Evidence map›Paper›PMID 32179550›Full record

ArticleMolecular and cellular biology2020

TWIST1 Homodimers and Heterodimers Orchestrate Lineage-Specific Differentiation.

Xiaochen Fan, Ashley J Waardenberg, Madeleine Demuth, Pierre Osteil, Jane Q J Sun, David A F Loebel, Mark Graham, Patrick P L Tam, Nicolas Fossat

Open access · greenAbstract read
In one paragraph

Article in Molecular and cellular biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed, 1 pooled it
1.7field-weighted citation impact, top 16% 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

24 citing papers in PubMed, 1 synthesis or guideline pooled it, 30 citations in OpenAlex.

  1. Genetics versus environment in the pathophysiology of sagittal synostosis.Child's nervous system : ChNS : official journal of the International Society for Pediatric Neurosurgery · 2026
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  13. Diagnostic Significance of HypomethylatedAdvanced biomedical research · 2023
    Article
  14. Cranium growth, patterning and homeostasis.Development (Cambridge, England) · 2022
    Article
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  18. Nutrients · 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

9 authors at 2 institutions in 1 country.

Xiaochen FanEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia x6fan@ucsd.edu.
Ashley J WaardenbergBioinformatics Group, The University of Sydney, Sydney, Australia.
Madeleine DemuthEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Pierre OsteilEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Jane Q J SunEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
David A F LoebelEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Mark GrahamSynapse Proteomics Group, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Patrick P L TamEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
Nicolas FossatEmbryology Unit, Children's Medical Research Institute, The University of Sydney, Sydney, Australia.
University of Sydney · AUChildren's Medical Research Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The extensive array of basic helix-loop-helix (bHLH) transcription factors and their combinations as dimers underpin the diversity of molecular function required for cell type specification during embryogenesis. The bHLH factor TWIST1 plays pleiotropic roles during development. However, which combinations of TWIST1 dimers are involved and what impact each dimer imposes on the gene regulation network controlled by TWIST1 remain elusive. In this work, proteomic profiling of human TWIST1-expressing cell lines and transcriptome analysis of mouse cranial mesenchyme have revealed that TWIST1 homodimers and heterodimers with TCF3, TCF4, and TCF12 E-proteins are the predominant dimer combinations. Disease-causing mutations in TWIST1 can impact dimer formation or shift the balance of different types of TWIST1 dimers in the cell, which may underpin the defective differentiation of the craniofacial mesenchyme. Functional analyses of the loss and gain of TWIST1-E-protein dimer activity have revealed previously unappreciated roles in guiding lineage differentiation of embryonic stem cells: TWIST1-E-protein heterodimers activate the differentiation of mesoderm and neural crest cells, which is accompanied by the epithelial-to-mesenchymal transition. At the same time, TWIST1 homodimers maintain the stem cells in a progenitor state and block entry to the endoderm lineage.

Indexed as

Cell DifferentiationProtein MultimerizationAnimalsCell LineDogsEpithelial-Mesenchymal TransitionGene Expression Regulation, DevelopmentalHumansMadin Darby Canine Kidney CellsMesodermMice, Inbred C57BLMutationNeural CrestNuclear ProteinsTranscriptomeTwist-Related Protein 1Nuclear ProteinsTWIST1 protein, humanTwist1 protein, mouseTwist-Related Protein 1bHLH factorembryonic stem cellsE-proteinlineage differentiationTWIST1

Identifiers

PMID32179550
PMCPMC7225560
OpenAlexW3011274279

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.