ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2010
Organization of myelinated axons by Caspr and Caspr2 requires the cytoskeletal adapter protein 4.1B.
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 68 papers.
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Who cites it
68 citing papers in PubMed, 108 citations in OpenAlex.
- CNTNAP2: isoform- and context-specific functions in neurological disorders and cancer.Frontiers in cellular neuroscience · 2026Review
- Paranodal instability driven by axonal mitochondrial accumulation in ischemic demyelination and cognitive decline.Molecular psychiatry · 2025Article
- Identification of candidate genes involved in Zika virus-induced reversible paralysis of mice.Scientific reports · 2025Article
- Age-dependent regulation of axoglial interactions and behavior by oligodendrocyte AnkyrinG.Nature communications · 2024Article
- Biallelic EPB41L3 variants underlie a developmental disorder with seizures and myelination defects.Brain : a journal of neurology · 2024Article
- Age-dependent regulation of axoglial interactions and behavior by oligodendrocyte AnkyrinG.bioRxiv : the preprint server for biology · 2024Article
- Glia trigger endocytic clearance of axonal proteins to promote rodent myelination.Developmental cell · 2024Article
- A class-specific effect of dysmyelination on the excitability of hippocampal interneurons.eLife · 2023Article
- LGI3/2-ADAM23 interactions cluster Kv1 channels in myelinated axons to regulate refractory period.The Journal of cell biology · 2023Article
- The Role of Cytoskeleton Protein 4.1 in Immunotherapy.International journal of molecular sciences · 2023Review
- Pathology of Initial Axon Segments in Chronic Inflammatory Demyelinating Polyradiculoneuropathy and Related Disorders.International journal of molecular sciences · 2022Review
- Review
- Cortical overgrowth in a preclinical forebrain organoid model of CNTNAP2-associated autism spectrum disorder.Nature communications · 2021Article
- A CADM3 variant causes Charcot-Marie-Tooth disease with marked upper limb involvement.Brain : a journal of neurology · 2021Article
- Differential Contribution of Cadm1-Cadm3 Cell Adhesion Molecules to Peripheral Myelinated Axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Implication of Contactins in Demyelinating Pathologies.Life (Basel, Switzerland) · 2021Review
- Impact of Neurofascin on Chronic Inflammatory Demyelinating PolyneuropathyFrontiers in molecular neuroscience · 2021Review
- Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021Review
- Assembly and Function of the Juxtaparanodal Kv1 Complex in Health and Disease.Life (Basel, Switzerland) · 2020Review
- Review
8 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
Caspr and Caspr2 regulate the formation of distinct axonal domains around the nodes of Ranvier. Caspr is required for the generation of a membrane barrier at the paranodal junction (PNJ), whereas Caspr2 serves as a membrane scaffold that clusters Kv1 channels at the juxtaparanodal region (JXP). Both Caspr and Caspr2 interact with protein 4.1B, which may link the paranodal and juxtaparanodal adhesion complexes to the axonal cytoskeleton. To determine the role of protein 4.1B in the function of Caspr proteins, we examined the ability of transgenic Caspr and Caspr2 mutants lacking their 4.1-binding sequence (d4.1) to restore Kv1 channel clustering in Caspr- and Caspr2-null mice, respectively. We found that Caspr-d4.1 was localized to the PNJ and is able to recruit the paranodal adhesion complex components contactin and NF155 to this site. Nevertheless, in axons expressing Caspr-d4.1, Kv1 channels were often detected at paranodes, suggesting that the interaction of Caspr with protein 4.1B is necessary for the generation of an efficient membrane barrier at the PNJ. We also found that the Caspr2-d4.1 transgene did not accumulate at the JXP, even though it was targeted to the axon, demonstrating that the interaction with protein 4.1B is required for the accumulation of Caspr2 and Kv1 channels at the juxtaparanodal axonal membrane. In accordance, we show that Caspr2 and Kv1 channels are not clustered at the JXP in 4.1B-null mice. Our results thus underscore the functional importance of protein 4.1B in the organization of peripheral myelinated axons.
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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.