Evidence map›Paper›PMID 31024003›Full record

ArticleCell death & disease2019

AP endonuclease 1 (Apex1) influences brain development linking oxidative stress and DNA repair.

De-Sheng Pei, Pan-Pan Jia, Juan-Juan Luo, Wei Liu, Phyllis R Strauss

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing 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

31 citing papers in PubMed, 51 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Role of cytokines and reactive oxygen species in brain aging.Mechanisms of ageing and development · 2023
    Review
  19. Article
  20. Unraveling DNA Repair Processes In Vivo: Insights from Zebrafish Studies.International journal of molecular sciences · 2023
    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

5 authors at 2 institutions in 2 countries.

De-Sheng PeiCollege of Life Science, Henan Normal University, Xinxiang, 453007, China. deshengpei@gmail.comM.ORCID http://orcid.org/0000-0001-6408-9575
Pan-Pan JiaKey Laboratory of Reservoir Aquatic Environment, Chongqing Institute of Green and Intelligent Technology, Chinese Academy of Sciences, Chongqing, 400714, China.
Juan-Juan LuoKey Laboratory of Reservoir Aquatic Environment, Chongqing Institute of Green and Intelligent Technology, Chinese Academy of Sciences, Chongqing, 400714, China.
Wei LiuDepartment of Biology, College of Science, Northeastern University, Boston, MA, 02115, USA.
Phyllis R StraussDepartment of Biology, College of Science, Northeastern University, Boston, MA, 02115, USA. p.strauss@northeastern.edu.
Chongqing Institute of Green and Intelligent Technology · CNNortheastern University · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Brain and neurons are particularly sensitive to reactive oxygen species (ROS). Oxidative damage from ROS results in increased 8-oxoguanine in DNA followed by repair through the base excision repair (BER) pathway. We reported earlier that AP endonuclease 1 (Apex1) not only participates directly in BER but also regulates transcription factor Creb1. Here, we investigated how Apex1 affects brain to respond effectively to oxidative damage during zebrafish development. Loss of Apex1 resulted in increased ROS, 8-oxoguanine, and abasic sites as well as loss of Ogg1, which recognizes 8-oxoguanine and is required for its repair. Moreover, knock-down of Apex1 not only resulted in reduction of expression of several major proteins in the BER pathway (Polb and Ogg1), and it also resulted in maldistribution and loss of four key brain transcription factors (fezf2, otx2, egr2a, and pax2a), leading to abnormal brain development. These results were independent of p53 protein level. In contrast, exposure to exogenous H

Indexed as

DNA RepairOxidative StressAnimalsBrainCyclic AMP Response Element-Binding ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseDNA Polymerase betaGuanineMorpholinosReactive Oxygen SpeciesTranscription FactorsTumor Suppressor Protein p53ZebrafishZebrafish Proteins8-hydroxyguanineCyclic AMP Response Element-Binding ProteinDNA-(Apurinic or Apyrimidinic Site) LyaseDNA Polymerase betaGuanineMorpholinosReactive Oxygen SpeciesTranscription FactorsTumor Suppressor Protein p53Zebrafish Proteins

Identifiers

PMID31024003
PMCPMC6484078
OpenAlexW2941697941

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.