Evidence map›Paper›PMID 28494938›Full record

ArticleStem cell reports2017

PI3K/AKT/mTOR Signaling Mediates Valproic Acid-Induced Neuronal Differentiation of Neural Stem Cells through Epigenetic Modifications.

Xi Zhang, Xiaosong He, Qingqing Li, Xuejian Kong, Zhenri Ou, Le Zhang, Zhuo Gong, Dahong Long, Jianhua Li, Meng Zhang and 4 more

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 42 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 1 pooled it
3.7field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.

  1. Pooled it
  2. 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

14 authors at 5 institutions in 2 countries.

Xi ZhangKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Xiaosong HeKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Qingqing LiKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Xuejian KongKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Zhenri OuKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Le ZhangKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Zhuo GongKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Dahong LongKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Jianhua LiDepartment of Physiology, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China.
Meng ZhangDepartment of Physiology, Augusta University, Augusta 30912, USA.
Weidong JiThe First Affiliated Hospital, Center for Translational Medicine, Sun Yat-sen University, Guangzhou 510080, China.
Wenjuan ZhangDepartment of Preventive Medicine, School of Medicine, Jinan University, Guangzhou, 510632, China.
Liping XuKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China.
Aiguo XuanKey Laboratory of Neuroscience, Key Laboratory of Protein Modification and Degradation, Department of Anatomy, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou 511436, China; Department of Neurology, Institute of Neuroscience, The Second Affiliated Hospital of Guangzhou Medical University, Key Laboratory of Neurogenetics and Channelopathies of Guangdong Province and the Ministry of Education of China, Guangzhou 510260, China. Electronic address: xag2005@sohu.com.
Guangzhou Medical University · CNSecond Affiliated Hospital of Guangzhou Medical University · CNAugusta University · USJinan University · CNSun Yat-sen University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Although valproic acid (VPA), has been shown to induce neuronal differentiation of neural stem cells (NSCs), the underlying mechanisms remain poorly understood. Here we investigated if and how mammalian target of rapamycin (mTOR) signaling is involved in the neuronal differentiation of VPA-induced NSCs. Our data demonstrated that mTOR activation not only promoted but also was necessary for the neuronal differentiation of NSCs induced by VPA. We further found that inhibition of mTOR signaling blocked demethylation of neuron-specific gene neurogenin 1 (Ngn1) regulatory element in induced cells. These are correlated with the significant alterations of passive DNA demethylation and the active DNA demethylation pathway in the Ngn1 promoter, but not the suppression of lysine-specific histone methylation and acetylation in the promoter region of Ngn1. These findings highlight a potentially important role for mTOR signaling, by working together with DNA demethylation, to influence the fate of NSCs via regulating the expression of Ngn1 in VPA-induced neuronal differentiation of NSCs.

Indexed as

Epigenesis, GeneticNeurogenesisSignal TransductionAnimalsBasic Helix-Loop-Helix ProteinsCells, CulturedDNA MethylationEnzyme InhibitorsHistone CodeNerve Tissue ProteinsNeural Stem CellsPhosphatidylinositol 3-KinasesPromoter Regions, GeneticProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyBasic Helix-Loop-Helix ProteinsEnzyme InhibitorsNerve Tissue ProteinsNeurog1 protein, mousePhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktTOR Serine-Threonine KinasesValproic Aciddifferentiationepigeneticsmammalian target of rapamycinneural stem cellsvalproic acid

Identifiers

PMID28494938
PMCPMC5425725
OpenAlexW2613060378

What OpenQuestion holds

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LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

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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.