ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Genetic deletion of Cadm4 results in myelin abnormalities resembling Charcot-Marie-Tooth neuropathy.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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Who cites it
47 citing papers in PubMed, 71 citations in OpenAlex.
- Multiple adhesion molecules act together in oligodendrocyte-mediated axonal selection and myelin formation.PLoS biology · 2026Article
- LPCAT1, the Enzyme Responsible for Converting LPC to PC, Promotes OPC Differentiation In Vitro.Journal of cellular and molecular medicine · 2025Article
- Palmitoylation regulates myelination by modulating the ZDHHC3-Cadm4 axis in the central nervous system.Signal transduction and targeted therapy · 2024Article
- Peripheral Nervous System (PNS) Myelin Diseases.Cold Spring Harbor perspectives in biology · 2024Review
- SynCAMs in Normal Vertebrate Neural Development and Neuropsychiatric Disorders: from the Perspective of the OCAs.Molecular neurobiology · 2024Review
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- IL-12 sensing in neurons induces neuroprotective CNS tissue adaptation and attenuates neuroinflammation in mice.Nature neuroscience · 2023Article
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- Transcriptomic changes associated with maternal care in the brain of mouthbrooding cichlid Astatotilapia burtoni reflect adaptation to self-induced metabolic stress.The Journal of experimental biology · 2023Article
- Identification of early neurodegenerative pathways in progressive multiple sclerosis.Nature neuroscience · 2022Article
- Synaptic Cell Adhesion Molecule 3 (SynCAM3) Deletion Promotes Recovery from Spinal Cord Injury by Limiting Glial Scar Formation.International journal of molecular sciences · 2022Article
- Myelin Biology.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Schwann cell interactions during the development of the peripheral nervous system.Developmental neurobiology · 2021Review
- Review
- A CADM3 variant causes Charcot-Marie-Tooth disease with marked upper limb involvement.Brain : a journal of neurology · 2021Article
- Dysregulation of myelin synthesis and actomyosin function underlies aberrant myelin in CMT4B1 neuropathy.Proceedings of the National Academy of Sciences of the United States of America · 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
- Defective minor spliceosomes induce SMA-associated phenotypes through sensitive intron-containing neural genes in Drosophila.Nature communications · 2020Article
- Not Just Another Scaffolding Protein Family: The Multifaceted MPPs.Molecules (Basel, Switzerland) · 2020Review
- Dominant mutations of the Notch ligand Jagged1 cause peripheral neuropathy.The Journal of clinical investigation · 2020Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
The interaction between myelinating Schwann cells and the axons they ensheath is mediated by cell adhesion molecules of the Cadm/Necl/SynCAM family. This family consists of four members: Cadm4/Necl4 and Cadm1/Necl2 are found in both glia and axons, whereas Cadm2/Necl3 and Cadm3/Necl1 are expressed by sensory and motor neurons. By generating mice lacking each of the Cadm genes, we now demonstrate that Cadm4 plays a role in the establishment of the myelin unit in the peripheral nervous system. Mice lacking Cadm4 (PGK-Cre/Cadm4(fl/fl)), but not Cadm1, Cadm2, or Cadm3, develop focal hypermyelination characterized by tomacula and myelin outfoldings, which are the hallmark of several Charcot-Marie-Tooth neuropathies. The absence of Cadm4 also resulted in abnormal axon-glial contact and redistribution of ion channels along the axon. These neuropathological features were also found in transgenic mice expressing a dominant-negative mutant of Cadm4 lacking its cytoplasmic domain in myelinating glia Tg(mbp-Cadm4dCT), as well as in mice lacking Cadm4 specifically in Schwann cells (DHH-Cre/Cadm4(fl/fl)). Consistent with these abnormalities, both PGK-Cre/Cadm4(fl/fl) and Tg(mbp-Cadm4dCT) mice exhibit impaired motor function and slower nerve conduction velocity. These findings indicate that Cadm4 regulates the growth of the myelin unit and the organization of the underlying axonal membrane.
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