Evidence map›Paper›PMID 31623112›Full record

ReviewGenes2019

Ubiquitin Ligases Involved in the Regulation of Wnt, TGF-β, and Notch Signaling Pathways and Their Roles in Mouse Development and Homeostasis.

Nikol Baloghova, Tomas Lidak, Lukas Cermak

Abstract readReview
In one paragraph

Review in Genes, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
–field-weighted citation impact
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

17 citing papers in PubMed.

  1. Article
  2. Targeting ubiquitination in disease and therapy.Signal transduction and targeted therapy · 2025
    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

3 authors.

Nikol BaloghovaLaboratory of Cancer Biology, Division BIOCEV, Institute of Molecular Genetics of the Czech Academy of Sciences, 252 42 Vestec, Czech Republic. nikol.baloghova@img.cas.cz.
Tomas LidakLaboratory of Cancer Biology, Division BIOCEV, Institute of Molecular Genetics of the Czech Academy of Sciences, 252 42 Vestec, Czech Republic. tomas.lidak@img.cas.cz.
Lukas CermakLaboratory of Cancer Biology, Division BIOCEV, Institute of Molecular Genetics of the Czech Academy of Sciences, 252 42 Vestec, Czech Republic. lukas.cermak@img.cas.cz.ORCID 0000-0002-8777-3692

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The Wnt, TGF-β, and Notch signaling pathways are essential for the regulation of cellular polarity, differentiation, proliferation, and migration. Differential activation and mutual crosstalk of these pathways during animal development are crucial instructive forces in the initiation of the body axis and the development of organs and tissues. Due to the ability to initiate cell proliferation, these pathways are vulnerable to somatic mutations selectively producing cells, which ultimately slip through cellular and organismal checkpoints and develop into cancer. The architecture of the Wnt, TGF-β, and Notch signaling pathways is simple. The transmembrane receptor, activated by the extracellular stimulus, induces nuclear translocation of the transcription factor, which subsequently changes the expression of target genes. Nevertheless, these pathways are regulated by a myriad of factors involved in various feedback mechanisms or crosstalk. The most prominent group of regulators is the ubiquitin-proteasome system (UPS). To open the door to UPS-based therapeutic manipulations, a thorough understanding of these regulations at a molecular level and rigorous confirmation in vivo are required. In this quest, mouse models are exceptional and, thanks to the progress in genetic engineering, also an accessible tool. Here, we reviewed the current understanding of how the UPS regulates the Wnt, TGF-β, and Notch pathways and we summarized the knowledge gained from related mouse models.

Indexed as

Animalsbeta CateninCell DifferentiationCell ProliferationGene Expression Regulation, DevelopmentalHomeostasisLigasesMiceReceptors, NotchTranscription FactorsTransforming Growth Factor betaUbiquitinUbiquitin-Protein LigasesWnt ProteinsWnt Signaling Pathwaybeta CateninLigasesReceptors, NotchTranscription FactorsTransforming Growth Factor betaUbiquitinUbiquitin-Protein LigasesWnt Proteinscancergene inactivationmouse modelubiquitin–proteasome system

Identifiers

PMID31623112
PMCPMC6826584

What OpenQuestion holds

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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.