Evidence map›Paper›PMID 24698271›Full record

ArticleNeuron2014

Calcineurin signaling regulates neural induction through antagonizing the BMP pathway.

Ahryon Cho, Yitai Tang, Jonathan Davila, Suhua Deng, Lei Chen, Erik Miller, Marius Wernig, Isabella A Graef

Open access · bronzeAbstract read
In one paragraph

Article in Neuron, 2014. 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
2.0field-weighted citation impact, top 14% 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, 30 citations in OpenAlex.

  1. Article
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  11. Calcium Signaling in Vertebrate Development and Its Role in Disease.International journal of molecular sciences · 2018
    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

8 authors at 1 institution in 1 country.

Ahryon ChoDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA.
Yitai Tang *Department of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA.
Jonathan Davila *Institute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.
Suhua DengDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA.
Lei ChenDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA.
Erik MillerDepartment of Genetics, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA.
Marius WernigInstitute for Stem Cell Biology and Regenerative Medicine, Stanford University School of Medicine, Stanford, California 94305, USA.
Isabella A GraefDepartment of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA.
Stanford University · US

Funding

Center for Protein Folding Machinery (RMI)PN2EY016525 · NEI · BAYLOR COLLEGE OF MEDICINE · PI CHIU, WAH · 2005 to 2015
$33.6M
TRAINING & OUTREACH COREP50GM107615 · NIGMS · STANFORD UNIVERSITY · PI FERRELL, JAMES E. · 2013 to 2017
$10.9M
Role of Calcineurin/NFAT signaling in the pathogenesis of neurodegeneration in DoR01AG039099 · NIA · STANFORD UNIVERSITY · PI GRAEF, ISABELLA A · 2010 to 2014
$1.6M
NEI NIH HHS PN2 EY016525NIA NIH HHS R01 AG039099NIA NIH HHS R01AG039099NIGMS NIH HHS P50 GM107615
6 · The paper itself

Abstract

Development of the nervous system begins with neural induction, which is controlled by complex signaling networks functioning in concert with one another. Fine-tuning of the bone morphogenetic protein (BMP) pathway is essential for neural induction in the developing embryo. However, the molecular mechanisms by which cells integrate the signaling pathways that contribute to neural induction have remained unclear. We find that neural induction is dependent on the Ca(2+)-activated phosphatase calcineurin (CaN). Fibroblast growth factor (FGF)-regulated Ca(2+) entry activates CaN, which directly and specifically dephosphorylates BMP-regulated Smad1/5 proteins. Genetic and biochemical analyses revealed that CaN adjusts the strength and transcriptional output of BMP signaling and that a reduction of CaN activity leads to an increase of Smad1/5-regulated transcription. As a result, FGF-activated CaN signaling opposes BMP signaling during gastrulation, thereby promoting neural induction and the development of anterior structures.

Indexed as

AnimalsBone Morphogenetic ProteinsCalcineurinCell DifferentiationCyclosporineEmbryo, MammalianEmbryonic DevelopmentEmbryonic Stem CellsFibroblast Growth FactorsGene Expression ProfilingGene Expression Regulation, DevelopmentalHumansImmunosuppressive AgentsMiceMice, TransgenicMutationBone Morphogenetic ProteinsCalcineurinCyclosporineFibroblast Growth FactorsImmunosuppressive AgentsTacrolimus

Identifiers

PMID24698271
PMCPMC4011666
OpenAlexW2051705519

What OpenQuestion holds

Textmetadata
LicenceTDM
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.