ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Assessing the role of the cadherin/catenin complex at the Schwann cell-axon interface and in the initiation of myelination.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
47 citing papers in PubMed, 65 citations in OpenAlex.
- Article
- Schwann Cell Development and Myelination.Cold Spring Harbor perspectives in biology · 2024Review
- Keratinocyte-Derived Exosomes in Painful Diabetic Neuropathy.bioRxiv : the preprint server for biology · 2024Article
- Cellular mechanisms of heterogeneity in NF2-mutant schwannoma.Nature communications · 2023Article
- A novel mouse model of CMT1B identifies hyperglycosylation as a new pathogenetic mechanism.Human molecular genetics · 2022Article
- Review
- Transcriptome Analysis of Schwann Cells at Various Stages of Myelination Implicates Chromatin Regulator Sin3A in Control of Myelination Identity.Neuroscience bulletin · 2022Article
- Peripheral Nerve Development and the Pathogenesis of Peripheral Neuropathy: the Sorting Point.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
- Adult tissue-derived neural crest-like stem cells: Sources, regulatory networks, and translational potential.Stem cells translational medicine · 2020Review
- Myelinating Schwann cells ensheath multiple axons in the absence of E3 ligase component Fbxw7.Nature communications · 2019Article
- RalGTPases contribute to Schwann cell repair after nerve injury via regulation of process formation.The Journal of cell biology · 2019Article
- Article
- Transcriptome analysis of adherens junction pathway-related genes after peripheral nerve injury.Neural regeneration research · 2018Article
- PKD1 Promotes Functional Synapse Formation Coordinated with N-Cadherin in Hippocampus.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The Pseudopod System for Axon-Glia Interactions: Stimulation and Isolation of Schwann Cell Protrusions that Form in Response to Axonal Membranes.Methods in molecular biology (Clifton, N.J.) · 2018Article
- N-Cadherin is Involved in Neuronal Activity-Dependent Regulation of Myelinating Capacity of Zebrafish Individual Oligodendrocytes In Vivo.Molecular neurobiology · 2017Article
- Sox2 expression in Schwann cells inhibits myelinationDevelopment (Cambridge, England) · 2017Article
- PLD1 promotes dendritic spine development by inhibiting ADAM10-mediated N-cadherin cleavage.Scientific reports · 2017Article
- Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
Abstract
Myelination is dependent on complex reciprocal interactions between the Schwann cell (SC) and axon. Recent evidence suggests that the SC-axon interface represents a membrane specialization essential for myelination; however, the manner in which this polarized-apical domain is generated remains a mystery. The cell adhesion molecule N-cadherin is enriched at the SC-axon interface and colocalizes with the polarity protein Par-3. The asymmetric localization is induced on SC-SC and SC-axon contact. Knockdown of N-cadherin in SCs cocultured with DRG neurons disrupts Par-3 localization and delays the initiation of myelination. However, knockdown or overexpression of neuronal N-cadherin does not influence the distribution of Par-3 or myelination, suggesting that homotypic interactions between SC and axonal N-cadherin are not essential for the events surrounding myelination. To further investigate the role of N-cadherin, mice displaying SC-specific gene ablation of N-cadherin were generated and characterized. Surprisingly, myelination is only slightly delayed, and mice are viable without any detectable myelination defects. β-Catenin, a downstream effector of N-cadherin, colocalizes and coimmunoprecipitates with N-cadherin on the initiation of myelination. To determine whether β-catenin mediates compensation on N-cadherin deletion, SC-specific gene ablation of β-catenin was generated and characterized. Consistent with our hypothesis, myelination is more severely delayed than when manipulating N-cadherin alone, but without any defect to the myelin sheath. Together, our results suggest that N-cadherin interacts with β-catenin in establishing SC polarity and the timely initiation of myelination, but they are nonessential components for the formation and maturation of the myelin sheath.
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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.