ArticleThe EMBO journal2002
Alternative splicing modulates the frequency-dependent response of CaMKII to Ca(2+) oscillations.
Article in The EMBO journal, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed.
- CAMKV kinase drives neuroblastoma growth and acts as a novel therapeutic target.The Journal of experimental medicine · 2026Article
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- A domain-swapped CaMKII conformation facilitates linker-mediated allosteric regulation.Nature communications · 2025Article
- CaMKIIβ deregulation contributes to neuromuscular junction destabilization in Myotonic Dystrophy type I.Skeletal muscle · 2024Article
- Studying CaMKII: Tools and standards.Cell reports · 2024Review
- CAMKV Kinase Signaling Is a Novel Therapeutic Avenue with Prognostic Relevance in Neuroblastoma.bioRxiv : the preprint server for biology · 2024Article
- Synaptic memory and CaMKII.Physiological reviews · 2023Review
- Excitotoxic glutamate levels drive spinal cord ependymal stem cell proliferation and fate specification through CP-AMPAR signaling.Stem cell reports · 2023Article
- Branch point strength controls species-specificLife science alliance · 2023Article
- Review
- Splicing signature database development to delineate cancer pathways using literature mining and transcriptome machine learning.Computational and structural biotechnology journal · 2023Article
- A Critical Role for γCaMKII in Decoding NMDA Signaling to Regulate AMPA Receptors in Putative Inhibitory Interneurons.Neuroscience bulletin · 2022Article
- The role of calcium and CaMKII in sleep.Frontiers in systems neuroscience · 2022Review
- CaMKII holoenzyme mechanisms that govern the LTP versus LTD decision.Science advances · 2021Article
- Phosphorylation of α-dystrobrevin is essential for αkap accumulation and acetylcholine receptor stability.The Journal of biological chemistry · 2020Article
- Heterogeneity in human hippocampal CaMKII transcripts reveals allosteric hub-dependent regulation.Science signaling · 2020Article
- Structural Insights into the Regulation of CaCold Spring Harbor perspectives in biology · 2020Review
- Characterization of CaMKIIα holoenzyme stability.Protein science : a publication of the Protein Society · 2020Article
- CaM Kinase: Still Inspiring at 40.Neuron · 2019Review
- FRET-based sensor for CaMKII activity (FRESCA): A useful tool for assessing CaMKII activity in response to CaThe Journal of biological chemistry · 2019Article
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Authors and funding
3 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Ca(2+) oscillations are required in various signal trans duction pathways, and contain information both in their amplitude and frequency. Remarkably, the Ca(2+)/calmodulin(CaM)-dependent protein kinase II (CaMKII) can decode such frequencies. A Ca(2+)/CaM-stimulated autophosphorylation leads to Ca(2+)/CaM-independent (autonomous) activity of the kinase that outlasts the initial stimulation. This autonomous activity increases exponentially with the frequency of Ca(2+) oscillations. Here we show that three beta-CaMKII splice variants (beta(M), beta and beta(e)') have very similar specific activity and maximal autonomy. However, their autonomy generated by Ca(2+) oscillations differs significantly. A mechanistic basis was found in alterations of the CaM activation constant and of the initial rate of autophosphorylation. Structurally, the splice variants differ only in a variable 'linker' region between the kinase and association domains. Therefore, we propose that differences in relative positioning of kinase domains within multimeric holoenzymes are responsible for the observed effects. Notably, the beta-CaMKII splice variants are differentially expressed, even among individual hippocampal neurons. Taken together, our results suggest that alternative splicing provides cells with a mechanism to modulate their sensitivity to Ca(2+) oscillations.
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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 OpenQuestion graph.