Loss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore opening - Wikidata - wikimedia - TriplyDB

Loss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore opening

Loss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore opening

http://www.wikidata.org/entity/Q34336431

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Parkinson's disease proteins: Novel mitochondrial targets for cardioprotection Electron Transport Disturbances and Neurodegeneration: From Albert Szent-Györgyi's Concept (Szeged) till Novel Approaches to Boost Mitochondrial Bioenergetics Oxidative stress and Parkinson's disease Mitochondrial dysfunction and oxidative stress in Parkinson's disease Use of cysteine-reactive cross-linkers to probe conformational flexibility of human DJ-1 demonstrates that Glu18 mutations are dimers Mitochondrial permeability transition pore regulates Parkinson's disease development in mutant α-synuclein transgenic mice.Mechanisms of Parkinson's disease-related proteins in mediating secondary brain damage after cerebral ischemia.Products of the Parkinson's disease-related glyoxalase DJ-1, D-lactate and glycolate, support mitochondrial membrane potential and neuronal survival Decreased DJ-1 leads to impaired Nrf2-regulated antioxidant defense and increased UV-A-induced apoptosis in corneal endothelial cells.Monomer DJ-1 and its N-terminal sequence are necessary for mitochondrial localization of DJ-1 mutants.Gender-dimorphic regulation of DJ1 and its interactions with metabolic proteins in streptozotocin-induced diabetic rats.Penicillium chrysogenum as a model system for studying cellular effects of methylglyoxal.DJ-1 links muscle ROS production with metabolic reprogramming and systemic energy homeostasis in mice.TRNA mutations that affect decoding fidelity deregulate development and the proteostasis network in zebrafish Neuroprotective function of DJ-1 in Parkinson's disease.Hyperglycemia-induced inhibition of DJ-1 expression compromised the effectiveness of ischemic postconditioning cardioprotection in rats.Subcellular localization of DJ-1 in human HL-60 leukemia cells in response to diallyl disulfide treatment.DJ-1 protects against cell death following acute cardiac ischemia-reperfusion injury.Mitochondrial dysfunction and mitophagy: the beginning and end to diabetic nephropathy?Relative importance of βcyto- and γcyto-actin in primary mouse embryonic fibroblasts.Calcium signaling in Parkinson's disease.Impaired mitochondrial homeostasis and neurodegeneration: towards new therapeutic targets?Mitochondrial control of cell bioenergetics in Parkinson's disease.Defects in GABA metabolism affect selective autophagy pathways and are alleviated by mTOR inhibition.Diallyl sulfide as a potential dietary agent to reduce TNF-α- and histamine-induced proinflammatory responses in A7r5 cells.Cyclosporine A Treatment Abrogates Ischemia-Induced Neuronal Cell Death by Preserving Mitochondrial Integrity through Upregulation of the Parkinson's Disease-Associated Protein DJ-1.Hexokinases link DJ-1 to the PINK1/parkin pathway.Parkinson's disease-related DJ-1 functions in thiol quality control against aldehyde attack in vitro.Evidence of oxidative stress in young and aged DJ-1-deficient mice.The Parkinson's disease-associated protein DJ-1 plays a positive nonmitochondrial role in endocytosis in Dictyostelium cells.Mitochondria: A Common Target for Genetic Mutations and Environmental Toxicants in Parkinson's Disease.DJ-1/PARK7, But Not Its L166P Mutant Linked to Autosomal Recessive Parkinsonism, Modulates the Transcriptional Activity of the Orphan Nuclear Receptor Nurr1 In Vitro and In Vivo.Unexpected mitochondrial matrix localization of Parkinson's disease-related DJ-1 mutants but not wild-type DJ-1.Natural Molecules From Chinese Herbs Protecting Against Parkinson's Disease via Anti-oxidative Stress

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P2860

Loss of DJ-1 does not affect mitochondrial respiration but increases ROS production and mitochondrial permeability transition pore opening

http://www.wikidata.org/entity/Q34336431

description

2012 nî lūn-bûn

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2012 թուականի Յուլիսին հրատարակուած գիտական յօդուած

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2012 թվականի հուլիսին 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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Loss of DJ-1 does not affect m ...... bility transition pore opening

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Loss of DJ-1 does not affect m ...... bility transition pore opening

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Loss of DJ-1 does not affect m ...... bility transition pore opening

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Loss of DJ-1 does not affect m ...... bility transition pore opening

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Loss of DJ-1 does not affect m ...... bility transition pore opening

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Loss of DJ-1 does not affect m ...... bility transition pore opening

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Loss of DJ-1 does not affect m ...... bility transition pore opening

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Clement A Gautier

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Emilie Giaime

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Hiroo Yamaguchi

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Jie Shen

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Tohru Kitada

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P2860

Down regulation of DJ-1 enhances cell death by oxidative stress, ER stress, and proteasome inhibition

DJ-1, a cancer- and Parkinson's disease-associated protein, stabilizes the antioxidant transcriptional master regulator Nrf2

DJ-1 has a role in antioxidative stress to prevent cell death

Mutations in the parkin gene cause autosomal recessive juvenile parkinsonism

RNA binding activity of the recessive parkinsonism protein DJ-1 supports involvement in multiple cellular pathways

Mutations in the DJ-1 gene associated with autosomal recessive early-onset parkinsonism

Mitochondrial localization of DJ-1 leads to enhanced neuroprotection

Hereditary early-onset Parkinson's disease caused by mutations in PINK1

Presenilins are essential for regulating neurotransmitter release

Redox mechanisms in hepatic chronic wound healing and fibrogenesis

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