ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience1999
Peripheral myelin protein 22 and protein zero: a novel association in peripheral nervous system myelin.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
42 citing papers in PubMed, 162 citations in OpenAlex.
- Peripheral Myelin Protein-22 and Its Prominence in Charcot-Marie-Tooth Disease.Chemical reviews · 2026Review
- Advances in PMP22 sequence variant-associated hereditary neuropathy with liability to pressure palsies: from gene dosage effects to mechanism-informed variant interpretation.Frontiers in neurology · 2026Review
- On the synergy between myelin proteins P0, MBP, and P2 in peripheral nerve major dense line formation.The FEBS journal · 2025Article
- Disrupting the transmembrane domain interface between PMP22 and MPZ causes peripheral neuropathy.iScience · 2024Article
- Targeting PI3K/Akt/mTOR signaling in rodent models of PMP22 gene-dosage diseases.EMBO molecular medicine · 2024Article
- Disrupted extracellular matrix and cell cycle genes in autism-associated Shank3 deficiency are targeted by lithium.Molecular psychiatry · 2024Article
- Review
- Mechanisms and treatment strategies of demyelinating and dysmyelinating Charcot-Marie-Tooth disease.Neural regeneration research · 2023Review
- Article
- Clinical and Genetic Survey for Charcot-Marie-Tooth Neuropathy Based on the Findings in Turkey, a Country with a High Rate of Consanguineous MarriagesBalkan medical journal · 2022Article
- Development of a common peroneal nerve injury model in domestic swine for the study of translational neuropathic pain treatments.Journal of neurosurgery · 2021Article
- The differentiation state of the Schwann cell progenitor drives phenotypic variation between two contagious cancers.PLoS pathogens · 2021Article
- Mechanisms and Treatments in Demyelinating CMT.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021Review
- Ion mobility-mass spectrometry reveals the role of peripheral myelin protein dimers in peripheral neuropathy.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- How Does Protein Zero Assemble Compact Myelin?Cells · 2020Article
- Peripheral myelin protein 22 preferentially partitions into ordered phase membrane domains.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Functional Recovery Occurs Even After Partial Remyelination of Axon-Meshed Median and Ulnar Nerves in Mice.Neurochemical research · 2019Article
- Peripheral myelin protein 22 modulates store-operated calcium channel activity, providing insights into Charcot-Marie-Tooth disease etiology.The Journal of biological chemistry · 2019Article
- PMP22 Regulates Cholesterol Trafficking and ABCA1-Mediated Cholesterol Efflux.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Molecular structure and function of myelin protein P0 in membrane stacking.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations found in the two major glycosylated transmembrane proteins of the PNS myelin, the peripheral myelin protein zero (P0) and peripheral myelin protein 22 (PMP22), have been independently associated with the most common hereditary demyelinating peripheral neuropathies. Genotype-phenotype correlations in humans and transgenic animals have provided functional evidence that P0 and PMP22 are involved in formation and maintenance of compact myelin. Here, we demonstrate for the first time that P0 and PMP22 proteins form complexes in the myelin membrane, as shown by coimmunoprecipitation experiments, and that glycosylation is not involved in mediating these interactions. Complex formation was also detected when the two proteins were coexpressed in heterologous cells. In transfected cells, P0 and PMP22 are recruited and colocalize at the apposed plasma membranes of expressors as shown by confocal microscopy. These findings provide a new basis for a better understanding of myelin assembly and of the pathomechanisms involved in demyelinating peripheral neuropathies. Furthermore, these results propose a possible explanation why alterations in either of these molecules are sufficient to destabilize the myelin structure and cause a similar disease phenotype.
Indexed as
Identifiers
10212299PMC6782240W1962850894What 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.