Overstimulation of PrPC signaling pathways by prion peptide 106-126 causes oxidative injury of bioaminergic neuronal cells. - Wikidata - awgldk - TriplyDB

Overstimulation of PrPC signaling pathways by prion peptide 106-126 causes oxidative injury of bioaminergic neuronal cells.

Overstimulation of PrPC signaling pathways by prion peptide 106-126 causes oxidative injury of bioaminergic neuronal cells.

http://www.wikidata.org/entity/Q40251968

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Neuroprotective Effects Against POCD by Photobiomodulation: Evidence from Assembly/Disassembly of the Cytoskeleton The ubiquitin-proteasome system in spongiform degenerative disorders Neurotoxicity of prion peptides mimicking the central domain of the cellular prion protein Functions of the cellular prion protein, the end of Moore's law, and Ockham's razor theory Glimepiride reduces the expression of PrPc, prevents PrPSc formation and protects against prion mediated neurotoxicity in cell lines.Redox control of prion and disease pathogenesis.The extracellular regulated kinase-1 (ERK1) controls regulated alpha-secretase-mediated processing, promoter transactivation, and mRNA levels of the cellular prion protein.Prions impair bioaminergic functions through serotonin- or catecholamine-derived neurotoxins in neuronal cells.Double-Edge Sword of Sustained ROCK Activation in Prion Diseases through Neuritogenesis Defects and Prion Accumulation Prion protein at the crossroads of physiology and disease.The cellular prion protein (PrP(C)): its physiological function and role in disease Prion protein expression differences in microglia and astroglia influence scrapie-induced neurodegeneration in the retina and brain of transgenic mice Antioxidant peroxiredoxin 6 protein rescues toxicity due to oxidative stress and cellular hypoxia in vitro, and attenuates prion-related pathology in vivo Induction of ligand-specific PrP (C) signaling in human neuronal cells Pathogenic prions deviate PrP(C) signaling in neuronal cells and impair A-beta clearance Molecular nexopathies: a new paradigm of neurodegenerative disease.Lipid rafts and caveolae and their role in compartmentation of redox signaling.Caveolin regulation of neuronal intracellular signaling.Metal attenuating therapies in neurodegenerative disease.Prion protein and its role in signal transduction.Modelling neurodegeneration in prion disease - applications for drug development.Review of studies that have used knockout mice to assess normal function of prion protein under immunological or pathophysiological stress.Protective role of cellular prion protein against TNFα-mediated inflammation through TACE α-secretase.Membrane Disruption Mechanism of a Prion Peptide (106-126) Investigated by Atomic Force Microscopy, Raman and Electron Paramagnetic Resonance Spectroscopy.Dysfunction of the PI3K-Akt-GSK-3 pathway is a common feature in cell culture and in vivo models of prion disease.Aberrant ERK 1/2 complex activation and localization in scrapie-infected GT1-1 cells.The mechanism of membrane disruption by cytotoxic amyloid oligomers formed by prion protein(106-126) is dependent on bilayer composition.Reelin Expression in Creutzfeldt-Jakob Disease and Experimental Models of Transmissible Spongiform Encephalopathies.Regulation of Amyloid β Oligomer Binding to Neurons and Neurotoxicity by the Prion Protein-mGluR5 Complex.Secretory pathway retention of mutant prion protein induces p38-MAPK activation and lethal disease in mice.PrP(106-126) does not interact with membranes under physiological conditions.Interactions of the prion peptide (PrP 106-126) with brain capillary endothelial cells: coordinated cell killing and remodeling of intercellular junctions.PDK1 decreases TACE-mediated α-secretase activity and promotes disease progression in prion and Alzheimer's diseases.Prion protein regulates glutathione metabolism and neural glutamate and cysteine uptake via excitatory amino acid transporter 3.[From prion diseases to Alzheimer's disease: a common therapeutic target, PDK1].p62-Keap1-NRF2-ARE Pathway: A Contentious Player for Selective Targeting of Autophagy, Oxidative Stress and Mitochondrial Dysfunction in Prion Diseases Neuroprotective Effects of Radix Scrophulariae on Cerebral Ischemia and Reperfusion Injury via MAPK Pathways

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P2860

Overstimulation of PrPC signaling pathways by prion peptide 106-126 causes oxidative injury of bioaminergic neuronal cells.

http://www.wikidata.org/entity/Q40251968

description

2006 nî lūn-bûn

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2006年の論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年論文

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2006年论文

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2006年论文

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2006年论文

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name

Overstimulation of PrPC signal ...... f bioaminergic neuronal cells.

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type

label

Overstimulation of PrPC signal ...... f bioaminergic neuronal cells.

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Overstimulation of PrPC signal ...... f bioaminergic neuronal cells.

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P1433

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P1433

Journal of Biological Chemistry

P1476

Overstimulation of PrPC signal ...... f bioaminergic neuronal cells.

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P2093

Andréa Caprini

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Benoit Schneider

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Elodie Pradines

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Jacques Grassi

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Mathéa Pietri

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Myriam Ermonval

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Odile Kellermann

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Sophie Mouillet-Richard

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P2860

Mice devoid of PrP are resistant to scrapie

Anchorless prion protein results in infectious amyloid disease without clinical scrapie

Protein aggregation and neurodegenerative disease

Oxidative stress in neurodegeneration: cause or consequence?

Sustained extracellular signal-regulated kinase activation by 6-hydroxydopamine: implications for Parkinson's disease

Prolonged nuclear retention of activated extracellular signal-regulated protein kinase promotes cell death generated by oxidative toxicity or proteasome inhibition in a neuronal cell line

Protofibrils, pores, fibrils, and neurodegeneration: separating the responsible protein aggregates from the innocent bystanders

Molecular pathways of neurodegeneration in Parkinson's disease

Dendritic and synaptic alterations of hippocampal pyramidal neurones in scrapie-infected mice.

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28470-28479

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10.1074/JBC.M602774200

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38

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281

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6920870

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16864581

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P921

Prion protein family