Dopamine-modified alpha-synuclein blocks chaperone-mediated autophagy.

By Marta Martínez-Vicente, Z. Tallóczy, Susmita Kaushik, Ashish C. Massey, Joseph R. Mazzulli, E. Mosharov, R. Hodara, R. Fredenburg, D. Wu, A. Follenzi and 6 more. Journal of Clinical Investigation, 2008

604 citations recorded by the source corpus.

Subfields: Epidemiology, Neurology, Physiology

View Paper: https://www.semanticscholar.org/paper/6374429b9f713e87c67cb05dc066f7b4548416ea

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Epidemiology

1. P. Boya
2. M. Wood
3. A. Schapira
4. Leonidas Stefanis

In Neurology

1. M. Mouradian
2. V. Dias
3. E. Junn
4. A. Schapira
5. Leonidas Stefanis
6. J. Bové
7. C. Perier

In Physiology

1. P. Boya
2. M. Wood
3. Leonidas Stefanis

Citations in the corpus

• α-Synuclein in Parkinson's disease. (2012, result): “WTAS, in an adduct with dopamine, can cause a similar effect (Martinez-Vicente et al. 2008).”
• Pathogenic Lysosomal Depletion in Parkinson's Disease (2010, background): “…in CMA have been linked to PD because of the ability of mutant and posttranslationally modified -synuclein to block CMA in vitro (Cuervo et al., 2004; Martinez-Vicente et al., 2008), macroautophagy dysregulation is increasingly recognized as a potential pathogenic factor in neurodegeneration.”
• The Role of Oxidative Stress in Parkinson’s Disease (2013, background): “Studies with cultured cells and isolated lysosomes have shown that dopamine-modified alpha-synuclein is not only poorly degraded by CMA but also blocks the degradation of other substrates that utilize this pathway, thus, causing considerable cellular stress [291].”
• Role of Oxidative Stress in Parkinson's Disease (2013, background): “The DA quinonemodified α-synuclein is not only poorly degraded but also inhibits the normal degradation of other proteins by chaperonemediated autophagy [8].”
• Lysosomal dysfunction increases exosome-mediated alpha-synuclein release and transmission (2011, methodology): “…lysosomal function described in PD (Alvarez-Erviti et al., 2010) we inhibited lysosomal function in normal and WT alpha-synuclein over-expressing SH-SY5Y cells with ammonium chloride for 7 days or with the vacuolar H+ATPase inhibitor bafilomycin A1 for 24 and 72 h (Martinez-Vicente et al., 2008).”