Evidence map›Paper›PMID 28199214›Full record

ReviewFrontiers in bioscience (Landmark edition)2017

Base excision repair of oxidative DNA damage: from mechanism to disease.

Amy M Whitaker, Matthew A Schaich, Mallory R Smith, Tony S Flynn, Bret D Freudenthal

Abstract readReview
In one paragraph

Review in Frontiers in bioscience (Landmark edition), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 124 papers.

0numbers the graph read from it
0cells of the map it votes in
124citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

124 citing papers in PubMed.

  1. Cadmium inhibits hSMUG1-mediated uracil excision: quantitative analysis and mitigation byJournal of enzyme inhibition and medicinal chemistry · 2026
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64 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors.

Amy M WhitakerDepartment of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, 66160.
Matthew A SchaichDepartment of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, 66160.
Mallory R SmithDepartment of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, 66160.
Tony S FlynnDepartment of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, 66160.
Bret D FreudenthalDepartment of Biochemistry and Molecular Biology, University of Kansas Medical Center, Kansas City, Kansas, 66160, bfreudenthal@kumc.edu.

Funding

DNA Repair Strategies that Impact Genomic Stability During Oxidative StressR00ES024431 · NIEHS · UNIVERSITY OF KANSAS MEDICAL CENTER · PI FREUDENTHAL, BRET D · 2015 to 2017
$734k
NIEHS NIH HHS R00 ES024431
6 · The paper itself

Abstract

Reactive oxygen species continuously assault the structure of DNA resulting in oxidation and fragmentation of the nucleobases. Both oxidative DNA damage itself and its repair mediate the progression of many prevalent human maladies. The major pathway tasked with removal of oxidative DNA damage, and hence maintaining genomic integrity, is base excision repair (BER). The aphorism that structure often dictates function has proven true, as numerous recent structural biology studies have aided in clarifying the molecular mechanisms used by key BER enzymes during the repair of damaged DNA. This review focuses on the mechanistic details of the individual BER enzymes and the association of these enzymes during the development and progression of human diseases, including cancer and neurological diseases. Expanding on these structural and biochemical studies to further clarify still elusive BER mechanisms, and focusing our efforts toward gaining an improved appreciation of how these enzymes form co-complexes to facilitate DNA repair is a crucial next step toward understanding how BER contributes to human maladies and how it can be manipulated to alter patient outcomes.

Indexed as

DNA DamageDNA RepairAnimalsDNADNA GlycosylasesDNA Polymerase betaGene Knockout TechniquesHumansMiceModels, MolecularMutationNeoplasmsNervous System DiseasesOxidation-ReductionReactive Oxygen SpeciesDNADNA GlycosylasesDNA Polymerase betaPOLB protein, humanReactive Oxygen Species

Identifiers

PMID28199214
PMCPMC5567671

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.