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dc.contributor.authorMargiotta, Azzurra
dc.date.accessioned2023-07-05T11:37:41Z
dc.date.available2023-07-05T11:37:41Z
dc.date.created2023-06-29T13:24:58Z
dc.date.issued2023-06-05
dc.identifier.issn1661-6596
dc.identifier.urihttps://hdl.handle.net/11250/3076072
dc.description.abstractThe myelin sheath is an insulating layer around the nerves of the brain and spinal cord which allows a fast and efficient nerve conduction. Myelin is made of protein and fatty substances and gives protection for the propagation of the electrical impulse. The myelin sheath is formed by oligodendrocytes in the central nervous system (CNS) and by Schwann cells in the peripheral nervous system (PNS). The myelin sheath presents a highly organized structure and expands both radially and longitudinally, but in a different way and with a different composition. Myelin alterations determine the onset of several neuropathies, as the electrical signal can be slowed or stopped. Soluble N-ethylmaleimide-sensitive factor attachment protein receptors (SNAREs) and ras (rat sarcoma)-associated binding proteins (rabs) have been proved to contribute to several aspects regarding the formation of myelin or dysmyelination. Here, I will describe the role of these proteins in regulating membrane trafficking and nerve conduction, myelin biogenesis and maintenance.en_US
dc.language.isoengen_US
dc.publisherMDPIen_US
dc.rightsNavngivelse 4.0 Internasjonal*
dc.rights.urihttp://creativecommons.org/licenses/by/4.0/deed.no*
dc.titleRole of SNAREs and Rabs in Myelin Regulationen_US
dc.typeJournal articleen_US
dc.typePeer revieweden_US
dc.description.versionpublishedVersionen_US
dc.rights.holderCopyright 2023 the authorsen_US
dc.source.articlenumber9772en_US
cristin.ispublishedtrue
cristin.fulltextoriginal
cristin.qualitycode1
dc.identifier.doi10.3390/ijms24119772
dc.identifier.cristin2159466
dc.source.journalInternational Journal of Molecular Sciencesen_US
dc.identifier.citationInternational Journal of Molecular Sciences. 2023, 24 (11), 9772.en_US
dc.source.volume24en_US
dc.source.issue11en_US


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