PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
2539976-0	1989	Interleukin-1 alpha exerts glucose-dependent stimulatory and inhibitory effects on islet cell phosphoinositide hydrolysis and insulin secretion.	Phosphatidylinositols	94-110	interleukin 1 alpha	Homo sapiens	0-19	
31605740-12	2020	Deletion or inhibition of LAT1 efficiently controls IL-23- and IL-1beta-induced phosphatidylinositol 3-kinase/AKT/mTOR activation independent of T-cell receptor signaling.	Phosphatidylinositols	80-100	interleukin 1 alpha	Homo sapiens	63-71	
31766427-6	2019	RESULTS: The expression of several genes involved in the cell cycle regulation, migration, inflammation, phosphatidylinositol 3-kinase (PI3K) and mitogen activated kinase-like protein (MAPK) pathway were found to be modulated including CCNB1, TWIST1, MMP14, TERT, AKT1, PTPRR, FOS and IL1A.	Phosphatidylinositols	105-125	interleukin 1 alpha	Homo sapiens	285-289	
1845871-2	1991	We studied the effects of IL-1 on phosphatidylinositol (PtdIns) metabolism and confirmed reports indicating that IL-1 does not stimulate increased PtdIns turnover; however, we observed the accumulation of PtdIns-4-phosphate (PtdInsP) in response to IL-1.	Phosphatidylinositols	34-54	interleukin 1 alpha	Homo sapiens	26-30	
1845871-2	1991	We studied the effects of IL-1 on phosphatidylinositol (PtdIns) metabolism and confirmed reports indicating that IL-1 does not stimulate increased PtdIns turnover; however, we observed the accumulation of PtdIns-4-phosphate (PtdInsP) in response to IL-1.	Phosphatidylinositols	56-62	interleukin 1 alpha	Homo sapiens	26-30	
1845871-9	1991	IL-1-stimulated PtdIns kinase activity represents an important physiological regulatory effect by IL-1 as it could control the synthesis and/or maintenance of phosphorylated derivatives of PtdIns which comprise only a very small pool of substrates for the generation of the second messengers inositol 1,4,5-triphosphate and diacylglycerol.	Phosphatidylinositols	16-22	interleukin 1 alpha	Homo sapiens	0-4	
1845871-9	1991	IL-1-stimulated PtdIns kinase activity represents an important physiological regulatory effect by IL-1 as it could control the synthesis and/or maintenance of phosphorylated derivatives of PtdIns which comprise only a very small pool of substrates for the generation of the second messengers inositol 1,4,5-triphosphate and diacylglycerol.	Phosphatidylinositols	16-22	interleukin 1 alpha	Homo sapiens	98-102	
2398032-3	1990	Phosphorylated truncated pre IL 1 alpha selectively binds to acidic phospholipids including phosphatidic acid, phosphatidylserine, and phosphatidylinositol, but not to other phospholipids (phosphatidylcholine and phosphatidylethanolamine).	Phosphatidylinositols	135-155	interleukin 1 alpha	Homo sapiens	29-39	
2157429-2	1990	IL1 itself raised neither the cAMP level nor the intracellular Ca2+ level nor did it induce phosphatidylinositol (PI) breakdown.	Phosphatidylinositols	92-112	interleukin 1 alpha	Homo sapiens	0-3	
8276785-8	1994	While confirming the existence of an autonomous nuclear phosphoinositide signaling system, our data clearly indicate that in SaOS-2 cells one of the earliest events following IL-1 alpha treatment is the breakdown of nuclear phosphatidylinositol monophosphate and phosphatidylinositol bisphosphate because of the activation of a specific nuclear PLC isoform.	Phosphatidylinositols	56-72	interleukin 1 alpha	Homo sapiens	175-185	
1665456-1	1991	The monokine interleukin-1 alpha (IL-1) induces a glucose-dependent increase in insulin secretion, an effect tentatively attributed to its ability to increase beta cell phosphoinositide (PI) hydrolysis.	Phosphatidylinositols	169-185	interleukin 1 alpha	Homo sapiens	13-32	
1665456-1	1991	The monokine interleukin-1 alpha (IL-1) induces a glucose-dependent increase in insulin secretion, an effect tentatively attributed to its ability to increase beta cell phosphoinositide (PI) hydrolysis.	Phosphatidylinositols	169-185	interleukin 1 alpha	Homo sapiens	34-38	
3028403-2	1987	Analysis of [3H]-arachidonic acid labeled phospholipids showed that interleukin-1 and tumor necrosis factor diminished [3H]-arachidonic acid in phosphatidyl-choline phosphatidylserine and phosphatidylinositol.	Phosphatidylinositols	188-208	interleukin 1 alpha	Homo sapiens	68-107