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GCLC — INS

Text-mined interactions from Literome

Kim et al., J Pharmacol Exp Ther 2004 : The signaling pathways responsible for mediating insulin effects on GCLC expression and GSH levels, however, are unknown ... The phosphatidylinositol 3-kinase (PI3K) inhibitors, wortmannin and LY294002 [ 2- ( 4-morpholinyl ) -9-phenyl-4H-1-benzopyran-4-one ], dominant negative Akt, or rapamycin, an inhibitor of mTOR ( mammalian target of rapamycin ) and ribosomal p70 S6 kinase (p70S6K) phosphorylation, inhibited the insulin mediated increase in GCLC protein and GSH levels ... Although the mitogen activated protein kinases ( MAPKs ) extracellular signal regulated kinase, p38 MAPK, and JNK ( c-Jun N-terminal kinase ) were activated in response to insulin, PD98059 ( 2'-amino-3'-methoxyflavone ), an inhibitor of mitogen activated protein kinase kinase, SP600125 ( 1,9-pyrazoloanthrone ), an inhibitor of JNK, and SB203580 [ 4- ( 4-fluorophenyl ) -2- ( 4-methylsulfinylphenyl ) -5- ( 4-pyridyl ) 1H-imidazole ], an inhibitor of p38 MAPK, failed to inhibit the insulin mediated increase in GCLC protein levels
Langston et al., Free Radic Biol Med 2008 : Collectively, these results support the functional importance of insulin in Nrf2 dependent transcriptional upregulation of GCLc in GSH recovery during oxidative challenge and suggest a possible role for hypoglycemia in promoting insulin mediated GCLc upregulation
Langston et al., Free Radic Biol Med 2011 : Here, using IHECs stably transfected with promoter-luciferase reporter vectors, we found that insulin increased GCLc promoter activity, which required a prerequisite increase or decrease in medium glucose