Evidence map›Paper›PMID 21779366›Full record

ArticlePloS one2011

Interplay between SIN3A and STAT3 mediates chromatin conformational changes and GFAP expression during cellular differentiation.

Pei-Yi Cheng, Yu-Ping Lin, Ya-Ling Chen, Yi-Ching Lee, Chia-Chen Tai, Yi-Ting Wang, Yu-Ju Chen, Cheng-Fu Kao, John Yu

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
2.3field-weighted citation impact, top 12% 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

33 citing papers in PubMed, 55 citations in OpenAlex.

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  15. Epigenetic regulation of astrocyte function in neuroinflammation and neurodegeneration.Biochimica et biophysica acta. Molecular basis of disease · 2018
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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

9 authors at 5 institutions in 1 country.

Pei-Yi ChengGraduate Institute of Life Sciences, National Defense Medical Center, Taipei, Taiwan.
Yu-Ping Lin
Ya-Ling Chen
Yi-Ching Lee
Chia-Chen Tai
Yi-Ting Wang
Yu-Ju Chen
Cheng-Fu Kao
John Yu
Institute of Cellular and Organismic Biology, Academia Sinica · TWInstitute of Biomedical Sciences, Academia Sinica · TWInstitute of Chemistry, Academia Sinica · TWGenomics Research Center, Academia Sinica · TWNational Defense Medical Center · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundNeurons and astrocytes are generated from common neural precursors, yet neurogenesis precedes astrocyte formation during embryogenesis. The mechanisms of neural development underlying suppression and de-suppression of differentiation-related genes for cell fate specifications are not well understood. METHODOLOGY/PRINCIPAL

findingsBy using an in vitro system in which NTera-2 cells were induced to differentiate into an astrocyte-like lineage, we revealed a novel role for Sin3A in maintaining the suppression of GFAP in NTera-2 cells. Sin3A coupled with MeCP2 bound to the GFAP promoter and their occupancies were correlated with repression of GFAP transcription. The repression by Sin3A and MeCP2 may be an essential mechanism underlying the inhibition of cell differentiation. Upon commitment toward an astrocyte-like lineage, Sin3A- MeCP2 departed from the promoter and activated STAT3 simultaneously bound to the promoter and exon 1 of GFAP; meanwhile, olig2 was exported from nuclei to the cytoplasm. This suggested that a three-dimensional or higher-order structure was provoked by STAT3 binding between the promoter and proximal coding regions. STAT3 then recruited CBP/p300 to exon 1 and targeted the promoter for histone H3K9 and H3K14 acetylation. The CBP/p300-mediated histone modification further facilitates chromatin remodeling, thereby enhancing H3K4 trimethylation and recruitment of RNA polymerase II to activate GFAP gene transcription. CONCLUSIONS/SIGNIFICANCE: These results provide evidence that exchange of repressor and activator complexes and epigenetic modifications are critical strategies for cellular differentiation and lineage-specific gene expression.

Indexed as

AnimalsBasic Helix-Loop-Helix ProteinsBlotting, WesternCell CycleCell DifferentiationCell LineCell NucleusChromatinChromatin ImmunoprecipitationDNA MethylationGlial Fibrillary Acidic ProteinHumansImmunohistochemistryImmunoprecipitationLentivirusMethyl-CpG-Binding Protein 2Basic Helix-Loop-Helix ProteinsChromatinGlial Fibrillary Acidic ProteinMethyl-CpG-Binding Protein 2Nerve Tissue ProteinsOLIG2 protein, humanOligodendrocyte Transcription Factor 2STAT3 protein, humanSTAT3 Transcription Factor

Identifiers

PMID21779366
PMCPMC3136934
OpenAlexW2135785283

What OpenQuestion holds

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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.