Evidence map›Paper›PMID 22179133›Full record

ArticleNature genetics2011

A chromatin-modifying function of JNK during stem cell differentiation.

Vijay K Tiwari, Michael B Stadler, Christiane Wirbelauer, Renato Paro, Dirk Schübeler, Christian Beisel

Abstract read
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In one paragraph

Article in Nature genetics, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 90 papers.

0numbers the graph read from it
0cells of the map it votes in
90citing papers in PubMed
5.9field-weighted citation impact, top 3% 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

90 citing papers in PubMed, 136 citations in OpenAlex.

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30 more citing papers are in PubMed but not listed here.

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

6 authors at 3 institutions in 1 country.

Vijay K TiwariFriedrich Miescher Institute for Biomedical Research, Basel, Switzerland.
Michael B Stadler
Christiane Wirbelauer
Renato Paro
Dirk Schübeler
Christian Beisel
Friedrich Miescher Institute · CHBoard of the Swiss Federal Institutes of Technology · CHUniversity of Basel · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Signaling mediates cellular responses to extracellular stimuli. The c-Jun NH(2)-terminal kinase (JNK) pathway exemplifies one subgroup of the mitogen-activated protein (MAP) kinases, which, besides having established functions in stress response, also contribute to development by an unknown mechanism. We show by genome-wide location analysis that JNK binds to a large set of active promoters during the differentiation of stem cells into neurons. JNK-bound promoters are enriched with binding motifs for the transcription factor NF-Y but not for AP-1. NF-Y occupies these predicted sites, and overexpression of dominant-negative NF-YA reduces the JNK presence on chromatin. We find that histone H3 Ser10 (H3S10) is a substrate for JNK, and JNK-bound promoters are enriched for H3S10 phosphorylation. Inhibition of JNK signaling in post-mitotic neurons reduces phosphorylation at H3S10 and the expression of target genes. These results establish MAP kinase binding and function on chromatin at a novel class of target genes during stem cell differentiation.

Indexed as

Cell DifferentiationAnimalsCCAAT-Binding FactorChromatinEmbryonic Stem CellsGene Expression RegulationMAP Kinase Kinase 4MAP Kinase Signaling SystemMiceNeural Stem CellsNeuronsPhosphorylationPromoter Regions, GeneticProtein BindingStem CellsUp-RegulationCCAAT-Binding FactorChromatinMAP Kinase Kinase 4nuclear factor Y

Identifiers

PMID22179133
OpenAlexW2022966544

What OpenQuestion holds

Textmetadata
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.