohydrolase (PARG), allowing the whole event to repeat [55,66].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“In contrast, poly [ADP-ribose] polymerases (PARPs) work as signaling molecules in single-strand break repair.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“PARPs catalyze an evolutionary conserved posttranslational modification in which ADP-ribose residues from nicotinamide adenine dinucleotide (NAD+) molecules are transferred onto amino acid moieties of various proteins, including histone proteins and PARP itself, leading to polymeric ADP-ribose chains formation.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“In fact, PARP1 is responsible for the majority of ADP-ribosylation events in cell.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“PARP binding is only temporary due to emerging electrostatic interactions.”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“Double-strand break repair protein (MRE11), one of the components of MRN possess endo and exonucleolytic activity that enables single strand DNA (ssDNA) formation [55,118].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“ssDNA is then coated with RPA protein that comprise to the stability of DNA fragments and form a platform for DNA repair protein RAD51 (RAD51) protein [55].”
From Focus on UV-Induced DNA Damage and Repair—Disease Relevance and Protective Strategies (2020) · cites this paper as [55]
In the citing paper
“The checkpoints also actively stimulate the repair processes [1–9] and, in higher eukaryotes, trigger the apoptotic response, if damage cannot be dealt with successfully [10–12].”
From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [9]
In the citing paper
“These observations suggest that DDR pathways, evolved to safeguard genomic integrity and maximize survival of the organism13,44–46, may show reduced activity in stem cells with age.”
From Stem cell aging: mechanisms, regulators and therapeutic opportunities (2014) · cites this paper as [44]
In the citing paper
“ATR (ATM and Rad3-related) is critical to UV DNA damage signaling (Ciccia and Elledge, 2010) and is intimately linked with NER”
From RETRACTED: PKA-Mediated Phosphorylation of ATR Promotes Recruitment of XPA to UV-Induced DNA Damage (2014) · cites this paper as Ciccia and Elledge, 2010
In the citing paper
“It is estimated that oxidative stress may induce approximately 10,000 DNA alterations per cell per day, representing a major portion of endogenous DNA damage [17–20].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [19]
In the citing paper
“Oxidative stress can induce a variety of different types of DNA damage or replication stress, such as base (purine and pyrimidine) damage, sugar moiety damage, Apurinic/apyrimidinic (AP) sites, DNA single-strand breaks (SSBs), DNA double-strand breaks (DSBs), tandem base modifications (e.g., DNA intrastrand crosslink), DNA interstrand crosslinks, protein–DNA crosslinks, mismatched pairs with dam”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [19]
In the citing paper
“In response to oxidative DNA damage, various DNA repair and DNA damage response (DDR) pathways are employed by cells to maintain genomic integrity [12, 18, 19, 31]”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [19]
In the citing paper
“To maintain genome stability, the DDR pathways are conserved surveillance mechanisms coordinating DNA repair, cell cycle progression, transcription, apoptosis, and senescence [19, 39–41].”
From Functional interplay between ATM/ATR-mediated DNA damage response and DNA repair pathways in oxidative stress (2014) · cites this paper as [19]
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Metadata
- Authors
- Ciccia, A., & Elledge, S. J.
- Affiliations
- Brigham and Women's Hospital (US)
- Corresponding author
- Elledge, Stephen J.
- Venue
- Molecular Cell
- Publisher
- Elsevier BV
- Published
- 2010-10
- Volume
- 40
- Issue
- 2
- Pages
- 179-204
- ISSN
- 1097-2765 (ISSN-L)
- PMC
- PMC2988877
- OpenAlex
- W2077436902
- Cited by
- 4,368
- References
- 246
- Citations by year
- 2026: 198 · 2025: 240 · 2024: 246 · 2023: 301 · 2022: 292 · 2021: 335 · 2020: 343 · 2019: 308 · 2018: 292 · 2017: 303 · 2016: 329 · 2015: 289 · 2014: 288 · 2013: 269 · 2012: 201
- FWCI
- 16.84
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Molecular Cell (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Howard Hughes Medical Institute
- National Institute of General Medical Sciences (R37GM044664)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
- Health Sciences › Medicine › Oncology › Cancer-related Molecular Pathways
- Health Sciences › Medicine › Oncology › PARP inhibition in cancer therapy
- Keywords
- DNA damage response, DNA repair, signal transduction, DNA damage recognition, DNA repair regulation, mammalian cells, genetic stability, genome stability
- MeSH terms
- Animals, DNA, DNA Damage, DNA Repair, Models, Genetic, Recombination, Genetic, Signal Transduction, DNA Breaks, Double-Stranded, Eukaryota
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