PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16885208-4	2006	We demonstrate that adenoviral-mediated gene transfer of AC6 in human umbilical vein endothelial cells preferentially enhances prostacyclin receptor (versus other GPCR)-stimulated cAMP synthesis and, in parallel, inhibits thrombin-stimulated increases in endothelial cell barrier function.	Cyclic AMP	180-184	adenylate cyclase 6	Homo sapiens	57-60	
16885208-4	2006	We demonstrate that adenoviral-mediated gene transfer of AC6 in human umbilical vein endothelial cells preferentially enhances prostacyclin receptor (versus other GPCR)-stimulated cAMP synthesis and, in parallel, inhibits thrombin-stimulated increases in endothelial cell barrier function.	Cyclic AMP	180-184	prostaglandin I2 receptor	Homo sapiens	127-148	
16885208-5	2006	Using multiple strategies, including prostacyclin receptor-targeted small interfering RNA, we identify that the enhancement of endothelial barrier function by AC6 overexpression is dependent on an autocrine/paracrine feedback pathway involving the release of prostacyclin and activation of prostacyclin receptors.	Epoprostenol	37-49	adenylate cyclase 6	Homo sapiens	159-162	
16885208-6	2006	AC6 overexpression in endothelial cells may have use as a means to enhance prostacyclin function and reduce endothelial barrier permeability.	Epoprostenol	75-87	adenylate cyclase 6	Homo sapiens	0-3