| Literature DB >> 33886091 |
Ana Cazurro-Gutiérrez1,2, Anna Marcé-Grau1, Marta Correa-Vela1,2, Ainara Salazar1,3, María I Vanegas1,4, Alfons Macaya1,2,3, Àlex Bayés2,5, Belén Pérez-Dueñas6,7,8.
Abstract
Myoclonus-dystonia (MD) is a rare childhood-onset movement disorder, with an estimated prevalence of about 2 per 1,000,.000 in Europe, characterized by myoclonic jerks in combination with focal or segmental dystonia. Pathogenic variants in the gene encoding ε-sarcoglycan (SGCE), a maternally imprinted gene, are the most frequent genetic cause of MD. To date, the exact role of ε-sarcoglycan and the pathogenic mechanisms that lead to MD are still unknown. However, there are more than 40 reported isoforms of human ε-sarcoglycan, pointing to a complex biology of this protein. Additionally, some of these are brain-specific isoforms, which may suggest an important role within the central nervous system. In the present review, we aim to provide an overview of the current state of knowledge of ε-sarcoglycan. We will focus on the genetic landscape of SGCE and the presence and plausible role of ε-sarcoglycan in the brain. Finally, we discuss the importance of the brain-specific isoforms and hypothesize that SGCE may play essential roles in normal synaptic functioning and their alteration will be strongly related to MD.Entities:
Keywords: Epsilon-sarcoglycan; Isoform; Myoclonus-dystonia; PDZ-motif; Synapse
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Year: 2021 PMID: 33886091 DOI: 10.1007/s12035-021-02391-0
Source DB: PubMed Journal: Mol Neurobiol ISSN: 0893-7648 Impact factor: 5.590