ArticleNeuron2011
Nodes of Ranvier act as barriers to restrict invasion of flanking paranodal domains in myelinated axons.
Article in Neuron, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers, 1 of them a synthesis that pooled it.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
52 citing papers in PubMed, 1 synthesis or guideline pooled it, 81 citations in OpenAlex.
- Association of neurofascin IgG4 and atypical chronic inflammatory demyelinating polyneuropathy: A systematic review and meta-analysis.Brain and behavior · 2018Pooled it
- Branching of O-mannose glycans regulates node of Ranvier organization and saltatory conduction.Communications biology · 2026Article
- Neurofascin Antibodies in a Large Cohort of Inflammatory Neuropathies from India.Annals of Indian Academy of Neurology · 2026Article
- Autoimmune nodopathy and focal segmental glomerulosclerosis mediated by anti-NF186 antibody: a case report and literature review.BMC neurology · 2026Review
- Clinical and immunological features of auto-immune nodopathies.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2026Article
- Purkinje cell-specific loss of Neurofascin and Ankyrin G causes disruption of axon initial segments, neurodegeneration, and cerebellar ataxia.Frontiers in cellular neuroscience · 2026Article
- Article
- A Novel Mutation in CNTNAP1 Gene Causes Disorganization of Axonal Domains, Hypomyelination and Severe Neurological Deficits.Journal of neuroscience research · 2025Article
- 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
- Compromised Myelin and Axonal Molecular Organization Following Adult-Onset Sulfatide Depletion.Biomedicines · 2023Article
- Paraneoplastic Syndrome Presenting Combined Central and Peripheral Demyelination Associated with Anti-CV2/CRMP5 and Anti-NF186 Antibodies: A Case Report.Brain sciences · 2023Article
- Distinguish CIDP with autoantibody from that without autoantibody: pathogenesis, histopathology, and clinical features.Journal of neurology · 2021Review
- Impact of Neurofascin on Chronic Inflammatory Demyelinating PolyneuropathyFrontiers in molecular neuroscience · 2021Review
- Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021Review
- Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo.The Journal of clinical investigation · 2019Article
- Astrocytic connexin 43 potentiates myelin injury in ischemic white matter disease.Theranostics · 2019Article
- Diagnostic insights into chronic-inflammatory demyelinating polyneuropathies.Annals of translational medicine · 2018Review
- Reorganization of Destabilized Nodes of Ranvier in βThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Accumulation of voltage-gated sodium (Na(v)) channels at nodes of Ranvier is paramount for action potential propagation along myelinated fibers, yet the mechanisms governing nodal development, organization, and stabilization remain unresolved. Here, we report that genetic ablation of the neuron-specific isoform of Neurofascin (Nfasc(NF¹⁸⁶)) in vivo results in nodal disorganization, including loss of Na(v) channel and ankyrin-G (AnkG) enrichment at nodes in the peripheral nervous system (PNS) and central nervous system (CNS). Interestingly, the presence of paranodal domains failed to rescue nodal organization in the PNS and the CNS. Most importantly, using ultrastructural analysis, we demonstrate that the paranodal domains invade the nodal space in Nfasc(NF¹⁸⁶) mutant axons and occlude node formation. Our results suggest that Nfasc(NF¹⁸⁶)-dependent assembly of the nodal complex acts as a molecular boundary to restrict the movement of flanking paranodal domains into the nodal area, thereby facilitating the stereotypic axonal domain organization and saltatory conduction along myelinated axons.
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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.