Protein aggregation and proteasome dysfunction after brain ischemia. - Wikidata - wikimedia - TriplyDB

Protein aggregation and proteasome dysfunction after brain ischemia.

Protein aggregation and proteasome dysfunction after brain ischemia.

http://www.wikidata.org/entity/Q37161571

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The ubiquitin proteasome system and myocardial ischemia Neuroinflammation and cerebrovascular disease in old age: a translational medicine perspective SOD1 aggregation in astrocytes following ischemia/reperfusion injury: a role of NO-mediated S-nitrosylation of protein disulfide isomerase (PDI)Heat shock proteins: cellular and molecular mechanisms in the central nervous system.Ischemic preconditioning induces chaperone hsp70 expression and inhibits protein aggregation in the CA1 neurons of rats Aging is not associated with proteasome impairment in UPS reporter mice.The ubiquitin-proteasome system in myocardial ischaemia and preconditioning.Role of the proteasome in excitotoxicity-induced cleavage of glutamic acid decarboxylase in cultured hippocampal neurons.Protein aggregation in neurons following OGD: a role for Na+ and Ca2+ ionic dysregulation.Ubiquitin C-terminal hydrolase-L1 as a biomarker for ischemic and traumatic brain injury in rats.Ischemic postconditioning protects neuronal death caused by cerebral ischemia and reperfusion via attenuating protein aggregation.Effects of N-stearoyl-L-tyrosine on the hippocampal ubiquitin-proteasome system in rats with chronic cerebral hypoperfusion.Implication of snail in metabolic stress-induced necrosis.Ischemic tolerance in an in vivo model of glutamate preconditioning.Reperfusion rather than ischemia drives the formation of ubiquitin aggregates after middle cerebral artery occlusion Ubiquitin C-terminal hydrolase is a novel biomarker in humans for severe traumatic brain injury Inhibition of immunoproteasome reduces infarction volume and attenuates inflammatory reaction in a rat model of ischemic stroke.Autophagy and protein aggregation after brain ischemia Role of oxygen consumption in hypoxia protection by translation factor depletion.Subcellular stress response and induction of molecular chaperones and folding proteins after transient global ischemia in rats.TAT-Hsp70 induces neuroprotection against stroke via anti-inflammatory actions providing appropriate cellular microenvironment for transplantation of neural precursor cells E2-25K SUMOylation inhibits proteasome for cell death during cerebral ischemia/reperfusion Ubiquilin-1 protects cells from oxidative stress and ischemic stroke caused tissue injury in mice.Molecular chaperones and hypoxic-ischemic encephalopathy Loss of endoplasmic reticulum Ca2+ homeostasis: contribution to neuronal cell death during cerebral ischemia.The novel proteasome inhibitor BSc2118 protects against cerebral ischaemia through HIF1A accumulation and enhanced angioneurogenesis.Protein misfolding, aggregation, and autophagy after brain ischemia.'Functional histology' in brain ischemia studies Short Chemical Ischemia Triggers Phosphorylation of eIF2α and Death of SH-SY5Y Cells but not Proteasome Stress and Heat Shock Protein Response in both SH-SY5Y and T98G Cells.Life and death in the trash heap: The ubiquitin proteasome pathway and UCHL1 in brain aging, neurodegenerative disease and cerebral Ischemia.rAAV8-733-Mediated Gene Transfer of CHIP/Stub-1 Prevents Hippocampal Neuronal Death in Experimental Brain Ischemia.USP14 inhibitor attenuates cerebral ischemia/reperfusion-induced neuronal injury in mice Enhanced Proteostasis in Post-ischemic Stroke Mouse Brains by Ubiquilin-1 Promotes Functional Recovery.Physiological and Pathological Roles of 15-Deoxy-Δ12,14-Prostaglandin J2 in the Central Nervous System and Neurological Diseases.Modification of ubiquitin-C-terminal hydrolase-L1 by cyclopentenone prostaglandins exacerbates hypoxic injury.Curcumin inhibits endoplasmic reticulum stress induced by cerebral ischemia-reperfusion injury in rats.The γ-secretase blocker DAPT reduces the permeability of the blood-brain barrier by decreasing the ubiquitination and degradation of occludin during permanent brain ischemia.Disease of mRNA Regulation: Relevance for Ischemic Brain Injury.Protein Modifications with Ubiquitin as Response to Cerebral Ischemia-Reperfusion Injury.Role of mitochondrial function in the protective effects of ischaemic postconditioning on ischaemia/reperfusion cerebral damage.

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P2860

Protein aggregation and proteasome dysfunction after brain ischemia.

http://www.wikidata.org/entity/Q37161571

description

2007 nî lūn-bûn

@nan

2007年の論文

@ja

2007年学术文章

@wuu

2007年学术文章

@zh-cn

2007年学术文章

@zh-hans

2007年学术文章

@zh-my

2007年学术文章

@zh-sg

2007年學術文章

@yue

2007年學術文章

@zh

2007年學術文章

@zh-hant

name

Protein aggregation and proteasome dysfunction after brain ischemia.

@en

Protein aggregation and proteasome dysfunction after brain ischemia.

@nl

type

label

Protein aggregation and proteasome dysfunction after brain ischemia.

@en

Protein aggregation and proteasome dysfunction after brain ischemia.

@nl

prefLabel

Protein aggregation and proteasome dysfunction after brain ischemia.

@en

Protein aggregation and proteasome dysfunction after brain ischemia.

@nl

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STROKEAHA.107.487108

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Protein aggregation and proteasome dysfunction after brain ischemia.

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Bingren Hu

http://www.w3.org/2001/XMLSchema#string

Cindy L Liu

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Pengfei Ge

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Yinan Luo

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P2860

The ubiquitin-proteasome proteolytic pathway: destruction for the sake of construction

Protein aggregation after focal brain ischemia and reperfusion.

Insoluble detergent-resistant aggregates form between pathological and nonpathological lengths of polyglutamine in mammalian cells

Protein denaturation and aggregation: Cellular responses to denatured and aggregated proteins.

Role and mechanisms of secondary mitochondrial failure.

Delayed neuronal death in the gerbil hippocampus following ischemia.

Global organization and function of mammalian cytosolic proteasome pools: Implications for PA28 and 19S regulatory complexes.

Co-translational protein aggregation after transient cerebral ischemia.

Ischemic preconditioning prevents protein aggregation after transient cerebral ischemia.

Protein ubiquitination in postsynaptic densities after transient cerebral ischemia.

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3230-3236

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10.1161/STROKEAHA.107.487108

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