Evidence map›Paper›PMID 21454484›Full record

ArticleThe Journal of biological chemistry2011

AMP-activated protein kinase regulates beta-catenin transcription via histone deacetylase 5.

Jun-Xing Zhao, Wan-Fu Yue, Mei-Jun Zhu, Min Du

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

31 citing papers in PubMed, 55 citations in OpenAlex.

  1. Article
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  12. Reciprocal Regulation of AMPK/SNF1 and Protein Acetylation.International journal of molecular sciences · 2018
    Review
  13. Article
  14. Article
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  17. Suppression of NF-κB activity via nanoparticle-based siRNA delivery alters early cartilage responses to injury.Proceedings of the National Academy of Sciences of the United States of America · 2016
    Article
  18. Article
  19. Article
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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

4 authors at 1 institution in 1 country.

Jun-Xing ZhaoDepartment of Animal Science, University of Wyoming, Laramie, Wyoming 82071, USA.
Wan-Fu Yue
Mei-Jun Zhu
Min Du
University of Wyoming · US

Funding

Wyoming IDeA Networks of Biomedical Research ExcellenceP20RR016474 · NCRR · UNIVERSITY OF WYOMING · PI LIBERLES, DAVID A. · 2001 to 2011
$28.2M
Maternal obesity, AMPK and fetal brown adipogenesisR01HD067449 · NICHD · WASHINGTON STATE UNIVERSITY · PI MIN DU · 2010 to 2026
$4.6M
A novel model for studying fetal skeletal muscle developmentR03HD057506 · NICHD · UNIVERSITY OF WYOMING · PI DU, MIN · 2008 to 2009
$189k
NCRR NIH HHS P20 RR016474NCRR NIH HHS P20RR016474NICHD NIH HHS 1R01HD067449NICHD NIH HHS 1R03HD057506NICHD NIH HHS R01 HD067449NICHD NIH HHS R03 HD057506
6 · The paper itself

Abstract

AMP-activated protein kinase (AMPK) is a key regulator of energy metabolism; it is inhibited under obese conditions and is activated by exercise and by many anti-diabetic drugs. Emerging evidence also suggests that AMPK regulates cell differentiation, but the underlying mechanisms are unclear. We hypothesized that AMPK regulates cell differentiation via altering β-catenin expression, which involves phosphorylation of class IIa histone deacetylase 5 (HDAC5). In both C3H10T1/2 cells and mouse embryonic fibroblasts (MEFs), AMPK activity was positively correlated with β-catenin content. Chemical inhibition of HDAC5 increased β-catenin mRNA expression. HDAC5 overexpression reduced and HDAC5 knockdown increased H3K9 acetylation and cellular β-catenin content. HDAC5 formed a complex with myocyte enhancer factor-2 to down-regulate β-catenin mRNA expression. AMPK phosphorylated HDAC5, which promoted HDAC5 exportation from the nucleus; mutation of two phosphorylation sites in HDAC5, Ser-259 and -498, abolished the regulatory role of AMPK on β-catenin expression. In conclusion, AMPK promotes β-catenin expression through phosphorylation of HDAC5, which reduces HDAC5 interaction with the β-catenin promoter via myocyte enhancer factor-2. Thus, the data indicate that AMPK regulates cell differentiation and development via cross-talk with the wingless and Int (Wnt)/β-catenin signaling pathway.

Indexed as

AcetylationActive Transport, Cell NucleusAMP-Activated Protein Kinase KinasesAnimalsbeta CateninCell DifferentiationCell LineCell NucleusGene Expression RegulationGene Knockdown TechniquesHistone DeacetylasesMiceMyogenic Regulatory FactorsPhosphorylationPromoter Regions, GeneticProtein KinasesAMP-Activated Protein Kinase Kinasesbeta CateninHdac5 protein, mouseHistone DeacetylasesMyogenic Regulatory FactorsProtein KinasesWnt Proteins

Identifiers

PMID21454484
PMCPMC3091248
OpenAlexW2135504542

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.