Title : Differential role of glutaredoxin and thioredoxin in metabolic oxidative stress-induced activation of apoptosis signal-regulating kinase 1.

Pub. Date : 2003 Aug 1

PMID : 12723971






6 Functional Relationships(s)
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1 L-Buthionine-( S, R )-sulphoximine, which decreases intracellular glutathione content, enhanced glucose deprivation-induced activation of JNK1 by promoting the dissociation of TRX, but not GRX, from ASK1. l-buthionine-( s, r )-sulphoximine mitogen-activated protein kinase kinase kinase 5 Homo sapiens
2 L-Buthionine-( S, R )-sulphoximine, which decreases intracellular glutathione content, enhanced glucose deprivation-induced activation of JNK1 by promoting the dissociation of TRX, but not GRX, from ASK1. Glucose mitogen-activated protein kinase kinase kinase 5 Homo sapiens
3 Treatment of cells with exogenous glutathione disulphide ester resulted in the dissociation of GRX, but not TRX, from ASK1 and the subsequent activation of JNK1. glutathione disulphide ester mitogen-activated protein kinase kinase kinase 5 Homo sapiens
4 Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways. Glucose mitogen-activated protein kinase kinase kinase 5 Homo sapiens
5 Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways. Glutathione mitogen-activated protein kinase kinase kinase 5 Homo sapiens
6 Taken together, glucose deprivation-induced metabolic oxidative stress may activate ASK1 through two different pathways: glutathione-dependent GRX-ASK1 and glutathione-independent TRX-ASK1 pathways. Glutathione mitogen-activated protein kinase kinase kinase 5 Homo sapiens