ArticleFrontiers in molecular neuroscience2013
CASK regulates CaMKII autophosphorylation in neuronal growth, calcium signaling, and learning.
Article in Frontiers in molecular neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 55 citations in OpenAlex.
- CASK promotes non-small cell lung cancer growth through coordinated regulation of EGFR expression, trafficking, and p21 expression.Journal of biomedical science · 2026Article
- CaMKII as a Multimodal Signalling Hub in Neural Connectivity and Vulnerability.Molecular neurobiology · 2026Review
- Viral modulation of synaptic pruning: implications for neuropathology and brain function.Journal of virology · 2026Review
- Drosophila CASK regulates brain size and neuronal morphogenesis, providing a genetic model of postnatal microcephaly suitable for drug discovery.Neural development · 2023Article
- Calcium/Calmodulin-Dependent Serine Protein Kinase (Animals : an open access journal from MDPI · 2023Article
- An oligogenic architecture underlying ecological and reproductive divergence in sympatric populations.eLife · 2023Article
- Arc ubiquitination regulates endoplasmic reticulum-mediated CaFrontiers in cellular neuroscience · 2023Article
- Article
- Review
- PSMD14 Targeting Triggers Paraptosis in Breast Cancer Cells by Inducing Proteasome Inhibition and CaInternational journal of molecular sciences · 2022Article
- Functional Dissection of Protein Kinases in Sexual Development and Female Receptivity ofFrontiers in cell and developmental biology · 2022Article
- The gut-microbiota-brain axis in autism: what Drosophila models can offer?Journal of neurodevelopmental disorders · 2021Review
- Loss of CASK Accelerates Heart Failure Development.Circulation research · 2021Article
- A role for alternative splicing in circadian control of exocytosis and glucose homeostasis.Genes & development · 2020Article
- Baicalin ameliorates chronic mild stress-induced depression-like behaviors in mice and attenuates inflammatory cytokines and oxidative stress.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2019Article
- Alzheimer's Disease Associated Genes Ankyrin and Tau Cause Shortened Lifespan and Memory Loss inFrontiers in cellular neuroscience · 2019Article
- Restoration of Olfactory Memory inFrontiers in cellular neuroscience · 2019Article
- FMRFa receptor stimulated Ca2+ signals alter the activity of flight modulating central dopaminergic neurons in Drosophila melanogaster.PLoS genetics · 2018Article
- MicroRNA interactome analysis predicts post-transcriptional regulation of ADRB2 and PPP3R1 in the hypercholesterolemic myocardium.Scientific reports · 2018Article
- Regulation of Eag by CaJournal of neurophysiology · 2018Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Calcium (Ca(2+))/calmodulin (CaM)-dependent kinase II (CaMKII) activity plays a fundamental role in learning and memory. A key feature of CaMKII in memory formation is its ability to be regulated by autophosphorylation, which switches its activity on and off during synaptic plasticity. The synaptic scaffolding protein CASK (calcium (Ca(2+))/calmodulin (CaM) associated serine kinase) is also important for learning and memory, as mutations in CASK result in intellectual disability and neurological defects in humans. We show that in Drosophila larvae, CASK interacts with CaMKII to control neuronal growth and calcium signaling. Furthermore, deletion of the CaMK-like and L27 domains of CASK (CASK β null) or expression of overactive CaMKII (T287D) produced similar effects on synaptic growth and Ca(2+) signaling. CASK overexpression rescues the effects of CaMKII overactivity, consistent with the notion that CASK and CaMKII act in a common pathway that controls these neuronal processes. The reduction in Ca(2+) signaling observed in the CASK β null mutant caused a decrease in vesicle trafficking at synapses. In addition, the decrease in Ca(2+) signaling in CASK mutants was associated with an increase in Ether-à-go-go (EAG) potassium (K(+)) channel localization to synapses. Reducing EAG restored the decrease in Ca(2+) signaling observed in CASK mutants to the level of wildtype, suggesting that CASK regulates Ca(2+) signaling via EAG. CASK knockdown reduced both appetitive associative learning and odor evoked Ca(2+) responses in Drosophila mushroom bodies, which are the learning centers of Drosophila. Expression of human CASK in Drosophila rescued the effect of CASK deletion on the activity state of CaMKII, suggesting that human CASK may also regulate CaMKII autophosphorylation.
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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.