ArticleProceedings of the National Academy of Sciences of the United States of America2007
Deletion of CASK in mice is lethal and impairs synaptic function.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 122 papers.
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Who cites it
122 citing papers in PubMed, 211 citations in OpenAlex.
- The development of FEDUPP: feeding experimentation device users processing package to assess learning and cognitive flexibility.Translational psychiatry · 2026Article
- Cerebellar hypoplasia caused by calcium/calmodulin-dependent serine protein kinase deficiency.Molecules and cells · 2026Review
- Neurological Effects ofNutrients · 2026Article
- CASK hypomorph mice display cone photoreceptor dysfunction.bioRxiv : the preprint server for biology · 2026Article
- Patient-Derived Variants Define Constraints for Ligand Binding at the PDZ Domain of CASK.Journal of neurochemistry · 2025Article
- CASKIN2 mediates PTPσ-orchestrated transsynaptic mechanisms at excitatory synapses.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cardioprotective effects of semaglutide on isolated human ventricular myocardium.European journal of heart failure · 2025Article
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- Genetic evidence for splicing-dependent structural and functional plasticity in CASK protein.Journal of medical genetics · 2024Article
- Analyses of the autism-associated neuroligin-3 R451C mutation in human neurons reveal a gain-of-function synaptic mechanism.Molecular psychiatry · 2024Article
- Review
- Regulation of interferon alpha production by the MAGUK-family protein CASK under H5N1 infection.Frontiers in immunology · 2024Article
- Drosophila CASK regulates brain size and neuronal morphogenesis, providing a genetic model of postnatal microcephaly suitable for drug discovery.Neural development · 2023Article
- Diverse Clinical Phenotypes ofGenes · 2023Review
- An impaired splicing program underlies differentiation defects in hSOD1Cellular and molecular life sciences : CMLS · 2023Article
- Calcium/Calmodulin-Dependent Serine Protein Kinase (Animals : an open access journal from MDPI · 2023Article
- Microglial targeted therapy relieves cognitive impairment caused byExploration (Beijing, China) · 2023Article
- Article
- Hypoxic Preconditioned Neural Stem Cell-Derived Extracellular Vesicles Contain Distinct Protein Cargo from Their Normal Counterparts.Current issues in molecular biology · 2023Article
62 more citing papers are in PubMed but not listed here.
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
CASK is an evolutionarily conserved multidomain protein composed of an N-terminal Ca2+/calmodulin-kinase domain, central PDZ and SH3 domains, and a C-terminal guanylate kinase domain. Many potential activities for CASK have been suggested, including functions in scaffolding the synapse, in organizing ion channels, and in regulating neuronal gene transcription. To better define the physiological importance of CASK, we have now analyzed CASK "knockdown" mice in which CASK expression was suppressed by approximately 70%, and CASK knockout (KO) mice, in which CASK expression was abolished. CASK knockdown mice are viable but smaller than WT mice, whereas CASK KO mice die at first day after birth. CASK KO mice exhibit no major developmental abnormalities apart from a partially penetrant cleft palate syndrome. In CASK-deficient neurons, the levels of the CASK-interacting proteins Mints, Veli/Mals, and neurexins are decreased, whereas the level of neuroligin 1 (which binds to neurexins that in turn bind to CASK) is increased. Neurons lacking CASK display overall normal electrical properties and form ultrastructurally normal synapses. However, glutamatergic spontaneous synaptic release events are increased, and GABAergic synaptic release events are decreased in CASK-deficient neurons. In contrast to spontaneous neurotransmitter release, evoked release exhibited no major changes. Our data suggest that CASK, the only member of the membrane-associated guanylate kinase protein family that contains a Ca2+/calmodulin-dependent kinase domain, is required for mouse survival and performs a selectively essential function without being in itself required for core activities of neurons, such as membrane excitability, Ca2+-triggered presynaptic release, or postsynaptic receptor functions.
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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.