Evidence map›Paper›PMID 35589804›Full record

ArticleScientific reports2022

DVL1 and DVL3 require nuclear localisation to regulate proliferation in human myoblasts.

Johanna Pruller, Nicolas Figeac, Peter S Zammit

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

10 citing papers in PubMed, 17 citations in OpenAlex.

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  8. Identification of SNPs inFrontiers in genetics · 2023
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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 at 1 institution in 1 country.

Johanna PrullerKing's College London, Randall Centre for Cell and Molecular Biophysics, London, SE1 1UL, UK.
Nicolas FigeacKing's College London, Randall Centre for Cell and Molecular Biophysics, London, SE1 1UL, UK.
Peter S ZammitKing's College London, Randall Centre for Cell and Molecular Biophysics, London, SE1 1UL, UK. peter.zammit@kcl.ac.uk.
King's College London · GB

Funding

Medical Research Council MR/P023215/1Wellcome Trust WT 203949/Z/16/Z
6 · The paper itself

Abstract

WNT signalling is essential for regulating a diverse range of cellular processes. In skeletal muscle, the WNT pathway plays crucial roles in maintenance of the stem cell pool and myogenic differentiation. Focus is usually directed at examining the function of central components of the WNT pathway, including β-CATENIN and the GSK3β complex and TCF/LEF transcription factors, in tissue homeostasis and cancer. Other core components of the WNT pathway though, are three dishevelled (DVL) proteins: membrane associated proteins that propagate WNT signalling from membrane to nucleus. Here we examined DVL function in human myogenesis and the muscle-related cancer alveolar rhabdomyosarcoma. We demonstrate that DVL1 and DVL3 are necessary for efficient proliferation in human myoblasts and are important for timely myogenic differentiation. DVL1 and DVL3 also contribute to regulation of proliferation in rhabdomyosarcoma. DVL1 or DVL3 must be present in the nucleus to regulate proliferation, but they operate through different protein domains: DVL3 requires the DIX and PDZ domains, while DVL1 does not. Importantly, DVL1 and DVL3 activity is independent of markedly increased translocation of β-CATENIN to the nucleus, normally a hallmark of active canonical WNT signalling.

Indexed as

beta CateninNeoplasmsCell ProliferationDishevelled ProteinsHumansMyoblastsPhosphoproteinsWnt Signaling Pathwaybeta CateninDishevelled ProteinsDVL3 protein, humanPhosphoproteins

Identifiers

PMID35589804
PMCPMC9120025
OpenAlexW4280542414

What OpenQuestion holds

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Registered trials

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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.