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ACCEPTED MANUSCRIPT National Academy of Sciences of the United States of America 105 (2008) 1716-1721. [120] A. Wood-Kaczmar, S. Gandhi, Z. Yao, A.Y. Abramov, E.A. Miljan, G. Keen, L. Stanyer, I. Hargreaves, K. Klupsch, E. Deas, J. Downward, L. Mansfield, P. Jat, J. Taylor, S. Heales, M.R. Duchen, D. Latchman, S.J. Tabrizi, N.W. Wood, PINK1 is necessary for long term survival and mitochondrial function in human dopaminergic neurons, PLoS ONE 3 (2008) e2455. [121] S. Gandhi, A. Wood-Kaczmar, Z. Yao, H. Plun-Favreau, E. Deas, K. Klupsch, J. Downward, D.S. Latchman, S.J. Tabrizi, N.W. Wood, M.R. Duchen, A.Y. Abramov, PINK1-associated Parkinson's disease is caused by neuronal vulnerability to calcium-induced cell death, Molecular cell 33 (2009) 627-638. [122] C.A. Gautier, T. Kitada, J. Shen, Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress, Proceedings of the National Academy of Sciences of the United States of America 105 (2008) 11364-11369. [123] M.E. Gegg, J.M. Cooper, A.H. Schapira, J.W. Taanman, Silencing of PINK1 expression affects mitochondrial DNA and oxidative phosphorylation in ACCEPTED MANUSCRIPT dopaminergic cells, PLoS ONE 4 (2009) e4756. [124] S. Gispert, F. Ricciardi, A. Kurz, M. Azizov, H.H. Hoepken, D. Becker, W. Voos, K. Leuner, W.E. Muller, A.P. Kudin, W.S. Kunz, A. Zimmermann, J. Roeper, D. Wenzel, M. Jendrach, M. Garcia-Arencibia, J. Fernandez-Ruiz, L. Huber, H. Rohrer, M. Barrera, A.S. Reichert, U. Rub, A. Chen, R.L. Nussbaum, G. Auburger, Parkinson phenotype in aged PINK1-deficient mice is accompanied by progressive mitochondrial dysfunction in absence of neurodegeneration, PLoS ONE 4 (2009) e5777. 55
ACCEPTED MANUSCRIPT [125] A. Grunewald, M.E. Gegg, J.W. Taanman, R.H. King, N. Kock, C. Klein, A.H. Schapira, Differential effects of PINK1 nonsense and missense mutations on mitochondrial function and morphology, Experimental neurology (2009). [126] H.H. Hoepken, S. Gispert, B. Morales, O. Wingerter, D. Del Turco, A. Mulsch, R.L. Nussbaum, K. Muller, S. Drose, U. Brandt, T. Deller, B. Wirth, A.P. Kudin, W.S. Kunz, G. Auburger, Mitochondrial dysfunction, peroxidation damage and changes in glutathione metabolism in PARK6, Neurobiology of disease 25 (2007) 401-411. [127] W. Liu, C. Vives-Bauza, R. Acin-Perez, A. Yamamoto, Y. Tan, Y. Li, J. Magrane, M.A. Stavarache, S. Shaffer, S. Chang, M.G. Kaplitt, X.Y. Huang, M.F. Beal, G. Manfredi, C. Li, PINK1 defect causes mitochondrial dysfunction, proteasomal deficit and alpha-synuclein aggregation in cell culture models of Parkinson's disease, PLoS ONE 4 (2009) e4597. [128] R. Marongiu, B. Spencer, L. Crews, A. Adame, C. Patrick, M. Trejo, B. Dallapiccola, E.M. Valente, E. Masliah, Mutant Pink1 induces mitochondrial dysfunction in a neuronal cell model of Parkinson's disease by disturbing ACCEPTED MANUSCRIPT calcium flux, Journal of neurochemistry 108 (2009) 1561-1574. [129] R.K. Dagda, S.J. Cherra, 3rd, S.M. Kulich, A. Tandon, D. Park, C.T. Chu, Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission, The Journal of biological chemistry 284 (2009) 13843-13855. [130] A. Sandebring, K.J. Thomas, A. Beilina, M. van der Brug, M.M. Cleland, R. Ahmad, D.W. Miller, I. Zambrano, R.F. Cowburn, H. Behbahani, A. Cedazo- Minguez, M.R. Cookson, Mitochondrial alterations in PINK1 deficient cells 56
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Page 83 and 84: ACCEPTED MANUSCRIPT Ferrante, N.W.
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