PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
1637304-2	1992	Here I examined possible stimulation of PtdEtn hydrolysis by various growth-stimulatory agents, including serum, bombesin, platelet-derived growth factor (PDGF), fibroblast growth factor (FGF) and insulin.	phosphatidylethanolamine	40-46	insulin	Homo sapiens	197-204	
8643029-1	1995	The compound 3-amino-1-propanol which replaces ethanolamine in phosphatidyl-ethanolamine and inhibits transformation of it, hindered insulin imprinting of Tetrahymena.	phosphatidylethanolamine	63-88	insulin	Homo sapiens	133-140	
6373768-2	1984	Subsequent treatment with physiological concentrations of insulin provoked 40-70% increases in 32PO4 levels (reflecting increases in mass) in phosphatidic acid, phosphatidylinositol, and polyphosphoinositides, and, lesser, 20-25% increases in phosphatidylserine and the combined chromatographic area containing phosphatidylethanolamine plus phosphatidylcholine plus phosphatidylcholine.	phosphatidylethanolamine	311-335	insulin	Homo sapiens	58-65	
3146971-3	1988	In studies of the effect on PA synthesis de novo, insulin stimulated [2-3H]glycerol incorporation into PA, DAG, PC/PE and total glycerolipids of BC3H-1 myocytes, regardless of whether insulin was added simultaneously with, or after 2 h or 3 or 10 days of prelabelling with, [2-3H]glycerol.	phosphatidylethanolamine	115-117	insulin	Homo sapiens	50-57	
2829843-2	1987	Reconstitution of the receptor kinase into leaky vesicles containing phosphatidylcholine and phosphatidylethanolamine (1:1, w/w) by detergent removal on Sephadex G-50 results in the complete loss of receptor kinase sensitivity to activation by insulin.	phosphatidylethanolamine	93-117	insulin	Homo sapiens	244-251	
2829843-9	1987	These data indicate that the phospholipid environment of insulin receptors can modulate its binding and kinase activity, and phosphatidylserine acts to restore insulin-sensitivity to the receptor kinase incorporated into phosphatidylcholine/phosphatidylethanolamine vesicles.	phosphatidylethanolamine	241-265	insulin	Homo sapiens	57-64	
2829843-9	1987	These data indicate that the phospholipid environment of insulin receptors can modulate its binding and kinase activity, and phosphatidylserine acts to restore insulin-sensitivity to the receptor kinase incorporated into phosphatidylcholine/phosphatidylethanolamine vesicles.	phosphatidylethanolamine	241-265	insulin	Homo sapiens	160-167	
23039070-7	2012	Insulin was the main hormone inducing compositional differences in membrane lipids, increasing phosphatidylethanolamine and phosphatidylinositol and decreasing sphingomyelin and cholesterol.	phosphatidylethanolamine	95-119	insulin	Homo sapiens	0-7	
665365-3	1978	Insulin enhances these activities within phosphatidylethanolamine.	phosphatidylethanolamine	41-65	insulin	Homo sapiens	0-7	
5158903-11	1971	Insulin decreased the [(14)C]glucose solubilized by phosphatidylcholine, phosphatidylethanolamine and phosphatidic acid, but not by sphingomyelin.	phosphatidylethanolamine	73-97	insulin	Homo sapiens	0-7	
28740220-4	2017	Here, we demonstrate that insulin temporally induces Tnfaip8, which mediates the anti-autophagic action of insulin through formation of a novel ternary complex including Tnfaip8, phosphatidylethanolamine (PE) and Galphai3.	phosphatidylethanolamine	179-203	insulin	Homo sapiens	26-33	
28740220-4	2017	Here, we demonstrate that insulin temporally induces Tnfaip8, which mediates the anti-autophagic action of insulin through formation of a novel ternary complex including Tnfaip8, phosphatidylethanolamine (PE) and Galphai3.	phosphatidylethanolamine	179-203	insulin	Homo sapiens	107-114	
28740220-4	2017	Here, we demonstrate that insulin temporally induces Tnfaip8, which mediates the anti-autophagic action of insulin through formation of a novel ternary complex including Tnfaip8, phosphatidylethanolamine (PE) and Galphai3.	phosphatidylethanolamine	205-207	insulin	Homo sapiens	26-33	
28740220-4	2017	Here, we demonstrate that insulin temporally induces Tnfaip8, which mediates the anti-autophagic action of insulin through formation of a novel ternary complex including Tnfaip8, phosphatidylethanolamine (PE) and Galphai3.	phosphatidylethanolamine	205-207	insulin	Homo sapiens	107-114	
27032901-0	2016	Skeletal muscle phosphatidylcholine and phosphatidylethanolamine are related to insulin sensitivity and respond to acute exercise in humans.	phosphatidylethanolamine	40-64	insulin	Homo sapiens	80-87	
27032901-10	2016	In summary, total muscle PC and PE are positively related to insulin sensitivity while PC:PE ratio is inversely related to insulin sensitivity in humans.	phosphatidylethanolamine	32-34	insulin	Homo sapiens	61-68	
26499445-5	2016	RESULTS: In omental adipose tissue of obese, insulin-resistant women, adipocyte hypertrophy and macrophage infiltration were accompanied by an increase in GM3 ganglioside and its synthesis enzyme ST3GAL5; in addition, phosphatidylethanolamine (PE) lipids were increased and their degradation enzyme, phosphatidylethanolamine methyl transferase (PEMT), decreased.	phosphatidylethanolamine	244-246	insulin	Homo sapiens	45-52	
29695812-0	2018	Skeletal muscle phosphatidylcholine and phosphatidylethanolamine respond to exercise and influence insulin sensitivity in men.	phosphatidylethanolamine	40-64	insulin	Homo sapiens	99-106	
29695812-1	2018	Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) composition in skeletal muscle have been linked to insulin sensitivity.	phosphatidylethanolamine	29-53	insulin	Homo sapiens	110-117	
29695812-1	2018	Phosphatidylcholine (PC) and phosphatidylethanolamine (PE) composition in skeletal muscle have been linked to insulin sensitivity.	phosphatidylethanolamine	55-57	insulin	Homo sapiens	110-117	
26499445-0	2016	GM3 ganglioside and phosphatidylethanolamine-containing lipids are adipose tissue markers of insulin resistance in obese women.	phosphatidylethanolamine	20-44	insulin	Homo sapiens	93-100