ArticleDevelopment (Cambridge, England)2020
Connexin 43 gap junctional intercellular communication inhibits
Article in Development (Cambridge, England), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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.
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.
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Who cites it
7 citing papers in PubMed, 12 citations in OpenAlex.
- Injury-induced electrochemical coupling triggers organ growth.Science advances · 2026Article
- Overexpression of potassium channel Kcna5 alters skeletal patterning in the zebrafish regenerating fin.Developmental biology · 2025Article
- Ccn2a acts downstream of cx43 to influence joint formation during zebrafish fin regeneration.Biology open · 2025Article
- Retinoic Acid InfluencesBioelectricity · 2023Article
- The Role of Connexin 43 in Renal Disease: Insights from In Vivo Models of Experimental Nephropathy.International journal of molecular sciences · 2022Review
- Regenerating zebrafish scales express a subset of evolutionary conserved genes involved in human skeletal disease.BMC biology · 2022Article
- Impaired Cx43 gap junction endocytosis causes morphological and functional defects in zebrafish.Molecular biology of the cell · 2021Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
The gap junction protein Connexin 43 (Cx43) contributes to cell fate decisions that determine the location of fin ray joints during regeneration. Here, we provide insights into how Cx43, expressed medially, influences changes in gene expression in lateral skeletal precursor cells. Using the Gap27 peptide inhibitor specific to Cx43, we show that Cx43-gap junctional intercellular communication (GJIC) influences Cx43-dependent skeletal phenotypes, including segment length. We also demonstrate that Cx43-GJIC influences the expression of the Smp/β-catenin pathway in the lateral skeletal precursor cells, and does not influence the Sema3d pathway. Moreover, we show that the
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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 Socratic graph.