ArticlePLoS biology2015
HDAC1/2-Dependent P0 Expression Maintains Paranodal and Nodal Integrity Independently of Myelin Stability through Interactions with Neurofascins.
Article in PLoS biology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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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Who cites it
23 citing papers in PubMed, 38 citations in OpenAlex.
- Article
- Phenotypic spectrum of myelin protein zero-related neuropathies: a large cohort study from five mutation clusters across Italy.Journal of neurology, neurosurgery, and psychiatry · 2024Article
- Schwann Cell Development and Myelination.Cold Spring Harbor perspectives in biology · 2024Review
- Myelin protein zero mutation-related hereditary neuropathies: Neuropathological insight from a new nerve biopsy cohort.Brain pathology (Zurich, Switzerland) · 2024Article
- Mechanisms and treatment strategies of demyelinating and dysmyelinating Charcot-Marie-Tooth disease.Neural regeneration research · 2023Review
- A new mouse model of Charcot-Marie-Tooth 2J neuropathy replicates human axonopathy and suggest alteration in axo-glia communication.PLoS genetics · 2022Article
- Theophylline Induces Remyelination and Functional Recovery in a Mouse Model of Peripheral Neuropathy.Biomedicines · 2022Article
- Emerging Role of HDACs in Regeneration and Ageing in the Peripheral Nervous System: Repair Schwann Cells as Pivotal Targets.International journal of molecular sciences · 2022Review
- Mechanisms and Treatments in Demyelinating CMT.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Wrestling and Wrapping: A Perspective on SUMO Proteins in Schwann Cells.Biomolecules · 2021Review
- [Role and mechanism of histone deacetylases in mouse neuronal development].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2021Article
- New evidence for secondary axonal degeneration in demyelinating neuropathies.Neuroscience letters · 2021Review
- Mechanisms of Schwann cell plasticity involved in peripheral nerve repair after injury.Cellular and molecular life sciences : CMLS · 2020Review
- EEF1A1 deacetylation enables transcriptional activation of remyelination.Nature communications · 2020Article
- Insights Into the Role and Potential of Schwann Cells for Peripheral Nerve Repair From Studies of Development and Injury.Frontiers in molecular neuroscience · 2020Article
- Mutation update for myelin protein zero-related neuropathies and the increasing role of variants causing a late-onset phenotype.Journal of neurology · 2019Article
- Article
- Regulation of Central Nervous System Development by Class I Histone Deacetylases.Developmental neuroscience · 2019Review
- HDAC3 Regulates the Transition to the Homeostatic Myelinating Schwann Cell State.Cell reports · 2018Article
- Delaying histone deacetylase response to injury accelerates conversion into repair Schwann cells and nerve regeneration.Nature communications · 2017Article
Corrections and comments
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Authors and funding
19 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The pathogenesis of peripheral neuropathies in adults is linked to maintenance mechanisms that are not well understood. Here, we elucidate a novel critical maintenance mechanism for Schwann cell (SC)-axon interaction. Using mouse genetics, ablation of the transcriptional regulators histone deacetylases 1 and 2 (HDAC1/2) in adult SCs severely affected paranodal and nodal integrity and led to demyelination/remyelination. Expression levels of the HDAC1/2 target gene myelin protein zero (P0) were reduced by half, accompanied by altered localization and stability of neurofascin (NFasc)155, NFasc186, and loss of Caspr and septate-like junctions. We identify P0 as a novel binding partner of NFasc155 and NFasc186, both in vivo and by in vitro adhesion assay. Furthermore, we demonstrate that HDAC1/2-dependent P0 expression is crucial for the maintenance of paranodal/nodal integrity and axonal function through interaction of P0 with neurofascins. In addition, we show that the latter mechanism is impaired by some P0 mutations that lead to late onset Charcot-Marie-Tooth disease.
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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.