Evidence map›Paper›PMID 25514808›Full record

ArticlePloS one2014

Shoc2/Sur8 protein regulates neurite outgrowth.

Gonzalo Leon, Lucia Sanchez-Ruiloba, Andrea Perez-Rodriguez, Teresa Gragera, Natalia Martinez, Silvia Hernandez, Berta Anta, Olga Calero, Carlota A Garcia-Dominguez, Lara M Dura and 8 more

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.3field-weighted citation impact, top 41% 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

1 citing paper in PubMed, 5 citations in OpenAlex.

  1. 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

18 authors at 4 institutions in 1 country.

Gonzalo LeonUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Lucia Sanchez-RuilobaInstituto de Investigaciones Biomédicas "Alberto Sols," Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, 28029 Madrid, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, CIBERNED, Madrid, Spain.
Andrea Perez-RodriguezUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Teresa GrageraUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Natalia MartinezUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Silvia HernandezUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Berta AntaUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Olga CaleroCentro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, CIBERNED, Madrid, Spain; Unidad de Encefalopatías Espongiformes, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Carlota A Garcia-DominguezUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Lara M DuraUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Daniel Peña-JimenezUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Judit CastroUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Natasha ZarichUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Pilar Sanchez-GomezUnidad de Neuro-Oncología, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Miguel CaleroCentro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, CIBERNED, Madrid, Spain; Unidad de Encefalopatías Espongiformes, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Teresa IglesiasInstituto de Investigaciones Biomédicas "Alberto Sols," Consejo Superior de Investigaciones Científicas-Universidad Autónoma de Madrid, 28029 Madrid, Spain; Centro de Investigación Biomédica en Red sobre Enfermedades Neurodegenerativas, CIBERNED, Madrid, Spain.
Jose L OlivaUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Jose M RojasUnidad de Biología Celular, Unidad Funcional de Investigación de Enfermedades Crónicas, Instituto de Salud Carlos III, 28220 Majadahonda, Madrid, Spain.
Unidad Funcional de Investigación de Enfermedades Crónicas · ESInstituto de Salud Carlos III · ESBiomedical Research Networking Center on Neurodegenerative Diseases · ESUniversidad Autónoma de Madrid · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Shoc2 protein has been implicated in the positive regulation of the Ras-ERK pathway by increasing the functional binding interaction between Ras and Raf, leading to increased ERK activity. Here we found that Shoc2 overexpression induced sustained ERK phosphorylation, notably in the case of EGF stimulation, and Shoc2 knockdown inhibited ERK activation. We demonstrate that ectopic overexpression of human Shoc2 in PC12 cells significantly promotes neurite extension in the presence of EGF, a stimulus that induces proliferation rather than differentiation in these cells. Finally, Shoc2 depletion reduces both NGF-induced neurite outgrowth and ERK activation in PC12 cells. Our data indicate that Shoc2 is essential to modulate the Ras-ERK signaling outcome in cell differentiation processes involved in neurite outgrowth.

Indexed as

AnimalsCell Line, TumorEnzyme ActivationEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsMAP Kinase Signaling SystemNeuritesPC12 CellsPhosphorylationras ProteinsRatsRNA InterferenceRNA, Small InterferingEpidermal Growth FactorExtracellular Signal-Regulated MAP KinasesIntracellular Signaling Peptides and Proteinsras ProteinsRNA, Small InterferingSHOC2 protein, humanShoc2 protein, rat

Identifiers

PMID25514808
PMCPMC4267731
OpenAlexW2032818594

What OpenQuestion holds

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LicenceCC BY
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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.