ArticleNature communications2014
Fragile X mental retardation protein controls synaptic vesicle exocytosis by modulating N-type calcium channel density.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 95 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
95 citing papers in PubMed, 134 citations in OpenAlex.
- Contribution of astrocytic calcium signaling to auditory hypersensitivity in a mouse model of fragile X syndrome.Neurobiology of disease · 2026Article
- Gene Therapy for Fragile X Syndrome, Challenges, and Promises.The journal of gene medicine · 2025Review
- Stress-Induced Membraneless Organelles in Neurons: Bridging Liquid-Liquid Phase Separation and Neurodevelopmental Dysfunction.International journal of molecular sciences · 2025Review
- Neuronal potassium channel activity triggers initiation of mRNA translation through binding of translation regulators.Science advances · 2025Article
- Early postnatal exposure to bicuculline modulates E/I balance and induces ASD-like behavioral phenotypes in mice.Animal cells and systems · 2025Article
- Molecular Profiling of Mouse Models of Loss or Gain of Function of the KCNT1 (Slack) Potassium Channel and Antisense Oligonucleotide Treatment.Biomolecules · 2024Article
- Region-Related Differences in Short-Term Synaptic Plasticity and Synaptotagmin-7 in the Male and Female Hippocampus of a Rat Model of Fragile X Syndrome.International journal of molecular sciences · 2024Article
- Functional remodeling of presynaptic voltage-gated calcium channels in superficial layers of the dorsal horn during neuropathic pain.iScience · 2024Article
- Astroglial Kir4.1 potassium channel deficit drives neuronal hyperexcitability and behavioral defects in Fragile X syndrome mouse model.Nature communications · 2024Article
- Fragile X Messenger Ribonucleoprotein Protein and Its Multifunctionality: From Cytosol to Nucleolus and Back.Biomolecules · 2024Review
- Review
- Characterization of Fragile X Mental Retardation Protein expression in human nociceptors and their axonal projections to the spinal dorsal horn.The Journal of comparative neurology · 2023Article
- The activation of mGluR4 rescues parallel fiber synaptic transmission and LTP, motor learning and social behavior in a mouse model of Fragile X Syndrome.Molecular autism · 2023Article
- Axonal and presynaptic FMRP: Localization, signal, and functional implications.Hearing research · 2023Review
- Efficient Delivery ofGenes · 2023Article
- Directly reprogrammed fragile X syndrome dorsal forebrain precursor cells generate cortical neurons exhibiting impaired neuronal maturation.Frontiers in cellular neuroscience · 2023Article
- From circuits to behavior: Amygdala dysfunction in fragile X syndrome.Frontiers in integrative neuroscience · 2023Review
- Deletion of Fmr1 in parvalbumin-expressing neurons results in dysregulated translation and selective behavioral deficits associated with fragile X syndrome.Molecular autism · 2022Article
- Mechanisms Driving the Emergence of Neuronal Hyperexcitability in Fragile X Syndrome.International journal of molecular sciences · 2022Review
- The role of altered translation in intellectual disability and epilepsy.Progress in neurobiology · 2022Review
35 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Fragile X syndrome (FXS), the most common heritable form of mental retardation, is characterized by synaptic dysfunction. Synaptic transmission depends critically on presynaptic calcium entry via voltage-gated calcium (Ca(V)) channels. Here we show that the functional expression of neuronal N-type Ca(V) channels (Ca(V)2.2) is regulated by fragile X mental retardation protein (FMRP). We find that FMRP knockdown in dorsal root ganglion neurons increases Ca(V) channel density in somata and in presynaptic terminals. We then show that FMRP controls Ca(V)2.2 surface expression by targeting the channels to the proteasome for degradation. The interaction between FMRP and Ca(V)2.2 occurs between the carboxy-terminal domain of FMRP and domains of Ca(V)2.2 known to interact with the neurotransmitter release machinery. Finally, we show that FMRP controls synaptic exocytosis via Ca(V)2.2 channels. Our data indicate that FMRP is a potent regulator of presynaptic activity, and its loss is likely to contribute to synaptic dysfunction in FXS.
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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.