PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12692077-7	2003	Furthermore, N-(n-butyl)deoxynojirimycin, a potent and non-toxic GCS inhibitor, had no chemosensitizing effect on wild-type melanoma cells.	miglustat	13-40	UDP-glucose ceramide glucosyltransferase	Mus musculus	65-68	
18387328-4	2008	The imino sugars N-butyldeoxynojirimycin (NB-DNJ, miglustat, Zavesca) and N-butyldeoxygalactonojirimycin (NB-DGJ) used for SRT inhibit glucosylceramide synthase (GlcCerS) that catalyses the first committed step in glycosphingolipid biosynthesis.	miglustat	17-40	UDP-glucose ceramide glucosyltransferase	Mus musculus	135-160	
25915583-4	2015	Glucosylceramide synthase (GCS) inhibitors, including the clinically approved agent N-butyl-deoxynojirimycin (NB-DNJ), prevented OC development and activation by disrupting RANKL-induced localization of TRAF6 and c-SRC into lipid rafts and preventing nuclear accumulation of transcriptional activator NFATc1.	miglustat	84-108	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-25	
11525744-5	2001	To evaluate this possibility, we treated murine and feline NPC models with N-butyldeoxynojirimycin (NB-DNJ), an inhibitor of glucosylceramide synthase, a pivotal enzyme in the early GSL synthetic pathway.	miglustat	75-98	UDP-glucose ceramide glucosyltransferase	Mus musculus	125-150	
11525744-5	2001	To evaluate this possibility, we treated murine and feline NPC models with N-butyldeoxynojirimycin (NB-DNJ), an inhibitor of glucosylceramide synthase, a pivotal enzyme in the early GSL synthetic pathway.	miglustat	100-106	UDP-glucose ceramide glucosyltransferase	Mus musculus	125-150	
34697142-4	2021	MATERIALS AND METHODS: We analyzed the expression of glycosphingolipids and cell growth in MC3T3-E1 mouse osteoblast cells treated with the GCS inhibitors miglustat, D-PDMP and D-PPMP.	miglustat	155-164	UDP-glucose ceramide glucosyltransferase	Mus musculus	140-143	
27106513-4	2016	N-butyldeoxynojirimycin, an inhibitor of ceramide glucosyltransferase activity and therefore of ganglioside synthesis, was administered to MPS IIIA mice both prior to maximal GM2 and GM3 accumulation (early treatment) and after the maximum level of ganglioside had accumulated in the brain (late treatment) to determine if behaviour was altered by ganglioside level.	miglustat	0-23	UDP-glucose ceramide glucosyltransferase	Mus musculus	41-69	
10841515-6	2000	Complications observed with another glucosylceramide synthase inhibitor, N-butyldeoxynojirimycin, including weight loss and acellularity of lymphatic organs, were not observed with D-t-EtDO-P4.	miglustat	73-96	UDP-glucose ceramide glucosyltransferase	Mus musculus	36-61	
28610891-5	2017	Several studies have demonstrated that N-butyldeoxynojirimycin (NB-DNJ, also known as miglustat), an inhibitor of the enzyme glucosylceramide synthase (GCS), successfully delays the onset of motor deficits, improves longevity, and rescues some of the cerebellar abnormalities (e.g., Purkinje cell death) seen in another lysosomal disease known as Niemann-Pick type C (NPC).	miglustat	39-62	UDP-glucose ceramide glucosyltransferase	Mus musculus	125-150	
28610891-5	2017	Several studies have demonstrated that N-butyldeoxynojirimycin (NB-DNJ, also known as miglustat), an inhibitor of the enzyme glucosylceramide synthase (GCS), successfully delays the onset of motor deficits, improves longevity, and rescues some of the cerebellar abnormalities (e.g., Purkinje cell death) seen in another lysosomal disease known as Niemann-Pick type C (NPC).	miglustat	39-62	UDP-glucose ceramide glucosyltransferase	Mus musculus	152-155	
28610891-5	2017	Several studies have demonstrated that N-butyldeoxynojirimycin (NB-DNJ, also known as miglustat), an inhibitor of the enzyme glucosylceramide synthase (GCS), successfully delays the onset of motor deficits, improves longevity, and rescues some of the cerebellar abnormalities (e.g., Purkinje cell death) seen in another lysosomal disease known as Niemann-Pick type C (NPC).	miglustat	64-70	UDP-glucose ceramide glucosyltransferase	Mus musculus	125-150	
28610891-5	2017	Several studies have demonstrated that N-butyldeoxynojirimycin (NB-DNJ, also known as miglustat), an inhibitor of the enzyme glucosylceramide synthase (GCS), successfully delays the onset of motor deficits, improves longevity, and rescues some of the cerebellar abnormalities (e.g., Purkinje cell death) seen in another lysosomal disease known as Niemann-Pick type C (NPC).	miglustat	64-70	UDP-glucose ceramide glucosyltransferase	Mus musculus	152-155	
26771826-9	2016	Inhibition of GSL synthesis with the glucosylceramide synthase (GCS) inhibitor N-butyl-1-deoxynojirimycin prevented U18666A-induced Gpnmb induction and secretion.	miglustat	79-105	UDP-glucose ceramide glucosyltransferase	Mus musculus	37-62	
26771826-9	2016	Inhibition of GSL synthesis with the glucosylceramide synthase (GCS) inhibitor N-butyl-1-deoxynojirimycin prevented U18666A-induced Gpnmb induction and secretion.	miglustat	79-105	UDP-glucose ceramide glucosyltransferase	Mus musculus	64-67	
25915583-4	2015	Glucosylceramide synthase (GCS) inhibitors, including the clinically approved agent N-butyl-deoxynojirimycin (NB-DNJ), prevented OC development and activation by disrupting RANKL-induced localization of TRAF6 and c-SRC into lipid rafts and preventing nuclear accumulation of transcriptional activator NFATc1.	miglustat	84-108	UDP-glucose ceramide glucosyltransferase	Mus musculus	27-30	
21738789-7	2011	Similar results were observed with NB-DNJ, another iminosugar-based GCS inhibitor.	miglustat	35-41	UDP-glucose ceramide glucosyltransferase	Mus musculus	68-71