ArticleGlia2013
The 4.1B cytoskeletal protein regulates the domain organization and sheath thickness of myelinated axons.
Article in Glia, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 51 citations in OpenAlex.
- 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
- Biallelic EPB41L3 variants underlie a developmental disorder with seizures and myelination defects.Brain : a journal of neurology · 2024Article
- Glia trigger endocytic clearance of axonal proteins to promote rodent myelination.Developmental cell · 2024Article
- SynCAMs in Normal Vertebrate Neural Development and Neuropsychiatric Disorders: from the Perspective of the OCAs.Molecular neurobiology · 2024Review
- A class-specific effect of dysmyelination on the excitability of hippocampal interneurons.eLife · 2023Article
- The Node of Ranvier as an Interface for Axo-Glial Interactions: Perturbation of Axo-Glial Interactions in Various Neurological Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2023Review
- Article
- LGI3/2-ADAM23 interactions cluster Kv1 channels in myelinated axons to regulate refractory period.The Journal of cell biology · 2023Article
- 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
- Mechanisms of node of Ranvier assembly.Nature reviews. Neuroscience · 2021Review
- 4.1N-Mediated Interactions and Functions in Nerve System and Cancer.Frontiers in molecular biosciences · 2021Review
- Assembly and Function of the Juxtaparanodal Kv1 Complex in Health and Disease.Life (Basel, Switzerland) · 2020Review
- 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
- Article
- Ablation of cytoskeletal scaffolding proteins, Band 4.1B and Whirlin, leads to cerebellar purkinje axon pathology and motor dysfunction.Journal of neuroscience research · 2019Article
- Selective Axonal Expression of the Kv1 Channel Complex in Pre-myelinated GABAergic Hippocampal Neurons.Frontiers in cellular neuroscience · 2019Article
- Structure and function of the contactin-associated protein family in myelinated axons and their relationship with nerve diseases.Neural regeneration research · 2017Review
- Axonal transport deficits in multiple sclerosis: spiraling into the abyss.Acta neuropathologica · 2017Review
Corrections and comments
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Authors and funding
10 authors at 6 institutions in 1 country.
Funding
Abstract
Myelinated axons are organized into specialized domains critical to their function in saltatory conduction, i.e., nodes, paranodes, juxtaparanodes, and internodes. Here, we describe the distribution and role of the 4.1B protein in this organization. 4.1B is expressed by neurons, and at lower levels by Schwann cells, which also robustly express 4.1G. Immunofluorescence and immuno-EM demonstrates 4.1B is expressed subjacent to the axon membrane in all domains except the nodes. Mice deficient in 4.1B have preserved paranodes, based on marker staining and EM in contrast to the juxtaparanodes, which are substantially affected in both the PNS and CNS. The juxtaparanodal defect is evident in developing and adult nerves and is neuron-autonomous based on myelinating cocultures in which wt Schwann cells were grown with 4.1B-deficient neurons. Despite the juxtaparanodal defect, nerve conduction velocity is unaffected. Preservation of paranodal markers in 4.1B deficient mice is associated with, but not dependent on an increase of 4.1R at the axonal paranodes. Loss of 4.1B in the axon is also associated with reduced levels of the internodal proteins, Necl-1 and Necl-2, and of alpha-2 spectrin. Mutant nerves are modestly hypermyelinated and have increased numbers of Schmidt-Lanterman incisures, increased expression of 4.1G, and express a residual, truncated isoform of 4.1B. These results demonstrate that 4.1B is a key cytoskeletal scaffold for axonal adhesion molecules expressed in the juxtaparanodal and internodal domains that unexpectedly regulates myelin sheath thickness.
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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.