ArticleScientific reports2015
Neurogranin regulates CaM dynamics at dendritic spines.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers, 2 of them syntheses that pooled it.
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Who cites it
33 citing papers in PubMed, 2 syntheses or guidelines pooled it, 62 citations in OpenAlex.
- Associations between cerebrospinal fluid markers and cognition in ageing and dementia: A systematic review.The European journal of neuroscience · 2022Pooled it
- Neurogranin and VILIP-1 as Molecular Indicators of Neurodegeneration in Alzheimer's Disease: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2020Pooled it
- Longitudinal Alterations in Sleep EEG Biomarkers of Memory Consolidation in Middle-Aged and Older Adults.bioRxiv : the preprint server for biology · 2026Article
- Neurogranin negatively regulates gene expression and proinflammatory mediator release in allergen-activated mast cells.ImmunoHorizons · 2026Article
- CaMK2rep: A Highly Sensitive Genetically Encoded Biosensor for Monitoring CaMKII Activity in Mammalian Cells.Analytical chemistry · 2025Article
- HDAC4 Inhibits NMDA Receptor-mediated Stimulation of Neurogranin Expression.Molecular neurobiology · 2025Article
- CSF neurogranin levels as a biomarker in Alzheimer's disease and frontotemporal lobar degeneration: a cross-sectional analysis.Alzheimer's research & therapy · 2024Article
- Temporal-Specific Sex and Injury-Dependent Changes on Neurogranin-Associated Synaptic Signaling After Controlled Cortical Impact in Rats.Molecular neurobiology · 2024Article
- TauCell death & disease · 2024Article
- Molecular Characterization of Neurogranin (NRGN) Gene from Red‑Bellied Pacu (Piaractus brachypomus).Molecular neurobiology · 2024Article
- Monitoring synaptic pathology in Alzheimer's disease through fluid and PET imaging biomarkers: a comprehensive review and future perspectives.Molecular psychiatry · 2024Review
- Calcium- and calmodulin-dependent inhibition of NMDA receptor currents.Biophysical journal · 2024Review
- Alzheimer's Disease beyond Calcium Dysregulation: The Complex Interplay between Calmodulin, Calmodulin-Binding Proteins and Amyloid Beta from Disease Onset through Progression.Current issues in molecular biology · 2023Review
- Molecular Biomarkers of Neuronal Injury in Epilepsy Shared with Neurodegenerative Diseases.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Pathological (Dis)Similarities in Neuronal Exosome-Derived Synaptic and Organellar Marker Levels Between Alzheimer's Disease and Frontotemporal Dementia.Journal of Alzheimer's disease : JAD · 2023Article
- Neurogranin regulates calcium-dependent cardiac hypertrophy.Experimental and molecular pathology · 2022Article
- Neurogranin and Neuronal Pentraxin Receptor as Synaptic Dysfunction Biomarkers in Alzheimer's Disease.Journal of clinical medicine · 2021Article
- Synaptic tau: A pathological or physiological phenomenon?Acta neuropathologica communications · 2021Review
- Neurogranin Regulates Adult-Born Olfactory Granule Cell Spine Density and Odor-Reward Associative Memory in Mice.International journal of molecular sciences · 2021Article
- Cerebrospinal Fluid Biomarkers of Alzheimer's Disease: Current Evidence and Future Perspectives.Brain sciences · 2021Review
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Calmodulin (CaM) plays a key role in synaptic function and plasticity due to its ability to mediate Ca(2+) signaling. Therefore, it is essential to understand the dynamics of CaM at dendritic spines. In this study we have explored CaM dynamics using live-cell confocal microscopy and fluorescence recovery after photobleaching (FRAP) to study CaM diffusion. We find that only a small fraction of CaM in dendritic spines is immobile. Furthermore, the diffusion rate of CaM was regulated by neurogranin (Ng), a CaM-binding protein enriched at dendritic spines. Interestingly, Ng did not influence the immobile fraction of CaM at recovery plateau. We have previously shown that Ng enhances synaptic strength in a CaM-dependent manner. Taken together, these data indicate that Ng-mediated enhancement of synaptic strength is due to its ability to target, rather than sequester, CaM within dendritic spines.
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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.