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. 2020 May 27;21(11):3779. doi: 10.3390/ijms21113779

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© 2020 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Schematic model of the molecular mechanism of the loss of tyrosine hydroxylase (TH) protein in the dopaminergic neurons. (A) A balanced state between the recycling TH protein and degrading TH protein. (B) Dopamine/biopterin deficient state activates PKA (red), and α-Synuclein aggregation presumably activates MAPKAPK and MSK1 (purple). Both activations accelerate TH phosphorylation (pSer40-TH), which is accompanied by proteasomal degradation. PKA, cAMP-dependent protein kinase; PP2A, protein phosphatase 2a. MAPKAPK, mitogen-activated protein kinase activated protein kinase; MSK1, mitogen- and stress-activated kinase 1.