Decreased proteolysis caused by protein aggregates, inclusion bodies, plaques, lipofuscin, ceroid, and 'aggresomes' during oxidative stress, aging, and disease.
about
Rule-based cell systems model of aging using feedback loop motifs mediated by stress responsesThe concept of translocational regulationPML clastosomes prevent nuclear accumulation of mutant ataxin-7 and other polyglutamine proteinsAdaptive preconditioning in neurological diseases – therapeutic insights from proteostatic perturbationsThe Ubiquitin-Proteasome System: Potential Therapeutic Targets for Alzheimer's Disease and Spinal Cord InjuryThe role of ALFY in selective autophagyAutophagy and heterophagy dysregulation leads to retinal pigment epithelium dysfunction and development of age-related macular degenerationMitochondrial quality control: decommissioning power plants in neurodegenerative diseasesRoles for the ubiquitin-proteasome pathway in protein quality control and signaling in the retina: implications in the pathogenesis of age-related macular degenerationHsp70.1 and related lysosomal factors for necrotic neuronal deathPostnatal proteasome inhibition induces neurodegeneration and cognitive deficiencies in adult mice: a new model of neurodevelopment syndromeProtective coupling of mitochondrial function and protein synthesis via the eIF2α kinase GCN-2Metacaspase Yca1 is required for clearance of insoluble protein aggregates.Accelerated aging and failure to segregate damaged proteins in Sir2 mutants can be suppressed by overproducing the protein aggregation-remodeling factor Hsp104pProtein carbonylation, cellular dysfunction, and disease progressionAcute decreases in proteasome pathway activity after inhalation of fresh diesel exhaust or secondary organic aerosolRegulation of proteasome activity in health and diseaseOxygen consumption and usage during physical exercise: the balance between oxidative stress and ROS-dependent adaptive signalingDynamic impacts of the inhibition of the molecular chaperone Hsp90 on the T-cell proteome have implications for anti-cancer therapyAutophagy in cell death: an innocent convict?Effect of thermal treatment on meat proteins with special reference to heterocyclic aromatic amines (HAAs).Microscopic analysis of protein oxidative damage: effect of carbonylation on structure, dynamics, and aggregability of villin headpieceOxidative stress resistance in Deinococcus radiodurans.Stress and aging induce distinct polyQ protein aggregation statesRole of proteasomes in disease.Proteasomes remain intact, but show early focal alteration in their composition in a mouse model of amyotrophic lateral sclerosis.Increased endoplasmic reticulum stress and decreased proteasomal function in lafora disease models lacking the phosphatase laforinThe ubiquitin-proteasome system in myocardial ischaemia and preconditioning.On to the road to degradation: atherosclerosis and the proteasomeThe age- and sex-specific decline of the 20s proteasome and the Nrf2/CncC signal transduction pathway in adaption and resistance to oxidative stress in Drosophila melanogasterRole of oxidative carbonylation in protein quality control and senescence.Defense against protein carbonylation by DnaK/DnaJ and proteases of the heat shock regulon.Proteasome inhibition modulates kinase activation in neural cells: relevance to ubiquitination, ribosomes, and survival.Lifelong calorie restriction alleviates age-related oxidative damage in peripheral nerves.Killer proteases and little strokes--how the things that do not kill you make you stronger.Novel bio-spectroscopic imaging reveals disturbed protein homeostasis and thiol redox with protein aggregation prior to hippocampal CA1 pyramidal neuron death induced by global brain ischemia in the rat.Posttranslational modification of differentially expressed mitochondrial proteins in the retina during early experimental autoimmune uveitis.Impairment of immunoproteasome function by β5i/LMP7 subunit deficiency results in severe enterovirus myocarditis.Pathological aspects of lipid peroxidation.Establishment of a novel fluorescence-based method to evaluate chaperone-mediated autophagy in a single neuron.
P2860
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P2860
Decreased proteolysis caused by protein aggregates, inclusion bodies, plaques, lipofuscin, ceroid, and 'aggresomes' during oxidative stress, aging, and disease.
description
2004 nî lūn-bûn
@nan
2004年の論文
@ja
2004年論文
@yue
2004年論文
@zh-hant
2004年論文
@zh-hk
2004年論文
@zh-mo
2004年論文
@zh-tw
2004年论文
@wuu
2004年论文
@zh
2004年论文
@zh-cn
name
Decreased proteolysis caused b ...... ve stress, aging, and disease.
@ast
Decreased proteolysis caused b ...... ve stress, aging, and disease.
@en
type
label
Decreased proteolysis caused b ...... ve stress, aging, and disease.
@ast
Decreased proteolysis caused b ...... ve stress, aging, and disease.
@en
prefLabel
Decreased proteolysis caused b ...... ve stress, aging, and disease.
@ast
Decreased proteolysis caused b ...... ve stress, aging, and disease.
@en
P50
P1476
Decreased proteolysis caused b ...... ive stress, aging, and disease
@en
P2093
Katrin Merker
P304
P356
10.1016/J.BIOCEL.2004.04.020
P577
2004-12-01T00:00:00Z