PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
18678787-3	2008	Levels of the p85-alpha subunit and reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits, including p47phox, p22phox, and Rac-1, increased in the membrane fraction from arteries treated with D-glucose (20 mmol/L) accompanied by increased intracellular superoxide production.	Glucose	207-216	phosphoinositide-3-kinase regulatory subunit 1	Homo sapiens	14-23	
18678787-3	2008	Levels of the p85-alpha subunit and reduced nicotinamide-adenine dinucleotide phosphate oxidase subunits, including p47phox, p22phox, and Rac-1, increased in the membrane fraction from arteries treated with D-glucose (20 mmol/L) accompanied by increased intracellular superoxide production.	Superoxides	268-278	phosphoinositide-3-kinase regulatory subunit 1	Homo sapiens	14-23	
18678787-4	2008	High glucose simultaneously augmented Akt phosphorylation at Ser 473, as well as Thr 308 in the human vascular smooth muscle cells.	Glucose	5-12	AKT serine/threonine kinase 1	Homo sapiens	38-41	
18678787-4	2008	High glucose simultaneously augmented Akt phosphorylation at Ser 473, as well as Thr 308 in the human vascular smooth muscle cells.	Serine	61-64	AKT serine/threonine kinase 1	Homo sapiens	38-41	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Superoxides	190-200	AKT serine/threonine kinase 1	Homo sapiens	88-91	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Superoxides	190-200	neutrophil cytosolic factor 1	Homo sapiens	142-149	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Superoxides	190-200	cytochrome b-245 alpha chain	Homo sapiens	151-158	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Superoxides	190-200	Rac family small GTPase 1	Homo sapiens	164-169	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Glucose	228-235	AKT serine/threonine kinase 1	Homo sapiens	88-91	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Glucose	228-235	neutrophil cytosolic factor 1	Homo sapiens	142-149	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Glucose	228-235	Rac family small GTPase 1	Homo sapiens	164-169	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Adenosine Triphosphate	268-271	AKT serine/threonine kinase 1	Homo sapiens	88-91	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Adenosine Triphosphate	268-271	neutrophil cytosolic factor 1	Homo sapiens	142-149	
18678787-6	2008	Therefore, it can be concluded that the activation of the phosphatidylinositol 3-kinase-Akt pathway, in combination with the translocation of p47phox, p22phox, and Rac-1, contributes to the superoxide production induced by high glucose, resulting in the impairment of ATP-sensitive K(+) channel function in the human visceral artery.	Adenosine Triphosphate	268-271	Rac family small GTPase 1	Homo sapiens	164-169