Evidence map›Paper›PMID 31835537›Full record

ArticleInternational journal of molecular sciences2019

Evidence for the Desmosomal Cadherin Desmoglein-3 in Regulating YAP and Phospho-YAP in Keratinocyte Responses to Mechanical Forces.

Jutamas Uttagomol, Usama Sharif Ahmad, Ambreen Rehman, Yunying Huang, Ana C Laly, Angray Kang, Jan Soetaert, Randy Chance, Muy-Teck Teh, John T Connelly and 1 more

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
2.2field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 29 citations in OpenAlex.

  1. Keratinocytes: A key player in skin immunity and their emerging roles in secondary lymphedema.JID innovations : skin science from molecules to population health · 2026
    Review
  2. Article
  3. YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024
    Review
  4. Review
  5. Desmosomes at a glance.Journal of cell science · 2024
    Review
  6. Article
  7. Regulation of Photosensitivity by the Hippo Pathway in Lupus Skin.Arthritis & rheumatology (Hoboken, N.J.) · 2023
    Article
  8. Review
  9. Review
  10. Review
  11. Article
  12. Article
  13. Desmosomal Cadherins in Health and Disease.Annual review of pathology · 2022
    Review
  14. Review
  15. Review
  16. Article
  17. Article
  18. Article
  19. Desmosomes as Signaling Hubs in the Regulation of Cell Behavior.Frontiers in cell and developmental biology · 2021
    Review
  20. Review
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

11 authors at 1 institution in 1 country.

Jutamas UttagomolCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.ORCID 0000-0002-1407-9771
Usama Sharif AhmadCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.ORCID 0000-0003-4204-0476
Ambreen RehmanCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Yunying HuangCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Ana C LalyCentre for Cell Biology and Cutaneous Research, Blizard Institute; Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Angray KangCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Jan SoetaertCentre for Cell Biology and Cutaneous Research, Blizard Institute; Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Randy ChanceCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Muy-Teck TehCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
John T ConnellyCentre for Cell Biology and Cutaneous Research, Blizard Institute; Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.
Hong WanCentre for Oral Immunobiology and Regenerative Medicine, Institute of Dentistry, Barts and The London School of Medicine and Dentistry, Queen Mary University of London, London E1 2AT, UK.ORCID 0000-0003-3794-5692
Queen Mary University of London · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Desmoglein 3 (Dsg3) plays a crucial role in cell-cell adhesion and tissue integrity. Increasing evidence suggests that Dsg3 acts as a regulator of cellular mechanotransduction, but little is known about its direct role in mechanical force transmission. The present study investigated the impact of cyclic strain and substrate stiffness on Dsg3 expression and its role in mechanotransduction in keratinocytes. A direct comparison was made with E-cadherin, a well-characterized mechanosensor. Exposure of oral and skin keratinocytes to equiaxial cyclic strain promoted changes in the expression and localization of junction assembly proteins. The knockdown of Dsg3 by siRNA blocked strain-induced junctional remodeling of E-cadherin and Myosin IIa. Importantly, the study demonstrated that Dsg3 regulates the expression and localization of yes-associated protein (YAP), a mechanosensory, and an effector of the Hippo pathway. Furthermore, we showed that Dsg3 formed a complex with phospho-YAP and sequestered it to the plasma membrane, while Dsg3 depletion had an impact on both YAP and phospho-YAP in their response to mechanical forces, increasing the sensitivity of keratinocytes to the strain or substrate rigidity-induced nuclear relocation of YAP and phospho-YAP. Plakophilin 1 (PKP1) seemed to be crucial in recruiting the complex containing Dsg3/phospho-YAP to the cell surface since its silencing affected Dsg3 junctional assembly with concomitant loss of phospho-YAP at the cell periphery. Finally, we demonstrated that this Dsg3/YAP pathway has an influence on the expression of

Indexed as

Adaptor Proteins, Signal TransducingAntigens, CDCadherinsCell LineCell MembraneCell ProliferationDesmoglein 3DesmosomesGene Knockdown TechniquesHumansKeratinocytesMechanotransduction, CellularNonmuscle Myosin Type IIAPhosphorylationSignal TransductionTranscription FactorsAdaptor Proteins, Signal TransducingAntigens, CDCadherinsCDH1 protein, humanDesmoglein 3DSG3 protein, humanNonmuscle Myosin Type IIATranscription FactorsYAP1 protein, humanYAP-Signaling Proteinsadherens junctioncyclic straindesmogleindesmosomekeratinocytePhospho-YAPsubstrate stiffnessYAP

Identifiers

PMID31835537
PMCPMC6940936
OpenAlexW2986581405

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.