Evidence map›Paper›PMID 26867947›Full record

ArticleScientific reports2016

MAZ mediates the cross-talk between CT-1 and NOTCH1 signaling during gliogenesis.

Bin Liu, Anyun Ma, Feng Zhang, Yumeng Wang, Zengmin Li, Qingyu Li, Zhiheng Xu, Yufang Zheng

Erratum issuedOpen access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.2field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 20 citations in OpenAlex.

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  10. Rare mutations ofClinical science (London, England : 1979) · 2019
    Article
  11. 16p11.2 transcription factorProceedings of the National Academy of Sciences of the United States of America · 2018
    Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

8 authors at 3 institutions in 1 country.

Bin LiuState Key Laboratory of Genetic Engineering and Ministry of Education (MOE) Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University.
Anyun MaState Key Laboratory of Genetic Engineering and Ministry of Education (MOE) Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University.
Feng ZhangState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China 100101.
Yumeng WangState Key Laboratory of Genetic Engineering and Ministry of Education (MOE) Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University.
Zengmin LiState Key Laboratory of Genetic Engineering and Ministry of Education (MOE) Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University.
Qingyu LiState Key Laboratory of Genetic Engineering and Ministry of Education (MOE) Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University.
Zhiheng XuState Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing, China 100101.
Yufang ZhengState Key Laboratory of Genetic Engineering and Ministry of Education (MOE) Key Laboratory of Contemporary Anthropology, School of Life Sciences, Fudan University.
Fudan University · CNChinese Academy of Sciences · CNState Key Laboratory of Genetic Engineering

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Neurons and glia cells are differentiated from neural stem/progenitor cells (NSCs/NPCs) during brain development. Concomitant activation of JAK/STAT and NOTCH1 signaling is required for gliogenesis, a process to generate glia cells to ensure proper brain functions. NOTCH1 signaling is down-regulated during neurogenesis and up-regulated during gliogenesis. However, the underlying mechanism remains elusive. We report here that cardiotrophin-1 (CT-1) activates NOTCH1 signaling through the up-regulation of ADAM10, a rate-limiting factor of NOTCH1 signaling activation. We found that a transcriptional factor, Myc-associated zinc finger protein (MAZ), plays an important role in ADAM10 transcription in response to CT-1 in NPCs. MAZ knockdown inhibits CT-1 stimulated gliogenesis and it can be rescued by over-expressing human NICD. Our results provide a link between NOTCH1 activation and neuronal secreted CT-1, suggesting that CT-1 plays an important role in ensuring the coordinated activation of NOTCH1 signaling during gliogenesis.

Indexed as

ADAM10 ProteinAmyloid Precursor Protein SecretasesAnimalsCytokinesDNA-Binding ProteinsHumansMembrane ProteinsMiceNeural Stem CellsNeurogliaNIH 3T3 CellsReceptor, Notch1Signal TransductionTranscription FactorsADAM10 ProteinADAM10 protein, humanAmyloid Precursor Protein Secretasescardiotrophin 1c-MYC-associated zinc finger proteinCytokinesDNA-Binding ProteinsMembrane ProteinsNOTCH1 protein, humanReceptor, Notch1Transcription Factors

Identifiers

PMID26867947
PMCPMC4751466
OpenAlexW2411559597

What OpenQuestion holds

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LicenceCC BY
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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.