Evidence map›Paper›PMID 28559431›Full record

ArticleMolecular and cellular biology2017

DNA Polymerase Beta Participates in Mitochondrial DNA Repair.

P Sykora, S Kanno, M Akbari, T Kulikowicz, B A Baptiste, G S Leandro, H Lu, J Tian, A May, K A Becker and 5 more

Open access · bronzeAbstract read
In one paragraph

Article in Molecular and cellular biology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
5.7field-weighted citation impact, top 3% 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

74 citing papers in PubMed, 106 citations in OpenAlex.

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  19. Cardiovascular aging: spotlight on mitochondria.American journal of physiology. Heart and circulatory physiology · 2024
    Review
  20. Decoding mitochondrial DNA damage and repair associated withFrontiers in cellular and infection microbiology · 2024
    Review

14 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

15 authors at 6 institutions in 4 countries.

P SykoraLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
S KannoDivision of Dynamic Proteome in Cancer and Aging, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
M AkbariCenter for Healthy Aging, University of Copenhagen, Copenhagen, Denmark.
T KulikowiczLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
B A BaptisteLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
G S LeandroLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
H LuLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
J TianLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
A MayLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
K A BeckerLaboratory of Genetics, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
D L CroteauLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
D M WilsonLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA.
R W SobolDepartment of Oncologic Sciences, Mitchell Cancer Institute, University of South Alabama, Mobile, Alabama, USA.ORCID http://orcid.org/0000-0001-7385-3563
A YasuiDivision of Dynamic Proteome in Cancer and Aging, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan.
V A BohrLaboratory of Molecular Gerontology, National Institute on Aging, Intramural Research Program, Baltimore, Maryland, USA BohrV@grc.nia.nih.gov.
National Institute on Aging · USTohoku University · JPUSA Mitchell Cancer Institute · USInstitute on Aging · USUniversidade de São Paulo · BRUniversity of Copenhagen · DK

Funding

Analysis of complex biological systems by microarray based gene expressionZICAG000616 · NIA · NATIONAL INSTITUTE ON AGING · PI DE, SUPRIYO · 2009 to 2025
$15.5M
Mitochondrial DNA Repair Processes In Oxidative Stress And AgingZIAAG000733 · NIA · NATIONAL INSTITUTE ON AGING · PI FERRUCCI, LUIGI · 2009 to 2022
$9.2M
Base Excision DNA Repair in Disease Susceptibility and TreatmentZIAAG000750 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 2009 to 2019
$5.4M
Novel approaches to enhance tumor cell cytotoxicity of alkylating agentsR01CA148629 · NCI · UNIVERSITY OF SOUTH ALABAMA · PI SOBOL, ROBERT W · 2010 to 2021
$3.4M
PROCESSING OF OXIDATIVE STRESS IN ALZHEIMER'S DISEASEZ01AG000735 · NIA · NATIONAL INSTITUTE ON AGING · PI BOHR, VILHELM A · 1997 to 2008
$565k
Intramural NIH HHS Z01 AG000735NCI NIH HHS R01 CA148629
6 · The paper itself

Abstract

We have detected DNA polymerase beta (Polβ), known as a key nuclear base excision repair (BER) protein, in mitochondrial protein extracts derived from mammalian tissue and cells. Manipulation of the N-terminal sequence affected the amount of Polβ in the mitochondria. Using Polβ fragments, mitochondrion-specific protein partners were identified, with the interactors functioning mainly in DNA maintenance and mitochondrial import. Of particular interest was the identification of the proteins TWINKLE, SSBP1, and TFAM, all of which are mitochondrion-specific DNA effectors and are known to function in the nucleoid. Polβ directly interacted functionally with the mitochondrial helicase TWINKLE. Human kidney cells with Polβ knockout (KO) had higher endogenous mitochondrial DNA (mtDNA) damage. Mitochondrial extracts derived from heterozygous Polβ mouse tissue and KO cells had lower nucleotide incorporation activity. Mouse-derived Polβ null fibroblasts had severely affected metabolic parameters. Indeed, gene knockout of Polβ caused mitochondrial dysfunction, including reduced membrane potential and mitochondrial content. We show that Polβ is a mitochondrial polymerase involved in mtDNA maintenance and is required for mitochondrial homeostasis.

Indexed as

base excision repairDNA polymerase betamitochondriamitochondrial DNA repairmitochondrial healthmutational studiesTFAM

Identifiers

PMID28559431
PMCPMC5533889
OpenAlexW2620067343

What OpenQuestion holds

Textmetadata
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.