ArticleThe Journal of biological chemistry2009
Ca2+/calmodulin-dependent protein kinase IV links group I metabotropic glutamate receptors to fragile X mental retardation protein in cingulate cortex.
Article in The Journal of biological chemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 22 citations in OpenAlex.
- Decreased H3K79 acetylation and dysregulation of neurodevelopmental genes in fetal down syndrome.Translational pediatrics · 2026Article
- Research advances on CaMKs-mediated neurodevelopmental injury.Archives of toxicology · 2024Review
- Acamprosate in a mouse model of fragile X syndrome: modulation of spontaneous cortical activity, ERK1/2 activation, locomotor behavior, and anxiety.Journal of neurodevelopmental disorders · 2017Article
- Aquaporin 4-Mediated Glutamate-Induced Astrocyte Swelling Is Partially Mediated through Metabotropic Glutamate Receptor 5 Activation.Frontiers in cellular neuroscience · 2017Article
- Neuron class-specific requirements for Fragile X Mental Retardation Protein in critical period development of calcium signaling in learning and memory circuitry.Neurobiology of disease · 2016Article
- Synaptic Plasticity, a Prominent Contributor to the Anxiety in Fragile X Syndrome.Neural plasticity · 2016Review
- Independent role for presynaptic FMRP revealed by an FMR1 missense mutation associated with intellectual disability and seizures.Proceedings of the National Academy of Sciences of the United States of America · 2015Article
- Gestational and early postnatal hypothyroidism alters VGluT1 and VGAT bouton distribution in the neocortex and hippocampus, and behavior in rats.Frontiers in neuroanatomy · 2015Article
- Common variants in genes of the postsynaptic FMRP signalling pathway are risk factors for autism spectrum disorders.Human genetics · 2014Article
- An evo-devo approach to thyroid hormones in cerebral and cerebellar cortical development: etiological implications for autism.Frontiers in endocrinology · 2014Review
- Roles of CREB in the regulation of FMRP by group I metabotropic glutamate receptors in cingulate cortex.Molecular brain · 2012Article
- Therapeutic strategies in fragile X syndrome: dysregulated mGluR signaling and beyond.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Review
- Group I metabotropic glutamate receptor-mediated gene transcription and implications for synaptic plasticity and diseases.Frontiers in pharmacology · 2012Article
- Evidence of mitochondrial dysfunction in fragile X-associated tremor/ataxia syndrome.The Biochemical journal · 2010Article
- Roles of fragile X mental retardation protein in dopaminergic stimulation-induced synapse-associated protein synthesis and subsequent alpha-amino-3-hydroxyl-5-methyl-4-isoxazole-4-propionate (AMPA) receptor internalization.The Journal of biological chemistry · 2010Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fragile X syndrome is caused by a lack of fragile X mental retardation protein (FMRP) due to silencing of the FMR1 gene. The metabotropic glutamate receptors (mGluRs) in the central nervous system contribute to higher brain functions including learning/memory, persistent pain, and mental disorders. Our recent study has shown that activation of Group I mGluR up-regulated FMRP in anterior cingulate cortex (ACC), a key region for brain cognitive and executive functions; Ca(2+) signaling pathways could be involved in the regulation of FMRP by Group I mGluRs. In this study we demonstrate that stimulating Group I mGluRs activates Ca(2+)/calmodulin-dependent protein kinase IV (CaMKIV) in ACC neurons. In ACC neurons of adult mice overexpressing CaMKIV, the up-regulation of FMRP by stimulating Group I mGluR is enhanced. The enhancement occurs at the transcriptional level as the Fmr1 mRNA level was further elevated compared with wild-type mice. Using pharmacological approaches, we found that inhibition of CaMKIV could attenuate the up-regulation of FMRP by Group I mGluRs. CaMKIV contribute to the regulation of FMRP by Group I mGluRs probably through cyclic AMP-responsive element binding protein (CREB) activation, as manipulation of CaMKIV could simultaneously cause the change of CREB phosphorylation induced by Group I mGluR activation. Our study has provided strong evidence for CaMKIV as a molecular link between Group I mGluRs and FMRP in ACC neurons and may help us to elucidate the pathogenesis of fragile X syndrome.
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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.