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An in vivo paradigm to study the role of PINK1-SIAH3 intra-mitochondrial aggregation in promoting the accumulation of pathogenic - synuclein in Parkinson’s disease

Our lab investigates the molecular mechanisms that lead to Parkinson’s disease. We study the main proteins involved in the disease, including a-synuclein, LRRK2 and PINK1. We discovered that ubiquitination and SUMOylation regulate a-synuclein degradation and aggregation. Also, that LRRK2 helps maintain nuclear lamina organization, and synphilin-1, in concert with PINK1, represents a novel pathway to promote mitophagy.

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