PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34490270-0	2021	alpha1-nAchR-Mediated Signaling Through Lipid Raft Is Required for Nicotine-Induced NLRP3 Inflammasome Activation and Nicotine-Accelerated Atherosclerosis.	Nicotine	67-75	brain protein 1	Mus musculus	0-6	
34490270-0	2021	alpha1-nAchR-Mediated Signaling Through Lipid Raft Is Required for Nicotine-Induced NLRP3 Inflammasome Activation and Nicotine-Accelerated Atherosclerosis.	Nicotine	118-126	brain protein 1	Mus musculus	0-6	
34490270-7	2021	Mechanically, nicotine increased the expression of alpha1-nAChR and stimulated the accumulation of alpha1-nAChR in lipid raft, leading to NLRP3 inflammasome activation in macrophage.	Nicotine	14-22	brain protein 1	Mus musculus	99-105	
34490270-8	2021	Conversely, silencing of alpha1-nAChR in macrophage sufficiently blocked the pro-inflammasome activation effect of nicotine, indicating that alpha1-nAChR was the specific receptor for nicotine in triggering NLRP3 inflammasome in macrophage.	Nicotine	115-123	brain protein 1	Mus musculus	141-147	
34490270-8	2021	Conversely, silencing of alpha1-nAChR in macrophage sufficiently blocked the pro-inflammasome activation effect of nicotine, indicating that alpha1-nAChR was the specific receptor for nicotine in triggering NLRP3 inflammasome in macrophage.	Nicotine	184-192	brain protein 1	Mus musculus	141-147	
34490270-9	2021	Furthermore, both the destruction of lipid raft by methyl-beta-cyclodextrin and the interference of lipid raft clustering by silencing acid sphingomyelinase reversed nicotine-induced NLRP3 inflammasome activation by reducing the accumulation of alpha1-nAChR in lipid raft in macrophage, suggesting lipid raft-mediated accumulation of alpha1-nAChR was the key event in regulating the pro-inflammatory effects of nicotine in macrophage.	Nicotine	166-174	brain protein 1	Mus musculus	334-340	
34490270-9	2021	Furthermore, both the destruction of lipid raft by methyl-beta-cyclodextrin and the interference of lipid raft clustering by silencing acid sphingomyelinase reversed nicotine-induced NLRP3 inflammasome activation by reducing the accumulation of alpha1-nAChR in lipid raft in macrophage, suggesting lipid raft-mediated accumulation of alpha1-nAChR was the key event in regulating the pro-inflammatory effects of nicotine in macrophage.	Nicotine	411-419	brain protein 1	Mus musculus	334-340	
34490270-11	2021	Conclusion: alpha1-nAChR-mediated signaling through lipid raft is required for NLRP3 inflammasome activation and pro-atherosclerotic property of nicotine.	Nicotine	145-153	brain protein 1	Mus musculus	12-18