Title : Dipeptidyl peptidase-4 inhibition attenuates arrhythmias via a protein kinase A-dependent pathway in infarcted hearts.

Pub. Date : 2015

PMID : 26399925






3 Functional Relationships(s)
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1 Ex vivo studies showed that sitagliptin increased the phosphorylated cAMP response element-binding protein (CREB), which can be reversed by H-89 (a PKA inhibitor), not brefeldin A (an Epac inhibitor).Heme oxygenase-1(HO-1) expression was increased by a PKA agonist but not by an Epac agonist.HO-1expression was attenuated in KG-501 (a CREB inhibitor)-treated infarcted rats in the presence of a PKA agonist. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus
2 Ex vivo studies showed that sitagliptin increased the phosphorylated cAMP response element-binding protein (CREB), which can be reversed by H-89 (a PKA inhibitor), not brefeldin A (an Epac inhibitor).Heme oxygenase-1(HO-1) expression was increased by a PKA agonist but not by an Epac agonist.HO-1expression was attenuated in KG-501 (a CREB inhibitor)-treated infarcted rats in the presence of a PKA agonist. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus
3 Ex vivo studies showed that sitagliptin increased the phosphorylated cAMP response element-binding protein (CREB), which can be reversed by H-89 (a PKA inhibitor), not brefeldin A (an Epac inhibitor).Heme oxygenase-1(HO-1) expression was increased by a PKA agonist but not by an Epac agonist.HO-1expression was attenuated in KG-501 (a CREB inhibitor)-treated infarcted rats in the presence of a PKA agonist. N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide protein kinase cAMP-activated catalytic subunit alpha Rattus norvegicus