Evidence map›Paper›PMID 20952396›Full record

ArticleThe Journal of biological chemistry2010

A phosphorylation switch regulates the transcriptional activation of cell cycle regulator p21 by histone deacetylase inhibitors.

Elisabeth Simboeck, Anna Sawicka, Gordin Zupkovitz, Silvia Senese, Stefan Winter, Franck Dequiedt, Egon Ogris, Luciano Di Croce, Susanna Chiocca, Christian Seiser

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

35 citing papers in PubMed, 58 citations in OpenAlex.

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  10. Epigenetic Activation ofMolecular pharmacology · 2017
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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

10 authors at 5 institutions in 4 countries.

Elisabeth SimboeckDepartment of Medical Biochemistry, Max F. Perutz Laboratories, Medical University of Vienna, Vienna Biocenter, A-1030 Vienna, Austria.
Anna Sawicka
Gordin Zupkovitz
Silvia Senese
Stefan Winter
Franck Dequiedt
Egon Ogris
Luciano Di Croce
Susanna Chiocca
Christian Seiser
Vienna Biocenter · ATEuropean Institute of Oncology · ITMedical University of Vienna · ATCentre for Genomic Regulation · ESGembloux Agro-Bio Tech · BE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Histone deacetylase inhibitors induce cell cycle arrest and apoptosis in tumor cells and are, therefore, promising anti-cancer drugs. The cyclin-dependent kinase inhibitor p21 is activated in histone deacetylase (HDAC) inhibitor-treated tumor cells, and its growth-inhibitory function contributes to the anti-tumorigenic effect of HDAC inhibitors. We show here that induction of p21 by trichostatin A involves MAP kinase signaling. Activation of the MAP kinase signaling pathway by growth factors or stress signals results in histone H3 serine 10 phosphorylation at the p21 promoter and is crucial for acetylation of the neighboring lysine 14 and recruitment of activated RNA polymerase II in response to trichostatin A treatment. In non-induced cells, the protein phosphatase PP2A is associated with the p21 gene and counteracts its activation. Induction of p21 is linked to simultaneous acetylation and phosphorylation of histone H3. The dual modification mark H3S10phK14ac at the activated p21 promoter is recognized by the phospho-binding protein 14-3-3ζ, which protects the phosphoacetylation mark from being processed by PP2A. Taken together we have revealed a cross-talk of reversible phosphorylation and acetylation signals that controls the activation of p21 by HDAC inhibitors and identify the phosphatase PP2A as chromatin-associated transcriptional repressor in mammalian cells.

Indexed as

14-3-3 ProteinsAcetylationAnimalsCyclin-Dependent Kinase Inhibitor p21Histone Deacetylase InhibitorsHistonesHydroxamic AcidsMAP Kinase Signaling SystemMicePhosphorylationRNA Polymerase IISwiss 3T3 CellsTranscriptional ActivationTranscription, Genetic14-3-3 ProteinsCdkn1a protein, mouseCyclin-Dependent Kinase Inhibitor p21Histone Deacetylase InhibitorsHistonesHydroxamic AcidsRNA Polymerase IItrichostatin A

Identifiers

PMID20952396
PMCPMC3003405
OpenAlexW2075428343

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.