PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17079137-5	2007	The use of a selective inhibitor of PKA (H-89) prevented the effects of calcitriol on CYP27B1 gene and hCG secretion, but not on CYP24A1 transcription.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	41-45	hypertrichosis 2 (generalised, congenital)	Homo sapiens	103-106	
14636638-10	2003	The hCG (15IU/ml)- and forskolin (10microM)-induced follistatin expression could be blocked by H89 (10microM), a specific protein kinase A (PKA) inhibitor.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	95-98	hypertrichosis 2 (generalised, congenital)	Homo sapiens	4-7	
9260834-13	1997	Interestingly, H89 (2 microM), a specific protein kinase-A inhibitor, dramatically decreased the responses to hCG (500 mIU/ml) and the 8Br-cAMP (0.5 mM) stimulation of trophoblastic gap junctional communication.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	15-18	hypertrichosis 2 (generalised, congenital)	Homo sapiens	110-113	
12606479-4	2003	Gonadotropin-stimulated VEGF production was mediated by cAMP-dependent protein kinase A (PKA), as evidenced by the effect of hCG being mimicked by 8Br-cAMP and being abolished in the presence of a PKA-specific inhibitor, H-89.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	221-225	hypertrichosis 2 (generalised, congenital)	Homo sapiens	125-128	
10645245-4	1999	In contrast, hCG-induced MAP kinase activation was sensitive to PD098059 and protein kinase A inhibitor, H-89, but not to wortmannin.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	105-109	hypertrichosis 2 (generalised, congenital)	Homo sapiens	13-16	
26116232-4	2015	Pretreatment with H89, a specific inhibitor of PKA, and U0126, a specific inhibitor of ERK1/2 significantly inhibited both hCG-induced eIF5A mRNA expression and hypusination of eIF5A protein.	N-(2-(4-bromocinnamylamino)ethyl)-5-isoquinolinesulfonamide	18-21	hypertrichosis 2 (generalised, congenital)	Homo sapiens	123-126