Evidence map›Paper›PMID 20512937›Full record

ArticleJournal of cellular biochemistry2010

Enhanced connexin 43 expression delays intra-mitotic duration and cell cycle traverse independently of gap junction channel function.

Scott R Johnstone, Angela K Best, Catherine S Wright, Brant E Isakson, Rachel J Errington, Patricia E Martin

Open access · greenAbstract read
In one paragraph

Article in Journal of cellular biochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.8field-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

18 citing papers in PubMed, 41 citations in OpenAlex.

  1. Injury-induced connexin 43 expression regulates endothelial wound healing.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  2. Correlations of the expression of Cx43, SCFWorld journal of gastrointestinal oncology · 2025
    Article
  3. Mutations of theMedicina (Kaunas, Lithuania) · 2024
    Article
  4. Article
  5. Review
  6. Mechanisms of Connexin Regulating Peptides.International journal of molecular sciences · 2021
    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

6 authors at 3 institutions in 2 countries.

Scott R JohnstoneDepartment of Biological and Biomedical Sciences, School of Life Sciences, Glasgow Caledonian University, 70 Cowcaddens Rd, Glasgow, Scotland G4 0BA, UK.
Angela K Best
Catherine S Wright
Brant E Isakson
Rachel J Errington
Patricia E Martin
University of Virginia · USGlasgow Caledonian University · GBCardiff University · GB

Funding

Mechanisms of Heterocellular Signaling at the Myoenothelial JunctionR01HL088554 · NHLBI · UNIVERSITY OF VIRGINIA · PI ISAKSON, BRANT E, WEISS, MITCHELL J · 2008 to 2017
$3.8M
Biotechnology and Biological Sciences Research Council BB/E012574/1Biotechnology and Biological Sciences Research Council C23049Chief Scientist Office CZB/606/04NHLBI NIH HHS R01 HL088554PHS HHS R01088554
6 · The paper itself

Abstract

Connexins (Cxs) and gap junction (GJ)-mediated communication have been linked with the regulation of cell cycle traverse. However, it is not clear whether Cx expression or GJ channel function are the key mediators in this process or at what stage this regulation may occur. We therefore tested the hypothesis that enhanced Cx expression could alter the rate of cell cycle traverse independently of GJ channel function. Sodium butyrate (NaBu) or anti-arrhythmic peptide (AAP10) were used to enhance Cx expression in HeLa cells stably expressing Cx43 (HeLa-43) and primary cultures of human fibroblasts (HFF) that predominantly express Cx43. To reduce GJ-mediated communication, 18-alpha-glycyrrhetinic acid (GA) was used. In HeLa-43 and HFF cells, NaBu and AAP10 enhanced Cx43 expression and increased channel function, while GA reduced GJ-mediated communication but did not significantly alter Cx43 expression levels. Timelapse microscopy and flow cytometry of HeLa-WT (wild-type, Cx deficient) and HeLa-43 cells dissected cell cycle traverse and enabled measurements of intra-mitotic time and determined levels of G1 arrest. Enhanced Cx43 expression increased mitotic durations corresponding with a G1 delay in cell cycle, which was linked to an increase in expression of the cell cycle inhibitor p21(waf1/cip1) in both HeLa-43 and HFF cells. Reductions in Cx43 channel function did not abrogate these responses, indicating that GJ channel function was not a critical factor in reducing cell proliferation in either cell type. We conclude that enhanced Cx43 expression and not GJ-mediated communication, is involved in regulating cell cycle traverse.

Indexed as

Blotting, WesternCell CycleCell SeparationConnexin 43Flow CytometryFluorescent Antibody TechniqueGap JunctionsHeLa CellsHumansImmunohistochemistryMicroscopyMitosisTimeConnexin 43

Identifiers

PMID20512937
PMCPMC3030924
OpenAlexW2076273115

What OpenQuestion holds

Textmetadata
LicenceTDM
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.