PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18664325-1	2008	AIM: The present study was designed to explore the endogenous production and localization of the sulfur dioxide (SO2)/aspartate aminotransferase pathway in vascular tissues of rats and to examine its vasorelaxant effect on isolated aortic rings,as well as the possible mechanisms.	Sulfur Dioxide	97-111	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	118-144	
18664325-1	2008	AIM: The present study was designed to explore the endogenous production and localization of the sulfur dioxide (SO2)/aspartate aminotransferase pathway in vascular tissues of rats and to examine its vasorelaxant effect on isolated aortic rings,as well as the possible mechanisms.	Sulfur Dioxide	113-116	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	118-144	
18664325-8	2008	The aortic aspartate aminotransferase mRNA located in endothelia and vascular smooth muscle cells beneath the endothelial layer.Furthermore, a physiological dose of the SO2 derivatives (Na2SO3/NaHSO3) relaxed isolated artery rings slightly, whereas higher doses (1-12 mmol/L) relaxed rings in a concentration-dependent manner.	Sulfur Dioxide	169-172	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	11-37	
29760703-5	2018	We found that endogenous H2S deficiency caused by cystathionine-gamma-lyase (CSE) knockdown increased endogenous SO2 level in endothelial cells and enhanced the enzymatic activity of AAT, a major SO2 synthesis enzyme, without affecting the expressions of AAT1 and AAT2.	Sulfur Dioxide	113-116	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	183-186	
29760703-9	2018	Furthermore, an AAT inhibitor l-aspartate-beta-hydroxamate (HDX), which blocked the upregulation of endogenous SO2/AAT generation induced by CSE knockdown, aggravated CSE knockdown-activated nuclear factor-kappaB pathway in the endothelial cells and its downstream inflammatory factors including ICAM-1, TNF-alpha, and IL-6.	Sulfur Dioxide	111-114	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	16-19	
29760703-9	2018	Furthermore, an AAT inhibitor l-aspartate-beta-hydroxamate (HDX), which blocked the upregulation of endogenous SO2/AAT generation induced by CSE knockdown, aggravated CSE knockdown-activated nuclear factor-kappaB pathway in the endothelial cells and its downstream inflammatory factors including ICAM-1, TNF-alpha, and IL-6.	Sulfur Dioxide	111-114	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	115-118	
29760703-10	2018	In in vivo experiment, H2S donor restored the deficiency of endogenous H2S production induced by MCT, and reversed the upregulation of endogenous SO2/AAT pathway via sulfhydrating AAT1 and AAT2.	Sulfur Dioxide	146-149	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	150-153	
29760703-12	2018	In conclusion, for the first time, the present study showed that H2S inhibited endogenous SO2 generation by inactivating AAT via the sulfhydration of AAT1/2; and the increased endogenous SO2 generation might play a compensatory role when H2S/CSE pathway was downregulated, thereby exerting protective effects in endothelial inflammatory responses in vitro and in vivo.	Sulfur Dioxide	90-93	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	121-124	
29760703-5	2018	We found that endogenous H2S deficiency caused by cystathionine-gamma-lyase (CSE) knockdown increased endogenous SO2 level in endothelial cells and enhanced the enzymatic activity of AAT, a major SO2 synthesis enzyme, without affecting the expressions of AAT1 and AAT2.	Sulfur Dioxide	196-199	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	183-186