PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22489671-11	2012	Nicotine treatment led to the downregulation of ECM molecules, including collagen type I, elastin and fibronectin, and upregulation of MMPs (MMP-1, MMP-2, MMP-8 and MMP-9).	Nicotine	0-8	matrix metallopeptidase 1	Homo sapiens	135-139	
22489671-11	2012	Nicotine treatment led to the downregulation of ECM molecules, including collagen type I, elastin and fibronectin, and upregulation of MMPs (MMP-1, MMP-2, MMP-8 and MMP-9).	Nicotine	0-8	matrix metallopeptidase 1	Homo sapiens	141-146	
22489671-12	2012	Inhibition of ER stress by salubrinal and transfection of CHOP small interfering RNA attenuated the nicotine-induced cell death, ECM degradation and production of MMPs.	Nicotine	100-108	matrix metallopeptidase 1	Homo sapiens	163-167	
22489671-14	2012	CONCLUSION: These results indicate that nicotine-induced cell death is mediated by the ER stress pathway, involving ECM degradation by MMPs, in human periodontal ligament cells.	Nicotine	40-48	matrix metallopeptidase 1	Homo sapiens	135-139	
17151781-4	2006	We also examined the effect of the nicotine antagonist D-tubocurarine on nicotine-induced expression of MMP-1.	Nicotine	35-43	matrix metallopeptidase 1	Homo sapiens	104-109	
18986645-7	2009	RESULTS: The addition of nicotine and/or LPS to the culture medium increased the expression of MMP-1, -2, and -3 and tissue-type PA (tPA); decreased the expression of TIMP-1, -3, and -4; and did not affect expression of TIMP-2 or PAI-1.	Nicotine	25-33	matrix metallopeptidase 1	Homo sapiens	95-112	
18986645-9	2009	In the presence of NS398 or celecoxib, the stimulatory effects of nicotine and LPS on MMP-1 expression were unchanged, but they were unable to stimulate PGE(2) production.	Nicotine	66-74	matrix metallopeptidase 1	Homo sapiens	86-91	
18986645-10	2009	CONCLUSION: These results suggest that nicotine and LPS stimulate the resorption process that occurs during turnover of osteoid by increasing the production of MMPs and tPA and by decreasing the production of TIMPs.	Nicotine	39-47	matrix metallopeptidase 1	Homo sapiens	160-164	
17151781-4	2006	We also examined the effect of the nicotine antagonist D-tubocurarine on nicotine-induced expression of MMP-1.	Nicotine	73-81	matrix metallopeptidase 1	Homo sapiens	104-109	
17151781-7	2006	Nicotine treatment caused expression of MMP-1, 2, 3, and 13, but not MMP-14, to increase significantly after 5 or 10 d of culture; MMP-14 expression did not change through day 14.	Nicotine	0-8	matrix metallopeptidase 1	Homo sapiens	40-51	
17151781-8	2006	Enhancement of MMP-1 expression by nicotine treatment was eliminated by simultaneous treatment with D-tubocurarine.	Nicotine	35-43	matrix metallopeptidase 1	Homo sapiens	15-20	
17151781-11	2006	These results suggest that nicotine stimulates bone matrix turnover by increasing production of tPA and MMP-1, 2, 3, and 13, thereby tipping the balance between bone matrix formation and resorption toward the latter process.	Nicotine	27-35	matrix metallopeptidase 1	Homo sapiens	104-123	
30260034-8	2019	Besides, the 0.15 muM nicotine-2 muM cotinine mixture also reduced matrix metalloproteinase (MMP)-1 and MMP-9 expressions in pterygium cells by 1.56- ( P = 0.043) and 1.27-fold ( P = 0.012), respectively.	Nicotine	22-30	matrix metallopeptidase 1	Homo sapiens	67-99	
26553320-10	2016	Compared with the monoculture, MMP-1, MMP-3, interleukin (IL)-1beta, IL-6, IL-17, and IL-21 in supernatant of cocultures were markedly elevated after treatment with nicotine.	Nicotine	165-173	matrix metallopeptidase 1	Homo sapiens	31-36	
25914226-6	2016	We confirmed the increased secretion by nicotine of matrix metalloproteinase 1 and two proposed markers of OA, fibronectin, and chitinase 3-like protein 1.	Nicotine	40-48	matrix metallopeptidase 1	Homo sapiens	52-78	
26530054-8	2016	We showed that nicotine increased LOVO and SW620 colorectal cancer cell invasion along with enhanced activity and expression of MMP-1, -2 and -9.	Nicotine	15-23	matrix metallopeptidase 1	Homo sapiens	128-144