Evidence map›Paper›PMID 30382077›Full record

ArticleCell death & disease2018

Plau and Tgfbr3 are YAP-regulated genes that promote keratinocyte proliferation.

Susan M Corley, Veronica Mendoza-Reinoso, Nichole Giles, Emma Suwanun Singer, John E Common, Marc R Wilkins, Annemiek Beverdam

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.6field-weighted citation impact, top 35% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
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  7. YAP/TAZ Signalling Controls Epidermal Keratinocyte Fate.International journal of molecular sciences · 2024
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  14. Wnt5a/β-catenin axis is involved in the downregulation of AT2 lineage by PAI-1.American journal of physiology. Lung cellular and molecular physiology · 2022
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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 3 institutions in 2 countries.

Susan M CorleySystems Biology Initiative, School of Biotechnology and Biomolecular Sciences, UNSW Australia, Sydney, New South Wales, Australia. s.corley@unsw.edu.au.ORCID http://orcid.org/0000-0003-0605-6411
Veronica Mendoza-ReinosoSchool of Medical Sciences, UNSW Australia, Sydney, New South Wales, Australia.
Nichole GilesSchool of Medical Sciences, UNSW Australia, Sydney, New South Wales, Australia.
Emma Suwanun SingerSchool of Medical Sciences, UNSW Australia, Sydney, New South Wales, Australia.
John E CommonInstitute of Medical Biology, A*STAR, 8A Biomedical Grove, Immunos, Singapore, 138648, Singapore.
Marc R WilkinsSystems Biology Initiative, School of Biotechnology and Biomolecular Sciences, UNSW Australia, Sydney, New South Wales, Australia.
Annemiek BeverdamSchool of Medical Sciences, UNSW Australia, Sydney, New South Wales, Australia. a.beverdam@unsw.edu.au.ORCID http://orcid.org/0000-0003-4893-0162
UNSW Sydney · AUAgency for Science, Technology and Research · SGThe University of Queensland · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Yes-associated protein (YAP) is a mechanosensor protein and a downstream effector of the Hippo kinase pathway, which controls organ growth, cell proliferation, survival, maintenance and regeneration. Unphosphorylated YAP translocates to the nucleus where it acts as a cofactor of primarily the TEAD transcription factors to activate target gene transcription and cell proliferation. Perturbed YAP activation results in tumorigenesis. The pathways downstream of activated YAP that drive cell proliferation remain relatively unexplored. In this study, we employed YAP2-5SA-∆C transgenic mice, which overexpress a mildly activated YAP mutant protein in basal keratinocytes leading to increased proliferation of the epidermal stem/progenitor cell populations. We performed massively-parallel sequencing of skin biopsy mRNA (RNA-Seq) and found dysregulation of 1491 genes in YAP2-5SA-∆C skin, including many with roles in cell activation and proliferation. Furthermore, we found that 150 of these dysregulated genes harbored YAP/TEAD binding motifs in the 3' UTR, suggesting that these may be direct YAP/TEAD target genes in the control of epidermal regeneration. Further validation and functional characterization assays identified Plau and Tgfbr3 as prime candidate genes that may be activated by epidermal YAP activity in the mouse skin in vivo to promote keratinocyte proliferation. This study provides novel insights into the mechanisms regulated by YAP that control tissue homeostasis, and in particular in conditions where YAP is aberrantly activated such as in neoplastic and regenerative skin disease.

Indexed as

TranscriptomeAdaptor Proteins, Signal TransducingAnimalsCell Cycle ProteinsCell ProliferationEpidermisGene Expression ProfilingGene Expression RegulationHumansKeratinocytesMiceMice, TransgenicNucleotide MotifsProtein BindingProteoglycansReceptors, Transforming Growth Factor betaAdaptor Proteins, Signal TransducingbetaglycanCell Cycle ProteinsProteoglycansReceptors, Transforming Growth Factor betaRNA, MessengerUrokinase-Type Plasminogen ActivatorYap1 protein, mouseYAP-Signaling Proteins

Identifiers

PMID30382077
PMCPMC6208416
OpenAlexW2899315626

What OpenQuestion holds

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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.