Evidence map›Paper›PMID 31540330›Full record

ArticleInternational journal of molecular sciences2019

Enhanced Function and Overexpression of Metabotropic Glutamate Receptors 1 and 5 in the Spinal Cord of the SOD1

Tiziana Bonifacino, Claudia Rebosio, Francesca Provenzano, Carola Torazza, Matilde Balbi, Marco Milanese, Luca Raiteri, Cesare Usai, Ernesto Fedele, Giambattista Bonanno

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

20 citing papers in PubMed, 25 citations in OpenAlex.

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  16. Blocking glutamate mGluBritish journal of pharmacology · 2021
    Article
  17. Perspective of mesenchymal transformation in glioblastoma.Acta neuropathologica communications · 2021
    Review
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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

10 authors at 3 institutions in 1 country.

Tiziana BonifacinoDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, 16148 Genova, Italy. bonifacino@difar.unige.it.
Claudia RebosioDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, 16148 Genova, Italy. claudiarebosio@gmail.com.
Francesca ProvenzanoDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, 16148 Genova, Italy. provenzano.phd@difar.unige.it.
Carola TorazzaDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, 16148 Genova, Italy. torazza@difar.unige.it.
Matilde BalbiDepartment of Pharmacy, Unit of Pharmacology and Toxicology, University of Genoa, 16148 Genova, Italy. balbi.phd@difar.unige.it.
Marco MilaneseDepartment of Pharmacy, Unit of Pharmacology and Toxicology and Center of Excellence for Biomedical Research (CEBR), University of Genoa, 16132 Genova, Italy. milanese@difar.unige.it.
Luca RaiteriDepartment of Pharmacy, Unit of Pharmacology and Toxicology and Center of Excellence for Biomedical Research (CEBR), University of Genoa, 16132 Genova, Italy. lraiter@difar.unige.it.
Cesare UsaiInstitute of Biophysics, National Research Council (CNR), 16149 Genova, Italy. usai@ge.ibf.cnr.it.ORCID 0000-0001-8863-7759
Ernesto FedeleDepartment of Pharmacy, Unit of Pharmacology and Toxicology and Center of Excellence for Biomedical Research (CEBR), University of Genoa, 16132 Genova, Italy. fedele@difar.unige.it.ORCID 0000-0002-0386-0925
Giambattista BonannoDepartment of Pharmacy, Unit of Pharmacology and Toxicology and Center of Excellence for Biomedical Research (CEBR), University of Genoa, 16132 Genova, Italy. bonanno@difar.unige.it.ORCID 0000-0003-3744-5786
University of Genoa · ITOspedale Policlinico San Martino · ITNational Research Council · IT

Funding

Compagnia di San Paolo 2018.AAI629.U730/SD/pvMinistero dell'Istruzione, dell'Università e della Ricerca RBSI14B1Z1
6 · The paper itself

Abstract

Glutamate (Glu)-mediated excitotoxicity is a major cause of amyotrophic lateral sclerosis (ALS) and our previous work highlighted that abnormal Glu release may represent a leading mechanism for excessive synaptic Glu. We demonstrated that group I metabotropic Glu receptors (mGluR1, mGluR5) produced abnormal Glu release in SOD1

Indexed as

Amyotrophic Lateral SclerosisAnimalsDisease Models, AnimalDisease ProgressionGlutamic AcidGlycineHumansMiceMutationReceptor, Metabotropic Glutamate 5Receptors, Metabotropic GlutamateResorcinolsSpinal CordSuperoxide Dismutase-1Up-Regulation3,5-dihydroxyphenylglycineGlutamic AcidGlycineGrm5 protein, mousemetabotropic glutamate receptor type 1Receptor, Metabotropic Glutamate 5Receptors, Metabotropic GlutamateResorcinolsSod1 protein, mouseSuperoxide Dismutase-1amyotrophic lateral sclerosisdisease progressionglutamate releasemetabotropic glutamate receptor 1 (mGluR1)metabotropic glutamate receptor 5 (mGluR5)mGluR1/mGluR5 expressionSOD1G93A micespinal cord

Identifiers

PMID31540330
PMCPMC6774337
OpenAlexW2972753038

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.