PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24744867-5	2013	Thrombin treatment of PASMC resulted in a transient increase in Akt phosphorylation and had similar effects on the downstream targets of the Akt/mTOR pathway.	pasmc	22-27	coagulation factor II, thrombin	Homo sapiens	0-8	
24744867-10	2013	Thrombin has direct effects on PASMC increasing intracellular [Ca(2+)] and PASMC proliferation, an effect attributed to Akt phosphorylation.	pasmc	31-36	coagulation factor II, thrombin	Homo sapiens	0-8	
24744867-10	2013	Thrombin has direct effects on PASMC increasing intracellular [Ca(2+)] and PASMC proliferation, an effect attributed to Akt phosphorylation.	pasmc	75-80	coagulation factor II, thrombin	Homo sapiens	0-8	
18836030-8	2008	Notably, thrombin-induced receptor-mediated calcium influx was still observed in PASMC after CPA pretreatment in the presence of extracellular Ca(2+).	pasmc	81-86	coagulation factor II, thrombin	Homo sapiens	9-17	
18836030-9	2008	Ca(2+) oscillations were triggered by thrombin in PASMC resulting from a balance of extracellular Ca(2+) influx and Ca(2+) reuptake by the sarcoplasmic reticulum.	pasmc	50-55	coagulation factor II, thrombin	Homo sapiens	38-46	
18836030-10	2008	The data show that thrombin induces increases in intracellular calcium in PASMC and PAEC with a distinct CPA-, caffeine-, and ryanodine-insensitive release existing only in PAEC.	pasmc	74-79	coagulation factor II, thrombin	Homo sapiens	19-27	
18836030-11	2008	Furthermore, a dynamic balance between Ca(2+) influx, intracellular Ca(2+) release, and reuptake underlie the Ca(2+) transients evoked by thrombin in some PASMC.	pasmc	155-160	coagulation factor II, thrombin	Homo sapiens	138-146	
15134338-5	2004	Stimulation of PASMC with thrombin or CoCl2 increased ROS production and enhanced HIF-alpha protein and VEGF mRNA levels as well as HIF-dependent reporter gene activity.	pasmc	15-20	coagulation factor II, thrombin	Homo sapiens	26-34	
20039838-8	2010	Thus, ROS derived from NOX4 in response to thrombin stabilize HIF-2alpha by preventing hydroxylation of the N- and C-TAD, thus allowing formation of transcriptionally active HIF-2alpha, which promotes PASMC proliferation.	pasmc	201-206	coagulation factor II, thrombin	Homo sapiens	43-51	
19363122-9	2009	Furthermore, chronic exposure to thrombin, an activator of PAR, significantly reduced the peak agonist-induced Ca(2+) release in PAEC, but increased it in PASMC.	pasmc	155-160	coagulation factor II, thrombin	Homo sapiens	33-41	
19363122-12	2009	In conclusion, chronic exposure to fibrinogen, fibrin, and thrombin caused differential changes in [Ca(2+)](cyt) in PAEC and PASMC.	pasmc	125-130	coagulation factor II, thrombin	Homo sapiens	59-67	
18836030-4	2008	Thrombin increased the [Ca(2+)](cyt) in both cell types; however, the transient response was significantly higher and recovered quicker in the PASMC, suggesting different mechanisms may contribute to thrombin-mediated increases in [Ca(2+)](cyt) in these cell types.	pasmc	143-148	coagulation factor II, thrombin	Homo sapiens	200-208	
18836030-6	2008	Interestingly, CPA pretreatment significantly attenuated thrombin-induced Ca(2+) release in PASMC; this attenuation was not apparent in PAEC, indicating that a PAEC-specific mechanism was targeted by thrombin.	pasmc	92-97	coagulation factor II, thrombin	Homo sapiens	57-65	
19132225-9	2008	Finally, upregulation of PAI-1 by Rac-1 and HIF-1 was essential for thrombin-stimulated proliferation of PASMC.	pasmc	105-110	coagulation factor II, thrombin	Homo sapiens	68-76	
19132225-10	2008	These findings indicate that Rac-1 is an important mediator of thrombin signaling and may contribute to pulmonary vascular remodeling via HIF-1-dependent upregulation of PAI-1 leading to enhanced proliferation of PASMC.	pasmc	213-218	coagulation factor II, thrombin	Homo sapiens	63-71