ArticleFrontiers in pharmacology2013
Together and apart: inhibition of DNA synthesis by connexin-43 and its relationship to transforming growth factor β.
Article in Frontiers in pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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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.
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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.
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Who cites it
2 citing papers in PubMed, 3 citations in OpenAlex.
- Article
- Mind the gap! Connexins and pannexins in physiology, pharmacology and disease.Frontiers in pharmacology · 2013Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The membrane and channel protein connexin-43 (Cx43), as well as the cytokine transforming growth factor (TGF) β, suppress proliferative growth in cardiomyocytes and other cell types. Previously we showed that the inhibitory effect of Cx43 is canceled when Cx43 becomes phosphorylated at serine (S) 262 in response to mitogen stimulation. We have now asked if the TGFβ-triggered inhibition of DNA synthesis is associated with changes in Cx43 phosphorylation at S262. Conversely, we investigated if inhibition of DNA synthesis by overexpressed Cx43 is dependent on engaging TGFβ signal transduction. We report that TGFβ acutely prevented mitogen-induced Cx43 phosphorylation at S262, while chronic inhibition of TGFβ signal transduction raised baseline levels of endogenous phospho-S262-Cx43 without affecting total Cx43. Inhibition of baseline TGFβ signal transduction through (a) inhibiting TGFβ receptor I (TGFβRI) with SB431542, (b) inhibiting TGFβ receptor II (TGFβRII) by overexpressing dominant-negative (DN) TGFβRII, (c) inhibiting the downstream signaling mediator Smad2 by overexpressing DN Smad2, each separately increased baseline cardiomyocyte DNA synthesis, but could not reverse DNA synthesis inhibition by overexpressed Cx43. It is suggested that inhibition of cardiomyocyte DNA synthesis by TGFβ/TGFβRI/II/phospho-Smad2 signaling is mediated, at least in part, by reducing endogenous phospho-S262-Cx43 levels.
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Registered trials
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.