ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2003
Expression of laminin receptors in schwann cell differentiation: evidence for distinct roles.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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Who cites it
51 citing papers in PubMed, 105 citations in OpenAlex.
- Molecular Mediators Associated With Myelination, Demyelination, and Remyelination in the Peripheral Nervous System.Journal of the peripheral nervous system : JPNS · 2026Review
- Roles and therapeutic prospects of the laminin family in disorders of the nervous system.Journal of translational medicine · 2026Review
- The STRIPAK complex is required for radial sorting and laminin receptor expression in Schwann cells.Cell reports · 2025Article
- GFRα1 Promotes Axon Regeneration after Peripheral Nerve Injury by Functioning as a Ligand.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Material matters: Degradation products affect regenerating Schwann cells.Biomaterials advances · 2024Article
- The Influence of Lysosomal Stress on Dental Pulp Stem Cell-Derived Schwann Cells.Biomolecules · 2024Article
- Polycaprolactone/graphene oxide/acellular matrix nanofibrous scaffolds with antioxidant and promyelinating features for the treatment of peripheral demyelinating diseases.Journal of materials science. Materials in medicine · 2023Article
- A novel mouse model of CMT1B identifies hyperglycosylation as a new pathogenetic mechanism.Human molecular genetics · 2022Article
- Peripheral Nerve Development and the Pathogenesis of Peripheral Neuropathy: the Sorting Point.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Review
- Astrocyte reactivity in spinal cord and functional impairment after tendon injury in rats.Heliyon · 2021Article
- αGlia · 2021Article
- LAMA2 Neuropathies: Human Findings and Pathomechanisms From Mouse Models.Frontiers in molecular neuroscience · 2020Article
- A mutation-independent approach for muscular dystrophy via upregulation of a modifier gene.Nature · 2019Article
- Laminin 211 inhibits protein kinase A in Schwann cells to modulate neuregulin 1 type III-driven myelination.PLoS biology · 2017Article
- A reciprocal regulatory loop between TAZ/YAP and G-protein Gαs regulates Schwann cell proliferation and myelination.Nature communications · 2017Article
- Implications of Schwann Cells Biomechanics and Mechanosensitivity for Peripheral Nervous System Physiology and Pathophysiology.Frontiers in molecular neuroscience · 2017Review
- YAP and TAZ control peripheral myelination and the expression of laminin receptors in Schwann cells.Nature neuroscience · 2016Article
- Exclusive expression of the Rab11 effector SH3TC2 in Schwann cells links integrin-α6 and myelin maintenance to Charcot-Marie-Tooth disease type 4C.Biochimica et biophysica acta · 2016Article
- How Schwann Cells Sort Axons: New Concepts.The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry · 2016Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
Abstract
Schwann cells require laminin-2 throughout nerve development, because mutations in the alpha2 chain in dystrophic mice interfere with sorting of axons before birth and formation of myelin internodes after birth. Mature Schwann cells express several laminin receptors, but their expression and roles in development are poorly understood. Therefore, we correlated the onset of myelination in nerve and synchronized myelinating cultures to the appearance of integrins and dystroglycan in Schwann cells. Only alpha6beta1 integrin is expressed before birth, whereas dystroglycan and alpha6beta4 integrin appear perinatally, just before myelination. Although dystroglycan is immediately polarized to the outer surface of Schwann cells, alpha6beta4 appears polarized only after myelination. We showed previously that Schwann cells lacking beta1 integrin do not relate properly to axons before birth. Here we show that the absence of beta1 before birth is not compensated by other laminin receptors, whereas coexpression of both dystroglycan and beta4 integrin is likely required for beta1-null Schwann cells to myelinate after birth. Finally, both beta1-null and dystrophic nerves contain bundles of unsorted axons, but they are predominant in different regions: in spinal roots in dystrophic mice and in nerves in beta1-null mice. We show that differential compensation by laminin-1, but not laminin receptors may partially explain this. These data suggest that the action of laminin is mediated by beta1 integrins during axonal sorting and by dystroglycan, alpha6beta1, and alpha6beta4 integrins during myelination.
Indexed as
Identifiers
12843252PMC6741230W2130618942What OpenQuestion holds
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.