Evidence map›Paper›PMID 27405641›Full record

ArticleNature communications2016

αE-catenin inhibits YAP/TAZ activity to regulate signalling centre formation during tooth development.

Chun-Ying Li, Jimmy Hu, Hongbing Lu, Jing Lan, Wei Du, Nicole Galicia, Ophir D Klein

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
2.7field-weighted citation impact, top 11% 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

40 citing papers in PubMed, 48 citations in OpenAlex.

  1. Mechanical control in dental and jaw morphogenesis and remodeling.International journal of oral science · 2026
    Review
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  10. Tooth number abnormality: from bench to bedside.International journal of oral science · 2023
    Review
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  12. Article
  13. Article
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  15. 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

7 authors at 2 institutions in 3 countries.

Chun-Ying LiThe Research Center and Department of Pathology, Zhongshan Hospital of Dalian University, Dalian 116001, China.
Jimmy HuDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
Hongbing LuDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
Jing LanDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
Wei DuDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
Nicole GaliciaDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.
Ophir D KleinDepartment of Orofacial Sciences and Program in Craniofacial Biology, University of California, San Francisco, California 94143, USA.ORCID 0000-0002-6254-7082
University of California, San Francisco · USInternational Craniofacial Institute · US

Funding

The role of Hippo and YAP/TAZ in dental renewalR01DE024988 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI KLEIN, OPHIR D · 2015 to 2016
$793k
The role of YAP/TAZ and Hippo signaling in mouse incisor stem cellsF32DE023705 · NIDCR · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI HU, JIMMY KUANG-HSIEN · 2013 to 2015
$161k
NIDCR NIH HHS F32 DE023705NIDCR NIH HHS R01 DE024988
6 · The paper itself

Abstract

Embryonic signalling centres are specialized clusters of non-proliferating cells that direct the development of many organs. However, the mechanisms that establish these essential structures in mammals are not well understood. Here we report, using the murine incisor as a model, that αE-catenin is essential for inhibiting nuclear YAP localization and cell proliferation. This function of αE-catenin is required for formation of the tooth signalling centre, the enamel knot (EK), which maintains dental mesenchymal condensation and epithelial invagination. EK formation depends primarily on the signalling function of αE-catenin through YAP and its homologue TAZ, as opposed to its adhesive function, and combined deletion of Yap and Taz rescues the EK defects caused by loss of αE-catenin. These findings point to a developmental mechanism by which αE-catenin restricts YAP/TAZ activity to establish a group of non-dividing and specialized cells that constitute a signalling centre.

Indexed as

Adaptor Proteins, Signal Transducingalpha CateninAmelogenesisAnimalsCell Cycle ProteinsCell ProliferationGene Expression Regulation, DevelopmentalIncisorMiceMice, KnockoutOdontogenesisPhosphoproteinsToothTrans-ActivatorsYAP-Signaling ProteinsAdaptor Proteins, Signal Transducingalpha CateninCell Cycle ProteinsCtnna1 protein, mousePhosphoproteinsTrans-ActivatorsWwtr1 protein, mouseYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID27405641
PMCPMC4947177
OpenAlexW2464048391

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.