MOESM5 of Exhaustion of mitochondrial and autophagic reserve may contribute to the development of LRRK2
G2019S
-Parkinson’s disease
Diana Juárez-Flores
Ingrid González-Casacuberta
Mario Ezquerra
María Bañó
Francesc Carmona-Pontaque
Marc Catalán-García
Mariona Guitart-Mampel
Juan Rivero
Ester Tobias
Jose Milisenda
Eduard Tolosa
Maria Marti
Ruben Fernández-Santiago
Francesc Cardellach
Constanza Morén
Glòria Garrabou
10.6084/m9.figshare.6465374.v1
https://springernature.figshare.com/articles/journal_contribution/MOESM5_of_Exhaustion_of_mitochondrial_and_autophagic_reserve_may_contribute_to_the_development_of_LRRK2___G2019S__-Parkinson_s_disease/6465374
Additional file 5: Figure S2. Genetics and mitochondrial protein synthesis. Results are represented by means ± SEM, comparing controls (white bars), non-manifesting carriers of LRRK2 G2019S -mutation, (NM-LRRK2 G2019S , grey bars) and patients with LRRK2 G2019S -mutation and clinically manifest PD (PD-LRRK2 G2019S , black bars) in glucose and galactose media. A. Mitochondrial DNA was conserved in both groups and media. B. Mitochondrial RNA levels were significantly decreased in NM-LRRK2 G2019S when compared to controls in galactose media C-E. Cell growth, mitochondrial content and protein synthesis did not show differences between groups, in either condition. F. Representative image of Western Blot of mitochondrial proteins in either glucose (Glu) or galactose (Gal) media of the three cohorts studied, the original Blott has been cropped for its better visualization, complete images can be provided at request.
2018-06-08 05:00:00
Parkinson’s disease
LRRK2
G2019S
Non-manifesting carriers
Mitochondrial dysfunction
Mitochondrial dynamics
Autophagy
Fibroblasts
Glucose
Galactose