PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31676444-16	2020	H-89, a PKA inhibitor, suppressed CREB activation, lipid accumulation and NOX activity in RAW264.7 cells.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	0-4	cAMP responsive element binding protein 1	Mus musculus	34-38	
34563511-9	2022	H89, an inhibitor of CREB signaling, abolished these effects of thioperamide to suppress gliosis and proinflammatory cytokine release.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	0-3	cAMP responsive element binding protein 1	Mus musculus	21-25	
32038255-6	2019	However, H89, an inhibitor of protein kinase A (PKA)/CREB, reverses the effects of thioperamide on either BDNF expression and release or cell proliferation in NE-4C stem cells.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	9-12	cAMP responsive element binding protein 1	Mus musculus	53-57	
25453775-4	2015	Pre-treatment with H89, a PKA inhibitor, prevented the activation of CREB by ephrinB2-Fc.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	19-22	cAMP responsive element binding protein 1	Mus musculus	69-73	
31555361-7	2019	Compared with the SCF single stimulation group, the production of IL-13 was significantly reduced in P815 cells stimulated with U0126 (ERK-MEK/pathway inhibitor) or H-89 (CREB inhibitor) combined with SCF stimulation group (P<0.01).	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	165-169	cAMP responsive element binding protein 1	Mus musculus	171-175	
16785762-7	2006	The PKA inhibitor H89 inhibited CREB activation, but the PLC inhibitor U73122 did not.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	18-21	cAMP responsive element binding protein 1	Mus musculus	32-36	
21782812-8	2011	PKA inhibitor, H-89, reduced CREB (S133) phosphorylation and mBAFF expression in control and LPS-stimulated macrophages.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	15-19	cAMP responsive element binding protein 1	Mus musculus	29-33	
17645870-5	2007	Treatment with H89, a PKA inhibitor, markedly decreased IL-4-induced AID expression, and over-expression of CREB enhanced it.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	15-18	cAMP responsive element binding protein 1	Mus musculus	108-112	
16845490-14	2006	In addiction, PKA inhibitor H89 also inhibits c-Fos induction in 3T3-AR7 cells by ACTH(39), implicating activation of the cAMP/PKA/CREB pathway in c-Fos induction by ACTH(39).	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	28-31	cAMP responsive element binding protein 1	Mus musculus	131-135	
16873684-3	2006	We observed that 10 mmol/l glucose-induced CREB phosphorylation was totally inhibited by the protein kinase A (PKA) inhibitor H89 (2 micromol/l) and reduced by 50% with the extracellular signal-regulated kinase (ERK)1/2 inhibitor PD98059 (20 micromol/l).	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	126-129	cAMP responsive element binding protein 1	Mus musculus	43-47	
18577515-8	2008	Although the protein kinase A inhibitor H-89 abolished forskolin-stimulated CREB phosphorylation, it did not modify forskolin-induced GTP-Rap1 levels, excluding PKA participation.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	40-44	cAMP responsive element binding protein 1	Mus musculus	76-80	
17651699-7	2007	This result was further confirmed by the fact that rosmarinic acid-induced phosphorylation of CREB was inhibited by H-89, but not by PD98059, a MEK1 inhibitor, or by LY294002, a phosphatidylinositol-3-kinase (PI3K) inhibitor.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	116-120	cAMP responsive element binding protein 1	Mus musculus	94-98	
15855635-5	2005	Dibutyryl cAMP increased phosphorylation of Akt and CREB, both of which were reversed by H89, wortmannin and the Akt inhibitor SH-6.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	89-92	cAMP responsive element binding protein 1	Mus musculus	52-56	
15659802-4	2004	The observation that glucose-induced CREB phosphorylation was totally inhibited by the PKA inhibitor H89 (2 microM) and reduced by 50% with the ERK1/2 inhibitor PD98059 (20 microM) indicates that ERK1/2, located downstream of PKA, cooperates with PKA and is responsible for half of the PKA-mediated CREB phosphorylation elicited by glucose in MIN6 beta cells.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	101-104	cAMP responsive element binding protein 1	Mus musculus	37-41