Evidence map›Paper›PMID 34274951›Full record

ArticleCell death & disease2021

DJ-1 inhibits microglial activation and protects dopaminergic neurons in vitro and in vivo through interacting with microglial p65.

Zixuan Lin, Chen Chen, Dongqin Yang, Jianqing Ding, Guanghui Wang, Haigang Ren

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

35 citing papers in PubMed, 52 citations in OpenAlex.

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  14. Long-term exposure to PMScientific reports · 2025
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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.

Zixuan LinJiangsu Key Laboratory of Translational Research and Therapy for Neuropsychiatric disorders & Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, 199 Ren'ai Road, Suzhou, Jiangsu, 215123, China.
Chen ChenJiangsu Key Laboratory of Translational Research and Therapy for Neuropsychiatric disorders & Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, 199 Ren'ai Road, Suzhou, Jiangsu, 215123, China.
Dongqin YangJiangsu Key Laboratory of Translational Research and Therapy for Neuropsychiatric disorders & Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, 199 Ren'ai Road, Suzhou, Jiangsu, 215123, China.
Jianqing DingDepartment of Neurology & Institute of Neurology, Ruijin Hospital affiliated to Shanghai Jiao Tong University School of Medicine, Shanghai, 200025, China.
Guanghui WangJiangsu Key Laboratory of Translational Research and Therapy for Neuropsychiatric disorders & Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, 199 Ren'ai Road, Suzhou, Jiangsu, 215123, China. wanggh@suda.edu.cn.ORCID http://orcid.org/0000-0001-8551-6468
Haigang RenJiangsu Key Laboratory of Translational Research and Therapy for Neuropsychiatric disorders & Department of Pharmacology, College of Pharmaceutical Sciences, Soochow University, 199 Ren'ai Road, Suzhou, Jiangsu, 215123, China. rhg@suda.edu.cn.ORCID http://orcid.org/0000-0001-8844-4754
Soochow University · CNShanghai Jiao Tong University · CN

Funding

National Natural Science Foundation of China (National Science Foundation of China) 31970966National Natural Science Foundation of China (National Science Foundation of China) 32070970
6 · The paper itself

Abstract

Parkinson's disease (PD), one of the most common neurodegenerative disorders, is characterized by progressive neurodegeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc). DJ-1 acts essential roles in neuronal protection and anti-neuroinflammatory response, and its loss of function is tightly associated with a familial recessive form of PD. However, the molecular mechanism of DJ-1 involved in neuroinflammation is largely unclear. Here, we found that wild-type DJ-1, rather than the pathogenic L166P mutant DJ-1, directly binds to the subunit p65 of nuclear factor-κB (NF-κB) in the cytoplasm, and loss of DJ-1 promotes p65 nuclear translocation by facilitating the dissociation between p65 and NF-κB inhibitor α (IκBα). DJ-1 knockout (DJ-1

Indexed as

AnimalsCell NucleusCells, CulturedDopaminergic NeuronsHEK293 CellsHumansInflammationLipopolysaccharidesMiceMicrogliaModels, BiologicalMutationNeuroprotective AgentsNeurotoxinsProtein BindingProtein Deglycase DJ-1LipopolysaccharidesNeuroprotective AgentsNeurotoxinsPARK7 protein, mouseProtein Deglycase DJ-1Protein SubunitsTranscription Factor RelA

Identifiers

PMID34274951
PMCPMC8286256
OpenAlexW3186026575

What OpenQuestion holds

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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.