ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2015
Oligodendroglial maturation is dependent on intracellular protein shuttling.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 37 citations in OpenAlex.
- p57International journal of molecular sciences · 2024Article
- Review
- Signal enhancement in spark-assisted laser-induced breakdown spectroscopy for discrimination of glioblastoma and oligodendroglioma lesions.Biomedical optics express · 2023Article
- A Novel Ex Vivo Model to Study Therapeutic Treatments for Myelin Repair following Ischemic Damage.International journal of molecular sciences · 2023Article
- Teriflunomide as a therapeutic means for myelin repair.Journal of neuroinflammation · 2023Article
- Insights into myelin dysfunction in schizophrenia and bipolar disorder.World journal of psychiatry · 2022Review
- The p21-activated kinases in neural cytoskeletal remodeling and related neurological disorders.Protein & cell · 2022Review
- Identification of novel myelin repair drugs by modulation of oligodendroglial differentiation competence.EBioMedicine · 2021Article
- TLR4 Associated Signaling Disrupters as a New Means to Overcome HERV-W Envelope-Mediated Myelination Deficits.Frontiers in cellular neuroscience · 2021Article
- C21orf91 Regulates Oligodendroglial Precursor Cell Fate-A Switch in the Glial Lineage?Frontiers in cellular neuroscience · 2021Article
- RNA-binding protein altered expression and mislocalization in MS.Neurology(R) neuroimmunology & neuroinflammation · 2020Article
- Functional Versatility of the CDK Inhibitor p57Frontiers in cell and developmental biology · 2020Review
- pHERV-W envelope protein fuels microglial cell-dependent damage of myelinated axons in multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- TDP-43 proteinopathy in Theiler's murine encephalomyelitis virus infection.PLoS pathogens · 2019Article
- Teriflunomide promotes oligodendroglial differentiation and myelination.Journal of neuroinflammation · 2018Article
- Heterogeneous populations of neural stem cells contribute to myelin repair.Neural regeneration research · 2017Review
- Article
- Taking Advantage of Nature's Gift: Can Endogenous Neural Stem Cells Improve Myelin Regeneration?International journal of molecular sciences · 2016Review
- Article
- [New therapeutic strategies for remyelination in multiple sclerosis].Der Nervenarzt · 2015Article
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis is an autoimmune disease of the CNS resulting in degeneration of myelin sheaths and loss of oligodendrocytes, which means that protection and electrical insulation of axons and rapid signal propagation are impaired, leading to axonal damage and permanent disabilities. Partial replacement of lost oligodendrocytes and remyelination can occur as a result of activation and recruitment of resident oligodendroglial precursor cells. However, the overall remyelination capacity remains inefficient because precursor cells often fail to generate new oligodendrocytes. Increasing evidence points to the existence of several molecular inhibitors that act on these cells and interfere with their cellular maturation. The p57kip2 gene encodes one such potent inhibitor of oligodendroglial differentiation and this study sheds light on the underlying mode of action. We found that subcellular distribution of the p57kip2 protein changed during differentiation of rat, mouse, and human oligodendroglial cells both in vivo and in vitro. Nuclear export of p57kip2 was correlated with promoted myelin expression, higher morphological phenotypes, and enhanced myelination in vitro. In contrast, nuclear accumulation of p57kip2 resulted in blocked oligodendroglial differentiation. Experimental evidence suggests that the inhibitory role of p57kip2 depends on specific interactions with binding proteins such as LIMK-1, CDK2, Mash1, and Hes5 either by controlling their site of action or their activity. Because functional restoration in demyelinating diseases critically depends on the successful generation of oligodendroglial cells, a therapeutic need that is currently unmet, the regulatory mechanism described here might be of particular interest for identifying suitable drug targets and devising novel therapeutic approaches.
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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.