Evidence map›Paper›PMID 27818219›Full record

ReviewFree radical biology & medicine2017

Removal of oxidatively generated DNA damage by overlapping repair pathways.

Vladimir Shafirovich, Nicholas E Geacintov

Abstract readReview
In one paragraph

Review in Free radical biology & medicine, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
3.5field-weighted citation impact, top 7% 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

37 citing papers in PubMed, 53 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
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  6. Article
  7. Article
  8. Telomere Attrition in Chronic Kidney Diseases.Antioxidants (Basel, Switzerland) · 2023
    Review
  9. Review
  10. Article
  11. Article
  12. Nucleotide excision repair: a versatile and smart toolkit.Acta biochimica et biophysica Sinica · 2022
    Review
  13. Article
  14. Article
  15. Review
  16. Review
  17. Review
  18. The Multiple Cellular Roles of SMUG1 in Genome Maintenance and Cancer.International journal of molecular sciences · 2021
    Review
  19. Article
  20. 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

2 authors at 1 institution in 1 country.

Vladimir ShafirovichChemistry Department, New York University, 31 Washington Place, New York, NY 10003-5180, USA. Electronic address: vs5@nyu.edu.
Nicholas E GeacintovChemistry Department, New York University, 31 Washington Place, New York, NY 10003-5180, USA.
New York University · US

Funding

Interplay between DNA repair mechanisms in human cells and extractsR01ES027059 · NIEHS · NEW YORK UNIVERSITY · PI SHAFIROVICH, VLADIMIR · 2016 to 2020
$1.8M
Recognition of Environmental Carcinogen-DNA lesions by NER ProteinsR01ES024050 · NIEHS · NEW YORK UNIVERSITY · PI GEACINTOV, NICHOLAS E · 2014 to 2018
$1.8M
SHARED INSTR FACILITIY FOR THE LIFE SCIC06RR016572 · NCRR · NEW YORK UNIVERSITY · PI LENNIE, PETER · 2001 to 2001
$665k
NCRR NIH HHS C06 RR016572NIEHS NIH HHS R01 ES024050NIEHS NIH HHS R01 ES027059
6 · The paper itself

Abstract

It is generally believed that the mammalian nucleotide excision repair pathway removes DNA helix-distorting bulky DNA lesions, while small non-bulky lesions are repaired by base excision repair (BER). However, recent work demonstrates that the oxidativly generated guanine oxidation products, spiroimininodihydantoin (Sp), 5-guanidinohydantoin (Gh), and certain intrastrand cross-linked lesions, are good substrates of NER and BER pathways that compete with one another in human cell extracts. The oxidation of guanine by peroxynitrite is known to generate 5-guanidino-4-nitroimidazole (NIm) which is structurally similar to Gh, except that the 4-nitro group in NIm is replaced by a keto group in Gh. However, unlike Gh, NIm is an excellent substrate of BER, but not of NER. These and other related results are reviewed and discussed in this article.

Indexed as

DNA DamageDNA RepairOxidative StressDNA, B-FormDNA GlycosylasesGuanidinesHumansHydantoinsNitroimidazolesOxidation-ReductionSubstrate Specificity5-guanidino-4-nitroimidazoleDNA, B-FormDNA GlycosylasesGuanidinesguanidinohydantoinHydantoinsNitroimidazolesBase excision repairDNA damageNucleotide excision repairOxidative stressReactive oxygen species

Identifiers

PMID27818219
PMCPMC5418118
OpenAlexW2548878692

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.