A pivotal role for PINK1 and autophagy in mitochondrial quality control: implications for Parkinson disease

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The Parkinson-associated protein PINK1 interacts with Beclin1 and promotes autophagy

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Parkin stabilizes PINK1 through direct interaction

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c-Jun NH2-Terminal Kinase Activation Is Essential for DRAM-Dependent Induction of Autophagy and Apoptosis in 2-Methoxyestradiol-Treated Ewing Sarcoma Cells

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Atg32 Is a Mitochondrial Protein that Confers Selectivity during Mitophagy

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Parkinson's disease mutations in PINK1 result in decreased Complex I activity and deficient synaptic function

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Mitochondrial Gene Therapy Augments Mitochondrial Physiology in a Parkinson's Disease Cell Model

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Mitochondrial quality control: insights on how Parkinson’s disease related genes PINK1, parkin, and Omi/HtrA2 interact to maintain mitochondrial homeostasis

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The PINK1/Parkin pathway: a mitochondrial quality control system?

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Loss of Parkin or PINK1 Function Increases Drp1-dependent Mitochondrial Fragmentation

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Loss of PINK1 Function Promotes Mitophagy through Effects on Oxidative Stress and Mitochondrial Fission

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Parkin, PINK1, and DJ-1 form a ubiquitin E3 ligase complex promoting unfolded protein degradation

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Mutant Pink1 induces mitochondrial dysfunction in a neuronal cell model of Parkinson’s disease by disturbing calcium flux

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Loss-of-Function Analysis Suggests That Omi/HtrA2 Is Not an Essential Component of the pink1/parkin Pathway In Vivo

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Mitochondrial kinases in Parkinson’s disease: Converging insights from neurotoxin and genetic models

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Molecular interaction between parkin and PINK1 in mammalian neuronal cells

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PINK1-Associated Parkinson's Disease Is Caused by Neuronal Vulnerability to Calcium-Induced Cell Death

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Discovery of Atg5/Atg7-independent alternative macroautophagy

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PINK1 Defect Causes Mitochondrial Dysfunction, Proteasomal Deficit and α-Synuclein Aggregation in Cell Culture Models of Parkinson's Disease

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Silencing of PINK1 Expression Affects Mitochondrial DNA and Oxidative Phosphorylation in DOPAMINERGIC Cells

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Mitochondrial Alterations in PINK1 Deficient Cells Are Influenced by Calcineurin-Dependent Dephosphorylation of Dynamin-Related Protein 1

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Parkinson Phenotype in Aged PINK1-Deficient Mice Is Accompanied by Progressive Mitochondrial Dysfunction in Absence of Neurodegeneration

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FOXO3a-dependent regulation of Pink1 (Park6) mediates survival signaling in response to cytokine deprivation

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Mitochondrial protein homeostasis: the cooperative roles of chaperones and proteases

(2009) Wolfgang Voos   RESEARCH IN MICROBIOLOGY

Autophagy activation and enhanced mitophagy characterize the Purkinje cells of pcd mice prior to neuronal death

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PINK1 controls mitochondrial localization of Parkin through direct phosphorylation

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Role of non-canonical Beclin 1-independent autophagy in cell death induced by resveratrol in human breast cancer cells

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Rhomboid-7 and HtrA2/Omi act in a common pathway with the Parkinson's disease factors Pink1 and Parkin

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Fission and selective fusion govern mitochondrial segregation and elimination by autophagy

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Shaping mitochondria: The complex posttranslational regulation of the mitochondrial fission protein DRP1

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Parkin is recruited selectively to impaired mitochondria and promotes their autophagy

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Characterization of PINK1 processing, stability, and subcellular localization

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Role of autophagy in G2019S-LRRK2-associated neurite shortening in differentiated SH-SY5Y cells

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Neuroinflammation and Oxidation/Nitration of  -Synuclein Linked to Dopaminergic Neurodegeneration

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Mitochondrial localization of alpha-synuclein protein in alpha-synuclein overexpressing cells

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PINK1 Is Necessary for Long Term Survival and Mitochondrial Function in Human Dopaminergic Neurons

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Cytoplasmic Pink1 activity protects neurons from dopaminergic neurotoxin MPTP

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Loss of PINK1 causes mitochondrial functional defects and increased sensitivity to oxidative stress

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The kinase domain of mitochondrial PINK1 faces the cytoplasm

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