Tshianda N. M. Alerte

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α-synuclein (α-Syn) is a chaperone-like protein that is highly implicated in Parkinson's disease (PD) as well as in dementia with Lewy bodies (DLB). Rare forms of PD occur in individuals with mutations of α-Syn or triplication of wild type α-Syn, and in both PD and DLB the intraneuronal inclusions known as Lewy bodies contain aggregated α-Syn that is highly(More)
Tyrosine hydroxylase (TH), the rate limiting enzyme in catecholamine synthesis, is frequently used as a marker of dopaminergic neuronal loss in animal models of Parkinson's disease (PD). We have been exploring the normal function of the PD-related protein alpha-synuclein (alpha-Syn) with regard to dopamine synthesis. TH is activated by the phosphorylation(More)
Alpha-synuclein (a-Syn), a protein implicated in Parkinson disease, contributes significantly to dopamine metabolism. a-Syn binding inhibits the activity of tyrosine hydroxylase (TH), the rate-limiting enzyme in catecholamine synthesis. Phosphorylation of TH stimulates its activity, an effect that is reversed by protein phosphatase 2A (PP2A). In cells,(More)
Aging, the main risk factor for Parkinson's disease (PD), is associated with increased α-synuclein levels in substantia nigra pars compacta (SNc). Excess α-synuclein spurs Lewy-like pathology and dysregulates the activity of protein phosphatase 2A (PP2A). PP2A dephosphorylates many neuroproteins, including the catecholamine rate-limiting enzyme, tyrosine(More)
SERINE 129 PHOSPHORYLATION REDUCES α-SYNUCLEIN’S ABILITY TO REGULATE TYROSINE HYDROXYLASE AND PROTEIN PHOSPHATASE 2A IN VITRO AND IN VIVO Haiyan Lou*, Susana E. Montoya*, Tshianda N. M. Alerte*, Jian Wang, Jianjun Wu, Xiangmin Peng, Chang-Sook Hong, Emily E. Friedrich, Samantha A. Mader, Courtney J. Pedersen, Brian S. Marcus, Alison L. McCormack, Donato A.(More)
Haiyan Lou, Susana E. Montoya, Tshianda N. M. Alerte, Jian Wang, Jianjun Wu, Xiangmin Peng, Chang-Sook Hong, Emily E. Friedrich, Samantha A. Mader, Courtney J. Pedersen, Brian S. Marcus, Alison L. McCormack, Donato A. Di Monte, S. Colette Daubner , and Ruth G. Perez** From the Pittsburgh Institute for Neurodegenerative Diseases, University of Pittsburgh,(More)
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