ArticleScientific reports2016
The molecular, temporal and region-specific requirements of the beta isoform of Calcium/Calmodulin-dependent protein kinase type 2 (CAMK2B) in mouse locomotion.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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19 citing papers in PubMed, 34 citations in OpenAlex.
- CaMKIIβ insufficiency disrupts cortical networks, producing aberrant low-gamma oscillations and seizure susceptibility.Epilepsia · 2026Article
- A chromosome region linked to neurodevelopmental disorders influences locomotor behavior through sex-specific neural circuits.Nature communications · 2026Article
- MuSK is a substrate for CaMK2β but this interaction is dispensable for MuSK activation in vivo.Scientific reports · 2025Article
- Pharmacological Enhancement of Adult Hippocampal Neurogenesis Improves Behavioral Pattern Separation in Young and Aged Male Mice.Biological psychiatry global open science · 2025Article
- CAMK2B Impacts the Proliferation, Invasion, and Migration of Glioma Cells via the Ras/Raf/MEK/ERK Signaling Pathway.Oncology research · 2025Article
- Role of CAMK2D in neurodevelopment and associated conditions.American journal of human genetics · 2024Article
- MiR-188-5p regulates the proliferation and differentiation of goat skeletal muscle satellite cells by targeting calcium/calmodulin dependent protein kinase II beta.Animal bioscience · 2023Article
- An Exploratory Data Analysis from Ovine and Bovine RNA-Seq Identifies Pathways and Key Genes Related to Cervical Dilatation.Animals : an open access journal from MDPI · 2023Article
- Role of CaFrontiers in molecular neuroscience · 2022Review
- Loss of CAMK2G affects intrinsic and motor behavior but has minimal impact on cognitive behavior.Frontiers in neuroscience · 2022Article
- CaMKIIβ in Neuronal Development and Plasticity: An Emerging Candidate in Brain Diseases.International journal of molecular sciences · 2020Review
- Hemispheric asymmetry in the human brain and in Parkinson's disease is linked to divergent epigenetic patterns in neurons.Genome biology · 2020Article
- A neuroscientist's guide to transgenic mice and other genetic tools.Neuroscience and biobehavioral reviews · 2020Review
- The Wnt/CaThe EMBO journal · 2019Article
- CAMK2-Dependent Signaling in Neurons Is Essential for Survival.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Localization of Retinal CaFrontiers in molecular neuroscience · 2019Article
- Article
- De Novo Mutations in Protein Kinase Genes CAMK2A and CAMK2B Cause Intellectual Disability.American journal of human genetics · 2017Article
- Article
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Authors and funding
5 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Genetic approaches using temporal and brain region-specific restricted gene deletions have provided a wealth of insight in the brain regions and temporal aspects underlying spatial and associative learning. However, for locomotion such extensive studies are still scarce. Previous studies demonstrated that Camk2b(-/-) mice, which lack the β isoform of Calcium/Calmodulin-dependent protein kinase 2 (CAMK2B), show very severe locomotion deficits. However, where these locomotion deficits originate is unknown. Here we made use of novel Camk2b mutants (Camk2b(f/f) and Camk2b(T287A)), to explore the molecular, temporal and brain region-specific requirements of CAMK2B for locomotion. At the molecular level we found that normal locomotion requires Calcium/Calmodulin mediated activation of CAMK2B, but CAMK2B autonomous activity is largely dispensable. At a systems level, we found that global deletion of Camk2b in the adult mouse causes only mild locomotion deficits, suggesting that the severe locomotion deficits of Camk2b(-/-) mice are largely of developmental origin. However, early onset deletion of Camk2b in cerebellum, striatum or forebrain did not recapitulate the locomotion deficits, suggesting that these deficits cannot be attributed to a single brain area. Taken together, these results provide the first insights into the molecular, temporal and region-specific role of CAMK2B in locomotion.
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