Next Article in Journal
Retinal Cell Death Caused by Sodium Iodate Involves Multiple Caspase-Dependent and Caspase-Independent Cell-Death Pathways
Next Article in Special Issue
Interferon Beta-1a (AVONEX®) as a Treatment Option for Untreated Patients with Multiple Sclerosis (AXIOM): A Prospective, Observational Study
Previous Article in Journal
Differences between Mice and Humans in Regulation and the Molecular Network of Collagen, Type III, Alpha-1 at the Gene Expression Level: Obstacles that Translational Research Must Overcome
Previous Article in Special Issue
Cutaneous Adverse Events Associated with Interferon-β Treatment of Multiple Sclerosis
Review

Intracellular Protein Shuttling: A Mechanism Relevant for Myelin Repair in Multiple Sclerosis?

Department of Neurology, Medical Faculty, University of Düsseldorf, 40225 Düsseldorf, Germany
*
Author to whom correspondence should be addressed.
Academic Editors: Christoph Kleinschnitz and Sven Meuth
Int. J. Mol. Sci. 2015, 16(7), 15057-15085; https://doi.org/10.3390/ijms160715057
Received: 29 May 2015 / Revised: 23 June 2015 / Accepted: 25 June 2015 / Published: 3 July 2015
(This article belongs to the Special Issue Advances in Multiple Sclerosis)
A prominent feature of demyelinating diseases such as multiple sclerosis (MS) is the degeneration and loss of previously established functional myelin sheaths, which results in impaired signal propagation and axonal damage. However, at least in early disease stages, partial replacement of lost oligodendrocytes and thus remyelination occur as a result of resident oligodendroglial precursor cell (OPC) activation. These cells represent a widespread cell population within the adult central nervous system (CNS) that can differentiate into functional myelinating glial cells to restore axonal functions. Nevertheless, the spontaneous remyelination capacity in the adult CNS is inefficient because OPCs often fail to generate new oligodendrocytes due to the lack of stimulatory cues and the presence of inhibitory factors. Recent studies have provided evidence that regulated intracellular protein shuttling is functionally involved in oligodendroglial differentiation and remyelination activities. In this review we shed light on the role of the subcellular localization of differentiation-associated factors within oligodendroglial cells and show that regulation of intracellular localization of regulatory factors represents a crucial process to modulate oligodendroglial maturation and myelin repair in the CNS. View Full-Text
Keywords: multiple sclerosis; myelin repair; nucleocytoplasmic shuttling; oligodendrocyte; differentiation inhibitors; transcription factors; remyelination multiple sclerosis; myelin repair; nucleocytoplasmic shuttling; oligodendrocyte; differentiation inhibitors; transcription factors; remyelination
Show Figures

Figure 1

MDPI and ACS Style

Göttle, P.; Küry, P. Intracellular Protein Shuttling: A Mechanism Relevant for Myelin Repair in Multiple Sclerosis? Int. J. Mol. Sci. 2015, 16, 15057-15085. https://doi.org/10.3390/ijms160715057

AMA Style

Göttle P, Küry P. Intracellular Protein Shuttling: A Mechanism Relevant for Myelin Repair in Multiple Sclerosis? International Journal of Molecular Sciences. 2015; 16(7):15057-15085. https://doi.org/10.3390/ijms160715057

Chicago/Turabian Style

Göttle, Peter, and Patrick Küry. 2015. "Intracellular Protein Shuttling: A Mechanism Relevant for Myelin Repair in Multiple Sclerosis?" International Journal of Molecular Sciences 16, no. 7: 15057-15085. https://doi.org/10.3390/ijms160715057

Find Other Styles

Article Access Map by Country/Region

1
Only visits after 24 November 2015 are recorded.
Back to TopTop