Evidence map›Paper›PMID 30123078›Full record

ArticleInternational journal of biological sciences2018

Preliminary Observation about Alteration of Proteins and Their Potential Functions in Spinal Cord of SOD1 G93A Transgenic Mice.

Jie Zhang, Ping Huang, Chengsi Wu, Huiting Liang, Yue Li, Lei Zhu, Yi Lu, Chunyan Tang, Renshi Xu

Open access · goldAbstract read
In one paragraph

Article in International journal of biological sciences, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.8field-weighted citation impact, top 26% 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

11 citing papers in PubMed, 13 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

9 authors at 2 institutions in 1 country.

Jie ZhangDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Ping HuangDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Chengsi WuDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Huiting LiangDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Yue LiDepartment of Health Statistics, Nanchang University, Nanchang 330006, Jiangxi, China.
Lei ZhuDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Yi LuDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Chunyan TangDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
Renshi XuDepartment of Neurology, the First Affiliated Hospital of Nanchang University, Nanchang 330006, Jiangxi, China.
First Affiliated Hospital of Nanchang University · CNNanchang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The protein abnormality participates in the development of ALS that meets with the widespread approval from major researchers. However, these currently found abnormal proteins aren't far enough to explain all pathogenesis of ALS. Therefore, the search of novel abnormal proteins participated in the pathogenesis of ALS is very necessary. In this study, we screened, compared and analyzed the differentially expressed proteins in the spinal cord of the SOD1 G93A transgenic and wild-type (WT) mice applying the isobaric tags for relative and absolute quantitation (iTRAQ) and the bioinformatics methods. The results revealed the details of significantly differentially expressed proteins between the SOD1 G93A transgenic and WT mice, and the damaged and/or regulated cellular components, molecular functions and biological processes and the significant enrichment pathways of these proteins. Our study comprehensively described the details of the possible abnormal proteins participated in the pathogenesis of SOD1 G93A transgenic mice, extensively explored their possible molecular mechanisms how to play the role in the development in this animal model, and provided some evidences and clues for further and deeply studying the relationship between the abnormal proteins and the pathogenesis of ALS in the other animal models and ALS patients.

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalGene OntologyMaleMiceMice, Inbred C57BLMice, TransgenicMotor NeuronsProteomicsSpinal CordSuperoxide DismutaseSuperoxide Dismutase-1Tandem Mass SpectrometrySuperoxide DismutaseSuperoxide Dismutase-1Amyotrophic lateral sclerosisCluster of orthologous groupsGene ontologyiTRAQProteomics

Identifiers

PMID30123078
PMCPMC6097476
OpenAlexW2886755253

What OpenQuestion holds

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LicenceCC BY-NC
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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.