ArticleFrontiers in cellular neuroscience2017
Postnatal Loss of Neuronal and Glial Neurofascins Differentially Affects Node of Ranvier Maintenance and Myelinated Axon Function.
Article in Frontiers in cellular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 30 citations in OpenAlex.
- Purkinje cell-specific loss of Neurofascin and Ankyrin G causes disruption of axon initial segments, neurodegeneration, and cerebellar ataxia.Frontiers in cellular neuroscience · 2026Article
- Antibody-Mediated Nodo- and Paranodopathies.Journal of clinical medicine · 2024Review
- Mouse models of human CNTNAP1-associated congenital hypomyelinating neuropathy and genetic restoration of murine neurological deficits.Cell reports · 2023Article
- Clinical profile of autoimmune nodopathy with anti-neurofascin 186 antibody.Annals of clinical and translational neurology · 2023Article
- Anti-pan-neurofascin antibodies induce subclass-related complement activation and nodo-paranodal damage.Brain : a journal of neurology · 2023Article
- Schwann cell nodal membrane disruption triggers bystander axonal degeneration in a Guillain-Barré syndrome mouse model.The Journal of clinical investigation · 2022Article
- Neurofascin antibodies in chronic inflammatory demyelinating polyradiculoneuropathy: from intrinsic genetic background to clinical manifestations.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Review
- Impact of Neurofascin on Chronic Inflammatory Demyelinating PolyneuropathyFrontiers in molecular neuroscience · 2021Review
- Focal loss of the paranodal domain protein Neurofascin155 in the internal capsule impairs cortically induced muscle activity in vivo.Molecular brain · 2020Article
- Accumulation of Neurofascin at Nodes of Ranvier Is Regulated by a Paranodal Switch.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2020Article
- Review
- Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo.The Journal of clinical investigation · 2019Article
- Ablation of cytoskeletal scaffolding proteins, Band 4.1B and Whirlin, leads to cerebellar purkinje axon pathology and motor dysfunction.Journal of neuroscience research · 2019Article
- Glial Sulfatides and Neuronal Complex Gangliosides Are Functionally Interdependent in Maintaining Myelinating Axon Integrity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Dysregulation of schizophrenia-related aquaporin 3 through disruption of paranode influences neuronal viability.Journal of neurochemistry · 2018Article
- Genome-Wide Association Study of Circadian Rhythmicity in 71,500 UK Biobank Participants and Polygenic Association with Mood Instability.EBioMedicine · 2018Article
- Reorganization of Destabilized Nodes of Ranvier in βThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Glial βII Spectrin Contributes to Paranode Formation and Maintenance.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- mTORC1 Activation by Loss ofFrontiers in cellular neuroscience · 2018Article
- Regulation and dysregulation of axon infrastructure by myelinating glia.The Journal of cell biology · 2017Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Intricate molecular interactions between neurons and glial cells underlie the creation of unique domains that are essential for saltatory conduction of action potentials by myelinated axons. Previously, the cell surface adhesion molecule Neurofascin (Nfasc) has been shown to have a dual-role in the establishment of axonal domains from both the glial and neuronal interface. While the neuron-specific isoform of Neurofascin (NF186) is indispensable for clustering of voltage-gated sodium channels at nodes of Ranvier; the glial-specific isoform of Neurofascin (NF155) is required for myelinating glial cells to organize the paranodal domain. Although many studies have addressed the individual roles of NF155 and NF186 in assembling paranodes and nodes, respectively; critical questions about their roles in the maintenance and long-term health of the myelinated axons remain, which we aimed to address in these studies. Here using spatiotemporal ablation of Neurofascin in neurons alone or together with myelinating glia, we report that loss of NF186 individually from postnatal mice leads to progressive nodal destabilization and axonal degeneration. While individual ablation of paranodal NF155 does not disrupt nodes of Ranvier; loss of NF186 combined with NF155 causes more accelerated nodal destabilization than loss of NF186 alone, providing strong evidence regarding a supporting role for paranodes in nodal maintenance. In both cases of NF186 loss, myelinating axons show ultrastructural changes and degeneration. Our studies reveal that long-term maintenance of nodes and ultimately the health of axons is correlated with the stability of NF186 within the nodal complex and the presence of auxiliary paranodes.
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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.