PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18817806-0	2009	Intracerebroventricular fluvoxamine administration inhibited pain behavior but increased Fos expression in affective pain pathways.	Fluvoxamine	24-35	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	89-92	
18817806-7	2009	Moreover, fluvoxamine alone increased Fos in the BL and PFC.	Fluvoxamine	10-21	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	38-41	
18817806-9	2009	The results indicated that 5-HT2 receptor activities participate minimally in Fos induction by fluvoxamine in the PFC and BL.	Fluvoxamine	95-106	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	78-81	
18817806-10	2009	In contrast, WAY-100635 affected the Fos expression produced by fluvoxamine.	Fluvoxamine	64-75	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-40	
18817806-11	2009	In the portion of the brain with affectional pain pathways, 5-HT1 receptor activities induced anti-nociceptive effects and decreased Fos expression with fluvoxamine, while 5-HT2 receptor activation affected to anti-nociceptive effects but did not induce Fos expression.	Fluvoxamine	153-164	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	133-136