ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2008
Tumor suppressor schwannomin/merlin is critical for the organization of Schwann cell contacts in peripheral nerves.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 26 citations in OpenAlex.
- Conformational flexibility determines the Nf2/merlin tumor suppressor functions.Matrix biology plus · 2021Article
- Wrestling and Wrapping: A Perspective on SUMO Proteins in Schwann Cells.Biomolecules · 2021Review
- Proximity biotinylation identifies a set of conformation-specific interactions between Merlin and cell junction proteins.Science signaling · 2019Article
- Nf2 Mutation in Schwann Cells Delays Functional Neural Recovery Following Injury.Neuroscience · 2018Article
- Schwannomin-interacting Protein 1 Isoform IQCJ-SCHIP1 Is a Multipartner Ankyrin- and Spectrin-binding Protein Involved in the Organization of Nodes of Ranvier.The Journal of biological chemistry · 2017Article
- Merlin controls the repair capacity of Schwann cells after injury by regulating Hippo/YAP activity.The Journal of cell biology · 2017Article
- Myelinating Schwann Cell Polarity and Mechanically-Driven Myelin Sheath Elongation.Frontiers in cellular neuroscience · 2017Review
- Optimal myelin elongation relies on YAP activation by axonal growth and inhibition by Crb3/Hippo pathway.Nature communications · 2016Article
- Merlin status regulates p75(NTR) expression and apoptotic signaling in Schwann cells following nerve injury.Neurobiology of disease · 2015Article
- A neuronal function of the tumor suppressor protein merlin.Acta neuropathologica communications · 2014Review
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- Rac1 controls Schwann cell myelination through cAMP and NF2/merlin.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- A mouse model of Schwartz-Jampel syndrome reveals myelinating Schwann cell dysfunction with persistent axonal depolarization in vitro and distal peripheral nerve hyperexcitability when perlecan is lacking.The American journal of pathology · 2012Article
- Schwannomin/merlin promotes Schwann cell elongation and influences myelin segment length.Molecular and cellular neurosciences · 2011Article
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- Signals to promote myelin formation and repair.Nature reviews. Neurology · 2010Review
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Schwannomin/merlin is the product of a tumor suppressor gene mutated in neurofibromatosis type 2 (NF2). Although the consequences of NF2 mutations on Schwann cell proliferation are well established, the physiological role of schwannomin in differentiated cells is not known. To unravel this role, we studied peripheral nerves in mice overexpressing in Schwann cells schwannomin with a deletion occurring in NF2 patients (P0-SCH-Delta39-121) or a C-terminal deletion. The myelin sheath and nodes of Ranvier were essentially preserved in both lines. In contrast, the ultrastructural and molecular organization of contacts between Schwann cells and axons in paranodal and juxtaparanodal regions were altered, with irregular juxtaposition of normal and abnormal areas of contact. Similar but more severe alterations were observed in mice with conditional deletion of the Nf2 gene in Schwann cells. The number of Schmidt-Lanterman incisures, which are cytoplasmic channels interrupting the compact myelin and characterized by distinct autotypic contacts, was increased in the three mutant lines. P0-SCH-Delta39-121 and conditionally deleted mice displayed exuberant wrapping of nonmyelinated fibers and short internodes, an abnormality possibly related to altered control of Schwann cell proliferation. In support of this hypothesis, Schwann cell number was increased along fibers before myelination in P0-SCH-Delta39-121 mice but not in those with C-terminal deletion. Schwann cell numbers were also more numerous in mice with conditional deletion. Thus, schwannomin plays an important role in the control of Schwann cell number and is necessary for the correct organization and regulation of axoglial heterotypic and glio-glial autotypic contacts.
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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.