Evidence map›Paper›PMID 29358575›Full record

ArticleCell death & disease2018

Pathological hydrogen peroxide triggers the fibrillization of wild-type SOD1 via sulfenic acid modification of Cys-111.

Wen-Chang Xu, Jin-Zhao Liang, Cheng Li, Zhi-Xin He, Han-Ye Yuan, Ben-Yan Huang, Xiao-Ling Liu, Bo Tang, Dai-Wen Pang, Hai-Ning Du and 5 more

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.

0numbers the graph read from it
0cells of the map it votes in
38citing papers in PubMed
5.4field-weighted citation impact, top 4% 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

38 citing papers in PubMed, 72 citations in OpenAlex.

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  15. DnaJs are enriched in tau regulators.International journal of biological macromolecules · 2023
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  17. Excess PrPNature communications · 2023
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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

15 authors at 4 institutions in 1 country.

Wen-Chang XuState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Jin-Zhao LiangNational Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.
Cheng LiState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Zhi-Xin HeState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Han-Ye YuanState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Ben-Yan HuangDepartment of Neurology Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China.
Xiao-Ling LiuState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Bo TangCollege of Chemistry and Molecular Sciences, State Key Laboratory of Virology, Wuhan University, Wuhan, 430072, China.
Dai-Wen PangCollege of Chemistry and Molecular Sciences, State Key Laboratory of Virology, Wuhan University, Wuhan, 430072, China.
Hai-Ning DuHubei Key Laboratory of Cell Homeostasis, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Yi YangState Key Laboratory of Bioreactor Engineering, School of Pharmacy, East China University of Science and Technology, Shanghai, 200237, China.ORCID 0000-0002-7349-8300
Jie ChenState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China.
Lei WangNational Laboratory of Biomacromolecules, CAS Center for Excellence in Biomacromolecules, Institute of Biophysics, Chinese Academy of Sciences, Beijing, 100101, China.ORCID 0000-0002-5071-5800
Min ZhangDepartment of Neurology Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430030, China. zhang_min_3464@126.com.
Yi LiangState Key Laboratory of Virology, College of Life Sciences, Wuhan University, Wuhan, 430072, China. liangyi@whu.edu.cn.
Wuhan University · CNChinese Academy of Sciences · CNTongji Hospital · CNEast China University of Science and Technology · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) involves the abnormal posttranslational modifications and fibrillization of copper, zinc superoxide dismutase (SOD1) and TDP-43. However, how SOD1-catalyzed reaction product hydrogen peroxide affects amyloid formation of SOD1 and TDP-43 remains elusory. 90% of ALS cases are sporadic and the remaining cases are familial ALS. In this paper, we demonstrate that H

Indexed as

AmyloidAmyotrophic Lateral SclerosisApoptosisCell Line, TumorCysteineDNA-Binding ProteinsHumansHydrogen PeroxideModels, BiologicalProtein MultimerizationSulfenic AcidsSuperoxide Dismutase-1AmyloidCysteineDNA-Binding ProteinsHydrogen PeroxideSulfenic AcidsSuperoxide Dismutase-1TARDBP protein, human

Identifiers

PMID29358575
PMCPMC5833406
OpenAlexW2792470718

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.