Evidence map›Paper›PMID 29879444›Full record

ArticleFree radical biology & medicine2018

Enhanced mitochondrial DNA repair of the common disease-associated variant, Ser326Cys, of hOGG1 through small molecule intervention.

Beverly A Baptiste, Steven R Katchur, Elayne M Fivenson, Deborah L Croteau, William L Rumsey, Vilhelm A Bohr

Abstract read
In one paragraph

Article in Free radical biology & medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
0.6field-weighted citation impact, top 32% of its field
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

26 citing papers in PubMed, 35 citations in OpenAlex.

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  16. Review
  17. There's more to enzyme antagonism than inhibition.Bioorganic & medicinal chemistry · 2023
    Review
  18. Chemical Tools for the Study of DNA Repair.Accounts of chemical research · 2022
    Article
  19. Article
  20. Mitochondrial CaArteriosclerosis, thrombosis, and vascular biology · 2022
    Article
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

6 authors at 3 institutions in 1 country.

Beverly A BaptisteLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, United States.
Steven R KatchurRespiratory Therapy Area, GSK R&D, Collegeville, PA, United States.
Elayne M FivensonLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, United States.
Deborah L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, United States.
William L RumseyRespiratory Therapy Area, GSK R&D, Collegeville, PA, United States.
Vilhelm A BohrLaboratory of Molecular Gerontology, National Institute on Aging, National Institutes of Health, Baltimore, MD, United States. Electronic address: BohrV@grc.nia.nih.gov.
National Institutes of Health · USGlaxoSmithKline (United States) · USNational Institute on Aging · US

Funding

DNA repair dysfunction in neurodegeneration and Alzheimer's DiseaseZIAAG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BROSH, ROBERT · 2009 to 2025
$9.5M
Mitochondrial DNA Repair Processes In Oxidative Stress And AgingZIAAG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.2M
Oxidative DNA Damage And Its ProcessingZIAAG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$8.4M
REPAIR OF OXIDATIVE DNA DAMAGEZ01AG000727 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1994 to 2008
$1.3M
GROWTH ARREST AND DNA DAMAGE INDUCIBLE GENE GADD153--REGULATION BY DNA DAMAGEZ01AG000723 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM · 1992 to 2008
$310k
Intramural NIH HHS Z01 AG000723Intramural NIH HHS Z01 AG000727
6 · The paper itself

Abstract

The common oxidatively generated lesion, 8-oxo-7,8-dihydroguanine (8-oxoGua), is removed from DNA by base excision repair. The glycosylase primarily charged with recognition and removal of this lesion is 8-oxoGuaDNA glycosylase 1 (OGG1). When left unrepaired, 8-oxodG alters transcription and is mutagenic. Individuals homozygous for the less active OGG1 allele, Ser326Cys, have increased risk of several cancers. Here, small molecule enhancers of OGG1 were identified and tested for their ability to stimulate DNA repair and protect cells from the environmental hazard paraquat (PQ). PQ-induced mtDNA damage was inversely proportional to the levels of OGG1 expression whereas stimulation of OGG1, in some cases, entirely abolished its cellular effects. The PQ-mediated decline of mitochondrial membrane potential or nuclear condensation were prevented by the OGG1 activators. In addition, in Ogg1

Indexed as

DNA RepairA549 CellsAnimalsCells, CulturedDNA DamageDNA GlycosylasesDNA, MitochondrialFibroblastsHerbicidesHumansMiceMice, KnockoutMitochondriaMutationOxidation-ReductionOxidative StressDNA GlycosylasesDNA, MitochondrialHerbicidesOgg1 protein, mouseoxoguanine glycosylase 1, humanParaquatReactive Oxygen SpeciesSerineSmall Molecule Libraries8-dihydroguanine8-oxo-78-Oxoguanine DNA glycosylase-1Base excision repairMitochondriaOGG1(S326C)Oxidative stress

Identifiers

PMID29879444
PMCPMC6098717
OpenAlexW2805889381

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.