Evidence map›Paper›PMID 35013445›Full record

ArticleScientific reports2022

Effects of intracellular calcium accumulation on proteins encoded by the major genes underlying amyotrophic lateral sclerosis.

Giovanni De Marco, Annarosa Lomartire, Umberto Manera, Antonio Canosa, Maurizio Grassano, Federico Casale, Giuseppe Fuda, Paolina Salamone, Maria Teresa Rinaudo, Sebastiano Colombatto and 3 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
3.0field-weighted citation impact, top 8% 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

18 citing papers in PubMed, 25 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

13 authors at 2 institutions in 1 country.

Giovanni De Marco *Department of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy. giovanni.demarco@unito.it.ORCID 0000-0002-3966-8695
Annarosa Lomartire *Department of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Umberto ManeraDepartment of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Antonio CanosaDepartment of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Maurizio GrassanoDepartment of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Federico CasaleDepartment of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Giuseppe FudaDepartment of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Paolina SalamoneDepartment of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Maria Teresa RinaudoDepartment of Oncology, University of Turin, via Michelangelo 27/b, 10126, Turin, Italy.
Sebastiano ColombattoDepartment of Oncology, University of Turin, via Michelangelo 27/b, 10126, Turin, Italy.
Cristina MogliaDepartment of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Adriano Chiò *Department of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
Andrea Calvo *Department of Neuroscience, ALS Centre, "Rita Levi Montalcini", University of Turin, Via Cherasco 15, 10126, Turin, Italy.
University of Turin · ITAzienda Ospedaliera Citta' della Salute e della Scienza di Torino · IT

Funding

Ministero della Salute RF-2016-02362405Ministero della Salute RF-2018-12365614Ministero dell'Istruzione, dell'Università e della Ricerca 2017SNW5MB
6 · The paper itself

Abstract

The aetiology of Amyotrophic Lateral Sclerosis (ALS) is still poorly understood. The discovery of genetic forms of ALS pointed out the mechanisms underlying this pathology, but also showed how complex these mechanisms are. Excitotoxicity is strongly suspected to play a role in ALS pathogenesis. Excitotoxicity is defined as neuron damage due to excessive intake of calcium ions (Ca

Indexed as

Calcium SignalingAmyotrophic Lateral SclerosisAutophagyC9orf72 ProteinCalciumCalpainCaspasesDNA-Binding ProteinsGene Expression RegulationHeLa CellsHumansNerve Tissue ProteinsNeuronsNuclear Matrix-Associated ProteinsProfilinsProteolysisC9orf72 ProteinC9orf72 protein, humanCalciumCalpainCaspasesDNA-Binding ProteinsFUS protein, humanMATR3 protein, humanNerve Tissue ProteinsNuclear Matrix-Associated ProteinsPFN1 protein, humanProfilinsRNA-Binding Protein FUSRNA-Binding ProteinsSequestosome-1 ProteinSOD1 protein, humanSQSTM1 protein, humanSuperoxide Dismutase-1TARDBP protein, humanValosin Containing ProteinVCP protein, human

Identifiers

PMID35013445
PMCPMC8748718
OpenAlexW4205369585

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.