Evidence map›Paper›PMID 29843805›Full record

ArticleMolecular brain2018

Systemic overexpression of SQSTM1/p62 accelerates disease onset in a SOD1

Shun Mitsui, Asako Otomo, Masahisa Nozaki, Suzuka Ono, Kai Sato, Ryohei Shirakawa, Hiroaki Adachi, Masashi Aoki, Gen Sobue, Hui-Fang Shang and 1 more

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
3.9field-weighted citation impact, top 6% 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

30 citing papers in PubMed, 45 citations in OpenAlex.

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  20. SQSTM1eNeurologicalSci · 2021
    Article
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

11 authors at 5 institutions in 2 countries.

Shun MitsuiDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Asako OtomoDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Masahisa NozakiDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Suzuka OnoDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Kai SatoDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Ryohei ShirakawaDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan.
Hiroaki AdachiDepartment of Neurology, University of Occupational and Environmental Health School of Medicine, Kitakyushu, Fukuoka, 807-0804, Japan.
Masashi AokiDepartment of Neurology, Tohoku University Graduate School of Medicine, Sendai, Miyagi, 980-8575, Japan.
Gen SobueDepartment of Neurology, Nagoya University Graduate School of Medicine, Nagoya, Aichi, 466-8550, Japan.
Hui-Fang ShangDepartment of Neurology, West China Hospital, Sichuan University, Chengdu, 610041, Sichuan, China.
Shinji HadanoDepartment of Molecular Life Sciences, Tokai University School of Medicine, Isehara, Kanagawa, 259-1193, Japan. shinji@is.icc.u-tokai.ac.jp.ORCID 0000-0002-4997-3968
Tokai University · JPNagoya University · JPSichuan University · CNTohoku University · JPUniversity of Occupational and Environmental Health Japan · JP

Funding

Japanese Society for Promotion of Science 24650189Japanese Society for Promotion of Science 26290018
6 · The paper itself

Abstract

Amyotrophic lateral sclerosis (ALS) is a progressive neurodegenerative disease characterized by a selective loss of upper and lower motor neurons. Recent studies have shown that mutations in SQSTM1 are linked to ALS. SQSTM1 encodes SQSTM1/p62 that regulates not only autophagy via the association with MAP1LC3/LC3 and ubiquitinated proteins but also the KEAP1-NFE2L2/Nrf2 anti-oxidative stress pathway by interacting with KEAP1. Previously, we have demonstrated that loss of SQSTM1 exacerbates disease phenotypes in a SOD1

Indexed as

Disease ProgressionAmyotrophic Lateral SclerosisAnimalsAnterior Horn CellsBody WeightCell CountDisease Models, AnimalFemaleLongevityLumbar VertebraeMice, Inbred C57BLMice, TransgenicMotor NeuronsNeurogliaPhosphorylationPolyubiquitinPolyubiquitinProtein AggregatesSequestosome-1 ProteinSqstm1 protein, mouseSuperoxide Dismutase-1Amyotrophic lateral sclerosisSOD1SQSTM1/p62Ubiquitin-positive aggregates

Identifiers

PMID29843805
PMCPMC5975400
OpenAlexW2805146185

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.