Evidence map›Paper›PMID 29141232›Full record

ArticleStem cell reports2017

FOXP1 Promotes Embryonic Neural Stem Cell Differentiation by Repressing Jagged1 Expression.

Luca Braccioli, Stephin J Vervoort, Youri Adolfs, Cobi J Heijnen, Onur Basak, R Jeroen Pasterkamp, Cora H Nijboer, Paul J Coffer

Open access · goldAbstract read
In one paragraph

Article in Stem cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
2.9field-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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 79 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

8 authors at 2 institutions in 2 countries.

Luca BraccioliLaboratory of Neuroimmunology and Developmental Origins of Disease (NIDOD), University Medical Center Utrecht, Utrecht 3508 AB, the Netherlands; Center for Molecular Medicine and Regenerative Medicine Center, University Medical Center Utrecht, Utrecht 3584 CT, the Netherlands.
Stephin J VervoortCenter for Molecular Medicine and Regenerative Medicine Center, University Medical Center Utrecht, Utrecht 3584 CT, the Netherlands.
Youri AdolfsDepartment of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht 3584 CX, the Netherlands.
Cobi J HeijnenLaboratory of Neuroimmunology, Department of Symptom Research, Division of Internal Medicine, University of Texas MD Anderson Cancer Center, Houston, TX 77030, USA.
Onur BasakHubrecht Institute, Royal Netherlands Academy of Arts and Sciences (KNAW) and University Medical Center Utrecht, 3584 CT Utrecht, the Netherlands.
R Jeroen PasterkampDepartment of Translational Neuroscience, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht 3584 CX, the Netherlands.
Cora H NijboerLaboratory of Neuroimmunology and Developmental Origins of Disease (NIDOD), University Medical Center Utrecht, Utrecht 3508 AB, the Netherlands. Electronic address: c.nijboer@umcutrecht.nl.
Paul J CofferCenter for Molecular Medicine and Regenerative Medicine Center, University Medical Center Utrecht, Utrecht 3584 CT, the Netherlands. Electronic address: p.j.coffer@umcutrecht.nl.
University Medical Center Utrecht · NLThe University of Texas MD Anderson Cancer Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in FOXP1 have been linked to neurodevelopmental disorders including intellectual disability and autism; however, the underlying molecular mechanisms remain ill-defined. Here, we demonstrate with RNA and chromatin immunoprecipitation sequencing that FOXP1 directly regulates genes controlling neurogenesis. We show that FOXP1 is expressed in embryonic neural stem cells (NSCs), and modulation of FOXP1 expression affects both neuron and astrocyte differentiation. Using a murine model of cortical development, FOXP1-knockdown in utero was found to reduce NSC differentiation and migration during corticogenesis. Furthermore, transplantation of FOXP1-knockdown NSCs in neonatal mice after hypoxia-ischemia challenge demonstrated that FOXP1 is also required for neuronal differentiation and functionality in vivo. FOXP1 was found to repress the expression of Notch pathway genes including the Notch-ligand Jagged1, resulting in inhibition of Notch signaling. Finally, blockade of Jagged1 in FOXP1-knockdown NSCs rescued neuronal differentiation in vitro. Together, these data support a role for FOXP1 in regulating embryonic NSC differentiation by modulating Notch signaling.

Indexed as

NeurogenesisAnimalsAstrocytesCells, CulturedCerebral CortexForkhead Transcription FactorsHypoxia-Ischemia, BrainJagged-1 ProteinMiceMice, Inbred C57BLMouse Embryonic Stem CellsNeural Stem CellsReceptors, NotchRepressor ProteinsStem Cell TransplantationForkhead Transcription FactorsFoxp1 protein, mouseJagged-1 ProteinReceptors, NotchRepressor Proteinsdifferentiationembryonic neural stem cellsFOXP1NotchNSCtranscription

Identifiers

PMID29141232
PMCPMC5688236
OpenAlexW2768911594

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.