Evidence map›Paper›PMID 25199838›Full record

ArticleCell reports2014

PTEN interacts with histone H1 and controls chromatin condensation.

Zhu Hong Chen, Minglu Zhu, Jingyi Yang, Hui Liang, Jinxue He, Shiming He, Pan Wang, Xi Kang, Michael A McNutt, Yuxin Yin and 1 more

Open access · goldAbstract read
In one paragraph

Article in Cell reports, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 66 papers.

0numbers the graph read from it
0cells of the map it votes in
66citing 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

66 citing papers in PubMed, 117 citations in OpenAlex.

  1. Article
  2. PTEN Subcellular Localization Dictates Function.bioRxiv : the preprint server for biology · 2026
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6 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Zhu Hong ChenInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China; Department of Radiation Oncology, Weill Medical College of Cornell University, New York, NY 10065, USA.
Minglu ZhuInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China; Department of Radiation Oncology, Weill Medical College of Cornell University, New York, NY 10065, USA.
Jingyi YangInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China.
Hui LiangInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China.
Jinxue HeDepartment of Radiation Oncology, Weill Medical College of Cornell University, New York, NY 10065, USA.
Shiming HeInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China.
Pan WangInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China.
Xi KangInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China; Department of Radiation Oncology, Weill Medical College of Cornell University, New York, NY 10065, USA.
Michael A McNuttInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China.
Yuxin YinInstitute of Systems Biomedicine, Department of Pathology, School of Basic Medical Sciences, Beijing Key Laboratory of Tumor Systems Biology, Peking-Tsinghua Center for Life Sciences, Peking University Health Science Center, Beijing 100191, China; Department of Radiation Oncology, Weill Medical College of Cornell University, New York, NY 10065, USA. Electronic address: yinyuxin@hsc.pku.edu.cn.
Wen H ShenDepartment of Radiation Oncology, Weill Medical College of Cornell University, New York, NY 10065, USA. Electronic address: wes2007@med.cornell.edu.
Center for Life Sciences · CNCornell University · USPeking University · CN

Funding

Role of PTEN in Mitosis and Chromosome StabilityR01GM100478 · NIGMS · WEILL MEDICAL COLL OF CORNELL UNIV · PI SHEN, WEN H. · 2012 to 2020
$2.9M
PTEN Deficiency and Tumor DevelopmentR01CA133008 · NCI · WEILL MEDICAL COLL OF CORNELL UNIV · PI YIN, YUXIN · 2009 to 2012
$1.4M
NCI NIH HHS R01 CA133008NCI NIH HHS R01CA133008NIGMS NIH HHS R01 GM100478NIGMS NIH HHS R01GM100478
6 · The paper itself

Abstract

Chromatin organization and dynamics are integral to global gene transcription. Histone modification influences chromatin status and gene expression. PTEN plays multiple roles in tumor suppression, development, and metabolism. Here, we report on the interplay of PTEN, histone H1, and chromatin. We show that loss of PTEN leads to dissociation of histone H1 from chromatin and decondensation of chromatin. PTEN deletion also results in elevation of histone H4 acetylation at lysine 16, an epigenetic marker for chromatin activation. We found that PTEN and histone H1 physically interact through their C-terminal domains. Disruption of the PTEN C terminus promotes the chromatin association of MOF acetyltransferase and induces H4K16 acetylation. Hyperacetylation of H4K16 impairs the association of PTEN with histone H1, which constitutes regulatory feedback that may reduce chromatin stability. Our results demonstrate that PTEN controls chromatin condensation, thus influencing gene expression. We propose that PTEN regulates global gene transcription profiling through histones and chromatin remodeling.

Indexed as

AcetylationAnimalsCell LineChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneGene Expression ProfilingHistonesMicePromoter Regions, GeneticProtein BindingProtein Structure, TertiaryPTEN PhosphohydrolaseChromatinChromobox Protein Homolog 5Chromosomal Proteins, Non-HistoneHistonesPTEN Phosphohydrolase

Identifiers

PMID25199838
PMCPMC4201947
OpenAlexW2071086325

What OpenQuestion holds

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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.