PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16452470-0	2006	Prolonged activation of cAMP-response element-binding protein and ATF-2 needed for nicotine-triggered elevation of tyrosine hydroxylase gene transcription in PC12 cells.	Nicotine	83-91	tyrosine hydroxylase	Rattus norvegicus	115-135	
16452470-1	2006	Phosphorylation (P-) of cAMP-response element-binding protein (CREB) by protein kinase A or mitogen-activated protein kinases was implicated in mediating the increased tyrosine hydroxylase (TH) gene expression after prolonged exposure to nicotine in vivo and in cell culture.	Nicotine	238-246	tyrosine hydroxylase	Rattus norvegicus	168-188	
16452470-1	2006	Phosphorylation (P-) of cAMP-response element-binding protein (CREB) by protein kinase A or mitogen-activated protein kinases was implicated in mediating the increased tyrosine hydroxylase (TH) gene expression after prolonged exposure to nicotine in vivo and in cell culture.	Nicotine	238-246	tyrosine hydroxylase	Rattus norvegicus	190-192	
16452470-6	2006	In contrast, protein kinase A inhibitor H-89 or Ca(2+)/calmodulin-activated protein kinase inhibitor KN-93 reduced the nicotine-triggered rise in P-CREB and TH promoter activity.	Nicotine	119-127	tyrosine hydroxylase	Rattus norvegicus	157-159	
16452470-12	2006	The results suggest that both ATF-2 and CREB mediate activation of TH gene transcription by nicotine.	Nicotine	92-100	tyrosine hydroxylase	Rattus norvegicus	67-69