PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
21833718-2	2011	Pro-apoptotic ceramide mediates imatinib-induced apoptosis, and metabolism of ceramide by glucosylceramide synthase (GCS) activity, converting ceramide to glucosyl ceramide, might contribute to imatinib resistance.	Glucosylceramides	155-172	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-115
21986308-6	2012	Synthesis of both total lipids and individual lipid classes, including phospholipids, sphingolipids and neutral lipids, were found to be increased at 24 h in CHK treated with 1 mug/ml WG; in similarly treated fibroblasts, only the syntheses of sphingolipids (such as ceramides and glucosylceramides), but not other lipid species, were significantly increased.	Glucosylceramides	281-298	megakaryocyte-associated tyrosine kinase	Homo sapiens	158-161
21910967-7	2011	We found that the bile salts cholate, deoxycholate, taurocholate and taurodeoxycholate, cause glucosylceramide to become transferrable by GLTP.	Glucosylceramides	94-110	glycolipid transfer protein	Homo sapiens	138-142
21982627-3	2011	beta-glucocerebrosidase, the enzyme deficient in Gaucher disease, also has an essential role in maintaining epidermal permeability function, by regulating the ratio of ceramides to glucosylceramides in the stratum corneum of the skin.	Glucosylceramides	181-198	glucosylceramidase beta	Homo sapiens	0-23
23110086-0	2012	Age-dependent changes in the sphingolipid composition of mouse CD4+ T cell membranes and immune synapses implicate glucosylceramides in age-related T cell dysfunction.	Glucosylceramides	115-132	CD4 antigen	Mus musculus	63-66
23110086-8	2012	These results suggest that reductions in glucosylceramide abundance contribute to age-related impairments in CD4(+) T cell function.	Glucosylceramides	41-57	CD4 antigen	Mus musculus	109-112
21833718-2	2011	Pro-apoptotic ceramide mediates imatinib-induced apoptosis, and metabolism of ceramide by glucosylceramide synthase (GCS) activity, converting ceramide to glucosyl ceramide, might contribute to imatinib resistance.	Glucosylceramides	155-172	UDP-glucose ceramide glucosyltransferase	Homo sapiens	117-120
21538359-1	2011	BACKGROUND AND OBJECTIVES: Besides MDR1/P-glycoprotein (MDR1/P-gp), glucosylceramide synthase (GCS), an enzyme, which transfers UDP-glucose to ceramide to form glucosylceramide was also related with multidrug resistance (MDR) in breast cancer.	Glucosylceramides	68-84	UDP-glucose ceramide glucosyltransferase	Homo sapiens	95-98
21325339-1	2011	Ceramide glucosyltransferase (Ugcg) [uridine diphosphate (UDP)-glucose:N-acylsphingosine D-glucosyltransferase or UDP-glucose ceramide glucosyltransferase (GlcT): EC 2.4.1.80] catalyzes formation of glucosylceramide (GlcCer) from ceramide and UDP-glucose.	Glucosylceramides	199-215	UDP-glucose ceramide glucosyltransferase	Mus musculus	30-34
21558327-4	2011	Following TPA treatment, we observed a 3.5-fold increase in GlcCer levels that was caused by enhanced activity of ceramide glucosyltransferase (GlcT-1), which catalyses ceramide glycosylation.	Glucosylceramides	60-66	UDP-glucose ceramide glucosyltransferase	Homo sapiens	114-142
21558327-4	2011	Following TPA treatment, we observed a 3.5-fold increase in GlcCer levels that was caused by enhanced activity of ceramide glucosyltransferase (GlcT-1), which catalyses ceramide glycosylation.	Glucosylceramides	60-66	UDP-glucose ceramide glucosyltransferase	Homo sapiens	144-150
21550991-1	2011	Glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs).	Glucosylceramides	62-78	Glucosylceramide synthase	Drosophila melanogaster	0-25
21550991-1	2011	Glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs).	Glucosylceramides	62-78	Glucosylceramide synthase	Drosophila melanogaster	27-33
21550991-1	2011	Glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs).	Glucosylceramides	80-86	Glucosylceramide synthase	Drosophila melanogaster	0-25
21550991-1	2011	Glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs).	Glucosylceramides	80-86	Glucosylceramide synthase	Drosophila melanogaster	27-33
21550991-9	2011	Furthermore, we found that GlcCer is the sole GSL of the fat body, indicating that regulation of GlcCer synthesis by GlcT-1 in the fat body is responsible for regulating energy homeostasis.	Glucosylceramides	27-33	Glucosylceramide synthase	Drosophila melanogaster	117-123
21235447-2	2011	The absence of beta-glucocerebrosidase whose purpose is to cleave the glucose from ceramide results in accumulation of glucocerebroside; storage of this glycolipid results in Gaucher disease.	Glucosylceramides	119-135	glucosylceramidase beta	Homo sapiens	15-38
21457079-1	2011	INTRODUCTION: Mutations in the gene encoding for acid beta-glucosidase (beta-glucocerebrosidase, GlcCerase) are seen in Gaucher disease (GD), which give rise to significant protein misfolding effects and result in progressive accumulation of glucosyl ceramide.	Glucosylceramides	242-259	glucosylceramidase beta	Homo sapiens	49-70
21325339-1	2011	Ceramide glucosyltransferase (Ugcg) [uridine diphosphate (UDP)-glucose:N-acylsphingosine D-glucosyltransferase or UDP-glucose ceramide glucosyltransferase (GlcT): EC 2.4.1.80] catalyzes formation of glucosylceramide (GlcCer) from ceramide and UDP-glucose.	Glucosylceramides	217-223	UDP-glucose ceramide glucosyltransferase	Mus musculus	30-34
21325339-11	2011	From these results, we concluded that the Ugcg gene is indispensable in the germline and that an ample supply of GlcCer is needed for oocytes and fertilized eggs to maintain normal membranes and to proceed through the normal cell cycle.	Glucosylceramides	113-119	UDP-glucose ceramide glucosyltransferase	Mus musculus	42-46
21222241-0	2011	Oral glucosylceramide reduces 2,4-dinitrofluorobenzene induced inflammatory response in mice by reducing TNF-alpha levels and leukocyte infiltration.	Glucosylceramides	5-21	tumor necrosis factor	Mus musculus	105-114
20728381-2	2011	Deficiency of glucocerebrosidase (GBA), a beta-glucosidase degrading glucosylceramide, underlies Gaucher disease.	Glucosylceramides	69-85	glucosylceramidase beta	Homo sapiens	34-37
24900342-4	2011	Here we show that C6-OH appears of less important, which may set guidelines for the development of GCS inhibitors that have less affinity (in comparison with Zavesca) for other glycoprocessing enzymes, in particular those hydrolases that act on glucosylceramide.	Glucosylceramides	245-261	UDP-glucose ceramide glucosyltransferase	Homo sapiens	99-102
21257328-8	2011	In a chemically induced GCase deficiency, alpha-synuclein aggregates and glucosylceramide accumulation also occurred.	Glucosylceramides	73-89	glucosidase, beta, acid	Mus musculus	24-29
21257328-9	2011	These studies demonstrate a relationship between glucosylceramide accumulation and alpha-synuclein aggregates, and implicate glucosylceramide accumulation as risk factor for the alpha-synucleinopathies.	Glucosylceramides	49-65	synuclein, alpha	Mus musculus	83-98
21700325-3	2011	Glucosylceramide (GlcCer), the GCase substrate, directly influenced amyloid formation of purified alpha-syn by stabilizing soluble oligomeric intermediates.	Glucosylceramides	0-16	synuclein alpha	Homo sapiens	98-107
21700325-3	2011	Glucosylceramide (GlcCer), the GCase substrate, directly influenced amyloid formation of purified alpha-syn by stabilizing soluble oligomeric intermediates.	Glucosylceramides	18-24	synuclein alpha	Homo sapiens	98-107
21270676-9	2011	The C-9 also decreased Gb3 and glucosylceramide expression levels in rat kidneys.	Glucosylceramides	31-47	complement C9	Rattus norvegicus	4-7
21303904-5	2011	By preferring dihydroxy sphingoid bases and C(16)/C(18) acyl-coenzyme A as substrates, Bar1p produces a structurally well defined group of ceramide species, which is the exclusive precursor for glucosylceramide biosynthesis.	Glucosylceramides	194-210	aspartyl protease BAR1	Saccharomyces cerevisiae S288C	87-92
21303904-6	2011	Correlating with the absence of glucosylceramide in this yeast, a gene encoding Bar1p is missing in S. cerevisiae.	Glucosylceramides	32-48	aspartyl protease BAR1	Saccharomyces cerevisiae S288C	80-85
21366909-7	2011	RESULTS: Fa2h-/-/Cgt-/- double-deficient mice lack sulfatide, GalCer, and in addition HFA-GlcCer and sphingomyelin.	Glucosylceramides	90-96	fatty acid 2-hydroxylase	Mus musculus	9-13
21366909-7	2011	RESULTS: Fa2h-/-/Cgt-/- double-deficient mice lack sulfatide, GalCer, and in addition HFA-GlcCer and sphingomyelin.	Glucosylceramides	90-96	UDP galactosyltransferase 8A	Mus musculus	17-20
20728381-4	2011	Recombinant GBA3 was found to hydrolyze artificial substrates such as 4-methylumbelliferyl-beta-D-glucoside and C6-NBD-glucosylceramide, but hydrolysis of naturally occurring lipids like glucosylceramide and glucosylsphingosine was hardly detected.	Glucosylceramides	119-135	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	12-16
20728381-3	2011	We examined GBA3, which recently was proposed to degrade glucosylceramide and influence the clinical manifestation of Gaucher disease.	Glucosylceramides	57-73	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	12-16
20574042-8	2010	The amounts of LacCer and GM3 ganglioside were drastically reduced, while GlcCer accumulated in the beta4GalT-5-deficient XEN cells.	Glucosylceramides	74-80	UDP-Gal:betaGlcNAc beta 1,4-galactosyltransferase, polypeptide 5	Mus musculus	100-111
21576963-1	2011	BACKGROUND/AIMS: The non-lysosomal glucosylceramidase, beta-glucosidase (Gba2), hydrolyzes glucosylceramide to glucose and ceramide (Cer).	Glucosylceramides	91-107	glucosidase beta 2	Mus musculus	21-53
21576963-1	2011	BACKGROUND/AIMS: The non-lysosomal glucosylceramidase, beta-glucosidase (Gba2), hydrolyzes glucosylceramide to glucose and ceramide (Cer).	Glucosylceramides	91-107	glucosidase beta 2	Mus musculus	73-77
22112991-1	2011	Gaucher"s disease is a lysosomal storage disease caused by the lack of beta-glucocerebrosidase enzyme, leading to the accumulation of glucocerebroside.	Glucosylceramides	134-150	glucosylceramidase beta	Homo sapiens	71-94
21500096-4	2011	Glucosylceramide synthase (GCS) and sphingosine kinase-1 (SK-1) enzymes can convert ceramides to antiapoptotic molecules, glucosylceramide, and sphingosine-1-phosphate, respectively.	Glucosylceramides	122-138	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
21500096-4	2011	Glucosylceramide synthase (GCS) and sphingosine kinase-1 (SK-1) enzymes can convert ceramides to antiapoptotic molecules, glucosylceramide, and sphingosine-1-phosphate, respectively.	Glucosylceramides	122-138	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
21500096-4	2011	Glucosylceramide synthase (GCS) and sphingosine kinase-1 (SK-1) enzymes can convert ceramides to antiapoptotic molecules, glucosylceramide, and sphingosine-1-phosphate, respectively.	Glucosylceramides	122-138	sphingosine kinase 1	Homo sapiens	36-62
21738789-2	2011	A potential approach is substrate reduction therapy using inhibitors of glucosylceramide synthase (GCS) to decrease the synthesis of glucosylceramide and related glycosphingolipids that accumulate in the lysosomes.	Glucosylceramides	72-88	UDP-glucose ceramide glucosyltransferase	Mus musculus	99-102
21738789-6	2011	The increase in brain glucosylceramide levels might be due to concurrent inhibition of the non-lysosomal glucosylceramidase, Gba2.	Glucosylceramides	22-38	glucosidase beta 2	Mus musculus	91-123
21738789-6	2011	The increase in brain glucosylceramide levels might be due to concurrent inhibition of the non-lysosomal glucosylceramidase, Gba2.	Glucosylceramides	22-38	glucosidase beta 2	Mus musculus	125-129
24900289-3	2011	In particular, iminosugar type GCS inhibitors often also inhibit to some extent human acid glucosylceramidase (GBA1) and the nonlysosomal glucosylceramidase (GBA2), the two enzymes known to process glucosylceramide.	Glucosylceramides	198-214	UDP-glucose ceramide glucosyltransferase	Homo sapiens	31-34
24900289-3	2011	In particular, iminosugar type GCS inhibitors often also inhibit to some extent human acid glucosylceramidase (GBA1) and the nonlysosomal glucosylceramidase (GBA2), the two enzymes known to process glucosylceramide.	Glucosylceramides	198-214	glucosylceramidase beta	Homo sapiens	91-109
24900289-3	2011	In particular, iminosugar type GCS inhibitors often also inhibit to some extent human acid glucosylceramidase (GBA1) and the nonlysosomal glucosylceramidase (GBA2), the two enzymes known to process glucosylceramide.	Glucosylceramides	198-214	glucosylceramidase beta	Homo sapiens	111-115
24900289-3	2011	In particular, iminosugar type GCS inhibitors often also inhibit to some extent human acid glucosylceramidase (GBA1) and the nonlysosomal glucosylceramidase (GBA2), the two enzymes known to process glucosylceramide.	Glucosylceramides	198-214	glucosylceramidase beta	Homo sapiens	138-156
24900289-3	2011	In particular, iminosugar type GCS inhibitors often also inhibit to some extent human acid glucosylceramidase (GBA1) and the nonlysosomal glucosylceramidase (GBA2), the two enzymes known to process glucosylceramide.	Glucosylceramides	198-214	glucosylceramidase beta 2	Homo sapiens	158-162
24900289-5	2011	The physiological importance of GBA2 in glucosylceramide processing in relation to disease states is less clear, and here, selective inhibitors can be of use as chemical knockout entities.	Glucosylceramides	40-56	glucosylceramidase beta 2	Homo sapiens	32-36
20935456-4	2010	We hypothesized that increases in GCS activity and thus glucosylceramide, the product of GCS activity, represents an important resistance mechanism in glioblastoma.	Glucosylceramides	56-72	UDP-glucose ceramide glucosyltransferase	Homo sapiens	89-92
20872320-2	2010	Gaucher disease is an inherited defect of lysosomal functions caused by mutations in the GBA1 gene leading to accumulation of glucocerebroside, primarily in macrophages.	Glucosylceramides	126-142	glucosylceramidase beta	Homo sapiens	89-93
21057870-7	2010	However, when cell homogenates were incubated with glucosylceramide in the presence of UDP-[(3)H]Gal, Lac-Cer synthase activity in B4galt5 ( +/- ) - and B4galt5 ( -/- ) -derived MEF cells decreased to 41% and 11% of that of B4galt5 ( +/+ )-derived MEF cells.	Glucosylceramides	51-67	UDP-Gal:betaGlcNAc beta 1,4-galactosyltransferase, polypeptide 5	Mus musculus	131-160
21057870-7	2010	However, when cell homogenates were incubated with glucosylceramide in the presence of UDP-[(3)H]Gal, Lac-Cer synthase activity in B4galt5 ( +/- ) - and B4galt5 ( -/- ) -derived MEF cells decreased to 41% and 11% of that of B4galt5 ( +/+ )-derived MEF cells.	Glucosylceramides	51-67	UDP-Gal:betaGlcNAc beta 1,4-galactosyltransferase, polypeptide 5	Mus musculus	131-138
20714811-5	2010	Progressive storage of glucosylceramide in mononuclear cells and macrophages results in elevated levels of chitotriosidase and CCL18/PARC which may be used as biomarker to assess disease severity and efficacy of treatment.	Glucosylceramides	23-39	C-C motif chemokine ligand 18	Homo sapiens	127-132
20714811-5	2010	Progressive storage of glucosylceramide in mononuclear cells and macrophages results in elevated levels of chitotriosidase and CCL18/PARC which may be used as biomarker to assess disease severity and efficacy of treatment.	Glucosylceramides	23-39	C-C motif chemokine ligand 18	Homo sapiens	133-137
21221911-1	2010	Gaucher disease is a genetic disorder of sphingolipid metabolism resulting from dysfunction of the lysosomal membrane-associated glycoprotein glucocerebrosidase (GBA) and resulting in intracellular accumulation of glucosylceramide and other glycolipids.	Glucosylceramides	214-230	glucosylceramidase beta	Homo sapiens	162-165
20962279-1	2010	In nonneuronopathic type 1 Gaucher disease (GD1), mutations in the glucocerebrosidase gene (GBA1) gene result in glucocerebrosidase deficiency and the accumulation of its substrate, glucocerebroside (GL-1), in the lysosomes of mononuclear phagocytes.	Glucosylceramides	182-198	glucosidase, beta, acid	Mus musculus	67-85
20962279-1	2010	In nonneuronopathic type 1 Gaucher disease (GD1), mutations in the glucocerebrosidase gene (GBA1) gene result in glucocerebrosidase deficiency and the accumulation of its substrate, glucocerebroside (GL-1), in the lysosomes of mononuclear phagocytes.	Glucosylceramides	182-198	glucosidase, beta, acid	Mus musculus	92-96
22563139-2	2010	This glucosylceramide analogue acts as an inhibitor of glucosylceramide synthase, a Golgi complex enzyme that catalyzes the formation of glucosylceramide from ceramide and UDP-glucose and is the first step in the formation of glucocerebroside-based glycosphingolipids.	Glucosylceramides	5-21	UDP-glucose ceramide glucosyltransferase	Homo sapiens	55-80
20540746-5	2010	GCS converts ceramide to glucosylceramide, reducing the impact of ceramide-induced apoptosis and increasing glycosphingolipid (GSL) synthesis.	Glucosylceramides	25-41	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
20157020-5	2010	Although GST gene expression was higher under heat stress, SM4s synthesis decreased, which may have been due to increased GST sensitivity to a temperature higher than 37 degrees C. When we introduced the HSP70 gene into the expression vector and transfected the plasmid (pCDM-dHSP70) into kidney cells, GlcCer synthesis increased significantly.	Glucosylceramides	303-309	heat shock 70 kDa protein 1	Canis lupus familiaris	204-209
20157020-6	2010	From these results, we speculated that HSP70 may play a role in GluT gene expression to increase GlcCer and decrease intracellular ceramide level.	Glucosylceramides	97-103	heat shock 70 kDa protein 1	Canis lupus familiaris	39-44
20432257-4	2010	In those studies, ubiquitously acting inhibitors for GSL biosynthesis have been used to inhibit the enzyme Ugcg (UDP-glucose:ceramide glucosyltransferase), catalyzing the first step of the glucosylceramide-based GSL-synthesis pathway.	Glucosylceramides	189-205	UDP-glucose ceramide glucosyltransferase	Mus musculus	107-111
20425796-1	2010	In Gaucher disease (GD), inherited deficiency of lysosomal glucocerebrosidase due to mutations in GBA1 gene results in accumulation of glucosylceramide in tissue macrophages, systemic macrophage activation, and a complex multisystemic phenotype.	Glucosylceramides	135-151	glucosylceramidase beta	Homo sapiens	98-102
20167235-9	2010	Gaucher spleen cells accumulating glucosylceramide expressed very high levels of CD97 and EMR2.	Glucosylceramides	34-50	adhesion G protein-coupled receptor E5	Homo sapiens	81-85
20167235-9	2010	Gaucher spleen cells accumulating glucosylceramide expressed very high levels of CD97 and EMR2.	Glucosylceramides	34-50	adhesion G protein-coupled receptor E2	Homo sapiens	90-94
20432257-4	2010	In those studies, ubiquitously acting inhibitors for GSL biosynthesis have been used to inhibit the enzyme Ugcg (UDP-glucose:ceramide glucosyltransferase), catalyzing the first step of the glucosylceramide-based GSL-synthesis pathway.	Glucosylceramides	189-205	UDP-glucose ceramide glucosyltransferase	Mus musculus	113-153
19932170-8	2010	However, hypoxia also increased the cellular level of glucosylceramide, which was inhibited by a glucosylceramide synthase (GCS) inhibitor and specific siRNA, but not a ceramidase inhibitor.	Glucosylceramides	54-70	UDP-glucose ceramide glucosyltransferase	Homo sapiens	97-122
19932170-8	2010	However, hypoxia also increased the cellular level of glucosylceramide, which was inhibited by a glucosylceramide synthase (GCS) inhibitor and specific siRNA, but not a ceramidase inhibitor.	Glucosylceramides	54-70	UDP-glucose ceramide glucosyltransferase	Homo sapiens	124-127
19932170-9	2010	The increase in glucosylceramide was accompanied by increases in both PARP cleavage and DNA fragmentation.	Glucosylceramides	16-32	poly(ADP-ribose) polymerase 1	Homo sapiens	70-74
20148966-6	2010	IFG incubation also increased the lysosomal trafficking and in situ activity of L444P GCase in intact cells, as measured by reduction in endogenous glucosylceramide levels.	Glucosylceramides	148-164	glucosidase, beta, acid	Mus musculus	86-91
20216312-3	2010	RECENT FINDINGS: Who: ceramides and glucosylceramides are likely to be independent antagonists of insulin action.	Glucosylceramides	36-53	insulin	Homo sapiens	98-105
20216312-6	2010	What: ceramides and glucosylceramides inhibit different insulin signaling events, but it is unclear whether these actions account for the broad spectrum of therapeutic benefits resulting from sphingolipid depletion.	Glucosylceramides	20-37	insulin	Homo sapiens	56-63
19826105-1	2010	Glucosylceramide synthase (GCS or GlcT-1), converting ceramide to glucosylceramide, is a key enzyme for the synthesis of glycosphingolipids.	Glucosylceramides	66-82	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
19826105-1	2010	Glucosylceramide synthase (GCS or GlcT-1), converting ceramide to glucosylceramide, is a key enzyme for the synthesis of glycosphingolipids.	Glucosylceramides	66-82	UDP-glucose ceramide glucosyltransferase	Homo sapiens	34-40
20015957-2	2010	The few patients with saposin C deficiency develop a Gaucher disease-like central nervous system (CNS) phenotype attributed to diminished glucosylceramide (GC) cleavage activity by acid beta-glucosidase (GCase).	Glucosylceramides	138-154	glucosidase, beta, acid	Mus musculus	204-209
20177787-1	2010	In Gaucher disease, defective lysosomal glucocerebrosidase due to mutations in the GBA1 gene results in lysosomal accumulation of glucocerebroside in mononuclear phagocytes and a multisystemic phenotype.	Glucosylceramides	130-146	glucosylceramidase beta	Homo sapiens	83-87
20019081-3	2010	To investigate the importance of the methyl branch of the long-chain base in glucosylceramides in pathogenic fungi, we identified and characterized a sphingolipid C9-methyltransferase gene (MTS1, C9-MethylTransferase for Sphingolipid 1) in the pathogenic yeast Candida albicans.	Glucosylceramides	77-94	mRNA-binding protein NPL3	Saccharomyces cerevisiae S288C	190-194
20019081-4	2010	The mts1 disruptant lacked (E,E)-9-methylsphinga-4,8-dienine in its glucosylceramides and contained (E)-sphing-4-enine and (E,E)-sphinga-4,8-dienine.	Glucosylceramides	68-85	mRNA-binding protein NPL3	Saccharomyces cerevisiae S288C	4-8
20015957-2	2010	The few patients with saposin C deficiency develop a Gaucher disease-like central nervous system (CNS) phenotype attributed to diminished glucosylceramide (GC) cleavage activity by acid beta-glucosidase (GCase).	Glucosylceramides	156-158	glucosidase, beta, acid	Mus musculus	186-202
19576930-2	2009	The aim of this study was to determine whether there is a relationship between alpha-synuclein (alpha-syn), a key protein in Parkinson"s disease pathogenesis, and abnormalities in glucocerebroside (GC) catabolism that lead to the development of Gaucher disease.	Glucosylceramides	180-196	synuclein, alpha	Mus musculus	79-94
20169998-0	2010	[Novel metabolic pathway of glucosylceramide that involves Klotho-related protein KLrP].	Glucosylceramides	28-44	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	82-86
20156351-8	2010	On the other hand, mAb MEST-2 specifically directed to fungal glucosylceramide (GlcCer) was able to promote only a weak inhibition on fungal differentiation and colony formation.	Glucosylceramides	62-78	mesoderm specific transcript	Homo sapiens	23-27
20156351-8	2010	On the other hand, mAb MEST-2 specifically directed to fungal glucosylceramide (GlcCer) was able to promote only a weak inhibition on fungal differentiation and colony formation.	Glucosylceramides	80-86	mesoderm specific transcript	Homo sapiens	23-27
19824038-1	2009	Five glucosylceramides (GlcCers) were isolated by reversed phase high-performance liquid chromatography from the MeOH extracts of a marine sponge, Haliclona (Reniera) sp., collected from the coast of Ulleung Island, Korea, and analyzed by fast atom bombardment mass spectrometry (FAB-MS) in positive-ion mode.	Glucosylceramides	5-22	FA complementation group B	Homo sapiens	280-283
19824038-1	2009	Five glucosylceramides (GlcCers) were isolated by reversed phase high-performance liquid chromatography from the MeOH extracts of a marine sponge, Haliclona (Reniera) sp., collected from the coast of Ulleung Island, Korea, and analyzed by fast atom bombardment mass spectrometry (FAB-MS) in positive-ion mode.	Glucosylceramides	24-31	FA complementation group B	Homo sapiens	280-283
19940249-1	2009	The Golgi-associated four-phosphate adaptor protein 2 (FAPP2) has been shown to possess transfer activity for glucosylceramide both in vitro and in cells.	Glucosylceramides	110-126	pleckstrin homology domain containing A8	Canis lupus familiaris	21-53
19940249-1	2009	The Golgi-associated four-phosphate adaptor protein 2 (FAPP2) has been shown to possess transfer activity for glucosylceramide both in vitro and in cells.	Glucosylceramides	110-126	pleckstrin homology domain containing A8	Canis lupus familiaris	55-60
19576930-2	2009	The aim of this study was to determine whether there is a relationship between alpha-synuclein (alpha-syn), a key protein in Parkinson"s disease pathogenesis, and abnormalities in glucocerebroside (GC) catabolism that lead to the development of Gaucher disease.	Glucosylceramides	198-200	synuclein, alpha	Mus musculus	79-94
19429679-1	2009	ABCA12 (ATP binding cassette transporter, family 12) is a cellular membrane transporter that facilitates the delivery of glucosylceramides to epidermal lamellar bodies in keratinocytes, a process that is critical for permeability barrier formation.	Glucosylceramides	121-138	ATP binding cassette subfamily A member 12	Homo sapiens	0-6
19052561-5	2009	Silencing of either VDR, SRC2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids such as cholesterol and free fatty acids.	Glucosylceramides	73-89	vitamin D (1,25-dihydroxyvitamin D3) receptor	Mus musculus	20-23
19052561-5	2009	Silencing of either VDR, SRC2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids such as cholesterol and free fatty acids.	Glucosylceramides	73-89	nuclear receptor coactivator 2	Mus musculus	25-29
19052561-5	2009	Silencing of either VDR, SRC2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids such as cholesterol and free fatty acids.	Glucosylceramides	73-89	nuclear receptor coactivator 3	Mus musculus	34-38
19052561-5	2009	Silencing of either VDR, SRC2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids such as cholesterol and free fatty acids.	Glucosylceramides	91-97	vitamin D (1,25-dihydroxyvitamin D3) receptor	Mus musculus	20-23
19052561-5	2009	Silencing of either VDR, SRC2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids such as cholesterol and free fatty acids.	Glucosylceramides	91-97	nuclear receptor coactivator 2	Mus musculus	25-29
19052561-5	2009	Silencing of either VDR, SRC2, or SRC3 resulted in decreases in specific glucosylceramide (GlcCer) species but not other lipids such as cholesterol and free fatty acids.	Glucosylceramides	91-97	nuclear receptor coactivator 3	Mus musculus	34-38
18459163-5	2008	On the other hand, FAPP2 transfers glucosylceramide (GlcCer) to appropriate sites for the synthesis of complex glycosphingolipids.	Glucosylceramides	35-51	pleckstrin homology domain containing A8	Homo sapiens	19-24
18783340-1	2008	In mammalian cells, glucosylceramide (GlcCer), the simplest glycosphingolipid, is hydrolyzed by the lysosomal enzyme acid beta-glucosidase (GlcCerase).	Glucosylceramides	20-36	glucosylceramidase beta	Homo sapiens	117-138
18783340-1	2008	In mammalian cells, glucosylceramide (GlcCer), the simplest glycosphingolipid, is hydrolyzed by the lysosomal enzyme acid beta-glucosidase (GlcCerase).	Glucosylceramides	38-44	glucosylceramidase beta	Homo sapiens	117-138
19279008-1	2009	Activation of protein kinase C (PKC) by the phorbol ester (phorbol 12-myristate 13-acetate) induces ceramide formation through the salvage pathway involving, in part, acid beta-glucosidase 1 (GBA1), which cleaves glucosylceramide to ceramide.	Glucosylceramides	213-229	proline rich transmembrane protein 2	Homo sapiens	14-30
19279008-1	2009	Activation of protein kinase C (PKC) by the phorbol ester (phorbol 12-myristate 13-acetate) induces ceramide formation through the salvage pathway involving, in part, acid beta-glucosidase 1 (GBA1), which cleaves glucosylceramide to ceramide.	Glucosylceramides	213-229	proline rich transmembrane protein 2	Homo sapiens	32-35
19279008-1	2009	Activation of protein kinase C (PKC) by the phorbol ester (phorbol 12-myristate 13-acetate) induces ceramide formation through the salvage pathway involving, in part, acid beta-glucosidase 1 (GBA1), which cleaves glucosylceramide to ceramide.	Glucosylceramides	213-229	glucosylceramidase beta	Homo sapiens	192-196
19279011-6	2009	In the present study, we examined whether acid beta-glucosidase 1 (GBA1), which hydrolyzes glucosylceramide to form lysosomal ceramide, was involved in PKC-regulated formation of ceramide from recycled sphingosine.	Glucosylceramides	91-107	glucosylceramidase beta	Homo sapiens	67-71
19279011-6	2009	In the present study, we examined whether acid beta-glucosidase 1 (GBA1), which hydrolyzes glucosylceramide to form lysosomal ceramide, was involved in PKC-regulated formation of ceramide from recycled sphingosine.	Glucosylceramides	91-107	protein kinase C delta	Homo sapiens	152-155
19279011-7	2009	Glucosylceramide levels declined after treatment of MCF-7 cells with a potent PKC activator, phorbol 12-myristate 13-acetate (PMA).	Glucosylceramides	0-16	protein kinase C delta	Homo sapiens	78-81
19279011-9	2009	Silencing GBA1 blocked PMA-induced degradation of glucosylceramide and generation of sphingosine, the source for ceramide biosynthesis.	Glucosylceramides	50-66	glucosylceramidase beta	Homo sapiens	10-14
19279011-14	2009	Thus, PKCdelta activation is suggested to stimulate the degradation of both sphingomyelin and glucosylceramide leading to the salvage pathway of ceramide formation.	Glucosylceramides	94-110	protein kinase C delta	Homo sapiens	6-14
19337026-5	2009	The dissociation of the Beclin 1:Bcl-2 complex has also been observed in response to tamoxifen and PDMP (an inhibitor of the enzyme that converts ceramide to glucosylceramide), drugs that increase the intracellular level of long-chain ceramides.	Glucosylceramides	158-174	beclin 1	Homo sapiens	24-32
19337026-5	2009	The dissociation of the Beclin 1:Bcl-2 complex has also been observed in response to tamoxifen and PDMP (an inhibitor of the enzyme that converts ceramide to glucosylceramide), drugs that increase the intracellular level of long-chain ceramides.	Glucosylceramides	158-174	BCL2 apoptosis regulator	Homo sapiens	33-38
19285492-2	2009	Inhibition of glucosylceramide (GC) synthesis has been shown in cell lines to correlate with the expression and function of P-gp and sensitise cancer cells to cytotoxic agents.	Glucosylceramides	14-30	ATP binding cassette subfamily B member 1	Homo sapiens	124-128
19285492-2	2009	Inhibition of glucosylceramide (GC) synthesis has been shown in cell lines to correlate with the expression and function of P-gp and sensitise cancer cells to cytotoxic agents.	Glucosylceramides	32-34	ATP binding cassette subfamily B member 1	Homo sapiens	124-128
19122329-3	2009	The major new features of these glucocerebrosides are C15 and C19 acyl chains, long (C24-C28) acyl chains, or the S-configuration of the acyl chains.	Glucosylceramides	32-49	placenta associated 8	Homo sapiens	54-57
18662675-1	2008	Human cytosolic beta-glucosidase, also known as klotho-related protein (KLrP, GBA3), is an enzyme that hydrolyzes various beta-D-glucosides, including glucosylceramide.	Glucosylceramides	151-167	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	6-32
18662675-1	2008	Human cytosolic beta-glucosidase, also known as klotho-related protein (KLrP, GBA3), is an enzyme that hydrolyzes various beta-D-glucosides, including glucosylceramide.	Glucosylceramides	151-167	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	48-70
18662675-1	2008	Human cytosolic beta-glucosidase, also known as klotho-related protein (KLrP, GBA3), is an enzyme that hydrolyzes various beta-D-glucosides, including glucosylceramide.	Glucosylceramides	151-167	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	72-76
18662675-1	2008	Human cytosolic beta-glucosidase, also known as klotho-related protein (KLrP, GBA3), is an enzyme that hydrolyzes various beta-D-glucosides, including glucosylceramide.	Glucosylceramides	151-167	glucosylceramidase beta 3 (gene/pseudogene)	Homo sapiens	78-82
18631186-6	2008	When the amino acid sequences of ceramide synthase derived from eight yeast species were compared, LAC1 proteins from five species producing glucosylceramide were clearly discriminated from those of the other three species and all LAG1 proteins.	Glucosylceramides	141-157	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	99-103
18631186-7	2008	The LAC1 protein of K. lactis is the enzyme that plays a crucial role in the synthesis of glucosylceramide.	Glucosylceramides	90-106	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	4-8
18537822-8	2008	The AtGLTP1 variant Arg59Lys/Asn95Leu showed low BODIPY-glucosylceramide transfer activity, indicating that Arg59 and/or Asn95 are important for the specific binding of glucosylceramide to AtGLTP1.	Glucosylceramides	56-72	glycolipid transfer protein 1	Arabidopsis thaliana	4-11
18435913-10	2008	The addition of exogenous GD1a to FBJ-LL cells suppressed TNFalpha expression, and treatment of FBJ-S1 cells with D-PDMP (glucosylceramide synthesis inhibitor) led to an increase in TNFalpha, indicating that TNFalpha is negatively regulated by GD1a in FBJ cells.	Glucosylceramides	122-138	tumor necrosis factor	Mus musculus	182-190
18435913-10	2008	The addition of exogenous GD1a to FBJ-LL cells suppressed TNFalpha expression, and treatment of FBJ-S1 cells with D-PDMP (glucosylceramide synthesis inhibitor) led to an increase in TNFalpha, indicating that TNFalpha is negatively regulated by GD1a in FBJ cells.	Glucosylceramides	122-138	tumor necrosis factor	Mus musculus	182-190
18245173-5	2008	GCS catalyzes ceramide glycosylation, converting ceramide to glucosylceramide; this process hastens ceramide clearance and limits ceramide-induced apoptosis.	Glucosylceramides	61-77	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
18459163-5	2008	On the other hand, FAPP2 transfers glucosylceramide (GlcCer) to appropriate sites for the synthesis of complex glycosphingolipids.	Glucosylceramides	53-59	pleckstrin homology domain containing A8	Homo sapiens	19-24
17709137-2	2008	Glucosylceramide synthase (GCS) catalyzes glycosylation of ceramide and produces glucosylceramide.	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
18373728-6	2008	In conclusion, the lumenal domain contains sorting information that guides Tyrp1 and probably tyrosinase to melanosomes by an intracellular route that excludes lysosomal proteins and requires glucosylceramide.	Glucosylceramides	192-208	tyrosinase related protein 1	Homo sapiens	75-80
17709137-2	2008	Glucosylceramide synthase (GCS) catalyzes glycosylation of ceramide and produces glucosylceramide.	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
18003606-3	2008	MDR1 is also a translocase that flips glucosylceramide inside the Golgi to enhance neutral glycosphingolipid (GSL) synthesis.	Glucosylceramides	38-54	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
18035065-0	2007	Ceramide and glucosylceramide upregulate expression of the multidrug resistance gene MDR1 in cancer cells.	Glucosylceramides	13-29	ATP binding cassette subfamily B member 1	Homo sapiens	85-89
18288958-4	2008	P-gp regulated the translocation of sphingomyelin (SM) and GlcCer, and short chain C(6)-NBD-GlcCer was found in the apical medium of P-gp cells exclusively and not in the basolateral membrane.	Glucosylceramides	59-65	ATP binding cassette subfamily B member 1	Homo sapiens	0-4
17803231-1	2008	Gaucher disease, the most prevalent lysosomal storage disorder, is principally caused by malfunction of the lysosomal enzyme glucocerebrosidase (GBA), a 497-amino acid membrane glycoprotein that catalyzes the hydrolysis of glucosylceramide to ceramide and glucose in the presence of an essential 84-residue activator peptide named saposin C (SapC).	Glucosylceramides	223-239	glucosylceramidase beta	Homo sapiens	145-148
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	100-116	ATP binding cassette subfamily B member 1	Homo sapiens	139-143
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	100-116	ATP binding cassette subfamily B member 1	Homo sapiens	190-204
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	100-116	ATP binding cassette subfamily B member 1	Homo sapiens	206-210
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	100-116	ATP binding cassette subfamily B member 1	Homo sapiens	261-265
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	118-120	ATP binding cassette subfamily B member 1	Homo sapiens	139-143
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	118-120	ATP binding cassette subfamily B member 1	Homo sapiens	190-204
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	118-120	ATP binding cassette subfamily B member 1	Homo sapiens	206-210
18035065-1	2007	In the present study we used human breast cancer cell lines to assess the influence of ceramide and glucosylceramide (GC) on expression of MDR1, the multidrug resistance gene that codes for P-glycoprotein (P-gp), because GC has been shown to be a substrate for P-gp.	Glucosylceramides	118-120	ATP binding cassette subfamily B member 1	Homo sapiens	261-265
17919309-3	2007	The prosaposin PSAP gene codes for a single protein which undergoes post-translational cleavage to yield four proteins named saposins A, B, C and D. Saposin (SAP-) C is required for glucosylceramide degradation, and its deficiency results in a variant form of Gaucher disease.	Glucosylceramides	182-198	prosaposin	Homo sapiens	15-19
17848577-0	2007	Accumulation of glucosylceramide in murine testis, caused by inhibition of beta-glucosidase 2: implications for spermatogenesis.	Glucosylceramides	16-32	glucosidase beta 2	Mus musculus	75-93
17848577-5	2007	This enzyme cleaves glucosylceramide into glucose and ceramide, is sensitive to imino sugars in vitro, and has been characterized as beta-glucosidase 2 (GBA2).	Glucosylceramides	20-36	glucosidase beta 2	Mus musculus	133-151
17848577-5	2007	This enzyme cleaves glucosylceramide into glucose and ceramide, is sensitive to imino sugars in vitro, and has been characterized as beta-glucosidase 2 (GBA2).	Glucosylceramides	20-36	glucosidase beta 2	Mus musculus	153-157
17848577-8	2007	Both of these GlcCer species were also increased in the testes from GBA2-deficient mice.	Glucosylceramides	14-20	glucosidase beta 2	Mus musculus	68-72
17980653-10	2007	We propose that GLTP is not likely involved in the de novo synthesis of glycosphingolipids, but could rather have a role as a glycolipid sensor for the cellular levels of glucosylceramide.	Glucosylceramides	171-187	glycolipid transfer protein	Homo sapiens	16-20
17994285-1	2007	Sandhoff disease, Gaucher disease type I and sialidosis type I are lysosomal storage disorders caused, respectively, by deficiency of activity of beta-hexosaminidase (storage of GM(2) and GA(2) ganglioside), glucosylceramidase (storage of glucosylceramide) and alpha-neuraminidase (storage of glucopeptides and/or oligosaccharides).	Glucosylceramides	239-255	O-GlcNAcase	Homo sapiens	146-165
17923527-12	2007	449:62-67) agree that four-phosphate adaptor protein 2 (FAPP2) transfers glucosylceramide (GlcCer), a lipid that takes an unexpectedly circuitous route.	Glucosylceramides	73-89	pleckstrin homology domain containing A8	Homo sapiens	22-54
17923527-12	2007	449:62-67) agree that four-phosphate adaptor protein 2 (FAPP2) transfers glucosylceramide (GlcCer), a lipid that takes an unexpectedly circuitous route.	Glucosylceramides	73-89	pleckstrin homology domain containing A8	Homo sapiens	56-61
17923527-12	2007	449:62-67) agree that four-phosphate adaptor protein 2 (FAPP2) transfers glucosylceramide (GlcCer), a lipid that takes an unexpectedly circuitous route.	Glucosylceramides	91-97	pleckstrin homology domain containing A8	Homo sapiens	22-54
17923527-12	2007	449:62-67) agree that four-phosphate adaptor protein 2 (FAPP2) transfers glucosylceramide (GlcCer), a lipid that takes an unexpectedly circuitous route.	Glucosylceramides	91-97	pleckstrin homology domain containing A8	Homo sapiens	56-61
17923531-8	2007	Thus, GlcCer destined for glycolipid synthesis follows a different pathway and transports back into the endoplasmic reticulum (ER) via the late Golgi protein FAPP2.	Glucosylceramides	6-12	pleckstrin homology domain containing A8	Homo sapiens	158-163
17511990-4	2007	The effects of the GCS inhibitor on impairment of CXCL12-induced cell migration temporally correlated with a pronounced downregulation of neutral glycosphingolipids, particularly glucosylceramide, and with a delayed and more moderate downregulation of gangliosides; moreover, exogenously administered glycosphingolipids allowed resumption of CXCR4-dependent chemotaxis.	Glucosylceramides	179-195	UDP-glucose ceramide glucosyltransferase	Homo sapiens	19-22
17535804-5	2007	The levels of glucosylceramide and lactosylceramide increased in parallel with Gb3 levels in an age-dependent manner, whereas globotetraosylceramide (Gb4) levels reached maximal levels by 6 months of age and then rapidly decreased at older ages.	Glucosylceramides	14-30	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	79-82
17443679-7	2007	Both ROS and APE1/Ref-1 increases are due to GlcCer accumulation, being prevented by treatment of GD fibroblasts with Cerezyme and induced in healthy fibroblasts treated with conduritol-beta-epoxide.	Glucosylceramides	45-51	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	13-17
17443679-7	2007	Both ROS and APE1/Ref-1 increases are due to GlcCer accumulation, being prevented by treatment of GD fibroblasts with Cerezyme and induced in healthy fibroblasts treated with conduritol-beta-epoxide.	Glucosylceramides	45-51	apurinic/apyrimidinic endodeoxyribonuclease 1	Homo sapiens	18-23
17687330-0	2007	Glycosphingolipid synthesis requires FAPP2 transfer of glucosylceramide.	Glucosylceramides	55-71	pleckstrin homology domain containing A8	Homo sapiens	37-42
17511990-4	2007	The effects of the GCS inhibitor on impairment of CXCL12-induced cell migration temporally correlated with a pronounced downregulation of neutral glycosphingolipids, particularly glucosylceramide, and with a delayed and more moderate downregulation of gangliosides; moreover, exogenously administered glycosphingolipids allowed resumption of CXCR4-dependent chemotaxis.	Glucosylceramides	179-195	C-X-C motif chemokine ligand 12	Homo sapiens	50-56
17080196-6	2006	Recombinant GBA2 hydrolyzed glucosylceramide to glucose and ceramide; the same reaction catalyzed by the beta-glucosidase acid 1 (GBA1) defective in subjects with the Gaucher"s form of lysosomal storage disease.	Glucosylceramides	28-44	glucosidase beta 2	Mus musculus	12-16
17355976-9	2007	These results reveal that 1) differentiation-dependent up-regulation of ceramide synthesis and fatty acid elongation is accompanied by up-regulation of FA2H; 2) 2-hydroxylation of fatty acid by FA2H occurs prior to generation of ceramides/glucosylceramides; and 3) 2-hydroxyceramides/2-hydroxyglucosylceramides are required for epidermal lamellar membrane formation.	Glucosylceramides	239-256	fatty acid 2-hydroxylase	Homo sapiens	152-156
17355976-9	2007	These results reveal that 1) differentiation-dependent up-regulation of ceramide synthesis and fatty acid elongation is accompanied by up-regulation of FA2H; 2) 2-hydroxylation of fatty acid by FA2H occurs prior to generation of ceramides/glucosylceramides; and 3) 2-hydroxyceramides/2-hydroxyglucosylceramides are required for epidermal lamellar membrane formation.	Glucosylceramides	239-256	fatty acid 2-hydroxylase	Homo sapiens	194-198
17217920-1	2007	Gaucher disease is a lysosomal glycolipid storage disorder characterized by defects in acid-beta-glucosidase (GlcCerase), the enzyme responsible for the catabolism of glucosylceramide.	Glucosylceramides	167-183	glucosylceramidase beta	Homo sapiens	87-108
17287460-5	2007	Treatment of ob/ob mice with AMP-DNM normalized their elevated tissue glucosylceramide levels, markedly lowered circulating glucose levels, improved oral glucose tolerance, reduced A1C, and improved insulin sensitivity in muscle and liver.	Glucosylceramides	70-86	dynamin 1	Mus musculus	33-36
17105727-11	2007	In conclusion, GBA2 plays a role in cellular glucosylceramide metabolism.	Glucosylceramides	45-61	glucosidase beta 2	Mus musculus	15-19
17827975-1	2007	RsAFP2 (Raphanus sativus antifungal peptide 2), an antifungal plant defensin isolated from seed of R. sativus, interacts with glucosylceramides (GlcCer) in membranes of susceptible yeast and fungi and induces membrane permeabilization and fungal cell death.	Glucosylceramides	126-143	defensin-like protein 2	Raphanus sativus	0-6
17827975-1	2007	RsAFP2 (Raphanus sativus antifungal peptide 2), an antifungal plant defensin isolated from seed of R. sativus, interacts with glucosylceramides (GlcCer) in membranes of susceptible yeast and fungi and induces membrane permeabilization and fungal cell death.	Glucosylceramides	126-143	defensin-like protein 2	Raphanus sativus	8-45
17510414-2	2007	The enzyme glucosylceramide synthase (GCS), responsible for bioactivation of the proapoptotic mediator ceramide to a nonfunctional moiety glucosylceramide, is overexpressed in many MDR tumor types and has been implicated in cell survival in the presence of chemotherapy.	Glucosylceramides	11-27	UDP-glucose ceramide glucosyltransferase	Homo sapiens	38-41
17367758-3	2007	TNFalpha expression was increased by addition of GM3 to the B16 transfectants and decreased after treatment with D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol, an inhibitor of glucosylceramide synthesis.	Glucosylceramides	187-203	tumor necrosis factor	Mus musculus	0-8
17080196-6	2006	Recombinant GBA2 hydrolyzed glucosylceramide to glucose and ceramide; the same reaction catalyzed by the beta-glucosidase acid 1 (GBA1) defective in subjects with the Gaucher"s form of lysosomal storage disease.	Glucosylceramides	28-44	glucosidase, beta, acid	Mus musculus	130-134
17100636-13	2006	Several possible ligands for NKT cells have recently been suggested including CD1d bound Glucocerebroside.	Glucosylceramides	89-105	CD1d molecule	Homo sapiens	78-82
17100636-18	2006	CD1d-bound glucocerebroside does not activate NKT cells directly, and may inhibit activation of NKT cells by alpha-GalCer.	Glucosylceramides	11-27	CD1d molecule	Homo sapiens	0-4
16724420-2	2006	We have shown that the ABC transporter, multiple drug resistance protein 1 (MDR1, P-glycoprotein) translocates glucosyl ceramide from the cytosolic to the luminal Golgi surface for neutral, but not acidic, glycosphingolipid (GSL) synthesis.	Glucosylceramides	111-128	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	40-74
16929170-11	2006	D, L-Threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol (PPMP) an inhibitor of glucosylceramide synthesis was used to block Gb3 synthesis.	Glucosylceramides	84-100	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	129-132
16736095-1	2006	Glucosylceramide-laden tissue macrophages in Gaucher patients secrete large quantities of chitotriosidase and CC chemokine ligand 18 (CCL18), resulting in markedly increased plasma levels.	Glucosylceramides	0-16	C-C motif chemokine ligand 18	Homo sapiens	110-132
16736095-1	2006	Glucosylceramide-laden tissue macrophages in Gaucher patients secrete large quantities of chitotriosidase and CC chemokine ligand 18 (CCL18), resulting in markedly increased plasma levels.	Glucosylceramides	0-16	C-C motif chemokine ligand 18	Homo sapiens	134-139
16528760-2	2006	The primary manifestation is the accumulation of glucosylceramide (GL-1) in the macrophages of liver and spleen (Gaucher cells), due to a deficiency in the lysosomal hydrolase glucocerebrosidase (GC).	Glucosylceramides	49-65	glucosidase, beta, acid	Mus musculus	196-198
16724420-3	2006	Here we show that the MDR1 inhibitor, cyclosporin A (CsA) can deplete Gaucher lymphoid cell lines of accumulated glucosyl ceramide and Fabry cell lines of globotriaosyl ceramide (Gb3), by preventing de novo synthesis.	Glucosylceramides	113-130	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	22-26
16724420-2	2006	We have shown that the ABC transporter, multiple drug resistance protein 1 (MDR1, P-glycoprotein) translocates glucosyl ceramide from the cytosolic to the luminal Golgi surface for neutral, but not acidic, glycosphingolipid (GSL) synthesis.	Glucosylceramides	111-128	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	76-80
16416005-1	2006	Glucosylceramide synthase (GCS), the enzyme that converts ceramide to glucosylceramide, induce multidrug resistance (MDR) in cancer cells.	Glucosylceramides	70-86	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
16416005-1	2006	Glucosylceramide synthase (GCS), the enzyme that converts ceramide to glucosylceramide, induce multidrug resistance (MDR) in cancer cells.	Glucosylceramides	70-86	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
16109770-3	2005	To gain insight into the role of GSLs in brain development and function, a cell-specific disruption of Ugcg was performed as indicated by the absence of virtually all glucosylceramide-based GSLs.	Glucosylceramides	167-183	UDP-glucose ceramide glucosyltransferase	Mus musculus	103-107
16185907-2	2005	The pathology of this recessively inherited disease arises from the accumulation of glucocerebroside in tissues due to deficient activity of the enzyme glucocerebrosidase (E.C.	Glucosylceramides	84-100	glucosylceramidase beta	Homo sapiens	152-170
15799713-0	2005	The reconstituted P-glycoprotein multidrug transporter is a flippase for glucosylceramide and other simple glycosphingolipids.	Glucosylceramides	73-89	ATP binding cassette subfamily B member 1	Homo sapiens	18-32
16000318-1	2005	Gaucher disease (GD), an autosomal recessive disease, is characterized by accumulation of glucosylceramide mainly in cells of the reticuloendothelial system, due to mutations in the acid beta-glucocerebrosidase gene.	Glucosylceramides	90-106	glucosylceramidase beta	Homo sapiens	187-210
15799713-3	2005	Pgp has been shown to translocate fluorescent phospholipids, and it has been suggested that it may also interact with GlcCer (glucosylceramide).	Glucosylceramides	118-124	ATP binding cassette subfamily B member 1	Homo sapiens	0-3
15799713-3	2005	Pgp has been shown to translocate fluorescent phospholipids, and it has been suggested that it may also interact with GlcCer (glucosylceramide).	Glucosylceramides	126-142	ATP binding cassette subfamily B member 1	Homo sapiens	0-3
15912415-0	2005	An accumulation of glucosylceramide in the stratum corneum due to attenuated activity of beta-glucocerebrosidase is associated with the early phase of UVB-induced alteration in cutaneous barrier function.	Glucosylceramides	19-35	glucosidase, beta, acid	Mus musculus	89-112
15787810-8	2005	Next, the metabolic fate of the GlcCer was studied by pulse-labelling of CHK with L-[14C]-serine.	Glucosylceramides	32-38	megakaryocyte-associated tyrosine kinase	Homo sapiens	73-76
15625180-8	2005	Next, results showed that exogenous addition of a-series gangliosides (GM3, GM2, GM1, GD1a) and b-series ganglioside (GD3) caused a decrease of pericyte proliferation, whereas nonsialylated precursors glucosylceramide and lactosylceramide were without effect.	Glucosylceramides	201-217	GRDX	Homo sapiens	118-121
15342415-2	2004	In HL-60/ADR cells (but not in HL-60 cells), the levels of mRNA, protein, and activity in glucosylceramide synthase (GCS), which converts ceramide to glucosylceramide, were up-regulated in response to DOX.	Glucosylceramides	90-106	UDP-glucose ceramide glucosyltransferase	Homo sapiens	117-120
15869587-0	2005	Decreased plasma sensitivity to activated protein C by oral contraceptives is associated with decreases in plasma glucosylceramide.	Glucosylceramides	114-130	APC regulator of WNT signaling pathway	Homo sapiens	32-51
15869587-2	2005	Plasma glucosylceramide (GlcCer) deficiency is associated with VTE and GlcCer functions as an APC anticoagulant cofactor.	Glucosylceramides	7-23	APC regulator of WNT signaling pathway	Homo sapiens	94-97
15869587-2	2005	Plasma glucosylceramide (GlcCer) deficiency is associated with VTE and GlcCer functions as an APC anticoagulant cofactor.	Glucosylceramides	71-77	APC regulator of WNT signaling pathway	Homo sapiens	94-97
15869587-6	2005	The plasma GlcCer level correlated with the sensitivity of plasma to APC (P = 0.017, r = 0.51, n = 21 plasma samples).	Glucosylceramides	11-17	APC regulator of WNT signaling pathway	Homo sapiens	69-72
15661399-2	2005	P-glycoprotein (p-gp) might augment ceramide glycosylation by translocating glucosylceramide (GC) across the Golgi membrane.	Glucosylceramides	76-92	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
15661399-2	2005	P-glycoprotein (p-gp) might augment ceramide glycosylation by translocating glucosylceramide (GC) across the Golgi membrane.	Glucosylceramides	76-92	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
15661399-2	2005	P-glycoprotein (p-gp) might augment ceramide glycosylation by translocating glucosylceramide (GC) across the Golgi membrane.	Glucosylceramides	94-96	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
15661399-2	2005	P-glycoprotein (p-gp) might augment ceramide glycosylation by translocating glucosylceramide (GC) across the Golgi membrane.	Glucosylceramides	94-96	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
15661399-13	2005	Pgp"s efflux function in TF-1 but not KG1a cells was inhibited by glucosylceramide.	Glucosylceramides	66-82	phosphoglycolate phosphatase	Homo sapiens	0-3
15661399-16	2005	CONCLUSION: Our data suggests that ceramide induces apoptosis in AML cells and that p-gp confers resistance to ceramide-induced apoptosis, with modulation of the ceramide-glucosylceramide pathway making a marked contribution to this resistance in TF-1 cells.	Glucosylceramides	171-187	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
16125333-7	2005	Galactocerebrosides and glucocerebrosides are the primary products of the enzyme UDP-galactose:cerebroside galactosyl transferase (CGT).	Glucosylceramides	24-41	UDP glycosyltransferase 8	Homo sapiens	81-129
16125333-7	2005	Galactocerebrosides and glucocerebrosides are the primary products of the enzyme UDP-galactose:cerebroside galactosyl transferase (CGT).	Glucosylceramides	24-41	UDP glycosyltransferase 8	Homo sapiens	131-134
15494128-1	2004	Lysosomal acid beta-glucocerebrosidase hydrolyzes glucocerebroside to glucose ceramide.	Glucosylceramides	50-66	glucosylceramidase beta	Homo sapiens	15-38
15234332-9	2004	These findings match recent biochemical studies linking elevated glucosylceramide levels to sensitization of CA2-4 RyaR receptors and 300% potentiation of neuronal CICR sensitivity.	Glucosylceramides	65-81	carbonic anhydrase 2	Rattus norvegicus	109-114
15495792-3	2004	The spleen of homozygous TNFR1 knockout mice lacked glucosylceramide substituted with palmitic acid, GlcCer(C16), and showed severe reduction in the expression of GlcCer(C24).	Glucosylceramides	52-68	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	25-30
15495792-3	2004	The spleen of homozygous TNFR1 knockout mice lacked glucosylceramide substituted with palmitic acid, GlcCer(C16), and showed severe reduction in the expression of GlcCer(C24).	Glucosylceramides	101-107	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	25-30
15210713-1	2004	Glucosylceramide synthase (GlcT-1) catalyzes the formation of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs), from ceramide and UDP-glucose.	Glucosylceramides	62-78	Glucosylceramide synthase	Drosophila melanogaster	0-25
15210713-1	2004	Glucosylceramide synthase (GlcT-1) catalyzes the formation of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs), from ceramide and UDP-glucose.	Glucosylceramides	62-78	Glucosylceramide synthase	Drosophila melanogaster	27-33
15210713-1	2004	Glucosylceramide synthase (GlcT-1) catalyzes the formation of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs), from ceramide and UDP-glucose.	Glucosylceramides	80-86	Glucosylceramide synthase	Drosophila melanogaster	0-25
15210713-1	2004	Glucosylceramide synthase (GlcT-1) catalyzes the formation of glucosylceramide (GlcCer), the core structure of major glycosphingolipids (GSLs), from ceramide and UDP-glucose.	Glucosylceramides	80-86	Glucosylceramide synthase	Drosophila melanogaster	27-33
15122583-1	2004	Previously we have described a novel multidrug-resistant cell line, HT29(col), which displayed over expression of the multidrug-resistance protein 1 (MRP1) and an altered sphingolipid composition, including enhanced levels of glucosylceramide (GlcCer; Kok JW, Veldman RJ, Klappe K, Koning H, Filipeanu C, Muller M. Int J Cancer 2000;87:172-8).	Glucosylceramides	244-250	ATP binding cassette subfamily B member 1	Homo sapiens	150-154
15122583-12	2004	In conclusion, upregulation of MRP1 occurs in concert with upregulation of GlcCer during multidrug-resistance acquisition, and both are enriched in rafts.	Glucosylceramides	75-81	ATP binding cassette subfamily B member 1	Homo sapiens	31-35
12692077-1	2003	Conversion of ceramide, a putative mediator of anticancer drug-induced apoptosis, into glucosylceramide, by the action of glucosylceramide synthase (GCS), has been implicated in drug resistance.	Glucosylceramides	87-103	UDP-glucose ceramide glucosyltransferase	Mus musculus	122-147
14662772-1	2004	Transfection studies have implicated the multiple drug resistance pump, MDR1, as a glucosyl ceramide translocase within the Golgi complex (Lala, P., Ito, S., and Lingwood, C. A.	Glucosylceramides	83-100	ATP binding cassette subfamily B member 1	Homo sapiens	72-76
14662772-7	2004	Microsomal lactosyl ceramide and globotriaosyl ceramide synthesis from endogenous or exogenously added liposomal glucosyl ceramide was inhibited by cyclosporin A, consistent with a direct role for MDR1/glucosyl ceramide translocase activity in their synthesis.	Glucosylceramides	113-130	ATP binding cassette subfamily B member 1	Homo sapiens	197-201
14662772-9	2004	Metabolic labeling in wild type and knock-out (MDR1a, 1b, MRP1) mouse fibroblasts showed the same loss of neutral glycosphingolipid (glucosyl ceramide, lactosyl ceramide) but not ganglioside (GM3) synthesis, confirming the proposed role for MDR1 translocase activity.	Glucosylceramides	133-150	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	47-52
14662772-9	2004	Metabolic labeling in wild type and knock-out (MDR1a, 1b, MRP1) mouse fibroblasts showed the same loss of neutral glycosphingolipid (glucosyl ceramide, lactosyl ceramide) but not ganglioside (GM3) synthesis, confirming the proposed role for MDR1 translocase activity.	Glucosylceramides	133-150	chemokine (C-C motif) ligand 6	Mus musculus	58-62
14662772-9	2004	Metabolic labeling in wild type and knock-out (MDR1a, 1b, MRP1) mouse fibroblasts showed the same loss of neutral glycosphingolipid (glucosyl ceramide, lactosyl ceramide) but not ganglioside (GM3) synthesis, confirming the proposed role for MDR1 translocase activity.	Glucosylceramides	133-150	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	47-51
12813057-2	2003	In the lysosomal sphingolipid degradation pathway, acid beta-glucosidase (GCase) requires saposin C for optimal in vitro and in vivo hydrolysis of glucocerebroside.	Glucosylceramides	147-163	glucosidase, beta, acid	Mus musculus	74-79
12771140-7	2003	Compared with untreated cells, tyrosine phosphorylation of phospholipase C-gamma1 was enhanced by EGF stimulation in glucosylceramide-depleted cells, associated with enhanced tyrosine phosphorylation of the EGF receptor at Tyr-1068 and Tyr-1086 stimulated by EGF.	Glucosylceramides	117-133	phospholipase C gamma 1	Homo sapiens	59-81
12771140-8	2003	The Src inhibitor, PP2, significantly blocked EGF-induced tyrosine phosphorylation of phospholipase C-gamma1 in control cells, whereas in glucosylceramide-depleted cells, suppression of Src kinase activity by PP2 toward EGF-induced tyrosine phosphorylation of phospholipase C-gamma1 was less significant.	Glucosylceramides	138-154	phospholipase C gamma 1	Homo sapiens	86-108
12771140-8	2003	The Src inhibitor, PP2, significantly blocked EGF-induced tyrosine phosphorylation of phospholipase C-gamma1 in control cells, whereas in glucosylceramide-depleted cells, suppression of Src kinase activity by PP2 toward EGF-induced tyrosine phosphorylation of phospholipase C-gamma1 was less significant.	Glucosylceramides	138-154	phospholipase C gamma 1	Homo sapiens	260-282
12771140-9	2003	Thus the activation of Src kinase by depletion of glucosylceramide-based glycosphingolipids in cultured ECV304 cells is a critical up-stream event in the activation of phospholipase C-gamma1.	Glucosylceramides	50-66	phospholipase C gamma 1	Homo sapiens	168-190
12692077-1	2003	Conversion of ceramide, a putative mediator of anticancer drug-induced apoptosis, into glucosylceramide, by the action of glucosylceramide synthase (GCS), has been implicated in drug resistance.	Glucosylceramides	87-103	UDP-glucose ceramide glucosyltransferase	Mus musculus	149-152
12692077-6	2003	Although glucosylceramide formation was detected in doxorubicin-treated GM95/GCS cells, metabolism of drug-induced ceramide did not appear to be instrumental in cell survival.	Glucosylceramides	9-25	ankyrin repeat domain 29	Mus musculus	72-76
12692077-6	2003	Although glucosylceramide formation was detected in doxorubicin-treated GM95/GCS cells, metabolism of drug-induced ceramide did not appear to be instrumental in cell survival.	Glucosylceramides	9-25	UDP-glucose ceramide glucosyltransferase	Mus musculus	77-80
12560338-7	2003	These data suggest that APC binds to GlcCer, that PC/PS/GlcCer vesicles like PC/PS vesicles bind to the N-terminal gamma-carboxyglutamic acid domain of APC, and that one mechanism by which GlcCer enhances the activity of APC is by increasing its affinity for membrane surfaces containing negatively charged phospholipids.	Glucosylceramides	37-43	APC regulator of WNT signaling pathway	Homo sapiens	24-27
12560338-1	2003	The effect of glucosylceramide (GlcCer) on activated protein C (APC)-phospholipid interactions was examined using fluorescence resonance energy transfer.	Glucosylceramides	14-30	APC regulator of WNT signaling pathway	Homo sapiens	64-67
12606053-4	2003	The spleen lipid findings with a concurrent accumulation of cholesterol, sphingomyelin and glucosylceramide (Acc-CSG) allowed us to suggest NPC diagnoses for these patients, who were free of neurologic symptoms.	Glucosylceramides	91-107	NPC intracellular cholesterol transporter 1	Homo sapiens	140-143
12560338-1	2003	The effect of glucosylceramide (GlcCer) on activated protein C (APC)-phospholipid interactions was examined using fluorescence resonance energy transfer.	Glucosylceramides	32-38	APC regulator of WNT signaling pathway	Homo sapiens	64-67
12560338-3	2003	This 5-fold increase in apparent affinity was not species-specific since bovine DEGR-APC also showed a similar GlcCer-dependent enhancement of binding of APC to PC/PS vesicles.	Glucosylceramides	111-117	APC regulator of WNT signaling pathway	Homo sapiens	85-88
12560338-3	2003	This 5-fold increase in apparent affinity was not species-specific since bovine DEGR-APC also showed a similar GlcCer-dependent enhancement of binding of APC to PC/PS vesicles.	Glucosylceramides	111-117	APC regulator of WNT signaling pathway	Bos taurus	154-157
11894136-5	2002	In addition, hCPT and CPT may favor ceramide signaling by disturbing sites of synthesis (Golgi) and trafficking of glucosylceramide from Golgi to lipid droplets.	Glucosylceramides	115-131	choline phosphotransferase 1	Homo sapiens	13-17
12554947-1	2003	Acid beta-glucocerebrosidase (N-acylsphingosyl-1-O-beta-D-glucoside:glucohydrolase) is a lysosomal glycoprotein that catalyzes the hydrolysis of the glycolipid glucocerebroside to glucose and ceramide.	Glucosylceramides	160-176	glucosylceramidase beta	Homo sapiens	5-28
12540565-8	2003	The product of CGT (glucosylceramide) was also increased.	Glucosylceramides	20-36	UDP-glucose ceramide glucosyltransferase	Homo sapiens	15-18
12594829-5	2003	Furthermore, transfection of CD1A and CD1B genes in a mutant cell line unable to synthesize glucosylceramides and galactosylceramides showed normal surface expression of both CD1 molecules.	Glucosylceramides	92-109	CD1a molecule	Homo sapiens	29-33
12594829-5	2003	Furthermore, transfection of CD1A and CD1B genes in a mutant cell line unable to synthesize glucosylceramides and galactosylceramides showed normal surface expression of both CD1 molecules.	Glucosylceramides	92-109	CD1b molecule	Homo sapiens	38-42
12594829-5	2003	Furthermore, transfection of CD1A and CD1B genes in a mutant cell line unable to synthesize glucosylceramides and galactosylceramides showed normal surface expression of both CD1 molecules.	Glucosylceramides	92-109	CD1b molecule	Homo sapiens	29-32
12417405-3	2002	Glucosylceramide synthase converts ceramide to glucosylceramide, a core structure of the vast majority of GSLs.	Glucosylceramides	47-63	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-25
12223447-0	2002	Phosphatidylcholine synthesis is elevated in neuronal models of Gaucher disease due to direct activation of CTP:phosphocholine cytidylyltransferase by glucosylceramide.	Glucosylceramides	151-167	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	108-147
12223447-5	2002	Indeed, CCT activity was elevated in neurons that had accumulated GlcCer.	Glucosylceramides	66-72	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	8-11
12223447-6	2002	GlcCer, but not galactosylceramide (GalCer), stimulated CCT activity in rat brain homogenates, and significantly higher levels of CCT were membrane associated in cortical homogenates from a mouse model of Gaucher disease compared with wild-type mice.	Glucosylceramides	0-6	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	56-59
12223447-7	2002	Because CCT mRNA and protein levels were unaltered in either neurons or brain tissue that had accumulated GlcCer, it appeared likely that GlcCer activates CCT by a post-translational mechanism.	Glucosylceramides	138-144	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	155-158
12223447-9	2002	GlcCer stimulated CCT activity, with stimulation observed at levels as low as 2.5 mol% and with maximal activation reached at 10 mol%.	Glucosylceramides	0-6	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	18-21
12223447-11	2002	Together, these data demonstrate that GlcCer directly activates CCT, which results in elevated PC synthesis, which may account for some of the changes in growth rates observed upon neuronal GlcCer accumulation.	Glucosylceramides	38-44	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	64-67
12223447-11	2002	Together, these data demonstrate that GlcCer directly activates CCT, which results in elevated PC synthesis, which may account for some of the changes in growth rates observed upon neuronal GlcCer accumulation.	Glucosylceramides	190-196	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	64-67
12489486-3	2002	OBJECTIVES: To determine whether variation in the glucosylceramide synthase (UDPGlucose ceramide glucosyltransferase) gene, which encodes the enzyme that regulates the synthesis of glucocerebroside, could account for the variability and clinical manifestations.	Glucosylceramides	181-197	UDP-glucose ceramide glucosyltransferase	Homo sapiens	50-75
12177173-6	2002	Further evidence that GlcCer production is responsible for normalized CHK proliferation includes: a) attenuation of SMase-induced inhibition of proliferation by exogenous GlcCer; and b) enhancement of the SMase effect in cells cotreated with the GlcCer synthase inhibitor, PDMP (D-threo-1-phenyl-2(decanoylamino)-3-morpholino-1-propanol).	Glucosylceramides	22-28	megakaryocyte-associated tyrosine kinase	Homo sapiens	70-73
12208132-7	2002	Prosaposin knock-out (PS-/-) mice expressing N or CBC transgenes, even at low levels, had delayed onset of neurologic signs and neuropathology, and significant lengthening of life span (from 1.7- to 7-fold) with age dependent partial correction of GlcCer and LacCer accumulation in the brain.	Glucosylceramides	248-254	prosaposin	Mus musculus	0-10
12126932-1	2002	Saposin C is a biological activator of acid beta-glucosidase (GCase), the lysosomal hydrolase with activity towards glucosylceramide (GC).	Glucosylceramides	116-132	glucosidase, beta, acid	Mus musculus	44-60
12126932-1	2002	Saposin C is a biological activator of acid beta-glucosidase (GCase), the lysosomal hydrolase with activity towards glucosylceramide (GC).	Glucosylceramides	116-132	glucosidase, beta, acid	Mus musculus	62-67
12126932-1	2002	Saposin C is a biological activator of acid beta-glucosidase (GCase), the lysosomal hydrolase with activity towards glucosylceramide (GC).	Glucosylceramides	62-64	glucosidase, beta, acid	Mus musculus	44-60
11894136-5	2002	In addition, hCPT and CPT may favor ceramide signaling by disturbing sites of synthesis (Golgi) and trafficking of glucosylceramide from Golgi to lipid droplets.	Glucosylceramides	115-131	choline phosphotransferase 1	Homo sapiens	14-17
12036828-1	2002	In Gaucher disease, a genetic deficiency in the activity of the lysosomal enzyme beta-glucocerebrosidase (acid beta-glucosidase) causes monocytes and macrophages to store excessive amounts of glucocerebroside in lysosomes.	Glucosylceramides	192-208	glucosylceramidase beta	Homo sapiens	106-127
11829604-1	2002	The interaction of recombinant HIV-1 surface glycoprotein gp120 (rgp120) with natural isolates of lactosylceramide (LacCer), glucosylceramide (GlcCer), and galactosylceramide (GalCer) has been quantitatively measured under equilibrium conditions using total internal reflection fluorescence (TIRF) spectroscopy.	Glucosylceramides	143-149	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	58-63
10702281-5	2000	This was achieved by cellular transfection with glucosylceramide synthase (GCS), the enzyme that converts ceramide to glucosylceramide.	Glucosylceramides	48-64	UDP-glucose ceramide glucosyltransferase	Homo sapiens	75-78
12467215-10	2002	Given the intracellular distribution patterns of Pgp, we propose that this effect is related to glucosylceramide translocation across the Golgi bilayer.	Glucosylceramides	96-112	ATP binding cassette subfamily B member 1	Homo sapiens	49-52
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	17-33	UDP-glucose ceramide glucosyltransferase	Homo sapiens	44-50
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	17-33	beta-1,3-galactosyltransferase 4	Homo sapiens	164-170
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	97-103	UDP-glucose ceramide glucosyltransferase	Homo sapiens	17-42
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	97-103	UDP-glucose ceramide glucosyltransferase	Homo sapiens	44-50
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	97-103	beta-1,3-galactosyltransferase 4	Homo sapiens	164-170
11493433-4	2001	These pathways are themselves influenced by a number of lipid products (diacylglycerol, sphingosine-1 phosphate, and glucosyl ceramide), reactive oxygen species, oncogenes (such as the tumor suppressor gene p53), protein kinases (protein kinase C and phosphoinositide-3 kinase), and external stimuli (hematopoietic growth factors and the extracellular matrix).	Glucosylceramides	117-134	tumor protein p53	Homo sapiens	207-210
10951276-8	2000	These findings suggest that, in contrast to changes in sphingolipid metabolism due to aging, the hitherto undiscovered enzyme SM deacylase, is highly expressed in the epidermis of AD patients, and competes with sphingomyelinase or beta-glucocerebrosidase for the common substrate SM or glucosylceramide, which leads to the ceramide deficiency of the stratum corneum in AD.	Glucosylceramides	286-302	glucosylceramidase beta	Homo sapiens	231-254
10946011-3	2000	It has previously been shown that CGT-deficient mice do not synthesize GalCer and its sulfated derivative GalCer I(3)-sulfate (galactosylsulfatide, SM4s) but form myelin containing glucosylceramide (GlcCer) and sphingomyelin with 2-hydroxy fatty acids.	Glucosylceramides	181-197	UDP galactosyltransferase 8A	Mus musculus	34-37
10946011-3	2000	It has previously been shown that CGT-deficient mice do not synthesize GalCer and its sulfated derivative GalCer I(3)-sulfate (galactosylsulfatide, SM4s) but form myelin containing glucosylceramide (GlcCer) and sphingomyelin with 2-hydroxy fatty acids.	Glucosylceramides	199-205	UDP galactosyltransferase 8A	Mus musculus	34-37
11749048-1	2001	The hydrolysis of glucosylceramide (GC) to ceramide and glucose requires the action of the lysosomal enzyme, acid beta-glucosidase (GCase), encoded by gba in the mouse.	Glucosylceramides	18-34	glucosidase, beta, acid	Mus musculus	132-137
11749048-1	2001	The hydrolysis of glucosylceramide (GC) to ceramide and glucose requires the action of the lysosomal enzyme, acid beta-glucosidase (GCase), encoded by gba in the mouse.	Glucosylceramides	18-34	glucosidase, beta, acid	Mus musculus	151-154
11749048-1	2001	The hydrolysis of glucosylceramide (GC) to ceramide and glucose requires the action of the lysosomal enzyme, acid beta-glucosidase (GCase), encoded by gba in the mouse.	Glucosylceramides	36-38	glucosidase, beta, acid	Mus musculus	132-137
11749048-1	2001	The hydrolysis of glucosylceramide (GC) to ceramide and glucose requires the action of the lysosomal enzyme, acid beta-glucosidase (GCase), encoded by gba in the mouse.	Glucosylceramides	36-38	glucosidase, beta, acid	Mus musculus	151-154
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	196-202	UDP-glucose ceramide glucosyltransferase	Homo sapiens	17-42
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	196-202	UDP-glucose ceramide glucosyltransferase	Homo sapiens	44-50
11740154-5	2001	It is known that glucosylceramide synthase (GlcT-1) catalyzes the synthesis of glucosylceramide (GlcCer) from ceramide, and subsequently lactosylceramide synthase (GalT-2) synthesizes LacCer from GlcCer.	Glucosylceramides	196-202	beta-1,3-galactosyltransferase 4	Homo sapiens	164-170
11465673-11	2001	A novel inhibitor of glucosyl ceramide synthesis, D-threo-1-phenyl-2-palmitoylamino-3-pyrrolidino-1-propanol (D-t-P4) reduced expression of GD3 much more than CD60 on activated T lymphocytes.	Glucosylceramides	21-38	GRDX	Homo sapiens	140-143
11264150-6	2001	Exogenously added GlcCer and the homologous Glc-containing globotriaosylceramide (Gb3Cer), but not galactosylceramide, dose-dependently prolonged clotting times of normal plasma in the presence, but not absence, of APC:protein S, which suggests that GlcCer or Gb3Cer can enhance protein C pathway anticoagulant activity.	Glucosylceramides	18-24	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	82-85
11264150-6	2001	Exogenously added GlcCer and the homologous Glc-containing globotriaosylceramide (Gb3Cer), but not galactosylceramide, dose-dependently prolonged clotting times of normal plasma in the presence, but not absence, of APC:protein S, which suggests that GlcCer or Gb3Cer can enhance protein C pathway anticoagulant activity.	Glucosylceramides	250-256	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	82-85
10945987-6	2000	To evaluate the functional significance of this Cer pool, we aimed to convert it to glucosylceramide (GlcCer), by constitutive overexpression of glucosylceramide synthase (GCS).	Glucosylceramides	84-100	UDP-glucose ceramide glucosyltransferase	Homo sapiens	145-170
10945987-6	2000	To evaluate the functional significance of this Cer pool, we aimed to convert it to glucosylceramide (GlcCer), by constitutive overexpression of glucosylceramide synthase (GCS).	Glucosylceramides	84-100	UDP-glucose ceramide glucosyltransferase	Homo sapiens	172-175
10945987-6	2000	To evaluate the functional significance of this Cer pool, we aimed to convert it to glucosylceramide (GlcCer), by constitutive overexpression of glucosylceramide synthase (GCS).	Glucosylceramides	102-108	UDP-glucose ceramide glucosyltransferase	Homo sapiens	145-170
10945987-6	2000	To evaluate the functional significance of this Cer pool, we aimed to convert it to glucosylceramide (GlcCer), by constitutive overexpression of glucosylceramide synthase (GCS).	Glucosylceramides	102-108	UDP-glucose ceramide glucosyltransferase	Homo sapiens	172-175
10744663-0	2000	Up-regulation of glucosylceramide synthesis upon stimulation of axonal growth by basic fibroblast growth factor.	Glucosylceramides	17-33	fibroblast growth factor 2	Homo sapiens	81-111
10744663-2	2000	We have previously shown that ongoing glucosylceramide (GlcCer) synthesis is required for basic fibroblast growth factor (bFGF) and laminin to stimulate axonal growth in cultured hippocampal neurons (Boldin, S., and Futerman, A. H. (1997) J. Neurochem.	Glucosylceramides	38-54	fibroblast growth factor 2	Homo sapiens	90-127
10744663-2	2000	We have previously shown that ongoing glucosylceramide (GlcCer) synthesis is required for basic fibroblast growth factor (bFGF) and laminin to stimulate axonal growth in cultured hippocampal neurons (Boldin, S., and Futerman, A. H. (1997) J. Neurochem.	Glucosylceramides	56-62	fibroblast growth factor 2	Homo sapiens	90-127
10744663-4	2000	We now demonstrate that stimulation of axonal growth by bFGF leads to an increase in the rate of GlcCer synthesis.	Glucosylceramides	97-103	fibroblast growth factor 2	Homo sapiens	56-60
10744663-6	2000	In vitro analysis of GlcCer synthase activity revealed an approximately 2-fold increase in the rate of [(14)C]hexanoyl GlcCer synthesis upon incubation with either bFGF or laminin; other growth factors, which did not effect the rate of axon growth, had no effect on the rate of [(14)C]hexanoyl GlcCer synthesis.	Glucosylceramides	21-27	fibroblast growth factor 2	Homo sapiens	164-168
11201796-4	2000	However, the Src kinases were eliminated from DIMs after depletion of the major neutral GSLs of J5 cells, glucosylceramide and lactosylceramide, by an inhibitor of glucosylceramide synthase (D-PDMP), indicating that GSLs in general are required for Src kinase association to DIM.	Glucosylceramides	106-122	Rous sarcoma oncogene	Mus musculus	13-16
10801059-0	2000	The increased sensitivity of neurons with elevated glucocerebroside to neurotoxic agents can be reversed by imiglucerase.	Glucosylceramides	51-67	glucosylceramidase beta	Homo sapiens	108-120
10620326-7	2000	When the GPI-linked protein B61 was inducibly expressed in these cells, sorting to caveolar membranes occurred normally, even in the presence of glucosylceramide depletion.	Glucosylceramides	145-161	ephrin A1	Mus musculus	28-31
10653651-3	2000	SP-D binds phosphatidylinositol (PI) and glucosylceramide.	Glucosylceramides	41-57	surfactant protein D	Rattus norvegicus	0-4
10393098-1	1999	Glucosylceramide synthase (GCS) catalyses the transfer of glucose from UDP-glucose (UDP-Glc) to ceramide to form glucosylceramide, the common precursor of most higher-order glycosphingolipids.	Glucosylceramides	113-129	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	0-25
10440752-7	1999	In addition, LAMP-1 and LAMP-2 associate with the bilayer of stored glucosylceramide.	Glucosylceramides	68-84	lysosomal associated membrane protein 1	Homo sapiens	13-19
10440752-7	1999	In addition, LAMP-1 and LAMP-2 associate with the bilayer of stored glucosylceramide.	Glucosylceramides	68-84	lysosomal associated membrane protein 2	Homo sapiens	24-30
10527636-2	1999	Glucosylceramide synthase (GCS) catalyzes glycosylation of ceramide and produces glucosylceramide.	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
10527636-2	1999	Glucosylceramide synthase (GCS) catalyzes glycosylation of ceramide and produces glucosylceramide.	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
10393098-1	1999	Glucosylceramide synthase (GCS) catalyses the transfer of glucose from UDP-glucose (UDP-Glc) to ceramide to form glucosylceramide, the common precursor of most higher-order glycosphingolipids.	Glucosylceramides	113-129	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	27-30
9852101-3	1998	We found that TNF-alpha increased LacCer synthesis by way of stimulating the activity of UDP-galactose:glucosylceramide beta(1-->4)-galactosyltransferase in a time-dependent fashion.	Glucosylceramides	103-119	tumor necrosis factor	Homo sapiens	14-23
10196186-2	1999	Ceramides, the major components of these multilayered membranes, derive in large part from hydrolysis of glucosylceramides mediated by stratum corneum beta-glucocerebrosidase (beta-GlcCerase).	Glucosylceramides	105-122	glucosidase, beta, acid	Mus musculus	151-174
10196186-3	1999	Prosaposin (pSAP) is a large precursor protein that is proteolytically cleaved to form four distinct sphingolipid activator proteins, which stimulate enzymatic hydrolysis of sphingolipids, including glucosylceramide.	Glucosylceramides	199-215	prosaposin	Mus musculus	0-10
10196186-3	1999	Prosaposin (pSAP) is a large precursor protein that is proteolytically cleaved to form four distinct sphingolipid activator proteins, which stimulate enzymatic hydrolysis of sphingolipids, including glucosylceramide.	Glucosylceramides	199-215	prosaposin	Mus musculus	12-16
10196186-5	1999	In addition to the extracutaneous findings noted previously, our present data indicate that pSAP deficiency in the epidermis has significant consequences including: 1) an accumulation of epidermal glucosylceramides together with below normal levels of ceramides; 2) alterations in lipids that are bound by ester linkages to proteins of the cornified cell envelope; 3) a thickened stratum lucidum with evidence of scaling; and 4) a striking abnormality in lamellar membrane maturation within the interstices of the stratum corneum.	Glucosylceramides	197-214	prosaposin	Mus musculus	92-96
10214939-2	1999	Ceramides, the main components of these membranes, derive in large part from hydrolysis of glucosylceramides mediated by the lysosomal enzyme beta-glucocerebrosidase.	Glucosylceramides	91-108	glucosidase, beta, acid	Mus musculus	142-165
10037475-2	1999	Incubation of NG108-15 cells with conduritol-B-epoxide, a covalent inhibitor of glucosylceramidase, raised the intracellular concentration of glucosylceramide (GC) by more than fourfold, indicating a glycolipid composition equivalent to that of Gaucher"s cells.	Glucosylceramides	142-158	glucosidase, beta, acid	Mus musculus	80-98
10037475-2	1999	Incubation of NG108-15 cells with conduritol-B-epoxide, a covalent inhibitor of glucosylceramidase, raised the intracellular concentration of glucosylceramide (GC) by more than fourfold, indicating a glycolipid composition equivalent to that of Gaucher"s cells.	Glucosylceramides	160-162	glucosidase, beta, acid	Mus musculus	80-98
10084306-5	1999	In contrast, the normal developmental increases in activities of glucosylceramide synthase and cholesterol sulfotransferase, responsible for the synthesis of glucosylceramides and cholesterol sulfate, respectively, were accelerated further by air exposure.	Glucosylceramides	158-175	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	65-90
9988695-7	1999	We now demonstrate by in vitro analysis that inhibition of ceramide synthesis by FB1 for 5 days results in up-regulation of the activities of three enzymes in the pathway of Gb3 synthesis, namely glucosylceramide, lactosylceramide, and Gb3 synthases; up-regulation is due to an increase in Vmax, with no change in Km values toward lipid substrates.	Glucosylceramides	196-212	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	174-177
9867864-1	1999	Glucosylceramide synthase (GCS) catalyzes the transfer of glucose from UDP-glucose to ceramide to form glucosylceramide, the precursor of most higher order glycosphingolipids.	Glucosylceramides	103-119	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	0-25
9867864-1	1999	Glucosylceramide synthase (GCS) catalyzes the transfer of glucose from UDP-glucose to ceramide to form glucosylceramide, the precursor of most higher order glycosphingolipids.	Glucosylceramides	103-119	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	27-30
9852101-4	1998	The TNF-alpha-induced expression of ICAM-1 was abrogated by D-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of UDP-galactose:glucosylceramide beta(1-->4)-galactosyltransferase.	Glucosylceramides	151-167	tumor necrosis factor	Homo sapiens	4-13
9852101-4	1998	The TNF-alpha-induced expression of ICAM-1 was abrogated by D-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of UDP-galactose:glucosylceramide beta(1-->4)-galactosyltransferase.	Glucosylceramides	151-167	intercellular adhesion molecule 1	Homo sapiens	36-42
9535903-8	1998	1) Tyrosine phosphorylation in FAK was greatly enhanced in B16 cells adhered to Gg3-coated plates but was minimal in cells adhered to GM3-coated, GlcCer-coated, or noncoated plates.	Glucosylceramides	146-152	PTK2 protein tyrosine kinase 2	Mus musculus	31-34
9813032-4	1998	In parallel with ceramide generation, TNF-mediated inhibition of glucosylceramide and sphingomyelin (SM) synthase prevents the immediate metabolization of this lipid mediator.	Glucosylceramides	65-81	tumor necrosis factor	Homo sapiens	38-41
9851714-0	1998	Modulation of carcinoembryonic antigen release by glucosylceramide--implications for HT29 cell differentiation.	Glucosylceramides	50-66	CEA cell adhesion molecule 3	Homo sapiens	14-38
9748278-1	1998	Previous studies have shown that the ceramide analogue, D-threo-1-phenyl-2-decanoylamin-3-morpholino-propanol (D-PDMP), inhibits glucosylceramide synthase and thus leads to extensive depletion of glycosphingolipids derived from glucosyl ceramide.	Glucosylceramides	228-245	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	129-154
9623774-1	1998	Ceramide glucosyltransferase (EC 2.4.1.80) catalyzes the first glycosylation step of glycosphingolipid (GSL) synthesis, the transfer of glucose from UDP-Glucose to hydrophobic ceramide and generate glucosylceramide (GlcCer).	Glucosylceramides	198-214	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-28
9623774-1	1998	Ceramide glucosyltransferase (EC 2.4.1.80) catalyzes the first glycosylation step of glycosphingolipid (GSL) synthesis, the transfer of glucose from UDP-Glucose to hydrophobic ceramide and generate glucosylceramide (GlcCer).	Glucosylceramides	216-222	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-28
9468543-3	1998	In contrast, SP-D binds to phosphatidylinositol (PI) and glucosylceramide (GlcCer).	Glucosylceramides	57-73	surfactant protein D	Rattus norvegicus	13-17
9468543-3	1998	In contrast, SP-D binds to phosphatidylinositol (PI) and glucosylceramide (GlcCer).	Glucosylceramides	75-81	surfactant protein D	Rattus norvegicus	13-17
9468543-9	1998	From these results, we conclude that 1) the SP-A region of Glu195-Phe228 is required for lipid and type II cell interactions, 2) the SP-D region of Cys261-Phe355 is required for optimal lipid interactions, and 3) the structural requirement for the binding of SP-D to PI is different from that for GlcCer.	Glucosylceramides	297-303	surfactant protein D	Rattus norvegicus	133-137
9204210-5	1997	As observed for SV40-transformed fibroblasts from Farber disease, degradation of radioactive glucosylceramide or low density lipoprotein-associated radiolabelled sphingomyelin by the prosaposin-deficient cells in situ showed a clear impairment in the turnover of lysosomal ceramide.	Glucosylceramides	93-109	prosaposin	Homo sapiens	183-193
9201993-1	1997	The degradation of glucosylceramide in lysosomes is accomplished by glucosylceramidase with the assistance of, at least, another protein, saposin C (Sap C), which is generated from a large precursor together with three other similar proteins, saposins A, B, and D.	Glucosylceramides	19-35	glucosylceramidase beta	Homo sapiens	68-86
9201993-1	1997	The degradation of glucosylceramide in lysosomes is accomplished by glucosylceramidase with the assistance of, at least, another protein, saposin C (Sap C), which is generated from a large precursor together with three other similar proteins, saposins A, B, and D.	Glucosylceramides	19-35	SH2 domain containing 1A	Homo sapiens	149-152
9201993-3	1997	The glucosylceramide contained in large unilamellar vesicles (LUV) was degraded by glucosylceramidase at a rate 7-8-fold lower than glucosylceramide inserted in small unilamellar vesicles (SUV).	Glucosylceramides	4-20	glucosylceramidase beta	Homo sapiens	83-101
9201993-8	1997	Sap C increased the rate of hydrolysis of both the artificial water soluble substrate, 4-methylumbelliferyl-beta-D-glucopyranoside, and the lipid substrate, glucosylceramide, while Sap A only stimulated degradation of the sphingolipid.	Glucosylceramides	157-173	SH2 domain containing 1A	Homo sapiens	0-3
9201993-12	1997	In conclusion, our results show that both Sap A and Sap C are required for maximal hydrolysis of glucosylceramide inserted in PS-containing LUV, that their effects are synergistic, and that their mode of action is different.	Glucosylceramides	97-113	SH2 domain containing 1A	Homo sapiens	42-45
9201993-12	1997	In conclusion, our results show that both Sap A and Sap C are required for maximal hydrolysis of glucosylceramide inserted in PS-containing LUV, that their effects are synergistic, and that their mode of action is different.	Glucosylceramides	97-113	SH2 domain containing 1A	Homo sapiens	52-55
9201993-14	1997	It can be envisaged that Sap A in conjunction with Sap C might have a physiological role in glucosylceramide degradation.	Glucosylceramides	92-108	SH2 domain containing 1A	Homo sapiens	25-28
9201993-14	1997	It can be envisaged that Sap A in conjunction with Sap C might have a physiological role in glucosylceramide degradation.	Glucosylceramides	92-108	SH2 domain containing 1A	Homo sapiens	51-54
9403993-10	1997	Subsequent actions of GM1-beta-galactosidase, beta-hexosaminidase A, sialidase and again GM1-beta-galactosidase on these labeled analogues of SGM1 in the presence of taurodeoxycholate produced the respective analogues of GM2, GM3, lactosylceramide and glucosylceramide, respectively.	Glucosylceramides	252-268	growth differentiation factor 6	Homo sapiens	142-146
9363775-16	1997	Labeling studies with [1-(14)C]palmitic acid indicated that cell lines transfected with mLCB2 preferentially use the excess sphingoid bases for glucocerebroside and galactocerebroside synthesis.	Glucosylceramides	144-160	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	88-93
9003082-0	1997	Glucosylceramide synthesis is required for basic fibroblast growth factor and laminin to stimulate axonal growth.	Glucosylceramides	0-16	fibroblast growth factor 2	Homo sapiens	43-73
9343929-1	1997	We have previously shown that oxidized low density lipoproteins (Ox-LDL) at low concentrations (10 micrograms/ml) via activating a UDP-galactose: glucosylceramide, beta 1-->4 galactosyl-transferase (GalT-2) and producing lactosylceramide can stimulate the proliferation of aortic smooth muscle cells.	Glucosylceramides	146-162	beta-1,3-galactosyltransferase 4	Homo sapiens	202-208
9003082-3	1997	By using these inhibitors, together with two stereoisomers of short acyl chain derivatives of ceramide, only one of which is metabolized to glucosylceramide, we demonstrate that ongoing synthesis of glucosylceramide, the simplest glycosphingolipid, is a prerequisite for both bFGF and laminin to stimulate axon growth.	Glucosylceramides	199-215	fibroblast growth factor 2	Homo sapiens	276-280
7657695-5	1995	A glycosyl-phosphatidylinositol (GPI)-anchored protein (GP-2) and a glycosphingolipid (glucosylceramide, GlcCer) are preferentially transported to the apical membrane in clone II/G cells, but, in clone II/J cells, GP-2 and GlcCer are delivered equally to both apical and basal-lateral membranes, similar to Na/K-ATPase.	Glucosylceramides	87-103	glycoprotein 2	Canis lupus familiaris	56-60
8579607-2	1996	Murine IL-2-dependent T lymphocyte CTLL cells metabolize exogenously added Sph to GlcCer through Cer within 30 min, whereas fibroblast BALB/C A31 cells required more than 2 h. Thus, CTLL cells exhibiting the active conversion were used as recipient cells, whereas A31 cells where the conversion was slow and fumonisin B1 (inhibition of Cer biosynthesis)-treated CTLL cells being donor cells.	Glucosylceramides	82-88	interleukin 2	Mus musculus	7-11
7657695-5	1995	A glycosyl-phosphatidylinositol (GPI)-anchored protein (GP-2) and a glycosphingolipid (glucosylceramide, GlcCer) are preferentially transported to the apical membrane in clone II/G cells, but, in clone II/J cells, GP-2 and GlcCer are delivered equally to both apical and basal-lateral membranes, similar to Na/K-ATPase.	Glucosylceramides	87-103	glycoprotein 2	Canis lupus familiaris	214-229
7657695-5	1995	A glycosyl-phosphatidylinositol (GPI)-anchored protein (GP-2) and a glycosphingolipid (glucosylceramide, GlcCer) are preferentially transported to the apical membrane in clone II/G cells, but, in clone II/J cells, GP-2 and GlcCer are delivered equally to both apical and basal-lateral membranes, similar to Na/K-ATPase.	Glucosylceramides	105-111	glycoprotein 2	Canis lupus familiaris	56-60
7657695-5	1995	A glycosyl-phosphatidylinositol (GPI)-anchored protein (GP-2) and a glycosphingolipid (glucosylceramide, GlcCer) are preferentially transported to the apical membrane in clone II/G cells, but, in clone II/J cells, GP-2 and GlcCer are delivered equally to both apical and basal-lateral membranes, similar to Na/K-ATPase.	Glucosylceramides	105-111	glycoprotein 2	Canis lupus familiaris	214-229
7783943-5	1995	However, a higher rate of synthesis of short acyl chain-glucosyl ceramides is observed in the Trembler samples.	Glucosylceramides	56-74	peripheral myelin protein 22	Mus musculus	94-102
7782337-0	1995	Altered carbohydrate recognition specificity engineered into surfactant protein D reveals different binding mechanisms for phosphatidylinositol and glucosylceramide.	Glucosylceramides	148-164	surfactant protein D	Rattus norvegicus	61-81
7782337-1	1995	Pulmonary surfactant protein D (SP-D) is a member of the collection subgroup of the C-type lectin superfamily that binds glycosylated lipids such as phosphatidylinositol (PI) and glucosylceramide (GlcCer).	Glucosylceramides	179-195	surfactant protein D	Rattus norvegicus	0-30
7782337-1	1995	Pulmonary surfactant protein D (SP-D) is a member of the collection subgroup of the C-type lectin superfamily that binds glycosylated lipids such as phosphatidylinositol (PI) and glucosylceramide (GlcCer).	Glucosylceramides	179-195	surfactant protein D	Rattus norvegicus	32-36
7782337-1	1995	Pulmonary surfactant protein D (SP-D) is a member of the collection subgroup of the C-type lectin superfamily that binds glycosylated lipids such as phosphatidylinositol (PI) and glucosylceramide (GlcCer).	Glucosylceramides	197-203	surfactant protein D	Rattus norvegicus	0-30
7782337-1	1995	Pulmonary surfactant protein D (SP-D) is a member of the collection subgroup of the C-type lectin superfamily that binds glycosylated lipids such as phosphatidylinositol (PI) and glucosylceramide (GlcCer).	Glucosylceramides	197-203	surfactant protein D	Rattus norvegicus	32-36
7782337-12	1995	1) The carbohydrate binding specificity of SP-DE321Q,N323D was changed from a mannose-glucose type to a galactose type; 2) the GlcCer binding property of SP-D is closely related to its sugar binding activity; and 3) the PI binding activity is not completely dependent on its carbohydrate binding specificity.	Glucosylceramides	127-133	surfactant protein D	Rattus norvegicus	43-47
7769132-1	1995	Hydrolysis of glucosylceramides (GlcCer) by beta-glucocerebrosidase generates ceramides, critical components of the epidermal permeability barrier.	Glucosylceramides	14-31	glucosidase, beta, acid	Mus musculus	44-67
7769132-1	1995	Hydrolysis of glucosylceramides (GlcCer) by beta-glucocerebrosidase generates ceramides, critical components of the epidermal permeability barrier.	Glucosylceramides	33-39	glucosidase, beta, acid	Mus musculus	44-67
7961971-4	1994	SP-D binds to phosphatidylinositol (PI) and glucosylceramide (GlcCer), and its role in alveolar lipid metabolism remains to be clarified.	Glucosylceramides	44-60	surfactant protein D	Rattus norvegicus	0-4
7961971-4	1994	SP-D binds to phosphatidylinositol (PI) and glucosylceramide (GlcCer), and its role in alveolar lipid metabolism remains to be clarified.	Glucosylceramides	62-68	surfactant protein D	Rattus norvegicus	0-4
7961971-6	1994	The rSP-D effectively competed with 125I-labeled native rat SP-D in a solid phase binding assay to PI and GlcCer in a manner nearly identical to native SP-D.	Glucosylceramides	106-112	surfactant protein D	Rattus norvegicus	4-9
7961971-6	1994	The rSP-D effectively competed with 125I-labeled native rat SP-D in a solid phase binding assay to PI and GlcCer in a manner nearly identical to native SP-D.	Glucosylceramides	106-112	surfactant protein D	Rattus norvegicus	5-9
7961971-6	1994	The rSP-D effectively competed with 125I-labeled native rat SP-D in a solid phase binding assay to PI and GlcCer in a manner nearly identical to native SP-D.	Glucosylceramides	106-112	surfactant protein D	Rattus norvegicus	60-64
7961971-8	1994	Chimera A1A2D3D4 competed with iodinated SP-D in the solid phase binding assay to both PI and GlcCer.	Glucosylceramides	94-100	surfactant protein D	Rattus norvegicus	41-45
8057468-5	1994	We observed less efficient binding of gp120 to liposomes containing lactosylceramide, glucosylceramide, and galactosylsulfate, whereas no binding to liposomes containing mixed gangliosides, psychosine, or sphingomyelin was detected.	Glucosylceramides	86-102	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	38-43
7806975-4	1994	The neutral glycolipids, including glucosylceramide and lactosylceramide, displayed a striking increase in 3-week-old cpk/cpk mice as did the acidic lipid, ganglioside GM3.	Glucosylceramides	35-51	cystin 1	Mus musculus	118-121
7806975-4	1994	The neutral glycolipids, including glucosylceramide and lactosylceramide, displayed a striking increase in 3-week-old cpk/cpk mice as did the acidic lipid, ganglioside GM3.	Glucosylceramides	35-51	cystin 1	Mus musculus	122-125
8163674-2	1994	Hydrolysis of glucosylceramide by beta-glucocerebrosidase results in ceramide, a critical component of the intercellular lamellae that mediate the epidermal permeability barrier.	Glucosylceramides	14-30	glucosidase, beta, acid	Mus musculus	34-57
8062885-1	1994	Gaucher"s disease is an autosomal recessive disorder characterized by a functional deficiency in beta-glucocerebrosidase enzymatic activity and the resultant accumulation of the glycolipid glucocerebroside in macrophages.	Glucosylceramides	189-205	glucosylceramidase beta	Homo sapiens	97-120
2102487-6	1990	Among the several glycolipids tested, Lac-Cer, Gg-4-Cer and Glc-Cer showed inhibitory effect on proliferation of Had-1 cells, but did not show any appreciable effect on that of FM3A cells.	Glucosylceramides	60-67	solute carrier family 35 (UDP-galactose transporter), member A2	Mus musculus	113-118
8492969-1	1993	Gaucher"s disease is a lipidosis caused by deficiency of the enzyme glucocerebrosidase (glucosylceramidase) with secondary accumulation of glucocerebrosides in macrophage lysosomes.	Glucosylceramides	139-156	glucosylceramidase beta	Homo sapiens	88-106
2060627-1	1991	The lysosomal degradation of glucosylceramide requires the hydrolase, glucosylceramide-beta-glucosidase and a sphingolipid activator protein (Gaucher factor, SAP-2, saposin C).	Glucosylceramides	29-45	ETS transcription factor ELK3	Homo sapiens	158-163
8457606-1	1993	In addition to the lysosomal glucocerebrosidase, a distinct beta-glucosidase that is also active towards glucosylceramide could be demonstrated in various human tissues and cell types.	Glucosylceramides	105-121	glucosylceramidase beta	Homo sapiens	19-47
1530650-0	1992	Binding specificity of lung surfactant protein SP-D for glucosylceramide.	Glucosylceramides	56-72	surfactant protein D	Rattus norvegicus	47-51
1530650-2	1992	When the binding study was performed on TLC plates, SP-D bound exclusively to GlcCer, whereas it failed to bind to GalCer, GM1, GM2, asialo-GM1, asialo-GM2, sulfatide, Forssman antigen, ceramide dihexoside, ceramide trihexoside, globoside, paragloboside or ceramide.	Glucosylceramides	78-84	surfactant protein D	Rattus norvegicus	52-56
1530650-4	1992	Antibody to rat SP-D inhibited 125I-SP-D binding to GlcCer.	Glucosylceramides	52-58	surfactant protein D	Rattus norvegicus	16-20
1530650-4	1992	Antibody to rat SP-D inhibited 125I-SP-D binding to GlcCer.	Glucosylceramides	52-58	surfactant protein D	Rattus norvegicus	36-40
1530650-5	1992	Ca2+ was absolutely required for the binding of SP-D to GlcCer; Mg2+ failed to substitute for Ca2+.	Glucosylceramides	56-62	surfactant protein D	Rattus norvegicus	48-52
1834652-5	1991	Sepharose-immobilized ceramide and Sepharose-immobilized glucosylceramide were found to be suitable acceptors for GlcT and GalT-2, respectively, still using intact Golgi cisternae as the enzyme source.	Glucosylceramides	57-73	beta-1,3-galactosyltransferase 4	Homo sapiens	123-129
2229016-5	1990	In this paper, we report a modification of this HPLC/FAB/MS method, which was used for the separation and characterization of neutral glycosphingolipids (GlcCer, LacCer, Gb3Cer, Gb4Cer, and IV3 alpha GalNAc-Gb4Cer) and monosialogangliosides [GM3(NeuAc or NeuGc), GM2 (NeuAc or NeuGc), and GM1 (NeuAc or NeuGc)].	Glucosylceramides	154-160	FA complementation group B	Homo sapiens	53-56
2141287-1	1990	Human acid beta-glucosidase (D-glucosyl-N-acylsphingosine glucohydrolase, EC 3.2.1.45) cleaves the beta-glucosidic bonds of glucosylceramide and synthetic beta-glucosides.	Glucosylceramides	124-140	glucosylceramidase beta	Homo sapiens	6-27
34897099-1	2022	BACKGROUND: Glucocerebrosidase gene (GBA) mutations influence risk and prognosis of Parkinson"s disease (PD), possibly through accumulation of glycosphingolipids, including glucosylceramide (GL-1).	Glucosylceramides	173-189	glucosylceramidase beta	Homo sapiens	37-40
2302413-0	1990	Correlation between the activity of glucosylceramidase and its binding to glucosylceramide-containing liposomes.	Glucosylceramides	74-90	glucosylceramidase beta	Homo sapiens	36-54
33974284-6	2021	In analogy to human plasma, lipid analyses revealed an accumulation of glucosylceramides (GlcCer) in the DRGs and sciatic nerves, which was associated with pathologic mitochondria, impairment of mitochondrial respiration, and deregulation of transient receptor potential and TRPV and TRPA channels at mRNA, protein and functional levels in DRGs.	Glucosylceramides	71-88	tryptase gamma 1	Homo sapiens	284-288
33974284-6	2021	In analogy to human plasma, lipid analyses revealed an accumulation of glucosylceramides (GlcCer) in the DRGs and sciatic nerves, which was associated with pathologic mitochondria, impairment of mitochondrial respiration, and deregulation of transient receptor potential and TRPV and TRPA channels at mRNA, protein and functional levels in DRGs.	Glucosylceramides	90-96	tryptase gamma 1	Homo sapiens	284-288
33971917-5	2021	The Gba2 deletion in gba1 KO medaka resulted in the exacerbation of glucosylceramide accumulation and no improvement in neuronopathic GD pathological changes, asyn accumulation, or swimming abnormalities.	Glucosylceramides	68-84	non-lysosomal glucosylceramidase	Oryzias latipes	4-8
34919775-4	2022	Here, the mutation of alkaline ceramidase (ACER) in a ceramide kinase mutant acd5 resulted in spontaneous programmed cell death early in development and was accompanied by ceramide accumulation, while other types of sphingolipids, such as long chain base, glucosylceramide, and glycosylinositol phosphorylceramide, remained at the same level as the wild-type plants.	Glucosylceramides	256-272	Diacylglycerol kinase family protein	Arabidopsis thaliana	77-81
33939982-8	2021	Additionally, triple ORMDL1/2/3 knockout but not ORMDL3 single knockout dramatically increased levels of galactosylceramides, glucosylceramides, and lactosylceramides, the elevated N-acyl chain distributions of which broadly correlated with the increases in ceramide species.	Glucosylceramides	126-143	ORMDL sphingolipid biosynthesis regulator 1	Homo sapiens	21-31
33823526-1	2021	INTRODUCTION: Gaucher disease (GD) is a rare autosomal recessive lysosomal storage disorder, in which biallelic pathogenic variants in the Glucosidase beta acid (GBA) gene result in defective functioning of glucosylceramidase that causes deposition of glucocerebroside in cells.	Glucosylceramides	252-268	glucosylceramidase beta	Homo sapiens	162-165
33823526-1	2021	INTRODUCTION: Gaucher disease (GD) is a rare autosomal recessive lysosomal storage disorder, in which biallelic pathogenic variants in the Glucosidase beta acid (GBA) gene result in defective functioning of glucosylceramidase that causes deposition of glucocerebroside in cells.	Glucosylceramides	252-268	glucosylceramidase beta	Homo sapiens	207-225
33802460-2	2021	Similar to Gaucher disease (GD), patients deficient in glucocerebrosidase (GCase) degrading GlcCer, NPC patients show an elevated glucosylsphingosine and glucosylated cholesterol.	Glucosylceramides	92-98	glucosidase, beta, acid	Mus musculus	75-80
11741960-3	2002	Thus, certain neutral glycosphingolipids (e.g. GlcCer, LacCer, and Gb(3)Cer) can enhance anticoagulant activity of APC/protein S by mechanisms that are distinctly different from those of phospholipids alone.	Glucosylceramides	47-53	APC regulator of WNT signaling pathway	Homo sapiens	115-118
34811369-2	2021	GBA encodes the beta-glucocerebrosidase enzyme that hydrolyzes glucosylceramide.	Glucosylceramides	63-79	glucosylceramidase beta	Homo sapiens	0-3
34843781-6	2022	In the same cell model, the AhR agonists reduced the expression of glucose metabolism genes (PCK1, G6PC and PDK4), and they up-regulated levels of glucosylceramides, together with a concomitant induction of expression of UGCG, glucosylceramide synthesis enzyme.	Glucosylceramides	147-164	aryl hydrocarbon receptor	Homo sapiens	28-31
34843781-6	2022	In the same cell model, the AhR agonists reduced the expression of glucose metabolism genes (PCK1, G6PC and PDK4), and they up-regulated levels of glucosylceramides, together with a concomitant induction of expression of UGCG, glucosylceramide synthesis enzyme.	Glucosylceramides	227-243	aryl hydrocarbon receptor	Homo sapiens	28-31
34843781-6	2022	In the same cell model, the AhR agonists reduced the expression of glucose metabolism genes (PCK1, G6PC and PDK4), and they up-regulated levels of glucosylceramides, together with a concomitant induction of expression of UGCG, glucosylceramide synthesis enzyme.	Glucosylceramides	227-243	UDP-glucose ceramide glucosyltransferase	Homo sapiens	221-225
34811369-0	2021	Glucosylceramide in cerebrospinal fluid of patients with GBA-associated and idiopathic Parkinson"s disease enrolled in PPMI.	Glucosylceramides	0-16	glucosylceramidase beta	Homo sapiens	57-60
34883387-2	2022	An attractive hypothesis is that the lipid substrate of glucocerebrosidase, glucosylceramide, accumulates in patients with PD with a GBA mutation (PD-GBA).	Glucosylceramides	76-92	glucosylceramidase beta	Homo sapiens	133-136
34883387-2	2022	An attractive hypothesis is that the lipid substrate of glucocerebrosidase, glucosylceramide, accumulates in patients with PD with a GBA mutation (PD-GBA).	Glucosylceramides	76-92	glucosylceramidase beta	Homo sapiens	150-153
34927020-1	2021	Glucosylceramide (GluCer) was accumulated in sphingomyelin synthase 1 (SMS1) but not SMS2 deficient mouse tissues.	Glucosylceramides	0-16	sphingomyelin synthase 1	Mus musculus	45-69
34927020-1	2021	Glucosylceramide (GluCer) was accumulated in sphingomyelin synthase 1 (SMS1) but not SMS2 deficient mouse tissues.	Glucosylceramides	0-16	sphingomyelin synthase 1	Mus musculus	71-75
34927020-1	2021	Glucosylceramide (GluCer) was accumulated in sphingomyelin synthase 1 (SMS1) but not SMS2 deficient mouse tissues.	Glucosylceramides	18-24	sphingomyelin synthase 1	Mus musculus	45-69
34927020-1	2021	Glucosylceramide (GluCer) was accumulated in sphingomyelin synthase 1 (SMS1) but not SMS2 deficient mouse tissues.	Glucosylceramides	18-24	sphingomyelin synthase 1	Mus musculus	71-75
34927020-6	2021	Further, we found that direct GluCer treatment (in vitro and in vivo) promoted hepatocyte to secrete more activated TGFbeta1, which stimulated more collagen 1alpha1 production in hepatic stellate cells.	Glucosylceramides	30-36	transforming growth factor, beta 1	Mus musculus	116-124
34927020-7	2021	Additionally, GluCer promoted more beta-catenin translocation into the nucleus, thus promoting tumorigenesis.	Glucosylceramides	14-20	catenin (cadherin associated protein), beta 1	Mus musculus	35-47
34626204-9	2021	Furthermore, tumor markers such as FGF21 and EPCAM are lowered following UGCG OE, which could be related to glucosylceramide (GlcCer) and lactosylceramide (LacCer) accumulation in glycosphingolipid-enriched microdomains (GEMs) and subsequently altered signaling protein phosphorylation.	Glucosylceramides	108-124	fibroblast growth factor 21	Mus musculus	35-40
34626204-9	2021	Furthermore, tumor markers such as FGF21 and EPCAM are lowered following UGCG OE, which could be related to glucosylceramide (GlcCer) and lactosylceramide (LacCer) accumulation in glycosphingolipid-enriched microdomains (GEMs) and subsequently altered signaling protein phosphorylation.	Glucosylceramides	108-124	epithelial cell adhesion molecule	Mus musculus	45-50
34626204-9	2021	Furthermore, tumor markers such as FGF21 and EPCAM are lowered following UGCG OE, which could be related to glucosylceramide (GlcCer) and lactosylceramide (LacCer) accumulation in glycosphingolipid-enriched microdomains (GEMs) and subsequently altered signaling protein phosphorylation.	Glucosylceramides	126-132	fibroblast growth factor 21	Mus musculus	35-40
34626204-9	2021	Furthermore, tumor markers such as FGF21 and EPCAM are lowered following UGCG OE, which could be related to glucosylceramide (GlcCer) and lactosylceramide (LacCer) accumulation in glycosphingolipid-enriched microdomains (GEMs) and subsequently altered signaling protein phosphorylation.	Glucosylceramides	126-132	epithelial cell adhesion molecule	Mus musculus	45-50
34686867-3	2021	Here, we uncover that tumor-cell-derived glucosylceramide stimulated unconventional endoplasmic reticulum (ER) stress responses by inducing reshuffling of lipid composition and saturation on the ER membrane in macrophages, which induced IRE1-mediated spliced XBP1 production and STAT3 activation.	Glucosylceramides	41-57	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	237-241
34686867-3	2021	Here, we uncover that tumor-cell-derived glucosylceramide stimulated unconventional endoplasmic reticulum (ER) stress responses by inducing reshuffling of lipid composition and saturation on the ER membrane in macrophages, which induced IRE1-mediated spliced XBP1 production and STAT3 activation.	Glucosylceramides	41-57	X-box binding protein 1	Homo sapiens	259-263
34686867-3	2021	Here, we uncover that tumor-cell-derived glucosylceramide stimulated unconventional endoplasmic reticulum (ER) stress responses by inducing reshuffling of lipid composition and saturation on the ER membrane in macrophages, which induced IRE1-mediated spliced XBP1 production and STAT3 activation.	Glucosylceramides	41-57	signal transducer and activator of transcription 3	Homo sapiens	279-284
34509608-2	2021	GCase metabolizes the glycosphingolipids glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	41-57	glucosidase, beta, acid	Mus musculus	0-5
34509608-2	2021	GCase metabolizes the glycosphingolipids glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	59-65	glucosidase, beta, acid	Mus musculus	0-5
34509608-5	2021	The glycosphingolipid GlcCer is synthesized by a single enzyme, glucosylceramide synthase (GCS), and small molecule inhibitors (GCSi) reduce cellular glycosphingolipid levels.	Glucosylceramides	22-28	UDP-glucose ceramide glucosyltransferase	Mus musculus	64-89
34509608-5	2021	The glycosphingolipid GlcCer is synthesized by a single enzyme, glucosylceramide synthase (GCS), and small molecule inhibitors (GCSi) reduce cellular glycosphingolipid levels.	Glucosylceramides	22-28	UDP-glucose ceramide glucosyltransferase	Mus musculus	91-94
34811369-3	2021	We hypothesized that GBA mutations will lead to glucosylceramide accumulation in cerebrospinal fluid (CSF).	Glucosylceramides	48-64	glucosylceramidase beta	Homo sapiens	21-24
34811369-6	2021	The glucosylceramide fraction was increased (P = 0.0001), and the sphingomyelin fraction (a downstream metabolite) was reduced (P = 0.0001) in CSF of GBA-PD patients compared to healthy controls.	Glucosylceramides	4-20	glucosylceramidase beta	Homo sapiens	150-153
34811369-10	2021	The GlcCer/SM ratio was negatively associated with alpha-synuclein levels in CSF of PD patients.	Glucosylceramides	4-10	synuclein alpha	Homo sapiens	51-66
34811369-11	2021	This study highlights glucosylceramide as a pathway biomarker for GBA-PD patients and the GlcCer/SM ratio as a potential stratification tool for clinical trials of idiopathic PD patients.	Glucosylceramides	22-38	glucosylceramidase beta	Homo sapiens	66-69
34686711-4	2021	Here, we aim to alleviate the lipid storage burden by inhibiting the de novo synthesis of the primary glycosphingolipid substrate of GCase, glucosylceramide (GlcCer).	Glucosylceramides	140-156	glucosidase, beta, acid	Mus musculus	133-138
34686711-4	2021	Here, we aim to alleviate the lipid storage burden by inhibiting the de novo synthesis of the primary glycosphingolipid substrate of GCase, glucosylceramide (GlcCer).	Glucosylceramides	158-164	glucosidase, beta, acid	Mus musculus	133-138
34686711-5	2021	We have previously shown that systemic GCS inhibition reduced GlcCer and glucosylsphingosine (GlcSph) accumulation, slowed alpha-synuclein buildup in the hippocampus, and improved cognitive deficits.	Glucosylceramides	62-68	UDP-glucose ceramide glucosyltransferase	Mus musculus	39-42
34134921-3	2021	An autosomal recessive disorder is caused by variants in the human glucocerebrosidase gene (GBA; MIM*606463) located on chromosome 1q21, resulting from deficit or lack of activity of the beta-glucocerebrosidase enzyme, leading to the accumulation of glucocerebroside substrate in the cells of the macrophage-monocyte system.	Glucosylceramides	250-266	glucosylceramidase beta	Homo sapiens	92-95
34622801-3	2021	We developed an efficient strategy to screen for modulators of beta-glucocerebrosidase (GCase), a lysosomal enzyme that exhibits decreased activity in patients with PD, leading to accumulation of the substrate glucosylceramide and oxidized dopamine and alpha-synuclein, which contribute to PD pathogenesis.	Glucosylceramides	210-226	glucosylceramidase beta	Homo sapiens	63-86
34622801-3	2021	We developed an efficient strategy to screen for modulators of beta-glucocerebrosidase (GCase), a lysosomal enzyme that exhibits decreased activity in patients with PD, leading to accumulation of the substrate glucosylceramide and oxidized dopamine and alpha-synuclein, which contribute to PD pathogenesis.	Glucosylceramides	210-226	glucosidase, beta, acid	Mus musculus	88-93
34720832-1	2021	Gaucher disease is a rare genetic disorder caused by the deficiency of acid beta-glucosidase to effectively catalyze the degradation of glucosylceramide to glucose and ceramide.	Glucosylceramides	136-152	glucosylceramidase beta	Homo sapiens	71-92
34638955-7	2021	Interestingly, S1P and glucosylceramides, but not ceramides, were elevated in bile of Sgpl1HepKO mice.	Glucosylceramides	23-40	sphingosine phosphate lyase 1	Mus musculus	86-91
34760177-1	2021	Gaucher"s disease, the most prevalent lysosomal storage disorder, is caused by missense mutation of the GBA gene, ultimately resulting in deficient GCase activity, hence the excessive build-up of cellular glucosylceramide.	Glucosylceramides	205-221	glucosylceramidase beta	Homo sapiens	104-107
34213307-0	2021	Glucosylceramide Associated with Gaucher Disease Forms Amyloid-like Twisted Ribbon Fibrils That Induce alpha-Synuclein Aggregation.	Glucosylceramides	0-16	synuclein alpha	Homo sapiens	103-118
34485083-1	2021	In Gaucher disease (GD), genetic deficiency of acid beta-glucosidase leads to accumulation of its substrate glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	108-124	glucosylceramidase beta	Homo sapiens	47-68
34485083-1	2021	In Gaucher disease (GD), genetic deficiency of acid beta-glucosidase leads to accumulation of its substrate glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	126-132	glucosylceramidase beta	Homo sapiens	47-68
34417467-5	2021	Germline deficiency, a conserved lifespan-extending paradigm, induces somatic expression of the fatty acid elongase ELO-3, and behenic acid (22:0) generated by ELO-3 is incorporated into glucosylceramide for lifespan regulation.	Glucosylceramides	187-203	Putative fatty acid elongation protein 3	Caenorhabditis elegans	160-165
34458595-1	2021	The acid beta-glucocerebrosidase (GCase) enzyme cleaves glucosylceramide into glucose and ceramide.	Glucosylceramides	56-72	glucosidase, beta, acid	Mus musculus	9-32
34458595-1	2021	The acid beta-glucocerebrosidase (GCase) enzyme cleaves glucosylceramide into glucose and ceramide.	Glucosylceramides	56-72	glucosidase, beta, acid	Mus musculus	34-39
34686508-1	2021	OBJECTIVE: UDP-glucose ceramide glycosyltransferase (UGCG), a critical enzyme for the synthesis of glucosylceramide, is implicated in various cellular processes.	Glucosylceramides	99-115	UDP-glucose ceramide glucosyltransferase	Homo sapiens	11-51
34686508-1	2021	OBJECTIVE: UDP-glucose ceramide glycosyltransferase (UGCG), a critical enzyme for the synthesis of glucosylceramide, is implicated in various cellular processes.	Glucosylceramides	99-115	UDP-glucose ceramide glucosyltransferase	Homo sapiens	53-57
34213307-1	2021	A major risk factor for Gaucher"s disease is loss of function mutations in the GBA1 gene that encodes lysosomal beta-glucocerebrosidase, resulting in accumulation of glucosylceramide (GlcCer), a key lysosomal sphingolipid.	Glucosylceramides	166-182	glucosylceramidase beta	Homo sapiens	79-83
34213307-1	2021	A major risk factor for Gaucher"s disease is loss of function mutations in the GBA1 gene that encodes lysosomal beta-glucocerebrosidase, resulting in accumulation of glucosylceramide (GlcCer), a key lysosomal sphingolipid.	Glucosylceramides	184-190	glucosylceramidase beta	Homo sapiens	79-83
34151863-3	2021	Deficiency in the GBA1 encoded enzyme glucocerebrosidase (GCase) leads to the accumulation of the GCase glycolipid substrates glucosylceramide and glucosylsphingosine and ultimately results in toxicity and inflammation and negatively affect many aspects of Parkinson"s disease, including disease risk, the severity of presentation, age of onset, and likelihood of progression to dementia.	Glucosylceramides	126-142	glucosylceramidase beta	Homo sapiens	18-22
34106956-1	2021	Multiple mutations have been described in the human GBA1 gene, which encodes the lysosomal enzyme beta-glucocerebrosidase (GCase) that degrades glucosylceramide and is pivotal in glycosphingolipid substrate metabolism.	Glucosylceramides	144-160	glucosylceramidase beta	Homo sapiens	52-56
34106956-1	2021	Multiple mutations have been described in the human GBA1 gene, which encodes the lysosomal enzyme beta-glucocerebrosidase (GCase) that degrades glucosylceramide and is pivotal in glycosphingolipid substrate metabolism.	Glucosylceramides	144-160	glucosylceramidase beta	Homo sapiens	98-121
34106956-1	2021	Multiple mutations have been described in the human GBA1 gene, which encodes the lysosomal enzyme beta-glucocerebrosidase (GCase) that degrades glucosylceramide and is pivotal in glycosphingolipid substrate metabolism.	Glucosylceramides	144-160	glucosidase, beta, acid	Mus musculus	123-128
34066520-7	2021	In SYS1 KO Vero cells, expression of Gb3 and sphingomyelin was decreased, while that of glucosylceramide and lactosylceramide was increased.	Glucosylceramides	88-104	protein SYS1 homolog	Chlorocebus sabaeus	3-7
34597626-5	2021	Using one probe, XLB, here we identified ATP-binding cassette (ABC) transporters ABCA3, ABCB4, and ABCB10 as unfractionated microsomal GlcCer-binding proteins in DU-145 prostate tumor cells.	Glucosylceramides	135-141	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	41-61
34597626-5	2021	Using one probe, XLB, here we identified ATP-binding cassette (ABC) transporters ABCA3, ABCB4, and ABCB10 as unfractionated microsomal GlcCer-binding proteins in DU-145 prostate tumor cells.	Glucosylceramides	135-141	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	63-66
34597626-5	2021	Using one probe, XLB, here we identified ATP-binding cassette (ABC) transporters ABCA3, ABCB4, and ABCB10 as unfractionated microsomal GlcCer-binding proteins in DU-145 prostate tumor cells.	Glucosylceramides	135-141	ATP binding cassette subfamily A member 3	Homo sapiens	81-86
34597626-5	2021	Using one probe, XLB, here we identified ATP-binding cassette (ABC) transporters ABCA3, ABCB4, and ABCB10 as unfractionated microsomal GlcCer-binding proteins in DU-145 prostate tumor cells.	Glucosylceramides	135-141	ATP binding cassette subfamily B member 4	Homo sapiens	88-93
34597626-5	2021	Using one probe, XLB, here we identified ATP-binding cassette (ABC) transporters ABCA3, ABCB4, and ABCB10 as unfractionated microsomal GlcCer-binding proteins in DU-145 prostate tumor cells.	Glucosylceramides	135-141	ATP binding cassette subfamily B member 10	Homo sapiens	99-105
34597626-8	2021	Depletion of ABCA12, implicated in GlcCer transport, preferentially decreased neutral GSL levels, while ABCB1 KD preferentially reduced gangliosides, but increased neutral GSL Gb3.	Glucosylceramides	35-41	ATP binding cassette subfamily A member 12	Homo sapiens	13-19
34597626-9	2021	These results imply that multiple ABC transporters may provide distinct but overlapping GlcCer and LacCer pools within the Golgi lumen for anabolism of different GSL series by metabolic channeling.	Glucosylceramides	88-94	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	34-37
34993951-2	2022	In the stratum corneum (SC), beta- glucocerebrosidase (GBA) mediates transformation of glucosylceramide (GlcCER) into ceramide (CER) and cholesterol into glucosylcholesterol (GlcChol).	Glucosylceramides	87-103	glucosylceramidase beta	Homo sapiens	55-58
34993951-2	2022	In the stratum corneum (SC), beta- glucocerebrosidase (GBA) mediates transformation of glucosylceramide (GlcCER) into ceramide (CER) and cholesterol into glucosylcholesterol (GlcChol).	Glucosylceramides	105-111	glucosylceramidase beta	Homo sapiens	55-58
35637196-0	2022	GBA1-dependent membrane glucosylceramide reprogramming promotes liver cancer metastasis via activation of the Wnt/beta-catenin signalling pathway.	Glucosylceramides	24-40	glucosylceramidase beta	Homo sapiens	0-4
35637196-0	2022	GBA1-dependent membrane glucosylceramide reprogramming promotes liver cancer metastasis via activation of the Wnt/beta-catenin signalling pathway.	Glucosylceramides	24-40	catenin beta 1	Homo sapiens	114-126
35637196-2	2022	In this study, we demonstrated that the protein expression of GBA1, which catalyses the conversion of GlcCer to ceramide, was downregulated in liver cancer tissue.	Glucosylceramides	102-108	glucosylceramidase beta	Homo sapiens	62-66
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	44-50	glucosylceramidase beta	Homo sapiens	29-33
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	44-50	LDL receptor related protein 6	Homo sapiens	75-79
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	44-50	LDL receptor related protein 6	Homo sapiens	144-148
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	44-50	LDL receptor related protein 6	Homo sapiens	173-177
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	44-50	catenin beta 1	Homo sapiens	237-249
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	133-139	glucosylceramidase beta	Homo sapiens	29-33
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	133-139	LDL receptor related protein 6	Homo sapiens	75-79
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	133-139	LDL receptor related protein 6	Homo sapiens	144-148
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	133-139	LDL receptor related protein 6	Homo sapiens	173-177
35637196-6	2022	In the plasma membrane (PM), GBA1-dependent GlcCer reprogramming increased LRP6 location in the PM leading to an interaction between GlcCer and LRP6, subsequently promoting LRP6 phosphorylation at Ser1490, and finally activating the Wnt/beta-catenin signalling pathway.	Glucosylceramides	133-139	catenin beta 1	Homo sapiens	237-249
35637196-8	2022	In addition, the results of mass spectrometry indicated that GlcCer d18:1/18:0 was the most notably increased studied species in the PM when GBA1 was downregulated, suggesting that GlcCer d18:1/18:0 may be the major functional lipid that promotes GBA1-dependent liver cancer metastasis.	Glucosylceramides	61-67	glucosylceramidase beta	Homo sapiens	141-145
35637196-8	2022	In addition, the results of mass spectrometry indicated that GlcCer d18:1/18:0 was the most notably increased studied species in the PM when GBA1 was downregulated, suggesting that GlcCer d18:1/18:0 may be the major functional lipid that promotes GBA1-dependent liver cancer metastasis.	Glucosylceramides	61-67	glucosylceramidase beta	Homo sapiens	247-251
35637196-8	2022	In addition, the results of mass spectrometry indicated that GlcCer d18:1/18:0 was the most notably increased studied species in the PM when GBA1 was downregulated, suggesting that GlcCer d18:1/18:0 may be the major functional lipid that promotes GBA1-dependent liver cancer metastasis.	Glucosylceramides	181-187	glucosylceramidase beta	Homo sapiens	141-145
35637196-8	2022	In addition, the results of mass spectrometry indicated that GlcCer d18:1/18:0 was the most notably increased studied species in the PM when GBA1 was downregulated, suggesting that GlcCer d18:1/18:0 may be the major functional lipid that promotes GBA1-dependent liver cancer metastasis.	Glucosylceramides	181-187	glucosylceramidase beta	Homo sapiens	247-251
35637196-9	2022	Thus, GBA1-mediated GlcCer reprogramming in the PM promotes metastasis of liver cancer via activation of the Wnt/beta-catenin signalling pathway, upregulation of GBA1 may be a potential therapeutic strategy to combat liver cancer metastasis.	Glucosylceramides	20-26	glucosylceramidase beta	Homo sapiens	6-10
35637196-9	2022	Thus, GBA1-mediated GlcCer reprogramming in the PM promotes metastasis of liver cancer via activation of the Wnt/beta-catenin signalling pathway, upregulation of GBA1 may be a potential therapeutic strategy to combat liver cancer metastasis.	Glucosylceramides	20-26	catenin beta 1	Homo sapiens	113-125
35637196-9	2022	Thus, GBA1-mediated GlcCer reprogramming in the PM promotes metastasis of liver cancer via activation of the Wnt/beta-catenin signalling pathway, upregulation of GBA1 may be a potential therapeutic strategy to combat liver cancer metastasis.	Glucosylceramides	20-26	glucosylceramidase beta	Homo sapiens	162-166
35101134-6	2022	Mutations in GBA reduce glucocerebrosidase (GCase) activity, leading to glucosylceramide accumulation, alpha-syn aggregation and broad autophagic abnormalities.	Glucosylceramides	72-88	glucosylceramidase beta	Homo sapiens	13-16
35065083-1	2022	The lysosomal enzyme glucocerebrosidase (GCase), encoded by the GBA1 gene, is a membrane-associated protein catalyzing the cleavage of glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	135-151	glucosylceramidase beta	Homo sapiens	64-68
35065083-1	2022	The lysosomal enzyme glucocerebrosidase (GCase), encoded by the GBA1 gene, is a membrane-associated protein catalyzing the cleavage of glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	153-159	glucosylceramidase beta	Homo sapiens	64-68
35401150-2	2022	Mutations in the glucocerebrosidase (GBA) gene, which encodes the lysosomal enzyme glucocerebrosidase (GCase), which hydrolyzes glucosylceramide (GlcCer) to glucose and ceramide, are the most important and common genetic PD risk factors discovered to date.	Glucosylceramides	128-144	glucosylceramidase beta	Homo sapiens	37-40
35401150-2	2022	Mutations in the glucocerebrosidase (GBA) gene, which encodes the lysosomal enzyme glucocerebrosidase (GCase), which hydrolyzes glucosylceramide (GlcCer) to glucose and ceramide, are the most important and common genetic PD risk factors discovered to date.	Glucosylceramides	128-144	glucosylceramidase beta	Homo sapiens	83-101
35401150-2	2022	Mutations in the glucocerebrosidase (GBA) gene, which encodes the lysosomal enzyme glucocerebrosidase (GCase), which hydrolyzes glucosylceramide (GlcCer) to glucose and ceramide, are the most important and common genetic PD risk factors discovered to date.	Glucosylceramides	146-152	glucosylceramidase beta	Homo sapiens	17-35
35401150-2	2022	Mutations in the glucocerebrosidase (GBA) gene, which encodes the lysosomal enzyme glucocerebrosidase (GCase), which hydrolyzes glucosylceramide (GlcCer) to glucose and ceramide, are the most important and common genetic PD risk factors discovered to date.	Glucosylceramides	146-152	glucosylceramidase beta	Homo sapiens	37-40
35401150-2	2022	Mutations in the glucocerebrosidase (GBA) gene, which encodes the lysosomal enzyme glucocerebrosidase (GCase), which hydrolyzes glucosylceramide (GlcCer) to glucose and ceramide, are the most important and common genetic PD risk factors discovered to date.	Glucosylceramides	146-152	glucosylceramidase beta	Homo sapiens	83-101
35188773-7	2022	The ring opening of T-036 resulted in another potent GCS inhibitor with a lower toxicological risk, T-690, which reduced glucosylceramide in a dose-dependent manner in the plasma and cortex of mice.	Glucosylceramides	121-137	UDP-glucose ceramide glucosyltransferase	Mus musculus	53-56
35572168-7	2022	RT-PCR revealed that after damage repair by Cer/Glucosylceramide (GlcCer), the expression of two genes in the sterol regulatory element-binding protein and three in the peroxisome proliferator-activated receptor pathway significantly increased.	Glucosylceramides	48-64	CCHC-type zinc finger nucleic acid binding protein	Homo sapiens	110-151
35315333-1	2022	In Gaucher disease (GD), the deficiency of glucocerebrosidase (GCase/ GBA1) causes lysosomal accumulation of glucosylceramide (GlcCer), which is partly converted by acid ceramidase (ACase) to glucosylsphingosine (GlcSph) in the lysosome.	Glucosylceramides	109-125	glucosidase, beta, acid	Danio rerio	70-74
35315333-1	2022	In Gaucher disease (GD), the deficiency of glucocerebrosidase (GCase/ GBA1) causes lysosomal accumulation of glucosylceramide (GlcCer), which is partly converted by acid ceramidase (ACase) to glucosylsphingosine (GlcSph) in the lysosome.	Glucosylceramides	127-133	glucosidase, beta, acid	Danio rerio	70-74
35562868-4	2022	UDP-glucose ceramide glycosyltransferase (UGCG), a key enzyme in glycosphingolipid metabolism, generates glucosylceramide (GlcCer), which is the precursor for all glycosphingolipids (GSLs).	Glucosylceramides	105-121	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-40
35562868-4	2022	UDP-glucose ceramide glycosyltransferase (UGCG), a key enzyme in glycosphingolipid metabolism, generates glucosylceramide (GlcCer), which is the precursor for all glycosphingolipids (GSLs).	Glucosylceramides	123-129	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-40
3408492-1	1988	SAP-2 is a family of heat-stable, acidic glycoproteins which stimulate enzymatic hydrolysis of glucosylceramide.	Glucosylceramides	95-111	ETS transcription factor ELK3	Homo sapiens	0-5
2591351-4	1989	When a crude glucosylceramidase placental preparation is incubated with the assay mixture the enzyme is almost totally bound to the glucosylceramide-oleic acid particles.	Glucosylceramides	132-148	glucosylceramidase beta	Homo sapiens	13-31
3087971-2	1986	Human acid beta-glucosidase (glucosylceramidase; EC 3.2.1.45) cleaves the glycosidic bonds of glucosyl ceramide and synthetic beta-glucosides.	Glucosylceramides	94-111	glucosylceramidase beta	Homo sapiens	6-27
3771578-2	1986	SAP-2 has previously been demonstrated to activate the hydrolysis of glucosylceramide, galactosylceramide, and, possibly, sphingomyelin.	Glucosylceramides	69-85	ETS transcription factor ELK3	Homo sapiens	0-5
3392043-8	1988	With enzyme preparations from the other strains lactosylceramide was the single major degradation product from complex glycosphingolipids with less than 30% further degradation to glucosylceramide within 48 h. We conclude that glycosidases from mucin-degrading strains of human enteric bacteria degrade oligosaccharide chains of lactoseries fucolipids and gangliosides of intestinal origin primarily to lactosylceramide.	Glucosylceramides	180-196	LOC100508689	Homo sapiens	245-250
3582671-0	1987	The binding of glucosylceramidase to glucosylceramide is promoted by its activator protein.	Glucosylceramides	37-53	glucosylceramidase beta	Homo sapiens	15-33
3582671-5	1987	After the purification step which frees the enzyme of most of its activator protein (octyl-Sepharose 4B chromatography), the capacity of glucosylceramidase to bind to the glucosylceramide micelles is dramatically decreased.	Glucosylceramides	171-187	glucosylceramidase beta	Homo sapiens	137-155
3099851-1	1987	The activity of a galactosyltransferase (GalT-2) that catalyzes the transfer of galactose from uridinediphosphogalactose to glucosylceramide in cultured normal human proximal tubular (PT) cells was characterized with respect to substrate saturation and metal ion requirements.	Glucosylceramides	124-140	beta-1,3-galactosyltransferase 4	Homo sapiens	41-47
3099851-4	1987	The Vmax values for glucosylceramide and UDP[U-14C]galactose were 0.12 nmol/mg protein per 2 h and 173 nmol/mg protein per 2 h, respectively.	Glucosylceramides	20-36	period circadian regulator 2	Homo sapiens	87-92
3099851-4	1987	The Vmax values for glucosylceramide and UDP[U-14C]galactose were 0.12 nmol/mg protein per 2 h and 173 nmol/mg protein per 2 h, respectively.	Glucosylceramides	20-36	period circadian regulator 2	Homo sapiens	119-124
3666281-10	1987	GalCer and GlcCer contained considerable amounts of C16- and C18-acids, and of C18-phytosphingosine, whereas C24-acids and C18-sphingosine were predominant in the other GSLs.	Glucosylceramides	11-17	Bardet-Biedl syndrome 9	Homo sapiens	61-64
3666281-10	1987	GalCer and GlcCer contained considerable amounts of C16- and C18-acids, and of C18-phytosphingosine, whereas C24-acids and C18-sphingosine were predominant in the other GSLs.	Glucosylceramides	11-17	Bardet-Biedl syndrome 9	Homo sapiens	79-82
3666281-10	1987	GalCer and GlcCer contained considerable amounts of C16- and C18-acids, and of C18-phytosphingosine, whereas C24-acids and C18-sphingosine were predominant in the other GSLs.	Glucosylceramides	11-17	Bardet-Biedl syndrome 9	Homo sapiens	79-82
2939881-6	1986	The orientation of the newly synthesized glucosylceramide is studied by the ability of the enzyme glucosylceramidase to hydrolyse this compound both on intact and on disrupted vesicles.	Glucosylceramides	41-57	glucosylceramidase beta	Homo sapiens	98-116
3087971-2	1986	Human acid beta-glucosidase (glucosylceramidase; EC 3.2.1.45) cleaves the glycosidic bonds of glucosyl ceramide and synthetic beta-glucosides.	Glucosylceramides	94-111	glucosylceramidase beta	Homo sapiens	29-47
3456607-1	1986	Human acid beta-glucosidase (D-glucosyl-N-acylsphingosine glucohydrolase, EC 3.2.1.45) cleaves the glucosidic bonds of glucosylceramide and synthetic beta-glucosides.	Glucosylceramides	119-135	glucosylceramidase beta	Homo sapiens	6-27
7049116-6	1982	The migration inhibition factor (MIF) test performed with the lymphocytes of our patients was positive to glucocerebroside in four of 17 patients, to glucocerebrosidase in four of 19 patients, and to the extracts of the spleen of a patient with Gaucher"s disease in three of eight patients.	Glucosylceramides	106-122	macrophage migration inhibitory factor	Homo sapiens	4-31
9556662-1	1985	Sphingolipid activator protein-2 (SAP-2) has been found to stimulate the enzymatic hydrolysis of glucosylceramide, galactosylceramide, and sphingomyelin.	Glucosylceramides	97-113	ETS transcription factor ELK3	Homo sapiens	0-32
9556662-1	1985	Sphingolipid activator protein-2 (SAP-2) has been found to stimulate the enzymatic hydrolysis of glucosylceramide, galactosylceramide, and sphingomyelin.	Glucosylceramides	97-113	ETS transcription factor ELK3	Homo sapiens	34-39
3929764-3	1985	Lactase hydrolyzes, besides lactose, cellobiose and the synthetic substrates, 4-methylumbelliferyl-beta-galactoside and beta-glucoside, as well as phlorizin; but it does not hydrolyze glucocerebroside.	Glucosylceramides	184-200	lactase	Homo sapiens	0-7
3921288-0	1985	Studies on a sphingolipid activator protein (SAP-2) in fibroblasts from patients with lysosomal storage diseases, including Niemann-Pick disease Type C. Sphingolipid activator protein-2 (SAP-2) has been found to stimulate the enzymatic hydrolysis of at least three sphingolipids, glucosylceramide, galactosylceramide and sphingomyelin.	Glucosylceramides	280-296	ETS transcription factor ELK3	Homo sapiens	45-50
3921288-0	1985	Studies on a sphingolipid activator protein (SAP-2) in fibroblasts from patients with lysosomal storage diseases, including Niemann-Pick disease Type C. Sphingolipid activator protein-2 (SAP-2) has been found to stimulate the enzymatic hydrolysis of at least three sphingolipids, glucosylceramide, galactosylceramide and sphingomyelin.	Glucosylceramides	280-296	ETS transcription factor ELK3	Homo sapiens	153-185
3921288-0	1985	Studies on a sphingolipid activator protein (SAP-2) in fibroblasts from patients with lysosomal storage diseases, including Niemann-Pick disease Type C. Sphingolipid activator protein-2 (SAP-2) has been found to stimulate the enzymatic hydrolysis of at least three sphingolipids, glucosylceramide, galactosylceramide and sphingomyelin.	Glucosylceramides	280-296	ETS transcription factor ELK3	Homo sapiens	187-192
6626552-2	1983	This hydration level, representing strongly bound water, is identical to that observed previously for human glucocerebroside (Bach, D., Sela, B. and Miller, I.R.	Glucosylceramides	108-124	acyl-CoA thioesterase 7	Homo sapiens	126-130
6883703-1	1983	Our earlier observation that N-stearoyl- and N-lignoceroyl-glucosyl-dihydro-sphingosines have much lower affinity to the hydrolytic enzyme, glucosylceramidase, than the natural mixture of glucosylceramide [11] has been further pursued with catalytically hydrogenated natural substrate.	Glucosylceramides	188-204	glucosylceramidase beta	Homo sapiens	140-158
7049116-6	1982	The migration inhibition factor (MIF) test performed with the lymphocytes of our patients was positive to glucocerebroside in four of 17 patients, to glucocerebrosidase in four of 19 patients, and to the extracts of the spleen of a patient with Gaucher"s disease in three of eight patients.	Glucosylceramides	106-122	macrophage migration inhibitory factor	Homo sapiens	33-36
7076644-6	1982	One is the pathway to GM4 (NeuAc) from galactosylceramide, and the other is that for synthesizing GM2 (NeuGc) from glucosylceramide.	Glucosylceramides	115-131	T cell receptor alpha variable 6-3	Mus musculus	22-25
7053901-0	1982	Comparison of synthetic and natural glucosylceramides as substrate for glucosylceramidase assay.	Glucosylceramides	36-53	glucosylceramidase beta	Homo sapiens	71-89
7053901-2	1982	When such tritiated glucosylceramide was diluted with unlabelled glucosylceramide from different sources and used as the substrate for assays of glucosylceramidase, the apparent activities obtained differed drastically.	Glucosylceramides	20-36	glucosylceramidase beta	Homo sapiens	145-163
7053901-2	1982	When such tritiated glucosylceramide was diluted with unlabelled glucosylceramide from different sources and used as the substrate for assays of glucosylceramidase, the apparent activities obtained differed drastically.	Glucosylceramides	65-81	glucosylceramidase beta	Homo sapiens	145-163
508779-6	1979	Thus, the hypothesis that the difference in fatty acid composition found in glucocerebroside is obtained as a result of a mutation affecting the specificity of the residual glucosylceramidase must be rejected.	Glucosylceramides	76-92	glucosylceramidase beta	Homo sapiens	173-191
7284440-1	1981	Purified antithrombin III has been reported to have bound glucocerebroside, the major glycolipid of plasma.	Glucosylceramides	58-74	serpin family C member 1	Homo sapiens	9-25
4364062-0	1974	The occurrence of beta-glucocerebrosidase activity in the glucocerebroside-rich deposits of Gaucher"s disease.	Glucosylceramides	58-74	glucosylceramidase beta	Homo sapiens	18-41
618863-8	1978	Although it remains to be established whether the inhibitory actions of antithrombin III are affected by glucosylceramide, the relative amounts which are bound suggest that antithrombin III may be a significant carrier of the glycolipid.	Glucosylceramides	105-121	serpin family C member 1	Homo sapiens	72-88
836891-5	1977	The loaded cells can be ingested by macrophage in vitro and the glucocerebroside partially degraded by lysosomal glucocerebrosidase.	Glucosylceramides	64-80	glucosylceramidase beta	Homo sapiens	103-131
1002685-2	1976	Glucosylceramide was perbenzoylated and separated on a packed muBondapack C18 column, using methanol as eluting solvent.	Glucosylceramides	0-16	Bardet-Biedl syndrome 9	Homo sapiens	74-77
182248-0	1976	Uptake of radiolabeled galactosyl-(alpha1 goes to 4)-galactosyl-(beta1 goes to 4)-glucosylceramide by human serum lipoproteins in vitro.	Glucosylceramides	80-98	adrenoceptor alpha 1D	Homo sapiens	35-41
182248-0	1976	Uptake of radiolabeled galactosyl-(alpha1 goes to 4)-galactosyl-(beta1 goes to 4)-glucosylceramide by human serum lipoproteins in vitro.	Glucosylceramides	80-98	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	65-70
182248-1	1976	Human serum was exposed to various amounts of [6-3H] galactosyl-(alpha1 goes to 4)-galactosyl-(beta1 goes to 4)-glucosylceramide under standardized conditions in vitro, and the uptake of the lipid by serum lipoproteins was determined.	Glucosylceramides	110-128	adrenoceptor alpha 1D	Homo sapiens	65-71
182248-1	1976	Human serum was exposed to various amounts of [6-3H] galactosyl-(alpha1 goes to 4)-galactosyl-(beta1 goes to 4)-glucosylceramide under standardized conditions in vitro, and the uptake of the lipid by serum lipoproteins was determined.	Glucosylceramides	110-128	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	95-100
809441-8	1975	In contrast to the results with GL-la, the maximum incorporation of [6,6-2H2]hexose into lactosylceramide (galactosyl-(beta1 leads to 4)-glucosylceramide) was 2-fold higher in the Fabry patient (1.6%) than in the control (0.8%).	Glucosylceramides	32-37	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	119-124
1177668-0	1975	Enzymatic synthesis of glucocerebroside by UDP-glucose: ceramide glucosyltransferase during ontogenesis of chicken retina.	Glucosylceramides	23-39	UDP-glucose ceramide glucosyltransferase	Gallus gallus	56-84
33684145-8	2021	These findings indicate that BSG stimulates ceramide synthesis via the up-regulated expression levels of CerS3 and GCS in the glucosylceramide pathway, which results in a significantly increased level of total ceramides in the SC accompanied by significantly increased levels of acylceramide species such as Cer[EOS].	Glucosylceramides	126-142	ceramide synthase 3	Homo sapiens	105-110
33219714-5	2021	This gene encodes an essential lysosomal enzyme called beta-glucocerebrosidase (GCase), which is responsible for degrading the glycolipid glucocerebroside into glucose and ceramide.	Glucosylceramides	138-154	glucosylceramidase beta	Homo sapiens	55-78
33342090-1	2021	Gaucher disease, the most prevalent metabolic storage disorder, is caused by mutations in the glucocerebrosidase gene GBA1, which lead to the accumulation of glucosylceramide (GlcCer) in affected cells.	Glucosylceramides	158-174	glucosylceramidase beta	Homo sapiens	118-122
33342090-1	2021	Gaucher disease, the most prevalent metabolic storage disorder, is caused by mutations in the glucocerebrosidase gene GBA1, which lead to the accumulation of glucosylceramide (GlcCer) in affected cells.	Glucosylceramides	176-182	glucosylceramidase beta	Homo sapiens	118-122
33342090-6	2021	With this synthetic mRNA-based rapid differentiation method, we found that the metabolic defect in GD1 patient cells can be rescued by the overexpression of wild-type GBA1 or the treatment with an inhibitor for GlcCer synthesis.	Glucosylceramides	211-217	glucosylceramidase beta	Homo sapiens	167-171
33684145-8	2021	These findings indicate that BSG stimulates ceramide synthesis via the up-regulated expression levels of CerS3 and GCS in the glucosylceramide pathway, which results in a significantly increased level of total ceramides in the SC accompanied by significantly increased levels of acylceramide species such as Cer[EOS].	Glucosylceramides	126-142	UDP-glucose ceramide glucosyltransferase	Homo sapiens	115-118
33142037-11	2021	After treatment stop, GlcCer levels returned to baseline and increased above baseline at lowest doses, probably due to the higher potency of sinbaglustat on GBA2 compared to GCS.	Glucosylceramides	22-28	glucosylceramidase beta 2	Homo sapiens	157-161
33355876-7	2020	The metabolism of glucosylceramide is regulated by glucosylceramide synthase (EC: 2.4.1.80) which is the key enzyme in the glycosylation of ceramide.	Glucosylceramides	18-34	UDP-glucose ceramide glucosyltransferase	Homo sapiens	51-76
33539341-11	2021	Lipidomic analysis of nSMase knockdown on ceramide and glucosylceramide levels suggested that Gba1b mutant protein aggregation may depend on relative depletion of specific ceramide species often enriched in EVs.	Glucosylceramides	55-71	neutral sphingomyelinase	Drosophila melanogaster	22-28
33152398-4	2021	Gba-/-;Gbatg mice, which contain a Gba transgene regulated by doxycycline, accumulate moderate levels of the offending substrate in GD, glucosylceramide, and live for up to 10 months, i.e. significantly longer than mice which model type 2 GD.	Glucosylceramides	136-152	glucosidase, beta, acid	Mus musculus	0-3
33152398-4	2021	Gba-/-;Gbatg mice, which contain a Gba transgene regulated by doxycycline, accumulate moderate levels of the offending substrate in GD, glucosylceramide, and live for up to 10 months, i.e. significantly longer than mice which model type 2 GD.	Glucosylceramides	136-152	glucosidase, beta, acid	Mus musculus	7-10
32851809-1	2021	Venglustat is a small-molecule glucosylceramide synthase (GCS) inhibitor designed to reduce the production of glucosylceramide (GL-1) and thus is expected to substantially reduce formation of glucosylceramide-based glycosphingolipids.	Glucosylceramides	31-47	UDP-glucose ceramide glucosyltransferase	Homo sapiens	58-61
32851809-1	2021	Venglustat is a small-molecule glucosylceramide synthase (GCS) inhibitor designed to reduce the production of glucosylceramide (GL-1) and thus is expected to substantially reduce formation of glucosylceramide-based glycosphingolipids.	Glucosylceramides	110-126	UDP-glucose ceramide glucosyltransferase	Homo sapiens	31-56
32851809-1	2021	Venglustat is a small-molecule glucosylceramide synthase (GCS) inhibitor designed to reduce the production of glucosylceramide (GL-1) and thus is expected to substantially reduce formation of glucosylceramide-based glycosphingolipids.	Glucosylceramides	110-126	UDP-glucose ceramide glucosyltransferase	Homo sapiens	58-61
33216044-9	2021	Interestingly, CSF glucosylceramide (d18 : 1/C23 : 0) exhibited a significant correlation with CSF C5a levels in PD, but not ALS.	Glucosylceramides	19-35	complement C5a receptor 1	Homo sapiens	99-102
33562655-12	2021	SM deacylase competes with aSMase and beta-glucocerebrosidase (BGCase) to hydrolyze their common substrates, SM and GCer, to yield their lysoforms sphingosylphosphorylcholine (SPC) and glucosylsphingosine (GSP), respectively, instead of ceramide.	Glucosylceramides	116-120	sphingomyelin phosphodiesterase 1	Homo sapiens	27-33
34043191-1	2021	Glucocerebrosidase (GCase), which is encoded by the GBA1 gene, has lysosomal glycoside hydrolase activity that hydrolyzes glucosylceramide.	Glucosylceramides	122-138	glucosylceramidase beta	Homo sapiens	52-56
33355876-10	2020	The purpose of this paper is to address the relationship between glucosylceramide, glucosylceramide synthase, and their possible association with liver diseases at the theoretical level.	Glucosylceramides	65-81	UDP-glucose ceramide glucosyltransferase	Homo sapiens	83-108
33060204-6	2020	The primary substrates of Dnf2 are glucosylceramide (GlcCer) and phosphatidylcholine ((PC) or their lyso-lipid derivatives), and we find that these substrates compete with each other for transport.	Glucosylceramides	35-51	aminophospholipid-translocating P4-type ATPase DNF2	Saccharomyces cerevisiae S288C	26-30
33060204-6	2020	The primary substrates of Dnf2 are glucosylceramide (GlcCer) and phosphatidylcholine ((PC) or their lyso-lipid derivatives), and we find that these substrates compete with each other for transport.	Glucosylceramides	53-59	aminophospholipid-translocating P4-type ATPase DNF2	Saccharomyces cerevisiae S288C	26-30
33060204-10	2020	Surprisingly, application of lipids that are poor transport substrates differentially affect PC and GlcCer transport by Dnf2, thus altering substrate preference.	Glucosylceramides	100-106	aminophospholipid-translocating P4-type ATPase DNF2	Saccharomyces cerevisiae S288C	120-124
33189821-8	2020	Also, the levels of acid ceramidase (Asah1) and glucocerebrosidase (Gba)-lysosomal enzymes involved in the hydrolysis of glucosylceramides-were consistently elevated in the lungs after CS exposure.	Glucosylceramides	121-138	N-acylsphingosine amidohydrolase 1	Mus musculus	20-35
33189821-8	2020	Also, the levels of acid ceramidase (Asah1) and glucocerebrosidase (Gba)-lysosomal enzymes involved in the hydrolysis of glucosylceramides-were consistently elevated in the lungs after CS exposure.	Glucosylceramides	121-138	N-acylsphingosine amidohydrolase 1	Mus musculus	37-42
33189821-8	2020	Also, the levels of acid ceramidase (Asah1) and glucocerebrosidase (Gba)-lysosomal enzymes involved in the hydrolysis of glucosylceramides-were consistently elevated in the lungs after CS exposure.	Glucosylceramides	121-138	glucosidase, beta, acid	Mus musculus	48-66
33189821-8	2020	Also, the levels of acid ceramidase (Asah1) and glucocerebrosidase (Gba)-lysosomal enzymes involved in the hydrolysis of glucosylceramides-were consistently elevated in the lungs after CS exposure.	Glucosylceramides	121-138	glucosidase, beta, acid	Mus musculus	68-71
33163670-1	2020	Glucosylceramidase (GCase) is a lysosomal enzyme that catalyzes the cleavage of beta-glucosidic linkage of glucocerebroside (GC) into glucose and ceramide; thereby, plays an essential function in the degradation of complex lipids and the turnover of cellular membranes.	Glucosylceramides	20-22	glucosylceramidase beta	Homo sapiens	0-18
33261081-2	2020	GlcCer is mainly degraded by two enzymes, lysosomal acid beta-glucosidase (GBA) and nonlysosomal beta-glucosidase (GBA2), which may have different isoforms because of alternative splicing.	Glucosylceramides	0-6	glucosylceramidase beta	Homo sapiens	75-78
33261081-2	2020	GlcCer is mainly degraded by two enzymes, lysosomal acid beta-glucosidase (GBA) and nonlysosomal beta-glucosidase (GBA2), which may have different isoforms because of alternative splicing.	Glucosylceramides	0-6	glucosylceramidase beta 2	Homo sapiens	115-119
33261081-6	2020	Comparison of ratios of glucosylceramides to the corresponding ceramides in the extracts indicated that GBA2 isoform 1 has broad specificity for the lipid component of glucosylceramide, suggesting that only one GBA2 isoform 1 is active and affects sphingolipid levels in the cell.	Glucosylceramides	24-41	glucosylceramidase beta 2	Homo sapiens	104-108
33261081-6	2020	Comparison of ratios of glucosylceramides to the corresponding ceramides in the extracts indicated that GBA2 isoform 1 has broad specificity for the lipid component of glucosylceramide, suggesting that only one GBA2 isoform 1 is active and affects sphingolipid levels in the cell.	Glucosylceramides	24-40	glucosylceramidase beta 2	Homo sapiens	104-108
32739173-6	2020	We have shown that the glucosylceramide degrading enzyme, glucocerebrosidase (GBA) 2 is abnormally increased in the spinal cord of the SOD1G86R mouse model of ALS.	Glucosylceramides	23-39	glucosidase beta 2	Mus musculus	58-84
32705968-1	2020	The accumulation of glucosylceramide (GlcCer), which is synthesized by UDP-glucose ceramide glucosyltransferase (UGCG), is associated with several diseases, including Gaucher disease and Parkinson"s disease.	Glucosylceramides	20-36	UDP-glucose ceramide glucosyltransferase	Homo sapiens	71-111
32705968-1	2020	The accumulation of glucosylceramide (GlcCer), which is synthesized by UDP-glucose ceramide glucosyltransferase (UGCG), is associated with several diseases, including Gaucher disease and Parkinson"s disease.	Glucosylceramides	20-36	UDP-glucose ceramide glucosyltransferase	Homo sapiens	113-117
32705968-1	2020	The accumulation of glucosylceramide (GlcCer), which is synthesized by UDP-glucose ceramide glucosyltransferase (UGCG), is associated with several diseases, including Gaucher disease and Parkinson"s disease.	Glucosylceramides	38-44	UDP-glucose ceramide glucosyltransferase	Homo sapiens	71-111
32705968-1	2020	The accumulation of glucosylceramide (GlcCer), which is synthesized by UDP-glucose ceramide glucosyltransferase (UGCG), is associated with several diseases, including Gaucher disease and Parkinson"s disease.	Glucosylceramides	38-44	UDP-glucose ceramide glucosyltransferase	Homo sapiens	113-117
32705968-2	2020	Since the inhibition of UGCG can be used to treat diseases caused by GlcCer accumulation, several UGCG inhibitors have been developed.	Glucosylceramides	69-75	UDP-glucose ceramide glucosyltransferase	Homo sapiens	24-28
32705968-2	2020	Since the inhibition of UGCG can be used to treat diseases caused by GlcCer accumulation, several UGCG inhibitors have been developed.	Glucosylceramides	69-75	UDP-glucose ceramide glucosyltransferase	Homo sapiens	98-102
32946792-2	2020	GlcChol is generated from glucosylceramide (GlcCer) and cholesterol through transglucosylation by two retaining beta-glucosidases, GBA and GBA2.	Glucosylceramides	26-42	glucosylceramidase beta	Homo sapiens	131-134
32946792-2	2020	GlcChol is generated from glucosylceramide (GlcCer) and cholesterol through transglucosylation by two retaining beta-glucosidases, GBA and GBA2.	Glucosylceramides	26-42	glucosylceramidase beta 2	Homo sapiens	139-143
32946792-2	2020	GlcChol is generated from glucosylceramide (GlcCer) and cholesterol through transglucosylation by two retaining beta-glucosidases, GBA and GBA2.	Glucosylceramides	44-50	glucosylceramidase beta	Homo sapiens	131-134
32946792-2	2020	GlcChol is generated from glucosylceramide (GlcCer) and cholesterol through transglucosylation by two retaining beta-glucosidases, GBA and GBA2.	Glucosylceramides	44-50	glucosylceramidase beta 2	Homo sapiens	139-143
32739173-6	2020	We have shown that the glucosylceramide degrading enzyme, glucocerebrosidase (GBA) 2 is abnormally increased in the spinal cord of the SOD1G86R mouse model of ALS.	Glucosylceramides	23-39	superoxide dismutase 1, soluble	Mus musculus	135-139
33205006-1	2020	Glucosylceramide synthase (GCS) is a key enzyme catalyzing ceramide glycosylation to generate glucosylceramide (GlcCer), which in turn serves as the precursor for cells to produce glycosphingolipids (GSLs).	Glucosylceramides	94-110	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
33205006-1	2020	Glucosylceramide synthase (GCS) is a key enzyme catalyzing ceramide glycosylation to generate glucosylceramide (GlcCer), which in turn serves as the precursor for cells to produce glycosphingolipids (GSLs).	Glucosylceramides	94-110	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
33205006-1	2020	Glucosylceramide synthase (GCS) is a key enzyme catalyzing ceramide glycosylation to generate glucosylceramide (GlcCer), which in turn serves as the precursor for cells to produce glycosphingolipids (GSLs).	Glucosylceramides	112-118	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
33205006-1	2020	Glucosylceramide synthase (GCS) is a key enzyme catalyzing ceramide glycosylation to generate glucosylceramide (GlcCer), which in turn serves as the precursor for cells to produce glycosphingolipids (GSLs).	Glucosylceramides	112-118	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
32232851-3	2020	FAM134B (rs78314670) was associated with low plasma levels of anticoagulant glucosylceramide.	Glucosylceramides	76-92	reticulophagy regulator 1	Mus musculus	0-7
32172343-0	2020	Mutated ATP10B increases Parkinson"s disease risk by compromising lysosomal glucosylceramide export.	Glucosylceramides	76-92	ATPase phospholipid transporting 10B (putative)	Homo sapiens	8-14
32191378-1	2020	Gaucher disease is caused by mutations in human acid beta-glucosidase, the enzyme responsible for hydrolysis of glucosyl ceramide in the lysosomes.	Glucosylceramides	112-129	glucosylceramidase beta	Homo sapiens	48-69
32632018-5	2020	Interestingly, adiponectin selectively bound several anionic phospholipids and sphingolipids, including phosphatidylserine, ceramide-1-phosphate, glucosylceramide, and sulfatide, via the C1q domain in an oligomerization-dependent fashion.	Glucosylceramides	146-162	adiponectin, C1Q and collagen domain containing	Homo sapiens	15-26
32172343-4	2020	We established that ATP10B encodes a late endo-lysosomal lipid flippase that translocates the lipids glucosylceramide (GluCer) and phosphatidylcholine (PC) towards the cytosolic membrane leaflet.	Glucosylceramides	101-117	ATPase phospholipid transporting 10B (putative)	Homo sapiens	20-26
32172343-4	2020	We established that ATP10B encodes a late endo-lysosomal lipid flippase that translocates the lipids glucosylceramide (GluCer) and phosphatidylcholine (PC) towards the cytosolic membrane leaflet.	Glucosylceramides	119-125	ATPase phospholipid transporting 10B (putative)	Homo sapiens	20-26
32172343-9	2020	Both ATP10B and glucocerebrosidase 1, encoded by the PD risk gene GBA1, reduce lysosomal GluCer levels, emerging lysosomal GluCer accumulation as a potential PD driver.	Glucosylceramides	89-95	ATPase phospholipid transporting 10B (putative)	Homo sapiens	5-11
32172343-9	2020	Both ATP10B and glucocerebrosidase 1, encoded by the PD risk gene GBA1, reduce lysosomal GluCer levels, emerging lysosomal GluCer accumulation as a potential PD driver.	Glucosylceramides	89-95	glucosylceramidase beta	Homo sapiens	66-70
32172343-9	2020	Both ATP10B and glucocerebrosidase 1, encoded by the PD risk gene GBA1, reduce lysosomal GluCer levels, emerging lysosomal GluCer accumulation as a potential PD driver.	Glucosylceramides	123-129	ATPase phospholipid transporting 10B (putative)	Homo sapiens	5-11
32172343-9	2020	Both ATP10B and glucocerebrosidase 1, encoded by the PD risk gene GBA1, reduce lysosomal GluCer levels, emerging lysosomal GluCer accumulation as a potential PD driver.	Glucosylceramides	123-129	glucosylceramidase beta	Homo sapiens	66-70
32424263-1	2020	The only enzyme in the glycosphingolipid (GSL) metabolic pathway, which produces glucosylceramide (GlcCer) de novo is UDP-glucose ceramide glucosyltransferase (UGCG).	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	118-158
32424263-1	2020	The only enzyme in the glycosphingolipid (GSL) metabolic pathway, which produces glucosylceramide (GlcCer) de novo is UDP-glucose ceramide glucosyltransferase (UGCG).	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	160-164
32424263-1	2020	The only enzyme in the glycosphingolipid (GSL) metabolic pathway, which produces glucosylceramide (GlcCer) de novo is UDP-glucose ceramide glucosyltransferase (UGCG).	Glucosylceramides	99-105	UDP-glucose ceramide glucosyltransferase	Homo sapiens	118-158
32424263-1	2020	The only enzyme in the glycosphingolipid (GSL) metabolic pathway, which produces glucosylceramide (GlcCer) de novo is UDP-glucose ceramide glucosyltransferase (UGCG).	Glucosylceramides	99-105	UDP-glucose ceramide glucosyltransferase	Homo sapiens	160-164
32229586-4	2020	Glucosylceramide (GlcCer) is a ubiquitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	145-185
32229586-4	2020	Glucosylceramide (GlcCer) is a ubiquitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	187-191
32229586-4	2020	Glucosylceramide (GlcCer) is a ubiquitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	18-24	UDP-glucose ceramide glucosyltransferase	Homo sapiens	79-104
32229586-4	2020	Glucosylceramide (GlcCer) is a ubiquitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	18-24	UDP-glucose ceramide glucosyltransferase	Homo sapiens	145-185
32229586-4	2020	Glucosylceramide (GlcCer) is a ubiquitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	18-24	UDP-glucose ceramide glucosyltransferase	Homo sapiens	187-191
32229586-5	2020	Stressed cells increase de novo biosynthesis of ceramides, which return to sub-toxic levels after UGCG-mediate incorporation into GlcCer.	Glucosylceramides	130-136	UDP-glucose ceramide glucosyltransferase	Homo sapiens	98-102
32032363-3	2020	Here we examined the role of the sphingolipid, glucosylceramide, in influenza virus infection by knocking out the enzyme responsible for its synthesis, glucosylceramide synthase (UGCG).	Glucosylceramides	47-63	UDP-glucose ceramide glucosyltransferase	Homo sapiens	179-183
32229586-4	2020	Glucosylceramide (GlcCer) is a ubiquitous glycosphingolipid (GSL) generated by glucosylceramide synthase, a key regulatory enzyme encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	79-104
32144204-1	2020	beta-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide.	Glucosylceramides	41-57	glucosidase, beta, acid	Mus musculus	0-23
32144204-1	2020	beta-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide.	Glucosylceramides	41-57	glucosidase, beta, acid	Mus musculus	25-28
32144204-1	2020	beta-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide.	Glucosylceramides	59-65	glucosidase, beta, acid	Mus musculus	0-23
32144204-1	2020	beta-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide.	Glucosylceramides	59-65	glucosidase, beta, acid	Mus musculus	25-28
32144204-2	2020	Previously, we demonstrated that lysosomal GBA1 and non-lysosomal GBA2 possess not only GlcCer hydrolase activity, but also transglucosylation activity to transfer the glucose residue from GlcCer to cholesterol to form beta-cholesterylglucoside (beta-GlcChol) in vitro beta-GlcChol is a member of sterylglycosides present in diverse species.	Glucosylceramides	88-94	glucosidase, beta, acid	Mus musculus	43-47
32144204-2	2020	Previously, we demonstrated that lysosomal GBA1 and non-lysosomal GBA2 possess not only GlcCer hydrolase activity, but also transglucosylation activity to transfer the glucose residue from GlcCer to cholesterol to form beta-cholesterylglucoside (beta-GlcChol) in vitro beta-GlcChol is a member of sterylglycosides present in diverse species.	Glucosylceramides	88-94	glucosidase beta 2	Mus musculus	66-70
31972222-4	2020	Compared to parental cell lines, oxaliplatin-resistant cells have increased expression of GCS protein associated with increased levels of the pro-survival ceramide metabolite, glucosylceramide (GlcCer).	Glucosylceramides	176-192	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-93
31972222-4	2020	Compared to parental cell lines, oxaliplatin-resistant cells have increased expression of GCS protein associated with increased levels of the pro-survival ceramide metabolite, glucosylceramide (GlcCer).	Glucosylceramides	194-200	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-93
31972222-5	2020	Inhibition of GCS expression by RNAi-mediated gene knockdown resulted in a reduction in cellular GlcCer levels, with restored sensitivity to oxaliplatin.	Glucosylceramides	97-103	UDP-glucose ceramide glucosyltransferase	Homo sapiens	14-17
31972222-7	2020	GlcCer, formed by GCS-mediated ceramide glycosylation, is the precursor to a complex array of glycosphingolipids.	Glucosylceramides	0-6	UDP-glucose ceramide glucosyltransferase	Homo sapiens	18-21
32032363-3	2020	Here we examined the role of the sphingolipid, glucosylceramide, in influenza virus infection by knocking out the enzyme responsible for its synthesis, glucosylceramide synthase (UGCG).	Glucosylceramides	152-168	UDP-glucose ceramide glucosyltransferase	Homo sapiens	179-183
31138658-8	2019	sptl-1(c363g)-derived neuronal defects were copied in animals with defective sphingolipid biosynthetic enzymes downstream of SPTL-1, including ceramide glucosyltransferases, suggesting that SPTLC1C133W contributes to the HSAN1 pathogenesis by limiting the production of complex sphingolipids, including glucosylceramide.	Glucosylceramides	303-319	Aminotran_1_2 domain-containing protein;Serine palmitoyltransferase 1	Caenorhabditis elegans	0-6
31914593-3	2020	Here, we demonstrate that glucosylceramide (GlcCer) and its synthase, glucosylceramide synthase (GCS), are key determinants of MSC differentiation into adipocytes or osteoblasts.	Glucosylceramides	44-50	UDP-glucose ceramide glucosyltransferase	Homo sapiens	70-95
31914593-3	2020	Here, we demonstrate that glucosylceramide (GlcCer) and its synthase, glucosylceramide synthase (GCS), are key determinants of MSC differentiation into adipocytes or osteoblasts.	Glucosylceramides	44-50	UDP-glucose ceramide glucosyltransferase	Homo sapiens	97-100
31914593-6	2020	Treatment with GlcCer sufficiently rescued adipogenesis and inhibited osteogenesis in GCS knockdown MSCs.	Glucosylceramides	15-21	UDP-glucose ceramide glucosyltransferase	Homo sapiens	86-89
31914593-7	2020	Mechanistically, GlcCer interacted directly with PPARgamma through A/B domain and synergistically enhanced rosiglitazone-induced PPARgamma activation without changing PPARgamma expression, thereby treatment with exogenous GlcCer increased adipogenesis and inhibited osteogenesis.	Glucosylceramides	17-23	peroxisome proliferator activated receptor gamma	Homo sapiens	49-58
31914593-7	2020	Mechanistically, GlcCer interacted directly with PPARgamma through A/B domain and synergistically enhanced rosiglitazone-induced PPARgamma activation without changing PPARgamma expression, thereby treatment with exogenous GlcCer increased adipogenesis and inhibited osteogenesis.	Glucosylceramides	17-23	peroxisome proliferator activated receptor gamma	Homo sapiens	129-138
31914593-7	2020	Mechanistically, GlcCer interacted directly with PPARgamma through A/B domain and synergistically enhanced rosiglitazone-induced PPARgamma activation without changing PPARgamma expression, thereby treatment with exogenous GlcCer increased adipogenesis and inhibited osteogenesis.	Glucosylceramides	17-23	peroxisome proliferator activated receptor gamma	Homo sapiens	129-138
31914593-7	2020	Mechanistically, GlcCer interacted directly with PPARgamma through A/B domain and synergistically enhanced rosiglitazone-induced PPARgamma activation without changing PPARgamma expression, thereby treatment with exogenous GlcCer increased adipogenesis and inhibited osteogenesis.	Glucosylceramides	222-228	peroxisome proliferator activated receptor gamma	Homo sapiens	49-58
31727994-4	2019	Oral administration of plant glucosylceramide (GlcCer) to APP overexpressing mice markedly reduced Abeta levels and plaque burdens and improved cognition in a Y-maze learning task.	Glucosylceramides	29-45	amyloid beta (A4) precursor protein	Mus musculus	99-104
31727994-4	2019	Oral administration of plant glucosylceramide (GlcCer) to APP overexpressing mice markedly reduced Abeta levels and plaque burdens and improved cognition in a Y-maze learning task.	Glucosylceramides	47-53	amyloid beta (A4) precursor protein	Mus musculus	99-104
31727994-5	2019	Moreover, there were substantial increases in the neuronal marker NCAM-1, L1CAM, and Abeta in EVs isolated from serum and brain tissues of the GlcCer-treated AD model mice.	Glucosylceramides	143-149	neural cell adhesion molecule 1	Mus musculus	66-72
31727994-5	2019	Moreover, there were substantial increases in the neuronal marker NCAM-1, L1CAM, and Abeta in EVs isolated from serum and brain tissues of the GlcCer-treated AD model mice.	Glucosylceramides	143-149	L1 cell adhesion molecule	Mus musculus	74-79
31727994-5	2019	Moreover, there were substantial increases in the neuronal marker NCAM-1, L1CAM, and Abeta in EVs isolated from serum and brain tissues of the GlcCer-treated AD model mice.	Glucosylceramides	143-149	amyloid beta (A4) precursor protein	Mus musculus	85-90
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	47-63	glucosidase, beta, acid	Danio rerio	10-14
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	47-63	glucosidase, beta (bile acid) 2	Danio rerio	34-38
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	65-71	glucosidase, beta, acid	Danio rerio	10-14
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	65-71	glucosidase, beta (bile acid) 2	Danio rerio	34-38
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	65-71	glucosidase, beta, acid	Danio rerio	74-78
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	186-192	glucosidase, beta, acid	Danio rerio	10-14
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	186-192	glucosidase, beta (bile acid) 2	Danio rerio	34-38
31562193-2	2019	Lysosomal GBA1 and cytosol-facing GBA2 degrade glucosylceramide (GlcCer); GBA1 deficiency causes Gaucher disease, a lysosomal storage disorder characterized by lysosomal accumulation of GlcCer, which is partly converted to glucosylsphingosine (GlcSph).	Glucosylceramides	186-192	glucosidase, beta, acid	Danio rerio	74-78
31562193-3	2019	GBA1 and GBA2 also may transfer glucose from GlcCer to cholesterol, yielding glucosylated cholesterol (GlcChol).	Glucosylceramides	45-51	glucosidase, beta, acid	Danio rerio	0-4
31562193-3	2019	GBA1 and GBA2 also may transfer glucose from GlcCer to cholesterol, yielding glucosylated cholesterol (GlcChol).	Glucosylceramides	45-51	glucosidase, beta (bile acid) 2	Danio rerio	9-13
31666638-1	2019	UDP-glucose ceramide glucosyltransferase (UGCG) is the key enzyme in glycosphingolipid (GSL) metabolism by being the only enzyme that generates glucosylceramide (GlcCer) de novo.	Glucosylceramides	144-160	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-40
31666638-1	2019	UDP-glucose ceramide glucosyltransferase (UGCG) is the key enzyme in glycosphingolipid (GSL) metabolism by being the only enzyme that generates glucosylceramide (GlcCer) de novo.	Glucosylceramides	144-160	UDP-glucose ceramide glucosyltransferase	Homo sapiens	42-46
31666638-1	2019	UDP-glucose ceramide glucosyltransferase (UGCG) is the key enzyme in glycosphingolipid (GSL) metabolism by being the only enzyme that generates glucosylceramide (GlcCer) de novo.	Glucosylceramides	162-168	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-40
31666638-1	2019	UDP-glucose ceramide glucosyltransferase (UGCG) is the key enzyme in glycosphingolipid (GSL) metabolism by being the only enzyme that generates glucosylceramide (GlcCer) de novo.	Glucosylceramides	162-168	UDP-glucose ceramide glucosyltransferase	Homo sapiens	42-46
31660434-7	2019	An enhanced Gba1 activity elevates ceramide levels responsible for apoptosis and decreases glucosylceramides to overcome drug resistance.	Glucosylceramides	91-108	glucosidase, beta, acid	Mus musculus	12-16
31208914-2	2019	Here, we evaluated the potential of substrate reduction therapy (SRT) using an inhibitor of glucosylceramide synthase (GCS) to decrease the synthesis of glucosylceramide (GL1) and related glycosphingolipids.	Glucosylceramides	92-108	UDP-glucose ceramide glucosyltransferase	Mus musculus	119-122
31447678-4	2019	Glucosylceramide is the main precursor of complex glycosphingolipids that is degraded by lysosomal (GBA1) or non-lysosomal (GBA2) glucocerebrosidase.	Glucosylceramides	0-16	glucosidase, beta, acid	Mus musculus	100-104
31447678-4	2019	Glucosylceramide is the main precursor of complex glycosphingolipids that is degraded by lysosomal (GBA1) or non-lysosomal (GBA2) glucocerebrosidase.	Glucosylceramides	0-16	glucosidase beta 2	Mus musculus	124-128
31447678-4	2019	Glucosylceramide is the main precursor of complex glycosphingolipids that is degraded by lysosomal (GBA1) or non-lysosomal (GBA2) glucocerebrosidase.	Glucosylceramides	0-16	glucosidase, beta, acid	Mus musculus	130-148
31819005-4	2020	Although the GlcCer biosynthetic pathway has been elucidated, little is known about GlcCer catabolism, and a plant GlcCer-degrading enzyme (glucosylceramidase (GCD)) has yet to be identified.	Glucosylceramides	13-19	glucosylceramidase beta	Homo sapiens	160-163
31819005-11	2020	Our results indicate that AtGCD3 is a plant glucosylceramidase that participates in GlcCer catabolism by preferentially hydrolyzing long-acyl-chain GlcCers.	Glucosylceramides	84-90	glucosylceramidase beta	Homo sapiens	44-62
31819005-11	2020	Our results indicate that AtGCD3 is a plant glucosylceramidase that participates in GlcCer catabolism by preferentially hydrolyzing long-acyl-chain GlcCers.	Glucosylceramides	148-155	glucosylceramidase beta	Homo sapiens	44-62
31931749-4	2020	At the cellular level, deficiency of GBA1 disturbs lysosomal storage with buildup of glucocerebroside.	Glucosylceramides	85-101	glucosylceramidase beta	Homo sapiens	37-41
31914593-0	2020	Glucosylceramide synthase regulates adipo-osteogenic differentiation through synergistic activation of PPARgamma with GlcCer.	Glucosylceramides	118-124	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
31914593-3	2020	Here, we demonstrate that glucosylceramide (GlcCer) and its synthase, glucosylceramide synthase (GCS), are key determinants of MSC differentiation into adipocytes or osteoblasts.	Glucosylceramides	26-42	UDP-glucose ceramide glucosyltransferase	Homo sapiens	70-95
31914593-3	2020	Here, we demonstrate that glucosylceramide (GlcCer) and its synthase, glucosylceramide synthase (GCS), are key determinants of MSC differentiation into adipocytes or osteoblasts.	Glucosylceramides	26-42	UDP-glucose ceramide glucosyltransferase	Homo sapiens	97-100
31265321-4	2019	Glucosylceramide (GlcCer), the initial GSL synthesized from ceramide by glucosylceramide synthase (GCS), is required for embryonic survival, but its role in the lung is unknown.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Mus musculus	72-97
31265321-4	2019	Glucosylceramide (GlcCer), the initial GSL synthesized from ceramide by glucosylceramide synthase (GCS), is required for embryonic survival, but its role in the lung is unknown.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Mus musculus	99-102
31265321-4	2019	Glucosylceramide (GlcCer), the initial GSL synthesized from ceramide by glucosylceramide synthase (GCS), is required for embryonic survival, but its role in the lung is unknown.	Glucosylceramides	18-24	UDP-glucose ceramide glucosyltransferase	Mus musculus	72-97
31265321-4	2019	Glucosylceramide (GlcCer), the initial GSL synthesized from ceramide by glucosylceramide synthase (GCS), is required for embryonic survival, but its role in the lung is unknown.	Glucosylceramides	18-24	UDP-glucose ceramide glucosyltransferase	Mus musculus	99-102
31562193-8	2019	GlcCer was comparable in gba1 -/- and WT larvae but increased in gba2 -/- and gba1 -/- :gba2 -/- larvae.	Glucosylceramides	0-6	glucosidase, beta, acid	Danio rerio	25-29
31562193-8	2019	GlcCer was comparable in gba1 -/- and WT larvae but increased in gba2 -/- and gba1 -/- :gba2 -/- larvae.	Glucosylceramides	0-6	glucosidase, beta (bile acid) 2	Danio rerio	65-69
31562193-8	2019	GlcCer was comparable in gba1 -/- and WT larvae but increased in gba2 -/- and gba1 -/- :gba2 -/- larvae.	Glucosylceramides	0-6	glucosidase, beta, acid	Danio rerio	78-82
31562193-8	2019	GlcCer was comparable in gba1 -/- and WT larvae but increased in gba2 -/- and gba1 -/- :gba2 -/- larvae.	Glucosylceramides	0-6	glucosidase, beta (bile acid) 2	Danio rerio	88-92
31562193-11	2019	Inhibition of GlcCer synthase (GCS) in Gba1-deficient larvae reduced GlcCer and GlcSph, and concomitant inhibition of GCS and Gba2 with iminosugars also reduced excessive GlcChol.	Glucosylceramides	14-20	glucosidase, beta, acid	Danio rerio	39-43
33569519-1	2021	The nonlysosomal glucosylceramidase beta2 (GBA2) gene encode an enzyme that catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Glucosylceramides	104-120	glucosylceramidase beta 2	Homo sapiens	17-41
33569519-1	2021	The nonlysosomal glucosylceramidase beta2 (GBA2) gene encode an enzyme that catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Glucosylceramides	104-120	glucosylceramidase beta 2	Homo sapiens	43-47
31138658-11	2019	By showing that the phenotypes observed in a C. elegans model of HSAN1 disease could be caused by loss of a downstream product (glucosylceramide) rather than the accumulation of a toxic byproduct, our work provides new insights into the origins of the symptoms of inherited metabolic diseases while expanding the repertoire of sphingolipid functions, specifically, of glucosylceramides.	Glucosylceramides	128-144	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	65-70
31138658-11	2019	By showing that the phenotypes observed in a C. elegans model of HSAN1 disease could be caused by loss of a downstream product (glucosylceramide) rather than the accumulation of a toxic byproduct, our work provides new insights into the origins of the symptoms of inherited metabolic diseases while expanding the repertoire of sphingolipid functions, specifically, of glucosylceramides.	Glucosylceramides	368-385	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	65-70
31138658-9	2019	Overexpression of SPTL-1(C121W) led to similar epithelial and neuronal defects and to reduced levels of complex sphingolipids, specifically glucosylceramide, consistent with a dominant-negative effect of SPTL-1(C121W) that is mediated by loss of this downstream product.	Glucosylceramides	140-156	Aminotran_1_2 domain-containing protein;Serine palmitoyltransferase 1	Caenorhabditis elegans	18-24
31333408-6	2019	We previously demonstrated that glucosylceramide accumulated by GBA1 deficiency promotes the conversion of alphaSyn into a proteinase K-resistant conformation.	Glucosylceramides	32-48	glucosylceramidase beta	Homo sapiens	64-68
31333408-6	2019	We previously demonstrated that glucosylceramide accumulated by GBA1 deficiency promotes the conversion of alphaSyn into a proteinase K-resistant conformation.	Glucosylceramides	32-48	synuclein alpha	Homo sapiens	107-115
30689867-7	2019	Dm mice showed an increased level of glucosylsphingosine without any noticeable accumulation of glucosylceramide, a direct substrate of GBA.	Glucosylceramides	96-112	glucosidase, beta, acid	Mus musculus	136-139
31234327-1	2019	The role of glucosylsphingosine (lyso-Gb1), a downstream metabolic product of glucosylceramide, for monitoring treated and untreated children with Gaucher disease (GD) has not yet been studied.	Glucosylceramides	78-94	gamma-aminobutyric acid type B receptor subunit 1	Homo sapiens	38-41
30864417-0	2019	Assay of beta-glucosidase 2 (GBA2) activity using lithocholic acid beta-3-O-glucoside substrate for cultured fibroblasts and glucosylceramide for brain tissue.	Glucosylceramides	125-141	glucosylceramidase beta 2	Homo sapiens	29-33
30864417-4	2019	We studied GBA2 activity, using lithocholic acid beta-glucoside or glucosylceramide as natural beta-glucosidase substrates in murine tissues or cultured patient fibroblasts with the pathologic genotypes: Gba1-/-; Gba2-/-; GBA1-/-; GBA2+/- and found expected and unexpected deviations from normal controls.	Glucosylceramides	67-83	glucosidase beta 2	Mus musculus	11-15
31051284-10	2019	UDP-glucose ceramide glucosyltransferase (Ugcg), the first rate limiting step in the glucosylceramide biosynthesis pathway, was inhibited via chemical compounds and shRNA knockdown in vivo and in vitro.	Glucosylceramides	85-101	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-40
31051284-10	2019	UDP-glucose ceramide glucosyltransferase (Ugcg), the first rate limiting step in the glucosylceramide biosynthesis pathway, was inhibited via chemical compounds and shRNA knockdown in vivo and in vitro.	Glucosylceramides	85-101	UDP-glucose ceramide glucosyltransferase	Homo sapiens	42-46
31051284-11	2019	beta-1,4-Galactosyltransferase (B4Galt) 5 and 6, enzymes that convert glucosylceramides into potentially inactive lactosylceramides, were subjected to shRNA knock down.	Glucosylceramides	70-87	beta-1,4-galactosyltransferase 5	Homo sapiens	32-47
31363476-2	2019	It is a deficiency of lysosomal glucocerebrosidase (GBA) due to biallelic mutations in the GBA gene, characterized by the deposition of glucocerebroside in macrophage-monocyte system cells.	Glucosylceramides	136-152	glucosylceramidase beta	Homo sapiens	52-55
31363476-2	2019	It is a deficiency of lysosomal glucocerebrosidase (GBA) due to biallelic mutations in the GBA gene, characterized by the deposition of glucocerebroside in macrophage-monocyte system cells.	Glucosylceramides	136-152	glucosylceramidase beta	Homo sapiens	91-94
33654788-4	2019	GCS that converts ceramide into glucosylceramide is a limiting-enzyme in the syntheses of glycosphingolipids and is one cause of cancer drug resistance.	Glucosylceramides	32-48	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-3
31114500-3	2019	Alternatively, ceramide can be converted to glucosylceramide (GlcCer) by the GlcCer synthase (GCS), encoded by the UGCG gene.	Glucosylceramides	44-60	UDP-glucose ceramide glucosyltransferase	Homo sapiens	115-119
30895685-1	2019	beta-Glucocerebrosidase (GBA) is the enzyme that degrades glucosylceramide in lysosomes.	Glucosylceramides	58-74	glucosylceramidase beta	Homo sapiens	0-23
30895685-1	2019	beta-Glucocerebrosidase (GBA) is the enzyme that degrades glucosylceramide in lysosomes.	Glucosylceramides	58-74	glucosylceramidase beta	Homo sapiens	25-28
30895685-2	2019	Defects in GBA that result in overall loss of enzymatic activity give rise to the lysosomal storage disorder Gaucher disease, which is characterized by the accumulation of glucosylceramide in tissue macrophages.	Glucosylceramides	172-188	glucosylceramidase beta	Homo sapiens	11-14
31114500-3	2019	Alternatively, ceramide can be converted to glucosylceramide (GlcCer) by the GlcCer synthase (GCS), encoded by the UGCG gene.	Glucosylceramides	62-68	UDP-glucose ceramide glucosyltransferase	Homo sapiens	115-119
30231605-2	2019	Glucosylceramide synthase (GCS) is a key enzyme for the synthesis of glucosylceramide (GlcCer), which is a main ceramide metabolism pathway in mammalian cells.	Glucosylceramides	69-85	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
30639288-0	2019	Psd2 pea defensin shows a preference for mimetic membrane rafts enriched with glucosylceramide and ergosterol.	Glucosylceramides	78-94	pleckstrin and Sec7 domain containing 2	Homo sapiens	0-4
30639288-3	2019	Protein-lipid overlay assays indicated that Psd2 recognizes Fusarium solani glucosylceramide (GlcCerF.solani) and ergosterol (Erg) in addition to phosphatidylcholine (POPC) and some phosphatidylinositol species, such as PtdIns (3)P, (5)P and (3,5)P2, suggesting that these lipids may play important roles as Psd2 targets.	Glucosylceramides	76-92	pleckstrin and Sec7 domain containing 2	Homo sapiens	44-48
30639288-5	2019	Surface plasmon resonance analysis showed that Psd2 has a higher affinity for pure POPC and POPC-based vesicles containing GlcCer and Erg at a 70:30 proportion than for vesicles containing cholesterol (Chol).	Glucosylceramides	123-129	pleckstrin and Sec7 domain containing 2	Homo sapiens	47-51
30639288-8	2019	Furthermore, we showed that the presence of C8C9 double bonds and a methyl group at position C9 of the sphingoid base backbone of GlcCer was relevant to Psd2 activity against Aspergillus nidulans.	Glucosylceramides	130-136	pleckstrin and Sec7 domain containing 2	Homo sapiens	153-157
30662006-1	2019	The nonlysosomal glucosylceramidase beta2 (GBA2) catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Glucosylceramides	77-93	glucosidase beta 2	Mus musculus	43-47
30231605-2	2019	Glucosylceramide synthase (GCS) is a key enzyme for the synthesis of glucosylceramide (GlcCer), which is a main ceramide metabolism pathway in mammalian cells.	Glucosylceramides	87-93	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
30231605-2	2019	Glucosylceramide synthase (GCS) is a key enzyme for the synthesis of glucosylceramide (GlcCer), which is a main ceramide metabolism pathway in mammalian cells.	Glucosylceramides	87-93	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
29900534-3	2019	Gaucher disease is caused by the loss of activity of glucocerebrosidase, leading to accumulation of glucosylceramide.	Glucosylceramides	100-116	glucosidase, beta, acid	Mus musculus	53-71
30315684-2	2019	In the biallelic state (homozygous or compound heterozygous) mutations in the glucocerebrosidase gene (GBA) may cause GD, in which glucosylceramide, the sphingolipid substrate of the glucocerebrosidase enzyme (GCase), accumulates in visceral organs leading to a number of clinical phenotypes.	Glucosylceramides	131-147	glucosylceramidase beta	Homo sapiens	103-106
30231605-2	2019	Glucosylceramide synthase (GCS) is a key enzyme for the synthesis of glucosylceramide (GlcCer), which is a main ceramide metabolism pathway in mammalian cells.	Glucosylceramides	69-85	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
30530492-5	2019	Moreover, ATP10D SNPs are associated with elevated levels of glucosylceramide (GlcCer) in plasma from diverse European populations.	Glucosylceramides	61-77	ATPase phospholipid transporting 10D (putative)	Homo sapiens	10-16
30530492-5	2019	Moreover, ATP10D SNPs are associated with elevated levels of glucosylceramide (GlcCer) in plasma from diverse European populations.	Glucosylceramides	79-85	ATPase phospholipid transporting 10D (putative)	Homo sapiens	10-16
30530492-7	2019	Here, we identify a conserved clade of P4-ATPases from Saccharomyces cerevisiae (Dnf1, Dnf2), Schizosaccharomyces pombe (Dnf2), and Homo sapiens (ATP10A, ATP10D) that transport GlcCer bearing an sn2 acyl-linked fluorescent tag.	Glucosylceramides	177-183	aminophospholipid-translocating P4-type ATPase DNF1	Saccharomyces cerevisiae S288C	81-85
30530492-7	2019	Here, we identify a conserved clade of P4-ATPases from Saccharomyces cerevisiae (Dnf1, Dnf2), Schizosaccharomyces pombe (Dnf2), and Homo sapiens (ATP10A, ATP10D) that transport GlcCer bearing an sn2 acyl-linked fluorescent tag.	Glucosylceramides	177-183	aminophospholipid-translocating P4-type ATPase DNF2	Saccharomyces cerevisiae S288C	87-91
30530492-7	2019	Here, we identify a conserved clade of P4-ATPases from Saccharomyces cerevisiae (Dnf1, Dnf2), Schizosaccharomyces pombe (Dnf2), and Homo sapiens (ATP10A, ATP10D) that transport GlcCer bearing an sn2 acyl-linked fluorescent tag.	Glucosylceramides	177-183	aminophospholipid-translocating P4-type ATPase DNF2	Saccharomyces cerevisiae S288C	121-125
30530492-7	2019	Here, we identify a conserved clade of P4-ATPases from Saccharomyces cerevisiae (Dnf1, Dnf2), Schizosaccharomyces pombe (Dnf2), and Homo sapiens (ATP10A, ATP10D) that transport GlcCer bearing an sn2 acyl-linked fluorescent tag.	Glucosylceramides	177-183	ATPase phospholipid transporting 10A (putative)	Homo sapiens	146-152
30600575-1	2019	Glucocerebrosidase (GBA) is a lysosomal beta-glucosidase-degrading glucosylceramide.	Glucosylceramides	67-83	glucosidase, beta, acid	Mus musculus	0-18
30600575-1	2019	Glucocerebrosidase (GBA) is a lysosomal beta-glucosidase-degrading glucosylceramide.	Glucosylceramides	67-83	glucosidase, beta, acid	Mus musculus	20-23
29750412-0	2019	ACBD3 is required for FAPP2 transferring glucosylceramide through maintaining the Golgi integrity.	Glucosylceramides	41-57	acyl-CoA binding domain containing 3	Homo sapiens	0-5
29750412-0	2019	ACBD3 is required for FAPP2 transferring glucosylceramide through maintaining the Golgi integrity.	Glucosylceramides	41-57	pleckstrin homology domain containing A8	Homo sapiens	22-27
29750412-2	2019	The four-phosphate adaptor protein FAPP2-mediated glucosylceramide (GlcCer) transport for complex GSL synthesis has been studied extensively.	Glucosylceramides	50-66	pleckstrin homology domain containing A8	Homo sapiens	35-40
29750412-2	2019	The four-phosphate adaptor protein FAPP2-mediated glucosylceramide (GlcCer) transport for complex GSL synthesis has been studied extensively.	Glucosylceramides	68-74	pleckstrin homology domain containing A8	Homo sapiens	35-40
30627514-3	2019	GD is caused by decreased or absent activity of beta-glucosidase with subsequent accumulation of the substrate glucosylceramide in macrophages due to genetic alterations in the GBA gene.	Glucosylceramides	111-127	glucosylceramidase beta	Homo sapiens	177-180
30578288-1	2019	Gaucher disease (GD) is a rare lysosomal storage disorder caused by mutations in the GBA1 gene, encoding the lysosome-resident glucocerebrosidase enzyme involved in the hydrolysis of glucosylceramide.	Glucosylceramides	183-199	glucosylceramidase beta	Homo sapiens	85-89
30578288-1	2019	Gaucher disease (GD) is a rare lysosomal storage disorder caused by mutations in the GBA1 gene, encoding the lysosome-resident glucocerebrosidase enzyme involved in the hydrolysis of glucosylceramide.	Glucosylceramides	183-199	glucosidase, beta, acid	Mus musculus	127-145
30242129-0	2018	Complex formation of sphingomyelin synthase 1 with glucosylceramide synthase increases sphingomyelin and decreases glucosylceramide levels.	Glucosylceramides	51-67	sphingomyelin synthase 1	Homo sapiens	21-45
30242129-6	2018	Fusion of the SMS1 N terminus to the GCS C terminus via linkers of different lengths increased SM synthesis and decreased GlcCer synthesis in vivo These results suggest that formation of the SMS1-GCS heteromeric complex increases SM synthesis and decreases GlcCer synthesis.	Glucosylceramides	122-128	sphingomyelin synthase 1	Homo sapiens	14-18
30242129-6	2018	Fusion of the SMS1 N terminus to the GCS C terminus via linkers of different lengths increased SM synthesis and decreased GlcCer synthesis in vivo These results suggest that formation of the SMS1-GCS heteromeric complex increases SM synthesis and decreases GlcCer synthesis.	Glucosylceramides	122-128	UDP-glucose ceramide glucosyltransferase	Homo sapiens	37-40
30242129-6	2018	Fusion of the SMS1 N terminus to the GCS C terminus via linkers of different lengths increased SM synthesis and decreased GlcCer synthesis in vivo These results suggest that formation of the SMS1-GCS heteromeric complex increases SM synthesis and decreases GlcCer synthesis.	Glucosylceramides	122-128	sphingomyelin synthase 1	Homo sapiens	191-195
30242129-6	2018	Fusion of the SMS1 N terminus to the GCS C terminus via linkers of different lengths increased SM synthesis and decreased GlcCer synthesis in vivo These results suggest that formation of the SMS1-GCS heteromeric complex increases SM synthesis and decreases GlcCer synthesis.	Glucosylceramides	122-128	UDP-glucose ceramide glucosyltransferase	Homo sapiens	196-199
30461613-1	2018	RATIONALE: Gaucher disease (GD), characterized by glucosylceramide accumulation in the macrophage-monocyte system, is caused by glucosidase b acid (GBA) gene mutations which lead to the deficiency of lysosomal enzyme glucocerebrosidase.	Glucosylceramides	50-66	glucosylceramidase beta	Homo sapiens	148-151
30099023-1	2018	Gaucher disease (GD) is a rare autosomal recessive disorder caused by deficient activity of beta-glucocerebrosidase resulting in the accumulation of glucosylceramide.	Glucosylceramides	149-165	glucosylceramidase beta	Homo sapiens	92-115
30550553-3	2018	We have addressed the mechanisms that might regulate the association between GLTP and the VAP proteins by studying the capacity of GLTP to recognize different N-linked acyl chain species of glucosylceramide.	Glucosylceramides	190-206	glycolipid transfer protein	Homo sapiens	131-135
30242129-2	2018	Sphingomyelin synthase 1 (SMS1) and glucosylceramide synthase (GCS) are key enzymes that catalyze the conversion of Cer to SM and GlcCer, respectively.	Glucosylceramides	130-136	sphingomyelin synthase 1	Homo sapiens	0-24
30242129-2	2018	Sphingomyelin synthase 1 (SMS1) and glucosylceramide synthase (GCS) are key enzymes that catalyze the conversion of Cer to SM and GlcCer, respectively.	Glucosylceramides	130-136	sphingomyelin synthase 1	Homo sapiens	26-30
30242129-2	2018	Sphingomyelin synthase 1 (SMS1) and glucosylceramide synthase (GCS) are key enzymes that catalyze the conversion of Cer to SM and GlcCer, respectively.	Glucosylceramides	130-136	UDP-glucose ceramide glucosyltransferase	Homo sapiens	36-61
30242129-2	2018	Sphingomyelin synthase 1 (SMS1) and glucosylceramide synthase (GCS) are key enzymes that catalyze the conversion of Cer to SM and GlcCer, respectively.	Glucosylceramides	130-136	UDP-glucose ceramide glucosyltransferase	Homo sapiens	63-66
30206120-4	2018	Using this domain, FAPP2 transports glucosylceramide from its cis-Golgi synthesis site to the trans-Golgi for conversion into complex GSLs.	Glucosylceramides	36-52	pleckstrin homology domain containing A8	Homo sapiens	19-24
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	48-52
30308956-1	2018	The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.	Glucosylceramides	112-128	glucosylceramidase beta 2	Homo sapiens	4-8
30308956-1	2018	The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.	Glucosylceramides	112-128	glucosylceramidase beta 2	Homo sapiens	26-58
30308956-1	2018	The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.	Glucosylceramides	112-128	glucosylceramidase beta 2	Homo sapiens	60-66
30308956-1	2018	The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.	Glucosylceramides	130-136	glucosylceramidase beta 2	Homo sapiens	4-8
30308956-1	2018	The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.	Glucosylceramides	130-136	glucosylceramidase beta 2	Homo sapiens	26-58
30308956-1	2018	The GBA2 gene encodes the non-lysosomal glucosylceramidase (NLGase), an enzyme that catalyzes the conversion of glucosylceramide (GlcCer) to ceramide and glucose.	Glucosylceramides	130-136	glucosylceramidase beta 2	Homo sapiens	60-66
30308956-8	2018	We conclude that the c.1780G>C mutation results in NLGase loss of function with abolishment of the enzymatic activity and accumulation of GlcCer accompanied by a compensatory increase in GCase.	Glucosylceramides	138-144	glucosylceramidase beta 2	Homo sapiens	51-57
29385658-8	2018	It has also been suggested that accumulation of GCase substrates glucosylceramide/glucosylsphingosine may contribute to GBA-PD pathogenesis.	Glucosylceramides	65-81	glucosylceramidase beta	Homo sapiens	120-123
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	170-186	glucosylceramidase beta	Homo sapiens	84-104
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	170-186	glucosylceramidase beta	Homo sapiens	106-110
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	170-186	synuclein alpha	Homo sapiens	306-314
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	188-194	glucosylceramidase beta	Homo sapiens	84-104
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	188-194	glucosylceramidase beta	Homo sapiens	106-110
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	188-194	synuclein alpha	Homo sapiens	306-314
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	270-276	glucosylceramidase beta	Homo sapiens	84-104
29305919-5	2018	Furthermore, genetic and clinicopathological studies have revealed mutations in the glucocerebrosidase 1 (GBA1) gene, which encodes a degrading enzyme for the glycolipid glucosylceramide (GlcCer), as strong risk factors for PD and DLB, and we recently demonstrated that GlcCer promotes toxic conversion of alphaSyn.	Glucosylceramides	270-276	glucosylceramidase beta	Homo sapiens	106-110
30206272-0	2018	Glucosylceramide modifies the LPS-induced inflammatory response in macrophages and the orientation of the LPS/TLR4 complex in silico.	Glucosylceramides	0-16	toll like receptor 4	Homo sapiens	110-114
30237856-4	2018	By comparing parental MEC-2 cells, a human CLL cell line, we found that flu-resistant clonal cells were significantly increased lethal dose 50 of flu concentration, and up-regulated expression of P-glycoprotein, a drug-resistant marker, glucosylceramide synthase (GCS), an enzyme that can convert ceramide to glucosylceramide, and CD34, a leukemia stem cell marker.	Glucosylceramides	237-253	ATP binding cassette subfamily B member 1	Homo sapiens	196-210
30237856-5	2018	Overexpression of GCS leads to promptly elimination of cellular ceramide levels and accumulation of glucosylceramide, which reduces apoptosis and promotes survival and proliferation of flu-resistant clonal cells.	Glucosylceramides	100-116	UDP-glucose ceramide glucosyltransferase	Homo sapiens	18-21
30237856-7	2018	We also found that elevating glucosylceramide levels in flu-resistant clonal cells was associated with up-regulation of GCS and CD34 expression.	Glucosylceramides	29-45	UDP-glucose ceramide glucosyltransferase	Homo sapiens	120-123
30237856-7	2018	We also found that elevating glucosylceramide levels in flu-resistant clonal cells was associated with up-regulation of GCS and CD34 expression.	Glucosylceramides	29-45	CD34 molecule	Homo sapiens	128-132
29549423-1	2018	The UDP-glucose ceramide glucosyltransferase (UGCG) is a key enzyme in the synthesis of glycosylated sphingolipids, since this enzyme generates the precursor for all complex glycosphingolipids (GSL), the GlcCer.	Glucosylceramides	204-210	UDP-glucose ceramide glucosyltransferase	Homo sapiens	4-44
29549423-1	2018	The UDP-glucose ceramide glucosyltransferase (UGCG) is a key enzyme in the synthesis of glycosylated sphingolipids, since this enzyme generates the precursor for all complex glycosphingolipids (GSL), the GlcCer.	Glucosylceramides	204-210	UDP-glucose ceramide glucosyltransferase	Homo sapiens	46-50
29549423-6	2018	These cellular effects seem to be mediated by an altered composition of glycosphingolipid-enriched microdomains (GEMs), especially an accumulation of globotriaosylceramide (Gb3) and glucosylceramide (GlcCer), which leads to an activation of Akt and ERK1/2.	Glucosylceramides	200-206	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	173-176
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	224-228
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	224-228
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	224-228
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	48-52
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	224-228
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	224-228
30206272-4	2018	Atomistic molecular dynamics simulations of the TLR4 dimer complex (with and without LPS in its MD-2 binding pockets) in membranes (in the presence and absence of GluCer) showed that: (1) LPS induced a tilted orientation of TLR4 and increased dimer integrity; (2) GluCer did not affect the integrity of the LPS/TLR4 dimer but reduced the LPS-induced tilt; and (3) GluCer increased electrostatic interactions between the membrane and the TLR4 extracellular domain, which could potentially modulate the tilt.	Glucosylceramides	264-270	toll like receptor 4	Homo sapiens	224-228
30206272-6	2018	We conclude that the GluCer-induced effects on LPS/TLR4 orientation may influence the signaling capabilities of the LPS/TLR4 complex by affecting its interaction with downstream signaling proteins.	Glucosylceramides	21-27	toll like receptor 4	Homo sapiens	51-55
30206272-6	2018	We conclude that the GluCer-induced effects on LPS/TLR4 orientation may influence the signaling capabilities of the LPS/TLR4 complex by affecting its interaction with downstream signaling proteins.	Glucosylceramides	21-27	toll like receptor 4	Homo sapiens	120-124
29934064-1	2018	Gaucher disease (GD) is an inherited disorder in which mutations in the GBA1 gene lead to deficient beta-glucocerebrosidase activity and accumulation of its substrate glucosylceramide.	Glucosylceramides	167-183	glucosylceramidase beta	Homo sapiens	72-76
29530534-1	2018	Deficiency of beta-glucocerebrosidase (GBA) leads to Gaucher disease (GD), an inherited disorder characterised by storage of glucosylceramide (GlcCer) in lysosomes of tissue macrophages.	Glucosylceramides	125-141	glucosylceramidase beta	Homo sapiens	39-42
30061606-2	2018	Here, we observed that chronic high-fat and high-cholesterol diet intake in a mouse model of atherosclerosis (ApoE-/-) decreases the level of ceramides and glucosylceramide.	Glucosylceramides	156-172	apolipoprotein E	Mus musculus	110-114
29673590-3	2018	Ceramide, glucosylceramide and sphingosine levels were all increased in SK1-/- but less so in SK2-/- cells and S1P levels were not significantly reduced in either SK1-/- or SK2-/- cells.	Glucosylceramides	10-26	sphingosine kinase 1	Mus musculus	72-75
29699937-1	2018	Gaucher disease (GD) is the most common lysosomal storage disease caused by deficiency of beta-glucocerebrosidase (GCase) resulting in lysosomal accumulation of its glycolipid substrate glucosylceramide.	Glucosylceramides	186-202	glucosylceramidase beta	Homo sapiens	115-120
29579237-1	2018	GBA1 encodes the lysosomal enzyme beta-glucocerebrosidase (GCase) which converts glucosylceramide into ceramide and glucose.	Glucosylceramides	81-97	glucosylceramidase beta	Homo sapiens	0-4
29579237-1	2018	GBA1 encodes the lysosomal enzyme beta-glucocerebrosidase (GCase) which converts glucosylceramide into ceramide and glucose.	Glucosylceramides	81-97	glucosylceramidase beta	Homo sapiens	34-57
29627573-2	2018	Here, we report that phophatidylinositol-4-phosphate (PtdIns(4)P) downregulates the cellular glucosylceramide (GlcCer) level by inhibiting the interaction between GlcCer synthase (UGCG) and UDP-glucose in the Golgi apparatus.	Glucosylceramides	93-109	UDP-glucose ceramide glucosyltransferase	Homo sapiens	180-184
29627573-2	2018	Here, we report that phophatidylinositol-4-phosphate (PtdIns(4)P) downregulates the cellular glucosylceramide (GlcCer) level by inhibiting the interaction between GlcCer synthase (UGCG) and UDP-glucose in the Golgi apparatus.	Glucosylceramides	111-117	UDP-glucose ceramide glucosyltransferase	Homo sapiens	180-184
29627573-4	2018	The levels of GlcCer and lactosylceramide, but not of sphingomyelin (SM), were increased following expression of the FAPP1 PH domain in cells, accompanied by an increase in UGCG activity.	Glucosylceramides	14-20	pleckstrin homology domain containing A3	Homo sapiens	117-122
29627573-4	2018	The levels of GlcCer and lactosylceramide, but not of sphingomyelin (SM), were increased following expression of the FAPP1 PH domain in cells, accompanied by an increase in UGCG activity.	Glucosylceramides	14-20	UDP-glucose ceramide glucosyltransferase	Homo sapiens	173-177
29769046-8	2018	Additionally, the conversion of newly synthesized ceramide to sphingomyelin and glucosylceramide at the Golgi is prevented by the inhibition of CERT.	Glucosylceramides	80-96	ceramide transporter 1	Homo sapiens	144-148
29764947-5	2018	Neutral GSLs comprise glucosylceramide and galactosylceramide, which utilize Delta4-Delta8-9-methyl-sphingadienine as a sphingoid base, linked to a C16-18 fatty acid chain, forming ceramide, and to a sugar residue, such as glucose or galactose.	Glucosylceramides	22-38	delta like canonical Notch ligand 4	Homo sapiens	83-92
29272250-1	2018	Gaucher disease (GD) is a lysosomal storage disorder, caused by an impaired function of beta-glucocerebrosidase, which results in accumulation of glucocerebroside in cells, and altered membrane ordering.	Glucosylceramides	146-162	glucosylceramidase beta	Homo sapiens	88-111
30023299-1	2018	Gaucher disease (GD) is a lysosomal storage disorder caused by the deficiency of the beta-glucocerebrosidase enzyme due to disease causing mutations in the GBA1 (glucosidase beta acid) gene, leading to the abnormal accumulation of the lipid glucocerebroside in lysosomal macrophages.	Glucosylceramides	241-257	glucosylceramidase beta	Homo sapiens	156-160
30023299-1	2018	Gaucher disease (GD) is a lysosomal storage disorder caused by the deficiency of the beta-glucocerebrosidase enzyme due to disease causing mutations in the GBA1 (glucosidase beta acid) gene, leading to the abnormal accumulation of the lipid glucocerebroside in lysosomal macrophages.	Glucosylceramides	241-257	glucosylceramidase beta	Homo sapiens	162-183
29530534-1	2018	Deficiency of beta-glucocerebrosidase (GBA) leads to Gaucher disease (GD), an inherited disorder characterised by storage of glucosylceramide (GlcCer) in lysosomes of tissue macrophages.	Glucosylceramides	143-149	glucosylceramidase beta	Homo sapiens	39-42
29409484-1	2018	The UDP-glucose ceramide glycosyltransferase (UGCG) is a key enzyme in the sphingolipid metabolism by generating glucosylceramide (GlcCer), the precursor for all glycosphingolipids (GSL), which are essential for proper cell function.	Glucosylceramides	113-129	UDP-glucose ceramide glucosyltransferase	Homo sapiens	4-44
29438993-7	2018	Moreover, the PGRMC1 inhibitor AG-205 significantly reduced synthesis of hydroxylated ceramide and glucosylceramide in FA2H-expressing cells.	Glucosylceramides	99-115	progesterone receptor membrane component 1	Homo sapiens	14-20
29438993-7	2018	Moreover, the PGRMC1 inhibitor AG-205 significantly reduced synthesis of hydroxylated ceramide and glucosylceramide in FA2H-expressing cells.	Glucosylceramides	99-115	fatty acid 2-hydroxylase	Homo sapiens	119-123
29409484-1	2018	The UDP-glucose ceramide glycosyltransferase (UGCG) is a key enzyme in the sphingolipid metabolism by generating glucosylceramide (GlcCer), the precursor for all glycosphingolipids (GSL), which are essential for proper cell function.	Glucosylceramides	113-129	UDP-glucose ceramide glucosyltransferase	Homo sapiens	46-50
29409484-1	2018	The UDP-glucose ceramide glycosyltransferase (UGCG) is a key enzyme in the sphingolipid metabolism by generating glucosylceramide (GlcCer), the precursor for all glycosphingolipids (GSL), which are essential for proper cell function.	Glucosylceramides	131-137	UDP-glucose ceramide glucosyltransferase	Homo sapiens	4-44
29409484-1	2018	The UDP-glucose ceramide glycosyltransferase (UGCG) is a key enzyme in the sphingolipid metabolism by generating glucosylceramide (GlcCer), the precursor for all glycosphingolipids (GSL), which are essential for proper cell function.	Glucosylceramides	131-137	UDP-glucose ceramide glucosyltransferase	Homo sapiens	46-50
29290548-0	2018	Reversible Conformational Conversion of alpha-Synuclein into Toxic Assemblies by Glucosylceramide.	Glucosylceramides	81-97	synuclein alpha	Homo sapiens	40-55
29366988-5	2018	RESULTS: PCSK9 inhibition significantly decreased plasma levels of several lipid classes, including sphingolipids (dihydroceramides, glucosylceramides, sphingomyelins, ceramides), cholesteryl esters and free cholesterol.	Glucosylceramides	133-150	proprotein convertase subtilisin/kexin type 9	Homo sapiens	9-14
29290548-5	2018	Pathological alpha-syn assembly mainly occurred through the conversion of high molecular weight (HMW) physiological alpha-syn conformers into compact, assembly-state intermediates by glucosylceramide (GluCer), without apparent disassembly into free monomers.	Glucosylceramides	183-199	synuclein alpha	Homo sapiens	13-22
29290548-5	2018	Pathological alpha-syn assembly mainly occurred through the conversion of high molecular weight (HMW) physiological alpha-syn conformers into compact, assembly-state intermediates by glucosylceramide (GluCer), without apparent disassembly into free monomers.	Glucosylceramides	201-207	synuclein alpha	Homo sapiens	13-22
30143433-5	2018	RESULTS: Glucosylceramide C16GC (per 1 log muM increase) was associated with higher odds of having uncontrolled hypertension (odds ratio [OR]: 1.34; 95% confidential interval [CI]: 1.01-1.76), left ventricular hypertrophy (OR: 1.53; 95% CI: 1.11-2.13), and reduced ejection fraction (OR: 1.05; 95% CI: 1.00-1.11) in fully adjusted models.	Glucosylceramides	9-25	latexin	Homo sapiens	43-46
29053611-3	2017	The pathological role of the deacylated form of glucosylceramide, glucosylsphingosine (lyso-Gb1), a recently identified sensitive and specific biomarker for GD, is not well investigated.	Glucosylceramides	48-64	gamma-aminobutyric acid (GABA) B receptor, 1	Mus musculus	92-95
29232555-4	2017	In particular, mTORC2 stimulated sphingolipid (glucosylceramide) and glycerophospholipid (cardiolipin) synthesis.	Glucosylceramides	47-63	CREB regulated transcription coactivator 2	Mus musculus	15-21
29025868-1	2017	Epidermal beta-glucocerebrosidase (GBA1), an acid beta-glucosidase normally located in lysosomes, converts (glucosyl)ceramides into ceramides, which is crucial to generate an optimal barrier function of the outermost skin layer, the stratum corneum (SC).	Glucosylceramides	107-126	glucosylceramidase beta	Homo sapiens	10-33
29025868-1	2017	Epidermal beta-glucocerebrosidase (GBA1), an acid beta-glucosidase normally located in lysosomes, converts (glucosyl)ceramides into ceramides, which is crucial to generate an optimal barrier function of the outermost skin layer, the stratum corneum (SC).	Glucosylceramides	107-126	glucosylceramidase beta	Homo sapiens	35-39
29234271-1	2017	The non-lysosomal glucosylceramidase GBA2 catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Glucosylceramides	70-86	glucosylceramidase beta 2	Homo sapiens	37-41
29234271-2	2017	Loss of GBA2 function results in accumulation of glucosylceramide.	Glucosylceramides	49-65	glucosylceramidase beta 2	Homo sapiens	8-12
28019653-11	2017	Knockdown of GlcCer synthase in the SPG fails to suppress glial overgrowth in egh nerves, and slightly promotes overgrowth in wild type, suggesting that RTK hyperactivation is caused by absence of MacCer and not by GlcCer accumulation.	Glucosylceramides	13-19	Tie-like receptor tyrosine kinase	Drosophila melanogaster	153-156
28944894-2	2017	Glucosylceramide is generated by glucosylceramide synthase (GCS), which is encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	33-58
28944894-2	2017	Glucosylceramide is generated by glucosylceramide synthase (GCS), which is encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	60-63
28944894-2	2017	Glucosylceramide is generated by glucosylceramide synthase (GCS), which is encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-130
28944894-2	2017	Glucosylceramide is generated by glucosylceramide synthase (GCS), which is encoded by the UDP-glucose ceramide glucosyltransferase (UGCG) gene.	Glucosylceramides	0-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	132-136
28851512-1	2017	Gaucher disease (GD), an autosomal recessive lipid storage disorder, arises from mutations in the GBA1 (beta-glucocerebrosidase) gene, resulting in glucosylceramide accumulation in tissue macrophages.	Glucosylceramides	148-164	glucosylceramidase beta	Homo sapiens	98-102
28847804-4	2017	We show that, whereas GD-related sphingolipids (glucosylceramide, glucosylsphingosine, sphingosine, sphingosine-1-phosphate) promote alpha-synuclein aggregation in vitro, glucosylsphingosine triggers the formation of oligomeric alpha-synuclein species capable of templating in human cells and neurons.	Glucosylceramides	48-64	synuclein alpha	Homo sapiens	133-148
28847804-7	2017	With age, brains exhibit glucosylceramide accumulations colocalized with alpha-synuclein pathology.	Glucosylceramides	25-41	synuclein, alpha	Mus musculus	73-88
28646016-6	2017	TSHB mRNA was consistently detected in AT from euthyroid subjects, and positively associated with serum total- and LDL-cholesterol, and with AT-specific cholesterol metabolism-associated lipids [arachidonoyl cholesteryl ester, C8-dihydroceramide, N-stearoyl-d-sphingosine, and GlcCer(18:0, 24:1)].	Glucosylceramides	277-283	thyroid stimulating hormone subunit beta	Homo sapiens	0-4
28812093-1	2017	Gaucher disease (GD) is caused by mutations on the GBA1 gene leading to deficiency in acid beta-glucosidase (GCase) and subsequent accumulation of its substrates, glucosylceramide (GlcC) and glucosylsphingosine (GlcS).	Glucosylceramides	163-179	glucosylceramidase beta	Homo sapiens	51-55
28812093-1	2017	Gaucher disease (GD) is caused by mutations on the GBA1 gene leading to deficiency in acid beta-glucosidase (GCase) and subsequent accumulation of its substrates, glucosylceramide (GlcC) and glucosylsphingosine (GlcS).	Glucosylceramides	181-185	glucosylceramidase beta	Homo sapiens	51-55
28485919-1	2017	Glucocerebrosidase (GBA) is a lysosomal beta-glucosidase that degrades glucosylceramide.	Glucosylceramides	71-87	glucosidase, beta, acid	Mus musculus	0-18
28485919-1	2017	Glucocerebrosidase (GBA) is a lysosomal beta-glucosidase that degrades glucosylceramide.	Glucosylceramides	71-87	glucosidase, beta, acid	Mus musculus	20-23
28851512-1	2017	Gaucher disease (GD), an autosomal recessive lipid storage disorder, arises from mutations in the GBA1 (beta-glucocerebrosidase) gene, resulting in glucosylceramide accumulation in tissue macrophages.	Glucosylceramides	148-164	glucosylceramidase beta	Homo sapiens	104-127
28851512-2	2017	Lyso-Gb1 (glucosylsphingosine, lyso-GL1), a downstream metabolic product of glucosylceramide, has been identified as a promising biomarker for the diagnosis and monitoring of patients with GD.	Glucosylceramides	76-92	gamma-aminobutyric acid type B receptor subunit 1	Homo sapiens	5-8
28574511-8	2017	One top hit was GBA1, the Gaucher disease-associated gene, which encodes glucocerebrosidase, an enzyme that metabolizes glucosylceramide to ceramide and glucose.	Glucosylceramides	120-136	glucosylceramidase beta	Homo sapiens	16-20
28490444-5	2017	To determine the role of ceramide metabolism to hexosylceramides in kidney injury, we treated mice with a potent and highly specific inhibitor of glucosylceramide synthase, the enzyme responsible for catalyzing the glycosylation of ceramides to form glucosylceramides.	Glucosylceramides	250-267	UDP-glucose ceramide glucosyltransferase	Mus musculus	146-171
28686011-2	2017	Reduced GCase activity primarily leads to the accumulation of two substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	78-94	glucosidase, beta, acid	Mus musculus	8-13
28686011-2	2017	Reduced GCase activity primarily leads to the accumulation of two substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph).	Glucosylceramides	96-102	glucosidase, beta, acid	Mus musculus	8-13
28258214-1	2017	The lysosomal acid beta-glucosidase GBA1 and the non-lysosomal beta-glucosidase GBA2 degrade glucosylceramide (GlcCer) to glucose and ceramide in different cellular compartments.	Glucosylceramides	93-109	glucosylceramidase beta	Homo sapiens	36-40
28258214-1	2017	The lysosomal acid beta-glucosidase GBA1 and the non-lysosomal beta-glucosidase GBA2 degrade glucosylceramide (GlcCer) to glucose and ceramide in different cellular compartments.	Glucosylceramides	93-109	glucosylceramidase beta 2	Homo sapiens	80-84
28258214-1	2017	The lysosomal acid beta-glucosidase GBA1 and the non-lysosomal beta-glucosidase GBA2 degrade glucosylceramide (GlcCer) to glucose and ceramide in different cellular compartments.	Glucosylceramides	111-117	glucosylceramidase beta	Homo sapiens	36-40
28258214-1	2017	The lysosomal acid beta-glucosidase GBA1 and the non-lysosomal beta-glucosidase GBA2 degrade glucosylceramide (GlcCer) to glucose and ceramide in different cellular compartments.	Glucosylceramides	111-117	glucosylceramidase beta 2	Homo sapiens	80-84
28144704-1	2017	Gaucher disease is a hereditary lipid storage disorder that affects the enzyme beta glucocerebrosidase, causing accumulation of glucocerebroside in macrophages of the reticuloendothelial system.	Glucosylceramides	128-144	glucosylceramidase beta	Homo sapiens	79-102
27693344-1	2017	It was first discovered in 1992 that P-glycoprotein (Pgp, ABCB1), an ATP binding cassette (ABC) transporter, can transport phospholipids such as phosphatidylcholine, -ethanolamine and -serine as well as glucosylceramide and glycosphingolipids.	Glucosylceramides	203-219	ATP binding cassette subfamily B member 1	Homo sapiens	37-51
27693344-1	2017	It was first discovered in 1992 that P-glycoprotein (Pgp, ABCB1), an ATP binding cassette (ABC) transporter, can transport phospholipids such as phosphatidylcholine, -ethanolamine and -serine as well as glucosylceramide and glycosphingolipids.	Glucosylceramides	203-219	ATP binding cassette subfamily B member 1	Homo sapiens	53-56
27693344-1	2017	It was first discovered in 1992 that P-glycoprotein (Pgp, ABCB1), an ATP binding cassette (ABC) transporter, can transport phospholipids such as phosphatidylcholine, -ethanolamine and -serine as well as glucosylceramide and glycosphingolipids.	Glucosylceramides	203-219	ATP binding cassette subfamily B member 1	Homo sapiens	58-63
27693344-1	2017	It was first discovered in 1992 that P-glycoprotein (Pgp, ABCB1), an ATP binding cassette (ABC) transporter, can transport phospholipids such as phosphatidylcholine, -ethanolamine and -serine as well as glucosylceramide and glycosphingolipids.	Glucosylceramides	203-219	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	58-61
28223512-5	2017	Treatment of GbaD409V/D409V mice with the GCS inhibitor reduced levels of glucosylceramide and glucosylsphingosine in the central nervous system (CNS), demonstrating target engagement.	Glucosylceramides	74-90	UDP-glucose ceramide glucosyltransferase	Mus musculus	42-45
28166796-2	2017	In GD, partial or complete loss of GCase activity causes the accumulation of the glycolipids glucosylceramide (GlcCer) and glucosylsphingosine in the lysosomes of macrophages.	Glucosylceramides	93-109	glucosylceramidase beta	Homo sapiens	35-40
28126847-0	2017	Lipids regulate the hydrolysis of membrane bound glucosylceramide by lysosomal beta-glucocerebrosidase.	Glucosylceramides	49-65	glucosylceramidase beta	Homo sapiens	79-102
28126847-1	2017	Glucosylceramide (GlcCer) is the primary storage lipid in the lysosomes of Gaucher patients and a secondary one in Niemann-Pick disease types A, B, and C. The regulatory roles of lipids on the hydrolysis of membrane bound GlcCer by lysosomal beta-glucocerebrosidase (GBA1) was probed using a detergent-free liposomal assay.	Glucosylceramides	0-16	glucosylceramidase beta	Homo sapiens	242-265
28126847-1	2017	Glucosylceramide (GlcCer) is the primary storage lipid in the lysosomes of Gaucher patients and a secondary one in Niemann-Pick disease types A, B, and C. The regulatory roles of lipids on the hydrolysis of membrane bound GlcCer by lysosomal beta-glucocerebrosidase (GBA1) was probed using a detergent-free liposomal assay.	Glucosylceramides	0-16	glucosylceramidase beta	Homo sapiens	267-271
28126847-1	2017	Glucosylceramide (GlcCer) is the primary storage lipid in the lysosomes of Gaucher patients and a secondary one in Niemann-Pick disease types A, B, and C. The regulatory roles of lipids on the hydrolysis of membrane bound GlcCer by lysosomal beta-glucocerebrosidase (GBA1) was probed using a detergent-free liposomal assay.	Glucosylceramides	18-24	glucosylceramidase beta	Homo sapiens	242-265
28126847-1	2017	Glucosylceramide (GlcCer) is the primary storage lipid in the lysosomes of Gaucher patients and a secondary one in Niemann-Pick disease types A, B, and C. The regulatory roles of lipids on the hydrolysis of membrane bound GlcCer by lysosomal beta-glucocerebrosidase (GBA1) was probed using a detergent-free liposomal assay.	Glucosylceramides	18-24	glucosylceramidase beta	Homo sapiens	267-271
28225753-2	2017	GBA1 mutations drive extensive accumulation of glucosylceramide (GC) in multiple innate and adaptive immune cells in the spleen, liver, lung and bone marrow, often leading to chronic inflammation.	Glucosylceramides	47-63	glucosidase, beta, acid	Mus musculus	0-4
28225753-2	2017	GBA1 mutations drive extensive accumulation of glucosylceramide (GC) in multiple innate and adaptive immune cells in the spleen, liver, lung and bone marrow, often leading to chronic inflammation.	Glucosylceramides	65-67	glucosidase, beta, acid	Mus musculus	0-4
28166796-2	2017	In GD, partial or complete loss of GCase activity causes the accumulation of the glycolipids glucosylceramide (GlcCer) and glucosylsphingosine in the lysosomes of macrophages.	Glucosylceramides	111-117	glucosylceramidase beta	Homo sapiens	35-40
27775668-5	2016	VLC-sphingolipid expression was increased along with that of CERS2, and the proportion of VLC species in glucosylceramide (GlcCer) was higher than that in SM for all expression levels of CERS2.	Glucosylceramides	105-121	ceramide synthase 2	Homo sapiens	187-192
27476102-6	2016	We found that ARAP2 knockdown increased glucosylceramide and lactosylceramide levels without affecting ceramide levels, and thus speculated that the rate-limiting enzyme in glycosphingolipid synthesis, namely glucosylceramide synthase (GCS), could be modified by ARAP2.	Glucosylceramides	40-56	ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 2	Mus musculus	14-19
28052128-5	2017	Our studies show that a reduced activity of GBA2 is sufficient to elevate the levels of glucosylceramide to similar levels as seen in Gaucher disease.	Glucosylceramides	88-104	glucosylceramidase beta 2	Homo sapiens	44-48
27522145-4	2017	RESULTS: Eliglustat is a selective, potent inhibitor of glucosylceramide synthase, the enzyme responsible for biosynthesis of glucosylceramides which accumulate in Gaucher disease.	Glucosylceramides	126-143	UDP-glucose ceramide glucosyltransferase	Homo sapiens	56-81
29199207-2	2017	Addition of GlcCer or GalCer suppressed cell injury caused lipopolysaccharide (LPS)- and TNF-alpha-induced inflammatory stress and induction of apoptosis in differentiated Caco-2 cells.	Glucosylceramides	12-18	tumor necrosis factor	Homo sapiens	89-98
27955980-1	2017	Gaucher disease is caused by the defective catabolism of the simple glycosphingolipid, glucosylceramide (GlcCer), due to mutations in the GBA1 gene which encodes for acid beta-glucosidase (GCase), the lysosomal enzyme that degrades GlcCer.	Glucosylceramides	87-103	glucosylceramidase beta	Homo sapiens	138-142
27955980-1	2017	Gaucher disease is caused by the defective catabolism of the simple glycosphingolipid, glucosylceramide (GlcCer), due to mutations in the GBA1 gene which encodes for acid beta-glucosidase (GCase), the lysosomal enzyme that degrades GlcCer.	Glucosylceramides	105-111	glucosylceramidase beta	Homo sapiens	138-142
27955980-1	2017	Gaucher disease is caused by the defective catabolism of the simple glycosphingolipid, glucosylceramide (GlcCer), due to mutations in the GBA1 gene which encodes for acid beta-glucosidase (GCase), the lysosomal enzyme that degrades GlcCer.	Glucosylceramides	232-238	glucosylceramidase beta	Homo sapiens	138-142
27697915-4	2016	A key step in vertebrate GlcChol biosynthesis is the transglucosylation reaction catalyzed by glucocerebrosidase (GBA)1 or GBA2, utilizing GlcCer as a glucose donor.	Glucosylceramides	139-145	glucosylceramidase beta	Homo sapiens	114-119
27697915-4	2016	A key step in vertebrate GlcChol biosynthesis is the transglucosylation reaction catalyzed by glucocerebrosidase (GBA)1 or GBA2, utilizing GlcCer as a glucose donor.	Glucosylceramides	139-145	glucosylceramidase beta 2	Homo sapiens	123-127
27775668-5	2016	VLC-sphingolipid expression was increased along with that of CERS2, and the proportion of VLC species in glucosylceramide (GlcCer) was higher than that in SM for all expression levels of CERS2.	Glucosylceramides	123-129	ceramide synthase 2	Homo sapiens	187-192
26860955-4	2016	Glucosylceramide is suggested to stabilize toxic oligomeric forms of alpha-synuclein that negatively influence the activity of beta-glucocerebrosidase and to partially block export of newly synthesized beta-glucocerebrosidase from the endoplasmic reticulum to late endocytic compartments, amplifying the pathological effects of alpha-synuclein and ultimately resulting in neuronal cell death.	Glucosylceramides	0-16	synuclein alpha	Homo sapiens	69-84
27539961-2	2016	The activities of acid sphingomyelinase and lysosomal glucocerebrosidase (GCase), which degrade sphingomyelin and GlcCer, respectively, are down-regulated in NPC cells, however, changes in GlcCer synthase activity have not yet been elucidated.	Glucosylceramides	114-120	sphingomyelin phosphodiesterase 1	Homo sapiens	18-39
27539961-2	2016	The activities of acid sphingomyelinase and lysosomal glucocerebrosidase (GCase), which degrade sphingomyelin and GlcCer, respectively, are down-regulated in NPC cells, however, changes in GlcCer synthase activity have not yet been elucidated.	Glucosylceramides	114-120	glucosylceramidase beta	Homo sapiens	44-72
28933411-7	2016	Decreased catalytic activity and/or instability of GCase leads to accumulation of glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph) in the lysosomes of macrophage cells and visceral organs.	Glucosylceramides	82-98	glucosidase, beta, acid	Mus musculus	51-56
28933411-7	2016	Decreased catalytic activity and/or instability of GCase leads to accumulation of glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph) in the lysosomes of macrophage cells and visceral organs.	Glucosylceramides	100-106	glucosidase, beta, acid	Mus musculus	51-56
26860955-4	2016	Glucosylceramide is suggested to stabilize toxic oligomeric forms of alpha-synuclein that negatively influence the activity of beta-glucocerebrosidase and to partially block export of newly synthesized beta-glucocerebrosidase from the endoplasmic reticulum to late endocytic compartments, amplifying the pathological effects of alpha-synuclein and ultimately resulting in neuronal cell death.	Glucosylceramides	0-16	synuclein alpha	Homo sapiens	328-343
27539321-4	2016	In particular, heterozygous mutations in the gene encoding for glucocerebrosidase (GBA1), a lysosomal enzyme converting glucosyl-ceramides (Glc-Cer) into Cer, increase the risk of developing PD.	Glucosylceramides	120-138	glucosidase, beta, acid	Mus musculus	63-81
27539321-4	2016	In particular, heterozygous mutations in the gene encoding for glucocerebrosidase (GBA1), a lysosomal enzyme converting glucosyl-ceramides (Glc-Cer) into Cer, increase the risk of developing PD.	Glucosylceramides	120-138	glucosidase, beta, acid	Mus musculus	83-87
27412675-6	2016	GlcCer inhibited GLTP cross-linking.	Glucosylceramides	0-6	glycolipid transfer protein	Homo sapiens	17-21
27551807-8	2016	Reducing the intracellular levels of glucosylceramide with a glucosylceramide synthase inhibitor resulted in decreased secretion of KALLIKREIN proteases by wild type keratinocytes, but not by smsk mutant keratinocytes.	Glucosylceramides	37-53	kallikrein 1-related peptidase b9	Mus musculus	132-142
27642553-6	2016	In conclusion, gpNMB acts as a marker for glucosylceramide-laden macrophages in man and mouse and gpNMB should be considered as candidate biomarker for Gaucher disease in treatment monitoring.	Glucosylceramides	42-58	glycoprotein nmb	Homo sapiens	15-20
27547732-1	2016	Glucosylceramide (GL-1) level in human has been considered as a surrogate biomarker for enzyme replacement and substrate reduction therapies (ERT and SRT) for Gaucher and Fabry patients.	Glucosylceramides	0-16	E74 like ETS transcription factor 3	Homo sapiens	142-145
26724485-2	2016	Cells express two GlcCer-degrading beta-glucosidases, glucocerebrosidase (GBA) and GBA2, located in and outside the lysosome, respectively.	Glucosylceramides	18-24	glucosylceramidase beta	Homo sapiens	54-72
27482815-1	2016	Glucocerebrosidase is a lysosomal hydrolase involved in the breakdown of glucosylceramide.	Glucosylceramides	73-89	glucosidase, beta, acid	Mus musculus	0-18
27162249-1	2016	Gaucher disease (GD) results from mutations in the acid beta-glucocerebrosidase (GCase) encoding gene, GBA, which leads to accumulation of glucosylceramides.	Glucosylceramides	139-156	glucosylceramidase beta	Homo sapiens	103-106
26792850-1	2016	BACKGROUND: Gaucher disease (GD) is an autosomal recessive disorder produced by mutations in the glucocerebrosidase gene (GBA), causing storage of glucosylceramide in reticuloendothelial cells in multiple organs.	Glucosylceramides	147-163	glucosylceramidase beta	Homo sapiens	122-125
27098312-1	2016	Gaucher disease, caused by pathological mutations GBA1, encodes the lysosome-resident enzyme glucocerebrosidase, which cleaves glucosylceramide into glucose and ceramide.	Glucosylceramides	127-143	glucosylceramidase beta	Homo sapiens	50-54
26739815-4	2016	RESULTS: Muscle C18:0 ceramide (p = 0.029), dihydroceramide (p = 0.06) and glucosylceramide (p = 0.03) species were inversely related to insulin sensitivity without differences in total ceramide, dihydroceramide, and glucosylceramide concentration.	Glucosylceramides	75-91	insulin	Homo sapiens	137-144
26909767-3	2016	GBA2 is a glucosylceramide-degrading enzyme that is located on the plasma membrane/endoplasmic reticulum, and is distinct from the lysosomal enzyme glucocerebrosidase (GBA).	Glucosylceramides	10-26	glucosidase, beta (bile acid) 2	Danio rerio	0-4
26909767-3	2016	GBA2 is a glucosylceramide-degrading enzyme that is located on the plasma membrane/endoplasmic reticulum, and is distinct from the lysosomal enzyme glucocerebrosidase (GBA).	Glucosylceramides	10-26	glucosidase, beta, acid	Danio rerio	0-3
27098793-1	2016	BACKGROUND: Gaucher"s disease (GD) is an autosomal recessive disorder caused by a deficiency of acid beta-glucosidase (glucocerebrosidase [GBA]) that results in the accumulation of glucocerebroside within macrophages.	Glucosylceramides	181-197	glucosylceramidase beta	Homo sapiens	119-137
27098793-1	2016	BACKGROUND: Gaucher"s disease (GD) is an autosomal recessive disorder caused by a deficiency of acid beta-glucosidase (glucocerebrosidase [GBA]) that results in the accumulation of glucocerebroside within macrophages.	Glucosylceramides	181-197	glucosylceramidase beta	Homo sapiens	139-142
26724485-2	2016	Cells express two GlcCer-degrading beta-glucosidases, glucocerebrosidase (GBA) and GBA2, located in and outside the lysosome, respectively.	Glucosylceramides	18-24	glucosylceramidase beta	Homo sapiens	74-77
26724485-2	2016	Cells express two GlcCer-degrading beta-glucosidases, glucocerebrosidase (GBA) and GBA2, located in and outside the lysosome, respectively.	Glucosylceramides	18-24	glucosylceramidase beta 2	Homo sapiens	83-87
26724485-3	2016	Here we demonstrate that through transglucosylation both GBA and GBA2 are able to catalyze in vitro the transfer of glucosyl-moieties from GlcCer to cholesterol, and vice versa.	Glucosylceramides	139-145	glucosylceramidase beta	Homo sapiens	57-60
26724485-3	2016	Here we demonstrate that through transglucosylation both GBA and GBA2 are able to catalyze in vitro the transfer of glucosyl-moieties from GlcCer to cholesterol, and vice versa.	Glucosylceramides	139-145	glucosylceramidase beta 2	Homo sapiens	65-69
26861868-3	2016	The results of cell experiment indicated that all of three glucocerebroside series, CF-Cer and CF-LCB exhibited an inhibitory effects on cell proliferation.	Glucosylceramides	59-75	clathrin light chain B	Homo sapiens	98-101
26861868-4	2016	Moreover, CFC-3 was most effective in three glucocerebrosides to HepG-2 cell viability.	Glucosylceramides	44-61	mitogen-activated protein kinase kinase 1	Homo sapiens	10-15
26708635-5	2016	Correlation studies showed that in GD the alpha-Syn dimer/monomer ratio is positively correlated with the levels of glucosylceramide (GlcCer) and the glucosylceramide/ceramide (GlcCer/Cer) ratio and negatively with the levels of malonyldialdehyde (MDA) and plasmalogens.	Glucosylceramides	116-132	synuclein alpha	Homo sapiens	42-51
26853111-6	2016	Cordycerebroside A (1), the new cerebroside, along with soyacerebroside I (2) and glucocerebroside (3) inhibited the accumulation of pro-inflammatory iNOS protein and reduced the expression of COX-2 protein in LPS-stimulated RAW264.7 macrophages.	Glucosylceramides	82-98	cox2	Cordyceps militaris	193-198
26708635-5	2016	Correlation studies showed that in GD the alpha-Syn dimer/monomer ratio is positively correlated with the levels of glucosylceramide (GlcCer) and the glucosylceramide/ceramide (GlcCer/Cer) ratio and negatively with the levels of malonyldialdehyde (MDA) and plasmalogens.	Glucosylceramides	134-140	synuclein alpha	Homo sapiens	42-51
26708635-5	2016	Correlation studies showed that in GD the alpha-Syn dimer/monomer ratio is positively correlated with the levels of glucosylceramide (GlcCer) and the glucosylceramide/ceramide (GlcCer/Cer) ratio and negatively with the levels of malonyldialdehyde (MDA) and plasmalogens.	Glucosylceramides	150-166	synuclein alpha	Homo sapiens	42-51
26708635-5	2016	Correlation studies showed that in GD the alpha-Syn dimer/monomer ratio is positively correlated with the levels of glucosylceramide (GlcCer) and the glucosylceramide/ceramide (GlcCer/Cer) ratio and negatively with the levels of malonyldialdehyde (MDA) and plasmalogens.	Glucosylceramides	177-183	synuclein alpha	Homo sapiens	42-51
26708635-6	2016	In conclusion, we have shown that the increased tendency of alpha-Syn to form dimers in the RBC membrane of patients with GD, is correlated with both the level of lipids, including GlcCer, the primary lipid abnormality in GD, and the increased oxidative stress observed in this disorder.	Glucosylceramides	181-187	synuclein alpha	Homo sapiens	60-69
26387627-1	2016	In Gaucher disease, deficient activity of acid beta-glucosidase results in accumulation of its substrates, glucosylceramide and glucosylsphingosine, within the lysosomes of cells primarily in the spleen, liver, bone marrow, and occasionally the lung.	Glucosylceramides	107-123	glucosylceramidase beta	Homo sapiens	42-63
26811686-1	2016	Gaucher disease (GD) is a lysosomal storage disorder caused by the deficient activity of acid beta glucosidase, with consequent accumulation of glucosylceramide in the spleen, liver, bone marrow, and various organs and tissues.	Glucosylceramides	144-160	glucosylceramidase beta	Homo sapiens	89-110
26588331-2	2016	GD is a rare autosomal recessive disorder characterized by the defective function of the catabolic enzyme beta-glucocerebrosidase (GBA), leading to an accumulation of its substrate, glucocerebroside.	Glucosylceramides	182-198	glucosylceramidase beta	Homo sapiens	106-129
26603294-1	2016	The non-lysosomal beta-glucosylceramidase GBA2 (EC3.2.1.45, GH116) is ubiquitously expressed in various mammal tissues and cell types where it catalyzes the hydrolysis of glucosylceramide into glucose and ceramide.	Glucosylceramides	171-187	glucosylceramidase beta 2	Homo sapiens	42-46
26588331-2	2016	GD is a rare autosomal recessive disorder characterized by the defective function of the catabolic enzyme beta-glucocerebrosidase (GBA), leading to an accumulation of its substrate, glucocerebroside.	Glucosylceramides	182-198	glucosylceramidase beta	Homo sapiens	131-134
26492941-2	2015	Selective modulation of one of the glycoprocessing enzymes involved in glucosylceramide metabolism-glucosylceramide synthase (GCS), acid glucosylceramidase (GBA1), or neutral glucosylceramidase (GBA2)-is therefore an attractive research objective.	Glucosylceramides	71-87	glucosylceramidase beta 2	Homo sapiens	195-199
26483191-6	2015	HPLC analysis showed increased amounts of GlcCer and downstream glycosphingolipids (GSLs) in SOD1(G86R) muscle compared with wild-type littermates.	Glucosylceramides	42-48	superoxide dismutase 1, soluble	Mus musculus	93-97
26483191-7	2015	Glucosylceramide synthase (GCS), the enzyme responsible for GlcCer biosynthesis, was up-regulated in muscle of SOD1(G86R) mice and ALS patients, and in muscle of wild-type mice after surgically induced denervation.	Glucosylceramides	60-66	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-25
26483191-7	2015	Glucosylceramide synthase (GCS), the enzyme responsible for GlcCer biosynthesis, was up-regulated in muscle of SOD1(G86R) mice and ALS patients, and in muscle of wild-type mice after surgically induced denervation.	Glucosylceramides	60-66	UDP-glucose ceramide glucosyltransferase	Mus musculus	27-30
26483191-7	2015	Glucosylceramide synthase (GCS), the enzyme responsible for GlcCer biosynthesis, was up-regulated in muscle of SOD1(G86R) mice and ALS patients, and in muscle of wild-type mice after surgically induced denervation.	Glucosylceramides	60-66	superoxide dismutase 1, soluble	Mus musculus	111-115
26420838-1	2015	Defective lysosomal acid beta-glucosidase (GCase) in Gaucher disease causes accumulation of glucosylceramide (GC) and glucosylsphingosine (GS) that distress cellular functions.	Glucosylceramides	92-108	glucosidase, beta, acid	Mus musculus	43-48
25996484-3	2015	GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases.	Glucosylceramides	76-92	glucosidase, beta, acid	Mus musculus	0-4
25996484-3	2015	GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases.	Glucosylceramides	76-92	glucosidase, beta, acid	Mus musculus	0-3
25996484-3	2015	GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases.	Glucosylceramides	94-96	glucosidase, beta, acid	Mus musculus	0-4
25996484-3	2015	GBA1- and GBA2-deficient genetic conditions, with different phenotypes, are glucosylceramide (GC; the main GBA substrate) accumulating diseases.	Glucosylceramides	94-96	glucosidase, beta, acid	Mus musculus	0-3
26116408-4	2015	The purified recombinant Egh1 hydrolyzed various beta-glucosides including ergosteryl beta-glucoside (EG), cholesteryl beta-glucoside, sitosteryl beta-glucoside, para-nitrophenyl beta-glucoside, 4-methylumberifellyl beta-glucoside and glucosylceramide.	Glucosylceramides	235-251	hydrolase	Saccharomyces cerevisiae S288C	25-29
26220867-10	2015	Treatment of Molt-3, an acute lymphoblastic leukemia cell line, with 4-HPR revealed moderate ceramide production (5-fold over control), robust conversion of ceramide to GC and sphingomyelin, and resistance to 4-HPR and C6-ceramide.	Glucosylceramides	169-171	haptoglobin-related protein	Homo sapiens	71-74
26313010-8	2015	Consistent with a role for GlcCer in organ-specific cell differentiation, calli from gcs-1 mutants formed roots and leaves on media supplemented with the glucosylated sphingosine glucopsychosine, which was readily converted to GlcCer independent of GCS.	Glucosylceramides	27-33	glucosidase 1	Arabidopsis thaliana	85-90
26313010-8	2015	Consistent with a role for GlcCer in organ-specific cell differentiation, calli from gcs-1 mutants formed roots and leaves on media supplemented with the glucosylated sphingosine glucopsychosine, which was readily converted to GlcCer independent of GCS.	Glucosylceramides	227-233	glucosidase 1	Arabidopsis thaliana	85-90
26312487-2	2015	GBA1 cleaves glucosylceramide to form ceramide, an established bioactive lipid, and defects in GBA1 lead to aberrant accumulation in glucosylceramide and insufficient formation of ceramide.	Glucosylceramides	13-29	glucosidase, beta, acid	Mus musculus	0-4
26094487-2	2015	GBA1 encodes for the lysosomal hydrolase glucocerebrosidase and reductions in this enzyme result in the accumulation of the glycolipid substrates glucosylceramide and glucosylsphingosine.	Glucosylceramides	146-162	glucosidase, beta, acid	Mus musculus	0-4
26094487-2	2015	GBA1 encodes for the lysosomal hydrolase glucocerebrosidase and reductions in this enzyme result in the accumulation of the glycolipid substrates glucosylceramide and glucosylsphingosine.	Glucosylceramides	146-162	glucosidase, beta, acid	Mus musculus	41-59
26297139-5	2015	The amount of 2-hydroxy fatty acid-containing glucosylceramide increased in the detergent-resistant membrane (DRM; a biochemical counterpart of plasma membrane microdomains) fraction obtained from BI-1-overexpressing rice cells.	Glucosylceramides	46-62	BAX inhibitor 1	Arabidopsis thaliana	197-201
26418157-1	2015	Gaucher disease is characterized by lysosomal accumulation of glucosylceramide due to deficient activity of lysosomal glucocerebrosidase (GBA).	Glucosylceramides	62-78	glucosylceramidase beta	Rattus norvegicus	138-141
26418157-2	2015	In cells, glucosylceramide is also degraded outside lysosomes by the enzyme glucosylceramidase 2 (GBA2) of which inherited deficiency is associated with ataxias.	Glucosylceramides	10-26	glucosylceramidase beta 2	Rattus norvegicus	76-96
26418157-2	2015	In cells, glucosylceramide is also degraded outside lysosomes by the enzyme glucosylceramidase 2 (GBA2) of which inherited deficiency is associated with ataxias.	Glucosylceramides	10-26	glucosylceramidase beta 2	Rattus norvegicus	98-102
26418157-3	2015	The interest in GBA and glucosylceramide metabolism in the brain has grown following the notion that mutations in the GBA gene impose a risk factor for motor disorders such as alpha-synucleinopathies.	Glucosylceramides	24-40	glucosylceramidase beta	Rattus norvegicus	118-121
26220345-2	2015	Glucosylceramide is degraded to ceramide and glucose by distinct, non-homologous enzymes, including glucocerebrosidase (GBA), localized in the endolysosomal pathway, and beta-glucosidase 2 (GBA2), which is associated with the plasma membrane and/or the endoplasmic reticulum.	Glucosylceramides	0-16	glucosylceramidase beta	Homo sapiens	120-123
26220345-2	2015	Glucosylceramide is degraded to ceramide and glucose by distinct, non-homologous enzymes, including glucocerebrosidase (GBA), localized in the endolysosomal pathway, and beta-glucosidase 2 (GBA2), which is associated with the plasma membrane and/or the endoplasmic reticulum.	Glucosylceramides	0-16	glucosylceramidase beta 2	Homo sapiens	190-194
26220345-3	2015	It is well established that mutations in the GBA gene result in endolysosomal glucosylceramide accumulation, which triggers Gaucher disease.	Glucosylceramides	78-94	glucosylceramidase beta	Homo sapiens	45-48
26001295-4	2015	VNR treatment significantly converts ceramide to glucosylceramide in VNR-resistant cells; however, pharmacologically inhibiting GCS with (+-)-threo-1-Phenyl-2-decanoylamino-3-morpholino-1-propanol hydrochloride (PDMP) induced ceramide accumulation, accompanied by a decrease in glucosylceramide.	Glucosylceramides	278-294	UDP-glucose ceramide glucosyltransferase	Homo sapiens	128-131
26312487-2	2015	GBA1 cleaves glucosylceramide to form ceramide, an established bioactive lipid, and defects in GBA1 lead to aberrant accumulation in glucosylceramide and insufficient formation of ceramide.	Glucosylceramides	133-149	glucosidase, beta, acid	Mus musculus	0-4
26312487-2	2015	GBA1 cleaves glucosylceramide to form ceramide, an established bioactive lipid, and defects in GBA1 lead to aberrant accumulation in glucosylceramide and insufficient formation of ceramide.	Glucosylceramides	133-149	glucosidase, beta, acid	Mus musculus	95-99
26275242-1	2015	The enzyme glucocerebrosidase (GBA) hydrolyses glucosylceramide (GlcCer) in lysosomes.	Glucosylceramides	47-63	glucosidase, beta, acid	Mus musculus	11-29
26275242-1	2015	The enzyme glucocerebrosidase (GBA) hydrolyses glucosylceramide (GlcCer) in lysosomes.	Glucosylceramides	47-63	glucosidase, beta, acid	Mus musculus	31-34
26275242-1	2015	The enzyme glucocerebrosidase (GBA) hydrolyses glucosylceramide (GlcCer) in lysosomes.	Glucosylceramides	65-71	glucosidase, beta, acid	Mus musculus	11-29
26275242-1	2015	The enzyme glucocerebrosidase (GBA) hydrolyses glucosylceramide (GlcCer) in lysosomes.	Glucosylceramides	65-71	glucosidase, beta, acid	Mus musculus	31-34
26108617-6	2015	Inhibition of glucosylceramide and ganglioside synthesis results in improved insulin sensitivity and increased activatory tyrosine phosphorylation of IRS1 in the muscle.	Glucosylceramides	14-30	insulin	Homo sapiens	77-84
26108617-6	2015	Inhibition of glucosylceramide and ganglioside synthesis results in improved insulin sensitivity and increased activatory tyrosine phosphorylation of IRS1 in the muscle.	Glucosylceramides	14-30	insulin receptor substrate 1	Homo sapiens	150-154
25808625-7	2015	Hepatic overexpression of Sphk2 in mice fed a high-fat diet (HFD) led to elevated S1P and reduced ceramide, sphingomyelin, and glucosylceramide in plasma and liver.	Glucosylceramides	127-143	sphingosine kinase 2	Mus musculus	26-31
25797198-5	2015	Human GLTP-motifs have evolved to function not only as glucosylceramide binding/transferring domains for phosphoinositol 4-phosphate adaptor protein-2 during glycosphingolipid biosynthesis but also as selective binding/transfer proteins for ceramide-1-phosphate.	Glucosylceramides	55-71	glycolipid transfer protein	Homo sapiens	6-10
26115433-3	2015	This effect can be explained in part by altered sphingolipid levels, because reducing glucosylceramide biosynthesis restored the localization of MIG-14::GFP.	Glucosylceramides	86-102	Protein wntless homolog	Caenorhabditis elegans	145-151
25080062-10	2015	In tumor-invasive areas, VEGF and HIF-1alpha in the tumor cells, and VEGF receptor-2 in endothelial cells decreased after treatment with dietary glucosylceramides.	Glucosylceramides	145-162	vascular endothelial growth factor A	Mus musculus	25-29
26048992-0	2015	AMP-activated Protein Kinase Suppresses Biosynthesis of Glucosylceramide by Reducing Intracellular Sugar Nucleotides.	Glucosylceramides	56-72	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-28
26048992-5	2015	Here, we investigated whether AMPK affects GlcCer metabolism.	Glucosylceramides	43-49	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	30-34
26048992-6	2015	AMPK activators (5-aminoimidazole-4-carboxamide 1-beta-d-ribofuranoside and metformin) decreased intracellular GlcCer levels and synthase activity in mouse fibroblasts.	Glucosylceramides	111-117	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-4
26048992-7	2015	AMPK inhibitors or AMPK siRNA reversed these effects, suggesting that GlcCer synthesis is negatively regulated by an AMPK-dependent mechanism.	Glucosylceramides	70-76	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-4
26048992-7	2015	AMPK inhibitors or AMPK siRNA reversed these effects, suggesting that GlcCer synthesis is negatively regulated by an AMPK-dependent mechanism.	Glucosylceramides	70-76	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	19-23
26048992-7	2015	AMPK inhibitors or AMPK siRNA reversed these effects, suggesting that GlcCer synthesis is negatively regulated by an AMPK-dependent mechanism.	Glucosylceramides	70-76	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	19-23
26048992-11	2015	Because AMPK activators are capable of reducing GlcCer levels in cells from Gaucher disease patients, our findings suggest that reducing GlcCer through AMPK activation may lead to a new strategy for treating diseases caused by abnormal accumulation of GlcCer.	Glucosylceramides	48-54	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	8-12
26048992-11	2015	Because AMPK activators are capable of reducing GlcCer levels in cells from Gaucher disease patients, our findings suggest that reducing GlcCer through AMPK activation may lead to a new strategy for treating diseases caused by abnormal accumulation of GlcCer.	Glucosylceramides	48-54	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	152-156
26048992-11	2015	Because AMPK activators are capable of reducing GlcCer levels in cells from Gaucher disease patients, our findings suggest that reducing GlcCer through AMPK activation may lead to a new strategy for treating diseases caused by abnormal accumulation of GlcCer.	Glucosylceramides	137-143	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	8-12
26048992-11	2015	Because AMPK activators are capable of reducing GlcCer levels in cells from Gaucher disease patients, our findings suggest that reducing GlcCer through AMPK activation may lead to a new strategy for treating diseases caused by abnormal accumulation of GlcCer.	Glucosylceramides	137-143	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	152-156
26048992-11	2015	Because AMPK activators are capable of reducing GlcCer levels in cells from Gaucher disease patients, our findings suggest that reducing GlcCer through AMPK activation may lead to a new strategy for treating diseases caused by abnormal accumulation of GlcCer.	Glucosylceramides	137-143	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	8-12
26048992-11	2015	Because AMPK activators are capable of reducing GlcCer levels in cells from Gaucher disease patients, our findings suggest that reducing GlcCer through AMPK activation may lead to a new strategy for treating diseases caused by abnormal accumulation of GlcCer.	Glucosylceramides	137-143	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	152-156
25080062-10	2015	In tumor-invasive areas, VEGF and HIF-1alpha in the tumor cells, and VEGF receptor-2 in endothelial cells decreased after treatment with dietary glucosylceramides.	Glucosylceramides	145-162	hypoxia inducible factor 1, alpha subunit	Mus musculus	34-44
25080062-10	2015	In tumor-invasive areas, VEGF and HIF-1alpha in the tumor cells, and VEGF receptor-2 in endothelial cells decreased after treatment with dietary glucosylceramides.	Glucosylceramides	145-162	kinase insert domain protein receptor	Mus musculus	69-84
25080062-13	2015	CONCLUSION: These results suggest that dietary glucosylceramides trigger the de novo pathway of ceramide synthesis, indicating that sphingosine-based ceramide suppresses the growth of head and neck tumors through the inhibition of pro-angiogenic signals such as VEGF, VEGF receptor-2, and HIF-1alpha.	Glucosylceramides	47-64	vascular endothelial growth factor A	Mus musculus	262-266
25080062-13	2015	CONCLUSION: These results suggest that dietary glucosylceramides trigger the de novo pathway of ceramide synthesis, indicating that sphingosine-based ceramide suppresses the growth of head and neck tumors through the inhibition of pro-angiogenic signals such as VEGF, VEGF receptor-2, and HIF-1alpha.	Glucosylceramides	47-64	kinase insert domain protein receptor	Mus musculus	268-283
25080062-13	2015	CONCLUSION: These results suggest that dietary glucosylceramides trigger the de novo pathway of ceramide synthesis, indicating that sphingosine-based ceramide suppresses the growth of head and neck tumors through the inhibition of pro-angiogenic signals such as VEGF, VEGF receptor-2, and HIF-1alpha.	Glucosylceramides	47-64	hypoxia inducible factor 1, alpha subunit	Mus musculus	289-299
25661072-6	2015	We report that GlcCer inhibited messenger RNA and protein expression of tissue necrosis factor alpha and interleukin 1beta without cytotoxicity.	Glucosylceramides	15-21	interleukin 1 beta	Mus musculus	105-122
25655314-8	2015	Glucosylceramidase activity above levels required for clearance of glucosylceramide from tissues resulted in reversal of splenomegaly, reduced Gaucher cell infiltration and a restoration of hematological parameters.	Glucosylceramides	67-83	glucosylceramidase beta	Homo sapiens	0-18
25842368-1	2015	Deficiency of glucocerebrosidase (GBA) leads to Gaucher disease (GD), an inherited disorder characterised by storage of glucosylceramide (GlcCer) in lysosomes of tissue macrophages.	Glucosylceramides	120-136	glucosylceramidase beta	Homo sapiens	34-37
25842368-1	2015	Deficiency of glucocerebrosidase (GBA) leads to Gaucher disease (GD), an inherited disorder characterised by storage of glucosylceramide (GlcCer) in lysosomes of tissue macrophages.	Glucosylceramides	138-144	glucosylceramidase beta	Homo sapiens	34-37
26351046-2	2015	It results from an autosomal recessive deficiency of the lysosomal enzyme acid beta-glucosidase/ beta-glucocerebrosidase (GBA), which is responsible for hydrolysis of glucocerebroside/glucosylceramide (GlcCer) into glucose and ceramide.	Glucosylceramides	167-183	glucosylceramidase beta	Homo sapiens	97-120
26351046-2	2015	It results from an autosomal recessive deficiency of the lysosomal enzyme acid beta-glucosidase/ beta-glucocerebrosidase (GBA), which is responsible for hydrolysis of glucocerebroside/glucosylceramide (GlcCer) into glucose and ceramide.	Glucosylceramides	167-183	glucosylceramidase beta	Homo sapiens	122-125
26351046-2	2015	It results from an autosomal recessive deficiency of the lysosomal enzyme acid beta-glucosidase/ beta-glucocerebrosidase (GBA), which is responsible for hydrolysis of glucocerebroside/glucosylceramide (GlcCer) into glucose and ceramide.	Glucosylceramides	184-200	glucosylceramidase beta	Homo sapiens	97-120
26351046-2	2015	It results from an autosomal recessive deficiency of the lysosomal enzyme acid beta-glucosidase/ beta-glucocerebrosidase (GBA), which is responsible for hydrolysis of glucocerebroside/glucosylceramide (GlcCer) into glucose and ceramide.	Glucosylceramides	184-200	glucosylceramidase beta	Homo sapiens	122-125
25715344-1	2015	Glucosylceramide synthase (GCS) catalyzes the first committed step in the biosynthesis of glucosylceramide (GlcCer)-related glycosphingolipids (GSLs).	Glucosylceramides	90-106	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
25715344-1	2015	Glucosylceramide synthase (GCS) catalyzes the first committed step in the biosynthesis of glucosylceramide (GlcCer)-related glycosphingolipids (GSLs).	Glucosylceramides	90-106	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
25715344-1	2015	Glucosylceramide synthase (GCS) catalyzes the first committed step in the biosynthesis of glucosylceramide (GlcCer)-related glycosphingolipids (GSLs).	Glucosylceramides	108-114	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
25715344-1	2015	Glucosylceramide synthase (GCS) catalyzes the first committed step in the biosynthesis of glucosylceramide (GlcCer)-related glycosphingolipids (GSLs).	Glucosylceramides	108-114	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
25715344-6	2015	LacCer, the precursor of all GlcCer-related GSL, was significantly reduced only in BG1 cells treated with PPMP.	Glucosylceramides	29-35	cathepsin A	Homo sapiens	44-47
25715344-6	2015	LacCer, the precursor of all GlcCer-related GSL, was significantly reduced only in BG1 cells treated with PPMP.	Glucosylceramides	29-35	acyl-CoA synthetase bubblegum family member 1	Homo sapiens	83-86
25661072-8	2015	Glucosylceramide also suppressed prostaglandin E2 but not nitric oxide production, consistent with its inhibition of cyclooxygenase 2 but not of inducible nitric oxide synthase expression.	Glucosylceramides	0-16	prostaglandin-endoperoxide synthase 2	Mus musculus	117-133
25803043-4	2015	Here, we reveal that glucosylceramide accumulation in GBA2 knockout-mice alters cytoskeletal dynamics due to a more ordered lipid organization in the plasma membrane.	Glucosylceramides	21-37	glucosidase beta 2	Mus musculus	54-58
25661072-9	2015	The molecular mechanism of GlcCer-mediated inhibition of LPS-induced inflammation in RAW 264.7 cells is closely related to suppression of NF-kappaB p65 subunit nuclear translocation as well as to phosphorylation of extracellular signal-regulated kinase and, in particular, p38 MAPK.	Glucosylceramides	27-33	mitogen-activated protein kinase 14	Mus musculus	273-281
25661072-11	2015	In conclusion, GlcCer inhibits LPS-induced inflammation by blocking the nuclear translocation of NF-kappaB and inhibiting the phosphorylation of extracellular signal-regulated kinase/p38 MAPK pathways in macrophages, suggesting that it might be a promising potential drug candidate for various inflammatory diseases.	Glucosylceramides	15-21	mitogen-activated protein kinase 14	Mus musculus	183-191
25552189-14	2015	Ceramide, the product of hydrolysis of glucosylceramide by GBA and involved in the regulation of cell differentiation, survival and apoptosis, is another putative candidate linking increased GBA activity to preeclampsia.	Glucosylceramides	39-55	glucosylceramidase beta	Homo sapiens	59-62
25552189-14	2015	Ceramide, the product of hydrolysis of glucosylceramide by GBA and involved in the regulation of cell differentiation, survival and apoptosis, is another putative candidate linking increased GBA activity to preeclampsia.	Glucosylceramides	39-55	glucosylceramidase beta	Homo sapiens	191-194
25239269-1	2014	Eliglustat [Cerdelga  (US, EU)], a small-molecule oral glucosylceramide analogue that inhibits the enzyme glucosylceramide synthase has been developed by Genzyme Corporation (a subsidiary of Sanofi) for the treatment of Gaucher disease type 1 in adults.	Glucosylceramides	55-71	UDP-glucose ceramide glucosyltransferase	Homo sapiens	106-131
25145677-5	2015	Herein, we show that in a model of highly glycolytic cells, generation of the glycosphingolipid (GSL) glucosylceramide (GlcCer) by GCS was elevated in response to increased glucose availability, while glucose deprivation diminished GSL levels.	Glucosylceramides	120-126	UDP-glucose ceramide glucosyltransferase	Homo sapiens	131-134
25551612-1	2014	Gaucher disease is a lysosomal storage disease caused by defective activity of acid beta-glucosidase (GCase), which leads to the accumulation of its major substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph) in many cells.	Glucosylceramides	167-183	glucosidase, beta, acid	Mus musculus	84-100
25551612-1	2014	Gaucher disease is a lysosomal storage disease caused by defective activity of acid beta-glucosidase (GCase), which leads to the accumulation of its major substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph) in many cells.	Glucosylceramides	167-183	glucosidase, beta, acid	Mus musculus	102-107
25551612-1	2014	Gaucher disease is a lysosomal storage disease caused by defective activity of acid beta-glucosidase (GCase), which leads to the accumulation of its major substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph) in many cells.	Glucosylceramides	185-191	glucosidase, beta, acid	Mus musculus	84-100
25551612-1	2014	Gaucher disease is a lysosomal storage disease caused by defective activity of acid beta-glucosidase (GCase), which leads to the accumulation of its major substrates, glucosylceramide (GlcCer) and glucosylsphingosine (GlcSph) in many cells.	Glucosylceramides	185-191	glucosidase, beta, acid	Mus musculus	102-107
25551612-5	2014	GCStg/Gba1 mice showed 2-3 fold increases in tissue GCS activity as well as accelerated GlcCer accumulation and the appearance of lipid-laden CD68 positive macrophages in visceral organs.	Glucosylceramides	88-94	glucosidase, beta, acid	Mus musculus	6-10
25551612-5	2014	GCStg/Gba1 mice showed 2-3 fold increases in tissue GCS activity as well as accelerated GlcCer accumulation and the appearance of lipid-laden CD68 positive macrophages in visceral organs.	Glucosylceramides	88-94	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-3
25515322-1	2014	Gaucher disease is a rare autosomal recessive disorder of glycosphingolipid metabolism resulting from deficient activity of the lysosomal enzyme beta-glucocerebrosidase that causes accumulation of glucosylceramide in tissue macrophage with damage to hematological, visceral, and skeletal organ systems.	Glucosylceramides	197-213	glucosylceramidase beta	Homo sapiens	145-168
25374574-10	2014	The levels of several species of glucosylceramide and glycosylinositolphosphoceramide tended to be higher in pPLAIIIbeta-OE than in WT.	Glucosylceramides	33-49	patatin-like protein 6	Arabidopsis thaliana	109-120
24266736-7	2014	Inhibition of ceramide conversion into glucosylceramide promotes liberation of c-Src from microdomains, and inhibition of de novo ceramide synthesis restores the microdomain distribution of c-Src and suppresses malignant phenotypes such as increased cell motility and anchorage-independent cell growth.	Glucosylceramides	39-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	79-84
24960545-7	2014	We found upregulation of specific sphingolipid enzymes, namely sphingomyelin synthase 1 (SMS1), sphingomyelinase 3 (SMPD3), and glucosylceramide synthase (GCS) in the endometrium of endometriotic women with corresponding increased GlcCer, decreased sphingomyelin levels, and decreased apoptosis in the endometrium.	Glucosylceramides	231-237	sphingomyelin synthase 1	Homo sapiens	63-87
24960545-7	2014	We found upregulation of specific sphingolipid enzymes, namely sphingomyelin synthase 1 (SMS1), sphingomyelinase 3 (SMPD3), and glucosylceramide synthase (GCS) in the endometrium of endometriotic women with corresponding increased GlcCer, decreased sphingomyelin levels, and decreased apoptosis in the endometrium.	Glucosylceramides	231-237	sphingomyelin synthase 1	Homo sapiens	89-93
24960545-7	2014	We found upregulation of specific sphingolipid enzymes, namely sphingomyelin synthase 1 (SMS1), sphingomyelinase 3 (SMPD3), and glucosylceramide synthase (GCS) in the endometrium of endometriotic women with corresponding increased GlcCer, decreased sphingomyelin levels, and decreased apoptosis in the endometrium.	Glucosylceramides	231-237	sphingomyelin phosphodiesterase 3	Homo sapiens	116-121
24960545-7	2014	We found upregulation of specific sphingolipid enzymes, namely sphingomyelin synthase 1 (SMS1), sphingomyelinase 3 (SMPD3), and glucosylceramide synthase (GCS) in the endometrium of endometriotic women with corresponding increased GlcCer, decreased sphingomyelin levels, and decreased apoptosis in the endometrium.	Glucosylceramides	231-237	UDP-glucose ceramide glucosyltransferase	Homo sapiens	155-158
25122154-8	2014	Plants in which IPUT1 was silenced accumulated IPC, the immediate precursor, as well as ceramides and glucosylceramides.	Glucosylceramides	102-119	plant glycogenin-like starch initiation protein 6	Arabidopsis thaliana	16-21
24935484-3	2014	Lately, mutations in the GBA gene were recognized as a major cause for the development of PD.Mutations in the GBA gene, which encodes for lysosomal beta-glucocerebrosidase (GCase), lead to Gaucher disease (GD), an autosomal recessive sphingolipidosis characterized by accumulation of glucosylceramide, mainly in monocyte-derived cells.	Glucosylceramides	284-300	glucosylceramidase beta	Homo sapiens	25-28
24935484-3	2014	Lately, mutations in the GBA gene were recognized as a major cause for the development of PD.Mutations in the GBA gene, which encodes for lysosomal beta-glucocerebrosidase (GCase), lead to Gaucher disease (GD), an autosomal recessive sphingolipidosis characterized by accumulation of glucosylceramide, mainly in monocyte-derived cells.	Glucosylceramides	284-300	glucosylceramidase beta	Homo sapiens	110-113
24935484-3	2014	Lately, mutations in the GBA gene were recognized as a major cause for the development of PD.Mutations in the GBA gene, which encodes for lysosomal beta-glucocerebrosidase (GCase), lead to Gaucher disease (GD), an autosomal recessive sphingolipidosis characterized by accumulation of glucosylceramide, mainly in monocyte-derived cells.	Glucosylceramides	284-300	glucosylceramidase beta	Homo sapiens	148-171
24935484-3	2014	Lately, mutations in the GBA gene were recognized as a major cause for the development of PD.Mutations in the GBA gene, which encodes for lysosomal beta-glucocerebrosidase (GCase), lead to Gaucher disease (GD), an autosomal recessive sphingolipidosis characterized by accumulation of glucosylceramide, mainly in monocyte-derived cells.	Glucosylceramides	284-300	glucosylceramidase beta	Homo sapiens	173-178
24064337-2	2014	Gaucher disease is caused by the defective activity of the lysosomal enzyme, glucocerebrosidase (GCase; GBA1), resulting in intracellular accumulation of the glycosphingolipids, glucosylceramide and psychosine.	Glucosylceramides	178-194	glucosidase, beta, acid	Mus musculus	77-95
24064337-2	2014	Gaucher disease is caused by the defective activity of the lysosomal enzyme, glucocerebrosidase (GCase; GBA1), resulting in intracellular accumulation of the glycosphingolipids, glucosylceramide and psychosine.	Glucosylceramides	178-194	glucosidase, beta, acid	Mus musculus	97-102
24064337-2	2014	Gaucher disease is caused by the defective activity of the lysosomal enzyme, glucocerebrosidase (GCase; GBA1), resulting in intracellular accumulation of the glycosphingolipids, glucosylceramide and psychosine.	Glucosylceramides	178-194	glucosidase, beta, acid	Mus musculus	104-108
24824606-8	2014	Further, an up-regulation of GLTP caused a substantial increase in both the Gb3 and glucosylceramide levels compared to the controls.	Glucosylceramides	84-100	glycolipid transfer protein	Homo sapiens	29-33
24448832-8	2014	In agreement with previous data that demonstrated extrusion of (glucosyl)ceramides by ABCB1 (Lee et al.	Glucosylceramides	63-82	ATP binding cassette subfamily B member 1	Canis lupus familiaris	86-91
24448832-12	2014	In conclusion, nickel induces a ROS-ceramide pathway to cause apoptotic cell death as well as activate adaptive survival responses, including upregulation of ABCB1, which improves cell survival by extruding proapoptotic (glucosyl)ceramides.	Glucosylceramides	220-239	ATP binding cassette subfamily B member 1	Canis lupus familiaris	158-163
24214972-0	2014	Ceramides and glucosylceramides are independent antagonists of insulin signaling.	Glucosylceramides	14-31	insulin	Homo sapiens	63-70
24214972-5	2014	3) Overexpression of glucosylceramide synthase in myotubes induces glucosylceramide but enhances insulin signaling.	Glucosylceramides	21-37	insulin	Homo sapiens	97-104
23880767-1	2013	beta-Glucosidase 2 (GBA2) is an enzyme that cleaves the membrane lipid glucosylceramide into glucose and ceramide.	Glucosylceramides	71-87	glucosidase beta 2	Mus musculus	0-18
24070122-11	2013	GlcCer levels in the spleen from Gba1/Gba2 knockout mice were much higher than the sum of the single knockouts, indicating a cross-talk between the two glucosylceramidases and suggesting a partially compensation of the loss of one enzyme by the other.	Glucosylceramides	0-6	glucosidase, beta, acid	Mus musculus	33-37
24070122-11	2013	GlcCer levels in the spleen from Gba1/Gba2 knockout mice were much higher than the sum of the single knockouts, indicating a cross-talk between the two glucosylceramidases and suggesting a partially compensation of the loss of one enzyme by the other.	Glucosylceramides	0-6	glucosidase beta 2	Mus musculus	38-42
24058461-1	2013	BACKGROUND: Mutations in the gene coding for glucocerebrosidase (GBA), which metabolizes glucosylceramide (a monohexosylceramide) into glucose and ceramide, is the most common genetic risk factor for sporadic Parkinson"s disease (PD).	Glucosylceramides	89-105	glucosylceramidase beta	Homo sapiens	45-63
24058461-1	2013	BACKGROUND: Mutations in the gene coding for glucocerebrosidase (GBA), which metabolizes glucosylceramide (a monohexosylceramide) into glucose and ceramide, is the most common genetic risk factor for sporadic Parkinson"s disease (PD).	Glucosylceramides	89-105	glucosylceramidase beta	Homo sapiens	65-68
24977484-4	2014	Changes in glucosylceramide synthase (GCS) activity were identified by incorporation of radiolabeled UDP-glucose in glucosylceramide, changes in gene expression via real-time PCR and Western blot analysis.	Glucosylceramides	11-27	UDP-glucose ceramide glucosyltransferase	Mus musculus	38-41
23880767-1	2013	beta-Glucosidase 2 (GBA2) is an enzyme that cleaves the membrane lipid glucosylceramide into glucose and ceramide.	Glucosylceramides	71-87	glucosidase beta 2	Mus musculus	20-24
23880767-6	2013	Compared with the well characterized impact of CBE on the lysosomal glucosylceramide-degrading enzyme (glucocerebrosidase, GBA), CBE inactivated GBA2 less efficiently, due to a lower affinity for this enzyme (higher KI) and a lower rate of enzyme inactivation (k(inact)).	Glucosylceramides	68-84	glucosidase, beta, acid	Mus musculus	103-121
23880767-6	2013	Compared with the well characterized impact of CBE on the lysosomal glucosylceramide-degrading enzyme (glucocerebrosidase, GBA), CBE inactivated GBA2 less efficiently, due to a lower affinity for this enzyme (higher KI) and a lower rate of enzyme inactivation (k(inact)).	Glucosylceramides	68-84	glucosidase, beta, acid	Mus musculus	123-126
23880767-6	2013	Compared with the well characterized impact of CBE on the lysosomal glucosylceramide-degrading enzyme (glucocerebrosidase, GBA), CBE inactivated GBA2 less efficiently, due to a lower affinity for this enzyme (higher KI) and a lower rate of enzyme inactivation (k(inact)).	Glucosylceramides	68-84	glucosidase beta 2	Mus musculus	145-149
23913272-2	2013	We previously identified a non-vesicular intra-Golgi transport pathway for glucosylceramide (GlcCer)--the common precursor of the different series of glycosphingolipids-that is operated by the cytosolic GlcCer-transfer protein FAPP2 (also known as PLEKHA8) (ref.	Glucosylceramides	75-91	pleckstrin homology domain containing, family A (phosphoinositide binding specific) member 8	Mus musculus	227-232
23151684-3	2013	One factor may be the activity of the non-lysosomal beta-glucosidase (GBA2) which exhibits catalytic activity towards glucosylceramide and is reported to be highly expressed in brain tissue.	Glucosylceramides	118-134	glucosylceramidase beta 2	Homo sapiens	70-74
23894633-11	2013	We also found that an 80% loss of glucosylceramide due to glucosylceramide synthase knockdown resulted in a significant reduction in the expression of GLTP.	Glucosylceramides	34-50	UDP-glucose ceramide glucosyltransferase	Homo sapiens	58-83
23913272-2	2013	We previously identified a non-vesicular intra-Golgi transport pathway for glucosylceramide (GlcCer)--the common precursor of the different series of glycosphingolipids-that is operated by the cytosolic GlcCer-transfer protein FAPP2 (also known as PLEKHA8) (ref.	Glucosylceramides	75-91	pleckstrin homology domain containing, family A (phosphoinositide binding specific) member 8	Mus musculus	248-255
23913272-2	2013	We previously identified a non-vesicular intra-Golgi transport pathway for glucosylceramide (GlcCer)--the common precursor of the different series of glycosphingolipids-that is operated by the cytosolic GlcCer-transfer protein FAPP2 (also known as PLEKHA8) (ref.	Glucosylceramides	93-99	pleckstrin homology domain containing, family A (phosphoinositide binding specific) member 8	Mus musculus	227-232
23913272-2	2013	We previously identified a non-vesicular intra-Golgi transport pathway for glucosylceramide (GlcCer)--the common precursor of the different series of glycosphingolipids-that is operated by the cytosolic GlcCer-transfer protein FAPP2 (also known as PLEKHA8) (ref.	Glucosylceramides	93-99	pleckstrin homology domain containing, family A (phosphoinositide binding specific) member 8	Mus musculus	248-255
23913272-4	2013	However, the molecular determinants of the FAPP2-mediated transfer of GlcCer from the cis-Golgi to the trans-Golgi network, as well as the physiological relevance of maintaining two parallel transport pathways of GlcCer--vesicular and non-vesicular--through the Golgi, remain poorly defined.	Glucosylceramides	70-76	pleckstrin homology domain containing, family A (phosphoinositide binding specific) member 8	Mus musculus	43-48
23473748-8	2013	Thus, UDP-glucose:ceramide glucosyltransferase (Ugcg), catalyzing the basic step of the glucosylceramide-based GSL-biosynthesis, was genetically disrupted.	Glucosylceramides	88-104	UDP-glucose ceramide glucosyltransferase	Mus musculus	6-46
23573974-1	2013	Gaucher disease is a progressive lysosomal storage disorder caused by a deficiency in the activity of beta-glucocerebrosidase and is characterized by the accumulation of the glycosphingolipid glucosylceramide in the lysosomes of macrophages that leads to dysfunction in multiple organ system.	Glucosylceramides	192-208	glucosylceramidase beta	Homo sapiens	102-125
23501591-8	2013	Moreover, evidence in favor of CERKL binding to GlcCer, GalCer and sphingomyelin has been gathered.	Glucosylceramides	48-54	ceramide kinase-like	Mus musculus	31-36
23473748-8	2013	Thus, UDP-glucose:ceramide glucosyltransferase (Ugcg), catalyzing the basic step of the glucosylceramide-based GSL-biosynthesis, was genetically disrupted.	Glucosylceramides	88-104	UDP-glucose ceramide glucosyltransferase	Mus musculus	48-52
22609461-6	2013	ORP3 silencing affected most the glucosyl ceramides (GluCer, decrease) and PE-plasmalogens (PE-pl, decrease), while ORP8 silencing increased FC and CE, and decreased GluCer and PE-pl.	Glucosylceramides	33-51	oxysterol binding protein-like 3	Mus musculus	0-4
22609461-6	2013	ORP3 silencing affected most the glucosyl ceramides (GluCer, decrease) and PE-plasmalogens (PE-pl, decrease), while ORP8 silencing increased FC and CE, and decreased GluCer and PE-pl.	Glucosylceramides	53-59	oxysterol binding protein-like 3	Mus musculus	0-4
23073830-7	2013	We report that GBA2 is down-regulated in melanoma; inducible expression of GBA2 affects endogenous sphingolipid metabolism by promoting glucosylceramide degradation (decrease by 78%) and ceramide generation; this is followed by a UPR that causes apoptosis, subsequent decreased anchorage-independent cell growth, and reduced in vivo tumor growth (by 40%); and all these events are abrogated when expressing a catalytically inactive GBA2.	Glucosylceramides	136-152	glucosylceramidase beta 2	Homo sapiens	75-79
23332916-3	2013	GBA2 encodes a microsomal nonlysosomal glucosylceramidase that catalyzes the conversion of glucosylceramide to free glucose and ceramide and the hydrolysis of bile acid 3-O-glucosides.	Glucosylceramides	91-107	glucosylceramidase beta 2	Homo sapiens	0-4
23159414-1	2013	Phosphoinositol 4-phosphate adaptor protein-2 (FAPP2) plays a key role in glycosphingolipid (GSL) production using its C-terminal domain to transport newly synthesized glucosylceramide away from the cytosol-facing glucosylceramide synthase in the cis-Golgi for further anabolic processing.	Glucosylceramides	168-184	pleckstrin homology domain containing A8	Homo sapiens	47-52
23159414-5	2013	A structurally-based preference for other simple uncharged GSLs, in addition to glucosylceramide, makes human FAPP2-GLTP more similar to fungal HET-C2 than to plant AtGLTP1 (glucosylceramide-specific) or to broadly GSL-selective human GLTP.	Glucosylceramides	80-96	pleckstrin homology domain containing A8	Homo sapiens	110-115
23159414-5	2013	A structurally-based preference for other simple uncharged GSLs, in addition to glucosylceramide, makes human FAPP2-GLTP more similar to fungal HET-C2 than to plant AtGLTP1 (glucosylceramide-specific) or to broadly GSL-selective human GLTP.	Glucosylceramides	174-190	pleckstrin homology domain containing A8	Homo sapiens	110-115
23158495-1	2013	Gaucher disease (GD) is characterized by accumulation of glucosylceramide in lysosomes due to mutations in the GBA1 gene encoding the lysosomal hydrolase beta-glucocerebrosidase (GCase).	Glucosylceramides	57-73	glucosylceramidase beta	Homo sapiens	111-115
23158495-1	2013	Gaucher disease (GD) is characterized by accumulation of glucosylceramide in lysosomes due to mutations in the GBA1 gene encoding the lysosomal hydrolase beta-glucocerebrosidase (GCase).	Glucosylceramides	57-73	glucosylceramidase beta	Homo sapiens	154-177
23158495-1	2013	Gaucher disease (GD) is characterized by accumulation of glucosylceramide in lysosomes due to mutations in the GBA1 gene encoding the lysosomal hydrolase beta-glucocerebrosidase (GCase).	Glucosylceramides	57-73	glucosylceramidase beta	Homo sapiens	179-184
23073830-7	2013	We report that GBA2 is down-regulated in melanoma; inducible expression of GBA2 affects endogenous sphingolipid metabolism by promoting glucosylceramide degradation (decrease by 78%) and ceramide generation; this is followed by a UPR that causes apoptosis, subsequent decreased anchorage-independent cell growth, and reduced in vivo tumor growth (by 40%); and all these events are abrogated when expressing a catalytically inactive GBA2.	Glucosylceramides	136-152	glucosylceramidase beta 2	Homo sapiens	75-79
23563543-0	2013	Dietary glucosylceramide enhances tight junction function in skin epidermis via induction of claudin-1.	Glucosylceramides	8-24	claudin 1	Mus musculus	93-102
23290777-1	2013	Glucosylceramide synthase (GCS), converting ceramide to glucosylceramide, catalyzes the first reaction of ceramide glycosylation in sphingolipid metabolism.	Glucosylceramides	56-72	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
23290777-1	2013	Glucosylceramide synthase (GCS), converting ceramide to glucosylceramide, catalyzes the first reaction of ceramide glycosylation in sphingolipid metabolism.	Glucosylceramides	56-72	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
23250757-1	2013	GBA1 and GBA2 are both beta-glucosidases, which cleave glucosylceramide (GlcCer) to glucose and ceramide.	Glucosylceramides	55-71	glucosylceramidase beta	Homo sapiens	0-4
23250757-1	2013	GBA1 and GBA2 are both beta-glucosidases, which cleave glucosylceramide (GlcCer) to glucose and ceramide.	Glucosylceramides	55-71	glucosylceramidase beta 2	Homo sapiens	9-13
23250757-1	2013	GBA1 and GBA2 are both beta-glucosidases, which cleave glucosylceramide (GlcCer) to glucose and ceramide.	Glucosylceramides	73-79	glucosylceramidase beta	Homo sapiens	0-4
23250757-1	2013	GBA1 and GBA2 are both beta-glucosidases, which cleave glucosylceramide (GlcCer) to glucose and ceramide.	Glucosylceramides	73-79	glucosylceramidase beta 2	Homo sapiens	9-13
23250757-4	2013	Knocking out the non-lysosomal GBA2 in mice results in accumulation of GlcCer outside the lysosomes in various tissues (e.g. testis and liver) and impairs sperm development and liver regeneration.	Glucosylceramides	71-77	glucosidase beta 2	Mus musculus	31-35
23250757-10	2013	GBA2 is localized at the ER and Golgi, which puts GBA2 in a key position for a lysosome-independent route of GlcCer-dependent signaling.	Glucosylceramides	109-115	glucosylceramidase beta 2	Homo sapiens	0-4
23250757-10	2013	GBA2 is localized at the ER and Golgi, which puts GBA2 in a key position for a lysosome-independent route of GlcCer-dependent signaling.	Glucosylceramides	109-115	glucosylceramidase beta 2	Homo sapiens	50-54
23563543-1	2013	Dietary glucosylceramide increased the expression of claudin-1 in UVB-irradiated mouse epidermis.	Glucosylceramides	8-24	claudin 1	Mus musculus	53-62
23563543-3	2013	Our results indicate that the skin barrier improvement induced by dietary glucosylceramide might be due to enhancement of tight junction function, mediated by increased expression of claudin-1 induced by sphingoid metabolites.	Glucosylceramides	74-90	claudin 1	Mus musculus	183-192
23555901-4	2013	ARF6 knockdown also resulted in increased glucosylceramide levels and decreased sphingomyelin levels, but did not affect the levels of ceramide or phospholipids.	Glucosylceramides	42-58	ADP-ribosylation factor 6	Mus musculus	0-4
23073611-7	2013	GCS regulates the balance between apoptotic ceramide and antiapoptotic GlcCer.	Glucosylceramides	71-77	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
23377801-8	2013	Glucosylceramide (GlcCer), the GCase substrate, influenced formation of purified a-syn by stabilizing soluble oligomeric intermediates.	Glucosylceramides	0-16	synuclein, alpha	Mus musculus	81-86
23377801-8	2013	Glucosylceramide (GlcCer), the GCase substrate, influenced formation of purified a-syn by stabilizing soluble oligomeric intermediates.	Glucosylceramides	18-24	glucosidase, beta, acid	Mus musculus	31-36
23377801-8	2013	Glucosylceramide (GlcCer), the GCase substrate, influenced formation of purified a-syn by stabilizing soluble oligomeric intermediates.	Glucosylceramides	18-24	synuclein, alpha	Mus musculus	81-86
23690856-5	2013	Long-term treatment of glucosylceramide decreased the expression of iNOS and COX-2 in the brain of aged mice.	Glucosylceramides	23-39	nitric oxide synthase 2, inducible	Mus musculus	68-72
23690856-5	2013	Long-term treatment of glucosylceramide decreased the expression of iNOS and COX-2 in the brain of aged mice.	Glucosylceramides	23-39	cytochrome c oxidase II, mitochondrial	Mus musculus	77-82
23470440-2	2013	Three glucocerebroside molecular species (CFC-1, CFC-2 and CFC-3) were isolated from crude total cerebrosides with repeated column chromatography.	Glucosylceramides	6-22	mitogen-activated protein kinase kinase 1	Homo sapiens	59-64
23470440-9	2013	Moreover, CFC-3 was most effective in four glucocerebrosides to Caco-2 cell viability.	Glucosylceramides	43-60	mitogen-activated protein kinase kinase 1	Homo sapiens	10-15
23073611-6	2013	GlcCer, generated by glucosylceramide synthase (GCS) that transfers the glucose from UDP-glucose to ceramide, is an important glycosphingolipid metabolic intermediate.	Glucosylceramides	0-6	UDP-glucose ceramide glucosyltransferase	Homo sapiens	21-46
23073611-6	2013	GlcCer, generated by glucosylceramide synthase (GCS) that transfers the glucose from UDP-glucose to ceramide, is an important glycosphingolipid metabolic intermediate.	Glucosylceramides	0-6	UDP-glucose ceramide glucosyltransferase	Homo sapiens	48-51
23555901-5	2013	We speculated that the ARF6 knockdown-induced increase in glucosylceramide was caused by an effect on glucosylceramide synthase and, in agreement, showed that ARF6 knockdown increased the mRNA levels and activity of glucosylceramide synthase.	Glucosylceramides	58-74	ADP-ribosylation factor 6	Mus musculus	23-27
23555901-5	2013	We speculated that the ARF6 knockdown-induced increase in glucosylceramide was caused by an effect on glucosylceramide synthase and, in agreement, showed that ARF6 knockdown increased the mRNA levels and activity of glucosylceramide synthase.	Glucosylceramides	58-74	UDP-glucose ceramide glucosyltransferase	Mus musculus	102-127
23555901-5	2013	We speculated that the ARF6 knockdown-induced increase in glucosylceramide was caused by an effect on glucosylceramide synthase and, in agreement, showed that ARF6 knockdown increased the mRNA levels and activity of glucosylceramide synthase.	Glucosylceramides	58-74	UDP-glucose ceramide glucosyltransferase	Mus musculus	216-241
23555901-7	2013	Our results thus show that ARF6 regulates neuronal differentiation through an effect on glucosylceramide synthase and glucosylceramide levels.	Glucosylceramides	88-104	ADP-ribosylation factor 6	Mus musculus	27-31
23520473-1	2013	Gaucher disease results from GBA1 mutations that lead to defective acid beta-glucosidase (GCase) mediated cleavage of glucosylceramide (GC) and glucosylsphingosine as well as heterogeneous manifestations in the viscera and CNS.	Glucosylceramides	118-134	glucosidase, beta, acid	Mus musculus	29-33
23520473-1	2013	Gaucher disease results from GBA1 mutations that lead to defective acid beta-glucosidase (GCase) mediated cleavage of glucosylceramide (GC) and glucosylsphingosine as well as heterogeneous manifestations in the viscera and CNS.	Glucosylceramides	118-134	glucosidase, beta, acid	Mus musculus	72-88
23520473-1	2013	Gaucher disease results from GBA1 mutations that lead to defective acid beta-glucosidase (GCase) mediated cleavage of glucosylceramide (GC) and glucosylsphingosine as well as heterogeneous manifestations in the viscera and CNS.	Glucosylceramides	118-134	glucosidase, beta, acid	Mus musculus	90-95
23520473-1	2013	Gaucher disease results from GBA1 mutations that lead to defective acid beta-glucosidase (GCase) mediated cleavage of glucosylceramide (GC) and glucosylsphingosine as well as heterogeneous manifestations in the viscera and CNS.	Glucosylceramides	90-92	glucosidase, beta, acid	Mus musculus	29-33
23520473-1	2013	Gaucher disease results from GBA1 mutations that lead to defective acid beta-glucosidase (GCase) mediated cleavage of glucosylceramide (GC) and glucosylsphingosine as well as heterogeneous manifestations in the viscera and CNS.	Glucosylceramides	90-92	glucosidase, beta, acid	Mus musculus	72-88
22772462-1	2012	Gaucher"s disease is caused by a deficiency of glucocerebrosidase (GBA) and results in the accumulation of glucocerebroside within macrophages.	Glucosylceramides	107-123	glucosylceramidase beta	Homo sapiens	67-70
23690856-6	2013	The LPS-induced mRNA level of iNOS, COX-2, IL-1 beta , and TNF- alpha was reduced by the acute treatment with glucosylceramide in adult mice.	Glucosylceramides	110-126	nitric oxide synthase 2, inducible	Mus musculus	30-34
23690856-6	2013	The LPS-induced mRNA level of iNOS, COX-2, IL-1 beta , and TNF- alpha was reduced by the acute treatment with glucosylceramide in adult mice.	Glucosylceramides	110-126	cytochrome c oxidase II, mitochondrial	Mus musculus	36-41
23690856-6	2013	The LPS-induced mRNA level of iNOS, COX-2, IL-1 beta , and TNF- alpha was reduced by the acute treatment with glucosylceramide in adult mice.	Glucosylceramides	110-126	interleukin 1 beta	Mus musculus	43-52
23690856-6	2013	The LPS-induced mRNA level of iNOS, COX-2, IL-1 beta , and TNF- alpha was reduced by the acute treatment with glucosylceramide in adult mice.	Glucosylceramides	110-126	tumor necrosis factor	Mus musculus	59-69
22927247-5	2012	We identified BCR engagement to catalyze the crucial modification of ceramide to glucosylceramide via UDP-glucose ceramide glucosyltransferase (UGCG).	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	102-142
22927247-5	2012	We identified BCR engagement to catalyze the crucial modification of ceramide to glucosylceramide via UDP-glucose ceramide glucosyltransferase (UGCG).	Glucosylceramides	81-97	UDP-glucose ceramide glucosyltransferase	Homo sapiens	144-148
22623374-1	2012	Mutations in the GBA gene, encoding the lysosomal acid beta-glucocerebrosidase (GCase), lead to deficient activity of the enzyme in the lysosomes, to glucosylceramide accumulation and to development of Gaucher disease (GD).	Glucosylceramides	150-166	glucosylceramidase beta	Homo sapiens	17-20
22623374-1	2012	Mutations in the GBA gene, encoding the lysosomal acid beta-glucocerebrosidase (GCase), lead to deficient activity of the enzyme in the lysosomes, to glucosylceramide accumulation and to development of Gaucher disease (GD).	Glucosylceramides	150-166	glucosylceramidase beta	Homo sapiens	55-78
22623374-1	2012	Mutations in the GBA gene, encoding the lysosomal acid beta-glucocerebrosidase (GCase), lead to deficient activity of the enzyme in the lysosomes, to glucosylceramide accumulation and to development of Gaucher disease (GD).	Glucosylceramides	150-166	glucosylceramidase beta	Homo sapiens	80-85
22566609-1	2012	Gaucher"s disease, the most common lysosomal storage disorder, is caused by the defective activity of glucocerebrosidase, the lysosomal hydrolase that degrades glucosylceramide.	Glucosylceramides	160-176	glucosidase, beta, acid	Mus musculus	102-120
22764777-0	2012	Beta-glucosidase 2 knockout mice with increased glucosylceramide show impaired liver regeneration.	Glucosylceramides	48-64	glucosidase beta 2	Mus musculus	0-18
22764777-2	2012	We previously generated beta-glucosidase 2 (GBA2) knockout mice that accumulate the glycolipid glucosylceramide in various tissues, including the liver.	Glucosylceramides	95-111	glucosidase beta 2	Mus musculus	24-42
22764777-2	2012	We previously generated beta-glucosidase 2 (GBA2) knockout mice that accumulate the glycolipid glucosylceramide in various tissues, including the liver.	Glucosylceramides	95-111	glucosidase beta 2	Mus musculus	44-48
22764777-10	2012	Accumulation of glucosylceramide was associated with a delay in liver regeneration and reduced serum levels of IL-6 and TNF-alpha.	Glucosylceramides	16-32	interleukin 6	Mus musculus	111-115
22764777-10	2012	Accumulation of glucosylceramide was associated with a delay in liver regeneration and reduced serum levels of IL-6 and TNF-alpha.	Glucosylceramides	16-32	tumor necrosis factor	Mus musculus	120-129
22451348-4	2012	Similarly, conduritol B epoxide, an inhibitor of beta-glucocerebrosidase, significantly down-regulated SC ceramide levels and significantly increased glucosylceramide levels.	Glucosylceramides	150-166	glucosylceramidase beta	Homo sapiens	49-72
22659419-2	2012	Beta-glucosidase 1 (GBA1; lysosomal glucocerebrosidase) and beta-glucosidase 2 (GBA2, non-lysosomal glucocerebrosidase) both have glucosylceramide as a main natural substrate.	Glucosylceramides	130-146	glucosidase, beta, acid	Mus musculus	20-24
22659419-2	2012	Beta-glucosidase 1 (GBA1; lysosomal glucocerebrosidase) and beta-glucosidase 2 (GBA2, non-lysosomal glucocerebrosidase) both have glucosylceramide as a main natural substrate.	Glucosylceramides	130-146	glucosidase beta 2	Mus musculus	60-78
22659419-2	2012	Beta-glucosidase 1 (GBA1; lysosomal glucocerebrosidase) and beta-glucosidase 2 (GBA2, non-lysosomal glucocerebrosidase) both have glucosylceramide as a main natural substrate.	Glucosylceramides	130-146	glucosidase beta 2	Mus musculus	80-84
22659419-5	2012	Given that GBA2 hydrolyses both BG and glucosylceramide, it was asked whether vice versa GBA1 hydrolyses both glucosylceramide and BG.	Glucosylceramides	39-55	glucosidase beta 2	Mus musculus	11-15
22659419-5	2012	Given that GBA2 hydrolyses both BG and glucosylceramide, it was asked whether vice versa GBA1 hydrolyses both glucosylceramide and BG.	Glucosylceramides	110-126	glucosidase, beta, acid	Mus musculus	89-93
22927247-9	2012	In summary, we identified the mode of action of novel kinase inhibitors CAL-101 and PCI-32765 by controlling the UGCG-mediated ceramide/glucosylceramide equilibrium as a downstream molecular switch of BCR signaling, also providing novel targeted treatment options beyond current chemotherapy-based regimens.	Glucosylceramides	136-152	UDP-glucose ceramide glucosyltransferase	Homo sapiens	113-117
22563011-3	2012	Accumulating evidence suggests a pathogenic role for glucosylceramide (GlcCer) in multiple forms of PKD.	Glucosylceramides	53-69	protein kinase D1	Mus musculus	100-103
22563011-3	2012	Accumulating evidence suggests a pathogenic role for glucosylceramide (GlcCer) in multiple forms of PKD.	Glucosylceramides	71-77	protein kinase D1	Mus musculus	100-103
22563011-10	2012	Surprisingly, genetic loss of Sphk1 exacerbated cystogenesis and was associated with increased levels of GlcCer and GM3.	Glucosylceramides	105-111	sphingosine kinase 1	Mus musculus	30-35
22726258-9	2012	RESULTS: Oral GlcCer administration significantly suppressed mRNA expression of the pro-inflammatory cytokines IL-1beta and IL-6.	Glucosylceramides	14-20	interleukin 1 beta	Mus musculus	111-119
22726258-9	2012	RESULTS: Oral GlcCer administration significantly suppressed mRNA expression of the pro-inflammatory cytokines IL-1beta and IL-6.	Glucosylceramides	14-20	interleukin 6	Mus musculus	124-128
22508690-2	2012	In this study, we found that the expression of mutant-PS1 in stable transfectants of SH-SY5Y neuroblastoma cells results in a reduction of the biosynthesis and steady-state levels of glucosylceramide.	Glucosylceramides	183-199	presenilin 1	Homo sapiens	54-57
22595426-1	2012	Gaucher disease is a lysosomal storage disease resulting from insufficient acid beta-glucosidase (glucocerebrosidase, GCase, EC 4.2.1.25) activity and the resultant accumulation of glucosylceramide.	Glucosylceramides	181-197	glucosidase, beta, acid	Mus musculus	118-123
22388998-1	2012	Mutations in GBA1 gene result in defective acid beta-glucosidase and the complex phenotype of Gaucher disease (GD) related to the accumulation of glucosylceramide-laden macrophages.	Glucosylceramides	146-162	glucosylceramidase beta	Homo sapiens	13-17
22337770-1	2012	Gaucher disease is a lysosomal storage disorder caused by a defect in the degradation of glucosylceramide catalyzed by the lysosomal enzyme beta-glucocerebrosidase (GBA).	Glucosylceramides	89-105	glucosylceramidase beta	Homo sapiens	140-163
22337770-1	2012	Gaucher disease is a lysosomal storage disorder caused by a defect in the degradation of glucosylceramide catalyzed by the lysosomal enzyme beta-glucocerebrosidase (GBA).	Glucosylceramides	89-105	glucosylceramidase beta	Homo sapiens	165-168
22384976-4	2012	Consistent with these genetic data, we demonstrated that RsAFP2 interacts with the cell wall of C. albicans, which also contains glucosylceramides, and activates the cell wall integrity pathway.	Glucosylceramides	129-146	defensin-like protein 2	Raphanus sativus	57-63