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Auburger G, Gispert S, Brehm N. Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis. Parkinsons Dis. 2016;2016:4686185doi: 10.1155/2016/4686185.
Auburger, G., Gispert, S., & Brehm, N. (2016). Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis. Parkinson's disease, 20164686185. https://doi.org/10.1155/2016/4686185
Auburger, Georg, et al. "Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis." Parkinson's disease vol. 2016 (2016): 4686185. doi: https://doi.org/10.1155/2016/4686185
Auburger G, Gispert S, Brehm N. Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis. Parkinsons Dis. 2016;2016:4686185. doi: 10.1155/2016/4686185. Epub 2016 Mar 01. PMID: 27034888; PMCID: PMC4791501.
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Parkinsons Dis. 2016;2016:4686185. doi: 10.1155/2016/4686185. Epub 2016 Mar 01.

Methyl-Arginine Profile of Brain from Aged PINK1-KO+A53T-SNCA Mice Suggests Altered Mitochondrial Biogenesis.

Parkinson's disease

Georg Auburger, Suzana Gispert, Nadine Brehm

Affiliations

  1. Experimental Neurology, Goethe University Medical School, 60590 Frankfurt am Main, Germany.

PMID: 27034888 PMCID: PMC4791501 DOI: 10.1155/2016/4686185

Abstract

Hereditary Parkinson's disease can be triggered by an autosomal dominant overdose of alpha-Synuclein (SNCA) or the autosomal recessive deficiency of PINK1. We recently showed that the combination of PINK1-knockout with overexpression of A53T-SNCA in double mutant (DM) mice potentiates phenotypes and reduces survival. Now we studied brain hemispheres of DM mice at age of 18 months in a hypothesis-free approach, employing a quantitative label-free global proteomic mass spectrometry scan of posttranslational modifications focusing on methyl-arginine. The strongest effects were documented for the adhesion modulator CMAS, the mRNA decapping/deadenylation factor PATL1, and the synaptic plasticity mediator CRTC1/TORC1. In addition, an intriguing effect was observed for the splicing factor PSF/SFPQ, known to interact with the dopaminergic differentiation factor NURR1 as well as with DJ-1, the protein responsible for the autosomal recessive PARK7 variant of PD. CRTC1, PSF, and DJ-1 are modulators of PGC1alpha and of mitochondrial biogenesis. This pathway was further stressed by dysregulations of oxygen sensor EGLN3 and of nuclear TMPO. PSF and TMPO cooperate with dopaminergic differentiation factors LMX1B and NURR1. Further dysregulations concerned PRR18, TRIO, HNRNPA1, DMWD, WAVE1, ILDR2, DBNDD1, and NFM. Thus, we report selective novel endogenous stress responses in brain, which highlight early dysregulations of mitochondrial homeostasis and midbrain vulnerability.

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