Evidence map›Paper›PMID 24457961›Full record

ArticleCell death & disease2014

Cross-regulation of Connexin43 and β-catenin influences differentiation of human neural progenitor cells.

F Rinaldi, E M Hartfield, L A Crompton, J L Badger, C P Glover, C M Kelly, A E Rosser, J B Uney, M A Caldwell

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.

0numbers the graph read from it
0cells of the map it votes in
30citing papers in PubMed
2.0field-weighted citation impact, top 14% 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

30 citing papers in PubMed, 48 citations in OpenAlex.

  1. Article
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  6. Viability and Longevity of Human Miniaturized Living Myocardial Slices.Journal of cardiovascular development and disease · 2025
    Article
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  10. Review
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  13. Article
  14. Article
  15. Review
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  17. Review
  18. Article
  19. Article
  20. 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

9 authors at 2 institutions in 1 country.

F RinaldiStem Cells and Neuroregeneration Research Group, School of Clinical Sciences, Medical Sciences Building, University Walk, University of Bristol, Bristol, UK.
E M HartfieldStem Cells and Neuroregeneration Research Group, School of Clinical Sciences, Medical Sciences Building, University Walk, University of Bristol, Bristol, UK.
L A CromptonStem Cells and Neuroregeneration Research Group, School of Clinical Sciences, Medical Sciences Building, University Walk, University of Bristol, Bristol, UK.
J L BadgerStem Cells and Neuroregeneration Research Group, School of Clinical Sciences, Medical Sciences Building, University Walk, University of Bristol, Bristol, UK.
C P GloverStem Cells and Neuroregeneration Research Group, School of Clinical Sciences, Medical Sciences Building, University Walk, University of Bristol, Bristol, UK.
C M KellyBrain Repair Group, School of Biosciences, Life Science Building, University of Cardiff, Cardiff, UK.
A E Rosser1] Brain Repair Group, School of Biosciences, Life Science Building, University of Cardiff, Cardiff, UK [2] Department of Neurology, School of Medicine, University of Cardiff, Cardiff, UK.
J B UneyStem Cells and Neuroregeneration Research Group, School of Clinical Sciences, Medical Sciences Building, University Walk, University of Bristol, Bristol, UK.
M A CaldwellStem Cells and Neuroregeneration Research Group, School of Clinical Sciences, Medical Sciences Building, University Walk, University of Bristol, Bristol, UK.
University of Bristol · GBCardiff University · GB

Funding

Biotechnology and Biological Sciences Research Council BB/F022298/1Medical Research Council
6 · The paper itself

Abstract

Connexin43 (Cx43) is the most widely and abundantly expressed gap junction (GJ) protein and it is strongly associated with the regulation of cell cycle progression. Emerging roles for Cx43 in cell adhesion and migration during neural differentiation have also been recently recognized, and this has emphasized the involvement of Cx43 in different physiological process beyond its role as a GJ protein. In this study, we explore the function of Cx43 in the differentiation of human neural progenitor cells (hNPCs) using viral vectors that mediate the overexpression or knockdown of the protein. Results showed that in the absence of this protein fetal cortex-derived hNPCs differentiated toward a neuronal phenotype at expenses of a glial phenotype. Furthermore, the silencing of Cx43 did not affect hNPC proliferation rate or numbers of apoptotic cells. The increase in the number of neurons was not recapitulated when GJ intercellular communications were pharmacologically blocked, and this suggested that Cx43 was influencing hNPCs differentiation with a GJ-independent effect. In addition, Cx43 knockdown significantly increased β-catenin signaling, which has been shown to regulate the transcription of pro-neuronal genes during embryonic neural development. Our results add further support to the hypothesis that Cx43 protein itself regulates key signaling pathways during development and neurogenesis beyond its role as GJ protein.

Indexed as

Neurogenesisbeta CateninCells, CulturedConnexin 43Gap JunctionsHumansNeural Stem CellsSignal Transductionbeta CateninConnexin 43

Identifiers

PMID24457961
PMCPMC4040652
OpenAlexW2057317386

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.