Calmodulin-kinases: modulators of neuronal development and plasticity.
Open accessAbstract
In the nervous system, many intracellular responses to elevated calcium are mediated by CaM kinases (CaMKs), a family of protein kinases whose activities are initially modulated by binding Ca(2+)/calmodulin and subsequently by protein phosphorylation. One member of this family, CaMKII, is well-established for its effects on modulating synaptic plasticity and learning and memory. However, recent studies indicate that some actions on neuronal development and function attributed to CaMKII may instead or in addition be mediated by other members of the CaMK cascade, such as CaMKK, CaMKI, and CaMKIV. This review summarizes key neuronal functions of the CaMK cascade in signal transduction, gene transcription, synaptic development and plasticity, and behavior. The technical challenges of mapping cellular protein kinase signaling pathways are also discussed.
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This rephosphorylation was blocked by KT5720 (1 μM), a PKA inhibitor, but not by KN-93 (10 μM) and PD98059 (25 μM).
“This rephosphorylation was blocked by KT5720 (1 µM), a PKA inhibitor, but not by KN-93 (10 µM) and PD98059 (25 µM), which inhibit CaM kinases [41] and MEK, respectively (Figure 3F).”
From Regulated RalBP1 Binding to RalA and PSD-95 Controls AMPA Receptor Endocytosis and LTD (2009) · cites this paper as [41]
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- Authors
- Wayman, G. A., Lee, Y.-S., Tokumitsu, H., Silva, A., & Soderling, T. R.
- Affiliations
- Oregon Health & Science University (US)
- University of California, Los Angeles (US)
- Kagawa University (JP)
- Corresponding author
- Soderling, Thomas R.
- Venue
- Neuron
- Publisher
- Elsevier BV
- Published
- 2008-09
- Volume
- 59
- Issue
- 6
- Pages
- 914-931
- ISSN
- 0896-6273 (ISSN-L)
- PMC
- PMC2664743
- OpenAlex
- W2024035512
- Cited by
- 567
- References
- 15
- Citations by year
- 2026: 22 · 2025: 22 · 2024: 20 · 2023: 19 · 2022: 19 · 2021: 25 · 2020: 27 · 2019: 32 · 2018: 32 · 2017: 21 · 2016: 33 · 2015: 25 · 2014: 32 · 2013: 43 · 2012: 46
- FWCI
- 4.28
- Type
- journal article
- Language
- en
- Update notices
- erratum (2009-11-25)
- Open access
- bronze
- doi.org
- Licence
- www.elsevier.com/tdm/userlicense/1.0/ (tdm)
- www.elsevier.com/legal/tdmrep-license (tdm)
- www.elsevier.com/open-access/userlicense/1.0/ (vor, 1816 d)
- doi.org/10.15223/policy-017 (stm-asf)
- doi.org/10.15223/policy-037 (stm-asf)
- doi.org/10.15223/policy-012 (stm-asf)
- doi.org/10.15223/policy-029 (stm-asf)
- doi.org/10.15223/policy-004 (stm-asf)
- Locations
- Neuron (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Aging (R01AG013622)
- National Institute of General Medical Sciences (R01GM041292)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Signaling Pathways in Disease
- Keywords
- calcium/calmodulin-dependent protein kinase, CaMKII, CaMKI, CaMKIV, CaMKK, neuronal development, synaptic plasticity, learning and memory, calcium signaling, protein phosphorylation, gene transcription, signal transduction, synaptic development, behavior
- MeSH terms
- Animals, Cell Differentiation, Humans, Neuronal Plasticity, Neurons, Structure-Activity Relationship, Second Messenger Systems, Signal Transduction, Calcium-Calmodulin-Dependent Protein Kinases, Calcium Signaling
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