ArticleMolecular biology of the cell2007
Dual mechanism of a natural CaMKII inhibitor.
Article in Molecular biology of the cell, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 127 papers.
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Who cites it
127 citing papers in PubMed, 195 citations in OpenAlex.
- CBX4 stabilizes NEUROD1 through SUMO-ubiquitin crosstalk to delay β-cell senescence.Nature communications · 2026Article
- Identification of a Small Secretoneurin Derivative That Inhibits CaMKIIδ Activity.Journal of cellular and molecular medicine · 2025Article
- Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation.eLife · 2025Article
- Rab10 inactivation promotes AMPAR trafficking and spine enlargement during long-term potentiation.bioRxiv : the preprint server for biology · 2025Article
- Role of CaMKII/CREB pathway in rapid-antidepressant-like effect: comparison of ketamine with rapastinel.Experimental brain research · 2025Article
- LTP expression mediated by autonomous activity of GluN2B-bound CaMKII.Cell reports · 2024Article
- Remote Ischemia Postconditioning Mitigates Hippocampal Neuron Impairment by Modulating Cav1.2-CaMKIIα-Aromatase Signaling After Global Cerebral Ischemia in Ovariectomized Rats.Molecular neurobiology · 2024Article
- CaMKII autophosphorylation is the only enzymatic event required for synaptic memory.Proceedings of the National Academy of Sciences of the United States of America · 2024Article
- Unveiling the role of CaMKII in retinal degeneration: from biological mechanism to therapeutic strategies.Cell & bioscience · 2024Review
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- Rem2 interacts with CaMKII at synapses and restricts long-term potentiation in hippocampus.bioRxiv : the preprint server for biology · 2024Article
- Rem2 interacts with CaMKII at synapses and restricts long-term potentiation in hippocampus.PloS one · 2024Article
- Synaptic memory and CaMKII.Physiological reviews · 2023Review
- Sevoflurane anaesthesia induces cognitive impairment in young mice through sequential tau phosphorylation.British journal of anaesthesia · 2023Article
- Article
- The GHB analogue HOCPCA improves deficits in cognition and sensorimotor function after MCAO via CaMKIIα.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023Article
- An improved reporter identifies ruxolitinib as a potent and cardioprotective CaMKII inhibitor.Science translational medicine · 2023Article
- CaMKIIα as a Promising Drug Target for Ischemic Grey Matter.Brain sciences · 2022Review
- CaMKII: a central molecular organizer of synaptic plasticity, learning and memory.Nature reviews. Neuroscience · 2022Review
- Article
67 more citing papers are in PubMed but not listed here.
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
Ca(2+)/calmodulin (CaM)-dependent protein kinase II (CaMKII) is a major mediator of cellular Ca(2+) signaling. Several inhibitors are commonly used to study CaMKII function, but these inhibitors all lack specificity. CaM-KIIN is a natural, specific CaMKII inhibitor protein. CN21 (derived from CaM-KIIN amino acids 43-63) showed full specificity and potency of CaMKII inhibition. CNs completely blocked Ca(2+)-stimulated and autonomous substrate phosphorylation by CaMKII and autophosphorylation at T305. However, T286 autophosphorylation (the autophosphorylation generating autonomous activity) was only mildly affected. Two mechanisms can explain this unusual differential inhibitor effect. First, CNs inhibited activity by interacting with the CaMKII T-site (and thereby also interfered with NMDA-type glutamate receptor binding to the T-site). Because of this, the CaMKII region surrounding T286 competed with CNs for T-site interaction, whereas other substrates did not. Second, the intersubunit T286 autophosphorylation requires CaM binding both to the "kinase" and the "substrate" subunit. CNs dramatically decreased CaM dissociation, thus facilitating the ability of CaM to make T286 accessible for phosphorylation. Tat-fusion made CN21 cell penetrating, as demonstrated by a strong inhibition of filopodia motility in neurons and insulin secrection from isolated Langerhans' islets. These results reveal the inhibitory mechanism of CaM-KIIN and establish a powerful new tool for dissecting CaMKII function.
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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.