PINK1 Is Selectively Stabilized on Impaired Mitochondria to Activate Parkin

Mutations in PINK1 or Parkin lead to familial parkinsonism. The authors suggest that PINK1 and Parkin form a pathway that senses damaged mitochondria and selectively targets them for degradation.

[1]  A. Schapira Molecular and clinical pathways to neuroprotection of dopaminergic drugs in Parkinson disease , 2009, Neurology.

[2]  V. Hristova,et al.  Identification of a Novel Zn2+-binding Domain in the Autosomal Recessive Juvenile Parkinson-related E3 Ligase Parkin* , 2009, Journal of Biological Chemistry.

[3]  Bing Li,et al.  Respiratory Uncoupling Induces δ-Aminolevulinate Synthase Expression through a Nuclear Respiratory Factor-1-dependent Mechanism in HeLa Cells* , 1999, The Journal of Biological Chemistry.

[4]  A. Brice,et al.  A regulated interaction with the UIM protein Eps15 implicates parkin in EGF receptor trafficking and PI(3)K–Akt signalling , 2006, Nature Cell Biology.

[5]  S. Rodríguez-Enríquez,et al.  Tracker Dyes to Probe Mitochondrial Autophagy (Mitophagy) in Rat Hepatocytes , 2006, Autophagy.

[6]  A. Schapira Mitochondria in the aetiology and pathogenesis of Parkinson's disease , 2008, The Lancet Neurology.

[7]  Y. Agid,et al.  A wide variety of mutations in the parkin gene are responsible for autosomal recessive parkinsonism in Europe. French Parkinson's Disease Genetics Study Group and the European Consortium on Genetic Susceptibility in Parkinson's Disease. , 1999, Human molecular genetics.

[8]  M. Cookson,et al.  Pink1 forms a multiprotein complex with Miro and Milton, linking Pink1 function to mitochondrial trafficking. , 2009, Biochemistry.

[9]  Linda Hicke,et al.  Ubiquitin-binding domains , 2005, Nature Reviews Molecular Cell Biology.

[10]  H. M. Cochemé,et al.  Complex I Is the Major Site of Mitochondrial Superoxide Production by Paraquat* , 2008, Journal of Biological Chemistry.

[11]  Todd B. Sherer,et al.  Chronic systemic pesticide exposure reproduces features of Parkinson's disease , 2000, Nature Neuroscience.

[12]  David S. Park,et al.  Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission* , 2009, Journal of Biological Chemistry.

[13]  Kenneth Wu,et al.  Structure of the C-terminal RING finger from a RING-IBR-RING/TRIAD motif reveals a novel zinc-binding domain distinct from a RING. , 2004, Journal of molecular biology.

[14]  Joachim Klose,et al.  Mitochondrial Dysfunction and Oxidative Damage in parkin-deficient Mice* , 2004, Journal of Biological Chemistry.

[15]  N. Arnheim,et al.  Mosaicism for a specific somatic mitochondrial DNA mutation in adult human brain , 1992, Nature Genetics.

[16]  N. Wood,et al.  Mitochondrial function and morphology are impaired in parkin‐mutant fibroblasts , 2008, Annals of neurology.

[17]  R. D'Hooge,et al.  Mitochondrial Rhomboid PARL Regulates Cytochrome c Release during Apoptosis via OPA1-Dependent Cristae Remodeling , 2006, Cell.

[18]  Wei Jiang,et al.  Parkin, PINK1, and DJ-1 form a ubiquitin E3 ligase complex promoting unfolded protein degradation. , 2009, The Journal of clinical investigation.

[19]  William Lin,et al.  Characterization of PINK1 processing, stability, and subcellular localization , 2008, Journal of neurochemistry.

[20]  J. Langston,et al.  Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis. , 1983, Science.

[21]  Jie Shen,et al.  Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress , 2008, Proceedings of the National Academy of Sciences.

[22]  Y. Ohsumi,et al.  Mitochondria-anchored receptor Atg32 mediates degradation of mitochondria via selective autophagy. , 2009, Developmental cell.

[23]  Y. Tsujimoto,et al.  Intracellular ATP levels determine cell death fate by apoptosis or necrosis. , 1997, Cancer research.

[24]  C. Geula,et al.  Mitochondrial DNA deletions are abundant and cause functional impairment in aged human substantia nigra neurons , 2006, Nature Genetics.

[25]  J. C. Greene,et al.  Mitochondrial pathology and apoptotic muscle degeneration in Drosophila parkin mutants , 2003, Proceedings of the National Academy of Sciences of the United States of America.

[26]  S. Schreiber,et al.  Controlling protein association and subcellular localization with a synthetic ligand that induces heterodimerization of proteins. , 1996, Proceedings of the National Academy of Sciences of the United States of America.

[27]  Michael R. Duchen,et al.  PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death , 2009, Molecular cell.

[28]  YongSung Kim,et al.  PINK1 controls mitochondrial localization of Parkin through direct phosphorylation. , 2008, Biochemical and biophysical research communications.

[29]  A. Reichert,et al.  Loss-of-Function of Human PINK1 Results in Mitochondrial Pathology and Can Be Rescued by Parkin , 2007, The Journal of Neuroscience.

[30]  David W. Miller,et al.  Mutations in PTEN-induced putative kinase 1 associated with recessive parkinsonism have differential effects on protein stability. , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[31]  M. Beal,et al.  Mitochondrial pathology and muscle and dopaminergic neuron degeneration caused by inactivation of Drosophila Pink1 is rescued by Parkin. , 2006, Proceedings of the National Academy of Sciences of the United States of America.

[32]  C. Thompson,et al.  Ulk1 plays a critical role in the autophagic clearance of mitochondria and ribosomes during reticulocyte maturation. , 2008, Blood.

[33]  E. Schon,et al.  The kinase domain of mitochondrial PINK1 faces the cytoplasm , 2008, Proceedings of the National Academy of Sciences.

[34]  Robert W. Taylor,et al.  High levels of mitochondrial DNA deletions in substantia nigra neurons in aging and Parkinson disease , 2006, Nature Genetics.

[35]  D. James Surmeier,et al.  ‘Rejuvenation’ protects neurons in mouse models of Parkinson’s disease , 2007, Nature.

[36]  D. Klionsky,et al.  Atg32 is a mitochondrial protein that confers selectivity during mitophagy. , 2009, Developmental cell.

[37]  S. Budd,et al.  A Reevaluation of the Role of Mitochondria in Neuronal Ca2+ Homeostasis , 1996, Journal of neurochemistry.

[38]  R. Youle,et al.  Parkin is recruited selectively to impaired mitochondria and promotes their autophagy , 2008, The Journal of cell biology.

[39]  Changan Jiang,et al.  Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin , 2006, Nature.

[40]  P. Kapahi,et al.  Loss-of-Function Analysis Suggests That Omi/HtrA2 Is Not an Essential Component of the pink1/parkin Pathway In Vivo , 2008, The Journal of Neuroscience.

[41]  G. Shaw,et al.  A disease state mutation unfolds the parkin ubiquitin-like domain. , 2007, Biochemistry.

[42]  Sunhong Kim,et al.  Mitochondrial dysfunction in Drosophila PINK1 mutants is complemented by parkin , 2006, Nature.

[43]  J. Lee,et al.  Rhomboid-7 and HtrA 2 / Omi act in a common pathway with the Parkinson ’ s disease factors Pink 1 and Parkin , 2022 .

[44]  N. Quinn,et al.  A heterozygous effect for PINK1 mutations in Parkinson's disease? , 2006, Annals of neurology.

[45]  A. M. van der Bliek,et al.  Regulation of the mitochondrial dynamin-like protein Opa1 by proteolytic cleavage , 2007, The Journal of cell biology.

[46]  M. Müftüoğlu,et al.  Mitochondrial complex I and IV activities in leukocytes from patients with parkin mutations , 2004, Movement disorders : official journal of the Movement Disorder Society.

[47]  D. Chan,et al.  Disruption of Fusion Results in Mitochondrial Heterogeneity and Dysfunction* , 2005, Journal of Biological Chemistry.

[48]  David S. Park,et al.  Cytoplasmic Pink1 activity protects neurons from dopaminergic neurotoxin MPTP , 2008, Proceedings of the National Academy of Sciences.

[49]  V. Hristova,et al.  Structure of the Parkin in-between-ring domain provides insights for E3-ligase dysfunction in autosomal recessive Parkinson's disease , 2007, Proceedings of the National Academy of Sciences.

[50]  A. Whitworth,et al.  Drosophila HtrA2 is dispensable for apoptosis but acts downstream of PINK1 independently from Parkin , 2009, Cell Death and Differentiation.

[51]  David W. Miller,et al.  Mitochondrial Alterations in PINK1 Deficient Cells Are Influenced by Calcineurin-Dependent Dephosphorylation of Dynamin-Related Protein 1 , 2009, PloS one.

[52]  J. C. Greene,et al.  Increased glutathione S-transferase activity rescues dopaminergic neuron loss in a Drosophila model of Parkinson's disease , 2005, Proceedings of the National Academy of Sciences of the United States of America.

[53]  P. Flachs,et al.  Expression of the uncoupling protein 1 from the aP2 gene promoter stimulates mitochondrial biogenesis in unilocular adipocytes in vivo. , 2002, European journal of biochemistry.

[54]  F. Eisenhaber,et al.  The ring between ring fingers (RBR) protein family , 2007, Genome Biology.

[55]  Eva Lindqvist,et al.  Progressive parkinsonism in mice with respiratory-chain-deficient dopamine neurons , 2007, Proceedings of the National Academy of Sciences.

[56]  L. Peltonen,et al.  Parkinsonism, premature menopause, and mitochondrial DNA polymerase γ mutations: clinical and molecular genetic study , 2004, The Lancet.

[57]  A. Pestronk,et al.  Familial parkinsonism and ophthalmoplegia from a mutation in the mitochondrial DNA helicase twinkle. , 2007, Archives of neurology.

[58]  Douglas R. Porter,et al.  Impaired dopamine release and synaptic plasticity in the striatum of PINK1-deficient mice , 2007, Proceedings of the National Academy of Sciences.