ArticleThe Journal of cell biology2002
Retention of a cell adhesion complex at the paranodal junction requires the cytoplasmic region of Caspr.
Article in The Journal of cell biology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 99 citations in OpenAlex.
- Cytoskeletal scaffolding of NaCurrent opinion in cell biology · 2025Review
- Impact of Neurofascin on Chronic Inflammatory Demyelinating PolyneuropathyFrontiers in molecular neuroscience · 2021Review
- βII spectrin (SPTBN1): biological function and clinical potential in cancer and other diseases.International journal of biological sciences · 2021Review
- Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021Review
- 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
- Regulation and dysregulation of axon infrastructure by myelinating glia.The Journal of cell biology · 2017Review
- Structure and function of the contactin-associated protein family in myelinated axons and their relationship with nerve diseases.Neural regeneration research · 2017Review
- Assembly of CNS Nodes of Ranvier in Myelinated Nerves Is Promoted by the Axon Cytoskeleton.Current biology : CB · 2017Article
- The Nodes of Ranvier: Molecular Assembly and Maintenance.Cold Spring Harbor perspectives in biology · 2015Review
- Caspr and caspr2 are required for both radial and longitudinal organization of myelinated axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Long-term maintenance of Na+ channels at nodes of Ranvier depends on glial contact mediated by gliomedin and NrCAM.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Genetic deletion of Cadm4 results in myelin abnormalities resembling Charcot-Marie-Tooth neuropathy.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Organization and maintenance of molecular domains in myelinated axons.Journal of neuroscience research · 2013Review
- Article
- Contactin-associated protein 1 (Caspr1) regulates the traffic and synaptic content of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA)-type glutamate receptors.The Journal of biological chemistry · 2012Article
- The cytoskeletal adapter protein 4.1G organizes the internodes in peripheral myelinated nerves.The Journal of cell biology · 2012Article
- Paranodal reorganization results in the depletion of transverse bands in the aged central nervous system.Neurobiology of aging · 2012Article
- Characterization of the axon initial segment (AIS) of motor neurons and identification of a para-AIS and a juxtapara-AIS, organized by protein 4.1B.BMC biology · 2011Article
- The cytoskeletal adaptor protein band 4.1B is required for the maintenance of paranodal axoglial septate junctions in myelinated axons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2011Article
- Real-time CARS imaging reveals a calpain-dependent pathway for paranodal myelin retraction during high-frequency stimulation.PloS one · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
An axonal complex of cell adhesion molecules consisting of Caspr and contactin has been found to be essential for the generation of the paranodal axo-glial junctions flanking the nodes of Ranvier. Here we report that although the extracellular region of Caspr was sufficient for directing it to the paranodes in transgenic mice, retention of the Caspr-contactin complex at the junction depended on the presence of an intact cytoplasmic domain of Caspr. Using immunoelectron microscopy, we found that a Caspr mutant lacking its intracellular domain was often found within the axon instead of the junctional axolemma. We further show that a short sequence in the cytoplasmic domain of Caspr mediated its binding to the cytoskeleton-associated protein 4.1B. Clustering of contactin on the cell surface induced coclustering of Caspr and immobilized protein 4.1B at the plasma membrane. Furthermore, deletion of the protein 4.1B binding site accelerated the internalization of a Caspr-contactin chimera from the cell surface. These results suggest that Caspr serves as a "transmembrane scaffold" that stabilizes the Caspr/contactin adhesion complex at the paranodal junction by connecting it to cytoskeletal components within the axon.
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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.