Evidence map›Paper›PMID 33085215›Full record

ReviewWIREs mechanisms of disease2021

The WNT/β-catenin dependent transcription: A tissue-specific business.

Simon Söderholm, Claudio Cantù

Open access · hybridAbstract readReview
In one paragraph

Review in WIREs mechanisms of disease, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.

0numbers the graph read from it
0cells of the map it votes in
51citing papers in PubMed
4.3field-weighted citation impact, top 5% 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

51 citing papers in PubMed, 83 citations in OpenAlex.

  1. Article
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  10. Dujieqing decoction suppresses multiple myeloma growth by inhibiting the Wnt/β-catenin pathway.Journal of traditional Chinese medicine = Chung i tsa chih ying wen pan · 2025
    Article
  11. Review
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  17. Review
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  20. NOTUM-mediated WNT silencing drives extravillous trophoblast cell lineage development.Proceedings of the National Academy of Sciences of the United States of America · 2024
    Article
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.

Simon SöderholmWallenberg Centre for Molecular Medicine, Linköping University, Linköping, Sweden.ORCID 0000-0001-5350-7102
Claudio CantùWallenberg Centre for Molecular Medicine, Linköping University, Linköping, Sweden.ORCID 0000-0003-1547-5415
Linköping University · SE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

β-catenin-mediated Wnt signaling is an ancient cell-communication pathway in which β-catenin drives the expression of certain genes as a consequence of the trigger given by extracellular WNT molecules. The events occurring from signal to transcription are evolutionarily conserved, and their final output orchestrates countless processes during embryonic development and tissue homeostasis. Importantly, a dysfunctional Wnt/β-catenin pathway causes developmental malformations, and its aberrant activation is the root of several types of cancer. A rich literature describes the multitude of nuclear players that cooperate with β-catenin to generate a transcriptional program. However, a unified theory of how β-catenin drives target gene expression is still missing. We will discuss two types of β-catenin interactors: transcription factors that allow β-catenin to localize at target regions on the DNA, and transcriptional co-factors that ultimately activate gene expression. In contrast to the presumed universality of β-catenin's action, the ensemble of available evidence suggests a view in which β-catenin drives a complex system of responses in different cells and tissues. A malleable armamentarium of players might interact with β-catenin in order to activate the right "canonical" targets in each tissue, developmental stage, or disease context. Discovering the mechanism by which each tissue-specific β-catenin response is executed will be crucial to comprehend how a seemingly universal pathway fosters a wide spectrum of processes during development and homeostasis. Perhaps more importantly, this could ultimately inform us about which are the tumor-specific components that need to be targeted to dampen the activity of oncogenic β-catenin. This article is categorized under: Cancer > Molecular and Cellular Physiology Cancer > Genetics/Genomics/Epigenetics Cancer > Stem Cells and Development.

Indexed as

beta CateninWnt Signaling PathwayCarcinogenesisCell NucleusHumansTranscription Factorsbeta CateninTranscription Factorscell signalinggenomicstranscriptionWnt signalingβ-catenin

Identifiers

PMID33085215
PMCPMC9285942
OpenAlexW3094105865

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.