Title : Glucagon-like peptide-1 improves beta-cell antioxidant capacity via extracellular regulated kinases pathway and Nrf2 translocation.

Pub. Date : 2016 Jun

PMID : 26968794






3 Functional Relationships(s)
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1 Moreover, ERK activation seems to be protein kinase A (PKA)-dependent because inhibition of PKA with H-89 was sufficient to block the GLP-1-derived protective effect on beta cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus
2 Moreover, ERK activation seems to be protein kinase A (PKA)-dependent because inhibition of PKA with H-89 was sufficient to block the GLP-1-derived protective effect on beta cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus
3 Moreover, ERK activation seems to be protein kinase A (PKA)-dependent because inhibition of PKA with H-89 was sufficient to block the GLP-1-derived protective effect on beta cells. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus