Evidence map›Paper›PMID 23878621›Full record

ReviewOxidative medicine and cellular longevity2013

The role of the Keap1/Nrf2 pathway in the cellular response to methylmercury.

Yoshito Kumagai, Hironori Kanda, Yasuhiro Shinkai, Takashi Toyama

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.5field-weighted citation impact, top 10% 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

26 citing papers in PubMed, 62 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Article
  5. The Role of Toxic Metals and Metalloids in Nrf2 Signaling.Antioxidants (Basel, Switzerland) · 2021
    Review
  6. Unfolding Nrf2 in diabetes mellitus.Molecular biology reports · 2021
    Review
  7. Article
  8. Review
  9. Sulfhydryl groups as targets of mercury toxicity.Coordination chemistry reviews · 2020
    Article
  10. Review
  11. Review
  12. Review
  13. Post-translational modifications in MeHg-induced neurotoxicity.Biochimica et biophysica acta. Molecular basis of disease · 2019
    Review
  14. Article
  15. Article
  16. Protective Effects ofToxicological research · 2019
    Article
  17. C. elegans as a model in developmental neurotoxicology.Toxicology and applied pharmacology · 2018
    Review
  18. Review
  19. Review
  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

4 authors at 1 institution in 1 country.

Yoshito KumagaiEnvironmental Biology Section, Faculty of Medicine, University of Tsukuba, Tsukuba, Ibaraki 305-8575, Japan.
Hironori Kanda
Yasuhiro Shinkai
Takashi Toyama
University of Tsukuba · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Methylmercury (MeHg) is an environmental electrophile that covalently modifies cellular proteins with reactive thiols, resulting in the formation of protein adducts. While such protein modifications, referred to as S-mercuration, are thought to be associated with the enzyme dysfunction and cellular damage caused by MeHg exposure, the current consensus is that (1) there is a cellular response to MeHg through the activation of NF-E2-related factor 2 (Nrf2) coupled to S-mercuration of its negative regulator, Kelch-like ECH-associated protein 1 (Keap1), and (2) the Keap1/Nrf2 pathway protects against MeHg toxicity. In this review, we introduce our findings and discuss the observations of other workers concerning the S-mercuration of cellular proteins by MeHg and the importance of the Keap1/Nrf2 pathway in protection against MeHg toxicity in cultured cells and mice.

Indexed as

AnimalsHumansIntracellular Signaling Peptides and ProteinsKelch-Like ECH-Associated Protein 1Methylmercury CompoundsNF-E2-Related Factor 2Signal TransductionIntracellular Signaling Peptides and ProteinsKEAP1 protein, humanKelch-Like ECH-Associated Protein 1Methylmercury CompoundsNF-E2-Related Factor 2

Identifiers

PMID23878621
PMCPMC3710591
OpenAlexW2148525762

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.