Protein kinase Cδ mediates trimethyltin-induced neurotoxicity in mice in vivo via inhibition of glutathione defense mechanism
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Title
Protein kinase Cδ mediates trimethyltin-induced neurotoxicity in mice in vivo via inhibition of glutathione defense mechanism
Authors
Keywords
PKCδ gene, Oxidative burdens, Nrf-2, Glutathione, PI3K/Akt signaling, Trimethyltin
Journal
ARCHIVES OF TOXICOLOGY
Volume 90, Issue 4, Pages 937-953
Publisher
Springer Nature
Online
2015-04-17
DOI
10.1007/s00204-015-1516-7
References
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- Redox Control of Protein Kinase C: Cell- and Disease-Specific Aspects
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- Enhanced Expression of Glutathione S-Transferase in the Hippocampus Following Acute Treatment With Trimethyltin In Vivo
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- Endogenous and Exogenous Glucocorticoids Prevent Trimethyltin From Causing Neuronal Degeneration of the Mouse Brain In Vivo: Involvement of Oxidative Stress Pathways
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- Deficits in Phosphorylation of GABAA Receptors by Intimately Associated Protein Kinase C Activity Underlie Compromised Synaptic Inhibition during Status Epilepticus
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- In vivo depletion of endogenous glutathione facilitates trimethyltin-induced neuronal damage in the dentate gyrus of mice by enhancing oxidative stress
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