PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10320004-0	1999	Regulation of AP-1 gene transcription factor binding activity in the rat brain during nicotine dependence.	Nicotine	86-94	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	14-18	
17174071-3	2007	failed to attenuate KA-induced neurotoxicity, repeated nicotine infusions (1.0 microg/side/day for 10 days) attenuated the seizures, the severe loss of cells in hippocampal regions CA1 and CA3, the increase in activator protein (AP)-1 DNA binding activity, and mortality after KA administration.	Nicotine	55-63	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	210-234	
10320004-1	1999	The effects of acute and chronic nicotine treatment on activator protein-1 (AP-1) gene transcription factor binding activity in the rat cortex were investigated.	Nicotine	33-41	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	55-74	
10320004-1	1999	The effects of acute and chronic nicotine treatment on activator protein-1 (AP-1) gene transcription factor binding activity in the rat cortex were investigated.	Nicotine	33-41	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	76-80	
10320004-3	1999	It was observed that 1 h after acute nicotine treatment (single injection) AP-1 DNA binding activity was significantly increased in the rat cortex.	Nicotine	37-45	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	75-79	
10320004-5	1999	However, at 18 and 24 h of nicotine withdrawal after 10 days of nicotine treatment, AP-1 DNA binding activity was significantly decreased in the rat cortex.	Nicotine	27-35	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-88	
10320004-5	1999	However, at 18 and 24 h of nicotine withdrawal after 10 days of nicotine treatment, AP-1 DNA binding activity was significantly decreased in the rat cortex.	Nicotine	64-72	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	84-88	
10320004-6	1999	Thus, these findings suggest that desensitization of cortical AP-1 DNA binding activity may be involved in the neuroadaptational mechanisms to nicotine dependence.	Nicotine	143-151	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	62-66	
1400333-5	1992	Handling of rats for several days prior to sacrifice failed to affect protein expression or binding; on the other hand, repeated injections of nicotine increased AP-1 DNA binding.	Nicotine	143-151	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	162-166	
1400333-6	1992	A single nicotine injection 60 min prior to removing the adrenals caused a significant reduction in AP-1 DNA binding without any detectable changes in AP-1 protein expression.	Nicotine	9-17	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	100-104	
19063868-3	2009	In this study, we investigated the effects of inhibiting the alpha7 nAChR-JAK2 pro-survival cascade on the nicotine-induced production of the survival factor Bcl-2 and the transcriptional activation of NF-kappaB, AP-1, STAT1, STAT3, and STAT5.	Nicotine	107-115	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	213-217	
19063868-4	2009	We report that nicotine induced the production of Bcl-2 and increased the transcriptional activation of NF-kappaB, AP-1, STAT1, and STAT3, and with the exception of AP-1, the other transcription factors (NF-kappaB, STAT1, and STAT3) were significantly reduced by JAK2 inhibition.	Nicotine	15-23	Jun proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	115-119