Evidence map›Paper›PMID 27720608›Full record

ArticleDevelopmental cell2016

Acetylation of VGLL4 Regulates Hippo-YAP Signaling and Postnatal Cardiac Growth.

Zhiqiang Lin, Haidong Guo, Yuan Cao, Sylvia Zohrabian, Pingzhu Zhou, Qing Ma, Nathan VanDusen, Yuxuan Guo, Jin Zhang, Sean M Stevens and 8 more

Open access · bronzeAbstract read
In one paragraph

Article in Developmental cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 74 papers.

0numbers the graph read from it
0cells of the map it votes in
74citing papers in PubMed
6.4field-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

74 citing papers in PubMed, 106 citations in OpenAlex.

  1. Review
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  5. The role of mechanosignaling in the control of myocardial mass.American journal of physiology. Heart and circulatory physiology · 2025
    Review
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  13. SUMOylation of TEAD1 Modulates the Mechanism of Pathological Cardiac Hypertrophy.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Article
  14. Review
  15. Article
  16. Article
  17. Review
  18. Article
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14 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

18 authors at 5 institutions in 4 countries.

Zhiqiang LinDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA. Electronic address: zlin@enders.tch.harvard.edu.
Haidong GuoDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA; Department of Anatomy, School of Basic Medicine, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China.
Yuan CaoDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA; Peking University, Fifth School of Clinical Medicine, Beijing 100730, China.
Sylvia ZohrabianDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Pingzhu ZhouDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Qing MaDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Nathan VanDusenDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Yuxuan GuoDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Jin ZhangDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Sean M StevensDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
Feng LiangRowland Institute at Harvard, Harvard University, Cambridge, MA 02142, USA.
Qimin QuanRowland Institute at Harvard, Harvard University, Cambridge, MA 02142, USA.
Pim R van GorpDepartment of Cardiology, Leiden University Medical Center, 2300 RC Leiden, the Netherlands.
Amy LiDepartment of Anatomy & Histology, Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
Cristobal Dos RemediosDepartment of Anatomy & Histology, Bosch Institute, University of Sydney, Sydney, NSW 2006, Australia.
Aibin HeInstitute of Molecular Medicine, Peking University, PKU-Tsinghua U Joint Center for Life Sciences, Beijing 100871, China.
Vassilios J BezzeridesDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA.
William T PuDepartment of Cardiology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA 02115, USA; Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA. Electronic address: wpu@pulab.org.
Boston Children's Hospital · USHarvard University · USThe University of Sydney · AULeiden University Medical Center · NLPeking University · CN

Funding

RESEARCH METHODS IN PEDIATRICS HEART DISEASET32HL007572 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI Sarah D DE FERRANTI, Jane W. Newburger · 1985 to 2026
$13.0M
Microenvironmental control of progenitors in organ dysfunction and repairU01HL100401 · NHLBI · UT SOUTHWESTERN MEDICAL CENTER · PI OLSON, ERIC N, SCHNEIDER, JAY W · 2009 to 2015
$8.3M
Regulation of Cardiac Development in Health and DiseaseUM1HL098166 · NHLBI · HARVARD MEDICAL SCHOOL · PI PENNACCHIO, LEN ALEXANDER, PU, WILLIAM TSWENCHING · 2015 to 2019
$4.4M
YAP1 Regulation of cardiomyocyte proliferation, function, and regenerationR01HL116461 · NHLBI · BOSTON CHILDREN'S HOSPITAL · PI PU, WILLIAM TSWENCHING · 2013 to 2017
$2.6M
NHLBI NIH HHS R01 HL116461NHLBI NIH HHS T32 HL007572NHLBI NIH HHS U01 HL100401NHLBI NIH HHS UM1 HL098166
6 · The paper itself

Abstract

Binding of the transcriptional co-activator YAP with the transcription factor TEAD stimulates growth of the heart and other organs. YAP overexpression potently stimulates fetal cardiomyocyte (CM) proliferation, but YAP's mitogenic potency declines postnatally. While investigating factors that limit YAP's postnatal mitogenic activity, we found that the CM-enriched TEAD1 binding protein VGLL4 inhibits CM proliferation by inhibiting TEAD1-YAP interaction and by targeting TEAD1 for degradation. Importantly, VGLL4 acetylation at lysine 225 negatively regulated its binding to TEAD1. This developmentally regulated acetylation event critically governs postnatal heart growth, since overexpression of an acetylation-refractory VGLL4 mutant enhanced TEAD1 degradation, limited neonatal CM proliferation, and caused CM necrosis. Our study defines an acetylation-mediated, VGLL4-dependent switch that regulates TEAD stability and YAP-TEAD activity. These insights may improve targeted modulation of TEAD-YAP activity in applications from cardiac regeneration to cancer.

Indexed as

Signal TransductionAcetylationAdaptor Proteins, Signal TransducingAgingAmino Acid SequenceAnimalsAnimals, NewbornCell Cycle ProteinsCell ProliferationDNA-Binding ProteinsHeartHeart FailureHippo Signaling PathwayHumansPhosphoproteinsProtein BindingAdaptor Proteins, Signal TransducingCell Cycle ProteinsDNA-Binding ProteinsPhosphoproteinsProtein Serine-Threonine KinasesTead1 protein, mouseTEA Domain Transcription FactorsTranscription FactorsVGLL4 protein, mouseYap1 protein, mouseYAP-Signaling ProteinsacetylationcardiaccardiomyocytedegradationHippo-YAP pathwaynecrosisproliferationTEAD1VGLL4

Identifiers

PMID27720608
PMCPMC5121000
OpenAlexW2531585457

What OpenQuestion holds

Textmetadata
LicenceTDM
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.