ArticleThe Journal of cell biology2010
Sox10 is required for Schwann cell identity and progression beyond the immature Schwann cell stage.
Article in The Journal of cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 141 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
141 citing papers in PubMed, 234 citations in OpenAlex.
- Myelination and Remyelination in Peripheral Nerve Injury: Mechanisms, Regulation, and Therapeutic Perspectives.MedComm · 2026Review
- Article
- Protein arginine methyltransferases coordinate mitochondrial stress adaptation and neuromuscular function.Experimental & molecular medicine · 2026Review
- Mutant SOD1 expressed by oligodendrocytes aggregates in myelinic nanochannels and accelerates disease progression in familial ALS mice.bioRxiv : the preprint server for biology · 2026Article
- Comparative gene expression analysis of nestin-expressing hair follicle-derived cells.Scientific reports · 2026Article
- Clinical Importance of Autoantibodies to SOX10 and Lamin A/C as Potential Biomarkers in Sera From Vitiligo Patients.Annals of dermatology · 2026Article
- Divergent stem cell mechanisms govern the primary body axis and appendage regeneration in the axolotl.Science advances · 2026Article
- Plasticity, injury-induced reprogramming, and translational applications of Schwann cells in neural regeneration.Frontiers in cellular neuroscience · 2026Review
- Enhanced Schwann cell differentiation of skin-derived neural crest-like stem cells through the synergistic action of SOX10 and immobilized NRG1 signaling.Bioengineering & translational medicine · 2025Article
- Gtf2i-encoded transcription factor Tfii-i regulates myelination via Sox10 and Mbp regulatory elements.Nature communications · 2025Article
- Biphasic Electrical Stimulation of Schwann Cells on Conducting Polymer-Coated Carbon Microfibers.International journal of molecular sciences · 2025Article
- Strengthening monocarboxylate transporters by adiponectin receptor agonist ameliorates diabetic peripheral neuropathy.Cell communication and signaling : CCS · 2025Article
- Article
- Nageotte nodules in human dorsal root ganglia reveal neurodegeneration in diabetic peripheral neuropathy.Nature communications · 2025Article
- Schwann cells in regeneration and cancer: an epithelial-mesenchymal transition perspective.Open biology · 2025Review
- Current molecular understanding of central nervous system schwannomas.Acta neuropathologica communications · 2025Review
- High expression of SOX10 is correlated with poor prognosis and immune infiltrates in skin cutaneous melanoma.Frontiers in oncology · 2025Article
- Decoding the molecular, cellular, and functional heterogeneity of zebrafish intracardiac nervous system.Nature communications · 2024Article
- Schwann Cell Development and Myelination.Cold Spring Harbor perspectives in biology · 2024Review
- Transcription Factors Sox8 and Sox10 Contribute with Different Importance to the Maintenance of Mature Oligodendrocytes.International journal of molecular sciences · 2024Article
81 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 5 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in the transcription factor SOX10 cause neurocristopathies, including Waardenburg-Hirschsprung syndrome and peripheral neuropathies in humans. This is partly attributed to a requirement for Sox10 in early neural crest for survival, maintenance of pluripotency, and specification to several cell lineages, including peripheral glia. As a consequence, peripheral glia are absent in Sox10-deficient mice. Intriguingly, Sox10 continues to be expressed in these cells after specification. To analyze glial functions after specification, we specifically deleted Sox10 in immature Schwann cells by conditional mutagenesis. Mutant mice died from peripheral neuropathy before the seventh postnatal week. Nerve alterations included a thinned perineurial sheath, increased lipid and collagen deposition, and a dramatically altered cellular composition. Nerve conduction was also grossly aberrant, and neither myelinating nor nonmyelinating Schwann cells formed. Instead, axons of different sizes remained unsorted in large bundles. Schwann cells failed to develop beyond the immature stage and were unable to maintain identity. Thus, our study identifies a novel cause for peripheral neuropathies in patients with SOX10 mutations.
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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.