ArticleBiochemistry2009
Exploring damage recognition models in prokaryotic nucleotide excision repair with a benzo[a]pyrene-derived lesion in UvrB.
Article in Biochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
14 citing papers in PubMed.
- Mechanistic insight into the repair of C8-linked pyrrolobenzodiazepine monomer-mediated DNA damage.RSC medicinal chemistry · 2022Article
- Sequence specificity, energetics and mechanism of mismatch recognition by DNA damage sensing protein Rad4/XPC.Nucleic acids research · 2020Article
- The ATPase mechanism of UvrA2 reveals the distinct roles of proximal and distal ATPase sites in nucleotide excision repair.Nucleic acids research · 2019Article
- Mechanism of DNA Lesion Homing and Recognition by the Uvr Nucleotide Excision Repair System.Research (Washington, D.C.) · 2019Article
- Conservation and Divergence in Nucleotide Excision Repair Lesion Recognition.The Journal of biological chemistry · 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
- Investigation of bacterial nucleotide excision repair using single-molecule techniques.DNA repair · 2014Review
- Ribonucleotides as nucleotide excision repair substrates.DNA repair · 2014Article
- Prokaryotic nucleotide excision repair.Cold Spring Harbor perspectives in biology · 2013Review
- Surviving the sun: repair and bypass of DNA UV lesions.Protein science : a publication of the Protein Society · 2011Review
- Article
- Base flipping free energy profiles for damaged and undamaged DNA.Chemical research in toxicology · 2010Article
- DNA-Destabilizing Agents as an Alternative Approach for Targeting DNA: Mechanisms of Action and Cellular Consequences.Journal of nucleic acids · 2010Article
- Mechanistic and biological aspects of helicase action on damaged DNA.Cell cycle (Georgetown, Tex.) · 2010Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors.
Funding
Abstract
The UvrB protein is a central unit for damage recognition in the prokaryotic nucleotide excision repair system, which excises bulky DNA lesions. We have utilized molecular modeling and MD simulations based on crystal structures, mutagenesis, and fluorescence data, to model the 10R-(+)-cis-anti-B[a]P-N2-dG lesion, derived from the tumorigenic (+)-anti-B[a]PDE metabolite of benzo[a]pyrene, at different locations on the inner and outer strand in UvrB. Our results suggest that this lesion is accommodated on the inner strand where it might translocate through the tunnel created by the beta-hairpin and UvrB domain 1B and ultimately could be housed in the pocket behind the beta-hairpin prior to excision by UvrC. Lesions that vary in size and shape may be stopped at the gate to the tunnel, within the tunnel, or in the pocket when UvrC initiates excision. Common features of beta-hairpin intrusion between the two DNA strands and nucleotide flipping manifested in structures of prokaryotic and eukaryotic NER lesion recognition proteins are consistent with common recognition mechanisms, based on lesion-induced local thermodynamic distortion/destabilization and nucleotide flipping.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.