ArticleChemical research in toxicology2012
The efficiencies of damage recognition and excision correlate with duplex destabilization induced by acetylaminofluorene adducts in human nucleotide excision repair.
Article in Chemical research in toxicology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed.
- Active DNA damage eviction by HLTF stimulates nucleotide excision repair.Molecular cell · 2022Article
- A combination of direct reversion and nucleotide excision repair counters the mutagenic effects of DNA carboxymethylation.DNA repair · 2022Article
- Regulation of p53 Activity by (+)-Epiloliolide Isolated fromMarine drugs · 2021Article
- Light-induced modulation of DNA recognition by the Rad4/XPC damage sensor protein.RSC chemical biology · 2021Article
- The DNA damage-sensing NER repair factor XPC-RAD23B does not recognize bulky DNA lesions with a missing nucleotide opposite the lesion.DNA repair · 2020Article
- A key interaction with RPA orients XPA in NER complexes.Nucleic acids research · 2020Article
- Polynuclear ruthenium organometallic compounds induce DNA damage in human cells identified by the nucleotide excision repair factor XPC.Bioscience reports · 2019Article
- cAMP-mediated regulation of melanocyte genomic instability: A melanoma-preventive strategy.Advances in protein chemistry and structural biology · 2019Review
- Molecular basis for damage recognition and verification by XPC-RAD23B and TFIIH in nucleotide excision repair.DNA repair · 2018Review
- Repair-Resistant DNA Lesions.Chemical research in toxicology · 2017Review
- Single-Molecule Imaging Reveals that Rad4 Employs a Dynamic DNA Damage Recognition Process.Molecular cell · 2016Article
- Dissociation Dynamics of XPC-RAD23B from Damaged DNA Is a Determining Factor of NER Efficiency.PloS one · 2016Article
- Exposure of Human Lung Cells to Tobacco Smoke Condensate Inhibits the Nucleotide Excision Repair Pathway.PloS one · 2016Article
- Protein Recognition in Drug-Induced DNA Alkylation: When the Moonlight Protein GAPDH Meets S23906-1/DNA Minor Groove Adducts.International journal of molecular sciences · 2015Review
- Kinetic gating mechanism of DNA damage recognition by Rad4/XPC.Nature communications · 2015Article
- The relationships between XPC binding to conformationally diverse DNA adducts and their excision by the human NER system: is there a correlation?DNA repair · 2014Article
- Structural basis for the recognition of diastereomeric 5',8-cyclo-2'-deoxypurine lesions by the human nucleotide excision repair system.Nucleic acids research · 2014Article
- Base-displaced intercalation of the 2-amino-3-methylimidazo[4,5-f]quinolone N2-dG adduct in the NarI DNA recognition sequence.Nucleic acids research · 2014Article
- Article
- Ribonucleotides as nucleotide excision repair substrates.DNA repair · 2014Article
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Authors and funding
4 authors.
Funding
Abstract
Nucleotide excision repair (NER) removes lesions caused by environmental mutagens or UV light from DNA. A hallmark of NER is the extraordinarily wide substrate specificity, raising the question of how one set of proteins is able to recognize structurally diverse lesions. Two key features of good NER substrates are that they are bulky and thermodynamically destabilize DNA duplexes. To understand what the limiting step in damage recognition in NER is, we set out to test the hypothesis that there is a correlation of the degree of thermodynamic destabilization induced by a lesion, binding affinity to the damage recognition protein XPC-RAD23B, and overall NER efficiency. We chose to use acetylaminofluorene (AAF) and aminofluorene (AF) adducts at the C8 position of guanine in different positions within the NarI (GGCGCC) sequence, as it is known that the structures of the duplexes depend on the position of the lesion in this context. We found that the efficiency of NER and the binding affinity of the damage recognition factor XPC-RAD23B correlated with the thermodynamic destabilization induced by the lesion. Our study is the first systematic analysis correlating these three parameters and supports the idea that initial damage recognition by XPC-RAD23B is a key rate-limiting step in NER.
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