Evidence map›Paper›PMID 30108253›Full record

ArticleScientific reports2018

Keap1-MCM3 interaction is a potential coordinator of molecular machineries of antioxidant response and genomic DNA replication in metazoa.

Nele Tamberg, Siret Tahk, Sandra Koit, Kersti Kristjuhan, Sergo Kasvandik, Arnold Kristjuhan, Ivar Ilves

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.0field-weighted citation impact, top 24% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

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  14. The roles of KLHL family members in human cancers.American journal of cancer research · 2022
    Review
  15. Article
  16. The Keap1-Nrf2 System: A Mediator between Oxidative Stress and Aging.Oxidative medicine and cellular longevity · 2021
    Review
  17. Review
  18. Review
  19. Beyond repression of Nrf2: An update on Keap1.Free radical biology & medicine · 2020
    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

7 authors at 1 institution in 1 country.

Nele TambergInstitute of Technology, University of Tartu, Tartu, 50411, Estonia.
Siret TahkInstitute of Technology, University of Tartu, Tartu, 50411, Estonia.
Sandra KoitInstitute of Technology, University of Tartu, Tartu, 50411, Estonia.
Kersti KristjuhanInstitute of Molecular and Cell Biology, University of Tartu, Tartu, 51010, Estonia.
Sergo KasvandikInstitute of Technology, University of Tartu, Tartu, 50411, Estonia.ORCID 0000-0003-0218-2410
Arnold KristjuhanInstitute of Molecular and Cell Biology, University of Tartu, Tartu, 51010, Estonia.
Ivar IlvesInstitute of Technology, University of Tartu, Tartu, 50411, Estonia. ivar.ilves@ut.ee.
University of Tartu · EE

Funding

Eesti Teadusagentuur (Estonian Research Council) ETF9155Eesti Teadusagentuur (Estonian Research Council) IUT-20-23Eesti Teadusagentuur (Estonian Research Council) PUT1004Eesti Teadusagentuur (Estonian Research Council) PUT124European Molecular Biology Organization (EMBO) 2524
6 · The paper itself

Abstract

Coordination of DNA replication and cellular redox homeostasis mechanisms is essential for the sustained genome stability due to the sensitivity of replicating DNA to oxidation. However, substantial gaps remain in our knowledge of underlying molecular pathways. In this study, we characterise the interaction of Keap1, a central antioxidant response regulator in Metazoa, with the replicative helicase subunit protein MCM3. Our analysis suggests that structural determinants of the interaction of Keap1 with its critical downstream target - Nrf2 master transactivator of oxidative stress response genes - may have evolved in evolution to mimic the conserved helix-2-insert motif of MCM3. We show that this has led to a competition between MCM3 and Nrf2 proteins for Keap1 binding, and likely recruited MCM3 for the competitive binding dependent modulation of Keap1 controlled Nrf2 activities. We hypothesise that such mechanism could help to adjust the Keap1-Nrf2 antioxidant response pathway according to the proliferative and replicative status of the cell, with possible reciprocal implications also for the regulation of cellular functions of MCM3. Altogether this suggests about important role of Keap1-MCM3 interaction in the cross-talk between replisome and redox homeostasis machineries in metazoan cells.

Indexed as

DNA ReplicationAmino Acid MotifsAnimalsCell Line, TumorCHO CellsCricetulusEvolution, MolecularHumansKelch-Like ECH-Associated Protein 1KeratinocytesMinichromosome Maintenance Complex Component 3NF-E2-Related Factor 2Oxidative StressPrimary Cell CultureProtein BindingProtein Conformation, alpha-HelicalKEAP1 protein, humanKeap1 protein, mouseKelch-Like ECH-Associated Protein 1MCM3 protein, humanMcm3 protein, mouseMinichromosome Maintenance Complex Component 3NFE2L2 protein, humanNfe2l2 protein, mouseNF-E2-Related Factor 2Recombinant ProteinsTrans-Activators

Identifiers

PMID30108253
PMCPMC6092318
OpenAlexW2887564443

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Registered trials

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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.