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NATURE, ISSN 0028-0836, 06/2014, Volume 510, Issue 7503, pp. 44 - 44
Two enzymes implicated in Parkinson's disease, PINK1 and parkin1,2, are thought to be involved in the disposal of defective mitochondria, but how the two... 
MULTIDISCIPLINARY SCIENCES | Ubiquitin | Protein research | Parkinson's disease | Physiological aspects | Research | Neurological research | Health aspects | Nerve proteins | Protein-protein interactions | Proteins | Studies | Enzymes | Phosphorylation | Mitochondria | Parkinsons disease | Mutation | Kinases
Journal Article
Nature, ISSN 0028-0836, 2014, Volume 510, Issue 7503, pp. 44 - 45
Journal Article
Nature, ISSN 0028-0836, 02/2010, Volume 463, Issue 7282, pp. 744 - 745
Cells that are deficient in Parkin, or that have diseaseassociated Parkin mutations, fail to rid themselves of defective mitochondria; by contrast, Parkin... 
Mitochondria | Parkinson's disease | Gene mutations | Causes of | Genetic aspects | Health aspects | Protein kinases | Mutation | Kinases | Quality control | Parkinsons disease
Journal Article
Nature, ISSN 0028-0836, 05/2016, Volume 533, Issue 7601, pp. 40 - 41
Genome-wide association studies have identified swathes of the human genome in which DNA sequence changes are associated with an altered likelihood that an... 
Studies | Proteins | Brain | Medical research | Stem cells | Parkinsons disease | Genomes | Gene expression | Deoxyribonucleic acid--DNA
Journal Article
Neuron, ISSN 0896-6273, 11/2006, Volume 52, Issue 4, pp. 587 - 593
Mutations in underlie an autosomal-dominant, inherited form of Parkinson's disease (PD) that mimics the clinical features of the common “sporadic” form of PD.... 
HUMDISEASE | MOLNEURO | SIGNALING | AUTOSOMAL-DOMINANT PARKINSONISM | MECHANISM | TRANSCRIPTION | DISEASE | NEURONS | SYNUCLEIN | MUTATIONS | OUTGROWTH | PATHOLOGY | NEUROSCIENCES | Substantia Nigra - physiopathology | Substantia Nigra - pathology | Humans | Lysosomes - genetics | Nerve Degeneration - physiopathology | Nerve Degeneration - genetics | tau Proteins - metabolism | Apoptosis - genetics | Cell Shape - genetics | Substantia Nigra - metabolism | Nerve Degeneration - metabolism | Brain - metabolism | Parkinsonian Disorders - metabolism | Lysosomes - metabolism | tau Proteins - genetics | Lysosomes - pathology | Parkinsonian Disorders - genetics | Inclusion Bodies - metabolism | Animals, Newborn | Parkinsonian Disorders - physiopathology | Genetic Predisposition to Disease - genetics | Brain - physiopathology | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Rats | Neurites - metabolism | Mutation - genetics | Rats, Sprague-Dawley | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Neurites - pathology | Inclusion Bodies - genetics | Animals | Brain - pathology | Inclusion Bodies - pathology | Mice | Neurons | Genetic aspects | Parkinson's disease | Proteins | Pathology | Cell culture | Dopamine | Microscopy | Plasmids | Software | Mutation | Kinases | Polyclonal antibodies | Index Medicus
Journal Article
Neuron, ISSN 0896-6273, 02/2013, Volume 77, Issue 3, pp. 425 - 439
Recent genome-wide association studies have linked common variants in the human genome to Parkinson@s disease (PD) risk. Here we show that the consequences of... 
LOCALIZATION | RETROMER | TRANSPORT | COMPLEX | KINASE | GENE-EXPRESSION | TRAFFICKING | ALPHA | NEURODEGENERATION | MICE | NEUROSCIENCES | rab5 GTP-Binding Proteins - genetics | Immunoprecipitation | Humans | Middle Aged | Cerebral Cortex - pathology | Male | Tubulin - genetics | rab GTP-Binding Proteins - genetics | Green Fluorescent Proteins - genetics | Statistics as Topic | Vesicle-Associated Membrane Protein 2 - genetics | Cerebral Cortex - cytology | Tyrosine 3-Monooxygenase | rab5 GTP-Binding Proteins - metabolism | Tubulin - metabolism | Transfection | Aged, 80 and over | Female | Neurons - metabolism | Parkinson Disease - metabolism | Protein-Serine-Threonine Kinases - metabolism | Animals, Newborn | Synaptosomal-Associated Protein 25 - genetics | rab GTP-Binding Proteins - metabolism | Genetic Predisposition to Disease | Genome-Wide Association Study | Parkinson Disease - pathology | Animals, Genetically Modified | Drosophila | Cells, Cultured | Protein-Serine-Threonine Kinases - genetics | Rats | Parkinson Disease - genetics | Mutation - genetics | Rats, Sprague-Dawley | Protein Transport - genetics | Leucine-Rich Repeat Serine-Threonine Protein Kinase-2 | Animals | Polymorphism, Single Nucleotide - genetics | Aged | Mice | Synaptosomal-Associated Protein 25 - metabolism | Vesicle-Associated Membrane Protein 2 - metabolism | Parkinson's disease | Neurons | Genomics | Risk factors | Brain | Laboratories | Parkinsons disease | Kinases | Gene expression | Experiments | Defects | Proteins | Pathology | Insects | Neurodegeneration | Gene loci | Mutation | Index Medicus
Journal Article
Journal Article
Nature, ISSN 0028-0836, 08/2012, Volume 488, Issue 7413, pp. 652 - 655
Journal Article
Alzheimer's & Dementia: The Journal of the Alzheimer's Association, ISSN 1552-5260, 2011, Volume 7, Issue 4, pp. S119 - S119
Journal Article
Molecular Neurodegeneration, ISSN 1750-1326, 2012, Volume 7, Issue 1, pp. 48 - 48
Journal Article
Journal Article
Alzheimer's & Dementia: The Journal of the Alzheimer's Association, ISSN 1552-5260, 2010, Volume 6, Issue 4, pp. S167 - S167
Journal Article
Cell Reports, ISSN 2211-1247, 11/2017, Volume 21, Issue 7, pp. 1727 - 1736
Mutations in presenilin ( ) 1 and 2, which encode components of the γ-secretase (GS) complex, cause familial Alzheimer’s disease (FAD). It is hypothesized that... 
BACE1 | γ-secretase processivity | fibroblast | CRISPR/Cas9 | Alzheimer’s disease | induced neuronal cells | amyloid precursor protein | presenilin | synergistic activation mediator | β-amyloid | CRISPR | Presenilin | Synergistic Activation Mediator | Cas9
Journal Article