Evidence map›Paper›PMID 26370090›Full record

ArticleThe Journal of biological chemistry2015

WNT10B enhances proliferation through β-catenin and RAC1 GTPase in human corneal endothelial cells.

Jeong Goo Lee, Martin Heur

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 27% 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

16 citing papers in PubMed, 25 citations in OpenAlex.

  1. Article
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  4. The role of WNT10B in physiology and disease: A 10-year update.Frontiers in cell and developmental biology · 2023
    Review
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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

2 authors at 1 institution in 1 country.

Jeong Goo LeeFrom the University of Southern California Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90033.
Martin HeurFrom the University of Southern California Eye Institute, Keck School of Medicine, University of Southern California, Los Angeles, California 90033 heur@usc.edu.
University of Southern California · US

Funding

Zebrafish Model of Human Corneal Development and DiseaseK08EY021485 · NEI · UNIVERSITY OF SOUTHERN CALIFORNIA · PI HEUR, MARTIN · 2011 to 2015
$1.1M
NEI NIH HHS K08 EY021485
6 · The paper itself

Abstract

The cornea is the anterior, transparent tissue of the human eye that serves as its main refractive element. Corneal endothelial cells are arranged as a monolayer on the posterior surface of the cornea and function as a pump to counteract the leakiness of its basement membrane. Maintaining the cornea in a slightly dehydrated state is critical for the maintenance of corneal transparency. Adult human corneal endothelial cells are G1-arrested, even in response to injury, leading to an age-dependent decline in endothelial cell density. Corneal edema and subsequent vision loss ensues when endothelial cell density decreases below a critical threshold. Vision loss secondary to corneal endothelial dysfunction is a common indication for transplantation in developed nations. An impending increase in demand for and a current global shortage of donor corneas will necessitate the development of treatments for vision loss because of endothelial dysfunction that do not rely on donor corneas. Wnt ligands regulate many critical cellular functions, such as proliferation, making them attractive candidates for modulation in corneal endothelial dysfunction. We show that WNT10B causes nuclear transport and binding of RAC1 and β-catenin in human corneal endothelial cells, leading to the activation of Cyclin D1 expression and proliferation. Our findings indicate that WNT10B promotes proliferation in human corneal endothelial cells by simultaneously utilizing both β-catenin-dependent and -independent pathways and suggest that its modulation could be used to treat vision loss secondary to corneal endothelial dysfunction.

Indexed as

Active Transport, Cell NucleusAdaptor Proteins, Signal Transducingbeta CateninCell Line, TransformedCell ProliferationCorneaCyclin D1Dishevelled ProteinsEndothelial CellsG1 Phase Cell Cycle CheckpointsGene Expression RegulationHumansInterleukin-1betaPhosphoproteinsProtein BindingProto-Oncogene ProteinsAdaptor Proteins, Signal Transducingbeta CateninCyclin D1Dishevelled ProteinsInterleukin-1betaPhosphoproteinsProto-Oncogene Proteinsrac1 GTP-Binding ProteinRAC1 protein, humanRNA, Small InterferingWNT10B protein, humanWnt Proteinscell proliferationcorneaendotheliumRas-related C3 botulinum toxin substrate 1 (Rac1)β-catenin

Identifiers

PMID26370090
PMCPMC4646328
OpenAlexW2247247147

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.