Protein degradation pathways in Parkinson's disease: curse or blessing - Test2 - elhamkhani - TriplyDB

Protein degradation pathways in Parkinson's disease: curse or blessing

Protein degradation pathways in Parkinson's disease: curse or blessing

http://www.wikidata.org/entity/Q27026029

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Polo-like kinase 2 regulates selective autophagic α-synuclein clearance and suppresses its toxicity in vivo Linking F-box protein 7 and parkin to neuronal degeneration in Parkinson's disease (PD)Mitochondria-Targeted Protective Compounds in Parkinson's and Alzheimer's Diseases What is the Clinical Significance of Cerebrospinal Fluid Biomarkers in Parkinson's disease? Is the Significance Diagnostic or Prognostic?Proteotoxicity: an underappreciated pathology in cardiac disease Ambroxol improves lysosomal biochemistry in glucocerebrosidase mutation-linked Parkinson disease cells Interactions of iron, dopamine and neuromelanin pathways in brain aging and Parkinson's disease Nigral proteasome inhibition in mice leads to motor and non-motor deficits and increased expression of Ser129 phosphorylated α-synuclein Molecular chaperones and protein folding as therapeutic targets in Parkinson's disease and other synucleinopathies Antihypertensive agents and risk of Parkinson's disease: a nationwide cohort study Integrated molecular landscape of Parkinson's disease Increased LINGO1 in the cerebellum of essential tremor patients.Synergistic effects on dopamine cell death in a Drosophila model of chronic toxin exposure.Accumulation of α-synuclein in dementia with Lewy bodies is associated with decline in the α-synuclein-degrading enzymes kallikrein-6 and calpain-1.ATP6V0C knockdown in neuroblastoma cells alters autophagy-lysosome pathway function and metabolism of proteins that accumulate in neurodegenerative disease.Alpha-synuclein levels in blood plasma decline with healthy aging.Dissecting the genetics of the human transcriptome identifies novel trait-related trans-eQTLs and corroborates the regulatory relevance of non-protein coding loci†.Interplay between Leucine-Rich Repeat Kinase 2 (LRRK2) and p62/SQSTM-1 in Selective Autophagy A Novel Hsp90 Inhibitor Activates Compensatory Heat Shock Protein Responses and Autophagy and Alleviates Mutant A53T α-Synuclein Toxicity.Age-related changes in the proteostasis network in the brain of the naked mole-rat: Implications promoting healthy longevity The activation sequence of cellular protein handling systems after proteasomal inhibition in dopaminergic cells.Dopaminergic neurotoxicity of S-ethyl N,N-dipropylthiocarbamate (EPTC), molinate, and S-methyl-N,N-diethylthiocarbamate (MeDETC) in Caenorhabditis elegans.DOPAL derived alpha-synuclein oligomers impair synaptic vesicles physiological function.Mechanisms underlying synaptic vulnerability and degeneration in neurodegenerative disease.Mitophagy and neurodegeneration: the zebrafish model system.Emerging role of autophagy in pediatric neurodegenerative and neurometabolic diseases.Immunotherapy targeting α-synuclein, with relevance for future treatment of Parkinson's disease and other Lewy body disorders.Protective and toxic roles of dopamine in Parkinson's disease.Ubiquitin-dependent proteolysis in yeast cells expressing neurotoxic proteins.Sirtuins and proteolytic systems: implications for pathogenesis of synucleinopathies.Proteasome properties of hemocytes differ between the whiteleg shrimp Penaeus vannamei and the brown shrimp Crangon crangon (Crustacea, Decapoda).Prolyl oligopeptidase and its role in the organism: attention to the most promising and clinically relevant inhibitors.Congenital disorders of autophagy: an emerging novel class of inborn errors of neuro-metabolism.Clathrin-Dependent Uptake of Paraquat into SH-SY5Y Cells and Its Internalization into Different Subcellular Compartments.Endothelin-converting enzymes degrade α-synuclein and are reduced in dementia with Lewy bodies.Of Pesticides and Men: a California Story of Genes and Environment in Parkinson's Disease.Impact of Plant-Derived Flavonoids on Neurodegenerative Diseases.Therapeutic potential of autophagy-enhancing agents in Parkinson's disease.Investigational α-synuclein aggregation inhibitors: hope for Parkinson's disease.Epigenetic regulation in Parkinson's disease.

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P2860

Protein degradation pathways in Parkinson's disease: curse or blessing

http://www.wikidata.org/entity/Q27026029

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2012 nî lūn-bûn

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2012 թուականի Օգոստոսին հրատարակուած գիտական յօդուած

@hyw

2012 թվականի օգոստոսին հրատարակված գիտական հոդված

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2012年の論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年論文

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2012年论文

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name

Protein degradation pathways in Parkinson's disease: curse or blessing

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Protein degradation pathways in Parkinson's disease: curse or blessing

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Protein degradation pathways in Parkinson's disease: curse or blessing

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type

label

Protein degradation pathways in Parkinson's disease: curse or blessing

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Protein degradation pathways in Parkinson's disease: curse or blessing

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Protein degradation pathways in Parkinson's disease: curse or blessing

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Protein degradation pathways in Parkinson's disease: curse or blessing

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Protein degradation pathways in Parkinson's disease: curse or blessing

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Acta Neuropathologica

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Protein degradation pathways in Parkinson's disease: curse or blessing

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Pamela J. McLean

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P2860

Leucine-rich repeat kinase 2 regulates autophagy through a calcium-dependent pathway involving NAADP

Homeostatic levels of p62 control cytoplasmic inclusion body formation in autophagy-deficient mice

Gaucher disease glucocerebrosidase and α-synuclein form a bidirectional pathogenic loop in synucleinopathies

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

Pre-fibrillar alpha-synuclein variants with impaired beta-structure increase neurotoxicity in Parkinson's disease models

HDAC6 and microtubules are required for autophagic degradation of aggregated huntingtin

Disrupted autophagy leads to dopaminergic axon and dendrite degeneration and promotes presynaptic accumulation of α-synuclein and LRRK2 in the brain

mTOR: from growth signal integration to cancer, diabetes and ageing

α-Synuclein propagates from mouse brain to grafted dopaminergic neurons and seeds aggregation in cultured human cells.

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Parkinson's disease

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