Evidence map›Paper›PMID 25033834›Full record

ReviewExperimental & molecular medicine2014

APE1/Ref-1 as an emerging therapeutic target for various human diseases: phytochemical modulation of its functions.

Shweta Thakur, Bibekananda Sarkar, Ravi P Cholia, Nandini Gautam, Monisha Dhiman, Anil K Mantha

Open access · goldAbstract readReview
In one paragraph

Review in Experimental & molecular medicine, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 84 papers.

0numbers the graph read from it
0cells of the map it votes in
84citing papers in PubMed
6.3field-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

84 citing papers in PubMed, 161 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Article
  6. Association ofThe International journal of angiology : official publication of the International College of Angiology, Inc · 2025
    Article
  7. Article
  8. Biological Amyloids Chemically Damage DNA.ACS chemical neuroscience · 2025
    Article
  9. Article
  10. Review
  11. Article
  12. Nanoscale Interaction of Endonuclease APE1 with DNA.International journal of molecular sciences · 2024
    Article
  13. Article
  14. The APE1/REF-1 and the hallmarks of cancer.Molecular biology reports · 2024
    Review
  15. Article
  16. Review
  17. Article
  18. Article
  19. Article
  20. Article

24 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

6 authors at 2 institutions in 2 countries.

Shweta ThakurCenter for Biosciences, School of Basic and Applied Sciences, Central University of Punjab, Punjab, India.
Bibekananda SarkarCenter for Biosciences, School of Basic and Applied Sciences, Central University of Punjab, Punjab, India.
Ravi P CholiaCenter for Biosciences, School of Basic and Applied Sciences, Central University of Punjab, Punjab, India.
Nandini GautamCenter for Environmental Science and Technology, School of Environment and Earth Sciences, Central University of Punjab, Punjab, India.
Monisha DhimanCenter for Genetic Diseases and Molecular Medicine, School of Emerging Life Science Technologies, Central University of Punjab, Punjab, India.
Anil K Mantha1] Center for Biosciences, School of Basic and Applied Sciences, Central University of Punjab, Punjab, India [2] Department of Biochemistry and Molecular Biology, University of Texas Medical Branch, Galveston, TX, USA.
Central University of Punjab · INThe University of Texas Medical Branch at Galveston · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Apurinic/apyrimidinic endonuclease 1 (APE1) is a multifunctional enzyme involved in the base excision repair (BER) pathway, which repairs oxidative base damage caused by endogenous and exogenous agents. APE1 acts as a reductive activator of many transcription factors (TFs) and has also been named redox effector factor 1, Ref-1. For example, APE1 activates activator protein-1, nuclear factor kappa B, hypoxia-inducible factor 1α, paired box gene 8, signal transducer activator of transcription 3 and p53, which are involved in apoptosis, inflammation, angiogenesis and survival pathways. APE1/Ref-1 maintains cellular homeostasis (redox) via the activation of TFs that regulate various physiological processes and that crosstalk with redox balancing agents (for example, thioredoxin, catalase and superoxide dismutase) by controlling levels of reactive oxygen and nitrogen species. The efficiency of APE1/Ref-1's function(s) depends on pairwise interaction with participant protein(s), the functions regulated by APE1/Ref-1 include the BER pathway, TFs, energy metabolism, cytoskeletal elements and stress-dependent responses. Thus, APE1/Ref-1 acts as a 'hub-protein' that controls pathways that are important for cell survival. In this review, we will discuss APE1/Ref-1's versatile nature in various human etiologies, including neurodegeneration, cancer, cardiovascular and other diseases that have been linked with alterations in the expression, subcellular localization and activities of APE/Ref-1. APE1/Ref-1 can be targeted for therapeutic intervention using natural plant products that modulate the expression and functions of APE1/Ref-1. In addition, studies focusing on translational applications based on APE1/Ref-1-mediated therapeutic interventions are discussed.

Indexed as

Molecular Targeted TherapyAnimalsDNA-(Apurinic or Apyrimidinic Site) LyaseDNA DamageDNA RepairHumansNeoplasmsNeurodegenerative DiseasesOxidative StressPhytochemicalsPolymorphism, GeneticProtein Interaction MapsAPEX1 protein, humanDNA-(Apurinic or Apyrimidinic Site) LyasePhytochemicals

Identifiers

PMID25033834
PMCPMC4119211
OpenAlexW1963552571

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.