ArticleBrain research2012
Calmodulin dependent protein kinase increases conductance at gap junctions formed by the neuronal gap junction protein connexin36.
Article in Brain research, 2012. 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.
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Who cites it
35 citing papers in PubMed, 52 citations in OpenAlex.
- Uncovering the electrical synapse proteome in retinal neurons via in vivo proximity labeling.eLife · 2026Article
- Simultaneous Whole-Cell Recording and Calcium Imaging Does Not Reveal Electrically Coupled Neurons ineNeuro · 2026Article
- Diverse roles of connexins in the neuro-vasculature in homeostasis and disease.Translational neuroscience · 2026Review
- Cx47 Phosphorylation Exacerbates White Matter Damage and Kainic Acid Induced Epilepsy.CNS neuroscience & therapeutics · 2025Article
- The Amino Terminal Domain and Modulation of Connexin36 Gap Junction Channels by Intracellular Magnesium Ions.Frontiers in physiology · 2022Article
- Review
- Convergent NMDA receptor-Pannexin1 signaling pathways regulate the interaction of CaMKII with Connexin-36.Communications biology · 2021Article
- The Roles of Calmodulin and CaMKII in Cx36 Plasticity.International journal of molecular sciences · 2021Review
- Regulation of Connexin Gap Junctions and Hemichannels by Calcium and Calcium Binding Protein Calmodulin.International journal of molecular sciences · 2020Review
- Phosphorylation of Connexin36 near the C-terminus switches binding affinities for PDZ-domain and 14-3-3 proteins in vitro.Scientific reports · 2020Article
- Calmodulin Binding to Connexin 35: Specializations to Function as an Electrical Synapse.International journal of molecular sciences · 2020Article
- Endocytosis of Connexin 36 is Mediated by Interaction with Caveolin-1.International journal of molecular sciences · 2020Article
- Role of Connexins 30, 36, and 43 in Brain Tumors, Neurodegenerative Diseases, and Neuroprotection.Cells · 2020Review
- Effects of Propofol on Electrical Synaptic Strength in Coupling Reticular Thalamic GABAergic Parvalbumin-Expressing Neurons.Frontiers in neuroscience · 2020Article
- Tubulin-Dependent Transport of Connexin-36 Potentiates the Size and Strength of Electrical Synapses.Cells · 2019Article
- Design principles of electrical synaptic plasticity.Neuroscience letters · 2019Review
- Localization of Retinal CaFrontiers in molecular neuroscience · 2019Article
- Long-term potentiation in an innexin-based electrical synapse.Scientific reports · 2018Article
- Modulation of Connexin-36 Gap Junction Channels by Intracellular pH and Magnesium Ions.Frontiers in physiology · 2018Article
- Direct visualization of interaction between calmodulin and connexin45.The Biochemical journal · 2017Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
The major neuronal gap junction protein connexin36 (Cx36) exhibits the remarkable property of "run-up", in which junctional conductance typically increases by 10-fold or more within 5-10min following cell break-in with patch pipettes. Such conductance "run-up" is a unique property of Cx36, as it has not been seen in cell pairs expressing other connexins. Because of the recent observation describing CaMKII binding and phosphorylation sites in Cx36 and evidence that calmodulin dependent protein kinase II (CaMKII) may potentiate electrical coupling in neurons of teleosts, we have explored whether CaMKII activates mammalian Cx36. Consistent with this hypothesis, certain Cx36 mutants lacking the CaMKII binding and phosphorylation sites or wild type Cx36 treated with certain cognate peptides corresponding to binding or phosphorylation sites blocked or strongly attenuated run-up of junctional conductance. Likewise, KN-93, an inhibitor of CaMKII, blocked run-up, as did a membrane permeable peptide corresponding to the CaMKII autoinhibitory domain. Furthermore, run-up was blocked by phosphatase delivered within the pipette and not affected by treatment with the phosphatase inhibitor okadaic acid. These results imply that phosphorylation by CaMKII strengthens junctional currents of Cx36 channels, thereby conferring functional plasticity on electrical synapses formed of this protein.
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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.