ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
In vivo deletion of immunoglobulin domains 5 and 6 in neurofascin (Nfasc) reveals domain-specific requirements in myelinated axons.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers.
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Who cites it
39 citing papers in PubMed, 54 citations in OpenAlex.
- Chronic Inflammatory Demyelinating Polyneuropathy (CIDP): A Comprehensive Review of Types, Pathophysiology, and Treatment Approaches.Brain and behavior · 2026Review
- Purkinje cell-specific loss of Neurofascin and Ankyrin G causes disruption of axon initial segments, neurodegeneration, and cerebellar ataxia.Frontiers in cellular neuroscience · 2026Article
- A Novel Mutation in CNTNAP1 Gene Causes Disorganization of Axonal Domains, Hypomyelination and Severe Neurological Deficits.Journal of neuroscience research · 2025Article
- Mouse models of human CNTNAP1-associated congenital hypomyelinating neuropathy and genetic restoration of murine neurological deficits.Cell reports · 2023Article
- Anti-pan-neurofascin antibodies induce subclass-related complement activation and nodo-paranodal damage.Brain : a journal of neurology · 2023Article
- Altered plasma membrane abundance of the sulfatide-binding protein NF155 links glycosphingolipid imbalances to demyelination.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Structural insights into the contactin 1 - neurofascin 155 adhesion complex.Nature communications · 2022Article
- Developmental Cues and Molecular Drivers in Myelinogenesis: Revisiting Early Life to Re-Evaluate the Integrity of CNS Myelin.Current issues in molecular biology · 2022Review
- Gene and protein expression profiles of olfactory ensheathing cells from olfactory bulbNeural regeneration research · 2022Article
- From PNS to CNS: characteristics of anti-neurofascin 186 neuropathy in 16 cases.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2021Article
- Distinguish CIDP with autoantibody from that without autoantibody: pathogenesis, histopathology, and clinical features.Journal of neurology · 2021Review
- 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
- Deletion of the Thrombin Proteolytic Site in Neurofascin 155 Causes Disruption of Nodal and Paranodal Organization.Frontiers in cellular neuroscience · 2021Article
- Focal loss of the paranodal domain protein Neurofascin155 in the internal capsule impairs cortically induced muscle activity in vivo.Molecular brain · 2020Article
- mNeuron · 2020Article
- Anti-Neurofascin-155 IgG4 antibodies prevent paranodal complex formation in vivo.The Journal of clinical investigation · 2019Article
- Regulation of myelin structure and conduction velocity by perinodal astrocytes.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Genome-Wide Association Study of Circadian Rhythmicity in 71,500 UK Biobank Participants and Polygenic Association with Mood Instability.EBioMedicine · 2018Article
- Autoantibodies Against the Node of Ranvier in Seropositive Chronic Inflammatory Demyelinating Polyneuropathy: Diagnostic, Pathogenic, and Therapeutic Relevance.Frontiers in immunology · 2018Review
- Expanding the genetic heterogeneity of intellectual disability.Human genetics · 2017Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
Abstract
The formation of paranodal axo-glial junctions is critical for the rapid and efficient propagation of nerve impulses. Genetic ablation of genes encoding the critical paranodal proteins Caspr, contactin (Cont), and the myelinating glia-specific isoform of Neurofascin (Nfasc(NF155)) results in the disruption of the paranodal axo-glial junctions, loss of ion channel segregation, and impaired nerve conduction, but the mechanisms regulating their interactions remain elusive. Here, we report that loss of immunoglobulin (Ig) domains 5 and 6 in Nfasc(NF155) in mice phenocopies complete ablation of Nfasc(NF155). The mutant mice lack paranodal septate junctions, resulting in the diffusion of Caspr and Cont from the paranodes, and redistribution of the juxtaparanodal potassium channels toward the nodes. Although critical for Nfasc(NF155) function, we find that Ig5-6 are dispensable for nodal Nfasc(NF186) function. Moreover, in vitro binding assays using Ig5-6 deletion constructs reveal their importance for the association of Nfasc(NF155) with Cont. These findings provide the first molecular evidence demonstrating domain-specific requirements controlling the association of the paranodal tripartite complex in vivo. Our studies further emphasize that in vivo structure/function analysis is necessary to define the unique protein-protein interactions that differentially regulate the functions of Neurofascins during axonal domain organization.
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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.