ReviewThe Journal of membrane biology2012
Degradation of endocytosed gap junctions by autophagosomal and endo-/lysosomal pathways: a perspective.
Review in The Journal of membrane biology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Deceiving the gatekeepers: virus modulation of gap junctions.Microbiology and molecular biology reviews : MMBR · 2025Review
- Pseudorabies virus infection triggers pUL46-mediated phosphorylation of connexin-43 and closure of gap junctions to promote intercellular virus spread.PLoS pathogens · 2025Article
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
- Mitochondrial Connexins and Mitochondrial Contact Sites with Gap Junction Structure.International journal of molecular sciences · 2023Review
- Impaired Cx43 gap junction endocytosis causes morphological and functional defects in zebrafish.Molecular biology of the cell · 2021Article
- Dysregulation of the Retromer Complex in Brain Endothelial Cells Results in Accumulation of Phosphorylated Tau.Journal of inflammation research · 2021Article
- Degradation of group V secretory phospholipase AMicrovascular research · 2020Article
- Therapeutic strategies targeting connexins.Nature reviews. Drug discovery · 2018Review
- Connexins: Synthesis, Post-Translational Modifications, and Trafficking in Health and Disease.International journal of molecular sciences · 2018Review
- Defining the factors that affect solute permeation of gap junction channels.Biochimica et biophysica acta. Biomembranes · 2018Review
- Connexins in Cardiovascular and Neurovascular Health and Disease: Pharmacological Implications.Pharmacological reviews · 2017Review
- Nutrient Starvation Decreases Cx43 Levels and Limits Intercellular Communication in Primary Bovine Corneal Endothelial Cells.The Journal of membrane biology · 2016Article
- Connexins: substrates and regulators of autophagy.BMC cell biology · 2016Review
- Molecular mechanisms regulating formation, trafficking and processing of annular gap junctions.BMC cell biology · 2016Review
- Structural Studies of the Nedd4 WW Domains and Their Selectivity for the Connexin43 (Cx43) Carboxyl Terminus.The Journal of biological chemistry · 2016Article
- Adrenocortical Gap Junctions and Their Functions.Frontiers in endocrinology · 2016Review
- The Mammalian Blood-Testis Barrier: Its Biology and Regulation.Endocrine reviews · 2015Review
- Gap junctional protein Cx43 is involved in the communication between extracellular vesicles and mammalian cells.Scientific reports · 2015Article
- Degradation of connexins and gap junctions.FEBS letters · 2014Review
- How to take autophagy and endocytosis up a notch.BioMed research international · 2014Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Gap junctions (GJs) are composed of tens to many thousands of double-membrane spanning GJ channels that cluster together to form densely packed channel arrays (termed GJ plaques) in apposing plasma membranes of neighboring cells. In addition to providing direct intercellular communication (GJIC, their hallmark function), GJs, based on their characteristic double-membrane-spanning configuration, likely also significantly contribute to physical cell-to-cell adhesion. Clearly, modulation (up-/down-regulation) of GJIC and of physical cell-to-cell adhesion is as vitally important as the basic ability of GJ formation itself. Others and we have previously described that GJs can be removed from the plasma membrane via the internalization of entire GJ plaques (or portions thereof) in a cellular process that resembles clathrin-mediated endocytosis. GJ endocytosis results in the formation of double-membrane vesicles [termed annular gap junctions (AGJs) or connexosomes] in the cytoplasm of one of the coupled cells. Four recent independent studies, consistent with earlier ultrastructural analyses, demonstrate the degradation of endocytosed AGJ vesicles via autophagy. However, in TPA-treated cells others report degradation of AGJs via the endo-/lysosomal degradation pathway. Here we summarize evidence that supports the concept that autophagy serves as the cellular default pathway for the degradation of internalized GJs. Furthermore, we highlight and discuss structural criteria that seem required for an alternate degradation via the endo-/lysosomal pathway.
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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.