Evidence map›Paper›PMID 28806787›Full record

ArticlePloS one2017

Antagonism of proteasome inhibitor-induced heme oxygenase-1 expression by PINK1 mutation.

Xiang-Jun Sheng, Hunag-Ju Tu, Wei-Lin Chien, Kai-Hsiang Kang, Dai-Hua Lu, Horng-Huei Liou, Ming-Jen Lee, Wen-Mei Fu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.1field-weighted citation impact, top 13% 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

12 citing papers in PubMed, 17 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Article
  10. Review
  11. Mitochondrial Targeting in Neurodegeneration: A Heme Perspective.Pharmaceuticals (Basel, Switzerland) · 2018
    Review
  12. Astrocytes, Microglia, and Parkinson's Disease.Experimental neurobiology · 2018
    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 2 institutions in 1 country.

Xiang-Jun ShengPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Hunag-Ju TuPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Wei-Lin ChienPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Kai-Hsiang KangPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Dai-Hua LuPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Horng-Huei LiouPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.
Ming-Jen LeeDepartment of Neurology, National Taiwan University Hospital, Taipei, Taiwan.
Wen-Mei FuPharmacological Institute, College of Medicine, National Taiwan University, Taipei, Taiwan.ORCID http://orcid.org/0000-0003-4157-8987
National Taiwan University · TWNational Taiwan University Hospital · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

PTEN-induced putative kinase 1 (PINK1) is an integral protein in the mitochondrial membrane and maintains mitochondrial fidelity. Pathogenic mutations in PINK1 have been identified as a cause of early-onset autosomal recessive familial Parkinson's disease (PD). The ubiquitin proteasome pathway is associated with neurodegenerative diseases. In this study, we investigated whether mutations of PINK1 affects the cellular stress response following proteasome inhibition. Administration of MG132, a peptide aldehyde proteasome inhibitor, significantly increased the expression of heme oxygenase-1 (HO-1) in rat dopaminergic neurons in the substantia nigra and in the SH-SY5Y neuronal cell line. The induction of HO-1 expression by proteasome inhibition was reduced in PINK1 G309D mutant cells. MG132 increased the levels of HO-1 through the Akt, p38, and Nrf2 signaling pathways. Compared with the cells expressing WT-PINK1, the phosphorylation of Akt and p38 was lower in those cells expressing the PINK1 G309D mutant, which resulted in the inhibition of the nuclear translocation of Nrf2. Furthermore, MG132-induced neuronal death was enhanced by the PINK1 G309D mutation. In this study, we demonstrated that the G309D mutation impairs the neuroprotective function of PINK1 following proteasome inhibition, which may be related to the pathogenesis of PD.

Indexed as

AnimalsAntioxidant Response ElementsCell DeathCell LineCell NucleusGene Expression Regulation, EnzymologicHeme Oxygenase-1HumansLeupeptinsMaleModels, BiologicalMutant ProteinsMutationNeuronsNF-E2-Related Factor 2Proteasome Inhibitorsbenzyloxycarbonylleucyl-leucyl-leucine aldehydeHeme Oxygenase-1LeupeptinsMutant ProteinsNF-E2-Related Factor 2Proteasome InhibitorsProtein KinasesPTEN-Induced Putative Kinase

Identifiers

PMID28806787
PMCPMC5555616
OpenAlexW2750081153

What OpenQuestion holds

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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.