ArticleNucleic acids research2012
Defining the functional footprint for recognition and repair of deaminated DNA.
Article in Nucleic acids research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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.
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Who cites it
8 citing papers in PubMed, 11 citations in OpenAlex.
- UV-DDB as a Dynamic Regulator Linking Base Excision and Nucleotide Excision Repair via AAG Interaction.International journal of molecular sciences · 2026Article
- Functional Role of N-Terminal Extension of Human AP Endonuclease 1 In Coordination of Base Excision DNA Repair via Protein-Protein Interactions.International journal of molecular sciences · 2020Article
- Expansion of base excision repair compensates for a lack of DNA repair by oxidative dealkylation in budding yeast.The Journal of biological chemistry · 2019Article
- DNA scanning by base excision repair enzymes and implications for pathway coordination.DNA repair · 2018Review
- Distinguishing Specific and Nonspecific Complexes of Alkyladenine DNA Glycosylase.Biochemistry · 2018Article
- Repair of Alkylation Damage in Eukaryotic Chromatin Depends on Searching Ability of Alkyladenine DNA Glycosylase.ACS chemical biology · 2015Article
- Probing the DNA structural requirements for facilitated diffusion.Biochemistry · 2015Article
- Isolating contributions from intersegmental transfer to DNA searching by alkyladenine DNA glycosylase.The Journal of biological chemistry · 2013Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Spontaneous deamination of DNA is mutagenic, if it is not repaired by the base excision repair (BER) pathway. Crystallographic data suggest that each BER enzyme has a compact DNA binding site. However, these structures lack information about poorly ordered termini, and the energetic contributions of specific protein-DNA contacts cannot be inferred. Furthermore, these structures do not reveal how DNA repair intermediates are passed between enzyme active sites. We used a functional footprinting approach to define the binding sites of the first two enzymes of the human BER pathway for the repair of deaminated purines, alkyladenine DNA glycosylase (AAG) and AP endonuclease (APE1). Although the functional footprint for full-length AAG is explained by crystal structures of truncated AAG, the footprint for full-length APE1 indicates a much larger binding site than is observed in crystal structures. AAG turnover is stimulated in the presence of APE1, indicating rapid exchange of AAG and APE1 at the abasic site produced by the AAG reaction. The coordinated reaction does not require an extended footprint, suggesting that each enzyme engages the site independently. Functional footprinting provides unique information relative to traditional footprinting approaches and is generally applicable to any DNA modifying enzyme or system of enzymes.
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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.