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Regulation of ER stress proteins by valproate: therapeutic implications.

Regulation of ER stress proteins by valproate: therapeutic implications.

http://www.wikidata.org/entity/Q34692778

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Endoplasmic Reticulum Stress and Associated ROS Xenobiotic perturbation of ER stress and the unfolded protein response Conversion of psychological stress into cellular stress response: roles of the sigma-1 receptor in the process Bax inhibitor 1, a modulator of calcium homeostasis, confers affective resilience.A review of the mammalian unfolded protein response.Valproate Attenuates 25-kDa C-Terminal Fragment of TDP-43-Induced Neuronal Toxicity via Suppressing Endoplasmic Reticulum Stress and Activating Autophagy.Decreased gene expression activity as a result of a mutation in the calreticulin gene promoter in a family case of schizoaffective disorder.Epigenetic differences in monozygotic twins discordant for major depressive disorder Mechanism of the Inhibitory Effects of Eucommia ulmoides Oliv. Cortex Extracts (EUCE) in the CCl 4 -Induced Acute Liver Lipid Accumulation in Rats.Endoplasmic reticulum stress: its role in disease and novel prospects for therapy.Translating neurotrophic and cellular plasticity: from pathophysiology to improved therapeutics for bipolar disorder.Valproate and neuroprotective effects for bipolar disorder.Role of endoplasmic reticulum stress in metabolic disease and other disorders.Pathological parainflammation and endoplasmic reticulum stress in depression: potential translational targets through the CNS insulin, klotho and PPAR-γ systems.Challenges in drug target discovery in bipolar disorder.The unfolded protein response triggered by environmental factors.The rise of proteostasis promoters.Valproate attenuates diabetic nephropathy through inhibition of endoplasmic reticulum stress‑induced apoptosis.Valproate protects dopaminergic neurons in midbrain neuron/glia cultures by stimulating the release of neurotrophic factors from astrocytes.Valproic acid inhibits histone deacetylase activity and suppresses excitotoxicity-induced GAPDH nuclear accumulation and apoptotic death in neurons.Endoplasmic reticulum stress and apoptosis signaling in human temporal lobe epilepsy.

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Regulation of ER stress proteins by valproate: therapeutic implications.

http://www.wikidata.org/entity/Q34692778

description

2002 nî lūn-bûn

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2002 թուականի Ապրիլին հրատարակուած գիտական յօդուած

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2002 թվականի ապրիլին հրատարակված գիտական հոդված

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2002年の論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年論文

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2002年论文

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name

Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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Regulation of ER stress proteins by valproate: therapeutic implications.

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J.1399-5618.2002.T01-1-40201.X

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Bipolar Disorders

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Regulation of ER stress proteins by valproate: therapeutic implications

@en

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Biao Chen

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

Christopher D Bown

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L Trevor Young

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P2860

Identification of the cis-acting endoplasmic reticulum stress response element responsible for transcriptional induction of mammalian glucose-regulated proteins. Involvement of basic leucine zipper transcription factors

Chronic cardiac rejection: identification of five upregulated genes in transplanted hearts by differential mRNA display

An Hsp70-like protein in the ER: identity with the 78 kd glucose-regulated protein and immunoglobulin heavy chain binding protein

The mood-stabilizing agents lithium and valproate robustly increase the levels of the neuroprotective protein bcl-2 in the CNS

Chronic valproate treatment increases expression of endoplasmic reticulum stress proteins in the rat cerebral cortex and hippocampus

Abnormal processing of multiple proteins in Alzheimer disease.

Alterations of intracellular calcium homeostasis and mitochondrial function are involved in ruthenium red neurotoxicity in primary cortical cultures.

Long term lithium treatment suppresses p53 and Bax expression but increases Bcl-2 expression. A prominent role in neuroprotection against excitotoxicity.

Expression of heat shock proteins in Alzheimer's disease.

Chronic lithium treatment robustly protects neurons in the central nervous system against excitotoxicity by inhibiting N-methyl-D-aspartate receptor-mediated calcium influx

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145-151

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10.1034/J.1399-5618.2002.T01-1-40201.X

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