Literature DB >> 18322646

Mitochondrial association of alpha-synuclein causes oxidative stress.

M S Parihar1, A Parihar, M Fujita, M Hashimoto, P Ghafourifar.   

Abstract

Alpha-synuclein is a neuron-specific protein that contributes to the pathology of Parkinson's disease via mitochondria-related mechanisms. The present study investigated possible interaction of alpha-synuclein with mitochondria and consequences of such interaction. Using SHSY cells overexpressing alpha-synuclein A53T mutant or wild-type, as well as isolated rat brain mitochondria, the present study shows that alpha-synuclein localizes at the mitochondrial membrane. In both SHSY cells and isolated mitochondria, interaction of alpha-synuclein with mitochondria causes release of cytochrome c, increase of mitochondrial calcium and nitric oxide, and oxidative modification of mitochondrial components. These findings suggest a pivotal role for mitochondria in oxidative stress and apoptosis induced by alpha-synuclein.

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Year:  2008        PMID： 18322646     DOI： 10.1007/s00018-008-7589-1

Source DB:  PubMed          Journal:  Cell Mol Life Sci        ISSN： 1420-682X            Impact factor:   9.261


  118 in total

1.  Two different binding modes of α-synuclein to lipid vesicles depending on its aggregation state.

Authors:  Tobias Högen; Johannes Levin; Felix Schmidt; Mario Caruana; Neville Vassallo; Hans Kretzschmar; Kai Bötzel; Frits Kamp; Armin Giese
Journal:  Biophys J       Date:  2012-04-03       Impact factor: 4.033

2.  Interaction of α-synuclein and a cell penetrating fusion peptide with higher eukaryotic cell membranes assessed by ¹⁹F NMR.

Authors:  Imola G Zigoneanu; Gary J Pielak
Journal:  Mol Pharm       Date:  2012-03-13       Impact factor: 4.939

Review 3.  Mitochondrial dysfunction in Parkinson's disease: molecular mechanisms and pathophysiological consequences.

Authors:  Nicole Exner; Anne Kathrin Lutz; Christian Haass; Konstanze F Winklhofer
Journal:  EMBO J       Date:  2012-06-26       Impact factor: 11.598

Review 4.  Calcium dysregulation and homeostasis of neural calcium in the molecular mechanisms of neurodegenerative diseases provide multiple targets for neuroprotection.

Authors:  Gregor Zündorf; Georg Reiser
Journal:  Antioxid Redox Signal       Date:  2010-10-06       Impact factor: 8.401

Review 5.  Drug targets from genetics: α-synuclein.

Authors:  Karin M Danzer; Pamela J McLean
Journal:  CNS Neurol Disord Drug Targets       Date:  2011-09-01       Impact factor: 4.388

Review 6.  The role of lipids in α-synuclein misfolding and neurotoxicity.

Authors:  Cathryn L Ugalde; Victoria A Lawson; David I Finkelstein; Andrew F Hill
Journal:  J Biol Chem       Date:  2019-05-07       Impact factor: 5.157

7.  The mitochondrial chaperone protein TRAP1 mitigates α-Synuclein toxicity.

Authors:  Erin K Butler; Aaron Voigt; A Kathrin Lutz; Jane P Toegel; Ellen Gerhardt; Peter Karsten; Björn Falkenburger; Andrea Reinartz; Konstanze F Winklhofer; Jörg B Schulz
Journal:  PLoS Genet       Date:  2012-02-02       Impact factor: 5.917

8.  Enhanced mitochondrial inhibition by 3,4-dihydroxyphenyl-acetaldehyde (DOPAL)-oligomerized α-synuclein.

Authors:  Theodore A Sarafian; Amneh Yacoub; Anastasia Kunz; Burkan Aranki; Grigor Serobyan; Whitaker Cohn; Julian P Whitelegge; Joseph B Watson
Journal:  J Neurosci Res       Date:  2019-08-16       Impact factor: 4.164

9.  DJ-1 deficient mice demonstrate similar vulnerability to pathogenic Ala53Thr human alpha-syn toxicity.

Authors:  Chenere P Ramsey; Elpida Tsika; Harry Ischiropoulos; Benoit I Giasson
Journal:  Hum Mol Genet       Date:  2010-01-20       Impact factor: 6.150

10.  The transgenic overexpression of alpha-synuclein and not its related pathology associates with complex I inhibition.

Authors:  Virginie Loeb; Eugenia Yakunin; Ann Saada; Ronit Sharon
Journal:  J Biol Chem       Date:  2010-01-06       Impact factor: 5.157
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