ArticleAmerican journal of physiology. Cell physiology2020
Mechanisms involved in AMPK-mediated deposition of tight junction components to the plasma membrane.
Article in American journal of physiology. Cell physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 13 citations in OpenAlex.
- Phosphoproteomic Insights into TRPV4-AMPK Signaling Axis and Barrier Regulation in the Choroid Plexus Epithelium.International journal of molecular sciences · 2026Article
- VPS13B, gene responsible for Cohen syndrome, regulates gingival epithelial barrier function via intracellular trafficking of coxsackievirus and adenovirus receptor.Scientific reports · 2026Article
- Multi-Omics Profiles of Small Intestine Organoids in Reaction to Breast Milk and Different Infant Formula Preparations.Nutrients · 2024Article
- Tight junctions: from molecules to gastrointestinal diseases.Tissue barriers · 2023Article
- Junctional integrity and directional mobility of lymphatic endothelial cell monolayers are disrupted by saturated fatty acids.Molecular biology of the cell · 2023Article
- Irisin reduces inflammatory signaling pathways in inflammation-mediated metabolic syndrome.Molecular and cellular endocrinology · 2022Review
- Parallel kinase pathways stimulate actin polymerization at depolarized mitochondria.Current biology : CB · 2022Article
- Blueberry Stem Extract Prevents Lacrimal Hyposecretion in Non-obese Diabetic MiceIn vivo (Athens, Greece)Article
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Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
AMP-activated protein kinase (AMPK) activation promotes early stages of epithelial junction assembly. AMPK activation in MDCK renal epithelial cells facilitates localization of the junction-associated proteins aPKCζ and Par3 to the plasma membrane and promotes conversion of Cdc42, a key regulator of epithelial polarization and junction assembly, to its active GTP bound state. Furthermore, Par3 is an important regulator of AMPK-mediated aPKCζ localization. Both aPKCζ and Par3 serve as intermediates in AMPK-mediated junction assembly, with inhibition of aPKCζ activity or Par3 knockdown disrupting AMPK's ability to facilitate zonula occludens (ZO-1) localization. AMPK phosphorylates the adherens junction protein afadin and regulates its interaction with the tight-junction protein zonula occludens-1. Afadin is phosphorylated at two critical sites, S228 (residing within an aPKCζ consensus site) and S1102 (residing within an AMPK consensus site), that are differentially regulated during junction assembly and that exert different effects on the process. Expression of phospho-defective mutants (S228A and S1102A) perturbed ZO-1 localization to the plasma membrane during AMPK-induced junction assembly. Expression of S228A increased the ZO-1/afadin interaction, while S1102A reduced this interaction during extracellular calcium-induced junction assembly. Inhibition of aPKCζ activity also increased the ZO-1/afadin interaction. Taken together, these data suggest that aPKCζ phosphorylation of afadin terminates the ZO-1/afadin interaction and thus permits the later stages of junction assembly.
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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.