Evidence map›Paper›PMID 32152416›Full record

ArticleScientific reports2020

DJ-1 is indispensable for the S-nitrosylation of Parkin, which maintains function of mitochondria.

Kentaro Ozawa, Hiroki Tsumoto, Yuri Miura, Junji Yamaguchi, Sanae M M Iguchi-Ariga, Tetsushi Sakuma, Takashi Yamamoto, Yasuo Uchiyama

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2020. 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
2.4field-weighted citation impact, top 8% 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, 39 citations in OpenAlex.

  1. Review
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  9. Review
  10. Article
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  13. Nitrosative stress in Parkinson's disease.NPJ Parkinson's disease · 2022
    Review
  14. Review
  15. Article
  16. Review
  17. Review
  18. Frontiers in cell and developmental biology · 2021
    Review
  19. Review
  20. Autophagy and Redox Homeostasis in Parkinson's: A Crucial Balancing Act.Oxidative medicine and cellular longevity · 2020
    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

8 authors at 4 institutions in 1 country.

Kentaro Ozawa *Research Team for Mechanism of Aging, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan. ozawa.sno.man@gmail.com.
Hiroki Tsumoto *Research Team for Mechanism of Aging, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan.
Yuri Miura *Research Team for Mechanism of Aging, Tokyo Metropolitan Institute of Gerontology, 35-2 Sakae-cho, Itabashi-ku, Tokyo, 173-0015, Japan.
Junji YamaguchiDepartment of Cellular and Molecular Neuropathology, Juntendo University Graduate School of Medicine, Bunkyo-Ku 2-1-1, Tokyo, 113-8421, Japan.
Sanae M M Iguchi-ArigaFaculty of Pharmaceutical Sciences, Hokkaido University, Kita 12, Nishi 6, Kita-ku, Sapporo, 060-0812, Japan.
Tetsushi SakumaDivision of Integrated Sciences for Life, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, 739-8526, Japan.
Takashi YamamotoDivision of Integrated Sciences for Life, Graduate School of Integrated Sciences for Life, Hiroshima University, Hiroshima, 739-8526, Japan.
Yasuo UchiyamaDepartment of Cellular and Molecular Neuropathology, Juntendo University Graduate School of Medicine, Bunkyo-Ku 2-1-1, Tokyo, 113-8421, Japan.
Tokyo Metropolitan Institute of Gerontology · JPHiroshima University · JPJuntendo University · JPHokkaido University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The DJ-1 gene, a causative gene for familial Parkinson's disease (PD), has been reported to have various functions, including transcriptional regulation, antioxidant response, and chaperone and protease functions; however, the molecular mechanism associated with the pathogenesis of PD remains elusive. To further explore the molecular function of DJ-1 in the pathogenesis of PD, we compared protein expression profiles in brain tissues from wild-type and DJ-1-deficient mice. Two-dimensional difference gel electrophoresis analysis and subsequent analysis using data mining methods revealed alterations in the expression of molecules associated with energy production. We demonstrated that DJ-1 deletion inhibited S-nitrosylation of endogenous Parkin as well as overexpressed Parkin in neuroblastoma cells and mouse brain tissues. Thus, we used genome editing to generate neuroblastoma cells with DJ-1 deletion or S-nitrosylated cysteine mutation in Parkin and demonstrated that these cells exhibited similar phenotypes characterized by enhancement of cell death under mitochondrial depolarization and dysfunction of mitochondria. Our data indicate that DJ-1 is required for the S-nitrosylation of Parkin, which positively affects mitochondrial function, and suggest that the denitrosylation of Parkin via DJ-1 inactivation might contribute to PD pathogenesis and act as a therapeutic target.

Indexed as

AnimalsBrainCell LineHumansMiceMice, KnockoutMitochondriaModels, BiologicalParkinson DiseaseProtein Deglycase DJ-1Protein Interaction MappingProtein Interaction MapsProtein Processing, Post-TranslationalUbiquitin-Protein Ligasesparkin proteinProtein Deglycase DJ-1Ubiquitin-Protein Ligases

Identifiers

PMID32152416
PMCPMC7062835
OpenAlexW3010441603

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.