Evidence map›Paper›PMID 31439839›Full record

ArticleNature communications2019

Sp1-regulated expression of p11 contributes to motor neuron degeneration by membrane insertion of TASK1.

Victoria García-Morales, Guillermo Rodríguez-Bey, Laura Gómez-Pérez, Germán Domínguez-Vías, David González-Forero, Federico Portillo, Antonio Campos-Caro, Ángela Gento-Caro, Noura Issaoui, Rosa M Soler and 2 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 2 pooled it
1.7field-weighted citation impact, top 15% 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, 2 syntheses or guidelines pooled it, 29 citations in OpenAlex.

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  6. Female-specificMolecular neurodegeneration advances · 2026
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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

12 authors at 3 institutions in 1 country.

Victoria García-MoralesGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.ORCID http://orcid.org/0000-0002-8964-9935
Guillermo Rodríguez-BeyGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.ORCID http://orcid.org/0000-0003-3597-0245
Laura Gómez-PérezGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.ORCID http://orcid.org/0000-0001-8615-7241
Germán Domínguez-VíasGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.ORCID http://orcid.org/0000-0002-9546-9148
David González-ForeroGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.
Federico PortilloGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.
Antonio Campos-CaroInstituto de Investigación e Innovación Biomédica de Cádiz (INiBICA), Cádiz, Spain.ORCID http://orcid.org/0000-0001-8532-2153
Ángela Gento-CaroGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.
Noura IssaouiGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain.
Rosa M SolerUnitat de Senyalització Neuronal, Dept. Medicina Experimental, Universitat de Lleida-IRBLLEIDA, Lleida, Spain.ORCID http://orcid.org/0000-0003-0528-3102
Ana GarceraUnitat de Senyalització Neuronal, Dept. Medicina Experimental, Universitat de Lleida-IRBLLEIDA, Lleida, Spain.
Bernardo Moreno-LópezGrupo de Neurodegeneración y Neurorreparación (GRUNEDERE), Área de Fisiología, Facultad de Medicina, Universidad de Cádiz, 11003 Cádiz, Spain. bernardo.moreno@uca.es.ORCID http://orcid.org/0000-0003-2897-6227
Universidad de Cádiz · ESUniversitat de Lleida · ESBiomedical Research and Innovation Institute of Cadiz · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Disruption in membrane excitability contributes to malfunction and differential vulnerability of specific neuronal subpopulations in a number of neurological diseases. The adaptor protein p11, and background potassium channel TASK1, have overlapping distributions in the CNS. Here, we report that the transcription factor Sp1 controls p11 expression, which impacts on excitability by hampering functional expression of TASK1. In the SOD1-G93A mouse model of ALS, Sp1-p11-TASK1 dysregulation contributes to increased excitability and vulnerability of motor neurons. Interference with either Sp1 or p11 is neuroprotective, delaying neuron loss and prolonging lifespan in this model. Nitrosative stress, a potential factor in human neurodegeneration, stimulated Sp1 expression and human p11 promoter activity, at least in part, through a Sp1-binding site. Disruption of Sp1 or p11 also has neuroprotective effects in a traumatic model of motor neuron degeneration. Together our work suggests the Sp1-p11-TASK1 pathway is a potential target for treatment of degeneration of motor neurons.

Indexed as

Amyotrophic Lateral SclerosisAnimalsAnnexin A2Cell MembraneDisease Models, AnimalFemaleGene Expression RegulationGene Knockdown TechniquesHEK293 CellsHumansMaleMembrane PotentialsMiceMice, TransgenicMotor NeuronsNerve DegenerationAnnexin A2Nerve Tissue ProteinsPotassium Channels, Tandem Pore Domainpotassium channel subfamily K member 3S100 Calcium Binding Protein A10S100 ProteinsSp1 Transcription Factor

Identifiers

PMID31439839
PMCPMC6706379
OpenAlexW2969461081

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.