Evidence map›Paper›PMID 24242043›Full record

ArticleMolecular and cellular biochemistry2014

Upregulated Parkin expression protects mitochondrial homeostasis in DJ-1 konckdown cells and cells overexpressing the DJ-1 L166P mutation.

Chunyan Chang, Guolu Wu, Peiye Gao, Ling Yang, Wen Liu, Ji Zuo

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Article in Molecular and cellular biochemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.8field-weighted citation impact, top 15% 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

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3 · Its place in the literature

Who cites it

10 citing papers in PubMed, 19 citations in OpenAlex.

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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 1 country.

Chunyan ChangDepartment of Cellular and Genetic Medicine, School of Basic Medical Sciences Fudan University, Dong' an Road, BOX 239, Shanghai, 200032, People's Republic of China.
Guolu Wu
Peiye Gao
Ling Yang
Wen Liu
Ji Zuo
Fudan University · CNShanghai Medical College of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Rare genetic mutations in the DJ-1 and Parkin genes cause recessive Parkinsonism, however, the relationship between these two genes is not fully elucidated. Current emerging evidence suggests that these genes are involved in mitochondrial homeostasis, and that a deficiency in either of these two genes is associated with damages in mitochondrial function and morphology. In this study, we demonstrated that knockdown of DJ-1 expression or the overexpression of the DJ-1 L166P mutation results in a damaged phenotype in mitochondria and a hypersensitivity to H2O2-induced cell apoptosis. These phenotypes result from increased levels of endogenous oxidative stress. However, overexpression of wild-type Parkin rescued the phenotypes observed in the mitochondria of DJ-1 knockdown and DJ-1 L166P mutant cells. We also determined that there were differences between the two cell models. Furthermore, both H₂O₂ treatment and the DJ-1 L166P mutation weakened the interaction between DJ-1 and Parkin. Taken together, these findings suggested that DJ-1 and Parkin were linked through oxidative stress, and that overexpression of Parkin protects DJ-1 protein-deficient and DJ-1 L166P mutant-expressing cells via inhibition of oxidative stress.

Indexed as

HomeostasisAdenosine TriphosphateCell Line, TumorCell SurvivalGene ExpressionHumansIntracellular Signaling Peptides and ProteinsMembrane Potential, MitochondrialMitochondriaMutation, MissenseOncogene ProteinsOxidative StressProtein Deglycase DJ-1Reactive Oxygen SpeciesUbiquitin-Protein LigasesUp-RegulationAdenosine TriphosphateIntracellular Signaling Peptides and ProteinsOncogene ProteinsPARK7 protein, humanparkin proteinProtein Deglycase DJ-1Reactive Oxygen SpeciesUbiquitin-Protein Ligases

Identifiers

PMID24242043
OpenAlexW2004358416

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.