Evidence map›Paper›PMID 29129598›Full record

ReviewDNA repair2017

POLB: A new role of DNA polymerase beta in mitochondrial base excision repair.

Brett A Kaufman, Bennett Van Houten

Abstract readReview
In one paragraph

Review in DNA repair, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.5field-weighted citation impact, top 18% 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

29 citing papers in PubMed, 43 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Article
  5. Article
  6. Mitochondrial DNA Damage and Its Repair Mechanisms in Aging Oocytes.International journal of molecular sciences · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Decoding mitochondrial DNA damage and repair associated withFrontiers in cellular and infection microbiology · 2024
    Review
  11. Article
  12. Article
  13. Review
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Mitochondrial Epigenetics Regulating Inflammation in Cancer and Aging.Frontiers in cell and developmental biology · 2022
    Review
  20. Review
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

2 authors at 2 institutions in 1 country.

Brett A KaufmanCenter for Metabolism and Mitochondrial Medicine, Division of Cardiology, Vascular Medicine Institute, University of Pittsburgh School of Medicine, Pittsburgh PA USA. Electronic address: bkauf@pitt.edu.
Bennett Van HoutenHillman Cancer Center, Department of Pharmacology and Chemical Biology, University of Pittsburgh Cancer Institute, Pittsburgh PA USA. Electronic address: vanhoutenb@upmc.edu.
University of Pittsburgh · USUPMC Hillman Cancer Center · US

Funding

DNA damage recognition by nucleotide excision repair proteinsR01ES019566 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI VAN HOUTEN, BENNETT · 2011 to 2020
$3.9M
Molecular mechanisms of mitochondrial DNA deletion formationR01GM110424 · NIGMS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI KAUFMAN, BRETT A · 2015 to 2019
$1.9M
ROS driven mitochondrial-telomere dysfunction during environmental stressR33ES025606 · NIEHS · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI OPRESKO, PATRICIA L, VAN HOUTEN, BENNETT · 2017 to 2019
$1.6M
NIEHS NIH HHS R01 ES019566NIEHS NIH HHS R33 ES025606NIGMS NIH HHS R01 GM110424
6 · The paper itself

Abstract

The mitochondrial genome is a matrilineally inherited DNA that encodes numerous essential subunits of the respiratory chain in all metazoans. As such mitochondrial DNA (mtDNA) sequence integrity is vital to organismal survival, but it has a limited cadre of DNA repair activities, primarily base excision repair (BER). We have known that the mtDNA is significantly oxidized by both endogenous and exogenous sources, but this does not lead to the expected preferential formation of transversion mutations, which suggest a robust base excision repair (BER) system. This year, two different groups reported compelling evidence that what was believed to be exclusively nuclear DNA repair polymerase, POLB, is located in the mitochondria and plays a significant role in mitochondrial BER, mtDNA integrity and mitochondrial function. In this commentary, we review the findings and highlight remaining questions for the field.

Indexed as

DNA RepairDNA DamageDNA, MitochondrialDNA Polymerase betaHumansMitochondriaMitochondrial ProteinsDNA, MitochondrialDNA Polymerase betaMitochondrial ProteinsBERdRP lyasemtDNA repairMutagenesisPOLBSN-BER

Identifiers

PMID29129598
PMCPMC5713914
OpenAlexW2767657107

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.