Acetylome in Human Fibroblasts From Parkinson's Disease Patients

Sokhna M S Yakhine-Diop, Mario Rodríguez-Arribas, Guadalupe Martínez-Chacón, Elisabet Uribe-Carretero, Rubén Gómez-Sánchez, Ana Aiastui, Adolfo López de Munain, José M Bravo-San Pedro, Mireia Niso-Santano, Rosa A González-Polo, José M Fuentes

    OnderzoeksoutputAcademicpeer review

    13 Citaten (Scopus)
    259 Downloads (Pure)


    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 LRRK2 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.

    Originele taal-2English
    TijdschriftFrontiers in cellular neuroscience
    StatusPublished - 17-apr.-2018


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