Evidence map›Paper›PMID 20628604›Full record

ArticlePloS one2010

Activated Notch1 target genes during embryonic cell differentiation depend on the cellular context and include lineage determinants and inhibitors.

Franziska Meier-Stiegen, Ralf Schwanbeck, Kristina Bernoth, Simone Martini, Thomas Hieronymus, David Ruau, Martin Zenke, Ursula Just

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.

0numbers the graph read from it
0cells of the map it votes in
54citing papers in PubMed
5.0field-weighted citation impact, top 4% 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

54 citing papers in PubMed, 100 citations in OpenAlex.

  1. Article
  2. Review
  3. Article
  4. Review
  5. Ubiquitin Proteasome Gene Signatures in Ependymoma Molecular Subtypes.International journal of molecular sciences · 2022
    Review
  6. Optogenetic control of NOTCH1 signaling.Cell communication and signaling : CCS · 2022
    Article
  7. Article
  8. ZFP36L2 Role in Thyroid Functionality.International journal of molecular sciences · 2021
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Article
  17. NOTCH1 regulates the viability of cholangiocarcinoma cells via 14-3-3 theta.Journal of cell communication and signaling · 2019
    Article
  18. Article
  19. Article
  20. 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

8 authors at 2 institutions in 1 country.

Franziska Meier-StiegenDepartment of Biochemistry, Christian-Albrechts-University of Kiel, Kiel, Germany.
Ralf Schwanbeck
Kristina Bernoth
Simone Martini
Thomas Hieronymus
David Ruau
Martin Zenke
Ursula Just
Kiel University · DERWTH Aachen University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNotch receptor signaling controls developmental cell fates in a cell-context dependent manner. Although Notch signaling directly regulates transcription via the RBP-J/CSL DNA binding protein, little is known about the target genes that are directly activated by Notch in the respective tissues. METHODOLOGY/PRINCIPAL

findingsTo analyze how Notch signaling mediates its context dependent function(s), we utilized a Tamoxifen-inducible system to activate Notch1 in murine embryonic stem cells at different stages of mesodermal differentiation and performed global transcriptional analyses. We find that the majority of genes regulated by Notch1 are unique for the cell type and vary widely dependent on other signals. We further show that Notch1 signaling regulates expression of genes playing key roles in cell differentiation, cell cycle control and apoptosis in a context dependent manner. In addition to the known Notch1 targets of the Hes and Hey families of transcriptional repressors, Notch1 activates the expression of regulatory transcription factors such as Sox9, Pax6, Runx1, Myf5 and Id proteins that are critically involved in lineage decisions in the absence of protein synthesis. CONCLUSION/SIGNIFICANCE: We suggest that Notch signaling determines lineage decisions and expansion of stem cells by directly activating both key lineage specific transcription factors and their repressors (Id and Hes/Hey proteins) and propose a model by which Notch signaling regulates cell fate commitment and self renewal in dependence of the intrinsic and extrinsic cellular context.

Indexed as

AnimalsApoptosisBlotting, WesternCell CycleCell DifferentiationCell LineCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsEmbryonic Stem CellsEye ProteinsHomeodomain ProteinsMiceMyogenic Regulatory Factor 5Oligonucleotide Array Sequence AnalysisPaired Box Transcription FactorsPAX6 Transcription FactorCore Binding Factor Alpha 2 SubunitDNA-Binding ProteinsEye ProteinsHomeodomain ProteinsMyf5 protein, mouseMyogenic Regulatory Factor 5Paired Box Transcription FactorsPax6 protein, mousePAX6 Transcription FactorRbpsuhl protein, mouseReceptor, Notch1Repressor ProteinsRunx1 protein, mouseSox9 protein, mouseSOX9 Transcription Factor

Identifiers

PMID20628604
PMCPMC2900208
OpenAlexW1973784868

What OpenQuestion holds

Textmetadata
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.