Hormesis: protecting neurons against cellular stress in Parkinson disease. - Wikidata - awgldk - TriplyDB

Hormesis: protecting neurons against cellular stress in Parkinson disease.

Hormesis: protecting neurons against cellular stress in Parkinson disease.

http://www.wikidata.org/entity/Q39575131

about

Hormesis in aging and neurodegeneration-a prodigy awaiting dissection Functional contribution of the transcription factor ATF4 to the pathogenesis of amyotrophic lateral sclerosis Control of dopaminergic neuron survival by the unfolded protein response transcription factor XBP1 α-Synuclein is involved in manganese-induced ER stress via PERK signal pathway in organotypic brain slice cultures Hormetic effect of panaxatriol saponins confers neuroprotection in PC12 cells and zebrafish through PI3K/AKT/mTOR and AMPK/SIRT1/FOXO3 pathways.Differential adiponectin signalling couples ER stress with lipid metabolism to modulate ageing in C. elegans Pathogenic role of BECN1/Beclin 1 in the development of amyotrophic lateral sclerosis.Impairment of visual function and retinal ER stress activation in Wfs1-deficient mice.Getting the better of ER stress.Nur77 exacerbates PC12 cellular injury in vitro by aggravating mitochondrial impairment and endoplasmic reticulum stress.Berberine protects against 6-OHDA-induced neurotoxicity in PC12 cells and zebrafish through hormetic mechanisms involving PI3K/AKT/Bcl-2 and Nrf2/HO-1 pathways.Adaptation and sensitization to proteotoxic stress.The Caenorhabditis elegans HP1 family protein HPL-2 maintains ER homeostasis through the UPR and hormesis Disturbance of endoplasmic reticulum proteostasis in neurodegenerative diseases.A Comprehensive View of the Neurotoxicity Mechanisms of Cocaine and Ethanol.The role of endoplasmic reticulum stress in neurodegenerative disease.The Endoplasmic Reticulum Unfolded Protein Response in Neurodegenerative Disorders and Its Potential Therapeutic Significance ER Stress and Neurodegenerative Disease: A Cause or Effect Relationship?ER proteostasis disturbances in Parkinson's disease: novel insights.Gold nanoparticles reduce high glucose-induced oxidative-nitrosative stress regulated inflammation and apoptosis via tuberin-mTOR/NF-κB pathways in macrophages.mTORC1 activation decreases autophagy in aging and idiopathic pulmonary fibrosis and contributes to apoptosis resistance in IPF fibroblasts.Ameliorative Effect of Quercetin on Neurochemical and Behavioral Deficits in Rotenone Rat Model of Parkinson's Disease: Modulating Autophagy (Quercetin on Experimental Parkinson's Disease).Mild endoplasmic reticulum stress ameliorates lipopolysaccharide-induced neuroinflammation and cognitive impairment via regulation of microglial polarization.Evidence for cross-hemispheric preconditioning in experimental Parkinson's disease.Conditioning Against the Pathology of Parkinson's disease

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Hormesis: protecting neurons against cellular stress in Parkinson disease.

http://www.wikidata.org/entity/Q39575131

description

2012 nî lūn-bûn

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2012年の論文

@ja

2012年論文

@yue

2012年論文

@zh-hant

2012年論文

@zh-hk

2012年論文

@zh-mo

2012年論文

@zh-tw

2012年论文

@wuu

2012年论文

@zh

2012年论文

@zh-cn

name

Hormesis: protecting neurons against cellular stress in Parkinson disease.

@en

Hormesis: protecting neurons against cellular stress in Parkinson disease.

@nl

type

label

Hormesis: protecting neurons against cellular stress in Parkinson disease.

@en

Hormesis: protecting neurons against cellular stress in Parkinson disease.

@nl

prefLabel

Hormesis: protecting neurons against cellular stress in Parkinson disease.

@en

Hormesis: protecting neurons against cellular stress in Parkinson disease.

@nl

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Hormesis: protecting neurons against cellular stress in Parkinson disease.

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Claudio Hetz

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

Karen Castillo

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Soledad Matus

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P2860

Autophagy suppresses tumorigenesis through elimination of p62

XBP-1 deficiency in the nervous system protects against amyotrophic lateral sclerosis by increasing autophagy

Cellular stress responses, the hormesis paradigm, and vitagenes: novel targets for therapeutic intervention in neurodegenerative disorders

mTORC1 serves ER stress-triggered apoptosis via selective activation of the IRE1-JNK pathway

Autophagy and the integrated stress response

Autophagy is activated for cell survival after endoplasmic reticulum stress

The unfolded protein response: controlling cell fate decisions under ER stress and beyond

IRE1 signaling affects cell fate during the unfolded protein response

Autophagy and aging

Adaptation to ER stress is mediated by differential stabilities of pro-survival and pro-apoptotic mRNAs and proteins

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997-1001

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scholarly article

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10.4161/AUTO.20748

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6

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8

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2012-06-01T00:00:00Z

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230615139

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22858553

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Parkinson's disease

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3427272

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