ArticleThe Journal of biological chemistry2011
AMP-activated protein kinase (AMPK) activation and glycogen synthase kinase-3β (GSK-3β) inhibition induce Ca2+-independent deposition of tight junction components at the plasma membrane.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 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
35 citing papers in PubMed, 50 citations in OpenAlex.
- Phosphoproteomic Insights into TRPV4-AMPK Signaling Axis and Barrier Regulation in the Choroid Plexus Epithelium.International journal of molecular sciences · 2026Article
- Hydroxycarboxylic acid receptor 2 (GPR109A) and retinopathies: pathways and prospects.Frontiers in medicine · 2026Review
- AMPK in Intestinal Health and Disease: A Multifaceted Therapeutic Target for Metabolic and Inflammatory Disorders.Drug design, development and therapy · 2025Review
- Review
- α1AMP-Activated Protein Kinase Protects against Lipopolysaccharide-Induced Endothelial Barrier Disruption via Junctional Reinforcement and Activation of the p38 MAPK/HSP27 Pathway.International journal of molecular sciences · 2020Article
- Mechanisms involved in AMPK-mediated deposition of tight junction components to the plasma membrane.American journal of physiology. Cell physiology · 2020Article
- Spatial control of AMPK signaling at subcellular compartments.Critical reviews in biochemistry and molecular biology · 2020Review
- Roles of AMP-Activated Protein Kinase (AMPK) in Mammalian Reproduction.Frontiers in cell and developmental biology · 2020Review
- Reciprocal Association between the Apical Junctional Complex and AMPK: A Promising Therapeutic Target for Epithelial/Endothelial Barrier Function?International journal of molecular sciences · 2019Review
- AMPK Activation Promotes Tight Junction Assembly in Intestinal Epithelial Caco-2 Cells.International journal of molecular sciences · 2019Article
- Review
- Implications of AMPK in the Formation of Epithelial Tight Junctions.International journal of molecular sciences · 2018Review
- Akkermansia muciniphila-derived extracellular vesicles influence gut permeability through the regulation of tight junctions.Experimental & molecular medicine · 2018Article
- AMPK in regulation of apical junctions and barrier function of intestinal epithelium.Tissue barriers · 2018Review
- Article
- Review
- AF-6 Protects Against Dopaminergic Dysfunction and Mitochondrial Abnormalities inFrontiers in cellular neuroscience · 2017Article
- Mesenchymal Stromal Cells Accelerate Epithelial Tight Junction Assembly via the AMP-Activated Protein Kinase Pathway, Independently of Liver Kinase B1.Stem cells international · 2017Article
- Article
- Connexin43 hemichannels contributes to the disassembly of cell junctions through modulation of intracellular oxidative status.Redox biology · 2016Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
Extracellular Ca(2+) is essential for the development of stable epithelial tight junctions. We find that in the absence of extracellular Ca(2+), AMP-activated protein kinase (AMPK) activation and glycogen synthase kinase (GSK)-3β inhibition independently induce the localization of epithelial tight junction components to the plasma membrane. The Ca(2+)-independent deposition of junctional proteins induced by AMPK activation and GSK-3β inhibition is independent of E-cadherin. Furthermore, the nectin-afadin system is required for the deposition of tight junction components induced by AMPK activation, but it is not required for that induced by GSK-3β inhibition. Phosphorylation studies demonstrate that afadin is a substrate for AMPK. These data demonstrate that two kinases involved in regulating cell growth and metabolism act through distinct pathways to influence the deposition of the components of epithelial tight junctions.
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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.