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GCLC — JUN
Protein-Protein interactions - manually collected from original source literature:
Studies that report less than 10 interactions are marked with *
Text-mined interactions from Literome
Manna et al., Oncogene 1999
:
Overexpression of
gamma-glutamylcysteine synthetase suppresses tumor necrosis factor induced apoptosis and activation of nuclear transcription factor-kappa B and
activator protein-1
Urata et al., Free Radic Biol Med 1999
:
Melatonin induces
gamma-glutamylcysteine synthetase mediated by
activator protein-1 in human vascular endothelial cells
Rahman et al., Eur Respir J 2000
(Disease Susceptibility...) :
This review describes the redox control and
involvement of nuclear factor-kappaB and
activator protein-1 in the regulation of cellular glutathione and
gamma-glutamylcysteine synthetase under conditions of oxidative stress and inflammation, the role of glutathione in oxidant mediated susceptibility/tolerance, gamma-glutamylcysteine synthetase genetic susceptibility and the potential therapeutic role of glutathione and its precursors in protecting against lung oxidant stress, inflammation and injury
Li et al., J Cell Physiol 2006
:
To determine whether age related activation of
ERK1/2-AP-1 signaling is
responsible for the up-regulation of
GCLC , the MEK inhibitors, PD98059 and U0126, were used to block ERK1/2 in VSMC from old rats
Levy et al., Free Radic Biol Med 2009
(Carcinoma, Hepatocellular...) :
Despite the increase in binding of phosphorylated c-Jun, reporter assays for EpRE 's showed that inhibition of
c-Jun phosphorylation
had variable effects on basal and HNE induced transcription of
GCLC and GCLM in HBE1 cells
Bergelson et al., Cancer Res 1994
(Carcinoma, Hepatocellular) :
We observe that lowering the glutathione levels with buthionine sulfoximine, an inhibitor of
gamma-glutamylcysteine synthetase , or diamide, a thiol oxidizing agent,
stimulates both basal and chemical-inducible expression of chloramphenicol acetyltransferase activity from EpRE Ya-cat and the
AP-1 binding activity