IndraLab

Statements


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"Rokutan et al. [34] have reported that elevated levels of GSH inhibit the oxidant-induced activation of c-Jun and ATF-2."

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"In human hepatoma cells, GSH inhibited the egg product-induced activation of ERK, c-JUN, and STAT3 (Fig. 5A-C)."

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"We hypothesized that stretch induced cytokine production is dependent on oxidant release and is regulated by intracellular glutathione (GSH) inhibition of nuclear factor kappa B (NF-kappa B) and activator protein-1 (AP-1) binding."

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"Glutathione depletion inhibits oxidant induced activation of nuclear factor-kappa B, AP-1, and c-Jun and ATF -2 in cultured guinea-pig gastric epithelial cells."

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"The nuclear c-Jun phosphorylation was not observed in cells treated with reduced glutathione."

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"We hypothesized that stretch induced cytokine production is dependent on oxidant release and is regulated by intracellular glutathione (GSH) inhibition of nuclear factor kappa B (NF-kappa B) and activator protein-1 (AP-1) binding."

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"Conversely, there is also evidence that increased cellular glutathione levels by NAC inhibit the expression and transcriptional activity of c-Jun triggered by numerous stimuli XREF_BIBR, including the binding of c-Jun to the AP-1 element within the VEGF promoter XREF_BIBR."

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"GSH supplementation blocked JNK/c-Jun activation and cell death, demonstrating that JNK/c-Jun overactivation is the downstream effect of GSH depletion."

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"Besides, GSH depletion induced inflammation stress in neuronal tissues of PD patients by modulating IL-1 signaling and JNK- (c-Jun N-terminal kinase-) activated inflammatory pathways [105, 106]."

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"An increase in mitochondrial GSH levels in HepG2 cells protects cytochrome C and inhibits necroptosis via the c-Jun N-terminal kinases pathway [104]."