Acetylome in Human Fibroblasts From Parkinson's Disease Patients

Parkinson's disease (PD) is a multifactorial neurodegenerative disorder. The pathogenesis of this disease is associated with gene and environmental factors. Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most frequent genetic cause of familial and sporadic PD. Moreover, posttranslati...

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Bibliographic Details
Published in:Frontiers in cellular neuroscience 2018-04, Vol.12, p.97-97
Main Authors: Yakhine-Diop, Sokhna M S, Rodríguez-Arribas, Mario, Martínez-Chacón, Guadalupe, Uribe-Carretero, Elisabet, Gómez-Sánchez, Rubén, Aiastui, Ana, López de Munain, Adolfo, Bravo-San Pedro, José M, Niso-Santano, Mireia, González-Polo, Rosa A, Fuentes, José M
Format: Article
Language:English
Subjects:
Acetylation
Autophagy
Cell culture
Environmental factors
Epigenetics
Fibroblasts
Gene expression
Kinases
Leucine
LRRK2
LRRK2 protein
Lysine
Movement disorders
Mutation
Neurodegeneration
Neurodegenerative diseases
Neuroscience
Parkinson
Parkinson's disease
Peptides
Proteins
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Summary:Parkinson's disease (PD) is a multifactorial neurodegenerative disorder. The pathogenesis of this disease is associated with gene and environmental factors. Mutations in leucine-rich repeat kinase 2 (LRRK2) are the most frequent genetic cause of familial and sporadic PD. Moreover, posttranslational modifications, including protein acetylation, are involved in the molecular mechanism of PD. Acetylation of lysine proteins is a dynamic process that is modulated in PD. In this descriptive study, we characterized the acetylated proteins and peptides in primary fibroblasts from idiopathic PD (IPD) and genetic PD harboring G2019S or R1441G mutations. Identified acetylated peptides are modulated between individuals' groups. Although acetylated nuclear proteins are the most represented in cells, they are hypoacetylated in IPD. Results display that the level of hyperacetylated and hypoacetylated peptides are, respectively, enhanced in genetic PD and in IPD cells.
ISSN:1662-5102
1662-5102
DOI:10.3389/fncel.2018.00097