ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2000
Uncoupling of myelin assembly and schwann cell differentiation by transgenic overexpression of peripheral myelin protein 22.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
What it found
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Who cites it
20 citing papers in PubMed, 71 citations in OpenAlex.
- Peripheral Myelin Protein-22 and Its Prominence in Charcot-Marie-Tooth Disease.Chemical reviews · 2026Review
- Characterising PMP22-Proximal Partners in a Schwann Cell Model of Charcot-Marie-Tooth Disease Type1A.Biology · 2025Article
- Targeting PI3K/Akt/mTOR signaling in rodent models of PMP22 gene-dosage diseases.EMBO molecular medicine · 2024Article
- Animal Models as a Tool to Design Therapeutical Strategies for CMT-like Hereditary Neuropathies.Brain sciences · 2021Review
- Regulating PMP22 expression as a dosage sensitive neuropathy gene.Brain research · 2020Review
- Peripheral myelin protein 22 alters membrane architecture.Science advances · 2017Article
- Molecular regulators of nerve conduction - Lessons from inherited neuropathies and rodent genetic models.Experimental neurology · 2015Review
- Neural-specific deletion of Htra2 causes cerebellar neurodegeneration and defective processing of mitochondrial OPA1.PloS one · 2014Article
- Biochemical characterization of protein quality control mechanisms during disease progression in the C22 mouse model of CMT1A.ASN neuro · 2013Article
- The PMP22 gene and its related diseases.Molecular neurobiology · 2013Review
- CFTR-deficient pigs display peripheral nervous system defects at birth.Proceedings of the National Academy of Sciences of the United States of America · 2013Article
- Rapid genetic screening of Charcot-Marie-Tooth disease type 1A and hereditary neuropathy with liability to pressure palsies patients.Neural regeneration research · 2012Article
- MLCK regulates Schwann cell cytoskeletal organization, differentiation and myelination.Journal of cell science · 2011Article
- P2X7-mediated increased intracellular calcium causes functional derangement in Schwann cells from rats with CMT1A neuropathy.The Journal of biological chemistry · 2009Article
- Pathomechanisms of mutant proteins in Charcot-Marie-Tooth disease.Neuromolecular medicine · 2006Review
- Animal models of Charcot-Marie-Tooth disease type 1A.Neuromolecular medicine · 2006Review
- Association of calnexin with mutant peripheral myelin protein-22 ex vivo: a basis for "gain-of-function" ER diseases.Proceedings of the National Academy of Sciences of the United States of America · 2002Article
- Understanding Schwann cell-neurone interactions: the key to Charcot-Marie-Tooth disease?Journal of anatomy · 2002Review
- Functional analysis for peripheral myelin protein PASII/PMP22: is it a member of claudin superfamily?Neurochemical research · 2001Article
- The AN2 protein is a novel marker for the Schwann cell lineage expressed by immature and nonmyelinating Schwann cells.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2001Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We have generated previously transgenic rats that overexpress peripheral myelin protein 22 (PMP22) in Schwann cells. In the nerves of these animals, Schwann cells have segregated with axons to the normal 1:1 ratio but remain arrested at the promyelinating stage, apparently unable to elaborate myelin sheaths. We have examined gene expression of these dysmyelinating Schwann cells using semiquantitative reverse transcription-PCR and immunofluorescence analysis. Unexpectedly, Schwann cell differentiation appears to proceed normally at the molecular level when monitored by the expression of mRNAs encoding major structural proteins of myelin. Furthermore, an aberrant coexpression of early and late Schwann cell markers was observed. PMP22 itself acquires complex glycosylation, suggesting that trafficking of the myelin protein through the endoplasmic reticulum is not significantly impaired. We suggest that PMP22, when overexpressed, accumulates in a late Golgi-cell membrane compartment and uncouples myelin assembly from the underlying program of Schwann cell differentiation.
Indexed as
Identifiers
10818147PMC6772658W1591673341What 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.