ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009
Transient receptor potential canonical 5 channels activate Ca2+/calmodulin kinase Igamma to promote axon formation in hippocampal neurons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
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Who cites it
54 citing papers in PubMed, 87 citations in OpenAlex.
- Molecular architecture of the human TRPC1/C5 heteromeric channel.Nature communications · 2025Article
- The SphK1/S1P Axis Regulates Synaptic Vesicle Endocytosis via TRPC5 Channels.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Article
- A Role for Second Messengers in Axodendritic Neuronal Polarity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Review
- Lipidation states orchestrate CLICK-III/CaMKIγ's stepwise association with Golgi and rafts-enriched membranes and specify its functional coupling to STEF-Rac1-dependent neurite extension.Frontiers in cellular neuroscience · 2023Article
- Prox1 inhibits neurite outgrowth during central nervous system development.Cellular and molecular life sciences : CMLS · 2021Article
- Role of Oxidative Stress and CaFrontiers in cell and developmental biology · 2021Review
- TRPC1 Regulates the Activity of a Voltage-Dependent Nonselective Cation Current in Hippocampal CA1 Neurons.Cells · 2020Article
- TRP Channels Regulation of Rho GTPases in Brain Context and Diseases.Frontiers in cell and developmental biology · 2020Review
- Neuronal Signaling Involved in Neuronal Polarization and Growth: Lipid Rafts and Phosphorylation.Frontiers in molecular neuroscience · 2020Article
- Evidence of a Role for the TRPC Subfamily in Mediating Oxidative Stress in Parkinson's Disease.Frontiers in physiology · 2020Review
- Purinergic Signaling Pathway in Human Olfactory Neuronal Precursor Cells.Stem cells international · 2019Article
- Differential regulation of ion channels function by proteolysis.Biochimica et biophysica acta. Molecular cell research · 2018Review
- Heteromeric channels formed by TRPC1, TRPC4 and TRPC5 define hippocampal synaptic transmission and working memory.The EMBO journal · 2017Article
- A Feed-Forward Mechanism Involving the NOX Complex and RyR-Mediated Ca2+ Release During Axonal Specification.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2016Article
- TRPC Channels: Prominent Candidates of Underlying Mechanism in Neuropsychiatric Diseases.Molecular neurobiology · 2016Review
- Increased expression of TRPC5 in cortical lesions of the focal cortical dysplasia.Journal of molecular neuroscience : MN · 2015Article
- Acute Treatment with a Novel TRPC4/C5 Channel Inhibitor Produces Antidepressant and Anxiolytic-Like Effects in Mice.PloS one · 2015Article
- Mechanochemical regulation of growth cone motility.Frontiers in cellular neuroscience · 2015Review
- Article
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
Abstract
Functionality of neurons is dependent on their compartmentalized polarization of dendrites and an axon. The rapid and selective outgrowth of one neurite, relative to the others, to form the axon is critical in initiating neuronal polarity. Axonogenesis is regulated in part by an optimal intracellular calcium concentration. Our investigation of Ca(2+)-signaling pathways involved in axon formation using cultured hippocampal neurons demonstrates a role for Ca(2+)/calmodulin kinase kinase (CaMKK) and its downstream target Ca(2+)/calmodulin kinase I (CaMKI). Expression of constitutively active CaMKI induced formation of multiple axons, whereas blocking CaMKK or CaMKI activity with pharmacological, dominant-negative, or short hairpin RNA (shRNA) methods significantly inhibited axon formation. CaMKK signals via the gamma-isoform of CaMKI as shRNA to CaMKIgamma, but not the other CaMKI isoforms, inhibited axon formation. Furthermore, overexpression of wild-type CaMKIgamma, but not a mutant incapable of membrane association, accelerated the rate of axon formation. Pharmacological or small interfering RNA inhibition of transient receptor potential canonical 5 (TRPC5) channels, which are present in developing axonal growth cones, suppressed CaMKK-mediated activation of CaMKIgamma as well as axon formation. We demonstrate using biochemical fractionation and immunocytochemistry that CaMKIgamma and TRPC5 colocalize to lipid rafts. These results are consistent with a model in which highly localized calcium influx through the TRPC5 channels activates CaMKK and CaMKIgamma, which subsequently promote axon formation.
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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.