PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
24374347-1	2014	Sphingomyelin synthase (SMS), which catalyzes ceramide as one of the substrates to produce sphingomyelin, is a critical factor in the sphingolipid biosynthesis pathway.	Ceramides	46-54	spermine synthase	Homo sapiens	0-22
24374347-1	2014	Sphingomyelin synthase (SMS), which catalyzes ceramide as one of the substrates to produce sphingomyelin, is a critical factor in the sphingolipid biosynthesis pathway.	Ceramides	46-54	spermine synthase	Homo sapiens	24-27
24417605-10	2014	Both GM3 and GD3 were composed of heterogeneous ceramide lipid tails, including d18:1/16:0 and d18:1/23:0.	Ceramides	48-56	GRDX	Homo sapiens	13-16
24274756-14	2014	Impaired RV hypertrophy and triglyceride and ceramide deposition are present as a function of RV mutant Bmpr2 in mice; fatty acid oxidation impairment in human HPAH RVs may underlie this finding.	Ceramides	45-53	bone morphogenetic protein receptor, type II (serine/threonine kinase)	Mus musculus	104-109
25356388-6	2014	Compared to parental controls, levels of CERS2 mRNA, protein, and activity were reduced by ~50% in fibroblasts isolated from this proband, resulting in significantly reduced levels of ceramides and sphingomyelins containing the very long-chain fatty acids C24:0 and C26:0.	Ceramides	184-193	ceramide synthase 2	Homo sapiens	41-46
24422988-13	2014	CONCLUSION: We have identified xIAP and cIAP1 as molecular targets of ceramide and determined that ceramide analog LCL85 is an effective sensitizer in overcoming resistance of human cell lines established from metastatic colon and breast cancers to apoptosis induction to suppress metastasis in vivo.	Ceramides	70-78	X-linked inhibitor of apoptosis	Homo sapiens	31-35
24183824-5	2014	The neutral sphingomyelinase was found to be responsible for the increase of SM and the decrease of ceramide in plasma membranes of resveratrol-treated senescent hepatocytes.	Ceramides	100-108	sphingomyelin phosphodiesterase 2	Rattus norvegicus	4-28
24749054-2	2014	Among these lipid species, ceramides and more complex sphingolipids have gained recent attention as being pathophysiologically relevant for the development of insulin resistance and impaired glycemic control.	Ceramides	27-36	insulin	Homo sapiens	159-166
24749054-3	2014	Upon excess intake of saturated fat, ceramides accumulate in insulin sensitive tissues either as a consequence of de novo synthesis or through mobilization from complex sphingolipids.	Ceramides	37-46	insulin	Homo sapiens	61-68
24749054-4	2014	Clinical studies have confirmed positive correlation between plasma and tissue levels of several ceramide species and insulin resistance.	Ceramides	97-105	insulin	Homo sapiens	118-125
24749054-5	2014	At the cellular level, it has been demonstrated that ceramides impair insulin signaling and intracellular handling of glucose and lipids with resulting deleterious effects on cellular metabolism.	Ceramides	53-62	insulin	Homo sapiens	70-77
24482684-9	2014	Use of different PKC pharmacological inhibitors suggested that although all three classes of PKC molecules, i.e., classical, novel, and atypical, play roles in MgD-induced synthesis/release of ceramide, sphingosine, and cytokines as well as activation of NF-kB, to varying degrees, PKC-zeta appears to play a greater role in these events than any of the other PKC isoforms; a specific PKC-zeta inhibitory peptide inhibited formation of sphingosine.	Ceramides	193-201	protein kinase C zeta	Homo sapiens	93-96
24482684-9	2014	Use of different PKC pharmacological inhibitors suggested that although all three classes of PKC molecules, i.e., classical, novel, and atypical, play roles in MgD-induced synthesis/release of ceramide, sphingosine, and cytokines as well as activation of NF-kB, to varying degrees, PKC-zeta appears to play a greater role in these events than any of the other PKC isoforms; a specific PKC-zeta inhibitory peptide inhibited formation of sphingosine.	Ceramides	193-201	protein kinase C zeta	Homo sapiens	93-96
24422988-0	2014	Ceramide targets xIAP and cIAP1 to sensitize metastatic colon and breast cancer cells to apoptosis induction to suppress tumor progression.	Ceramides	0-8	X-linked inhibitor of apoptosis	Homo sapiens	17-21
24422988-13	2014	CONCLUSION: We have identified xIAP and cIAP1 as molecular targets of ceramide and determined that ceramide analog LCL85 is an effective sensitizer in overcoming resistance of human cell lines established from metastatic colon and breast cancers to apoptosis induction to suppress metastasis in vivo.	Ceramides	70-78	baculoviral IAP repeat containing 2	Homo sapiens	40-45
24422988-0	2014	Ceramide targets xIAP and cIAP1 to sensitize metastatic colon and breast cancer cells to apoptosis induction to suppress tumor progression.	Ceramides	0-8	baculoviral IAP repeat containing 2	Homo sapiens	26-31
24422988-11	2014	Silencing xIAP and cIAP1 with specific siRNAs significantly increased the metastatic human colon carcinoma cell sensitivity to Fas-mediated apoptosis, suggesting that IAP proteins mediate apoptosis resistance in metastatic human colon carcinoma cells and ceramide induces IAP protein degradation to sensitize the tumor cells to apoptosis induction.	Ceramides	255-263	X-linked inhibitor of apoptosis	Homo sapiens	10-14
24422988-13	2014	CONCLUSION: We have identified xIAP and cIAP1 as molecular targets of ceramide and determined that ceramide analog LCL85 is an effective sensitizer in overcoming resistance of human cell lines established from metastatic colon and breast cancers to apoptosis induction to suppress metastasis in vivo.	Ceramides	99-107	X-linked inhibitor of apoptosis	Homo sapiens	31-35
24422988-11	2014	Silencing xIAP and cIAP1 with specific siRNAs significantly increased the metastatic human colon carcinoma cell sensitivity to Fas-mediated apoptosis, suggesting that IAP proteins mediate apoptosis resistance in metastatic human colon carcinoma cells and ceramide induces IAP protein degradation to sensitize the tumor cells to apoptosis induction.	Ceramides	255-263	baculoviral IAP repeat containing 2	Homo sapiens	19-24
24139861-4	2014	Fatty acid 2-hydroxylase (FA2H) is one of the enzymes that introduce the hydroxyl group during de novo synthesis of ceramide.	Ceramides	116-124	fatty acid 2-hydroxylase	Mus musculus	0-24
24422988-11	2014	Silencing xIAP and cIAP1 with specific siRNAs significantly increased the metastatic human colon carcinoma cell sensitivity to Fas-mediated apoptosis, suggesting that IAP proteins mediate apoptosis resistance in metastatic human colon carcinoma cells and ceramide induces IAP protein degradation to sensitize the tumor cells to apoptosis induction.	Ceramides	255-263	alkaline phosphatase, intestinal	Homo sapiens	11-14
24259670-0	2014	Sphingomyelin synthase-related protein SMSr is a suppressor of ceramide-induced mitochondrial apoptosis.	Ceramides	63-71	sterile alpha motif domain containing 8	Homo sapiens	39-43
24259670-4	2014	Here we identify SMSr (SAMD8), an ER-resident ceramide phosphoethanolamine (CPE) synthase, as a suppressor of ceramide-mediated cell death.	Ceramides	46-54	sterile alpha motif domain containing 8	Homo sapiens	17-21
24259670-4	2014	Here we identify SMSr (SAMD8), an ER-resident ceramide phosphoethanolamine (CPE) synthase, as a suppressor of ceramide-mediated cell death.	Ceramides	46-54	sterile alpha motif domain containing 8	Homo sapiens	23-28
24259670-5	2014	Disruption of SMSr catalytic activity causes a rise in ER ceramides and their mislocalization to mitochondria, triggering a mitochondrial pathway of apoptosis.	Ceramides	58-67	sterile alpha motif domain containing 8	Homo sapiens	14-18
24259670-6	2014	Blocking de novo ceramide synthesis, stimulating ceramide export from the ER or targeting a bacterial ceramidase to mitochondria rescues SMSr-deficient cells from apoptosis.	Ceramides	17-25	sterile alpha motif domain containing 8	Homo sapiens	137-141
24259670-7	2014	We also show that SMSr-catalyzed CPE production, although essential, is not sufficient to suppress ceramide-induced cell death and that SMSr-mediated ceramide homeostasis requires the N-terminal sterile alpha-motif, or SAM domain, of the enzyme.	Ceramides	150-158	sterile alpha motif domain containing 8	Homo sapiens	136-140
24214972-0	2014	Ceramides and glucosylceramides are independent antagonists of insulin signaling.	Ceramides	0-9	insulin	Homo sapiens	63-70
24214972-3	2014	Of particular note, ceramides antagonize insulin signaling in both myotubes and adipocytes, whereas glucosyceramides are only efficacious in adipocytes: 1) In myotubes exposed to saturated fats, inhibitors of enzymes required for ceramide synthesis enhance insulin signaling, but those targeting glucosylceramide synthase have no effect.	Ceramides	20-29	insulin	Homo sapiens	41-48
24214972-3	2014	Of particular note, ceramides antagonize insulin signaling in both myotubes and adipocytes, whereas glucosyceramides are only efficacious in adipocytes: 1) In myotubes exposed to saturated fats, inhibitors of enzymes required for ceramide synthesis enhance insulin signaling, but those targeting glucosylceramide synthase have no effect.	Ceramides	20-28	insulin	Homo sapiens	41-48
24214972-4	2014	2) Exogenous ceramides antagonize insulin signaling in myotubes, whereas ganglioside precursors do not.	Ceramides	13-22	insulin	Homo sapiens	34-41
28357207-7	2014	We also provide evidence that TORC1 downstream effectors, the type 2A protein phosphatase Sit4p and the AGC protein kinase Sch9p, integrate nutrient and stress signals from TORC1 with ceramide signaling derived from Isc1p to regulate mitochondrial function and lifespan in yeast.	Ceramides	184-192	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	90-95
28357207-7	2014	We also provide evidence that TORC1 downstream effectors, the type 2A protein phosphatase Sit4p and the AGC protein kinase Sch9p, integrate nutrient and stress signals from TORC1 with ceramide signaling derived from Isc1p to regulate mitochondrial function and lifespan in yeast.	Ceramides	184-192	serine/threonine protein kinase SCH9	Saccharomyces cerevisiae S288C	123-128
28357207-7	2014	We also provide evidence that TORC1 downstream effectors, the type 2A protein phosphatase Sit4p and the AGC protein kinase Sch9p, integrate nutrient and stress signals from TORC1 with ceramide signaling derived from Isc1p to regulate mitochondrial function and lifespan in yeast.	Ceramides	184-192	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	216-221
24139861-4	2014	Fatty acid 2-hydroxylase (FA2H) is one of the enzymes that introduce the hydroxyl group during de novo synthesis of ceramide.	Ceramides	116-124	fatty acid 2-hydroxylase	Mus musculus	26-30
24422572-6	2014	The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.	Ceramides	81-89	NLR family pyrin domain containing 3	Homo sapiens	132-137
25151392-2	2014	Each GSL contains a complex carbohydrate chain linked to a ceramide moiety that anchors the molecule to biomembranes.	Ceramides	59-67	cathepsin A	Homo sapiens	5-8
24422572-6	2014	The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.	Ceramides	81-89	interleukin 1 beta	Homo sapiens	180-188
24422572-6	2014	The fact that the accumulation of metabolic substrates such as monosodium urate, ceramide, cholesterol, and glucose can trigger the NLRP3 inflammasome connects metabolic stress to IL-1beta-mediated inflammation and provides a rationale for therapeutically targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.	Ceramides	81-89	interleukin 1 beta	Homo sapiens	180-184
25280528-0	2014	Ceramide-mediated depression in cardiomyocyte contractility through PKC activation and modulation of myofilament protein phosphorylation.	Ceramides	0-8	protein kinase C, gamma	Rattus norvegicus	68-71
23725018-4	2014	Herein we aimed to study the possible role of nSMase-derived ceramide as a common factor in the acute oxygen-sensing function of specialized vascular tissues.	Ceramides	61-69	sphingomyelin phosphodiesterase 2	Gallus gallus	46-52
23725018-11	2014	INNOVATION: These data provide evidence for the proposal that nSMase-derived ceramide is a critical player in acute oxygen-sensing in specialized vascular tissues.	Ceramides	77-85	sphingomyelin phosphodiesterase 2	Gallus gallus	62-68
25280528-7	2014	Compared to controls, myocytes treated with ceramide exhibited increased phosphorylation of myosin binding protein-C (cMyBP-C), specifically at Ser273 and Ser302, and troponin I (cTnI) at sites apart from Ser23/24, which could be attenuated with PKC inhibition.	Ceramides	44-52	troponin I3, cardiac type	Rattus norvegicus	179-183
24417945-4	2014	Ceramide, a cytotoxic and insulin desensitizing lipid metabolite formed when peripheral tissues are exposed to excessive lipid deposition, is potently opposed by adiponectin.	Ceramides	0-8	adiponectin, C1Q and collagen domain containing	Homo sapiens	162-173
24417945-5	2014	Via adiponectin receptors, AdipoR1 and AdipoR2, adiponectin stimulates the deacylation of ceramide- yielding sphingosine for conversion to sphingosine 1-phosphate (S1P) by sphingosine kinase.	Ceramides	90-98	adiponectin, C1Q and collagen domain containing	Homo sapiens	4-15
24417945-5	2014	Via adiponectin receptors, AdipoR1 and AdipoR2, adiponectin stimulates the deacylation of ceramide- yielding sphingosine for conversion to sphingosine 1-phosphate (S1P) by sphingosine kinase.	Ceramides	90-98	adiponectin receptor 2	Homo sapiens	39-46
25280528-7	2014	Compared to controls, myocytes treated with ceramide exhibited increased phosphorylation of myosin binding protein-C (cMyBP-C), specifically at Ser273 and Ser302, and troponin I (cTnI) at sites apart from Ser23/24, which could be attenuated with PKC inhibition.	Ceramides	44-52	protein kinase C, gamma	Rattus norvegicus	246-249
25280528-8	2014	We conclude that the altered myofilament response to calcium resulting from multiple sites of PKC-dependent phosphorylation contributes to contractile dysfunction that is associated with cardiac diseases in which elevations in ceramides are present.	Ceramides	227-236	protein kinase C, gamma	Rattus norvegicus	94-97
24417945-5	2014	Via adiponectin receptors, AdipoR1 and AdipoR2, adiponectin stimulates the deacylation of ceramide- yielding sphingosine for conversion to sphingosine 1-phosphate (S1P) by sphingosine kinase.	Ceramides	90-98	adiponectin receptor 1	Homo sapiens	27-34
23969158-2	2014	However, mounting evidence implicates ceramides and their derivatives in various aspects of metabolism via directly impacting the insulin receptor as well as modulating cell survival and proliferation.	Ceramides	38-47	insulin receptor	Homo sapiens	130-146
24417945-5	2014	Via adiponectin receptors, AdipoR1 and AdipoR2, adiponectin stimulates the deacylation of ceramide- yielding sphingosine for conversion to sphingosine 1-phosphate (S1P) by sphingosine kinase.	Ceramides	90-98	adiponectin, C1Q and collagen domain containing	Homo sapiens	48-59
24977487-5	2014	Moreover, bioactive lipid intermediates such as diacylglycerol (DAG) and ceramides appear to accumulate in response to NEFA, which may interact with insulin signaling.	Ceramides	73-82	insulin	Homo sapiens	149-156
24141140-10	2014	In turn, TNFalpha induced an increase in SPT in these cells, linking de novo synthesis of ceramide to inflammation.	Ceramides	90-98	tumor necrosis factor	Homo sapiens	9-17
24141140-10	2014	In turn, TNFalpha induced an increase in SPT in these cells, linking de novo synthesis of ceramide to inflammation.	Ceramides	90-98	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	41-44
24977480-2	2014	Our studies using Cftr-deficient mice and human CF specimens showed that ceramide accumulates in CF lungs and mediates increased cell death, susceptibility to infections, and inflammation.	Ceramides	73-81	cystic fibrosis transmembrane conductance regulator	Mus musculus	18-22
24977480-9	2014	CONCLUSION: Our data suggest a signaling cascade from ceramide via the inflammasome to caspase 1, the release of cytokines and an alteration of tight junction proteins in CF epithelia.	Ceramides	54-62	caspase 1	Mus musculus	87-96
24190701-12	2014	Further, bortezomib-induced pro-apoptotic c-Jun N-terminal kinase (JNK) activation was also associated with ceramide production.	Ceramides	108-116	mitogen-activated protein kinase 8	Homo sapiens	42-65
24190701-12	2014	Further, bortezomib-induced pro-apoptotic c-Jun N-terminal kinase (JNK) activation was also associated with ceramide production.	Ceramides	108-116	mitogen-activated protein kinase 8	Homo sapiens	67-70
24977487-6	2014	However, recent work has also indicated that sphingosine 1-phosphate (S1P), a breakdown product of ceramide, modulate insulin signaling in different cell types.	Ceramides	99-107	insulin	Homo sapiens	118-125
24977483-1	2014	BACKGROUND: Acid sphingomyelinase (ASM) is a key regulator of ceramide-dependent signalling pathways.	Ceramides	62-70	sphingomyelin phosphodiesterase 1	Homo sapiens	12-33
24977483-1	2014	BACKGROUND: Acid sphingomyelinase (ASM) is a key regulator of ceramide-dependent signalling pathways.	Ceramides	62-70	sphingomyelin phosphodiesterase 1	Homo sapiens	35-38
24394822-6	2014	Ceramide upregulation was linked with vascular endothelial growth factor suppression and decreased surfactant protein B levels, pathways important for the development of BPD.	Ceramides	0-8	vascular endothelial growth factor A	Homo sapiens	38-72
25562160-3	2014	Acid sphingomyelinase (ASMase) is responsible for the production of ceramide via the hydrolysis of sphingomyelin.	Ceramides	68-76	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
25562160-3	2014	Acid sphingomyelinase (ASMase) is responsible for the production of ceramide via the hydrolysis of sphingomyelin.	Ceramides	68-76	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
24394822-7	2014	In a murine model of BPD, intervention with an S1P analog had a favorable effect on histologic abnormalities and ceramide levels.	Ceramides	113-121	sphingosine-1-phosphate receptor 1	Mus musculus	47-50
24164338-5	2014	Ceramide may be produced from sphingomyelin by acid sphingomyelinase (Asm).	Ceramides	0-8	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	47-68
25189947-1	2014	BACKGROUND: Glucosylceramide synthase (GCS), an enzyme responsible for ceramide glycosylation, plays an important role in multidrug resistance (MDR) in some tumors in vitro; however, its expression and clinicopathological significance in non-small cell lung cancer (NSCLC) remains unclear.	Ceramides	20-28	UDP-glucose ceramide glucosyltransferase	Homo sapiens	39-42
24164338-5	2014	Ceramide may be produced from sphingomyelin by acid sphingomyelinase (Asm).	Ceramides	0-8	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	70-73
24035150-0	2014	Sphingomyelin and ceramide are physiological ligands for human LMIR3/CD300f, inhibiting FcepsilonRI-mediated mast cell activation.	Ceramides	18-26	CD300 molecule like family member f	Homo sapiens	63-68
23832510-5	2014	Peripheral CB1 R blockade also attenuated the diet-induced increase in C14:0, C16:0, C18:0, and C20:0 ceramide species with either C16 or C18 sphingosine-base in the liver.	Ceramides	102-110	cannabinoid receptor 1 (brain)	Mus musculus	11-16
23832510-6	2014	Decreased ceramide levels reflected their reduced de novo synthesis, due to inhibition of the activity of serine-palmitoyl transferase (SPT) and the expression of its SPTLC3 catalytic subunit, as well as reduced ceramide synthase (CerS) activity related to reduced expression of CerS1 and CerS6.	Ceramides	10-18	serine palmitoyltransferase, long chain base subunit 3	Mus musculus	167-173
23832510-6	2014	Decreased ceramide levels reflected their reduced de novo synthesis, due to inhibition of the activity of serine-palmitoyl transferase (SPT) and the expression of its SPTLC3 catalytic subunit, as well as reduced ceramide synthase (CerS) activity related to reduced expression of CerS1 and CerS6.	Ceramides	10-18	ceramide synthase 1	Mus musculus	279-284
23832510-6	2014	Decreased ceramide levels reflected their reduced de novo synthesis, due to inhibition of the activity of serine-palmitoyl transferase (SPT) and the expression of its SPTLC3 catalytic subunit, as well as reduced ceramide synthase (CerS) activity related to reduced expression of CerS1 and CerS6.	Ceramides	10-18	ceramide synthase 6	Mus musculus	289-294
23832510-11	2014	CONCLUSION: ECs induce CB1 R-mediated, endoplasmic reticulum stress-dependent synthesis of specific ceramide subspecies in the liver, which plays a key role in obesity-related hepatic insulin resistance.	Ceramides	100-108	cannabinoid receptor 1 (brain)	Mus musculus	23-26
25301364-1	2014	BACKGROUND: Acid sphingomyelinase (ASM) catalyses the hydrolysis of sphingomyelin into ceramide, which acts as a lipid messenger that regulates important cellular functions.	Ceramides	87-95	sphingomyelin phosphodiesterase 1	Homo sapiens	12-33
25301364-1	2014	BACKGROUND: Acid sphingomyelinase (ASM) catalyses the hydrolysis of sphingomyelin into ceramide, which acts as a lipid messenger that regulates important cellular functions.	Ceramides	87-95	sphingomyelin phosphodiesterase 1	Homo sapiens	35-38
23832510-1	2014	UNLABELLED: Obesity is associated with increased activity of two lipid signaling systems (endocannabinoids [ECs] and ceramides), with both being implicated in insulin resistance.	Ceramides	117-126	insulin	Homo sapiens	159-166
24035150-0	2014	Sphingomyelin and ceramide are physiological ligands for human LMIR3/CD300f, inhibiting FcepsilonRI-mediated mast cell activation.	Ceramides	18-26	CD300 molecule like family member f	Homo sapiens	69-75
24035150-0	2014	Sphingomyelin and ceramide are physiological ligands for human LMIR3/CD300f, inhibiting FcepsilonRI-mediated mast cell activation.	Ceramides	18-26	Fc epsilon receptor Ia	Homo sapiens	88-99
25276436-1	2014	The lysosomal acid ceramidase, an enzyme known to limit intracellular ceramide accumulation, has been reported to be defective in neurodegenerative disorders.	Ceramides	70-78	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	14-29
24196832-5	2014	In addition, we establish that Sch9 affects the activity of the inositol phosphosphingolipid phospholipase C, Isc1, which is required for ceramide production by hydrolysis of complex sphingolipids.	Ceramides	138-146	serine/threonine protein kinase SCH9	Saccharomyces cerevisiae S288C	31-35
24196832-5	2014	In addition, we establish that Sch9 affects the activity of the inositol phosphosphingolipid phospholipase C, Isc1, which is required for ceramide production by hydrolysis of complex sphingolipids.	Ceramides	138-146	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	110-114
24949486-6	2014	This is likely partly due to an insulin-induced increase in expression of multiple enzymes, particularly SPT2, which, when knocked down, prevented the increase in ceramides.	Ceramides	163-172	mucin-like 1	Mus musculus	105-109
23846911-1	2014	Farber disease is an inherited metabolic disorder caused by mutations in the acid ceramidase gene, which leads to ceramide accumulation in lysosomes.	Ceramides	114-122	N-acylsphingosine amidohydrolase 1	Homo sapiens	77-92
25276436-6	2014	Collectively, these results provide experimental evidence that ceramides play an important role in regulating Tau phosphorylation in the hippocampus via a mechanism dependent on GluN2B receptor subunits and CaMKII activation.	Ceramides	63-72	glutamate ionotropic receptor NMDA type subunit 2B	Rattus norvegicus	178-184
24220030-7	2013	We have found that TER P182L mutant enzyme exhibits reduced trans-2-enoyl-CoA reductase activity and protein stability, thereby impairing VLCFA synthesis and, in turn, altering the sphingolipid profile (i.e. decreased level of C24 sphingomyelin and C24 ceramide) in the TER(P182L/P182L) B-lymphoblastoid cell line.	Ceramides	253-261	trans-2,3-enoyl-CoA reductase	Homo sapiens	19-22
24376889-10	2013	Observed changes in insulin signaling proteins were related to the content of specific sphingolipids, namely to the reduction of ceramide.	Ceramides	129-137	insulin	Homo sapiens	20-27
24367685-7	2013	Nanoliposomal ceramide inhibits both the RNA and protein expression of GAPDH, an enzyme in the glycolytic pathway, which is overexpressed in CLL.	Ceramides	14-22	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	71-76
24095693-1	2013	Nerve growth factor (NGF) augments the excitability of isolated rat sensory neurons through activation of the p75 neurotrophin receptor (p75(NTR)) and its downstream sphingomyelin signaling cascade, wherein neutral sphingomyelinase(s) (nSMase), ceramide, and the atypical protein-kinase C (aPKC), protein-kinase M zeta (PKMzeta), are key mediators.	Ceramides	245-253	nerve growth factor receptor	Rattus norvegicus	137-145
24095693-1	2013	Nerve growth factor (NGF) augments the excitability of isolated rat sensory neurons through activation of the p75 neurotrophin receptor (p75(NTR)) and its downstream sphingomyelin signaling cascade, wherein neutral sphingomyelinase(s) (nSMase), ceramide, and the atypical protein-kinase C (aPKC), protein-kinase M zeta (PKMzeta), are key mediators.	Ceramides	245-253	sphingomyelin phosphodiesterase 2	Rattus norvegicus	207-234
24095693-6	2013	A single injection of N-acetyl sphingosine (C2-ceramide), simulating the ceramide produced by nSMase activity, induced ipsilateral allodynia that persisted for 24h, and transient hyperalgesia that resolved by 2h.	Ceramides	47-55	sphingomyelin phosphodiesterase 2	Rattus norvegicus	94-100
24095693-1	2013	Nerve growth factor (NGF) augments the excitability of isolated rat sensory neurons through activation of the p75 neurotrophin receptor (p75(NTR)) and its downstream sphingomyelin signaling cascade, wherein neutral sphingomyelinase(s) (nSMase), ceramide, and the atypical protein-kinase C (aPKC), protein-kinase M zeta (PKMzeta), are key mediators.	Ceramides	245-253	nerve growth factor receptor	Rattus norvegicus	110-113
24367685-8	2013	To confirm that ceramide targets GAPDH, we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis.	Ceramides	16-24	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	33-38
24367685-8	2013	To confirm that ceramide targets GAPDH, we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis.	Ceramides	16-24	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	78-83
24367685-8	2013	To confirm that ceramide targets GAPDH, we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis.	Ceramides	16-24	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	78-83
24367685-8	2013	To confirm that ceramide targets GAPDH, we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis.	Ceramides	122-130	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	78-83
24367685-8	2013	To confirm that ceramide targets GAPDH, we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis.	Ceramides	122-130	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	78-83
24367685-8	2013	To confirm that ceramide targets GAPDH, we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis.	Ceramides	122-130	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	78-83
24367685-8	2013	To confirm that ceramide targets GAPDH, we demonstrate that downregulation of GAPDH potentiates the decrease in ATP after ceramide treatment and exogenous pyruvate treatment as well as GAPDH overexpression partially rescues ceramide-induced necrosis.	Ceramides	122-130	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	78-83
24367685-9	2013	Finally, an in vivo murine model of CLL shows that nanoliposomal C6-ceramide treatment elicits tumor regression, concomitant with GAPDH downregulation.	Ceramides	68-76	glyceraldehyde-3-phosphate dehydrogenase	Mus musculus	130-135
24358176-0	2013	Ceramide mediates Ox-LDL-induced human vascular smooth muscle cell calcification via p38 mitogen-activated protein kinase signaling.	Ceramides	0-8	mitogen-activated protein kinase 14	Homo sapiens	85-88
24358176-4	2013	The aim of this study is to investigate whether ceramide regulates Ox-LDL-induced calcification of VSMCs via activation of p38 mitogen-activated protein kinase (MAPK) pathway.	Ceramides	48-56	mitogen-activated protein kinase 14	Homo sapiens	123-159
24358176-13	2013	These data suggest that Ox-LDL activates N-SMase-ceramide signaling pathway, and stimulates phosphorylation of p38 MAPK, leading to apoptosis in VSMCs, which initiates VSMC calcification.	Ceramides	49-57	sphingomyelin phosphodiesterase 2	Homo sapiens	41-48
24256255-10	2013	BMP and ceramide stimulate NPC-2-mediated cholesterol transfer, whereas sphingomyelin inhibits it.	Ceramides	8-16	NPC intracellular cholesterol transporter 2	Homo sapiens	27-32
24073738-5	2013	This effect is likely to be a result of increased Drp1 (dynamin-related protein 1) action, as ceramide increased Drp1 expression and Drp1 inhibition prevented ceramide-induced mitochondrial fission.	Ceramides	94-102	dynamin 1 like	Homo sapiens	50-54
24073738-5	2013	This effect is likely to be a result of increased Drp1 (dynamin-related protein 1) action, as ceramide increased Drp1 expression and Drp1 inhibition prevented ceramide-induced mitochondrial fission.	Ceramides	94-102	dynamin 1 like	Homo sapiens	56-81
24073738-5	2013	This effect is likely to be a result of increased Drp1 (dynamin-related protein 1) action, as ceramide increased Drp1 expression and Drp1 inhibition prevented ceramide-induced mitochondrial fission.	Ceramides	94-102	dynamin 1 like	Homo sapiens	113-117
24073738-5	2013	This effect is likely to be a result of increased Drp1 (dynamin-related protein 1) action, as ceramide increased Drp1 expression and Drp1 inhibition prevented ceramide-induced mitochondrial fission.	Ceramides	94-102	dynamin 1 like	Homo sapiens	113-117
24073738-5	2013	This effect is likely to be a result of increased Drp1 (dynamin-related protein 1) action, as ceramide increased Drp1 expression and Drp1 inhibition prevented ceramide-induced mitochondrial fission.	Ceramides	159-167	dynamin 1 like	Homo sapiens	50-54
24073738-5	2013	This effect is likely to be a result of increased Drp1 (dynamin-related protein 1) action, as ceramide increased Drp1 expression and Drp1 inhibition prevented ceramide-induced mitochondrial fission.	Ceramides	159-167	dynamin 1 like	Homo sapiens	56-81
24073738-7	2013	Ceramide treatment also increased H2O2 levels and reduced Akt/PKB (protein kinase B) phosphorylation in myotubes.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	58-65
24048885-7	2013	The ceramide analogue, C6-ceramide, induced a decrease in decidual cell viability and of p38 MAPK phosphorylation.	Ceramides	4-12	mitogen activated protein kinase 14	Rattus norvegicus	89-92
24048885-8	2013	Additionally, the pharmacologic inhibition of de novo ceramide biosynthesis with L-cycloserine and fumonisin B reduced the AEA-effects on cell viability and p38 MAPK phosphorylation.	Ceramides	54-62	mitogen activated protein kinase 14	Rattus norvegicus	157-160
24048885-9	2013	Furthermore, AEA and C6-ceramide induced a drop in DeltaPsim, an increase in ROS production and caspase-3/-7 activation, effects partially reverted by inhibitors of ceramide synthesis and of p38 MAPK.	Ceramides	24-32	caspase 3	Rattus norvegicus	96-105
24048885-9	2013	Furthermore, AEA and C6-ceramide induced a drop in DeltaPsim, an increase in ROS production and caspase-3/-7 activation, effects partially reverted by inhibitors of ceramide synthesis and of p38 MAPK.	Ceramides	24-32	mitogen activated protein kinase 14	Rattus norvegicus	191-194
24048885-10	2013	Taken together, we showed that AEA induces a reduction in decidual cell viability by a mechanism involving CB1 activation, which results in ceramide synthesis de novo and p38 phosphorylation, followed by mitochondrial stress and ROS production, leading to apoptosis.	Ceramides	140-148	cannabinoid receptor 1	Rattus norvegicus	107-110
24073738-8	2013	However, inhibition of mitochondrial fission via Drp1 knockdown completely protected the myotubes and fibre bundles from ceramide-induced metabolic disruption, including maintained mitochondrial respiration, reduced H2O2 levels and unaffected insulin signalling.	Ceramides	121-129	dynamin 1 like	Homo sapiens	49-53
23982477-7	2013	Finally, activation of AMPK by AICAR or adiponectin also decreased ceramide accumulation in the neutrophil cell membrane, a process involved in the early stages of spontaneous apoptosis, giving another possible mechanism downstream of AMPK activation for the inhibition of neutrophil apoptosis.	Ceramides	67-75	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	23-27
23982477-7	2013	Finally, activation of AMPK by AICAR or adiponectin also decreased ceramide accumulation in the neutrophil cell membrane, a process involved in the early stages of spontaneous apoptosis, giving another possible mechanism downstream of AMPK activation for the inhibition of neutrophil apoptosis.	Ceramides	67-75	adiponectin, C1Q and collagen domain containing	Homo sapiens	40-51
23939396-1	2013	Acid ceramidase (AC), EC 3.5.1.23, a lysosomal enzyme, catalyzes the hydrolysis of ceramide to constituent sphingoid base, sphingosine, and fatty acid.	Ceramides	83-91	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
23939396-1	2013	Acid ceramidase (AC), EC 3.5.1.23, a lysosomal enzyme, catalyzes the hydrolysis of ceramide to constituent sphingoid base, sphingosine, and fatty acid.	Ceramides	83-91	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
23939396-2	2013	Because AC regulates the levels of pro-apoptotic ceramide and mitogenic sphingosine-1-phosphate, it is considered an apt target in cancer therapy.	Ceramides	49-57	N-acylsphingosine amidohydrolase 1	Homo sapiens	8-10
23989724-0	2013	Ceramide accumulation in L6 skeletal muscle cells due to increased activity of ceramide synthase isoforms has opposing effects on insulin action to those caused by palmitate treatment.	Ceramides	0-8	insulin	Homo sapiens	130-137
23989724-1	2013	AIMS/HYPOTHESIS: An accumulation of ceramides has been implicated in the generation of insulin resistance in skeletal muscle upon an oversupply of fatty acid.	Ceramides	36-45	insulin	Homo sapiens	87-94
23989724-15	2013	Conversely, certain isoforms promote insulin action, indicating the importance of ceramides in cell function.	Ceramides	82-91	insulin	Homo sapiens	37-44
24126464-12	2013	PDT alone decreased substantially sphingosine levels and inhibited the activity of acid ceramidase, an enzyme that converts ceramide to sphingosine.	Ceramides	124-132	N-acylsphingosine amidohydrolase 1	Mus musculus	83-98
23830072-4	2013	hTERT upregulation was accompanied by recruitment of ceramide, a known regulator of hTERT, to the chlamydial inclusion and was abrogated following doxycycline-mediated infection clearance.	Ceramides	53-61	telomerase reverse transcriptase	Homo sapiens	0-5
24120971-7	2013	The protection from palmitate-induced apoptosis by PTP1B inhibition was also accompanied by a decrease in protein level of serine palmitoyl transferase, thus resulting in lower ceramide content in muscle cells.	Ceramides	177-185	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	51-56
24120971-11	2013	In summary, our results indicate that PTP1B modulation results in (1) alterations in mitochondrial function by changes in the activity of SIRT1/NF-kappaB/PGC-1alpha pathways and (2) changes in apoptosis that result from either a direct effect of PTP1B on the insulin signaling pathway or an indirect influence on ceramide content, ROS generation, JNK activation, and FOXO-1 nuclear translocation.	Ceramides	313-321	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	38-43
23830072-4	2013	hTERT upregulation was accompanied by recruitment of ceramide, a known regulator of hTERT, to the chlamydial inclusion and was abrogated following doxycycline-mediated infection clearance.	Ceramides	53-61	telomerase reverse transcriptase	Homo sapiens	84-89
23640727-10	2013	Increases in ceramides were noted, which left unchecked may promote systemic insulin resistance.	Ceramides	13-22	insulin	Homo sapiens	77-84
24062078-1	2013	Sphingomyelin synthase 1 (SMS1) is an essential enzyme that catalyses the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide in eukaryotic cells.	Ceramides	149-157	sphingomyelin synthase 1	Homo sapiens	0-24
24062078-1	2013	Sphingomyelin synthase 1 (SMS1) is an essential enzyme that catalyses the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide in eukaryotic cells.	Ceramides	149-157	sphingomyelin synthase 1	Homo sapiens	26-30
28664064-6	2013	In addition, lipid intermediates (e.g., fatty acyl-coenzyme A, diacylglycerol, and ceramide) impair insulin signaling in skeletal muscle.	Ceramides	83-91	insulin	Homo sapiens	100-107
24001971-1	2013	Here we present a minimal mathematical model for the sphingomyelin synthase 1 (SMS1) driven conversion of ceramide to sphingomyelin based on chemical reaction kinetics.	Ceramides	106-114	sphingomyelin synthase 1	Homo sapiens	53-77
23988586-3	2013	Two separate views suggest that IMTG dynamics are determinant for skeletal muscle fat oxidation, and that disruption of IMTG dynamics facilitates the accumulation of lipotoxic intermediates such as diacylglycerols and ceramides that interfere with insulin signaling.	Ceramides	218-227	insulin	Homo sapiens	248-255
24239358-5	2013	Expression of nonphosphorylatable Elo2 profoundly alters the ceramide spectrum, reflecting aberrant VLCFA synthesis.	Ceramides	61-69	ELOVL fatty acid elongase 6	Homo sapiens	34-38
24505937-0	2013	[An inhibitory receptor LMIR3/CD300f recognizes ceramide].	Ceramides	48-56	CD300 molecule like family member f	Homo sapiens	24-29
24505937-0	2013	[An inhibitory receptor LMIR3/CD300f recognizes ceramide].	Ceramides	48-56	CD300 molecule like family member f	Homo sapiens	30-36
24001971-1	2013	Here we present a minimal mathematical model for the sphingomyelin synthase 1 (SMS1) driven conversion of ceramide to sphingomyelin based on chemical reaction kinetics.	Ceramides	106-114	sphingomyelin synthase 1	Homo sapiens	79-83
24634821-5	2014	Decreased LPL activity in both models was associated with increased de novo ceramide synthesis and neurogenesis in the hippocampus, while intrahippocampal infusion of de novo ceramide synthesis inhibitor myriocin completely prevented body weight gain.	Ceramides	76-84	lipoprotein lipase	Mus musculus	10-13
24634821-5	2014	Decreased LPL activity in both models was associated with increased de novo ceramide synthesis and neurogenesis in the hippocampus, while intrahippocampal infusion of de novo ceramide synthesis inhibitor myriocin completely prevented body weight gain.	Ceramides	175-183	lipoprotein lipase	Mus musculus	10-13
24019516-1	2013	Very long chain (C22-C24) ceramides are synthesized by ceramide synthase 2 (CerS2).	Ceramides	26-35	ceramide synthase 2	Mus musculus	55-74
24260258-1	2013	Ceramide transfer protein (CERT) is responsible for the nonvesicular trafficking of ceramide from the endoplasmic reticulum (ER) to the trans Golgi network where it is converted to sphingomyelin (SM).	Ceramides	84-92	ceramide transporter 1	Homo sapiens	0-25
24260258-1	2013	Ceramide transfer protein (CERT) is responsible for the nonvesicular trafficking of ceramide from the endoplasmic reticulum (ER) to the trans Golgi network where it is converted to sphingomyelin (SM).	Ceramides	84-92	ceramide transporter 1	Homo sapiens	27-31
23973755-7	2013	As CPT1C is known to regulate ceramide levels, we measured these biolipids in different motor areas in adult mice.	Ceramides	30-38	carnitine palmitoyltransferase 1c	Mus musculus	3-8
23973755-8	2013	Cerebellar, striatum, and motor cortex extracts from Cpt1c knockout mice showed reduced levels of ceramide and its derivative sphingosine when compared to wild-type animals.	Ceramides	98-106	carnitine palmitoyltransferase 1c	Mus musculus	53-58
23973755-9	2013	Our results indicate that altered ceramide metabolism in motor brain areas induced by Cpt1c deficiency causes progressive motor dysfunction from a young age.	Ceramides	34-42	carnitine palmitoyltransferase 1c	Mus musculus	86-91
23937324-1	2013	The regulation of protein kinase C (PKC) isoforms by ceramide is still controversial.	Ceramides	53-61	protein kinase C alpha	Homo sapiens	36-39
23937324-2	2013	In this work, the yeast Saccharomyces cerevisiae was used as a model to elucidate the effect of ceramide on the activity of mammalian PKC isoforms.	Ceramides	96-104	protein kinase C alpha	Homo sapiens	134-137
23633022-10	2013	Therefore, we conclude that a ceramide deficiency in the epidermis leads to psoriasis-like lesions in mice, probably mediated by IL-23-dependent IL-22-producing gammadelta-17 cells.	Ceramides	30-38	interleukin 23, alpha subunit p19	Mus musculus	129-134
23633022-10	2013	Therefore, we conclude that a ceramide deficiency in the epidermis leads to psoriasis-like lesions in mice, probably mediated by IL-23-dependent IL-22-producing gammadelta-17 cells.	Ceramides	30-38	interleukin 22	Mus musculus	145-150
24180579-0	2013	Membrane TNF-alpha-activated programmed necrosis is mediated by Ceramide-induced reactive oxygen species.	Ceramides	64-72	tumor necrosis factor	Mus musculus	9-18
24180579-13	2013	CONCLUSION: These findings demonstrate that the mTNF-alpha isoform is an effective inducer of programmed necrosis through a caspase independent, ceramide-related pathway.	Ceramides	145-153	tumor necrosis factor	Mus musculus	48-58
24044897-7	2013	Addition of ceramide analog induced caspase-8 activation leading to caspase-3 activation and apoptotic neuronal death.	Ceramides	12-20	caspase 8	Homo sapiens	36-45
24044897-7	2013	Addition of ceramide analog induced caspase-8 activation leading to caspase-3 activation and apoptotic neuronal death.	Ceramides	12-20	caspase 3	Homo sapiens	68-77
24141119-8	2013	These findings suggest that ceramide may play an important role in sAPPalpha processing by modulating PKC activity.	Ceramides	28-36	proline rich transmembrane protein 2	Homo sapiens	102-105
23896361-6	2013	Dyslipidemic small HDL particles were further distinguished not only as the primary carrier of ceramides, which promote inflammation and insulin resistance, but also by a subnormal plasmalogen/apoAI ratio, consistent with elevated oxidative stress typical of type 2 diabetes.	Ceramides	95-104	insulin	Homo sapiens	137-144
23937324-5	2013	Interestingly, in isc1Delta yeast cells expressing PKCdelta this phenotype was completely abrogated in the presence of exogenous ceramide.	Ceramides	129-137	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	18-22
23937324-6	2013	Moreover, using a yeast-based assay previously developed for the screening of PKC inhibitors, it was also shown that, like the known PKC inhibitor NPC 15437, ceramide reduced the PMA-induced growth inhibition, supporting an inhibitory effect of ceramide on PKCdelta.	Ceramides	158-166	protein kinase C alpha	Homo sapiens	78-81
23937324-6	2013	Moreover, using a yeast-based assay previously developed for the screening of PKC inhibitors, it was also shown that, like the known PKC inhibitor NPC 15437, ceramide reduced the PMA-induced growth inhibition, supporting an inhibitory effect of ceramide on PKCdelta.	Ceramides	158-166	protein kinase C alpha	Homo sapiens	133-136
23937324-7	2013	Altogether, these results may indicate that ceramide distinctly interfere with the activity of PKCalpha, delta and zeta.	Ceramides	44-52	protein kinase C alpha	Homo sapiens	95-103
24269881-1	2013	UNLABELLED: High lipid and ceramide concentrations are hallmarks of obese and/or insulin resistant skeletal muscle, yet little is known about its role on cell cycle and senescence.	Ceramides	27-35	insulin	Homo sapiens	81-88
24269881-4	2013	RESULTS: Ceramide treatment caused a dephosphorylation (p<0.05) of Akt and 4E-BP1, regardless of the presence of insulin.	Ceramides	9-17	AKT serine/threonine kinase 1	Homo sapiens	70-84
24269881-6	2013	Ceramide treatment also upregulated (p<0.05) p53 and p21 protein expression, that was reversed by either pifithrin-alpha or shRNA for p53.	Ceramides	0-8	tumor protein p53	Homo sapiens	48-51
24269881-6	2013	Ceramide treatment also upregulated (p<0.05) p53 and p21 protein expression, that was reversed by either pifithrin-alpha or shRNA for p53.	Ceramides	0-8	H3 histone pseudogene 16	Homo sapiens	56-59
24269881-6	2013	Ceramide treatment also upregulated (p<0.05) p53 and p21 protein expression, that was reversed by either pifithrin-alpha or shRNA for p53.	Ceramides	0-8	tumor protein p53	Homo sapiens	137-140
24269881-7	2013	Metformin limited (p<0.05) ceramide"s effects on insulin signaling, senescence, and cell cycle regulation.	Ceramides	30-38	insulin	Homo sapiens	52-59
24044897-8	2013	In conclusion, our results suggest that cPLA2alpha activity plays a crucial role in the signaling cascade leading to apoptotic neuronal death by aggregated Abeta1-42 probably via activation of N-SMase, ceramide production and caspases-3 and -8.	Ceramides	202-210	phospholipase A2 group IVA	Homo sapiens	40-50
24019516-1	2013	Very long chain (C22-C24) ceramides are synthesized by ceramide synthase 2 (CerS2).	Ceramides	26-35	ceramide synthase 2	Mus musculus	76-81
24019516-2	2013	A CerS2 null mouse displays hepatopathy because of depletion of C22-C24 ceramides, elevation of C16-ceramide, and/or elevation of sphinganine.	Ceramides	72-81	ceramide synthase 2	Mus musculus	2-7
23524027-5	2013	In this review we present the two key examples of ceramide and cardiolipin in apoptosis, focusing particularly on BCL-2 family-regulated pathways at the mitochondrial level.	Ceramides	50-58	BCL2 apoptosis regulator	Homo sapiens	114-119
23921144-8	2013	To further elucidate the regulatory mechanism whereby PA amplifies LPS signal, our studies showed that PA and LPS synergistically increased hydrolysis of sphingomyelin by stimulating acid sphingomyelinase (ASMase) activity, which contributed to a marked increase in ceramide production and IL-6 upregulation.	Ceramides	266-274	sphingomyelin phosphodiesterase 1	Homo sapiens	183-204
23921144-8	2013	To further elucidate the regulatory mechanism whereby PA amplifies LPS signal, our studies showed that PA and LPS synergistically increased hydrolysis of sphingomyelin by stimulating acid sphingomyelinase (ASMase) activity, which contributed to a marked increase in ceramide production and IL-6 upregulation.	Ceramides	266-274	sphingomyelin phosphodiesterase 1	Homo sapiens	206-212
23988346-14	2013	Of relevance, in the arcuate nucleus, CPT-1c may link malonyl-CoA to ceramide metabolism to affect food intake.	Ceramides	69-77	carnitine palmitoyltransferase 1C	Homo sapiens	38-44
24025258-7	2013	Our data indicated that targeting cancer related signaling pathways through I2PP2A using ceramide as an anti-I2PP2A agent could have beneficial effects as a therapeutic approach to prevent prostate cancer.	Ceramides	89-97	SET nuclear proto-oncogene	Homo sapiens	76-82
24025258-7	2013	Our data indicated that targeting cancer related signaling pathways through I2PP2A using ceramide as an anti-I2PP2A agent could have beneficial effects as a therapeutic approach to prevent prostate cancer.	Ceramides	89-97	SET nuclear proto-oncogene	Homo sapiens	109-115
24025252-8	2013	(4) PP2A activity is known to be regulated by the bioactive lipid ceramide, and this occurs through both I2PP2A inhibition and PP2A de-repression and through ceramide actions on subunits of the PP2A enzyme complex.	Ceramides	66-74	protein phosphatase 2 phosphatase activator	Homo sapiens	4-8
24091326-3	2013	In this study, we demonstrate that ceramide-deacylating enzyme acid ceramidase (AC) was preferentially upregulated in irradiated PCa cells.	Ceramides	35-43	N-acylsphingosine amidohydrolase 1	Homo sapiens	63-78
24025252-8	2013	(4) PP2A activity is known to be regulated by the bioactive lipid ceramide, and this occurs through both I2PP2A inhibition and PP2A de-repression and through ceramide actions on subunits of the PP2A enzyme complex.	Ceramides	66-74	SET nuclear proto-oncogene	Homo sapiens	105-111
24025252-8	2013	(4) PP2A activity is known to be regulated by the bioactive lipid ceramide, and this occurs through both I2PP2A inhibition and PP2A de-repression and through ceramide actions on subunits of the PP2A enzyme complex.	Ceramides	66-74	protein phosphatase 2 phosphatase activator	Homo sapiens	107-111
24025252-8	2013	(4) PP2A activity is known to be regulated by the bioactive lipid ceramide, and this occurs through both I2PP2A inhibition and PP2A de-repression and through ceramide actions on subunits of the PP2A enzyme complex.	Ceramides	66-74	protein phosphatase 2 phosphatase activator	Homo sapiens	107-111
24025252-8	2013	(4) PP2A activity is known to be regulated by the bioactive lipid ceramide, and this occurs through both I2PP2A inhibition and PP2A de-repression and through ceramide actions on subunits of the PP2A enzyme complex.	Ceramides	158-166	protein phosphatase 2 phosphatase activator	Homo sapiens	4-8
24025252-10	2013	They determined whether ceramide could decrease accumulation of the oncogene c-Myc through inhibition of I2PP2A and activation of PP2A.	Ceramides	24-32	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	77-82
24025252-10	2013	They determined whether ceramide could decrease accumulation of the oncogene c-Myc through inhibition of I2PP2A and activation of PP2A.	Ceramides	24-32	SET nuclear proto-oncogene	Homo sapiens	105-111
24025252-10	2013	They determined whether ceramide could decrease accumulation of the oncogene c-Myc through inhibition of I2PP2A and activation of PP2A.	Ceramides	24-32	protein phosphatase 2 phosphatase activator	Homo sapiens	107-111
24025252-11	2013	As I2PP2A is also an inhibitor of histone acetylation they determined whether ceramide could block the epigenetic action of I2PP2A.	Ceramides	78-86	SET nuclear proto-oncogene	Homo sapiens	124-130
23712032-5	2013	Finally, we found that exogenously-added short-chain ceramide (C6) enhances plumbagin-induced AMPK activation and facilitates cell apoptosis and growth inhibition.	Ceramides	53-61	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	94-98
24091326-3	2013	In this study, we demonstrate that ceramide-deacylating enzyme acid ceramidase (AC) was preferentially upregulated in irradiated PCa cells.	Ceramides	35-43	N-acylsphingosine amidohydrolase 1	Homo sapiens	80-82
24091326-4	2013	Radiation-induced AC gene transactivation by activator protein 1 (AP-1) binding on the proximal promoter was sensitive to inhibition of de novo ceramide biosynthesis, as demonstrated by promoter reporter and ChIP-qPCR analyses.	Ceramides	144-152	N-acylsphingosine amidohydrolase 1	Homo sapiens	18-20
24091326-4	2013	Radiation-induced AC gene transactivation by activator protein 1 (AP-1) binding on the proximal promoter was sensitive to inhibition of de novo ceramide biosynthesis, as demonstrated by promoter reporter and ChIP-qPCR analyses.	Ceramides	144-152	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	45-64
23802886-9	2013	CONCLUSIONS: In ALD, the histopathology and impairments in insulin/IGF responsiveness can be substantially resolved by ceramide inhibitor treatments, even in the context of continued chronic ethanol exposure.	Ceramides	119-127	insulin-like growth factor 1	Rattus norvegicus	67-70
24091326-4	2013	Radiation-induced AC gene transactivation by activator protein 1 (AP-1) binding on the proximal promoter was sensitive to inhibition of de novo ceramide biosynthesis, as demonstrated by promoter reporter and ChIP-qPCR analyses.	Ceramides	144-152	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-70
24183051-1	2013	Neutral sphingomyelinase 2 (nSMase2), which located mainly on the plasma membrane, hydrolyzes sphingomyelin into ceramide and plays an important role in the physiological and pathological regulation of cell apoptosis, cell growth arrest, and inflammation.	Ceramides	113-121	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
23919525-5	2013	Treatment with neuronal lysates and ceramide, a lipid intermediate elevated in the JNCL brain, led to inflammasome activation and IL-1beta release in CLN3(Deltaex7/8) microglia but not WT cells, as well as increased expression of additional pro-inflammatory mediators.	Ceramides	36-44	interleukin 1 alpha	Mus musculus	130-138
23919525-5	2013	Treatment with neuronal lysates and ceramide, a lipid intermediate elevated in the JNCL brain, led to inflammasome activation and IL-1beta release in CLN3(Deltaex7/8) microglia but not WT cells, as well as increased expression of additional pro-inflammatory mediators.	Ceramides	36-44	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	150-154
24183051-1	2013	Neutral sphingomyelinase 2 (nSMase2), which located mainly on the plasma membrane, hydrolyzes sphingomyelin into ceramide and plays an important role in the physiological and pathological regulation of cell apoptosis, cell growth arrest, and inflammation.	Ceramides	113-121	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
24406179-12	2013	CONCLUSION: TNF-alpha can induce DUOX-1 expression increasing in lipid raft, then the DUOX-1 can be activated to increase reactive oxygen species level; acidic sphingomyelinase inhibitor desipramine can inhibit this process, the results disclose that the process will depend on the ceramide of lipid raft.	Ceramides	282-290	tumor necrosis factor	Homo sapiens	12-21
24086643-7	2013	Altogether, our findings establish the existence of a functional partnership PAF-R/eNOS on EC plasma membrane, at the level of PAF-induced ceramide plasma membrane microdomains, outside recognized vesicular profiles.	Ceramides	139-147	platelet-activating factor receptor	Mus musculus	77-82
24406179-12	2013	CONCLUSION: TNF-alpha can induce DUOX-1 expression increasing in lipid raft, then the DUOX-1 can be activated to increase reactive oxygen species level; acidic sphingomyelinase inhibitor desipramine can inhibit this process, the results disclose that the process will depend on the ceramide of lipid raft.	Ceramides	282-290	dual oxidase 1	Homo sapiens	33-39
24406179-12	2013	CONCLUSION: TNF-alpha can induce DUOX-1 expression increasing in lipid raft, then the DUOX-1 can be activated to increase reactive oxygen species level; acidic sphingomyelinase inhibitor desipramine can inhibit this process, the results disclose that the process will depend on the ceramide of lipid raft.	Ceramides	282-290	dual oxidase 1	Homo sapiens	86-92
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).	Ceramides	97-105	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).	Ceramides	97-105	glucosylceramidase beta	Homo sapiens	65-68
24058461-3	2013	We hypothesized that plasma levels of lipids involved in ceramide metabolism would also be altered in PD non-GBA mutation carriers and associated with worse cognition.	Ceramides	57-65	glucosylceramidase beta	Homo sapiens	109-112
24058461-7	2013	CONCLUSION: These results suggest that plasma ceramide and monohexosylceramide metabolism is altered in PD non-GBA mutation carriers and that higher levels are associated with worse cognition.	Ceramides	46-54	glucosylceramidase beta	Homo sapiens	111-114
23763823-3	2013	We found increased phosphatidylcholine and decreased ceramides in the brain of PGC1a-deficient mice.	Ceramides	53-62	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	79-84
23880767-1	2013	beta-Glucosidase 2 (GBA2) is an enzyme that cleaves the membrane lipid glucosylceramide into glucose and ceramide.	Ceramides	79-87	glucosidase beta 2	Mus musculus	0-18
23880767-1	2013	beta-Glucosidase 2 (GBA2) is an enzyme that cleaves the membrane lipid glucosylceramide into glucose and ceramide.	Ceramides	79-87	glucosidase beta 2	Mus musculus	20-24
23096778-4	2013	PKCzeta can be activated by lipid components, such as phosphatidylinositols, phosphatidic acid, arachidonic acid, and ceramide.	Ceramides	118-126	protein kinase C zeta	Homo sapiens	0-7
24040340-1	2013	We previously reported that fenretinide (4-HPR) was cytotoxic to acute lymphoblastic leukemia (ALL) cell lines in vitro in association with increased levels of de novo synthesized dihydroceramides, the immediate precursors of ceramides.	Ceramides	187-196	haptoglobin-related protein	Homo sapiens	43-46
24040340-4	2013	A novel method employing supplementation of individual fatty acids, sphinganine, and the dihydroceramide desaturase-1 (DES) inhibitor, GT-11, was used to increase de novo dihydroceramide synthesis and absolute levels of specific dihydroceramides and ceramides.	Ceramides	236-245	delta 4-desaturase, sphingolipid 1	Homo sapiens	89-117
24039766-3	2013	However, in obesity little is known about the plasma concentrations of sphinogsine-1-phosphate (S1P), the breakdown product of ceramide, which is an important signaling molecule in mammalian biology.	Ceramides	127-135	sphingosine-1-phosphate receptor 1	Mus musculus	96-99
24007266-0	2013	Early activation of nSMase2/ceramide pathway in astrocytes is involved in ischemia-associated neuronal damage via inflammation in rat hippocampi.	Ceramides	28-36	sphingomyelin phosphodiesterase 3	Rattus norvegicus	20-27
24007266-7	2013	The inhibition of nSMase2 activity effectively reduced ceramide accumulation in astrocytes and alleviated neuronal damage to some extent.	Ceramides	55-63	sphingomyelin phosphodiesterase 3	Rattus norvegicus	18-25
24007266-8	2013	Meanwhile, the expression levels of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta) and IL-6, were found to be upregulated, which may have played an import role in neuronal damage mediated by the nSMase2/ceramide pathway.	Ceramides	263-271	tumor necrosis factor	Rattus norvegicus	73-100
24007266-8	2013	Meanwhile, the expression levels of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta) and IL-6, were found to be upregulated, which may have played an import role in neuronal damage mediated by the nSMase2/ceramide pathway.	Ceramides	263-271	tumor necrosis factor	Rattus norvegicus	102-111
24007266-8	2013	Meanwhile, the expression levels of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta) and IL-6, were found to be upregulated, which may have played an import role in neuronal damage mediated by the nSMase2/ceramide pathway.	Ceramides	263-271	interleukin 1 beta	Rattus norvegicus	114-131
24007266-8	2013	Meanwhile, the expression levels of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta) and IL-6, were found to be upregulated, which may have played an import role in neuronal damage mediated by the nSMase2/ceramide pathway.	Ceramides	263-271	interleukin 1 beta	Rattus norvegicus	133-141
24007266-8	2013	Meanwhile, the expression levels of proinflammatory cytokines, including tumor necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta) and IL-6, were found to be upregulated, which may have played an import role in neuronal damage mediated by the nSMase2/ceramide pathway.	Ceramides	263-271	interleukin 6	Rattus norvegicus	147-151
24007266-12	2013	CONCLUSIONS: These results indicate that the inhibition of ceramide production in astrocytes by targeting A2BAR/p38MAPK/nSMase2 signaling may represent a viable approach for attenuating inflammatory responses and neuronal damage after cerebral ischemia.	Ceramides	59-67	mitogen activated protein kinase 14	Rattus norvegicus	112-119
24007266-12	2013	CONCLUSIONS: These results indicate that the inhibition of ceramide production in astrocytes by targeting A2BAR/p38MAPK/nSMase2 signaling may represent a viable approach for attenuating inflammatory responses and neuronal damage after cerebral ischemia.	Ceramides	59-67	sphingomyelin phosphodiesterase 3	Rattus norvegicus	120-127
23774624-4	2013	It has been previously proposed that the multidrug transporter P-glycoprotein (Pgp) might play a role in resistance of cells to intrinsic apoptotic pathways by interfering with components of ceramide metabolism or by modulating the electrochemical gradient across the plasma membrane.	Ceramides	191-199	ATP binding cassette subfamily B member 1	Homo sapiens	63-77
23774624-4	2013	It has been previously proposed that the multidrug transporter P-glycoprotein (Pgp) might play a role in resistance of cells to intrinsic apoptotic pathways by interfering with components of ceramide metabolism or by modulating the electrochemical gradient across the plasma membrane.	Ceramides	191-199	ATP binding cassette subfamily B member 1	Homo sapiens	79-82
23763823-4	2013	An analysis of lipid raft fractions revealed increased ceramide, glucocylceramides and GM1 ganglioside in the PGC1a mutants.	Ceramides	55-63	peroxisome proliferative activated receptor, gamma, coactivator 1 alpha	Mus musculus	110-115
25206527-7	2013	Compared with wild-type pups, the expression level of the important activator protein of the ceramide/ceramide-1-phosphate pathway, protein kinase C alpha, was reduced in the hippocampus of sphingomyelin synthase 2 knockouts.	Ceramides	93-101	protein kinase C, alpha	Mus musculus	132-154
23549421-5	2013	Moreover, we show a specific loss of ceramides with very long acyl chains from C26 up to C34 in terminally differentiating patient keratinocytes, which is in line with findings from a recent CerS3-deficient mouse model.	Ceramides	37-46	ceramide synthase 3	Homo sapiens	191-196
23549421-7	2013	Our findings demonstrate that synthesis of very long chain ceramides by CerS3 is a crucial early step for the skin barrier formation and link disorders presenting with congenital ichthyosis to defects in sphingolipid metabolism and the epidermal lipid architecture.	Ceramides	59-68	ceramide synthase 3	Homo sapiens	72-77
25206527-3	2013	In this study, we established an alcohol exposure model in wild-type mice and in knockout mice for the key enzyme involved in ceramide metabolism, sphingomyelin synthase 2.	Ceramides	126-134	sphingomyelin synthase 2	Mus musculus	147-171
23813961-4	2013	This is accompanied by the accumulation of LDLR in enlarged EEA1-positive endosomes that contain numerous intraluminal vesicles and sequester ceramide.	Ceramides	142-150	low density lipoprotein receptor	Mus musculus	43-47
23813961-4	2013	This is accompanied by the accumulation of LDLR in enlarged EEA1-positive endosomes that contain numerous intraluminal vesicles and sequester ceramide.	Ceramides	142-150	early endosome antigen 1	Mus musculus	60-64
23851680-8	2013	Furthermore, activation of glycogen synthase kinase-3beta (GSK-3beta) was required for ceramide-induced NF-kappaB activation and iNOS expression.	Ceramides	87-95	glycogen synthase kinase 3 beta	Mus musculus	59-68
25206527-7	2013	Compared with wild-type pups, the expression level of the important activator protein of the ceramide/ceramide-1-phosphate pathway, protein kinase C alpha, was reduced in the hippocampus of sphingomyelin synthase 2 knockouts.	Ceramides	93-101	sphingomyelin synthase 2	Mus musculus	190-214
25206527-8	2013	Our findings illustrate that ceramide is involved in alcohol-induced neural proliferation in the hippocampal dentate gyrus of pups after prenatal ethanol exposure, and the mechanism may be associated with increased pression of protein kinase C alpha activating the ceramide/ceramide-1-phosphate pathway.	Ceramides	29-37	protein kinase C, alpha	Mus musculus	227-249
25206527-8	2013	Our findings illustrate that ceramide is involved in alcohol-induced neural proliferation in the hippocampal dentate gyrus of pups after prenatal ethanol exposure, and the mechanism may be associated with increased pression of protein kinase C alpha activating the ceramide/ceramide-1-phosphate pathway.	Ceramides	265-273	protein kinase C, alpha	Mus musculus	227-249
23931754-1	2013	ABCA12 is involved in the transport of ceramides in skin, but it may play a wider role in lipid metabolism.	Ceramides	39-48	ATP-binding cassette, sub-family A (ABC1), member 12	Mus musculus	0-6
23651497-0	2013	A signaling cascade mediated by ceramide, src and PDGFRbeta coordinates the activation of the redox-sensitive neutral sphingomyelinase-2 and sphingosine kinase-1.	Ceramides	32-40	sphingomyelin phosphodiesterase 3	Homo sapiens	110-136
23651497-0	2013	A signaling cascade mediated by ceramide, src and PDGFRbeta coordinates the activation of the redox-sensitive neutral sphingomyelinase-2 and sphingosine kinase-1.	Ceramides	32-40	sphingosine kinase 1	Homo sapiens	141-161
23602992-2	2013	In cardiomyocytes, ceramides induce apoptosis by decreasing mitochondrial membrane potential and promoting cytochrome-c release.	Ceramides	19-28	cytochrome c, somatic	Homo sapiens	107-119
23651497-2	2013	The two redox-sensitive neutral sphingomyelinase-2 (nSMase2) and sphingosine kinase-1 (SK1) participate in transducing stress signaling to ceramide and S1P, respectively; however, whether these key enzymes are coordinately regulated is not known.	Ceramides	139-147	sphingomyelin phosphodiesterase 3	Homo sapiens	24-50
23651497-2	2013	The two redox-sensitive neutral sphingomyelinase-2 (nSMase2) and sphingosine kinase-1 (SK1) participate in transducing stress signaling to ceramide and S1P, respectively; however, whether these key enzymes are coordinately regulated is not known.	Ceramides	139-147	sphingomyelin phosphodiesterase 3	Homo sapiens	52-59
23651497-2	2013	The two redox-sensitive neutral sphingomyelinase-2 (nSMase2) and sphingosine kinase-1 (SK1) participate in transducing stress signaling to ceramide and S1P, respectively; however, whether these key enzymes are coordinately regulated is not known.	Ceramides	139-147	sphingosine kinase 1	Homo sapiens	65-90
23528227-4	2013	We previously reported that increased ceramide levels, regulated by increased serine palmitoyltransferase (SPT), directly mediate amyloid beta (Abeta) levels.	Ceramides	38-46	amyloid beta (A4) precursor protein	Mus musculus	144-149
23629860-4	2013	We recently showed that ceramide-induced activation of PP1alpha leads to dephosphorylation and inactivation of ERM proteins, while S1P results in phosphorylation and activation of ERM proteins.	Ceramides	24-32	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	55-63
23465595-10	2013	Finally, TLR4 activation by palmitate increased subsequent cellular uptake of palmitate, and inhibiting ceramide synthesis ablated palmitate effects on PCK1 mRNA abundance and promoter activity.	Ceramides	104-112	phosphoenolpyruvate carboxykinase 1	Homo sapiens	152-156
23481236-3	2013	We studied accumulation of lipid metabolites [triglycerides (TAGs), diglycerides (DAGs)] and ceramides in relation to insulin signaling and expression and phosphorylation of PTP1B by preincubating rat skeletal muscle cells (L6 myotubes) with three saturated and three unsaturated free fatty acids (FFAs) (200 muM).	Ceramides	93-102	protein tyrosine phosphatase, non-receptor type 1	Rattus norvegicus	174-179
23481236-9	2013	Only FFAs that increased ceramides caused impairment of AKt and PTP1B phosphorylation at Ser 50.	Ceramides	25-34	AKT serine/threonine kinase 1	Rattus norvegicus	56-59
23481236-9	2013	Only FFAs that increased ceramides caused impairment of AKt and PTP1B phosphorylation at Ser 50.	Ceramides	25-34	protein tyrosine phosphatase, non-receptor type 1	Rattus norvegicus	64-69
23495037-0	2013	Mechanisms of ceramide-induced COX-2-dependent apoptosis in human ovarian cancer OVCAR-3 cells partially overlapped with resveratrol.	Ceramides	14-22	prostaglandin-endoperoxide synthase 2	Homo sapiens	31-36
23495037-3	2013	Exposure to ceramide activates extracellular-signal-regulated kinases (ERK)1/2- and p38 kinase-dependent apoptosis in human ovarian cancer OVCAR-3 cells, concomitant with an increase in the expression of COX-2 and p53 phosphorylation.	Ceramides	12-20	mitogen-activated protein kinase 1	Homo sapiens	84-87
23495037-3	2013	Exposure to ceramide activates extracellular-signal-regulated kinases (ERK)1/2- and p38 kinase-dependent apoptosis in human ovarian cancer OVCAR-3 cells, concomitant with an increase in the expression of COX-2 and p53 phosphorylation.	Ceramides	12-20	prostaglandin-endoperoxide synthase 2	Homo sapiens	204-209
23495037-3	2013	Exposure to ceramide activates extracellular-signal-regulated kinases (ERK)1/2- and p38 kinase-dependent apoptosis in human ovarian cancer OVCAR-3 cells, concomitant with an increase in the expression of COX-2 and p53 phosphorylation.	Ceramides	12-20	tumor protein p53	Homo sapiens	214-217
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	90-98	prostaglandin-endoperoxide synthase 2	Homo sapiens	12-28
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	90-98	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-35
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	90-98	tumor protein p53	Homo sapiens	107-110
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	90-98	prostaglandin-endoperoxide synthase 2	Homo sapiens	154-159
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	90-98	mitogen-activated protein kinase 1	Homo sapiens	187-190
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	236-244	prostaglandin-endoperoxide synthase 2	Homo sapiens	12-28
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	236-244	prostaglandin-endoperoxide synthase 2	Homo sapiens	30-35
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	236-244	tumor protein p53	Homo sapiens	107-110
23495037-4	2013	Blockade of cyclooxygenase-2 (COX-2) activity by siRNA or NS398 correspondingly inhibited ceramide-induced p53 Ser-15 phosphorylation and apoptosis; thus COX-2 appears at the apex of the p38 kinase-mediated signaling cascade induced by ceramide.	Ceramides	236-244	prostaglandin-endoperoxide synthase 2	Homo sapiens	154-159
23495037-7	2013	Although both ceramide and resveratrol induced the expressions of caspase-3 and -7, the effect of inducible COX-2 was different in caspase-7 expression induced by ceramide compared to resveratrol.	Ceramides	14-22	caspase 3	Homo sapiens	66-82
23495037-7	2013	Although both ceramide and resveratrol induced the expressions of caspase-3 and -7, the effect of inducible COX-2 was different in caspase-7 expression induced by ceramide compared to resveratrol.	Ceramides	163-171	prostaglandin-endoperoxide synthase 2	Homo sapiens	108-113
23495037-7	2013	Although both ceramide and resveratrol induced the expressions of caspase-3 and -7, the effect of inducible COX-2 was different in caspase-7 expression induced by ceramide compared to resveratrol.	Ceramides	163-171	caspase 7	Homo sapiens	131-140
23495037-8	2013	In summary, resveratrol and ceramide converge on an endocytosis-requiring, ERK1/2-dependent signal transduction pathway and induction of COX-expression as an essential molecular antecedent for subsequent p53-dependent apoptosis.	Ceramides	28-36	mitogen-activated protein kinase 3	Homo sapiens	75-81
23495037-8	2013	In summary, resveratrol and ceramide converge on an endocytosis-requiring, ERK1/2-dependent signal transduction pathway and induction of COX-expression as an essential molecular antecedent for subsequent p53-dependent apoptosis.	Ceramides	28-36	tumor protein p53	Homo sapiens	204-207
23495037-10	2013	However, a p38 kinase-dependent signal transduction pathway and change in mitochondrial potential are also involved in ceramide-induced apoptosis.	Ceramides	119-127	mitogen-activated protein kinase 1	Homo sapiens	11-14
23665108-0	2013	Homocysteine induces cerebral endothelial cell death by activating the acid sphingomyelinase ceramide pathway.	Ceramides	93-101	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	71-92
23665108-2	2013	In this study we examined the role of the acid sphingomyelinase (Asm)-ceramide pathway in the molecular mechanism of Hcy-induced CEC dysfunction.	Ceramides	70-78	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	42-63
23665108-2	2013	In this study we examined the role of the acid sphingomyelinase (Asm)-ceramide pathway in the molecular mechanism of Hcy-induced CEC dysfunction.	Ceramides	70-78	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	65-68
24244808-5	2013	In this regard, AMP generation that is controlled by a key ceramide metabolite S1P-dependent mechanism could be considered as alternate therapeutic approaches to treat these skin disorders, i.e., Increased S1P levels strongly stimulated the CAMP expression which elevated the antimicrobial activity against multiple pathogens resulting the improved AD patient skin.	Ceramides	59-67	cathelicidin antimicrobial peptide	Homo sapiens	241-245
23840067-2	2013	Recent studies have suggested that saturated fatty acids induce hepatic insulin resistance through activation of the toll-like receptor 4 (TLR-4) receptor in the liver, which in turn transcriptionally activates hepatic ceramide synthesis leading to inhibition of insulin signaling.	Ceramides	219-227	toll-like receptor 4	Mus musculus	117-137
23840067-2	2013	Recent studies have suggested that saturated fatty acids induce hepatic insulin resistance through activation of the toll-like receptor 4 (TLR-4) receptor in the liver, which in turn transcriptionally activates hepatic ceramide synthesis leading to inhibition of insulin signaling.	Ceramides	219-227	toll-like receptor 4	Mus musculus	139-144
23889969-9	2013	During disruption of lipid rafts, PPD activated neutral sphingomyelinase 2 (nSMase 2) hydrolyzing membrane sphingomyelins into pro-apoptotic intracellular ceramides.	Ceramides	155-164	sphingomyelin phosphodiesterase 3	Homo sapiens	48-74
23889969-9	2013	During disruption of lipid rafts, PPD activated neutral sphingomyelinase 2 (nSMase 2) hydrolyzing membrane sphingomyelins into pro-apoptotic intracellular ceramides.	Ceramides	155-164	sphingomyelin phosphodiesterase 3	Homo sapiens	76-84
23889969-11	2013	CONCLUSIONS: This study demonstrates that neutral sphingomyelinase 2 is responsible for the cytotoxicity of PPD through production of apoptotic ceramides from membrane sphingomyelins.	Ceramides	144-153	sphingomyelin phosphodiesterase 3	Homo sapiens	42-68
23835113-5	2013	Studies using cultured cells, animal models, and human subjects demonstrate that ceramide is a key player in the induction of beta-cell apoptosis, insulin resistance, and reduction of insulin gene expression.	Ceramides	81-89	insulin	Homo sapiens	147-154
23894595-3	2013	HYL-1 function is required for synthesis of ceramides and sphingolipids containing very long acyl-chains (>=C24), while HYL-2 is required for synthesis of ceramides and sphingolipids containing shorter acyl-chains (<=C22).	Ceramides	44-53	Ceramide synthase hyl-1;TLC domain-containing protein	Caenorhabditis elegans	0-5
23894595-3	2013	HYL-1 function is required for synthesis of ceramides and sphingolipids containing very long acyl-chains (>=C24), while HYL-2 is required for synthesis of ceramides and sphingolipids containing shorter acyl-chains (<=C22).	Ceramides	158-167	Ceramide synthase hyl-1;TLC domain-containing protein	Caenorhabditis elegans	0-5
23894595-3	2013	HYL-1 function is required for synthesis of ceramides and sphingolipids containing very long acyl-chains (>=C24), while HYL-2 is required for synthesis of ceramides and sphingolipids containing shorter acyl-chains (<=C22).	Ceramides	158-167	Ceramide synthase hyl-2	Caenorhabditis elegans	123-128
23835113-6	2013	Ceramide induces beta-cell apoptosis by multiple mechanisms namely; activation of extrinsic apoptotic pathway, increasing cytochrome c release, free radical generation, induction of endoplasmic reticulum stress and inhibition of Akt.	Ceramides	0-8	cytochrome c, somatic	Homo sapiens	122-134
23835113-6	2013	Ceramide induces beta-cell apoptosis by multiple mechanisms namely; activation of extrinsic apoptotic pathway, increasing cytochrome c release, free radical generation, induction of endoplasmic reticulum stress and inhibition of Akt.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	229-232
23835113-7	2013	Ceramide also modulates many of the insulin signaling intermediates such as insulin receptor substrate, Akt, Glut-4, and it causes insulin resistance.	Ceramides	0-8	insulin	Homo sapiens	36-43
23835113-7	2013	Ceramide also modulates many of the insulin signaling intermediates such as insulin receptor substrate, Akt, Glut-4, and it causes insulin resistance.	Ceramides	0-8	insulin	Homo sapiens	76-83
23835113-7	2013	Ceramide also modulates many of the insulin signaling intermediates such as insulin receptor substrate, Akt, Glut-4, and it causes insulin resistance.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	104-107
23835113-7	2013	Ceramide also modulates many of the insulin signaling intermediates such as insulin receptor substrate, Akt, Glut-4, and it causes insulin resistance.	Ceramides	0-8	solute carrier family 2 member 4	Homo sapiens	109-115
23835113-7	2013	Ceramide also modulates many of the insulin signaling intermediates such as insulin receptor substrate, Akt, Glut-4, and it causes insulin resistance.	Ceramides	0-8	insulin	Homo sapiens	76-83
23835113-8	2013	Ceramide reduces the synthesis of insulin hormone by attenuation of insulin gene expression.	Ceramides	0-8	insulin	Homo sapiens	34-41
23835113-8	2013	Ceramide reduces the synthesis of insulin hormone by attenuation of insulin gene expression.	Ceramides	0-8	insulin	Homo sapiens	68-75
23861887-3	2013	According to the proposed rheostat theory, SPHK activity shifts the intracellular balance from the pro-apoptotic sphingolipids ceramide and sphingosine to the mitogenic S1P, thereby determining the susceptibility of a cell to apoptotic stress.	Ceramides	127-135	sphingosine kinase 1	Homo sapiens	43-47
23567871-5	2013	Rn xenocybrid cells were resistant to staurosporine-induced cell death, but exhibited a four-fold increase in sensitivity to ceramide-induced cell death that was caspase-3 independent and did not induce chromosomal DNA degradation.	Ceramides	125-133	caspase 3	Mus musculus	162-171
23535273-1	2013	The last step in sphingolipid biosynthesis is the conversion of ceramide (Cer) to sphingomyelin (SM), which is catalyzed by sphingomyelin synthase (SMS).	Ceramides	64-72	spermine synthase	Homo sapiens	124-146
23535273-1	2013	The last step in sphingolipid biosynthesis is the conversion of ceramide (Cer) to sphingomyelin (SM), which is catalyzed by sphingomyelin synthase (SMS).	Ceramides	64-72	spermine synthase	Homo sapiens	148-151
23535273-1	2013	The last step in sphingolipid biosynthesis is the conversion of ceramide (Cer) to sphingomyelin (SM), which is catalyzed by sphingomyelin synthase (SMS).	Ceramides	74-77	spermine synthase	Homo sapiens	124-146
23535273-1	2013	The last step in sphingolipid biosynthesis is the conversion of ceramide (Cer) to sphingomyelin (SM), which is catalyzed by sphingomyelin synthase (SMS).	Ceramides	74-77	spermine synthase	Homo sapiens	148-151
23640498-0	2013	Sphingomyelin synthase 2 activity and liver steatosis: an effect of ceramide-mediated peroxisome proliferator-activated receptor gamma2 suppression.	Ceramides	68-76	sphingomyelin synthase 2	Homo sapiens	0-24
23640498-0	2013	Sphingomyelin synthase 2 activity and liver steatosis: an effect of ceramide-mediated peroxisome proliferator-activated receptor gamma2 suppression.	Ceramides	68-76	peroxisome proliferator activated receptor gamma	Homo sapiens	86-135
23640498-7	2013	We found that Sms2 liver-specific transgenic livers have lower ceramide and higher sphingomyelin, whereas Sms2 knockout livers have higher ceramide and lower sphingomyelin.	Ceramides	63-71	sphingomyelin synthase 2	Homo sapiens	14-18
23640498-7	2013	We found that Sms2 liver-specific transgenic livers have lower ceramide and higher sphingomyelin, whereas Sms2 knockout livers have higher ceramide and lower sphingomyelin.	Ceramides	139-147	sphingomyelin synthase 2	Homo sapiens	106-110
23640498-9	2013	Importantly, the exogenous ceramide supplementation to Huh7 cells, a human hepatoma cell line, reduced the expression of peroxisome proliferator-activated receptor gamma2 and its target genes, Cd36 and Fsp27.	Ceramides	27-35	peroxisome proliferator activated receptor gamma	Homo sapiens	121-170
23640498-12	2013	CONCLUSIONS: We attributed these effects to ceramide that can suppress peroxisome proliferator-activated receptor gamma2, thus reducing the expression of Cd36 and Fsp27 and reducing liver steatosis.	Ceramides	44-52	peroxisome proliferator activated receptor gamma	Homo sapiens	71-120
23567871-8	2013	These results suggest that the interaction of ceramide with OXPHOS complex III is significantly enhanced by the presence of the xenotypic Rattus cytochrome b in complex III, likely due to the increased affinity for ceramide at the ubiquinone binding site.	Ceramides	46-54	cytochrome b, mitochondrial	Mus musculus	145-157
23567871-8	2013	These results suggest that the interaction of ceramide with OXPHOS complex III is significantly enhanced by the presence of the xenotypic Rattus cytochrome b in complex III, likely due to the increased affinity for ceramide at the ubiquinone binding site.	Ceramides	215-223	cytochrome b, mitochondrial	Mus musculus	145-157
23493572-4	2013	We also demonstrate that ghrelin elicits a marked upregulation of hypothalamic C18:0 ceramide levels mediated by CPT1C.	Ceramides	85-93	ghrelin	Mus musculus	25-32
23493572-0	2013	Hypothalamic ceramide levels regulated by CPT1C mediate the orexigenic effect of ghrelin.	Ceramides	13-21	carnitine palmitoyltransferase 1c	Mus musculus	42-47
23493572-4	2013	We also demonstrate that ghrelin elicits a marked upregulation of hypothalamic C18:0 ceramide levels mediated by CPT1C.	Ceramides	85-93	carnitine palmitoyltransferase 1c	Mus musculus	113-118
23493572-0	2013	Hypothalamic ceramide levels regulated by CPT1C mediate the orexigenic effect of ghrelin.	Ceramides	13-21	ghrelin	Mus musculus	81-88
23493572-5	2013	Notably, central inhibition of ceramide synthesis with myriocin negated the orexigenic action of ghrelin and normalized the levels of AgRP and NPY, as well as their key transcription factors phosphorylated cAMP-response element-binding protein and forkhead box O1.	Ceramides	31-39	ghrelin	Mus musculus	97-104
23493572-5	2013	Notably, central inhibition of ceramide synthesis with myriocin negated the orexigenic action of ghrelin and normalized the levels of AgRP and NPY, as well as their key transcription factors phosphorylated cAMP-response element-binding protein and forkhead box O1.	Ceramides	31-39	agouti related neuropeptide	Mus musculus	134-138
23493572-5	2013	Notably, central inhibition of ceramide synthesis with myriocin negated the orexigenic action of ghrelin and normalized the levels of AgRP and NPY, as well as their key transcription factors phosphorylated cAMP-response element-binding protein and forkhead box O1.	Ceramides	31-39	neuropeptide Y	Mus musculus	143-146
23493572-6	2013	Finally, central treatment with ceramide induced food intake and orexigenic neuropeptides expression in CPT1C KO mice.	Ceramides	32-40	carnitine palmitoyltransferase 1c	Mus musculus	104-109
23493572-7	2013	Overall, these data indicate that, in addition to formerly reported mechanisms, ghrelin also induces food intake through regulation of hypothalamic CPT1C and ceramide metabolism, a finding of potential importance for the understanding and treatment of obesity.	Ceramides	158-166	ghrelin	Mus musculus	80-87
23538298-1	2013	Ceramides are synthesized by six different ceramide synthases (CerS1-6), which differ in their specificity to produce ceramides of distinct chain length.	Ceramides	0-9	ceramide synthase 1	Homo sapiens	63-70
23538298-1	2013	Ceramides are synthesized by six different ceramide synthases (CerS1-6), which differ in their specificity to produce ceramides of distinct chain length.	Ceramides	118-127	ceramide synthase 1	Homo sapiens	63-70
23538298-6	2013	Interestingly, down-regulation of ELOVL1 had a comprehensive effect on the synthesis of very long chain ceramides which possibly point to a requirement for ELOVL1 expression for full CerS2-activity.	Ceramides	104-113	ELOVL fatty acid elongase 1	Homo sapiens	34-40
23538298-6	2013	Interestingly, down-regulation of ELOVL1 had a comprehensive effect on the synthesis of very long chain ceramides which possibly point to a requirement for ELOVL1 expression for full CerS2-activity.	Ceramides	104-113	ceramide synthase 2	Homo sapiens	183-188
23538298-7	2013	Co-expression of CerS2 with CerS4/CerS6 reversed the inhibitory effect of long chain ceramides on cell proliferation and the induction of apoptosis.	Ceramides	85-94	ceramide synthase 2	Homo sapiens	17-22
23538298-3	2013	Over-expression of CerS4 and CerS6 enhanced the level of C(16:0)-Cer twofold, that of C(18:0)- and C(20:0)-Cer up to sevenfold, in comparison to vector control transfected cells, whereas over-expression of CerS2 had no effect on the level of very long chain ceramide C(24:0)- and C(24:1)-Cer.	Ceramides	258-266	ceramide synthase 4	Homo sapiens	19-24
23538298-3	2013	Over-expression of CerS4 and CerS6 enhanced the level of C(16:0)-Cer twofold, that of C(18:0)- and C(20:0)-Cer up to sevenfold, in comparison to vector control transfected cells, whereas over-expression of CerS2 had no effect on the level of very long chain ceramide C(24:0)- and C(24:1)-Cer.	Ceramides	258-266	ceramide synthase 6	Homo sapiens	29-34
23538298-4	2013	Instead over-expression of CerS2 together with CerS4 or CerS6 increased the activity of CerS2 against very-long-chain ceramides about twofold.	Ceramides	118-127	ceramide synthase 2	Homo sapiens	27-32
23538298-4	2013	Instead over-expression of CerS2 together with CerS4 or CerS6 increased the activity of CerS2 against very-long-chain ceramides about twofold.	Ceramides	118-127	ceramide synthase 4	Homo sapiens	47-52
23538298-4	2013	Instead over-expression of CerS2 together with CerS4 or CerS6 increased the activity of CerS2 against very-long-chain ceramides about twofold.	Ceramides	118-127	ceramide synthase 6	Homo sapiens	56-61
23538298-7	2013	Co-expression of CerS2 with CerS4/CerS6 reversed the inhibitory effect of long chain ceramides on cell proliferation and the induction of apoptosis.	Ceramides	85-94	ceramide synthase 4	Homo sapiens	28-33
23538298-4	2013	Instead over-expression of CerS2 together with CerS4 or CerS6 increased the activity of CerS2 against very-long-chain ceramides about twofold.	Ceramides	118-127	ceramide synthase 2	Homo sapiens	88-93
23538298-7	2013	Co-expression of CerS2 with CerS4/CerS6 reversed the inhibitory effect of long chain ceramides on cell proliferation and the induction of apoptosis.	Ceramides	85-94	ceramide synthase 6	Homo sapiens	34-39
23543151-0	2013	Role of mitochondrial Bax, caspases, and MAPKs for ceramide-induced apoptosis in renal proximal tubular cells.	Ceramides	51-59	BCL2 associated X, apoptosis regulator	Homo sapiens	22-25
23543151-9	2013	Mitochondrial Bax and caspases, but not MAPKs, play a role for ceramide-induced apoptosis in RPTCs.	Ceramides	63-71	BCL2 associated X, apoptosis regulator	Homo sapiens	14-17
23543151-2	2013	Effect of ceramide on expression of mitochondrial Bax and phosphorylated (p)-ERK, p38MAPK and JNK, that of MAPKs inhibition, and of EGF in the presence or absence of MAPKs inhibition on ceramide-induced apoptosis were examined in HK-2 cells.	Ceramides	10-18	BCL2 associated X, apoptosis regulator	Homo sapiens	50-53
23543151-10	2013	EGF ameliorates ceramide-induced apoptosis in Bax- and MAPKs-independent pathways.	Ceramides	16-24	epidermal growth factor	Homo sapiens	0-3
23543151-2	2013	Effect of ceramide on expression of mitochondrial Bax and phosphorylated (p)-ERK, p38MAPK and JNK, that of MAPKs inhibition, and of EGF in the presence or absence of MAPKs inhibition on ceramide-induced apoptosis were examined in HK-2 cells.	Ceramides	10-18	mitogen-activated protein kinase 1	Homo sapiens	77-80
23543151-10	2013	EGF ameliorates ceramide-induced apoptosis in Bax- and MAPKs-independent pathways.	Ceramides	16-24	BCL2 associated X, apoptosis regulator	Homo sapiens	46-49
23543151-11	2013	The mechanism of ceramide-induced apoptosis and anti-apoptotic effect of EGF deserves further investigations.	Ceramides	17-25	epidermal growth factor	Homo sapiens	73-76
23543151-2	2013	Effect of ceramide on expression of mitochondrial Bax and phosphorylated (p)-ERK, p38MAPK and JNK, that of MAPKs inhibition, and of EGF in the presence or absence of MAPKs inhibition on ceramide-induced apoptosis were examined in HK-2 cells.	Ceramides	10-18	mitogen-activated protein kinase 8	Homo sapiens	94-97
23707712-2	2013	This gene codes for acid ceramidase, a lysosomal heterodimeric enzyme that hydrolyzes ceramide into sphingosine and fatty acid.	Ceramides	86-94	N-acylsphingosine amidohydrolase 1	Homo sapiens	20-35
23840630-1	2013	Activation of sphingomyelinase (SMase) by extracellular stimuli is the major pathway for cellular production of ceramide, a bioactive lipid mediator acting through sphingomyelin (SM) hydrolysis.	Ceramides	112-120	sphingomyelin phosphodiesterase 2	Homo sapiens	32-37
23770692-0	2013	Acid sphingomyelinase-ceramide system mediates effects of antidepressant drugs.	Ceramides	22-30	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
23770692-3	2013	We investigated the role of the acid sphingomyelinase (Asm)-ceramide system as a target for antidepressants.	Ceramides	60-68	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	32-53
23770692-3	2013	We investigated the role of the acid sphingomyelinase (Asm)-ceramide system as a target for antidepressants.	Ceramides	60-68	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	55-58
23770692-6	2013	Mice overexpressing Asm, heterozygous for acid ceramidase, treated with blockers of ceramide metabolism or directly injected with C16 ceramide in the hippocampus had higher ceramide concentrations and lower rates of neuronal proliferation, maturation and survival compared with controls and showed depression-like behavior even in the absence of stress.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	20-23
23770692-6	2013	Mice overexpressing Asm, heterozygous for acid ceramidase, treated with blockers of ceramide metabolism or directly injected with C16 ceramide in the hippocampus had higher ceramide concentrations and lower rates of neuronal proliferation, maturation and survival compared with controls and showed depression-like behavior even in the absence of stress.	Ceramides	84-92	N-acylsphingosine amidohydrolase 1	Mus musculus	42-57
23770692-6	2013	Mice overexpressing Asm, heterozygous for acid ceramidase, treated with blockers of ceramide metabolism or directly injected with C16 ceramide in the hippocampus had higher ceramide concentrations and lower rates of neuronal proliferation, maturation and survival compared with controls and showed depression-like behavior even in the absence of stress.	Ceramides	134-142	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	20-23
23770692-6	2013	Mice overexpressing Asm, heterozygous for acid ceramidase, treated with blockers of ceramide metabolism or directly injected with C16 ceramide in the hippocampus had higher ceramide concentrations and lower rates of neuronal proliferation, maturation and survival compared with controls and showed depression-like behavior even in the absence of stress.	Ceramides	134-142	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	20-23
23770692-7	2013	The decrease of ceramide abundance achieved by antidepressant-mediated inhibition of Asm normalized these effects.	Ceramides	16-24	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	85-88
23840630-8	2013	Furthermore, transfection of Hsp60 siRNA into PC12 cells effectively increased both N-SMase activity and ceramide production and increased dopamine re-uptake with paralleled increase.	Ceramides	105-113	heat shock protein family D (Hsp60) member 1	Rattus norvegicus	29-34
23640896-0	2013	Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance.	Ceramides	173-181	Rac family small GTPase 1	Homo sapiens	0-5
23640896-7	2013	This unique signaling capacity exerted by Rac-1 superactivation bypassed the defects imposed by JNK- and ceramide-induced insulin resistance and allowed full and partial restoration of the GLUT4 translocation response, respectively.	Ceramides	105-113	Rac family small GTPase 1	Homo sapiens	42-47
23640896-7	2013	This unique signaling capacity exerted by Rac-1 superactivation bypassed the defects imposed by JNK- and ceramide-induced insulin resistance and allowed full and partial restoration of the GLUT4 translocation response, respectively.	Ceramides	105-113	insulin	Homo sapiens	122-129
23445175-2	2013	Ypc1p can catalyse the reverse reaction, i.e. the condensation of non-esterified fatty acids with phytosphingosine or dihydrosphingosine and overexpression of YPC1 or YDC1 can provide enough ceramide synthesis to rescue the viability of cells lacking the normal acyl-CoA-dependent ceramide synthases.	Ceramides	191-199	phytoceramidase	Saccharomyces cerevisiae S288C	0-5
23445175-2	2013	Ypc1p can catalyse the reverse reaction, i.e. the condensation of non-esterified fatty acids with phytosphingosine or dihydrosphingosine and overexpression of YPC1 or YDC1 can provide enough ceramide synthesis to rescue the viability of cells lacking the normal acyl-CoA-dependent ceramide synthases.	Ceramides	191-199	phytoceramidase	Saccharomyces cerevisiae S288C	159-163
23445175-2	2013	Ypc1p can catalyse the reverse reaction, i.e. the condensation of non-esterified fatty acids with phytosphingosine or dihydrosphingosine and overexpression of YPC1 or YDC1 can provide enough ceramide synthesis to rescue the viability of cells lacking the normal acyl-CoA-dependent ceramide synthases.	Ceramides	191-199	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	167-171
23620586-7	2013	Oleate (C18:1) was the only fatty acid protecting isc1Delta cells from HU toxicity in a ceramide-dependent manner.	Ceramides	88-96	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	50-54
23640896-0	2013	Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance.	Ceramides	173-181	insulin	Homo sapiens	31-38
23640896-0	2013	Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance.	Ceramides	173-181	solute carrier family 2 member 4	Homo sapiens	51-72
23640896-0	2013	Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance.	Ceramides	173-181	solute carrier family 2 member 4	Homo sapiens	74-79
23640896-0	2013	Rac-1 superactivation triggers insulin-independent glucose transporter 4 (GLUT4) translocation that bypasses signaling defects exerted by c-Jun N-terminal kinase (JNK)- and ceramide-induced insulin resistance.	Ceramides	173-181	insulin	Homo sapiens	190-197
23545566-5	2013	It is reported that several bacterial sphingolipids composed of ceramide are recognized by CD1-restricted T and NKT cells and that a non-peptide antigen is recognized by gammadelta T cells.	Ceramides	64-72	CD1 antigen complex	Mus musculus	91-94
23732709-2	2013	AC modulates the cellular balance between ceramide, sphingosine and sphingosine 1-phosphate (S1P).	Ceramides	42-50	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-2
23681708-1	2013	Farber disease (FD) is a severe inherited disorder of lipid metabolism characterized by deficient lysosomal acid ceramidase (ACDase) activity, resulting in ceramide accumulation.	Ceramides	156-164	N-acylsphingosine amidohydrolase 1	Homo sapiens	125-131
23681708-4	2013	Homozygous Asah1(P361R/P361R) animals showed ACDase defects, accumulated ceramide, demonstrated FD manifestations and died within 7-13 weeks.	Ceramides	73-81	N-acylsphingosine amidohydrolase 1	Homo sapiens	11-16
23681708-6	2013	Treatment of neonates with a single injection of human ACDase-encoding lentivector diminished the severity of the disease as highlighted by enhanced growth, decreased ceramide, lessened cellular infiltrations and increased lifespans.	Ceramides	167-175	N-acylsphingosine amidohydrolase 1	Homo sapiens	55-61
23681708-7	2013	This model of ACDase deficiency offers insights into the pathophysiology of FD and the roles of ACDase, ceramide and related sphingolipids in cell signaling and growth, as well as facilitates the development of therapy.	Ceramides	104-112	N-acylsphingosine amidohydrolase 1	Homo sapiens	14-20
23529132-5	2013	Insulin-stimulated total glucose disposal (TGD), plasma FFA species, muscle insulin signalling, IBalpha protein, c-Jun phosphorylation, inflammatory gene (toll-like receptor 4 and monocyte chemotactic protein 1) expression, and ceramide and diacylglycerol (DAG) content were measured in muscle from a group of obese and T2DM subjects before and after administration of the antilipolytic drug acipimox for 7 days, and the results were compared to lean individuals.	Ceramides	228-236	insulin	Homo sapiens	0-7
23776401-1	2013	B13 is a ceramide analogue and apoptosis inducer with potent cytotoxic activity.	Ceramides	9-17	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	0-3
23547262-3	2013	Herein, we demonstrate that ablating dihydroceramide desaturase 1 (Des1), an enzyme that produces ceramides, leads to the simultaneous activation of both anabolic and catabolic signaling pathways.	Ceramides	98-107	delta 4-desaturase, sphingolipid 1	Homo sapiens	37-65
23547262-3	2013	Herein, we demonstrate that ablating dihydroceramide desaturase 1 (Des1), an enzyme that produces ceramides, leads to the simultaneous activation of both anabolic and catabolic signaling pathways.	Ceramides	98-107	delta 4-desaturase, sphingolipid 1	Homo sapiens	67-71
23833655-2	2013	We previously demonstrated that C6 ceramide and paclitaxel function synergistically to induce ovarian cancer cell death via modulation of the PI3/AKT cell survival pathway.	Ceramides	35-43	peptidase inhibitor 3	Homo sapiens	142-145
23754960-5	2013	However, analysis of additional patients with non-syndromic ARCI revealed a splice site mutation in CERS3 indicating that a defect in ceramide synthesis is causative for the present skin phenotype of our patients.	Ceramides	134-142	ceramide synthase 3	Homo sapiens	100-105
23754960-6	2013	Functional analysis of patient skin and in vitro differentiated keratinocytes demonstrated that mutations in CERS3 lead to a disturbed sphingolipid profile with reduced levels of epidermis-specific very long-chain ceramides that interferes with epidermal differentiation.	Ceramides	214-223	ceramide synthase 3	Homo sapiens	109-114
21862212-2	2013	Ceramide can be produced via multiple mechanisms including through the hydrolysis of sphingomyelin by acid and neutral sphingomyelinase or by a de novo synthesis pathway.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	111-135
23724146-3	2013	Recombinant human acid sphingomyelinase (rhASM), which hydrolyzes sphingomyelin to ceramide, is an orphan drug under development for the treatment of Type B Niemann-Pick disease (NPD).	Ceramides	83-91	sphingomyelin phosphodiesterase 1	Homo sapiens	18-39
23480852-0	2013	BAK activation is necessary and sufficient to drive ceramide synthase-dependent ceramide accumulation following inhibition of BCL2-like proteins.	Ceramides	52-60	BCL2 antagonist/killer 1	Homo sapiens	0-3
23480852-4	2013	In the present study we demonstrate that direct inhibition of anti-apoptotic BCL2 proteins with ABT-263 is sufficient to induce C(16)-ceramide synthesis in multiple cell lines, including human leukaemia and myeloma cells.	Ceramides	134-142	BCL2 apoptosis regulator	Homo sapiens	77-81
23480852-8	2013	Furthermore, we present a feed-forward model by which BAK activation of CerS by chemotherapeutic drugs leads to elevated ceramide levels that result in synergistic channel formation by ceramide (or one of its metabolites) and BAX/BAK.	Ceramides	121-129	BCL2 antagonist/killer 1	Homo sapiens	54-57
23480852-8	2013	Furthermore, we present a feed-forward model by which BAK activation of CerS by chemotherapeutic drugs leads to elevated ceramide levels that result in synergistic channel formation by ceramide (or one of its metabolites) and BAX/BAK.	Ceramides	121-129	BCL2 associated X, apoptosis regulator	Homo sapiens	226-229
23480852-8	2013	Furthermore, we present a feed-forward model by which BAK activation of CerS by chemotherapeutic drugs leads to elevated ceramide levels that result in synergistic channel formation by ceramide (or one of its metabolites) and BAX/BAK.	Ceramides	121-129	BCL2 antagonist/killer 1	Homo sapiens	230-233
23480852-8	2013	Furthermore, we present a feed-forward model by which BAK activation of CerS by chemotherapeutic drugs leads to elevated ceramide levels that result in synergistic channel formation by ceramide (or one of its metabolites) and BAX/BAK.	Ceramides	185-193	BCL2 antagonist/killer 1	Homo sapiens	54-57
23480852-8	2013	Furthermore, we present a feed-forward model by which BAK activation of CerS by chemotherapeutic drugs leads to elevated ceramide levels that result in synergistic channel formation by ceramide (or one of its metabolites) and BAX/BAK.	Ceramides	185-193	BCL2 associated X, apoptosis regulator	Homo sapiens	226-229
23480852-8	2013	Furthermore, we present a feed-forward model by which BAK activation of CerS by chemotherapeutic drugs leads to elevated ceramide levels that result in synergistic channel formation by ceramide (or one of its metabolites) and BAX/BAK.	Ceramides	185-193	BCL2 antagonist/killer 1	Homo sapiens	230-233
23690971-3	2013	We now show that C24- and C16-ceramides are the most abundant lung ceramide species, paralleled by high expression of their synthetic enzymes, ceramide synthase 2 (CerS2) and CerS5, respectively.	Ceramides	30-38	ceramide synthase 2	Mus musculus	143-162
23690971-3	2013	We now show that C24- and C16-ceramides are the most abundant lung ceramide species, paralleled by high expression of their synthetic enzymes, ceramide synthase 2 (CerS2) and CerS5, respectively.	Ceramides	30-38	ceramide synthase 2	Mus musculus	164-169
23690971-3	2013	We now show that C24- and C16-ceramides are the most abundant lung ceramide species, paralleled by high expression of their synthetic enzymes, ceramide synthase 2 (CerS2) and CerS5, respectively.	Ceramides	30-38	ceramide synthase 5	Mus musculus	175-180
23690971-4	2013	Furthermore, the ceramide species synthesis in the lung is homeostatically regulated, since mice lacking very long acyl chain C24-ceramides due to genetic deficiency of CerS2 displayed a ten-fold increase in C16-ceramides and C16-dihydroceramides along with elevation of acid sphingomyelinase and CerS5 activities.	Ceramides	17-25	ceramide synthase 2	Mus musculus	169-174
23690971-4	2013	Furthermore, the ceramide species synthesis in the lung is homeostatically regulated, since mice lacking very long acyl chain C24-ceramides due to genetic deficiency of CerS2 displayed a ten-fold increase in C16-ceramides and C16-dihydroceramides along with elevation of acid sphingomyelinase and CerS5 activities.	Ceramides	17-25	ceramide synthase 5	Mus musculus	297-302
23614460-1	2013	Acid ceramidase (AC) is an intracellular cysteine amidase that catalyzes the hydrolysis of the lipid messenger ceramide.	Ceramides	111-119	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	0-15
23614460-1	2013	Acid ceramidase (AC) is an intracellular cysteine amidase that catalyzes the hydrolysis of the lipid messenger ceramide.	Ceramides	111-119	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	17-19
23614460-2	2013	By regulating ceramide levels in cells, AC may contribute to the regulation of cancer cell proliferation and senescence and to the response to cancer therapy.	Ceramides	14-22	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	40-42
23663742-0	2013	An FGF21-adiponectin-ceramide axis controls energy expenditure and insulin action in mice.	Ceramides	21-29	fibroblast growth factor 21	Mus musculus	3-8
23663742-0	2013	An FGF21-adiponectin-ceramide axis controls energy expenditure and insulin action in mice.	Ceramides	21-29	adiponectin, C1Q and collagen domain containing	Mus musculus	9-20
23663742-5	2013	Here, we show that FGF21 rapidly and robustly stimulates adiponectin secretion in rodents while diminishing accumulation of ceramides in obese animals.	Ceramides	124-133	fibroblast growth factor 21	Mus musculus	19-24
23663742-6	2013	Importantly, adiponectin-knockout mice are refractory to changes in energy expenditure and ceramide-lowering effects evoked by FGF21 administration.	Ceramides	91-99	adiponectin, C1Q and collagen domain containing	Mus musculus	13-24
23663742-6	2013	Importantly, adiponectin-knockout mice are refractory to changes in energy expenditure and ceramide-lowering effects evoked by FGF21 administration.	Ceramides	91-99	fibroblast growth factor 21	Mus musculus	127-132
23667632-2	2013	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and glucosylceramide synthase (GCS) catalyzes ceramide metabolism.	Ceramides	56-64	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
23667632-2	2013	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and glucosylceramide synthase (GCS) catalyzes ceramide metabolism.	Ceramides	56-64	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
23667632-2	2013	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and glucosylceramide synthase (GCS) catalyzes ceramide metabolism.	Ceramides	77-85	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
23667632-2	2013	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and glucosylceramide synthase (GCS) catalyzes ceramide metabolism.	Ceramides	77-85	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
23667632-2	2013	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and glucosylceramide synthase (GCS) catalyzes ceramide metabolism.	Ceramides	77-85	UDP-glucose ceramide glucosyltransferase	Homo sapiens	96-99
23667632-6	2013	For in vitro studies, increases in ceramide levels were achieved either by ASM overexpression or by the GCS inhibitor DL-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol (PPMP) in human glioma cell lines.	Ceramides	35-43	sphingomyelin phosphodiesterase 1	Homo sapiens	75-78
23667632-6	2013	For in vitro studies, increases in ceramide levels were achieved either by ASM overexpression or by the GCS inhibitor DL-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol (PPMP) in human glioma cell lines.	Ceramides	35-43	UDP-glucose ceramide glucosyltransferase	Homo sapiens	104-107
23667632-11	2013	ASM overexpression or PPMP treatment alone led to ceramide accumulation but did not enhance the anti-glioma activity of alkylating chemotherapy or irradiation.	Ceramides	50-58	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
23667632-15	2013	CONCLUSION: Modulation of intrinsic glioma cell ceramide levels by ASM overexpression or GCS inhibition does not enhance the anti-glioma activity of alkylating chemotherapy or irradiation.	Ceramides	48-56	sphingomyelin phosphodiesterase 1	Homo sapiens	67-70
23519469-1	2013	We have investigated the role of ceramide in the cellular adaptation to folate stress induced by Aldh1l1, the enzyme involved in the regulation of folate metabolism.	Ceramides	33-41	aldehyde dehydrogenase 1 family member L1	Homo sapiens	97-104
23519469-4	2013	Pretreatment with ceramide synthesis inhibitors myriocin and fumonisin B1 or siRNA silencing of CerS6 prevented C16-ceramide accumulation and rescued cells supporting the role of CerS6/C16-ceramide as effectors of Aldh1l1-induced apoptosis.	Ceramides	115-124	ceramide synthase 6	Homo sapiens	96-101
23519469-5	2013	The CerS6 activation by Aldh1l1 and increased ceramide generation were p53-dependent; this effect was ablated in p53-null cells.	Ceramides	46-54	ceramide synthase 6	Homo sapiens	4-9
23519469-9	2013	Interestingly, ceramide elevation in response to Aldh1l1 was inhibited by silencing of PUMA, a proapoptotic downstream effector of p53 whereas the transient expression of CerS6 elevated PUMA in a p53-dependent manner indicating reciprocal relationships between ceramide and p53/PUMA pathways.	Ceramides	15-23	aldehyde dehydrogenase 1 family member L1	Homo sapiens	49-56
23519469-9	2013	Interestingly, ceramide elevation in response to Aldh1l1 was inhibited by silencing of PUMA, a proapoptotic downstream effector of p53 whereas the transient expression of CerS6 elevated PUMA in a p53-dependent manner indicating reciprocal relationships between ceramide and p53/PUMA pathways.	Ceramides	15-23	ceramide synthase 6	Homo sapiens	171-176
23519469-9	2013	Interestingly, ceramide elevation in response to Aldh1l1 was inhibited by silencing of PUMA, a proapoptotic downstream effector of p53 whereas the transient expression of CerS6 elevated PUMA in a p53-dependent manner indicating reciprocal relationships between ceramide and p53/PUMA pathways.	Ceramides	261-269	aldehyde dehydrogenase 1 family member L1	Homo sapiens	49-56
23519469-9	2013	Interestingly, ceramide elevation in response to Aldh1l1 was inhibited by silencing of PUMA, a proapoptotic downstream effector of p53 whereas the transient expression of CerS6 elevated PUMA in a p53-dependent manner indicating reciprocal relationships between ceramide and p53/PUMA pathways.	Ceramides	261-269	ceramide synthase 6	Homo sapiens	171-176
23519469-10	2013	Importantly, folate withdrawal also induced CerS6/C16-ceramide elevation accompanied by p53 accumulation.	Ceramides	54-62	ceramide synthase 6	Homo sapiens	44-49
23658784-1	2013	BACKGROUND: As a key enzyme in sphingolipid metabolism, acid sphingomyelinase (ASM) is involved in the regulation of cell fate and signaling via hydrolysis of sphingomyelin to form ceramide.	Ceramides	181-189	sphingomyelin phosphodiesterase 1	Homo sapiens	56-77
23658784-1	2013	BACKGROUND: As a key enzyme in sphingolipid metabolism, acid sphingomyelinase (ASM) is involved in the regulation of cell fate and signaling via hydrolysis of sphingomyelin to form ceramide.	Ceramides	181-189	sphingomyelin phosphodiesterase 1	Homo sapiens	79-82
23672204-3	2013	This implicates the enzyme dihydroceramide desaturase (DHC-DS), which converts dihydroceramide to ceramide, in a potential regulatory checkpoint in cardiomyocytes.	Ceramides	34-42	delta(4)-desaturase, sphingolipid 1	Mus musculus	55-61
23672204-11	2013	The regulation of de novo ceramide synthesis in response to hypoxia and this newly described interaction between E-box and NFATC transcription factors will pave the way to identify new pathways in the adaptation of the cardiomyocyte to stress.	Ceramides	26-34	nuclear factor of activated T cells, cytoplasmic, calcineurin dependent 1	Mus musculus	123-128
23181473-4	2013	GCS, a key enzyme of this pathway, neutralizes pro-apoptotic ceramide by transfer of a uridine diphosphate (UDP)-glucose.	Ceramides	61-69	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
23508272-0	2013	AMP-activated protein kinase (AMPK)/Ulk1-dependent autophagic pathway contributes to C6 ceramide-induced cytotoxic effects in cultured colorectal cancer HT-29 cells.	Ceramides	88-96	unc-51 like autophagy activating kinase 1	Homo sapiens	36-40
23508272-7	2013	Further, we indentified that AMP-activated protein kinase (AMPK)/Ulk1 signaling was required for autophagy induction by C6 ceramide, and AMPK silencing by a specific short hairpin RNA suppressed C6 ceramide-induced autophagy and cytotoxic effects.	Ceramides	123-131	unc-51 like autophagy activating kinase 1	Homo sapiens	65-69
23508272-7	2013	Further, we indentified that AMP-activated protein kinase (AMPK)/Ulk1 signaling was required for autophagy induction by C6 ceramide, and AMPK silencing by a specific short hairpin RNA suppressed C6 ceramide-induced autophagy and cytotoxic effects.	Ceramides	198-206	unc-51 like autophagy activating kinase 1	Homo sapiens	65-69
23545566-7	2013	Interestingly, this TLR 4-recognition pathway of bacterial SPLs involves the fatty acid composition of ceramide in addition to the sugar moiety.	Ceramides	103-111	toll-like receptor 4	Mus musculus	20-25
23501591-7	2013	Our results showed a consistent and notable decrease of the retinal SPL content (mainly ranging from 30% to 60%) in the Cerkl -/- compared to WT retinas, which was particularly evident in the glucosyl/galactosyl ceramide species (Glc/GalCer) whereas the phospholipids and neutral lipids remained unaltered.	Ceramides	212-220	plasma serotonin level	Mus musculus	68-71
23501591-7	2013	Our results showed a consistent and notable decrease of the retinal SPL content (mainly ranging from 30% to 60%) in the Cerkl -/- compared to WT retinas, which was particularly evident in the glucosyl/galactosyl ceramide species (Glc/GalCer) whereas the phospholipids and neutral lipids remained unaltered.	Ceramides	212-220	ceramide kinase-like	Mus musculus	120-125
23065519-3	2013	This study investigated the relationship between nSMase/ceramide and the NF-kappaB signaling pathway in PARs-mediated human platelet activation.	Ceramides	56-64	nuclear factor kappa B subunit 1	Homo sapiens	73-82
23065519-10	2013	We also found that C2-ceramide (a cell-permeable ceramide analog) activated p38 MAPK and IKKbeta phosphorylation in platelets and markedly shortened the occlusion time of platelet plug formation in vivo.	Ceramides	22-30	mitogen-activated protein kinase 14	Homo sapiens	76-79
23065519-10	2013	We also found that C2-ceramide (a cell-permeable ceramide analog) activated p38 MAPK and IKKbeta phosphorylation in platelets and markedly shortened the occlusion time of platelet plug formation in vivo.	Ceramides	22-30	inhibitor of nuclear factor kappa B kinase subunit beta	Homo sapiens	89-96
23065519-11	2013	This study demonstrated that thrombin activated nSMase by binding to PAR4, but not to PAR1, to increase the C24:0-ceramide level, followed by the activation of p38 MAPK-NF-kappaB signaling.	Ceramides	114-122	coagulation factor II, thrombin	Homo sapiens	29-37
23065519-11	2013	This study demonstrated that thrombin activated nSMase by binding to PAR4, but not to PAR1, to increase the C24:0-ceramide level, followed by the activation of p38 MAPK-NF-kappaB signaling.	Ceramides	114-122	sphingomyelin phosphodiesterase 2	Homo sapiens	48-54
23065519-12	2013	Our results showed a novel physiological significance of PAR4-nSMase/ceramide-p38 MAPK-NF-kappaB cascade in platelet activation.	Ceramides	69-77	F2R like thrombin or trypsin receptor 3	Homo sapiens	57-61
23065519-12	2013	Our results showed a novel physiological significance of PAR4-nSMase/ceramide-p38 MAPK-NF-kappaB cascade in platelet activation.	Ceramides	69-77	mitogen-activated protein kinase 14	Homo sapiens	78-81
23065519-12	2013	Our results showed a novel physiological significance of PAR4-nSMase/ceramide-p38 MAPK-NF-kappaB cascade in platelet activation.	Ceramides	69-77	nuclear factor kappa B subunit 1	Homo sapiens	87-96
23423838-1	2013	Acid ceramidase (AC) catalyzes the hydrolysis of ceramide into sphingosine, in turn a substrate of sphingosine kinases that catalyze its conversion into the mitogenic sphingosine-1-phosphate.	Ceramides	49-57	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
23423838-1	2013	Acid ceramidase (AC) catalyzes the hydrolysis of ceramide into sphingosine, in turn a substrate of sphingosine kinases that catalyze its conversion into the mitogenic sphingosine-1-phosphate.	Ceramides	49-57	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
23423838-4	2013	Stable knockdown of ASAH1 in PC-3/Mc cells caused an accumulation of ceramides, inhibition of clonogenic potential, increased requirement for growth factors, and inhibition of tumorigenesis and lung metastases.	Ceramides	69-78	N-acylsphingosine amidohydrolase 1	Homo sapiens	20-25
23423838-5	2013	We developed de novo ASAH1 inhibitors, which also caused a dose-dependent accumulation of ceramides in PC-3/Mc cells and inhibited their growth and clonogenicity.	Ceramides	90-99	N-acylsphingosine amidohydrolase 1	Homo sapiens	21-26
23582643-5	2013	TNF-induced necroptosis occurs through two pathways: modulation of mitochondrial cyclophilin D, implicated in mitochondrial permeability transition pore formation, and acid sphingomyelinase-mediated ceramide production.	Ceramides	199-207	tumor necrosis factor b (TNF superfamily, member 2)	Danio rerio	0-3
23675553-1	2013	The sphingolipid metabolites ceramide, sphingosine, and sphingosine-1-phosphate (S1P) and its enzyme sphingosine kinase (SphK) play an important role in the regulation of cell proliferation, survival, inflammation, and cell death.	Ceramides	29-37	sphingosine kinase 1	Homo sapiens	101-119
23638138-1	2013	Acid ceramidase is required to maintain the metabolic balance of several important bioactive lipids, including ceramide, sphingosine and sphingosine-1-phosphate.	Ceramides	111-119	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	0-15
23638138-2	2013	Here we show that addition of recombinant acid ceramidase (rAC) to primary chondrocyte culture media maintained low levels of ceramide and led to elevated sphingosine by 48 hours.	Ceramides	126-134	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	42-57
23353700-6	2013	The addition of either tamoxifen, VX-710, verapamil, or cyclosporin A, antagonists of P-gp, enhanced C6-ceramide cytotoxicity in all cell lines.	Ceramides	104-112	ATP binding cassette subfamily B member 1	Homo sapiens	86-90
23675553-1	2013	The sphingolipid metabolites ceramide, sphingosine, and sphingosine-1-phosphate (S1P) and its enzyme sphingosine kinase (SphK) play an important role in the regulation of cell proliferation, survival, inflammation, and cell death.	Ceramides	29-37	sphingosine kinase 1	Homo sapiens	121-125
23675553-5	2013	A central finding of these studies is that SphK is a critical regulator of the sphingolipid rheostat, as it not only produces the pro-growth, anti-apoptotic messenger S1P, but also decreases levels of pro-apoptotic ceramide and sphingosine.	Ceramides	215-223	sphingosine kinase 1	Homo sapiens	43-47
23353700-4	2013	Because intracellular P-glycoprotein (P-gp) plays a role in catalyzing the conversion of ceramide to higher sphingolipids, we hypothesized that administration of P-gp antagonists with C6-ceramide would magnify cell death cascades.	Ceramides	89-97	ATP binding cassette subfamily B member 1	Homo sapiens	22-36
23353700-4	2013	Because intracellular P-glycoprotein (P-gp) plays a role in catalyzing the conversion of ceramide to higher sphingolipids, we hypothesized that administration of P-gp antagonists with C6-ceramide would magnify cell death cascades.	Ceramides	89-97	ATP binding cassette subfamily B member 1	Homo sapiens	38-42
23353700-11	2013	The high frequency of expression of P-gp in CRC presents an adventitious target for complementing ceramide-based therapies, a strategy that could hold promise for treatment of resistant disease.	Ceramides	98-106	ATP binding cassette subfamily B member 1	Homo sapiens	36-40
23353700-4	2013	Because intracellular P-glycoprotein (P-gp) plays a role in catalyzing the conversion of ceramide to higher sphingolipids, we hypothesized that administration of P-gp antagonists with C6-ceramide would magnify cell death cascades.	Ceramides	89-97	ATP binding cassette subfamily B member 1	Homo sapiens	162-166
23593226-3	2013	In this study, we determine that the oxysterol binding protein family member Kes1 is required to maintain the ratio of complex sphingolipids and levels of ceramide, sphingosine-phosphate and sphingosine.	Ceramides	155-163	oxysterol-binding protein KES1	Saccharomyces cerevisiae S288C	77-81
23593476-1	2013	Sphingomyelin synthase 1 (SMS1) catalyzes the conversion of ceramide to sphingomyelin.	Ceramides	60-68	sphingomyelin synthase 1	Mus musculus	0-24
23593476-1	2013	Sphingomyelin synthase 1 (SMS1) catalyzes the conversion of ceramide to sphingomyelin.	Ceramides	60-68	sphingomyelin synthase 1	Mus musculus	26-30
23818862-2	2013	We demonstrate here that the AKT/FOXO pathway regulates survival in increased ceramide environment by metabolic adaptation involving changes in glycolysis and lipolysis through novel downstream targets.	Ceramides	78-86	thymoma viral proto-oncogene 1	Mus musculus	29-32
23393182-8	2013	Muscle ceramide content was significantly increased in insulin-resistant vs insulin-sensitive individuals (P = .04).	Ceramides	7-15	insulin	Homo sapiens	55-62
23393182-8	2013	Muscle ceramide content was significantly increased in insulin-resistant vs insulin-sensitive individuals (P = .04).	Ceramides	7-15	insulin	Homo sapiens	76-83
23417430-3	2013	Small molecule inhibitors of ceramide-specific glucosyltransferase, the first committed step in ganglioside biosynthesis, reduce storage of GM2 and GA2.	Ceramides	29-37	cytochrome b5 domain containing 2	Mus musculus	140-143
23433550-9	2013	Furthermore, the ceramide composition of the SC lipids and filaggrin processing were altered in Cldn1(-/-) mice.	Ceramides	17-25	claudin 1	Mus musculus	96-101
23421703-3	2013	Recent studies have identified that the GPI phospholipase A2 Per1p and O-acyltransferase Gup1p play essential roles in diacylglycerol-type lipid remodelling of GPI-anchored proteins, while Cwh43p is involved in the remodelling of lipid moieties to ceramide.	Ceramides	248-256	Per1p	Saccharomyces cerevisiae S288C	61-66
23421703-3	2013	Recent studies have identified that the GPI phospholipase A2 Per1p and O-acyltransferase Gup1p play essential roles in diacylglycerol-type lipid remodelling of GPI-anchored proteins, while Cwh43p is involved in the remodelling of lipid moieties to ceramide.	Ceramides	248-256	O-acyltransferase	Saccharomyces cerevisiae S288C	89-94
23421703-3	2013	Recent studies have identified that the GPI phospholipase A2 Per1p and O-acyltransferase Gup1p play essential roles in diacylglycerol-type lipid remodelling of GPI-anchored proteins, while Cwh43p is involved in the remodelling of lipid moieties to ceramide.	Ceramides	248-256	Cwh43p	Saccharomyces cerevisiae S288C	189-195
23421703-6	2013	Based on our analyses of single- and double-mutants of proteins involved in lipid remodelling, we demonstrate that an alternative pathway, in which lyso-phosphatidylinositol generated by Per1p is used as a substrate for Cwh43p, is involved in the remodelling of GPI lipid moieties to ceramide when the normal sequential pathway is inhibited.	Ceramides	284-292	Per1p	Saccharomyces cerevisiae S288C	187-192
23421703-6	2013	Based on our analyses of single- and double-mutants of proteins involved in lipid remodelling, we demonstrate that an alternative pathway, in which lyso-phosphatidylinositol generated by Per1p is used as a substrate for Cwh43p, is involved in the remodelling of GPI lipid moieties to ceramide when the normal sequential pathway is inhibited.	Ceramides	284-292	Cwh43p	Saccharomyces cerevisiae S288C	220-226
23421703-7	2013	In addition, mass spectrometric analysis of lipid species of Flag-tagged Gas1p revealed that Gas1p contains ceramide moieties in its GPI anchor.	Ceramides	108-116	1,3-beta-glucanosyltransferase GAS1	Saccharomyces cerevisiae S288C	73-78
23421703-7	2013	In addition, mass spectrometric analysis of lipid species of Flag-tagged Gas1p revealed that Gas1p contains ceramide moieties in its GPI anchor.	Ceramides	108-116	1,3-beta-glucanosyltransferase GAS1	Saccharomyces cerevisiae S288C	93-98
23350699-4	2013	Secretion of Scr3 was suppressed by 2-BP (2-bromopalmitate, a palmitoylation inhibitor) and by GW4869 (an inhibitor of ceramide synthesis).	Ceramides	119-127	RNA binding motif single stranded interacting protein 2	Homo sapiens	13-17
23550784-3	2013	Current evidence suggests that the inverse association between plasma PLP and inflammation may be the result of mobilization of this coenzyme to the site of inflammation, for use by the PLP-dependent enzymes of the kynurenine pathway of tryptophan degradation, metabolism of the immunomodulatory sphingolipids, ceramide and sphingosine 1-phosphate, and for serine hydroxymethylase for immune cell proliferation.	Ceramides	311-319	pyridoxal phosphatase	Homo sapiens	70-73
23550784-3	2013	Current evidence suggests that the inverse association between plasma PLP and inflammation may be the result of mobilization of this coenzyme to the site of inflammation, for use by the PLP-dependent enzymes of the kynurenine pathway of tryptophan degradation, metabolism of the immunomodulatory sphingolipids, ceramide and sphingosine 1-phosphate, and for serine hydroxymethylase for immune cell proliferation.	Ceramides	311-319	pyridoxal phosphatase	Homo sapiens	186-189
23395327-6	2013	Ischemia also significantly increased cell death mediator ceramides only in CA1.	Ceramides	58-67	carbonic anhydrase 1	Rattus norvegicus	76-79
23530619-0	2013	p53-independent early and late apoptosis is mediated by ceramide after exposure of tumor cells to photon or carbon ion irradiation.	Ceramides	56-64	tumor protein p53	Homo sapiens	0-3
23530619-1	2013	BACKGROUND: To determine whether ceramide is responsible for the induction of p53-independent early or late apoptosis in response to high- and low-Linear-Energy-Transfer (LET) irradiation.	Ceramides	33-41	tumor protein p53	Homo sapiens	78-81
23530619-7	2013	CONCLUSIONS: Ceramide is a determining factor in the onset of early and late apoptosis after low and high-LET irradiation and is the mediator of the p53-independent-apoptotic pathway.	Ceramides	13-21	tumor protein p53	Homo sapiens	149-152
23305978-0	2013	Adiponectin concentration is associated with muscle insulin sensitivity, AMPK phosphorylation, and ceramide content in skeletal muscles of men but not women.	Ceramides	99-107	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
23180825-5	2013	Moreover, Spns2 mice have decreased levels of both of these phosphorylated sphingoid bases in blood, accompanied by increases in very long chain ceramide species, and have defective lymphocyte trafficking.	Ceramides	145-153	spinster homolog 2	Mus musculus	10-15
23455468-2	2013	Some genotoxic stresses are able to induce p53-dependent ceramide accumulation leading to cell death.	Ceramides	57-65	tumor protein p53	Homo sapiens	43-46
23305978-7	2013	Serum adiponectin was also significantly, negatively associated with skeletal muscle ceramide content in men only, and interestingly, ceramide content was negatively associated with adiponectin receptor 1 (AdipoR1) expression in skeletal muscles of men.	Ceramides	85-93	adiponectin, C1Q and collagen domain containing	Homo sapiens	6-17
23305978-7	2013	Serum adiponectin was also significantly, negatively associated with skeletal muscle ceramide content in men only, and interestingly, ceramide content was negatively associated with adiponectin receptor 1 (AdipoR1) expression in skeletal muscles of men.	Ceramides	134-142	adiponectin receptor 1	Homo sapiens	182-204
23305978-7	2013	Serum adiponectin was also significantly, negatively associated with skeletal muscle ceramide content in men only, and interestingly, ceramide content was negatively associated with adiponectin receptor 1 (AdipoR1) expression in skeletal muscles of men.	Ceramides	134-142	adiponectin receptor 1	Homo sapiens	206-213
23305978-9	2013	These associations suggest that the insulin-sensitizing effect of adiponectin on human male skeletal muscles may be mediated via AdipoR1 to activation of AMPK, leading to lowering of ceramide content.	Ceramides	183-191	insulin	Homo sapiens	36-43
23305978-9	2013	These associations suggest that the insulin-sensitizing effect of adiponectin on human male skeletal muscles may be mediated via AdipoR1 to activation of AMPK, leading to lowering of ceramide content.	Ceramides	183-191	adiponectin, C1Q and collagen domain containing	Homo sapiens	66-77
23305978-9	2013	These associations suggest that the insulin-sensitizing effect of adiponectin on human male skeletal muscles may be mediated via AdipoR1 to activation of AMPK, leading to lowering of ceramide content.	Ceramides	183-191	adiponectin receptor 1	Homo sapiens	129-136
23386653-2	2013	In this study we measured whether GC-induced insulin resistance in humans is related to changes in muscle ceramide, GM3, and muscle mitochondrial function.	Ceramides	106-114	insulin	Homo sapiens	45-52
23455468-6	2013	Furthermore, after highlighting the role and mechanism of action of p53 in apoptosis, we review the association of ceramide and p53 with respect to apoptosis.	Ceramides	115-123	tumor protein p53	Homo sapiens	128-131
23455468-7	2013	Strikingly, the hypothesis for a direct interaction between ceramide and p53 is less favored.	Ceramides	60-68	tumor protein p53	Homo sapiens	73-76
23455468-8	2013	Recent data suggest that ceramide can act either upstream or downstream of p53 protein through posttranscriptional regulation or through many potential mediators, respectively.	Ceramides	25-33	tumor protein p53	Homo sapiens	75-78
23096701-5	2013	Here we adapted a targeted lipidomic approach using mass spectrometry and have determined that Ctip2(-/-) mice (germline deletion of the Ctip2 gene) display altered composition of major epidermal lipids, such as ceramides and sphingomyelins, compared with wild-type mice at different stages of skin development.	Ceramides	212-221	B cell leukemia/lymphoma 11B	Mus musculus	95-100
23319743-0	2013	Fatty acid synthase causes drug resistance by inhibiting TNF-alpha and ceramide production.	Ceramides	71-79	fatty acid synthase	Homo sapiens	0-19
23319743-6	2013	In this study, we show that FASN overexpression causes resistance to multiple anticancer drugs via inhibiting drug-induced ceramide production, caspase 8 activation, and apoptosis.	Ceramides	123-131	fatty acid synthase	Homo sapiens	28-32
23275342-0	2013	Fam57b (family with sequence similarity 57, member B), a novel peroxisome proliferator-activated receptor gamma target gene that regulates adipogenesis through ceramide synthesis.	Ceramides	160-168	TLC domain containing 3B	Mus musculus	0-6
23203344-0	2013	Ceramide PC102 inhibits melanin synthesis via proteasomal degradation of microphthalmia-associated transcription factor and tyrosinase.	Ceramides	0-8	melanocyte inducing transcription factor	Homo sapiens	73-119
23203344-0	2013	Ceramide PC102 inhibits melanin synthesis via proteasomal degradation of microphthalmia-associated transcription factor and tyrosinase.	Ceramides	0-8	tyrosinase	Homo sapiens	124-134
23312611-8	2013	In summary, this study shows that structural modification of the known ceramidase inhibitors B-13 and LCL-464 generates more potent ceramidase inhibitors that are active in intact cells and not only elevates the cellular ceramide levels, but also enhances cell death.	Ceramides	221-229	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	93-97
23283968-2	2013	We recently generated a ceramide synthase 2 (CerS2) null mouse that cannot synthesize very long acyl chain (C22-C24) ceramides.	Ceramides	117-126	ceramide synthase 2	Mus musculus	24-43
23283968-2	2013	We recently generated a ceramide synthase 2 (CerS2) null mouse that cannot synthesize very long acyl chain (C22-C24) ceramides.	Ceramides	117-126	ceramide synthase 2	Mus musculus	45-50
23275342-0	2013	Fam57b (family with sequence similarity 57, member B), a novel peroxisome proliferator-activated receptor gamma target gene that regulates adipogenesis through ceramide synthesis.	Ceramides	160-168	peroxisome proliferator activated receptor gamma	Mus musculus	63-111
23275342-7	2013	Analysis of the ceramide content by lipid assay found that ceramides were in fact augmented in FAM57B-overexpressing ST2 cells.	Ceramides	16-24	TLC domain containing 3B	Mus musculus	95-101
23275342-7	2013	Analysis of the ceramide content by lipid assay found that ceramides were in fact augmented in FAM57B-overexpressing ST2 cells.	Ceramides	59-68	TLC domain containing 3B	Mus musculus	95-101
23275342-9	2013	Therefore, the aforementioned results of FAM57B overexpression and siRNA experiments are reconciled by ceramide synthesis.	Ceramides	103-111	TLC domain containing 3B	Mus musculus	41-47
23275342-11	2013	In addition, our results suggest that PPARgamma activation contributes to the regulation of ceramide metabolism during adipogenesis via FAM57B.	Ceramides	92-100	peroxisome proliferator activated receptor gamma	Mus musculus	38-47
23275342-11	2013	In addition, our results suggest that PPARgamma activation contributes to the regulation of ceramide metabolism during adipogenesis via FAM57B.	Ceramides	92-100	TLC domain containing 3B	Mus musculus	136-142
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.	Ceramides	99-107	glucosylceramidase beta 2	Homo sapiens	0-4
22989773-0	2013	C(16)-Ceramide-induced F-actin regulation stimulates mouse embryonic stem cell migration: involvement of N-WASP/Cdc42/Arp2/3 complex and cofilin-1/alpha-actinin.	Ceramides	6-14	WASP like actin nucleation promoting factor	Mus musculus	105-111
23085009-8	2013	Inhibition of INS-1 apoptosis by over-expressed SphK1 was independent of sphingosine-1-phosphate receptors but was associated with a decreased formation of pro-apoptotic ceramides induced by gluco-lipotoxicity.	Ceramides	170-179	insulin 1	Rattus norvegicus	14-19
23085009-8	2013	Inhibition of INS-1 apoptosis by over-expressed SphK1 was independent of sphingosine-1-phosphate receptors but was associated with a decreased formation of pro-apoptotic ceramides induced by gluco-lipotoxicity.	Ceramides	170-179	sphingosine kinase 1	Rattus norvegicus	48-53
23085009-9	2013	Moreover, over-expression of SphK1 counteracted the defect in the ER-to-Golgi transport of proteins that contribute to the ceramide-dependent ER stress observed during gluco-lipotoxicity.	Ceramides	123-131	sphingosine kinase 1	Rattus norvegicus	29-34
23085009-10	2013	In conclusion, our results suggest that activation of palmitate-induced SphK1-mediated sphingoid base-1-phosphate formation in the ER of beta cells plays a protective role against palmitate-induced ceramide-dependent apoptotic beta cell death.	Ceramides	198-206	sphingosine kinase 1	Rattus norvegicus	72-77
22989773-0	2013	C(16)-Ceramide-induced F-actin regulation stimulates mouse embryonic stem cell migration: involvement of N-WASP/Cdc42/Arp2/3 complex and cofilin-1/alpha-actinin.	Ceramides	6-14	ARP2 actin-related protein 2	Mus musculus	118-122
22989773-0	2013	C(16)-Ceramide-induced F-actin regulation stimulates mouse embryonic stem cell migration: involvement of N-WASP/Cdc42/Arp2/3 complex and cofilin-1/alpha-actinin.	Ceramides	6-14	cell division cycle 42	Mus musculus	112-117
22989773-0	2013	C(16)-Ceramide-induced F-actin regulation stimulates mouse embryonic stem cell migration: involvement of N-WASP/Cdc42/Arp2/3 complex and cofilin-1/alpha-actinin.	Ceramides	6-14	cofilin 1, non-muscle	Mus musculus	137-146
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.	Ceramides	144-152	glucosylceramidase beta 2	Homo sapiens	75-79
23139352-2	2013	Here, we explored the role of circulating ceramide on the pathogenesis of insulin resistance.	Ceramides	42-50	insulin	Homo sapiens	74-81
23139352-3	2013	Ceramide transported in LDL is elevated in the plasma of obese patients with type 2 diabetes and correlated with insulin resistance but not with the degree of obesity.	Ceramides	0-8	insulin	Homo sapiens	113-120
23139352-4	2013	Treating cultured myotubes with LDL containing ceramide promoted ceramide accrual in cells and was accompanied by reduced insulin-stimulated glucose uptake, Akt phosphorylation, and GLUT4 translocation compared with LDL deficient in ceramide.	Ceramides	47-55	insulin	Homo sapiens	122-129
23139352-4	2013	Treating cultured myotubes with LDL containing ceramide promoted ceramide accrual in cells and was accompanied by reduced insulin-stimulated glucose uptake, Akt phosphorylation, and GLUT4 translocation compared with LDL deficient in ceramide.	Ceramides	47-55	solute carrier family 2 member 4	Homo sapiens	182-187
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.	Ceramides	144-152	glucosylceramidase beta 2	Homo sapiens	75-79
23250757-1	2013	GBA1 and GBA2 are both beta-glucosidases, which cleave glucosylceramide (GlcCer) to glucose and ceramide.	Ceramides	63-71	glucosylceramidase beta	Homo sapiens	0-4
23250746-3	2013	Ceramides are sphingolipids that modulate a variety of cellular responses including cell death, autophagy, insulin signaling, and inflammation.	Ceramides	0-9	insulin	Homo sapiens	107-114
23362869-0	2013	Ceramides stimulate caspase-14 expression in human keratinocytes.	Ceramides	0-9	caspase 14	Homo sapiens	20-30
23362869-4	2013	Here we demonstrate that ceramides (C(2) -Cer and C(6) -Cer), but not other sphingolipids (C(8) -glucosylceramides, sphinganine, sphingosine-1-phosphate or ceramide-1-phosphate), increase caspase-14 expression (mRNA and protein) in cultured human keratinocytes in a dose- and time-dependent manner.	Ceramides	25-34	caspase 14	Homo sapiens	188-198
23362869-5	2013	Inhibitors of glucosylceramide synthase and ceramidase increase endogenous ceramide levels and also increase caspase-14 expression, indicating an important regulatory role for ceramides and suggesting that the conversion of ceramides to other metabolites is not required.	Ceramides	22-30	caspase 14	Homo sapiens	109-119
23362869-5	2013	Inhibitors of glucosylceramide synthase and ceramidase increase endogenous ceramide levels and also increase caspase-14 expression, indicating an important regulatory role for ceramides and suggesting that the conversion of ceramides to other metabolites is not required.	Ceramides	176-185	UDP-glucose ceramide glucosyltransferase	Homo sapiens	14-39
23362869-5	2013	Inhibitors of glucosylceramide synthase and ceramidase increase endogenous ceramide levels and also increase caspase-14 expression, indicating an important regulatory role for ceramides and suggesting that the conversion of ceramides to other metabolites is not required.	Ceramides	176-185	caspase 14	Homo sapiens	109-119
23362869-5	2013	Inhibitors of glucosylceramide synthase and ceramidase increase endogenous ceramide levels and also increase caspase-14 expression, indicating an important regulatory role for ceramides and suggesting that the conversion of ceramides to other metabolites is not required.	Ceramides	224-233	UDP-glucose ceramide glucosyltransferase	Homo sapiens	14-39
23362869-5	2013	Inhibitors of glucosylceramide synthase and ceramidase increase endogenous ceramide levels and also increase caspase-14 expression, indicating an important regulatory role for ceramides and suggesting that the conversion of ceramides to other metabolites is not required.	Ceramides	224-233	caspase 14	Homo sapiens	109-119
23362869-6	2013	The increase in caspase-14 expression induced by ceramides is first seen at 16 h and requires new protein synthesis, suggesting that the ceramide-induced increase is likely an indirect effect.	Ceramides	49-58	caspase 14	Homo sapiens	16-26
23362869-6	2013	The increase in caspase-14 expression induced by ceramides is first seen at 16 h and requires new protein synthesis, suggesting that the ceramide-induced increase is likely an indirect effect.	Ceramides	49-57	caspase 14	Homo sapiens	16-26
23362869-7	2013	Furthermore, ceramides increase caspase-14 gene expression primarily by increasing transcription.	Ceramides	13-22	caspase 14	Homo sapiens	32-42
23362869-9	2013	These studies show that ceramides, an important structural lipid, stimulate caspase-14 expression providing a mechanism for coordinately regulating the formation of lipid lamellar membranes with the formation of corneocytes.	Ceramides	24-33	caspase 14	Homo sapiens	76-86
23250746-4	2013	In this study we investigated the intersection between TLR4-mediated inflammatory signaling and saturated fatty acids with regard to ceramide generation.	Ceramides	133-141	toll like receptor 4	Homo sapiens	55-59
23250746-9	2013	This ceramide response augmented IL-1beta and TNFalpha release, a process that may contribute to the enhanced inflammatory response in metabolic diseases characterized by dyslipidemia.	Ceramides	5-13	interleukin 1 beta	Homo sapiens	33-41
23250746-9	2013	This ceramide response augmented IL-1beta and TNFalpha release, a process that may contribute to the enhanced inflammatory response in metabolic diseases characterized by dyslipidemia.	Ceramides	5-13	tumor necrosis factor	Homo sapiens	46-54
23250757-1	2013	GBA1 and GBA2 are both beta-glucosidases, which cleave glucosylceramide (GlcCer) to glucose and ceramide.	Ceramides	63-71	glucosylceramidase beta 2	Homo sapiens	9-13
23290776-5	2013	For example, different fatty-acid chain lengths of ceramide, such as C(16)-ceramide that can be generated by ceramide synthase 6 (CerS6), have been implicated in cancer cell proliferation, whereas CerS1-generated C(18)-ceramide mediates cell death.	Ceramides	51-59	ceramide synthase 6	Homo sapiens	109-128
23298833-1	2013	Acid sphingomyelinase (ASM) regulates the homeostasis of sphingolipids, including ceramides and sphingosine-1-phosphate (S1P).	Ceramides	82-91	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
23298833-1	2013	Acid sphingomyelinase (ASM) regulates the homeostasis of sphingolipids, including ceramides and sphingosine-1-phosphate (S1P).	Ceramides	82-91	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
22727944-4	2013	This study demonstrates that serine palmitoyltransferase (SPT) in the astrocytes increases ceramide levels, which enhances the release of cytokines that mediate the activation of neural and acidic sphingomyelinase (SMase) in the neurons, to propagate the deleterious effects of PA (i.e., BACE1 upregulation).	Ceramides	91-99	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	29-56
22727944-4	2013	This study demonstrates that serine palmitoyltransferase (SPT) in the astrocytes increases ceramide levels, which enhances the release of cytokines that mediate the activation of neural and acidic sphingomyelinase (SMase) in the neurons, to propagate the deleterious effects of PA (i.e., BACE1 upregulation).	Ceramides	91-99	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	58-61
23290780-1	2013	Sphingosine kinase 1 (SK1) is a lipid enzyme with oncogenic properties that converts the proapoptotic lipids ceramide and sphingosine into the antiapoptotic lipid sphingosine-1-phosphate and activates the signal transduction pathways that lead to cell proliferation, migration, the activation of the inflammatory response, and the impairment of apoptosis.	Ceramides	109-117	sphingosine kinase 1	Homo sapiens	0-20
23290780-1	2013	Sphingosine kinase 1 (SK1) is a lipid enzyme with oncogenic properties that converts the proapoptotic lipids ceramide and sphingosine into the antiapoptotic lipid sphingosine-1-phosphate and activates the signal transduction pathways that lead to cell proliferation, migration, the activation of the inflammatory response, and the impairment of apoptosis.	Ceramides	109-117	sphingosine kinase 1	Homo sapiens	22-25
23230267-2	2013	ER stress also increases production of the proapoptotic lipid ceramide and its antiapoptotic metabolite, sphingosine-1-phosphate (S1P).	Ceramides	62-70	sphingosine-1-phosphate receptor 1	Mus musculus	130-133
23230267-4	2013	Cellular ceramide and S1P levels rose in parallel with CAMP levels following addition of either exogenous cell-permeating ceramide (C2Cer), which increases S1P production, or thapsigargin (an ER stressor), applied to cultured human skin keratinocytes or topically to mouse skin.	Ceramides	122-130	cathelicidin antimicrobial peptide	Homo sapiens	55-59
23230267-4	2013	Cellular ceramide and S1P levels rose in parallel with CAMP levels following addition of either exogenous cell-permeating ceramide (C2Cer), which increases S1P production, or thapsigargin (an ER stressor), applied to cultured human skin keratinocytes or topically to mouse skin.	Ceramides	122-130	sphingosine-1-phosphate receptor 1	Mus musculus	156-159
23290776-5	2013	For example, different fatty-acid chain lengths of ceramide, such as C(16)-ceramide that can be generated by ceramide synthase 6 (CerS6), have been implicated in cancer cell proliferation, whereas CerS1-generated C(18)-ceramide mediates cell death.	Ceramides	51-59	ceramide synthase 6	Homo sapiens	130-135
23290776-5	2013	For example, different fatty-acid chain lengths of ceramide, such as C(16)-ceramide that can be generated by ceramide synthase 6 (CerS6), have been implicated in cancer cell proliferation, whereas CerS1-generated C(18)-ceramide mediates cell death.	Ceramides	51-59	ceramide synthase 1	Homo sapiens	197-202
23290776-6	2013	The dichotomy of ceramides" function in cancer cells makes some of the metabolic enzymes of ceramide synthesis potential drug targets (such as Cers6) to prevent cancer growth in breast and head and neck cancers.	Ceramides	17-26	ceramide synthase 6	Homo sapiens	143-148
23290776-6	2013	The dichotomy of ceramides" function in cancer cells makes some of the metabolic enzymes of ceramide synthesis potential drug targets (such as Cers6) to prevent cancer growth in breast and head and neck cancers.	Ceramides	17-25	ceramide synthase 6	Homo sapiens	143-148
23290777-0	2013	Ceramide glycosylation catalyzed by glucosylceramide synthase and cancer drug resistance.	Ceramides	0-8	UDP-glucose ceramide glucosyltransferase	Homo sapiens	36-61
23290777-1	2013	Glucosylceramide synthase (GCS), converting ceramide to glucosylceramide, catalyzes the first reaction of ceramide glycosylation in sphingolipid metabolism.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
23290777-1	2013	Glucosylceramide synthase (GCS), converting ceramide to glucosylceramide, catalyzes the first reaction of ceramide glycosylation in sphingolipid metabolism.	Ceramides	44-52	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.	Ceramides	44-52	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
23290777-2	2013	This glycosylation by GCS is a critical step regulating the modulation of cellular activities by controlling ceramide and glycosphingolipids (GSLs).	Ceramides	109-117	UDP-glucose ceramide glucosyltransferase	Homo sapiens	22-25
23290777-6	2013	As ceramide glycosylation by GCS is a rate-limiting step in GSL synthesis, inhibition of GCS sensitizes cancer cells to anticancer drugs and eradicates cancer stem cells.	Ceramides	3-11	UDP-glucose ceramide glucosyltransferase	Homo sapiens	29-32
23290777-6	2013	As ceramide glycosylation by GCS is a rate-limiting step in GSL synthesis, inhibition of GCS sensitizes cancer cells to anticancer drugs and eradicates cancer stem cells.	Ceramides	3-11	UDP-glucose ceramide glucosyltransferase	Homo sapiens	89-92
22997409-5	2013	Liquid chromatography coupled with tandem mass spectrometry demonstrated altered ceramide profiles with higher levels of C14 and C18, and reduced C16 species in ethanol-exposed livers.	Ceramides	81-89	Bardet-Biedl syndrome 9	Homo sapiens	129-132
23290777-7	2013	Mechanistic studies indicate that uncoupling ceramide glycosylation can modulate gene expression, decreasing MDR1 through the cSrc/beta-catenin pathway and restoring p53 expression via RNA splicing.	Ceramides	45-53	ATP binding cassette subfamily B member 1	Homo sapiens	109-113
23290777-7	2013	Mechanistic studies indicate that uncoupling ceramide glycosylation can modulate gene expression, decreasing MDR1 through the cSrc/beta-catenin pathway and restoring p53 expression via RNA splicing.	Ceramides	45-53	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	126-130
23290777-7	2013	Mechanistic studies indicate that uncoupling ceramide glycosylation can modulate gene expression, decreasing MDR1 through the cSrc/beta-catenin pathway and restoring p53 expression via RNA splicing.	Ceramides	45-53	catenin beta 1	Homo sapiens	131-143
23290777-7	2013	Mechanistic studies indicate that uncoupling ceramide glycosylation can modulate gene expression, decreasing MDR1 through the cSrc/beta-catenin pathway and restoring p53 expression via RNA splicing.	Ceramides	45-53	tumor protein p53	Homo sapiens	166-169
23290778-1	2013	Acid sphingomyelinase (ASM) is a lipid hydrolase that cleaves the sphingolipid, sphingomyelin, into ceramide.	Ceramides	100-108	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
23290778-1	2013	Acid sphingomyelinase (ASM) is a lipid hydrolase that cleaves the sphingolipid, sphingomyelin, into ceramide.	Ceramides	100-108	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
24342307-1	2013	BACKGROUND: Glucosylceramide synthase (GCS) can reduce ceramide levels and help cells escape ceramide-induced apoptosis, thus leading to multidrug resistance (MDR).	Ceramides	20-28	UDP-glucose ceramide glucosyltransferase	Homo sapiens	39-42
23024063-0	2013	RTP801 is required for ceramide-induced cell-specific death in the murine lung.	Ceramides	23-31	DNA-damage-inducible transcript 4	Mus musculus	0-6
23024063-6	2013	RTP801 overexpression up-regulated lung ceramide levels 2.6-fold.	Ceramides	40-48	DNA-damage-inducible transcript 4	Mus musculus	0-6
23024063-7	2013	In turn, instillation of lung ceramides doubled the lung content of RTP801.	Ceramides	30-39	DNA-damage-inducible transcript 4	Mus musculus	68-74
23024063-9	2013	Interestingly, mice lacking rtp801 were protected against ceramide-induced apoptosis of epithelial type II cells, but not type I or endothelial cells.	Ceramides	58-66	DNA-damage-inducible transcript 4	Mus musculus	28-34
23024063-10	2013	Furthermore, rtp801-null mice were protected from ceramide-induced alveolar enlargement, and exhibited improved static lung compliance compared with wild-type mice.	Ceramides	50-58	DNA-damage-inducible transcript 4	Mus musculus	13-19
23073611-6	2013	GlcCer, generated by glucosylceramide synthase (GCS) that transfers the glucose from UDP-glucose to ceramide, is an important glycosphingolipid metabolic intermediate.	Ceramides	29-37	UDP-glucose ceramide glucosyltransferase	Homo sapiens	48-51
24335345-7	2013	The annexin-V-binding following geldanamycin treatment was not significantly modified by removal of extracellular Ca(2+) but was paralleled by significantly increased ceramide formation (50 microM).	Ceramides	167-175	annexin A5	Homo sapiens	4-13
23166225-2	2013	Alterations in the "sphingolipid rheostat"-the balance between the proapoptotic molecule ceramide and the mitogenic factor sphingosine-1-phosphate (S1P)-due to sphingosine kinase 1 (SphK1) overactivation have been involved in resistance to anticancer-targeted agents.	Ceramides	89-97	sphingosine kinase 1	Homo sapiens	160-180
23811568-0	2013	Increase in secretory sphingomyelinase activity and specific ceramides in the aorta of apolipoprotein E knockout mice during aging.	Ceramides	61-70	apolipoprotein E	Mus musculus	87-103
23811568-5	2013	Although the total plasma ceramide level was higher in apoE(-/-) than that in WT at all ages, it decreased with increasing age.	Ceramides	26-34	apolipoprotein E	Mus musculus	55-59
23811568-7	2013	When apoE(-/-) developed atherosclerosis at 15 w of age, C18:0, C22:0, and C24:0 ceramide levels in the apoE(-/-) aorta significantly increased.	Ceramides	81-89	apolipoprotein E	Mus musculus	5-9
23811568-7	2013	When apoE(-/-) developed atherosclerosis at 15 w of age, C18:0, C22:0, and C24:0 ceramide levels in the apoE(-/-) aorta significantly increased.	Ceramides	81-89	apolipoprotein E	Mus musculus	104-108
23073611-7	2013	GCS regulates the balance between apoptotic ceramide and antiapoptotic GlcCer.	Ceramides	44-52	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
23430142-6	2013	Serine palmitoyltransferase (SPT) is the rate-limiting enzyme in de novo ceramide synthesis, and the mRNA of its long-chain base subunit 1 (SPTLC1) was evaluated by quantitative reverse-transcription polymerase chain reaction.	Ceramides	73-81	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	140-146
23180565-2	2013	We show here that the tumour suppressor ceramide binds I2PP2A/SET selectively in the nucleus and including its K209 and Y122 residues as determined by molecular modelling/simulations and site-directed mutagenesis.	Ceramides	40-48	SET nuclear proto-oncogene	Homo sapiens	55-61
23180565-3	2013	Because I2PP2A/SET was found overexpressed, whereas ceramide was downregulated in lung tumours, a sphingolipid analogue drug, FTY720, was identified to mimick ceramide for binding and targeting I2PP2A/SET, leading to PP2A reactivation, lung cancer cell death, and tumour suppression in vivo.	Ceramides	159-167	SET nuclear proto-oncogene	Homo sapiens	8-14
23180565-3	2013	Because I2PP2A/SET was found overexpressed, whereas ceramide was downregulated in lung tumours, a sphingolipid analogue drug, FTY720, was identified to mimick ceramide for binding and targeting I2PP2A/SET, leading to PP2A reactivation, lung cancer cell death, and tumour suppression in vivo.	Ceramides	159-167	SET nuclear proto-oncogene	Homo sapiens	194-200
23180565-3	2013	Because I2PP2A/SET was found overexpressed, whereas ceramide was downregulated in lung tumours, a sphingolipid analogue drug, FTY720, was identified to mimick ceramide for binding and targeting I2PP2A/SET, leading to PP2A reactivation, lung cancer cell death, and tumour suppression in vivo.	Ceramides	159-167	protein phosphatase 2 phosphatase activator	Homo sapiens	10-14
24342307-1	2013	BACKGROUND: Glucosylceramide synthase (GCS) can reduce ceramide levels and help cells escape ceramide-induced apoptosis, thus leading to multidrug resistance (MDR).	Ceramides	55-63	UDP-glucose ceramide glucosyltransferase	Homo sapiens	12-37
24342307-1	2013	BACKGROUND: Glucosylceramide synthase (GCS) can reduce ceramide levels and help cells escape ceramide-induced apoptosis, thus leading to multidrug resistance (MDR).	Ceramides	55-63	UDP-glucose ceramide glucosyltransferase	Homo sapiens	39-42
23579450-1	2013	The enzyme acid sphingomyelinase catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	78-86	sphingomyelin phosphodiesterase 1	Homo sapiens	11-32
24489592-10	2013	Our results collectively demonstrate that andrographolide-reduced cell viability can be attributed to apoptosis in VSMCs, and this apoptosis-inducing activity was associated with the ceramide-p47phox-ROS signaling cascade.	Ceramides	183-191	neutrophil cytosolic factor 1	Rattus norvegicus	192-199
23563650-1	2013	Acid sphingomyelinase (ASMase) is a key initiator of sphingomyelin/ceramide signal transduction activated by many stress stimuli.	Ceramides	67-75	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
23563650-1	2013	Acid sphingomyelinase (ASMase) is a key initiator of sphingomyelin/ceramide signal transduction activated by many stress stimuli.	Ceramides	67-75	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
23563650-2	2013	Over the past two decades, much progress has been made in defining the clinical relevance of sphingomyelin/ceramide signaling in numerous diseases using ASMase knockout mice.	Ceramides	107-115	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	153-159
23563653-8	2013	One centers on the activation of neutral sphingomyelinase2 (nSMase2), an enzyme that hydrolyzes sphingomyelin to ceramide.	Ceramides	113-121	sphingomyelin phosphodiesterase 3	Homo sapiens	33-58
23563653-8	2013	One centers on the activation of neutral sphingomyelinase2 (nSMase2), an enzyme that hydrolyzes sphingomyelin to ceramide.	Ceramides	113-121	sphingomyelin phosphodiesterase 3	Homo sapiens	60-67
23563653-12	2013	demonstrated that during CS exposure, EGFR is favorably co-localized in ceramide-enriched regions of the plasma membrane, proposing that nSMase2/ceramide plays a role in the aberrant EGFR activation, leading to augmented tumorigenic signaling.	Ceramides	72-80	epidermal growth factor receptor	Homo sapiens	38-42
24489592-0	2013	Andrographolide, a Novel NF- kappa B Inhibitor, Induces Vascular Smooth Muscle Cell Apoptosis via a Ceramide-p47phox-ROS Signaling Cascade.	Ceramides	100-108	neutrophil cytosolic factor 1	Rattus norvegicus	109-116
23579452-4	2013	Bcl-2 family proteins control these channels in a manner expected from their physiological function: anti-apoptotic proteins destabilize the channels whereas pro-apoptotic proteins act synergistically with ceramide to increase membrane permeability.	Ceramides	206-214	BCL2 apoptosis regulator	Homo sapiens	0-5
23563653-12	2013	demonstrated that during CS exposure, EGFR is favorably co-localized in ceramide-enriched regions of the plasma membrane, proposing that nSMase2/ceramide plays a role in the aberrant EGFR activation, leading to augmented tumorigenic signaling.	Ceramides	72-80	sphingomyelin phosphodiesterase 3	Homo sapiens	137-144
23563653-12	2013	demonstrated that during CS exposure, EGFR is favorably co-localized in ceramide-enriched regions of the plasma membrane, proposing that nSMase2/ceramide plays a role in the aberrant EGFR activation, leading to augmented tumorigenic signaling.	Ceramides	145-153	epidermal growth factor receptor	Homo sapiens	38-42
23579452-6	2013	These analogs have also been useful in identifying the sites of interaction between ceramide and both Bax and Bcl-xL.	Ceramides	84-92	BCL2 associated X, apoptosis regulator	Homo sapiens	102-105
23563653-12	2013	demonstrated that during CS exposure, EGFR is favorably co-localized in ceramide-enriched regions of the plasma membrane, proposing that nSMase2/ceramide plays a role in the aberrant EGFR activation, leading to augmented tumorigenic signaling.	Ceramides	145-153	epidermal growth factor receptor	Homo sapiens	183-187
23563653-14	2013	Furthermore, structural anomalies of the CS-activated EGFR appear to be supported by the excess ceramide produced by the CS-activated nSMase2 in the plasma membrane of lung epithelial cells.We present in this chapter the progression of the sphingolipid field in lung cancer using ceramide as an example.	Ceramides	96-104	epidermal growth factor receptor	Homo sapiens	54-58
23579452-6	2013	These analogs have also been useful in identifying the sites of interaction between ceramide and both Bax and Bcl-xL.	Ceramides	84-92	BCL2 like 1	Homo sapiens	110-116
23563653-14	2013	Furthermore, structural anomalies of the CS-activated EGFR appear to be supported by the excess ceramide produced by the CS-activated nSMase2 in the plasma membrane of lung epithelial cells.We present in this chapter the progression of the sphingolipid field in lung cancer using ceramide as an example.	Ceramides	96-104	sphingomyelin phosphodiesterase 3	Homo sapiens	134-141
23563653-14	2013	Furthermore, structural anomalies of the CS-activated EGFR appear to be supported by the excess ceramide produced by the CS-activated nSMase2 in the plasma membrane of lung epithelial cells.We present in this chapter the progression of the sphingolipid field in lung cancer using ceramide as an example.	Ceramides	280-288	epidermal growth factor receptor	Homo sapiens	54-58
23579454-1	2013	In mammalian cells, cermide-1-phosphate (C1P) is produced via the ATP-dependent mechanism of converting ceramide to C1P by the enzyme, ceramide kinase (CERK).	Ceramides	104-112	ceramide kinase	Homo sapiens	135-150
23563653-14	2013	Furthermore, structural anomalies of the CS-activated EGFR appear to be supported by the excess ceramide produced by the CS-activated nSMase2 in the plasma membrane of lung epithelial cells.We present in this chapter the progression of the sphingolipid field in lung cancer using ceramide as an example.	Ceramides	280-288	sphingomyelin phosphodiesterase 3	Homo sapiens	134-141
23579454-1	2013	In mammalian cells, cermide-1-phosphate (C1P) is produced via the ATP-dependent mechanism of converting ceramide to C1P by the enzyme, ceramide kinase (CERK).	Ceramides	104-112	ceramide kinase	Homo sapiens	152-156
23579455-4	2013	The acid sphingomyelinase converts sphingomyelin to ceramide, a compound often involved in cell stress.	Ceramides	52-60	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
23230024-2	2013	Through the resultant increase in ceramides which interact with mTOR and Beclin1 (Atg6), this drug is also known to induce macroautophagy in mammalian cells.	Ceramides	34-43	mechanistic target of rapamycin kinase	Homo sapiens	64-68
23411472-9	2013	Our findings suggest that (1) iPLA2beta impacts upstream (UPR) and downstream (ceramide generation and mitochondrial) pathways in beta-cells and (2) both over- or under-expression of iPLA2beta is deleterious to the beta-cells.	Ceramides	79-87	phospholipase A2 group VI	Homo sapiens	30-39
22988930-3	2013	Herein, we demonstrate that treatment with a PPAR-delta agonist enhances insulin signaling and reduces the severities of ER stress and ceramide accumulation in an experimental model of ethanol-induced steatohepatitis.	Ceramides	135-143	peroxisome proliferator activated receptor alpha	Rattus norvegicus	45-49
23230024-2	2013	Through the resultant increase in ceramides which interact with mTOR and Beclin1 (Atg6), this drug is also known to induce macroautophagy in mammalian cells.	Ceramides	34-43	beclin 1	Homo sapiens	73-80
23230024-2	2013	Through the resultant increase in ceramides which interact with mTOR and Beclin1 (Atg6), this drug is also known to induce macroautophagy in mammalian cells.	Ceramides	34-43	beclin 1	Homo sapiens	82-86
23114219-9	2013	Postsynaptic blockade of ceramide production with fumonisin, a ceramide synthase inhibitor, blocked the effects of BDNF and d-erythro-sphingosine, implicating ceramide or ceramide phosphate as the active signal.	Ceramides	25-33	brain-derived neurotrophic factor	Rattus norvegicus	115-119
23108456-3	2013	We recently demonstrated that ceramide production via hydrolysis of membrane sphingomyelin by acid sphingomyelinase (ASM) results in membrane raft (MR) clustering and the formation of important redox signaling platforms, which play a crucial role in amplifying redox signaling in endothelial cells leading to endothelial dysfunction.	Ceramides	30-38	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	94-115
23108456-3	2013	We recently demonstrated that ceramide production via hydrolysis of membrane sphingomyelin by acid sphingomyelinase (ASM) results in membrane raft (MR) clustering and the formation of important redox signaling platforms, which play a crucial role in amplifying redox signaling in endothelial cells leading to endothelial dysfunction.	Ceramides	30-38	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	117-120
23108456-6	2013	Furthermore, TRAIL triggered ASM translocation, ceramide production, and NADPH oxidase aggregation in MR clusters in Smpd1 ( +/+ ) CAECs, whereas these observations were not found in Smpd1 (-/-) CAECs.	Ceramides	48-56	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	13-18
22832496-4	2013	Skin lipid analysis demonstrated that the severity of barrier failure is related to the loss of covalently bound ceramides in both 12R-LOX- and eLOX-3-null mice, confirming a proposed functional linkage of the LOX pathway to ceramide processing and formation of the corneocyte lipid envelope.	Ceramides	113-122	arachidonate 12-lipoxygenase, 12R type	Mus musculus	131-138
22832496-4	2013	Skin lipid analysis demonstrated that the severity of barrier failure is related to the loss of covalently bound ceramides in both 12R-LOX- and eLOX-3-null mice, confirming a proposed functional linkage of the LOX pathway to ceramide processing and formation of the corneocyte lipid envelope.	Ceramides	113-121	arachidonate 12-lipoxygenase, 12R type	Mus musculus	131-138
23114219-9	2013	Postsynaptic blockade of ceramide production with fumonisin, a ceramide synthase inhibitor, blocked the effects of BDNF and d-erythro-sphingosine, implicating ceramide or ceramide phosphate as the active signal.	Ceramides	63-71	brain-derived neurotrophic factor	Rattus norvegicus	115-119
24082981-0	2013	A novel Sit4 phosphatase complex is involved in the response to ceramide stress in yeast.	Ceramides	64-72	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	8-12
23612696-1	2013	Accumulation of ceramides within tissues induces insulin resistance.	Ceramides	16-25	insulin	Homo sapiens	49-56
23612696-2	2013	Moreover, adiponectin exerts its beneficial metabolic effects at least partially through ceramide catabolism.	Ceramides	89-97	adiponectin, C1Q and collagen domain containing	Homo sapiens	10-21
23612696-3	2013	We hypothesized that specific plasma ceramide subspecies are elevated in obese children and adolescents with type 2 diabetes (T2D), and that they inversely correlate with adiponectin and measures of insulin sensitivity.	Ceramides	37-45	adiponectin, C1Q and collagen domain containing	Homo sapiens	171-182
23612696-3	2013	We hypothesized that specific plasma ceramide subspecies are elevated in obese children and adolescents with type 2 diabetes (T2D), and that they inversely correlate with adiponectin and measures of insulin sensitivity.	Ceramides	37-45	insulin	Homo sapiens	199-206
23612696-8	2013	C22:0, C20:0 and C18:0 ceramide correlated with decreased adiponectin concentrations, increased HOMA-IR, BMI Z-score, triglyceride and fasting blood glucose concentrations (p<0.05).	Ceramides	23-31	adiponectin, C1Q and collagen domain containing	Homo sapiens	58-69
23246342-0	2013	Ceramide and its transport protein (CERT) contribute to deterioration of mitochondrial structure and function in aging oocytes.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	36-40
23246342-8	2013	In addition, ceramide localization was altered in old oocytes possibly due to downregulation of the ceramide transport protein (CERT).	Ceramides	13-21	ceramide transporter 1	Homo sapiens	100-126
23246342-8	2013	In addition, ceramide localization was altered in old oocytes possibly due to downregulation of the ceramide transport protein (CERT).	Ceramides	13-21	ceramide transporter 1	Homo sapiens	128-132
23246342-9	2013	However, knockdown of CERT alone was not sufficient to increase young oocyte"s susceptibility to death, because the sequential manipulation of ceramide levels (its chronic decrease, followed by downregulation of CERT, and finally a ceramide spike) were all necessary to replicate the aging phenotype.	Ceramides	143-151	ceramide transporter 1	Homo sapiens	22-26
23246342-9	2013	However, knockdown of CERT alone was not sufficient to increase young oocyte"s susceptibility to death, because the sequential manipulation of ceramide levels (its chronic decrease, followed by downregulation of CERT, and finally a ceramide spike) were all necessary to replicate the aging phenotype.	Ceramides	232-240	ceramide transporter 1	Homo sapiens	22-26
23457308-0	2013	Ceramide mediates inhibition of the Akt/eNOS pathway by high levels of glucose in human vascular endothelial cells.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	36-39
23457308-0	2013	Ceramide mediates inhibition of the Akt/eNOS pathway by high levels of glucose in human vascular endothelial cells.	Ceramides	0-8	nitric oxide synthase 3	Homo sapiens	40-44
23457308-1	2013	OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs).	Ceramides	30-38	AKT serine/threonine kinase 1	Homo sapiens	102-105
23457308-1	2013	OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs).	Ceramides	30-38	nitric oxide synthase 3	Homo sapiens	106-139
23457308-1	2013	OBJECTIVE: To investigate how ceramide mediates the effects of high-glucose-induced inhibition of the Akt/endothelial nitric oxide synthase (eNOS) signalling pathway in human vascular endothelial cells (HUVECs).	Ceramides	30-38	nitric oxide synthase 3	Homo sapiens	141-145
23457308-7	2013	Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05).	Ceramides	19-27	AKT serine/threonine kinase 1	Homo sapiens	104-107
23457308-7	2013	Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05).	Ceramides	19-27	nitric oxide synthase 3	Homo sapiens	108-112
23457308-7	2013	Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05).	Ceramides	19-27	AKT serine/threonine kinase 1	Homo sapiens	247-250
23457308-7	2013	Preventing de novo ceramide synthesis attenuated the antagonistic effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05); conversely, inducing ceramide build-up augmented the inhibitory effects of high-glucose levels on the Akt/eNOS signalling pathway (p<0.05).	Ceramides	19-27	nitric oxide synthase 3	Homo sapiens	251-255
23457308-8	2013	CONCLUSION: Ceramide is both necessary and sufficient for mediating the inhibition of the Akt/eNOS signalling pathway by high-glucose levels in endothelial cells.	Ceramides	12-20	AKT serine/threonine kinase 1	Homo sapiens	90-93
23457308-8	2013	CONCLUSION: Ceramide is both necessary and sufficient for mediating the inhibition of the Akt/eNOS signalling pathway by high-glucose levels in endothelial cells.	Ceramides	12-20	nitric oxide synthase 3	Homo sapiens	94-98
23135722-3	2013	The role of gangliosides in rotavirus cell entry was studied by silencing the expression of two key enzymes involved in their biosynthesis--the UDP-glucose:ceramide glucosyltransferase (UGCG), which transfers a glucose molecule to ceramide to produce glucosylceramide GlcCer, and the lactosyl ceramide-alpha-2,3-sialyl transferase 5 (GM3-s), which adds the first SA to lactoceramide-producing ganglioside GM3.	Ceramides	156-164	UDP-glucose ceramide glucosyltransferase	Homo sapiens	186-190
24082981-7	2013	We also find that the Sit4p target Elongator is not involved in the ceramide response but that cells deficient in Kti12p-an accessory protein with an undefined regulatory role-have similar ceramide phenotypes to sit4Delta mutants.	Ceramides	189-197	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	22-27
24082981-7	2013	We also find that the Sit4p target Elongator is not involved in the ceramide response but that cells deficient in Kti12p-an accessory protein with an undefined regulatory role-have similar ceramide phenotypes to sit4Delta mutants.	Ceramides	189-197	Kti12p	Saccharomyces cerevisiae S288C	114-120
24082981-8	2013	Therefore, Kti12p may play a similar secondary role in the ceramide response.	Ceramides	59-67	Kti12p	Saccharomyces cerevisiae S288C	11-17
24082981-9	2013	This evidence points to a novel Sit4-dependent regulatory mechanism in response to ceramide stress.	Ceramides	83-91	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	32-36
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.	Ceramides	50-58	ADP-ribosylation factor 6	Mus musculus	0-4
23342165-0	2013	Inhibition of ceramide metabolism sensitizes human leukemia cells to inhibition of BCL2-like proteins.	Ceramides	14-22	BCL2 apoptosis regulator	Homo sapiens	83-87
23372762-7	2013	Importantly, increased ceramide level activates AMP-activated protein kinase (AMPK), which then directly phosphorylates Ulk1 and eventually leads to cell autophagy.	Ceramides	23-31	unc-51 like autophagy activating kinase 1	Homo sapiens	120-124
22264909-11	2013	The ApoB100/ApoA1 ratio correlated with a reduction in ceramide subspecies (C18:0, C18:1, C20:0, C24:0, and C24:1; P < .05).	Ceramides	55-63	apolipoprotein B	Homo sapiens	4-11
23326540-13	2013	These data support the concept that increased de novo ceramide production causes alveolar septal cell apoptosis and causes emphysema via suppressing HIF-1alpha.	Ceramides	54-62	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	149-159
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	interleukin 10	Homo sapiens	18-23
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	tumor necrosis factor	Homo sapiens	48-57
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	tumor necrosis factor	Homo sapiens	96-105
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	tumor necrosis factor	Homo sapiens	96-105
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	interleukin 10	Homo sapiens	122-127
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	intercellular adhesion molecule 1	Homo sapiens	187-193
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	tumor necrosis factor	Homo sapiens	96-105
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	tumor necrosis factor	Homo sapiens	96-105
23247124-12	2013	Pretreatment with IL-10 significantly decreased TNF-alpha-induced increased levels of ceramide (TNF-alpha vs. TNF-alpha + IL-10: 6,278 +- 1,013 vs. 1,440 +- 130 pmol/mg prot), as well as ICAM-1 expression and leukocyte adhesion (TNF-alpha vs. TNF-alpha + IL-10: 26.8 +- 2.6 vs. 6.7 +- 0.4 adherent leukocytes/field at 15 min).	Ceramides	86-94	interleukin 10	Homo sapiens	122-127
23247124-14	2013	The antioxidant effect of IL-10 is mediated through PI3-kinase and is paralleled by a decrease in ceramide synthesis induced by TNF-alpha.	Ceramides	98-106	interleukin 10	Homo sapiens	26-31
23247124-14	2013	The antioxidant effect of IL-10 is mediated through PI3-kinase and is paralleled by a decrease in ceramide synthesis induced by TNF-alpha.	Ceramides	98-106	tumor necrosis factor	Homo sapiens	128-137
23301156-1	2013	The expression of acid ceramidase (AC) - a cysteine amidase that hydrolyses the proapoptotic lipid ceramide - is abnormally high in several human tumors, which is suggestive of a role in chemoresistance.	Ceramides	99-107	N-acylsphingosine amidohydrolase 1	Homo sapiens	18-33
23301156-1	2013	The expression of acid ceramidase (AC) - a cysteine amidase that hydrolyses the proapoptotic lipid ceramide - is abnormally high in several human tumors, which is suggestive of a role in chemoresistance.	Ceramides	99-107	N-acylsphingosine amidohydrolase 1	Homo sapiens	35-37
22264909-11	2013	The ApoB100/ApoA1 ratio correlated with a reduction in ceramide subspecies (C18:0, C18:1, C20:0, C24:0, and C24:1; P < .05).	Ceramides	55-63	apolipoprotein A1	Homo sapiens	12-17
23254292-5	2012	In H460 NSCLC cells, caspase-8 cleavage was shown to be induced by cisplatin and is dependent on death receptor 4, death receptor 5, Fas-associated protein with death domain, acid sphingomyelinase and ceramide synthesis.	Ceramides	201-209	caspase 8	Homo sapiens	21-30
23256041-2	2012	Here we report that doxorubicin stimulates de novo synthesis of ceramide, which in turn activates CREB3L1, a transcription factor synthesized as a membrane-bound precursor.	Ceramides	64-72	cAMP responsive element binding protein 3 like 1	Homo sapiens	98-105
23105111-1	2012	The glycosphingolipid biosynthesis is initiated by monoglycosylation of ceramides, the action of which is catalyzed either by UDP-glucose:ceramide glucosyltransferase or by UDP-galactose:ceramide galactosyltransferase (CGalT).	Ceramides	72-81	UDP glycosyltransferase 8	Homo sapiens	173-217
23105097-0	2012	Interleukin 1beta regulation of FoxO1 protein content and localization: evidence for a novel ceramide-dependent mechanism.	Ceramides	93-101	interleukin 1 beta	Homo sapiens	0-17
23105097-0	2012	Interleukin 1beta regulation of FoxO1 protein content and localization: evidence for a novel ceramide-dependent mechanism.	Ceramides	93-101	forkhead box O1	Homo sapiens	32-37
23105111-1	2012	The glycosphingolipid biosynthesis is initiated by monoglycosylation of ceramides, the action of which is catalyzed either by UDP-glucose:ceramide glucosyltransferase or by UDP-galactose:ceramide galactosyltransferase (CGalT).	Ceramides	72-81	UDP glycosyltransferase 8	Homo sapiens	219-224
23074226-6	2012	Expression of myelin-associated glycoprotein was also decreased by about 60% in cerebellum and forebrain, suggesting that interaction and stabilization of oligodendrocytic myelin-associated glycoprotein by neuronal gangliosides is due to the C18 acyl membrane anchor of CerS1-derived precursor ceramides.	Ceramides	294-303	myelin-associated glycoprotein	Mus musculus	14-44
23228165-10	2012	Detailed analyses demonstrated a causal link of ceramides and subsequent EGFR activation coupled with a loss of the receptor in the lipid raft fractions.	Ceramides	48-57	epidermal growth factor receptor	Homo sapiens	73-77
23228165-12	2012	Moreover, the compatible solute ectoine was able to prevent ceramide-mediated EGFR phosphorylation and subsequent signalling as well as lung inflammation in vivo.	Ceramides	60-68	epidermal growth factor receptor	Homo sapiens	78-82
23074226-6	2012	Expression of myelin-associated glycoprotein was also decreased by about 60% in cerebellum and forebrain, suggesting that interaction and stabilization of oligodendrocytic myelin-associated glycoprotein by neuronal gangliosides is due to the C18 acyl membrane anchor of CerS1-derived precursor ceramides.	Ceramides	294-303	myelin-associated glycoprotein	Mus musculus	172-202
23074226-8	2012	Our results reveal an essential function of CerS1-derived ceramide in the regulation of cerebellar development and neurodevelopmentally regulated behavior.	Ceramides	58-66	ceramide synthase 1	Mus musculus	44-49
23065795-5	2012	Inhibition of de novo ceramide synthesis using chemical inhibitors blocked the ability of gammaT and gammaT3 to induce apoptosis as detected by Annexin V-FITC/PI assay and to activate JNK/CHOP/DR5 pro-apoptotic signaling thereby demonstrating the involvement of de novo ceramide synthesis in gammaT- and gammaT3-induced apoptosis.	Ceramides	22-30	annexin A5	Homo sapiens	144-153
23007467-1	2012	Fabry disease is a lysosomal storage disorder (LSD) caused by deficiency             of alpha-galactosidase A (alpha-gal A), resulting in deposition of globotriaosylceramide             (Gb3; also known as ceramide trihexoside) in the vascular endothelium of many             organs.	Ceramides	165-173	galactosidase, alpha	Mus musculus	88-109
23007467-1	2012	Fabry disease is a lysosomal storage disorder (LSD) caused by deficiency             of alpha-galactosidase A (alpha-gal A), resulting in deposition of globotriaosylceramide             (Gb3; also known as ceramide trihexoside) in the vascular endothelium of many             organs.	Ceramides	165-173	galactosidase, alpha	Mus musculus	111-122
23054552-2	2012	Intramuscular lipid accumulation of ceramides, diacylglycerols, and long chain acyl-CoA is responsible for the induction of insulin resistance.	Ceramides	36-45	insulin	Homo sapiens	124-131
23074238-5	2012	Furthermore, we demonstrate that ER stress is associated with increases in islet iPLA(2)beta message, protein, and activity, iPLA(2)beta-dependent induction of neutral sphingomyelinase and ceramide accumulation, and subsequent loss of mitochondrial membrane potential.	Ceramides	189-197	phospholipase A2 group VI	Homo sapiens	125-136
22906436-5	2012	The elevation in ceramide levels was associated with activation of caspase 5 and the subsequent cleavage of HuR and apoptotic cell death.	Ceramides	17-25	caspase 5	Homo sapiens	67-76
22906436-5	2012	The elevation in ceramide levels was associated with activation of caspase 5 and the subsequent cleavage of HuR and apoptotic cell death.	Ceramides	17-25	ELAV like RNA binding protein 1	Homo sapiens	108-111
22981288-2	2012	Although the exact mechanisms by which IL-24 functions have not been completely elucidated, several pathways have consistently been identified: endoplasmic reticulum stress, ceramide-mediated events, and the generation of reactive oxygen species.	Ceramides	174-182	interleukin 24	Homo sapiens	39-44
22961081-0	2012	Overexpression of sphingosine kinase 1 prevents ceramide accumulation and ameliorates muscle insulin resistance in high-fat diet-fed mice.	Ceramides	48-56	sphingosine kinase 1	Mus musculus	18-38
22961081-2	2012	Intracellular ceramide accumulation causes insulin resistance, but sphingosine kinase 1 (SphK1) prevents ceramide accumulation, in part, by promoting its metabolism into S1P.	Ceramides	105-113	sphingosine kinase 1	Mus musculus	67-87
22961081-2	2012	Intracellular ceramide accumulation causes insulin resistance, but sphingosine kinase 1 (SphK1) prevents ceramide accumulation, in part, by promoting its metabolism into S1P.	Ceramides	105-113	sphingosine kinase 1	Mus musculus	89-94
22961081-5	2012	SphK1 Tg mice fed an HFD displayed increased SphK activity in skeletal muscle, which was associated with an attenuated intramuscular ceramide accumulation compared with wild-type (WT) littermates.	Ceramides	133-141	sphingosine kinase 1	Mus musculus	0-5
23160995-2	2012	CLN5-deficient (CLN5(-/-) ) fibroblasts demonstrate adhesion defects, increased growth, apoptosis, and decreased levels of ceramide, sphingomyelin, and glycosphingolipids.	Ceramides	123-131	CLN5 intracellular trafficking protein	Homo sapiens	0-4
23160995-7	2012	Similar to CLN5(-/-) cells, ceramide synthase activity, C16/C18:0/C24:0/C24:1 ceramide species, measured by MS is decreased in CLN8(-/-) cells.	Ceramides	28-36	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	127-131
23160995-13	2012	We explore the role of the CLN5/CLN8 proteins in ceramide species specific sphingolipid de novo synthesis, and suggest that CLN5/CLN8 proteins are more closely related than previously believed.	Ceramides	49-57	CLN5 intracellular trafficking protein	Homo sapiens	27-31
23160995-13	2012	We explore the role of the CLN5/CLN8 proteins in ceramide species specific sphingolipid de novo synthesis, and suggest that CLN5/CLN8 proteins are more closely related than previously believed.	Ceramides	49-57	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	32-36
23160995-13	2012	We explore the role of the CLN5/CLN8 proteins in ceramide species specific sphingolipid de novo synthesis, and suggest that CLN5/CLN8 proteins are more closely related than previously believed.	Ceramides	49-57	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	129-133
26052434-4	2012	Considerable evidence has accumulated to suggest that the cytosolic ectopic accumulation of fatty acid metabolites, including diacylglycerol and ceramides, underlies the development of insulin resistance in skeletal muscle.	Ceramides	145-154	insulin	Homo sapiens	185-192
23042913-4	2012	We hypothesized that the storage of ceramide would be increased in older individuals and this would be associated with increases in NFkappaB signaling and a decreased anabolic response to exercise.	Ceramides	36-44	nuclear factor kappa B subunit 1	Homo sapiens	132-140
23065795-5	2012	Inhibition of de novo ceramide synthesis using chemical inhibitors blocked the ability of gammaT and gammaT3 to induce apoptosis as detected by Annexin V-FITC/PI assay and to activate JNK/CHOP/DR5 pro-apoptotic signaling thereby demonstrating the involvement of de novo ceramide synthesis in gammaT- and gammaT3-induced apoptosis.	Ceramides	22-30	mitogen-activated protein kinase 8	Homo sapiens	184-187
23065795-5	2012	Inhibition of de novo ceramide synthesis using chemical inhibitors blocked the ability of gammaT and gammaT3 to induce apoptosis as detected by Annexin V-FITC/PI assay and to activate JNK/CHOP/DR5 pro-apoptotic signaling thereby demonstrating the involvement of de novo ceramide synthesis in gammaT- and gammaT3-induced apoptosis.	Ceramides	22-30	DNA damage inducible transcript 3	Homo sapiens	188-192
23065795-5	2012	Inhibition of de novo ceramide synthesis using chemical inhibitors blocked the ability of gammaT and gammaT3 to induce apoptosis as detected by Annexin V-FITC/PI assay and to activate JNK/CHOP/DR5 pro-apoptotic signaling thereby demonstrating the involvement of de novo ceramide synthesis in gammaT- and gammaT3-induced apoptosis.	Ceramides	22-30	TNF receptor superfamily member 10b	Homo sapiens	193-196
23065795-6	2012	CONCLUSION: Taken together, data show that both gammaT and gammaT3 induce apoptosis via de novo ceramide synthesis dependent activation of JNK/CHOP/DR5 pro-apoptotic signaling.	Ceramides	96-104	mitogen-activated protein kinase 8	Homo sapiens	139-142
22677645-1	2012	Ceramides (Cer) are implicated in obesity-associated skeletal muscle and perhaps adipocyte insulin resistance.	Ceramides	0-9	insulin	Homo sapiens	91-98
22677645-1	2012	Ceramides (Cer) are implicated in obesity-associated skeletal muscle and perhaps adipocyte insulin resistance.	Ceramides	0-3	insulin	Homo sapiens	91-98
23065795-6	2012	CONCLUSION: Taken together, data show that both gammaT and gammaT3 induce apoptosis via de novo ceramide synthesis dependent activation of JNK/CHOP/DR5 pro-apoptotic signaling.	Ceramides	96-104	DNA damage inducible transcript 3	Homo sapiens	143-147
23065795-6	2012	CONCLUSION: Taken together, data show that both gammaT and gammaT3 induce apoptosis via de novo ceramide synthesis dependent activation of JNK/CHOP/DR5 pro-apoptotic signaling.	Ceramides	96-104	TNF receptor superfamily member 10b	Homo sapiens	148-151
22677645-8	2012	For women only, there was a negative correlation between C16-Cer ceramide and plasma adiponectin (r = -0.77, P = 0.003) and a positive correlation between total ceramide content and HOMA(IR) (r = 0.74, P = 0.006).	Ceramides	65-73	adiponectin, C1Q and collagen domain containing	Homo sapiens	85-96
24957771-8	2012	Further interesting findings include: down-regulation of glucose export is postponed by TGFb, TGFb up-regulates the synthesis capacity of ketone bodies only as an early response, TGFb suppresses the strong up-regulation of Vanin, and TGFb induces re-formation of ceramides and sphingomyelin.	Ceramides	263-272	transforming growth factor, beta 1	Mus musculus	94-98
22940715-8	2012	Following DSS, ceramide levels were elevated in colon epithelium from WT and nCDase(-/-) mice, while S1P levels were significantly elevated only in the epithelium of nCDase(-/-) mice.	Ceramides	15-23	N-acylsphingosine amidohydrolase 2	Mus musculus	77-83
23066021-1	2012	BACKGROUND: The yeast Orm1/2 proteins regulate ceramide biosynthesis.	Ceramides	47-55	sphingolipid homeostasis protein ORM2	Saccharomyces cerevisiae S288C	22-28
23066021-2	2012	RESULTS: Depletion of the mammalian Orm1/2 homologues, ORMDL1-3, eliminates the negative feedback of exogenous ceramide on ceramide biosynthesis in HeLa cells.	Ceramides	111-119	orosomucoid 1	Homo sapiens	36-42
23066021-2	2012	RESULTS: Depletion of the mammalian Orm1/2 homologues, ORMDL1-3, eliminates the negative feedback of exogenous ceramide on ceramide biosynthesis in HeLa cells.	Ceramides	111-119	ORMDL sphingolipid biosynthesis regulator 1	Homo sapiens	55-61
23066021-2	2012	RESULTS: Depletion of the mammalian Orm1/2 homologues, ORMDL1-3, eliminates the negative feedback of exogenous ceramide on ceramide biosynthesis in HeLa cells.	Ceramides	123-131	orosomucoid 1	Homo sapiens	36-42
23066021-2	2012	RESULTS: Depletion of the mammalian Orm1/2 homologues, ORMDL1-3, eliminates the negative feedback of exogenous ceramide on ceramide biosynthesis in HeLa cells.	Ceramides	123-131	ORMDL sphingolipid biosynthesis regulator 1	Homo sapiens	55-61
23066021-5	2012	The mammalian ORMDL proteins are orthologues of the yeast Orm proteins (Orm1/2), which are regulators of ceramide biosynthesis.	Ceramides	105-113	sphingolipid homeostasis protein ORM2	Saccharomyces cerevisiae S288C	72-78
23066021-17	2012	We also tested the atypical sphingomyelin synthase isoform, SMSr, for its role in the regulation of ceramide biosynthesis.	Ceramides	100-108	sterile alpha motif domain containing 8	Homo sapiens	60-64
23066021-20	2012	We suggest that the role of SMSr may be in the regulation of downstream metabolism of ceramide.	Ceramides	86-94	sterile alpha motif domain containing 8	Homo sapiens	28-32
24957771-8	2012	Further interesting findings include: down-regulation of glucose export is postponed by TGFb, TGFb up-regulates the synthesis capacity of ketone bodies only as an early response, TGFb suppresses the strong up-regulation of Vanin, and TGFb induces re-formation of ceramides and sphingomyelin.	Ceramides	263-272	transforming growth factor, beta 1	Mus musculus	94-98
24957771-8	2012	Further interesting findings include: down-regulation of glucose export is postponed by TGFb, TGFb up-regulates the synthesis capacity of ketone bodies only as an early response, TGFb suppresses the strong up-regulation of Vanin, and TGFb induces re-formation of ceramides and sphingomyelin.	Ceramides	263-272	transforming growth factor, beta 1	Mus musculus	94-98
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.	Ceramides	127-135	UDP-glucose ceramide glucosyltransferase	Homo sapiens	113-117
23046545-1	2012	NSMase2 is associated to the plasma membrane, whereas ASMase is predominantly lysosomal; both hydrolyze sphingomyelin (SM) to ceramide and phosphocholine.	Ceramides	126-134	sphingomyelin phosphodiesterase 3	Homo sapiens	0-7
23046545-1	2012	NSMase2 is associated to the plasma membrane, whereas ASMase is predominantly lysosomal; both hydrolyze sphingomyelin (SM) to ceramide and phosphocholine.	Ceramides	126-134	sphingomyelin phosphodiesterase 1	Homo sapiens	54-60
23123064-0	2012	The receptor LMIR3 negatively regulates mast cell activation and allergic responses by binding to extracellular ceramide.	Ceramides	112-120	CD300 molecule like family member F	Mus musculus	13-18
23123064-5	2012	Both physical binding and functional reporter assays via an extracellular domain of LMIR3 showed that several extracellular lipids (including ceramide) and lipoproteins were possible ligands for LMIR3.	Ceramides	142-150	CD300 molecule like family member F	Mus musculus	84-89
23123064-5	2012	Both physical binding and functional reporter assays via an extracellular domain of LMIR3 showed that several extracellular lipids (including ceramide) and lipoproteins were possible ligands for LMIR3.	Ceramides	142-150	CD300 molecule like family member F	Mus musculus	195-200
23123064-7	2012	Upon engagement of high-affinity immunoglobulin E receptor, extracellular ceramide-LMIR3 binding inhibited MC activation via immunoreceptor tyrosine-based inhibitory and switch motifs of LMIR3.	Ceramides	74-82	CD300 molecule like family member F	Mus musculus	83-88
23123064-7	2012	Upon engagement of high-affinity immunoglobulin E receptor, extracellular ceramide-LMIR3 binding inhibited MC activation via immunoreceptor tyrosine-based inhibitory and switch motifs of LMIR3.	Ceramides	74-82	CD300 molecule like family member F	Mus musculus	187-192
22927247-3	2012	Applying liquid chromatography electrospray ionization tandem mass spectrometry, we revealed a significant decrease of proapoptotic ceramide in BCR/IL-4/CD40L-stimulated primary CLL cells compared with untreated controls.	Ceramides	132-140	interleukin 4	Homo sapiens	148-152
22927247-3	2012	Applying liquid chromatography electrospray ionization tandem mass spectrometry, we revealed a significant decrease of proapoptotic ceramide in BCR/IL-4/CD40L-stimulated primary CLL cells compared with untreated controls.	Ceramides	132-140	CD40 ligand	Homo sapiens	153-158
23035115-0	2012	Regulation of autophagy and its associated cell death by "sphingolipid rheostat": reciprocal role of ceramide and sphingosine 1-phosphate in the mammalian target of rapamycin pathway.	Ceramides	101-109	mechanistic target of rapamycin kinase	Homo sapiens	145-174
23035115-11	2012	These results indicate that S1P-S1P(3) plays a role in counteracting ceramide signals that mediate mTOR-controlled autophagy.	Ceramides	69-77	mechanistic target of rapamycin kinase	Homo sapiens	99-103
23035115-13	2012	Inhibition of CAPP by okadaic acid in AA(-)- or C(2)-ceramide-treated cells suppressed dephosphorylation/inactivation of mTOR, autophagy induction, and autophagy-associated cell death, indicating a novel role of ceramide-CAPPs in autophagy induction.	Ceramides	53-61	mechanistic target of rapamycin kinase	Homo sapiens	121-125
23035115-15	2012	Taken together, these results indicated that sphingolipid rheostat in ceramide-CAPPs and S1P-S1P(3) signaling modulates autophagy and its associated cell death through regulation of the mTOR pathway.	Ceramides	70-78	mechanistic target of rapamycin kinase	Homo sapiens	186-190
22927247-5	2012	We identified BCR engagement to catalyze the crucial modification of ceramide to glucosylceramide via UDP-glucose ceramide glucosyltransferase (UGCG).	Ceramides	69-77	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).	Ceramides	69-77	UDP-glucose ceramide glucosyltransferase	Homo sapiens	144-148
23134616-3	2012	The purpose of this study was to determine whether AICAR, an AMPK-activating drug, selectively reduces skeletal muscle ceramide synthesis.	Ceramides	119-127	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	61-65
23134616-9	2012	However, ceramide and SPT2 increased with the addition of compound C, an AMPK inhibitor.	Ceramides	9-17	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	73-77
23199915-2	2012	To study how such length variation affects the bilayer properties of ceramides, we synthesized ceramides consisting of a C12-, C14-, C16-, C18-, or C20-sphing-4-enin derivative coupled to palmitic acid.	Ceramides	95-104	Bardet-Biedl syndrome 9	Homo sapiens	139-142
23134616-12	2012	CONCLUSIONS: These results suggest that AICAR reduces ceramide synthesis by targeting SPT2 transcription, likely via AMPK activation as AMPK inhibition prevented the AICAR-induced improvements.	Ceramides	54-62	serine palmitoyltransferase, long chain base subunit 2	Rattus norvegicus	86-90
23134616-12	2012	CONCLUSIONS: These results suggest that AICAR reduces ceramide synthesis by targeting SPT2 transcription, likely via AMPK activation as AMPK inhibition prevented the AICAR-induced improvements.	Ceramides	54-62	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	117-121
23134616-12	2012	CONCLUSIONS: These results suggest that AICAR reduces ceramide synthesis by targeting SPT2 transcription, likely via AMPK activation as AMPK inhibition prevented the AICAR-induced improvements.	Ceramides	54-62	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	136-140
23134616-13	2012	Given the role of skeletal muscle ceramide in insulin resistance, it is tempting to speculate that interventions that activate AMPK may lead to long-term ceramide reduction and improved metabolic function.	Ceramides	34-42	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	127-131
23134616-13	2012	Given the role of skeletal muscle ceramide in insulin resistance, it is tempting to speculate that interventions that activate AMPK may lead to long-term ceramide reduction and improved metabolic function.	Ceramides	154-162	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	127-131
22728310-3	2012	We report that due to the difference of glucosylceramide synthase (GCS), catalyzing ceramide glycosylation, doxorubicin (Dox) eliminates bone marrow stem cells (BMSCs) and expands breast cancer stem cells (BCSCs).	Ceramides	48-56	UDP-glucose ceramide glucosyltransferase	Mus musculus	67-70
22989629-9	2012	Although neither HFD feeding nor AdipoR1 OE caused generalized changes in sphingolipids, AdipoR1 OE did reduce levels of sphingosine 1-phosphate, ceramide 18:1, ceramide 20:2, and dihydroceramide 20:0, plus mRNA levels of the ceramide synthetic enzymes serine palmitoyl transferase and sphingolipid Delta-4 desaturase, changes that are associated with increased insulin sensitivity.	Ceramides	146-154	adiponectin receptor 1	Rattus norvegicus	89-96
22989629-9	2012	Although neither HFD feeding nor AdipoR1 OE caused generalized changes in sphingolipids, AdipoR1 OE did reduce levels of sphingosine 1-phosphate, ceramide 18:1, ceramide 20:2, and dihydroceramide 20:0, plus mRNA levels of the ceramide synthetic enzymes serine palmitoyl transferase and sphingolipid Delta-4 desaturase, changes that are associated with increased insulin sensitivity.	Ceramides	161-169	adiponectin receptor 1	Rattus norvegicus	89-96
22989629-9	2012	Although neither HFD feeding nor AdipoR1 OE caused generalized changes in sphingolipids, AdipoR1 OE did reduce levels of sphingosine 1-phosphate, ceramide 18:1, ceramide 20:2, and dihydroceramide 20:0, plus mRNA levels of the ceramide synthetic enzymes serine palmitoyl transferase and sphingolipid Delta-4 desaturase, changes that are associated with increased insulin sensitivity.	Ceramides	161-169	adiponectin receptor 1	Rattus norvegicus	89-96
22935424-4	2012	Further, ceramide-induced cell death reduced significantly in stable SH-SY5Y cells expressing C/EBP homologous protein (CHOP) shRNA.	Ceramides	9-17	DNA damage inducible transcript 3	Homo sapiens	94-118
22899568-0	2012	Hyperosmolarity-induced lipid droplet formation depends on ceramide production by neutral sphingomyelinase 2.	Ceramides	59-67	sphingomyelin phosphodiesterase 3	Homo sapiens	82-108
22899568-6	2012	Both TG accumulation and IL-8 secretion were shown to be dependent on ceramide production by specific knock-down of NSM2.	Ceramides	70-78	C-X-C motif chemokine ligand 8	Homo sapiens	25-29
22899568-6	2012	Both TG accumulation and IL-8 secretion were shown to be dependent on ceramide production by specific knock-down of NSM2.	Ceramides	70-78	sphingomyelin phosphodiesterase 3	Homo sapiens	116-120
22322590-2	2012	The ceramide hydrolyzing enzyme acid ceramidase (AC), overexpressed in most prostate tumors, causes an aggressive and invasive phenotype through downstream effectors that have not yet been well characterized.	Ceramides	4-12	N-acylsphingosine amidohydrolase 1	Homo sapiens	32-47
22322590-2	2012	The ceramide hydrolyzing enzyme acid ceramidase (AC), overexpressed in most prostate tumors, causes an aggressive and invasive phenotype through downstream effectors that have not yet been well characterized.	Ceramides	4-12	N-acylsphingosine amidohydrolase 1	Homo sapiens	49-51
22980406-5	2012	Gene expression analyses revealed an up-regulation of genes known to be involved in apoptosis and ceramide-induced apoptotic pathways, including SMPD2, UGT8, COX6B1, Caspase 9 and MAP2K1 with ultrasound-stimulated microbubble exposure but not SMPD1.	Ceramides	98-106	sphingomyelin phosphodiesterase 2	Homo sapiens	145-150
22980406-5	2012	Gene expression analyses revealed an up-regulation of genes known to be involved in apoptosis and ceramide-induced apoptotic pathways, including SMPD2, UGT8, COX6B1, Caspase 9 and MAP2K1 with ultrasound-stimulated microbubble exposure but not SMPD1.	Ceramides	98-106	UDP glycosyltransferase 8	Homo sapiens	152-156
22980406-5	2012	Gene expression analyses revealed an up-regulation of genes known to be involved in apoptosis and ceramide-induced apoptotic pathways, including SMPD2, UGT8, COX6B1, Caspase 9 and MAP2K1 with ultrasound-stimulated microbubble exposure but not SMPD1.	Ceramides	98-106	cytochrome c oxidase subunit 6B1	Homo sapiens	158-164
22980406-5	2012	Gene expression analyses revealed an up-regulation of genes known to be involved in apoptosis and ceramide-induced apoptotic pathways, including SMPD2, UGT8, COX6B1, Caspase 9 and MAP2K1 with ultrasound-stimulated microbubble exposure but not SMPD1.	Ceramides	98-106	caspase 9	Homo sapiens	166-175
22980406-5	2012	Gene expression analyses revealed an up-regulation of genes known to be involved in apoptosis and ceramide-induced apoptotic pathways, including SMPD2, UGT8, COX6B1, Caspase 9 and MAP2K1 with ultrasound-stimulated microbubble exposure but not SMPD1.	Ceramides	98-106	mitogen-activated protein kinase kinase 1	Homo sapiens	180-186
22980406-5	2012	Gene expression analyses revealed an up-regulation of genes known to be involved in apoptosis and ceramide-induced apoptotic pathways, including SMPD2, UGT8, COX6B1, Caspase 9 and MAP2K1 with ultrasound-stimulated microbubble exposure but not SMPD1.	Ceramides	98-106	sphingomyelin phosphodiesterase 1	Homo sapiens	243-248
22935424-4	2012	Further, ceramide-induced cell death reduced significantly in stable SH-SY5Y cells expressing C/EBP homologous protein (CHOP) shRNA.	Ceramides	9-17	DNA damage inducible transcript 3	Homo sapiens	120-124
22935424-5	2012	Salubrinal inhibited ceramide-induced inositol-requiring enzyme 1alpha (IRE1alpha)/apoptosis signal regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) phosphorylation.	Ceramides	21-29	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	72-81
22935424-5	2012	Salubrinal inhibited ceramide-induced inositol-requiring enzyme 1alpha (IRE1alpha)/apoptosis signal regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) phosphorylation.	Ceramides	21-29	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	83-119
22935424-5	2012	Salubrinal inhibited ceramide-induced inositol-requiring enzyme 1alpha (IRE1alpha)/apoptosis signal regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) phosphorylation.	Ceramides	21-29	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	121-125
22935424-5	2012	Salubrinal inhibited ceramide-induced inositol-requiring enzyme 1alpha (IRE1alpha)/apoptosis signal regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) phosphorylation.	Ceramides	21-29	mitogen-activated protein kinase 8	Homo sapiens	152-155
22936806-0	2012	Ceramide glycosylation by glucosylceramide synthase selectively maintains the properties of breast cancer stem cells.	Ceramides	0-8	UDP-glucose ceramide glucosyltransferase	Homo sapiens	26-51
22936806-3	2012	Here, we report that ceramide glycosylation catalyzed by glucosylceramide synthase, which is enhanced in breast cancer stem cells (BCSCs) but not in normal mammary epithelial stem cells, maintains tumorous pluripotency of BCSCs.	Ceramides	21-29	UDP-glucose ceramide glucosyltransferase	Homo sapiens	57-82
22932257-11	2012	Moreover, the CPT1b(+/-) heart exhibited exacerbated mitochondrial abnormalities and myocardial lipid accumulation with elevated triglycerides and ceramide content, leading to greater cardiomyocyte apoptosis.	Ceramides	147-155	carnitine palmitoyltransferase 1b, muscle	Mus musculus	14-19
22652149-7	2012	Inhibition of the ceramide-responsive JNK and PP2A pathways did not abolish the effects of ceramide, and JNK phosphorylation was unresponsive to ceramide; however, ceramide significantly inhibited phosphorylation of Akt.	Ceramides	18-26	mitogen-activated protein kinase 8	Homo sapiens	38-41
22652149-7	2012	Inhibition of the ceramide-responsive JNK and PP2A pathways did not abolish the effects of ceramide, and JNK phosphorylation was unresponsive to ceramide; however, ceramide significantly inhibited phosphorylation of Akt.	Ceramides	18-26	protein phosphatase 2 phosphatase activator	Homo sapiens	46-50
22652149-7	2012	Inhibition of the ceramide-responsive JNK and PP2A pathways did not abolish the effects of ceramide, and JNK phosphorylation was unresponsive to ceramide; however, ceramide significantly inhibited phosphorylation of Akt.	Ceramides	18-26	AKT serine/threonine kinase 1	Homo sapiens	216-219
22738231-7	2012	The Lro1p-dependent transfer of oleic acid on to NBD-ceramide was confirmed by high-resolution Fourier transform and tandem MS. Immunopurified Lro1p was equally able to acylate NBD-ceramide.	Ceramides	53-61	phospholipid:diacylglycerol acyltransferase	Saccharomyces cerevisiae S288C	4-9
22738231-1	2012	The hydrolysis of ceramides in yeast is catalysed by the alkaline ceramidases Ypc1p and Ydc1p, two highly homologous membrane proteins localized to the ER (endoplasmic reticulum).	Ceramides	18-27	phytoceramidase	Saccharomyces cerevisiae S288C	78-83
22738231-7	2012	The Lro1p-dependent transfer of oleic acid on to NBD-ceramide was confirmed by high-resolution Fourier transform and tandem MS. Immunopurified Lro1p was equally able to acylate NBD-ceramide.	Ceramides	53-61	phospholipid:diacylglycerol acyltransferase	Saccharomyces cerevisiae S288C	143-148
22738231-1	2012	The hydrolysis of ceramides in yeast is catalysed by the alkaline ceramidases Ypc1p and Ydc1p, two highly homologous membrane proteins localized to the ER (endoplasmic reticulum).	Ceramides	18-27	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	88-93
22738231-2	2012	As observed with many enzymes, Ypc1p can also catalyse the reverse reaction, i.e. condense a non-esterified fatty acid with PHS (phytosphingosine) or DHS (dihydrosphingosine) and thus synthesize ceramides.	Ceramides	195-204	phytoceramidase	Saccharomyces cerevisiae S288C	31-36
22580159-0	2012	Palmitate-induced PTP1B expression is mediated by ceramide-JNK and nuclear factor kappaB (NF-kappaB) activation.	Ceramides	50-58	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	18-23
22712892-8	2012	ASMase-deficient mice (asm-/-/ldlr-/-) lacked S-SMase activity and were protected from diet-induced elevation in LDL ceramide.	Ceramides	117-125	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
22580159-0	2012	Palmitate-induced PTP1B expression is mediated by ceramide-JNK and nuclear factor kappaB (NF-kappaB) activation.	Ceramides	50-58	mitogen-activated protein kinase 8	Mus musculus	59-62
22580159-12	2012	Knockdown of PTP1B also prevented ceramide-reduced IRS-1 and Akt phosphorylations in the myotubes.	Ceramides	34-42	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	13-18
22580159-10	2012	Inhibitors of de novo ceramide synthesis prevented palmitate-induced PTP1B promoter activity in myotubes.	Ceramides	22-30	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	69-74
22580159-12	2012	Knockdown of PTP1B also prevented ceramide-reduced IRS-1 and Akt phosphorylations in the myotubes.	Ceramides	34-42	insulin receptor substrate 1	Mus musculus	51-56
22580159-11	2012	In addition, inhibitor of JNK pathway prevented ceramide-induced PTP1B promoter activity in myotubes.	Ceramides	48-56	mitogen-activated protein kinase 8	Mus musculus	26-29
22580159-12	2012	Knockdown of PTP1B also prevented ceramide-reduced IRS-1 and Akt phosphorylations in the myotubes.	Ceramides	34-42	thymoma viral proto-oncogene 1	Mus musculus	61-64
22580159-11	2012	In addition, inhibitor of JNK pathway prevented ceramide-induced PTP1B promoter activity in myotubes.	Ceramides	48-56	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	65-70
22580159-14	2012	Our data provide the evidence that the mechanism by which palmitate increased the expression of PTP1B seems to be through a mechanism involving the activation of ceramide-JNK and NF-kappaB pathways.	Ceramides	162-170	protein tyrosine phosphatase, non-receptor type 1	Mus musculus	96-101
22854889-2	2012	We hypothesised that plasma ceramide concentrations are increased in the presence of elevated fatty acid levels and are regulated by increased liver serine C-palmitoyltransferase (SPT) activity.	Ceramides	28-36	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	149-178
22580159-14	2012	Our data provide the evidence that the mechanism by which palmitate increased the expression of PTP1B seems to be through a mechanism involving the activation of ceramide-JNK and NF-kappaB pathways.	Ceramides	162-170	mitogen-activated protein kinase 8	Mus musculus	171-174
22854889-2	2012	We hypothesised that plasma ceramide concentrations are increased in the presence of elevated fatty acid levels and are regulated by increased liver serine C-palmitoyltransferase (SPT) activity.	Ceramides	28-36	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	180-183
22884781-5	2012	RESULTS: The addition of Th2 cytokines (IL-4/IL-6) at a concentration of 10nM resulted in a marked decrease in SC ceramide levels.	Ceramides	114-122	interleukin 6	Homo sapiens	45-49
22884781-3	2012	OBJECTIVE: We highlighted the effects of Th1/Th2 cytokines on ceramide levels in the SC.	Ceramides	62-70	negative elongation factor complex member C/D	Homo sapiens	41-44
22884781-6	2012	The reduced ceramide content in the SC was accompanied by the down-regulated expression of the genes encoding serine-palmitoyl transferase-2, acid sphingomyelinase and beta-glucocerebrosidase in the epidermis.	Ceramides	12-20	glucosylceramidase beta	Homo sapiens	168-191
22884781-5	2012	RESULTS: The addition of Th2 cytokines (IL-4/IL-6) at a concentration of 10nM resulted in a marked decrease in SC ceramide levels.	Ceramides	114-122	interleukin 4	Homo sapiens	40-44
22884781-7	2012	In contrast, the addition of Th1 cytokines (GM-CSF/IFN-gamma/TNF-alpha) at concentrations of 2.5 or 10nM resulted in a slight increase in SC ceramide levels, which were accompanied by no change or an increase in the expression of those genes encoding sphingolipid metabolic enzymes in the epidermis.	Ceramides	141-149	negative elongation factor complex member C/D	Homo sapiens	29-32
22884781-7	2012	In contrast, the addition of Th1 cytokines (GM-CSF/IFN-gamma/TNF-alpha) at concentrations of 2.5 or 10nM resulted in a slight increase in SC ceramide levels, which were accompanied by no change or an increase in the expression of those genes encoding sphingolipid metabolic enzymes in the epidermis.	Ceramides	141-149	colony stimulating factor 2	Homo sapiens	44-50
22884781-7	2012	In contrast, the addition of Th1 cytokines (GM-CSF/IFN-gamma/TNF-alpha) at concentrations of 2.5 or 10nM resulted in a slight increase in SC ceramide levels, which were accompanied by no change or an increase in the expression of those genes encoding sphingolipid metabolic enzymes in the epidermis.	Ceramides	141-149	interferon gamma	Homo sapiens	51-60
22884781-7	2012	In contrast, the addition of Th1 cytokines (GM-CSF/IFN-gamma/TNF-alpha) at concentrations of 2.5 or 10nM resulted in a slight increase in SC ceramide levels, which were accompanied by no change or an increase in the expression of those genes encoding sphingolipid metabolic enzymes in the epidermis.	Ceramides	141-149	tumor necrosis factor	Homo sapiens	61-70
22922758-6	2012	Thus, these data suggest a new receptor function of ceramide for anchoring LC3B-II autophagolysosomes to mitochondrial membranes, defining a key mechanism for the induction of lethal mitophagy.	Ceramides	52-60	microtubule associated protein 1 light chain 3 beta	Homo sapiens	75-79
22796112-5	2012	These results suggested that ACBD3 plays a pivotal role in ceramide transport regulation at the ER-Golgi interface.	Ceramides	59-67	acyl-CoA binding domain containing 3	Homo sapiens	29-34
22922758-5	2012	Moreover, knockdown of CerS1 abrogated sodium selenite-induced mitophagy, and stable LC3B knockdown protected against CerS1- and C(18)-ceramide-dependent mitophagy and blocked tumor suppression in vivo.	Ceramides	135-143	microtubule associated protein 1 light chain 3 beta	Homo sapiens	85-89
22922758-3	2012	C(18)-ceramide-induced lethal autophagy was regulated via microtubule-associated protein 1 light chain 3 beta-lipidation, forming LC3B-II, and selective targeting of mitochondria by LC3B-II-containing autophagolysosomes (mitophagy) through direct interaction between ceramide and LC3B-II upon Drp1-dependent mitochondrial fission, leading to inhibition of mitochondrial function and oxygen consumption.	Ceramides	6-14	microtubule associated protein 1 light chain 3 beta	Homo sapiens	58-109
22922758-3	2012	C(18)-ceramide-induced lethal autophagy was regulated via microtubule-associated protein 1 light chain 3 beta-lipidation, forming LC3B-II, and selective targeting of mitochondria by LC3B-II-containing autophagolysosomes (mitophagy) through direct interaction between ceramide and LC3B-II upon Drp1-dependent mitochondrial fission, leading to inhibition of mitochondrial function and oxygen consumption.	Ceramides	6-14	microtubule associated protein 1 light chain 3 beta	Homo sapiens	130-134
22922758-3	2012	C(18)-ceramide-induced lethal autophagy was regulated via microtubule-associated protein 1 light chain 3 beta-lipidation, forming LC3B-II, and selective targeting of mitochondria by LC3B-II-containing autophagolysosomes (mitophagy) through direct interaction between ceramide and LC3B-II upon Drp1-dependent mitochondrial fission, leading to inhibition of mitochondrial function and oxygen consumption.	Ceramides	6-14	microtubule associated protein 1 light chain 3 beta	Homo sapiens	182-186
22922758-3	2012	C(18)-ceramide-induced lethal autophagy was regulated via microtubule-associated protein 1 light chain 3 beta-lipidation, forming LC3B-II, and selective targeting of mitochondria by LC3B-II-containing autophagolysosomes (mitophagy) through direct interaction between ceramide and LC3B-II upon Drp1-dependent mitochondrial fission, leading to inhibition of mitochondrial function and oxygen consumption.	Ceramides	6-14	microtubule associated protein 1 light chain 3 beta	Homo sapiens	182-186
22922758-3	2012	C(18)-ceramide-induced lethal autophagy was regulated via microtubule-associated protein 1 light chain 3 beta-lipidation, forming LC3B-II, and selective targeting of mitochondria by LC3B-II-containing autophagolysosomes (mitophagy) through direct interaction between ceramide and LC3B-II upon Drp1-dependent mitochondrial fission, leading to inhibition of mitochondrial function and oxygen consumption.	Ceramides	6-14	collapsin response mediator protein 1	Homo sapiens	293-297
22922758-4	2012	Accordingly, expression of mutant LC3B with impaired ceramide binding, as predicted by molecular modeling, prevented CerS1-mediated mitochondrial targeting, recovering oxygen consumption.	Ceramides	53-61	microtubule associated protein 1 light chain 3 beta	Homo sapiens	34-38
22922758-4	2012	Accordingly, expression of mutant LC3B with impaired ceramide binding, as predicted by molecular modeling, prevented CerS1-mediated mitochondrial targeting, recovering oxygen consumption.	Ceramides	53-61	ceramide synthase 1	Homo sapiens	117-122
22869376-1	2012	Ceramide transport from the endoplasmic reticulum to the Golgi apparatus is crucial in sphingolipid biosynthesis, and the process relies on the ceramide trafficking protein (CERT), which contains pleckstrin homology (PH) and StAR-related lipid transfer domains.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	174-178
22869376-2	2012	The CERT PH domain specifically recognizes phosphatidylinositol 4-monophosphate (PtdIns(4)P), a characteristic phosphoinositide in the Golgi membrane, and is indispensable for the endoplasmic reticulum-to-Golgi transport of ceramide by CERT.	Ceramides	224-232	ceramide transporter 1	Homo sapiens	4-8
22869376-2	2012	The CERT PH domain specifically recognizes phosphatidylinositol 4-monophosphate (PtdIns(4)P), a characteristic phosphoinositide in the Golgi membrane, and is indispensable for the endoplasmic reticulum-to-Golgi transport of ceramide by CERT.	Ceramides	224-232	ceramide transporter 1	Homo sapiens	236-240
22828584-9	2012	OPCs inside the six axon/glia compartments were treated with a high concentration of ceramide (150 muM) to confirm the fluidic isolation among the satellite compartments.	Ceramides	85-93	latexin	Homo sapiens	99-102
22796112-2	2012	PPM1L, originally identified as a negative regulator of stress-activated protein kinase signaling, was recently shown to be involved in the regulation of ceramide trafficking at ER-Golgi membrane contact sites.	Ceramides	154-162	protein phosphatase, Mg2+/Mn2+ dependent 1L	Homo sapiens	0-5
22973882-0	2012	Ceramide sphingolipid signaling mediates Tumor Necrosis Factor (TNF)-dependent toxicity via caspase signaling in dopaminergic neurons.	Ceramides	0-8	tumor necrosis factor-like	Rattus norvegicus	41-62
22825003-2	2012	The present study investigated the role of ceramide production through acid sphingomyelinase (ASM) activation in the periaqueductal gray region, a brain region implicated in opioid analgesia and tolerance.	Ceramides	43-51	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	71-92
22825003-2	2012	The present study investigated the role of ceramide production through acid sphingomyelinase (ASM) activation in the periaqueductal gray region, a brain region implicated in opioid analgesia and tolerance.	Ceramides	43-51	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	94-97
22825003-4	2012	The effects of acute morphine treatment on ASM expression and ceramide generation in the periaqueductal gray region were completely blocked by pretreatment with naloxone and by silencing the ASM gene by plasmid-mediated transfection of ASM shRNA.	Ceramides	62-70	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	191-194
22825003-4	2012	The effects of acute morphine treatment on ASM expression and ceramide generation in the periaqueductal gray region were completely blocked by pretreatment with naloxone and by silencing the ASM gene by plasmid-mediated transfection of ASM shRNA.	Ceramides	62-70	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	191-194
22973882-0	2012	Ceramide sphingolipid signaling mediates Tumor Necrosis Factor (TNF)-dependent toxicity via caspase signaling in dopaminergic neurons.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	64-67
22973882-5	2012	Using lipidomics mass spectrometry we confirmed that TNF treatment not only promotes generation of ceramide, but also leads to accumulation of several atypical deoxy-sphingoid bases (DSBs).	Ceramides	99-107	tumor necrosis factor	Homo sapiens	53-56
22973882-7	2012	CONCLUSIONS: We conclude that TNF/TNFR1-dependent activation of SMases generates ceramide and sphingolipid species that promote degeneration and caspase-dependent cell death of DA neurons.	Ceramides	81-89	tumor necrosis factor	Homo sapiens	30-33
22973882-7	2012	CONCLUSIONS: We conclude that TNF/TNFR1-dependent activation of SMases generates ceramide and sphingolipid species that promote degeneration and caspase-dependent cell death of DA neurons.	Ceramides	81-89	TNF receptor superfamily member 1A	Homo sapiens	34-39
22974251-7	2012	Expression levels of SMPD3 mRNA correlated significantly with concentrations of different ceramides and sphingomyelins.	Ceramides	90-99	sphingomyelin phosphodiesterase 3	Homo sapiens	21-26
22727936-0	2012	Inhibition of sphingosine kinase 1 enhances cytotoxicity, ceramide levels and ROS formation in liver cancer cells treated with selenite.	Ceramides	58-66	sphingosine kinase 1	Homo sapiens	14-34
22810490-6	2012	Astrocytes isolated from MS lesions expressed enhanced mRNA levels of the ceramide-producing enzyme acid sphingomyelinase (ASM) compared to astrocytes isolated from control white matter.	Ceramides	74-82	sphingomyelin phosphodiesterase 1	Homo sapiens	100-121
22810490-6	2012	Astrocytes isolated from MS lesions expressed enhanced mRNA levels of the ceramide-producing enzyme acid sphingomyelinase (ASM) compared to astrocytes isolated from control white matter.	Ceramides	74-82	sphingomyelin phosphodiesterase 1	Homo sapiens	123-126
22810490-7	2012	In addition, TNF-alpha treatment induced ASM mRNA and ceramide levels in astrocytes isolated from control white matter.	Ceramides	54-62	tumor necrosis factor	Homo sapiens	13-22
22810490-8	2012	Incubation of astrocytes with Fingolimod prior to TNF-alpha treatment reduced ceramide production and mRNA expression of ASM to control levels in astrocytes.	Ceramides	78-86	tumor necrosis factor	Homo sapiens	50-59
22974230-7	2012	Two genes demonstrated increased expression during the bacterial challenge: a gene involved in hydrolytic breakdown of ceramide (acid ceramidase) and a gene involved in de novo generation of ceramide (3-ketodihydrosphingosine reductase), suggesting a possible role of ceramide in the invertebrate stress and immune responses.	Ceramides	119-127	acid ceramidase-like	Crassostrea gigas	129-144
22974230-7	2012	Two genes demonstrated increased expression during the bacterial challenge: a gene involved in hydrolytic breakdown of ceramide (acid ceramidase) and a gene involved in de novo generation of ceramide (3-ketodihydrosphingosine reductase), suggesting a possible role of ceramide in the invertebrate stress and immune responses.	Ceramides	191-199	acid ceramidase-like	Crassostrea gigas	129-144
22974230-7	2012	Two genes demonstrated increased expression during the bacterial challenge: a gene involved in hydrolytic breakdown of ceramide (acid ceramidase) and a gene involved in de novo generation of ceramide (3-ketodihydrosphingosine reductase), suggesting a possible role of ceramide in the invertebrate stress and immune responses.	Ceramides	191-199	acid ceramidase-like	Crassostrea gigas	129-144
22974230-10	2012	The gene expression pattern of acid ceramidase and 3-kethodihydrosphingosine reductase in response to bacterial exposure especially supports that ceramide and sphingolipid metabolism may be involved in the oyster"s stress and/or immune responses.	Ceramides	146-154	acid ceramidase-like	Crassostrea gigas	31-46
22727936-8	2012	Instead, 50 muM of SK1-II combined with 10 muM of selenite caused accumulation of cells in G1/S phases, but less apoptosis and accumulation of ceramides.	Ceramides	143-152	sphingosine kinase 1	Homo sapiens	19-22
22446749-4	2012	Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B.	Ceramides	123-132	NLR family pyrin domain containing 3	Homo sapiens	0-27
22446749-4	2012	Nod-like receptor protein 3 (NLRP3) is the major immune sensor for cellular stress signals, e.g., reactive oxygen species, ceramides, and cathepsin B.	Ceramides	123-132	NLR family pyrin domain containing 3	Homo sapiens	29-34
22169929-0	2012	NALP-3 inflammasome silencing attenuates ceramide-induced transepithelial permeability.	Ceramides	41-49	NLR family, pyrin domain containing 3	Mus musculus	0-6
22451348-4	2012	Similarly, conduritol B epoxide, an inhibitor of beta-glucocerebrosidase, significantly down-regulated SC ceramide levels and significantly increased glucosylceramide levels.	Ceramides	106-114	glucosylceramidase beta	Homo sapiens	49-72
22451348-6	2012	Using this model, we assessed the effects of the inflammatory cytokine interleukin-1alpha (IL-1alpha), several bioactive sphingolipids and all-trans retinoic acid (RA) on ceramide levels in the SC.	Ceramides	171-179	interleukin 1 alpha	Homo sapiens	91-100
22451348-7	2012	Whereas treatment with IL-1alpha (at 10 nM) significantly down-regulated ceramide levels, treatment with sphingosylphosphorylcholine (at 50 microM) or sphingosine-1-phosphate (at 10 or 20 microM) distinctly up-regulated ceramide levels.	Ceramides	73-81	interleukin 1 alpha	Homo sapiens	23-32
22451348-7	2012	Whereas treatment with IL-1alpha (at 10 nM) significantly down-regulated ceramide levels, treatment with sphingosylphosphorylcholine (at 50 microM) or sphingosine-1-phosphate (at 10 or 20 microM) distinctly up-regulated ceramide levels.	Ceramides	220-228	interleukin 1 alpha	Homo sapiens	23-32
22451348-9	2012	The increased levels of ceramide were accompanied by a significantly increased secretion of granulocyte-macrophage colony-stimulating factor as well as by a significantly down-regulated expression of acid-ceramidase at both the gene and protein levels.	Ceramides	24-32	colony stimulating factor 2	Homo sapiens	92-140
22451348-9	2012	The increased levels of ceramide were accompanied by a significantly increased secretion of granulocyte-macrophage colony-stimulating factor as well as by a significantly down-regulated expression of acid-ceramidase at both the gene and protein levels.	Ceramides	24-32	N-acylsphingosine amidohydrolase 1	Homo sapiens	200-215
22169929-8	2012	The effect of ceramide on activation of inflammasome and production of inflammatory cytokine was assessed in primary mouse alveolar macrophages and THP-1 cells.	Ceramides	14-22	GLI family zinc finger 2	Homo sapiens	148-153
22169929-10	2012	Our results reveal that ceramide causes inflammasome activation, induction of caspase-1, IL-1beta cleavage, and release of proinflammatory cytokines.	Ceramides	24-32	caspase 1	Mus musculus	78-87
22169929-10	2012	Our results reveal that ceramide causes inflammasome activation, induction of caspase-1, IL-1beta cleavage, and release of proinflammatory cytokines.	Ceramides	24-32	interleukin 1 beta	Mus musculus	89-97
23135655-0	2012	Adjunctive use of a facial moisturizer SPF 30 containing ceramide precursor improves tolerability of topical tretinoin 0.05%: a randomized, investigator-blinded, split-face study.	Ceramides	57-65	survival motor neuron domain containing 1	Homo sapiens	39-45
22801434-2	2012	Insulin-resistance dysregulates lipid metabolism, which promotes ceramide accumulation with attendant inflammation and endoplasmic reticulum (ER) stress.	Ceramides	65-73	insulin	Homo sapiens	0-7
21773820-5	2012	Blockage of intracellular ceramide production through the inhibition of de novo ceramide synthesis or the hydrolysis of sphingomyelin increased the invasive ability and upregulated MMP-9 protein levels.	Ceramides	26-34	matrix metallopeptidase 9	Homo sapiens	181-186
22784711-8	2012	In contrast, enforced expression of SPL sensitized cancer cells to irradiation or docetaxel by tilting the ceramide/S1P balance toward cell death.	Ceramides	107-115	sphingosine-1-phosphate lyase 1	Homo sapiens	36-39
22314624-4	2012	CD95 activation is caused by increased ceramide concentrations in cystic fibrosis lungs, as revealed by genetic modifications that normalize pulmonary ceramide concentrations.	Ceramides	39-47	Fas (TNF receptor superfamily member 6)	Mus musculus	0-4
22314624-4	2012	CD95 activation is caused by increased ceramide concentrations in cystic fibrosis lungs, as revealed by genetic modifications that normalize pulmonary ceramide concentrations.	Ceramides	151-159	Fas (TNF receptor superfamily member 6)	Mus musculus	0-4
22314624-5	2012	The activation of CD95 in cystic fibrosis lungs further increases pulmonary ceramide levels and results in a vicious feedback cycle of CD95 activation and ceramide accumulation.	Ceramides	76-84	Fas (TNF receptor superfamily member 6)	Mus musculus	18-22
22314624-5	2012	The activation of CD95 in cystic fibrosis lungs further increases pulmonary ceramide levels and results in a vicious feedback cycle of CD95 activation and ceramide accumulation.	Ceramides	155-163	Fas (TNF receptor superfamily member 6)	Mus musculus	18-22
23019415-0	2012	Metronomic ceramide analogs inhibit angiogenesis in pancreatic cancer through up-regulation of caveolin-1 and thrombospondin-1 and down-regulation of cyclin D1.	Ceramides	11-19	caveolin 1	Homo sapiens	95-105
23019415-0	2012	Metronomic ceramide analogs inhibit angiogenesis in pancreatic cancer through up-regulation of caveolin-1 and thrombospondin-1 and down-regulation of cyclin D1.	Ceramides	11-19	thrombospondin 1	Homo sapiens	110-126
23019415-0	2012	Metronomic ceramide analogs inhibit angiogenesis in pancreatic cancer through up-regulation of caveolin-1 and thrombospondin-1 and down-regulation of cyclin D1.	Ceramides	11-19	cyclin D1	Homo sapiens	150-159
23019415-7	2012	ERK1/2 and Akt phosphorylation were significantly decreased after metronomic ceramide analog treatment.	Ceramides	77-85	mitogen-activated protein kinase 3	Homo sapiens	0-6
23019415-7	2012	ERK1/2 and Akt phosphorylation were significantly decreased after metronomic ceramide analog treatment.	Ceramides	77-85	AKT serine/threonine kinase 1	Homo sapiens	11-14
22801434-3	2012	Mechanistically, we propose that toxic ceramides generated in extra-CNS tissues, e.g. liver, get released into peripheral blood, and subsequently transit across the blood-brain barrier into the brain where they induce brain insulin-resistance, inflammation, and cell death (extrinsic pathway).	Ceramides	39-48	insulin	Homo sapiens	224-231
22801434-4	2012	These abnormalities establish or help propagate a cascade of neurodegeneration associated with increased ER stress and ceramide generation, which exacerbate brain insulin-resistance, cell death, myelin degeneration, and neuro-inflammation.	Ceramides	119-127	insulin	Homo sapiens	163-170
22640955-6	2012	Increased monocyte surface CD11b and CD36 was inhibited by fumonisin B1, an inhibitor of de novo ceramide synthesis, but not by the superoxide dismutase mimetic MnTBap.	Ceramides	97-105	integrin subunit alpha M	Homo sapiens	27-32
22403805-3	2012	Inflammatory lung diseases are characterized by augmented acid sphingomyelinase (aSMase) activity leading to ceramide production, a pathway that promotes increased vascular permeability, apoptosis, and surfactant alterations.	Ceramides	109-117	sphingomyelin phosphodiesterase 1	Homo sapiens	58-79
21796379-7	2012	Effect of alpha- or gamma-tocopherol, but not of delta-tocopherol, on the newly synthesized ceramide content in old cells was correlated with the action of inhibitor of serine palmitoyl transferase (SPT) activity (myriocin) and SMase inhibitors (glutathione, imipramine).	Ceramides	92-100	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	199-202
22403805-3	2012	Inflammatory lung diseases are characterized by augmented acid sphingomyelinase (aSMase) activity leading to ceramide production, a pathway that promotes increased vascular permeability, apoptosis, and surfactant alterations.	Ceramides	109-117	sphingomyelin phosphodiesterase 1	Homo sapiens	81-87
22594559-2	2012	Using in vitro approaches, we analyzed the impact of sphingosine kinase-1 (SphK-1) inhibition on ceramide production, and evaluated SphK1 inhibitor II (SKI-II) as a potential curcumin chemo-sensitizer in ovarian cancer cells.	Ceramides	97-105	sphingosine kinase 1	Homo sapiens	75-81
22944681-4	2012	Prominent Gb3Cer and Gb4Cer lipoform heterogeneity was based on ceramides carrying predominantly C16:0 and C24:0/C24:1 fatty acids.	Ceramides	64-73	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	10-13
22944681-4	2012	Prominent Gb3Cer and Gb4Cer lipoform heterogeneity was based on ceramides carrying predominantly C16:0 and C24:0/C24:1 fatty acids.	Ceramides	64-73	beta-1,3-N-acetylgalactosaminyltransferase 1 (globoside blood group)	Homo sapiens	21-27
22615346-8	2012	In order to demonstrate more physiological activation of PP2Calpha by ceramide, phospho-p38delta was utilized as substrate.	Ceramides	70-78	protein phosphatase, Mg2+/Mn2+ dependent 1A	Homo sapiens	57-66
22615346-8	2012	In order to demonstrate more physiological activation of PP2Calpha by ceramide, phospho-p38delta was utilized as substrate.	Ceramides	70-78	mitogen-activated protein kinase 13	Homo sapiens	88-96
22628619-2	2012	We examined the changes in lipid homeostasis and gene expression in Huh7 hepatocytes when the synthesis of ceramide is perturbed by knocking down serine pal mitoyltransferase subunits 1, 2, and 3 (SPTLC123) or dihydroceramide desaturase 1 (DEGS1).	Ceramides	107-115	MIR7-3 host gene	Homo sapiens	68-72
22628619-2	2012	We examined the changes in lipid homeostasis and gene expression in Huh7 hepatocytes when the synthesis of ceramide is perturbed by knocking down serine pal mitoyltransferase subunits 1, 2, and 3 (SPTLC123) or dihydroceramide desaturase 1 (DEGS1).	Ceramides	107-115	delta 4-desaturase, sphingolipid 1	Homo sapiens	210-238
22619219-1	2012	Sulfatide is 3-O-sulfogalactosylceramide that is synthesized by two transferases (ceramide galactosyltransferase and cerebroside sulfotransferase) from ceramide and is specifically degraded by a sulfatase (arylsulfatase A).	Ceramides	32-40	arylsulfatase family member H	Homo sapiens	195-204
22628619-2	2012	We examined the changes in lipid homeostasis and gene expression in Huh7 hepatocytes when the synthesis of ceramide is perturbed by knocking down serine pal mitoyltransferase subunits 1, 2, and 3 (SPTLC123) or dihydroceramide desaturase 1 (DEGS1).	Ceramides	107-115	delta 4-desaturase, sphingolipid 1	Homo sapiens	240-245
22628619-8	2012	These studies are the first to provide a direct and comprehensive understanding at the lipidomic and transcriptomic levels of how Huh7 hepatocytes respond to changes in the inhibition of ceramide synthesis.	Ceramides	187-195	MIR7-3 host gene	Homo sapiens	130-134
22619219-1	2012	Sulfatide is 3-O-sulfogalactosylceramide that is synthesized by two transferases (ceramide galactosyltransferase and cerebroside sulfotransferase) from ceramide and is specifically degraded by a sulfatase (arylsulfatase A).	Ceramides	32-40	arylsulfatase A	Homo sapiens	206-221
22688512-4	2012	In addition, SMS1/SMS2 double-knockout cells had heightened sensitivity to CXCL12, which was significantly suppressed upon transfection with the SMS1 or SMS2 gene or when they were treated with exogenous sphingomyelin but not when they were treated with the SMS substrate ceramide.	Ceramides	272-280	sphingomyelin synthase 1	Mus musculus	13-17
22583777-5	2012	Co-administration phenoxodiol with doxorubicin synergistically inhibited SphK1 activity to trigger cellular ceramide accumulation, and achieved synergistic anti-OS growth effect, accompanied with a significant increased of apoptosis and cytotoxicity.	Ceramides	108-116	sphingosine kinase 1	Homo sapiens	73-78
22688512-4	2012	In addition, SMS1/SMS2 double-knockout cells had heightened sensitivity to CXCL12, which was significantly suppressed upon transfection with the SMS1 or SMS2 gene or when they were treated with exogenous sphingomyelin but not when they were treated with the SMS substrate ceramide.	Ceramides	272-280	chemokine (C-X-C motif) ligand 12	Mus musculus	75-81
22583777-6	2012	Increased cellular level of ceramide by the co-administration induced the association between Akt and Protein Phosphatase 1 (PP1) to dephosphorylate Akt, and to introduce a constitutively active Akt (CA-Akt) restored Akt activation and diminished cell growth inhibition.	Ceramides	28-36	AKT serine/threonine kinase 1	Homo sapiens	94-97
22583777-6	2012	Increased cellular level of ceramide by the co-administration induced the association between Akt and Protein Phosphatase 1 (PP1) to dephosphorylate Akt, and to introduce a constitutively active Akt (CA-Akt) restored Akt activation and diminished cell growth inhibition.	Ceramides	28-36	inorganic pyrophosphatase 1	Homo sapiens	102-123
22688512-4	2012	In addition, SMS1/SMS2 double-knockout cells had heightened sensitivity to CXCL12, which was significantly suppressed upon transfection with the SMS1 or SMS2 gene or when they were treated with exogenous sphingomyelin but not when they were treated with the SMS substrate ceramide.	Ceramides	272-280	spermine synthase	Mus musculus	13-16
22583777-6	2012	Increased cellular level of ceramide by the co-administration induced the association between Akt and Protein Phosphatase 1 (PP1) to dephosphorylate Akt, and to introduce a constitutively active Akt (CA-Akt) restored Akt activation and diminished cell growth inhibition.	Ceramides	28-36	inorganic pyrophosphatase 1	Homo sapiens	125-128
22583777-6	2012	Increased cellular level of ceramide by the co-administration induced the association between Akt and Protein Phosphatase 1 (PP1) to dephosphorylate Akt, and to introduce a constitutively active Akt (CA-Akt) restored Akt activation and diminished cell growth inhibition.	Ceramides	28-36	AKT serine/threonine kinase 1	Homo sapiens	149-152
22583777-6	2012	Increased cellular level of ceramide by the co-administration induced the association between Akt and Protein Phosphatase 1 (PP1) to dephosphorylate Akt, and to introduce a constitutively active Akt (CA-Akt) restored Akt activation and diminished cell growth inhibition.	Ceramides	28-36	AKT serine/threonine kinase 1	Homo sapiens	149-152
22609053-4	2012	We propose a mechanism through which ceramides contribute to the development of NAFLD and progression to NASH, due in part to second messenger effects via tumor necrosis factor (TNF)-alpha.	Ceramides	37-46	tumor necrosis factor	Homo sapiens	155-188
22583777-6	2012	Increased cellular level of ceramide by the co-administration induced the association between Akt and Protein Phosphatase 1 (PP1) to dephosphorylate Akt, and to introduce a constitutively active Akt (CA-Akt) restored Akt activation and diminished cell growth inhibition.	Ceramides	28-36	AKT serine/threonine kinase 1	Homo sapiens	149-152
22583777-6	2012	Increased cellular level of ceramide by the co-administration induced the association between Akt and Protein Phosphatase 1 (PP1) to dephosphorylate Akt, and to introduce a constitutively active Akt (CA-Akt) restored Akt activation and diminished cell growth inhibition.	Ceramides	28-36	AKT serine/threonine kinase 1	Homo sapiens	149-152
22718902-1	2012	We show that in Madin-Darby canine kidney (MDCK) cells, an apical ceramide-enriched compartment (ACEC) at the base of primary cilia is colocalized with Rab11a.	Ceramides	66-74	RAB11A, member RAS oncogene family	Canis lupus familiaris	152-158
22718902-2	2012	Ceramide and Rab11a vesicles isolated by magnetic sorting contain a highly similar profile of proteins (atypical protein kinase C [aPKC], Cdc42, Sec8, Rab11a, and Rab8) and ceramide species, suggesting the presence of a ciliogenic protein complex associated with ceramide at the ACEC.	Ceramides	0-8	cell division control protein 42 homolog	Canis lupus familiaris	138-143
22718902-2	2012	Ceramide and Rab11a vesicles isolated by magnetic sorting contain a highly similar profile of proteins (atypical protein kinase C [aPKC], Cdc42, Sec8, Rab11a, and Rab8) and ceramide species, suggesting the presence of a ciliogenic protein complex associated with ceramide at the ACEC.	Ceramides	0-8	RAB11A, member RAS oncogene family	Canis lupus familiaris	151-157
22718902-2	2012	Ceramide and Rab11a vesicles isolated by magnetic sorting contain a highly similar profile of proteins (atypical protein kinase C [aPKC], Cdc42, Sec8, Rab11a, and Rab8) and ceramide species, suggesting the presence of a ciliogenic protein complex associated with ceramide at the ACEC.	Ceramides	0-8	RAB8A, member RAS oncogene family	Canis lupus familiaris	163-167
22718902-3	2012	It is intriguing that C16 and C18 ceramide, although less abundant ceramide species in MDCK cells, are highly enriched in ceramide and Rab11a vesicles.	Ceramides	34-42	RAB11A, member RAS oncogene family	Canis lupus familiaris	135-141
22764099-2	2012	While investigating the mechanism of Akt inhibition, we found that short-term incubation with these compounds induced rapid shedding of cellular nanovesicles containing EGFR, IGFR and p-Akt that occurred in vitro and in vivo, while prolonged incubation led to cell detachment and death that depended on sphingomyelinase-mediated generation of ceramide.	Ceramides	343-351	AKT serine/threonine kinase 1	Homo sapiens	37-40
22605339-0	2012	Limonoid compounds inhibit sphingomyelin biosynthesis by preventing CERT protein-dependent extraction of ceramides from the endoplasmic reticulum.	Ceramides	105-114	ceramide transporter 1	Homo sapiens	68-72
22849442-6	2012	However, SMS2 but not SMS1 deficiency increased plasma ceramides.	Ceramides	55-64	sphingomyelin synthase 2	Homo sapiens	9-13
22678504-4	2012	However, so far there has been no evidence that CERKL phosphorylates ceramide or any other lipid substrate in vitro or in vivo.	Ceramides	69-77	ceramide kinase like	Homo sapiens	48-53
22764099-4	2012	Similarly, exogenous ceramide also decreased active Akt and induced nanovesicle release.	Ceramides	21-29	AKT serine/threonine kinase 1	Homo sapiens	52-55
22764099-6	2012	When transferred in vitro, PIA or Per-induced nanovesicles increased ceramide levels and death in recipient cells.	Ceramides	69-77	RPTOR independent companion of MTOR complex 2	Homo sapiens	27-30
22764099-7	2012	These results indicate ceramide generation underlies the Akt inhibition and cytotoxicity of this group of agents, and suggests nanovesicle shedding and uptake might potentially propagate their cytotoxicity in vivo.	Ceramides	23-31	AKT serine/threonine kinase 1	Homo sapiens	57-60
22673740-7	2012	PP2A can be directly activated by ceramide and SET/I2PP2A can be inhibited by ceramide.	Ceramides	34-42	protein phosphatase 2 phosphatase activator	Homo sapiens	0-4
22753704-7	2012	CERS1 knockdown was associated with global and selective decreases in ceramides and dihydroceramides, in particular C18-, C18:1- and C20-ceramide post-PDT.	Ceramides	70-79	ceramide synthase 1	Homo sapiens	0-5
22753704-7	2012	CERS1 knockdown was associated with global and selective decreases in ceramides and dihydroceramides, in particular C18-, C18:1- and C20-ceramide post-PDT.	Ceramides	70-78	ceramide synthase 1	Homo sapiens	0-5
22349266-2	2012	However, absence of a p53-mediated response does not necessarily abrogate programmed cell death, due to the existence of p53-independent apoptotic pathways, such as those mediated by the pro-apoptotic molecule ceramide.	Ceramides	210-218	tumor protein p53	Homo sapiens	22-25
22349266-2	2012	However, absence of a p53-mediated response does not necessarily abrogate programmed cell death, due to the existence of p53-independent apoptotic pathways, such as those mediated by the pro-apoptotic molecule ceramide.	Ceramides	210-218	tumor protein p53	Homo sapiens	121-124
22349266-4	2012	When treated with mitomycin C, p53-deficient cells, but not p53-expressing cells, showed a marked increase in ceramide levels.	Ceramides	110-118	tumor protein p53	Homo sapiens	31-34
22349266-5	2012	Microarray analysis of genes involved in ceramide metabolism identified acid ceramidase (ASAH1, up-regulated), ceramide glucosyltransferase (UGCG, down-regulated), and galactosylceramidase (GALC, up-regulated) as the three genes most affected.	Ceramides	41-49	N-acylsphingosine amidohydrolase 1	Homo sapiens	72-87
22349266-5	2012	Microarray analysis of genes involved in ceramide metabolism identified acid ceramidase (ASAH1, up-regulated), ceramide glucosyltransferase (UGCG, down-regulated), and galactosylceramidase (GALC, up-regulated) as the three genes most affected.	Ceramides	41-49	N-acylsphingosine amidohydrolase 1	Homo sapiens	89-94
22349266-5	2012	Microarray analysis of genes involved in ceramide metabolism identified acid ceramidase (ASAH1, up-regulated), ceramide glucosyltransferase (UGCG, down-regulated), and galactosylceramidase (GALC, up-regulated) as the three genes most affected.	Ceramides	41-49	UDP-glucose ceramide glucosyltransferase	Homo sapiens	111-139
22349266-5	2012	Microarray analysis of genes involved in ceramide metabolism identified acid ceramidase (ASAH1, up-regulated), ceramide glucosyltransferase (UGCG, down-regulated), and galactosylceramidase (GALC, up-regulated) as the three genes most affected.	Ceramides	41-49	UDP-glucose ceramide glucosyltransferase	Homo sapiens	141-145
22349266-5	2012	Microarray analysis of genes involved in ceramide metabolism identified acid ceramidase (ASAH1, up-regulated), ceramide glucosyltransferase (UGCG, down-regulated), and galactosylceramidase (GALC, up-regulated) as the three genes most affected.	Ceramides	41-49	galactosylceramidase	Homo sapiens	168-188
22349266-5	2012	Microarray analysis of genes involved in ceramide metabolism identified acid ceramidase (ASAH1, up-regulated), ceramide glucosyltransferase (UGCG, down-regulated), and galactosylceramidase (GALC, up-regulated) as the three genes most affected.	Ceramides	41-49	galactosylceramidase	Homo sapiens	190-194
22349266-6	2012	Experiments employing pharmacological and siRNA agents revealed that inhibition of UGCG is sufficient to increase ceramide levels and induce cell death.	Ceramides	114-122	UDP-glucose ceramide glucosyltransferase	Homo sapiens	83-87
22494048-3	2012	The stereochemistry of the headgroup and access to the amide group of ceramide is indispensible for Bax binding, indicating that Bax may interact with the polar portion of the ceramide channel facing the bulk phase.	Ceramides	70-78	BCL2 associated X, apoptosis regulator	Homo sapiens	100-103
22494048-3	2012	The stereochemistry of the headgroup and access to the amide group of ceramide is indispensible for Bax binding, indicating that Bax may interact with the polar portion of the ceramide channel facing the bulk phase.	Ceramides	70-78	BCL2 associated X, apoptosis regulator	Homo sapiens	129-132
22494048-3	2012	The stereochemistry of the headgroup and access to the amide group of ceramide is indispensible for Bax binding, indicating that Bax may interact with the polar portion of the ceramide channel facing the bulk phase.	Ceramides	176-184	BCL2 associated X, apoptosis regulator	Homo sapiens	100-103
22494048-3	2012	The stereochemistry of the headgroup and access to the amide group of ceramide is indispensible for Bax binding, indicating that Bax may interact with the polar portion of the ceramide channel facing the bulk phase.	Ceramides	176-184	BCL2 associated X, apoptosis regulator	Homo sapiens	129-132
22494048-5	2012	The present study also revealed that Bcl-xL has an optimal interaction with long-chain ceramides that are elevated early in apoptosis, whereas short-chain ceramides are not well regulated.	Ceramides	87-96	BCL2 like 1	Homo sapiens	37-43
22494048-7	2012	Molecular docking simulations of the lowest-energy binding poses of ceramides and Bcl-xL inhibitors to Bcl-xL were consistent with the results of our functional studies and propose potential binding modes.	Ceramides	68-77	BCL2 like 1	Homo sapiens	103-109
22579584-4	2012	We demonstrate that knockdown of ELOVL1 or CERS2, which catalyze synthesis of C24 acyl-CoAs and C24 ceramide, respectively, drastically reduced C24 sphingolipid levels with a complementary increase in C16 sphingolipids.	Ceramides	100-108	ELOVL fatty acid elongase 1	Homo sapiens	33-39
22579584-4	2012	We demonstrate that knockdown of ELOVL1 or CERS2, which catalyze synthesis of C24 acyl-CoAs and C24 ceramide, respectively, drastically reduced C24 sphingolipid levels with a complementary increase in C16 sphingolipids.	Ceramides	100-108	ceramide synthase 2	Homo sapiens	43-48
22673740-7	2012	PP2A can be directly activated by ceramide and SET/I2PP2A can be inhibited by ceramide.	Ceramides	78-86	protein phosphatase 2 phosphatase activator	Homo sapiens	0-4
22673740-7	2012	PP2A can be directly activated by ceramide and SET/I2PP2A can be inhibited by ceramide.	Ceramides	78-86	SET nuclear proto-oncogene	Homo sapiens	51-57
22673740-8	2012	Inhibition of the de novo ceramide synthase pathway blocked drug-induced ceramide generation, PP2A activation and tumor cell killing.	Ceramides	26-34	protein phosphatase 2 phosphatase activator	Homo sapiens	94-98
22586587-0	2012	Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex.	Ceramides	0-8	thymoma viral proto-oncogene 1	Mus musculus	110-113
22586587-0	2012	Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex.	Ceramides	0-8	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	66-70
22586587-5	2012	Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation.	Ceramides	49-57	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	87-101
22586587-0	2012	Ceramide mediates vascular dysfunction in diet-induced obesity by PP2A-mediated dephosphorylation of the eNOS-Akt complex.	Ceramides	0-8	nitric oxide synthase 3, endothelial cell	Mus musculus	105-109
22586587-5	2012	Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation.	Ceramides	49-57	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	103-107
22586587-5	2012	Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation.	Ceramides	49-57	nitric oxide synthase 3, endothelial cell	Mus musculus	139-172
22586587-5	2012	Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation.	Ceramides	49-57	nitric oxide synthase 3, endothelial cell	Mus musculus	174-178
22586587-5	2012	Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation.	Ceramides	49-57	thymoma viral proto-oncogene 1	Mus musculus	180-183
22586587-5	2012	Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation.	Ceramides	49-57	heat shock protein 86, pseudogene 1	Mus musculus	184-189
22586587-5	2012	Studies in endothelial cells reveal that de novo ceramide biosynthesis induced protein phosphatase 2A (PP2A) association directly with the endothelial nitric oxide synthase (eNOS)/Akt/Hsp90 complex that was concurrent with decreased basal and agonist-stimulated eNOS phosphorylation.	Ceramides	49-57	nitric oxide synthase 3, endothelial cell	Mus musculus	262-266
22586587-7	2012	Ceramide decreased the association between PP2A and the predominantly cytosolic inhibitor 2 of PP2A.	Ceramides	0-8	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	43-47
22586587-7	2012	Ceramide decreased the association between PP2A and the predominantly cytosolic inhibitor 2 of PP2A.	Ceramides	0-8	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	95-99
22586587-8	2012	We conclude that ceramide mediates obesity-related vascular dysfunction by a mechanism that involves PP2A-mediated disruption of the eNOS/Akt/Hsp90 signaling complex.	Ceramides	17-25	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	101-105
22586587-8	2012	We conclude that ceramide mediates obesity-related vascular dysfunction by a mechanism that involves PP2A-mediated disruption of the eNOS/Akt/Hsp90 signaling complex.	Ceramides	17-25	nitric oxide synthase 3, endothelial cell	Mus musculus	133-137
22586587-8	2012	We conclude that ceramide mediates obesity-related vascular dysfunction by a mechanism that involves PP2A-mediated disruption of the eNOS/Akt/Hsp90 signaling complex.	Ceramides	17-25	thymoma viral proto-oncogene 1	Mus musculus	138-141
22586587-8	2012	We conclude that ceramide mediates obesity-related vascular dysfunction by a mechanism that involves PP2A-mediated disruption of the eNOS/Akt/Hsp90 signaling complex.	Ceramides	17-25	heat shock protein 86, pseudogene 1	Mus musculus	142-147
22539351-0	2012	Ceramide levels regulated by carnitine palmitoyltransferase 1C control dendritic spine maturation and cognition.	Ceramides	0-8	carnitine palmitoyltransferase 1c	Mus musculus	29-62
22523228-3	2012	Ceramide is an essential second messenger in cells and regulates various cellular mechanisms, including PP2A activation and cytoskeleton destabilization.	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	104-108
22523228-7	2012	Furthermore, ceramide may mediate the MCLR-induced upregulation of PP2A activity and protein level of PP2A regulatory subunits in HEK293 cells.	Ceramides	13-21	protein phosphatase 2 phosphatase activator	Homo sapiens	67-71
22523228-7	2012	Furthermore, ceramide may mediate the MCLR-induced upregulation of PP2A activity and protein level of PP2A regulatory subunits in HEK293 cells.	Ceramides	13-21	protein phosphatase 2 phosphatase activator	Homo sapiens	102-106
22523228-10	2012	Our results suggest that ceramide may mediate MCLR-induced PP2A regulation and cytoskeleton destabilization.	Ceramides	25-33	protein phosphatase 2 phosphatase activator	Homo sapiens	59-63
22579584-8	2012	Apoptosis induced by UV radiation or C6 ceramides also increased in ELOVL1 or CERS2 knockdown cells.	Ceramides	40-49	ELOVL fatty acid elongase 1	Homo sapiens	68-74
22579584-8	2012	Apoptosis induced by UV radiation or C6 ceramides also increased in ELOVL1 or CERS2 knockdown cells.	Ceramides	40-49	ceramide synthase 2	Homo sapiens	78-83
22523228-0	2012	Microcystin-LR induces ceramide to regulate PP2A and destabilize cytoskeleton in HEK293 cells.	Ceramides	23-31	protein phosphatase 2 phosphatase activator	Homo sapiens	44-48
22993865-0	2012	[Effect of ceramide on GSTA1 in Caco-2 cells].	Ceramides	11-19	glutathione S-transferase alpha 1	Homo sapiens	23-28
22993865-1	2012	This study is to investigate the effects of ceramide on GSTA1 expression in Caco-2 cells.	Ceramides	44-52	glutathione S-transferase alpha 1	Homo sapiens	56-61
22993865-3	2012	The data showed that ceramide can significantly induce the expression of protein and GSTA1 mRNA, and increase transcriptional activity and enzyme activity of GSTA1.	Ceramides	21-29	glutathione S-transferase alpha 1	Homo sapiens	85-90
22993865-3	2012	The data showed that ceramide can significantly induce the expression of protein and GSTA1 mRNA, and increase transcriptional activity and enzyme activity of GSTA1.	Ceramides	21-29	glutathione S-transferase alpha 1	Homo sapiens	158-163
22993865-4	2012	The results demonstrated that ceramide may increase resistance to chemotherapeutics in Caco-2 cells by up-regulating the expression of GSTA1.	Ceramides	30-38	glutathione S-transferase alpha 1	Homo sapiens	135-140
22532571-3	2012	Apoptosis was also prevented by shRNA-mediated down-regulation of PAR-4, a protein sensitizing cells to the sphingolipid ceramide.	Ceramides	121-129	pro-apoptotic WT1 regulator	Homo sapiens	66-71
22532571-11	2012	Taken together, we report a novel mechanism of apoptosis induction by PAR-4/ceramide-enriched exosomes, which may critically contribute to Alzheimer disease.	Ceramides	76-84	pro-apoptotic WT1 regulator	Homo sapiens	70-75
22539351-5	2012	First, we analyzed the implication of CPT1C in ceramide metabolism.	Ceramides	47-55	carnitine palmitoyltransferase 1c	Mus musculus	38-43
22532571-5	2012	Apoptosis was not observed in astrocytes with deficient neutral sphingomyelinase 2 (nSMase2), indicating that ceramide generated by nSMase2 is critical for amyloid-induced apoptosis.	Ceramides	110-118	sphingomyelin phosphodiesterase 3	Homo sapiens	132-139
22539351-6	2012	CPT1C overexpression in primary hippocampal cultured neurons increased ceramide levels, whereas in CPT1C-deficient neurons, ceramide levels were diminished.	Ceramides	71-79	carnitine palmitoyltransferase 1c	Mus musculus	0-5
22532571-6	2012	Antibodies against PAR-4 and ceramide prevented amyloid-induced apoptosis in vitro and in vivo, suggesting that apoptosis was mediated by exogenous PAR-4 and ceramide, potentially associated with secreted lipid vesicles.	Ceramides	158-166	pro-apoptotic WT1 regulator	Homo sapiens	19-24
22532571-8	2012	Exosomes were not secreted by nSMase2-deficient astrocytes, indicating that ceramide generated by nSMase2 is critical for exosome secretion.	Ceramides	76-84	sphingomyelin phosphodiesterase 3	Homo sapiens	98-105
22539351-6	2012	CPT1C overexpression in primary hippocampal cultured neurons increased ceramide levels, whereas in CPT1C-deficient neurons, ceramide levels were diminished.	Ceramides	124-132	carnitine palmitoyltransferase 1c	Mus musculus	0-5
22532571-10	2012	Moreover, isolated PAR-4/ceramide-enriched exosomes were taken up by astrocytes and induced apoptosis in the absence of amyloid peptide.	Ceramides	25-33	pro-apoptotic WT1 regulator	Homo sapiens	19-24
22539351-7	2012	Correspondingly, CPT1C knock-out (KO) mice showed reduced ceramide levels in the hippocampus.	Ceramides	58-66	carnitine palmitoyltransferase 1c	Mus musculus	17-22
22539351-10	2012	Treatment of cultured neurons with exogenous ceramide reverted the KO phenotype, as did ectopic overexpression of CPT1C, indicating that CPT1C regulation of spine maturation is mediated by ceramide.	Ceramides	45-53	carnitine palmitoyltransferase 1c	Mus musculus	137-142
22539351-10	2012	Treatment of cultured neurons with exogenous ceramide reverted the KO phenotype, as did ectopic overexpression of CPT1C, indicating that CPT1C regulation of spine maturation is mediated by ceramide.	Ceramides	189-197	carnitine palmitoyltransferase 1c	Mus musculus	137-142
22539351-13	2012	All of these results demonstrate that CPT1C regulates the levels of ceramide in the endoplasmic reticulum of hippocampal neurons, and this is a relevant mechanism for the correct maturation of dendritic spines and for proper spatial learning.	Ceramides	68-76	carnitine palmitoyltransferase 1c	Mus musculus	38-43
22472120-4	2012	CERT transfers ceramide from the endoplasmic reticulum to the Golgi complex for conversion into sphingomyelin (SM).	Ceramides	15-23	ceramide transporter 1	Homo sapiens	0-4
22586279-4	2012	Systemic insulin resistance in heart failure was accompanied by decreased myocardial triglyceride and overall fatty acid content but increased toxic lipid intermediates, diacylglycerol, and ceramide.	Ceramides	190-198	insulin	Homo sapiens	9-16
22574859-7	2012	MX1 partially colocalized with exosomal protein CD63, and a ceramide inhibitor reduced numbers of MX1-associated exosomes.	Ceramides	60-68	MX dynamin like GTPase 1	Bos taurus	98-101
21935601-2	2012	Acid ceramidase (AC) hydrolyzes ceramide, and thus reduces intracellular levels of this proapoptotic lipid.	Ceramides	32-40	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
22271589-2	2012	This work was undertaken to study the role of ceramide and its metabolites in TNF-alpha action.	Ceramides	46-54	tumor necrosis factor	Homo sapiens	78-87
22112438-9	2012	T-bet expression was also decreased by NS-398 treatment, thereby indicating that C6 ceramide enhances Th1 responses via a COX-2 dependent pathway.	Ceramides	84-92	T-box transcription factor 21	Homo sapiens	0-5
22112438-9	2012	T-bet expression was also decreased by NS-398 treatment, thereby indicating that C6 ceramide enhances Th1 responses via a COX-2 dependent pathway.	Ceramides	84-92	complement C6	Homo sapiens	81-83
22112438-9	2012	T-bet expression was also decreased by NS-398 treatment, thereby indicating that C6 ceramide enhances Th1 responses via a COX-2 dependent pathway.	Ceramides	84-92	prostaglandin-endoperoxide synthase 2	Homo sapiens	122-127
22451680-1	2012	Neutral ceramidase (NCDase) is considered to be a critical enzyme for controlling the turnover of ceramide, an important bioactive lipid, which determines cell"s fate.	Ceramides	98-106	N-acylsphingosine amidohydrolase 2	Homo sapiens	0-18
22451680-1	2012	Neutral ceramidase (NCDase) is considered to be a critical enzyme for controlling the turnover of ceramide, an important bioactive lipid, which determines cell"s fate.	Ceramides	98-106	N-acylsphingosine amidohydrolase 2	Homo sapiens	20-26
22451680-5	2012	We examined whether the down-regulation of NCDase was involved in the increase in ceramide and cell differentiation.	Ceramides	82-90	N-acylsphingosine amidohydrolase 2	Homo sapiens	43-49
22451680-10	2012	These results demonstrate that down-regulation of NCDase through ATRA-induced GATA-2 decrease plays an important role in induction of ceramide accumulation and neuronal differentiation in SH-SY5Y cells.	Ceramides	134-142	N-acylsphingosine amidohydrolase 2	Homo sapiens	50-56
22451680-10	2012	These results demonstrate that down-regulation of NCDase through ATRA-induced GATA-2 decrease plays an important role in induction of ceramide accumulation and neuronal differentiation in SH-SY5Y cells.	Ceramides	134-142	GATA binding protein 2	Homo sapiens	78-84
22230689-3	2012	We established in neuronal cells that TNFalpha exposure dramatically increased Mg(2+)-dependent neutral sphingomyelinase (nSMase) activity thus generating the bioactive lipid mediator ceramide essential for subsequent NADPH oxidase (NOX) activation and oxidative stress.	Ceramides	184-192	tumor necrosis factor	Homo sapiens	38-46
22230689-3	2012	We established in neuronal cells that TNFalpha exposure dramatically increased Mg(2+)-dependent neutral sphingomyelinase (nSMase) activity thus generating the bioactive lipid mediator ceramide essential for subsequent NADPH oxidase (NOX) activation and oxidative stress.	Ceramides	184-192	sphingomyelin phosphodiesterase 2	Homo sapiens	122-128
22230689-4	2012	Since many of the pleiotropic effects of ceramide are attributable to its metabolites, we examined whether ceramide kinase (CerK), converting ceramide to ceramide-1-phosphate, is implicated both in NOX activation and enhanced eicosanoid production in neuronal cells.	Ceramides	107-115	ceramide kinase	Homo sapiens	124-128
22155483-2	2012	We previously studied microRNAs (miRNAs) in AD autopsy brain samples and reported a connection between miR-137, -181c, -9, -29a/b and AD, through the regulation of ceramides.	Ceramides	164-173	microRNA 137	Homo sapiens	103-129
22425588-1	2012	Data from studies in animal models indicate that certain lipid metabolites, particularly diacylglycerol, ceramide, and acylcarnitine, disrupt insulin action.	Ceramides	105-113	insulin	Homo sapiens	142-149
22469869-2	2012	Evidence is accumulating that ceramide, generated by acid sphingomyelinase (aSMase), and sphingosine-1-phosphate (S1-P) are important mediators in host defence as well as in pathologic processes of acute lung injury.	Ceramides	30-38	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	53-74
22393932-2	2012	In this study, we examined whether the formation of sphingosine 1-phosphate (S1P), a ceramide metabolite, is associated with this apoptotic pathway.	Ceramides	85-93	sphingosine-1-phosphate receptor 1	Mus musculus	77-80
22454477-5	2012	In the present study, we show that TNF/CHX increase lysosomal ceramide that is subsequently converted into sphingosine.	Ceramides	62-70	tumor necrosis factor	Rattus norvegicus	35-38
22469869-2	2012	Evidence is accumulating that ceramide, generated by acid sphingomyelinase (aSMase), and sphingosine-1-phosphate (S1-P) are important mediators in host defence as well as in pathologic processes of acute lung injury.	Ceramides	30-38	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	76-82
22493506-3	2012	Heart-specific Sptlc2-deficient (hSptlc2 KO) mice had a >35% reduction in ceramide, which was limited to C18:0 and very long chain ceramides.	Ceramides	77-85	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	15-21
22706115-10	2012	The ceramide pathway can directly stimulate biochemical changes in the brain noted at the onset of disease: tau overphosphorylation and beta-amyloid peptide accumulation.	Ceramides	4-12	microtubule associated protein tau	Homo sapiens	108-111
22706115-10	2012	The ceramide pathway can directly stimulate biochemical changes in the brain noted at the onset of disease: tau overphosphorylation and beta-amyloid peptide accumulation.	Ceramides	4-12	amyloid beta precursor protein	Homo sapiens	136-156
22493506-3	2012	Heart-specific Sptlc2-deficient (hSptlc2 KO) mice had a >35% reduction in ceramide, which was limited to C18:0 and very long chain ceramides.	Ceramides	77-85	serine palmitoyltransferase long chain base subunit 2	Homo sapiens	33-40
22493506-3	2012	Heart-specific Sptlc2-deficient (hSptlc2 KO) mice had a >35% reduction in ceramide, which was limited to C18:0 and very long chain ceramides.	Ceramides	134-143	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	15-21
22493506-9	2012	These results suggest that Sptlc2-mediated de novo ceramide synthesis is an essential source of C18:0 and very long chain, but not of shorter chain, ceramides in the heart.	Ceramides	51-59	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	27-33
22493506-9	2012	These results suggest that Sptlc2-mediated de novo ceramide synthesis is an essential source of C18:0 and very long chain, but not of shorter chain, ceramides in the heart.	Ceramides	149-158	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	27-33
22661954-5	2012	In addition, we describe the current understanding about the mechanism of P2X(7)-dependent MV formation and membrane abscission, which, by involving sphingomyelinase activity and ceramide formation, may share similarities with exosome biogenesis.	Ceramides	179-187	purinergic receptor P2X 7	Homo sapiens	74-80
22783238-4	2012	Previously we reported that the sphingolipid pathway gene, ISC1, which is responsible for ceramide production, is a major virulence factor in Cn infection.	Ceramides	90-98	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	59-63
22328531-8	2012	The sphingolipid intermediates (long chain base and ceramide) are decreased when ORM2 is overexpressed, suggesting that sphingolipid synthesis is repressed under ER stress conditions.	Ceramides	52-60	sphingolipid homeostasis protein ORM2	Saccharomyces cerevisiae S288C	81-85
22474281-2	2012	Recent in vitro data indicate that fenretinide inhibits dihydroceramide desaturase, an enzyme involved in the biosynthesis of lipotoxic ceramides that antagonize insulin action.	Ceramides	136-145	delta(4)-desaturase, sphingolipid 1	Mus musculus	56-82
22465662-1	2012	Ceramide kinase (CERK) is an enzyme that phosphorylates ceramide to produce ceramide 1-phosphate.	Ceramides	56-64	ceramide kinase	Mus musculus	0-15
22507982-5	2012	Co-administration of ceramide (C6) and genistein induced a significant Akt inhibition and c-jun-NH(2)-kinase (JNK) activation, caspase-3 cleavage and cytochrome c release.	Ceramides	21-29	thymoma viral proto-oncogene 1	Mus musculus	71-74
22507982-5	2012	Co-administration of ceramide (C6) and genistein induced a significant Akt inhibition and c-jun-NH(2)-kinase (JNK) activation, caspase-3 cleavage and cytochrome c release.	Ceramides	21-29	mitogen-activated protein kinase 8	Mus musculus	90-108
22507982-5	2012	Co-administration of ceramide (C6) and genistein induced a significant Akt inhibition and c-jun-NH(2)-kinase (JNK) activation, caspase-3 cleavage and cytochrome c release.	Ceramides	21-29	mitogen-activated protein kinase 8	Mus musculus	110-113
22507982-5	2012	Co-administration of ceramide (C6) and genistein induced a significant Akt inhibition and c-jun-NH(2)-kinase (JNK) activation, caspase-3 cleavage and cytochrome c release.	Ceramides	21-29	caspase 3	Mus musculus	127-136
22507982-6	2012	Caspase-3 inhibitor z-DVED-fmk, JNK inhibitor SP 600125, or to restore Akt activation by introducing a constitutively active form of Akt (CA-Akt) diminished ceramide (C6) and genistein co-administration-induced in vitro anti-melanoma effect.	Ceramides	157-165	caspase 3	Mus musculus	0-9
22507982-6	2012	Caspase-3 inhibitor z-DVED-fmk, JNK inhibitor SP 600125, or to restore Akt activation by introducing a constitutively active form of Akt (CA-Akt) diminished ceramide (C6) and genistein co-administration-induced in vitro anti-melanoma effect.	Ceramides	157-165	thymoma viral proto-oncogene 1	Mus musculus	71-74
22507982-6	2012	Caspase-3 inhibitor z-DVED-fmk, JNK inhibitor SP 600125, or to restore Akt activation by introducing a constitutively active form of Akt (CA-Akt) diminished ceramide (C6) and genistein co-administration-induced in vitro anti-melanoma effect.	Ceramides	157-165	thymoma viral proto-oncogene 1	Mus musculus	133-136
22507982-6	2012	Caspase-3 inhibitor z-DVED-fmk, JNK inhibitor SP 600125, or to restore Akt activation by introducing a constitutively active form of Akt (CA-Akt) diminished ceramide (C6) and genistein co-administration-induced in vitro anti-melanoma effect.	Ceramides	157-165	thymoma viral proto-oncogene 1	Mus musculus	138-144
22465662-1	2012	Ceramide kinase (CERK) is an enzyme that phosphorylates ceramide to produce ceramide 1-phosphate.	Ceramides	56-64	ceramide kinase	Mus musculus	17-21
22328778-0	2012	Intercellular adhesion molecule 1 engagement modulates sphingomyelinase and ceramide, supporting uptake of drug carriers by the vascular endothelium.	Ceramides	76-84	intercellular adhesion molecule 1	Mus musculus	0-33
22560211-0	2012	A ceramide-centric view of insulin resistance.	Ceramides	2-10	insulin	Homo sapiens	27-34
22560211-2	2012	In this review, we discuss from a historical perspective the most important discoveries produced over the last decade supporting a role for ceramide and its metabolites in the pathogenesis of insulin resistance and other obesity-associated metabolic diseases.	Ceramides	140-148	insulin	Homo sapiens	192-199
22560211-3	2012	Moreover, we describe how a ceramide-centric view of insulin resistance might be reconciled in the context of other prominent models of nutrient-induced insulin resistance.	Ceramides	28-36	insulin	Homo sapiens	53-60
22328778-7	2012	Acid sphingomyelinase (ASM), an acidic enzyme that hydrolyzes sphingomyelin into ceramide (involved in plasmalemma deformability and cytoskeletal reorganization), redistributed to ICAM-1-engagement sites at ceramide-enriched areas.	Ceramides	81-89	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
22328778-7	2012	Acid sphingomyelinase (ASM), an acidic enzyme that hydrolyzes sphingomyelin into ceramide (involved in plasmalemma deformability and cytoskeletal reorganization), redistributed to ICAM-1-engagement sites at ceramide-enriched areas.	Ceramides	81-89	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
22328778-7	2012	Acid sphingomyelinase (ASM), an acidic enzyme that hydrolyzes sphingomyelin into ceramide (involved in plasmalemma deformability and cytoskeletal reorganization), redistributed to ICAM-1-engagement sites at ceramide-enriched areas.	Ceramides	81-89	intercellular adhesion molecule 1	Mus musculus	180-186
22328778-7	2012	Acid sphingomyelinase (ASM), an acidic enzyme that hydrolyzes sphingomyelin into ceramide (involved in plasmalemma deformability and cytoskeletal reorganization), redistributed to ICAM-1-engagement sites at ceramide-enriched areas.	Ceramides	207-215	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
22328778-7	2012	Acid sphingomyelinase (ASM), an acidic enzyme that hydrolyzes sphingomyelin into ceramide (involved in plasmalemma deformability and cytoskeletal reorganization), redistributed to ICAM-1-engagement sites at ceramide-enriched areas.	Ceramides	207-215	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
22328778-7	2012	Acid sphingomyelinase (ASM), an acidic enzyme that hydrolyzes sphingomyelin into ceramide (involved in plasmalemma deformability and cytoskeletal reorganization), redistributed to ICAM-1-engagement sites at ceramide-enriched areas.	Ceramides	207-215	intercellular adhesion molecule 1	Mus musculus	180-186
22328778-9	2012	Inhibiting ASM impaired ceramide enrichment, engulfment structures, cytoskeletal reorganization, and carrier uptake, which was rescued by supplying this enzyme activity exogenously.	Ceramides	24-32	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	11-14
22328778-11	2012	CONCLUSIONS: These findings are consistent with the ability of endothelial cells to internalize relatively large ICAM- 1--targeted drug carriers and expand our knowledge on the regulation of the sphingomyelin/ceramide pathway by the vascular endothelium.	Ceramides	209-217	intercellular adhesion molecule 1	Mus musculus	113-120
22236141-4	2012	Sphingomyelin is a major constituent of cell membranes and lipoprotein particles and acid sphingomyelinase (ASMase) hydrolyses sphingomyelin to generate the bioactive lipid ceramide.	Ceramides	173-181	sphingomyelin phosphodiesterase 1	Homo sapiens	85-106
22103431-5	2012	We found that three related ceramide analogue GSL inhibitors, based on the PDMP (D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol) structure, reduced cellular Abeta production and in all cases this was correlated with inhibition of pERK (phosphorylated ERK) formation.	Ceramides	28-36	mitogen-activated protein kinase 1	Homo sapiens	241-244
22236141-4	2012	Sphingomyelin is a major constituent of cell membranes and lipoprotein particles and acid sphingomyelinase (ASMase) hydrolyses sphingomyelin to generate the bioactive lipid ceramide.	Ceramides	173-181	sphingomyelin phosphodiesterase 1	Homo sapiens	108-114
22452947-0	2012	Off-target function of the Sonic hedgehog inhibitor cyclopamine in mediating apoptosis via nitric oxide-dependent neutral sphingomyelinase 2/ceramide induction.	Ceramides	141-149	sonic hedgehog signaling molecule	Homo sapiens	27-41
22466649-6	2012	Moreover, we report the generation of 2A2, an anti-ceramide monoclonal antibody that binds to ceramide to prevent platform formation on the surface of irradiated endothelial cells of the murine GI tract.	Ceramides	51-59	serine (or cysteine) peptidase inhibitor, clade A, member 3G	Mus musculus	38-41
22466649-6	2012	Moreover, we report the generation of 2A2, an anti-ceramide monoclonal antibody that binds to ceramide to prevent platform formation on the surface of irradiated endothelial cells of the murine GI tract.	Ceramides	94-102	serine (or cysteine) peptidase inhibitor, clade A, member 3G	Mus musculus	38-41
22466649-8	2012	As such, we suggest that 2A2 represents a prototype of a new class of anti-ceramide therapeutics and an effective countermeasure against radiation GI syndrome mortality.	Ceramides	75-83	serine (or cysteine) peptidase inhibitor, clade A, member 3G	Mus musculus	25-28
22445853-2	2012	Isc1p functions upstream of the ceramide-activated protein phosphatase Sit4p through the modulation of ceramide levels.	Ceramides	32-40	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	0-5
22522453-8	2012	Inhibition of the PI3K or atypical PKC pathway induced a dramatic loss of SAP155 complex formation at ceramide-responsive RNA cis-element 1.	Ceramides	102-110	protein kinase C zeta	Homo sapiens	35-38
22445853-2	2012	Isc1p functions upstream of the ceramide-activated protein phosphatase Sit4p through the modulation of ceramide levels.	Ceramides	32-40	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	71-76
22445853-3	2012	Here, we show that both ceramide and loss of Isc1p lead to the activation of Hog1p, the MAPK of the high osmolarity glycerol (HOG) pathway that is functionally related to mammalian p38 and JNK.	Ceramides	24-32	mitogen-activated protein kinase HOG1	Saccharomyces cerevisiae S288C	77-82
22445853-3	2012	Here, we show that both ceramide and loss of Isc1p lead to the activation of Hog1p, the MAPK of the high osmolarity glycerol (HOG) pathway that is functionally related to mammalian p38 and JNK.	Ceramides	24-32	mitogen-activated protein kinase 14	Homo sapiens	181-184
22445853-3	2012	Here, we show that both ceramide and loss of Isc1p lead to the activation of Hog1p, the MAPK of the high osmolarity glycerol (HOG) pathway that is functionally related to mammalian p38 and JNK.	Ceramides	24-32	mitogen-activated protein kinase 8	Homo sapiens	189-192
22522453-8	2012	Inhibition of the PI3K or atypical PKC pathway induced a dramatic loss of SAP155 complex formation at ceramide-responsive RNA cis-element 1.	Ceramides	102-110	splicing factor 3b subunit 1	Homo sapiens	74-80
22452947-4	2012	Here, we report that cyclopamine mediates ceramide generation selectively via induction of neutral sphingomyelin phosphodiesterase 3, SMPD3 (nSMase2) in Daoy human medulloblastoma cells.	Ceramides	42-50	sphingomyelin phosphodiesterase 3	Homo sapiens	134-139
22452947-4	2012	Here, we report that cyclopamine mediates ceramide generation selectively via induction of neutral sphingomyelin phosphodiesterase 3, SMPD3 (nSMase2) in Daoy human medulloblastoma cells.	Ceramides	42-50	sphingomyelin phosphodiesterase 3	Homo sapiens	141-148
22452947-5	2012	Importantly, short interfering RNA-mediated knockdown of nSMase2 prevented cyclopamine-induced ceramide generation and protected Daoy cells from drug-induced apoptosis.	Ceramides	95-103	sphingomyelin phosphodiesterase 3	Homo sapiens	57-64
22257159-4	2012	We also found that EGCG induces aSMase translocation to the plasma membrane and PKCdelta (protein kinase Cdelta) phosphorylation at Ser664, which was necessary for aSMase/ceramide signalling via 67LR.	Ceramides	171-179	protein kinase C, delta	Mus musculus	80-88
22210893-4	2012	Previously, water-insoluble ceramides were shown to change alternative splicing and decrease SR-protein phosphorylation by activating protein phosphatase-1 (PP1).	Ceramides	28-37	RNA binding protein with serine rich domain 1	Homo sapiens	93-103
22210893-4	2012	Previously, water-insoluble ceramides were shown to change alternative splicing and decrease SR-protein phosphorylation by activating protein phosphatase-1 (PP1).	Ceramides	28-37	inorganic pyrophosphatase 1	Homo sapiens	134-155
22210893-4	2012	Previously, water-insoluble ceramides were shown to change alternative splicing and decrease SR-protein phosphorylation by activating protein phosphatase-1 (PP1).	Ceramides	28-37	inorganic pyrophosphatase 1	Homo sapiens	157-160
22812004-6	2012	Puerarin restrains the ceramide accumulation to block downstream p38 MAPK pathway and calcium ion rising, therefore reduces DNA damage in HaCaT cells induced by UVB.	Ceramides	23-31	mitogen-activated protein kinase 14	Homo sapiens	65-68
22383528-6	2012	We then showed that in fro/fro fibroblasts, the reduced ceramide was associated with decreased phosphorylation of protein phosphatase 2A (PP2A) and increased phosphorylation of its substrate Akt-p, together with PI3K, PDK1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.	Ceramides	56-64	protein phosphatase 2 phosphatase activator	Homo sapiens	138-142
22383528-6	2012	We then showed that in fro/fro fibroblasts, the reduced ceramide was associated with decreased phosphorylation of protein phosphatase 2A (PP2A) and increased phosphorylation of its substrate Akt-p, together with PI3K, PDK1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.	Ceramides	56-64	AKT serine/threonine kinase 1	Homo sapiens	191-194
22383528-6	2012	We then showed that in fro/fro fibroblasts, the reduced ceramide was associated with decreased phosphorylation of protein phosphatase 2A (PP2A) and increased phosphorylation of its substrate Akt-p, together with PI3K, PDK1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.	Ceramides	56-64	pyruvate dehydrogenase kinase 1	Homo sapiens	218-222
22383528-6	2012	We then showed that in fro/fro fibroblasts, the reduced ceramide was associated with decreased phosphorylation of protein phosphatase 2A (PP2A) and increased phosphorylation of its substrate Akt-p, together with PI3K, PDK1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.	Ceramides	56-64	mechanistic target of rapamycin kinase	Homo sapiens	224-228
22383528-6	2012	We then showed that in fro/fro fibroblasts, the reduced ceramide was associated with decreased phosphorylation of protein phosphatase 2A (PP2A) and increased phosphorylation of its substrate Akt-p, together with PI3K, PDK1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.	Ceramides	56-64	mechanistic target of rapamycin kinase	Homo sapiens	230-259
22383528-6	2012	We then showed that in fro/fro fibroblasts, the reduced ceramide was associated with decreased phosphorylation of protein phosphatase 2A (PP2A) and increased phosphorylation of its substrate Akt-p, together with PI3K, PDK1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.	Ceramides	56-64	ribosomal protein S6 kinase B1	Homo sapiens	266-272
22383528-6	2012	We then showed that in fro/fro fibroblasts, the reduced ceramide was associated with decreased phosphorylation of protein phosphatase 2A (PP2A) and increased phosphorylation of its substrate Akt-p, together with PI3K, PDK1, mTOR (mammalian target of rapamycin), and p70S6K, although PTEN was unaffected.	Ceramides	56-64	phosphatase and tensin homolog	Homo sapiens	283-287
22383528-7	2012	Exogenous ceramide, as well as inhibitors of Akt (Akt inhibitor VIII), PI 3-kinase (LY294002 and wortmannin), and mTOR (rapamycin) reduced secretion of HA, whereas the NSMase2 inhibitor GW4869 increased HA synthesis and secretion.	Ceramides	10-18	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	168-175
22383528-0	2012	Neutral sphingomyelinase 2 deficiency increases hyaluronan synthesis by up-regulation of Hyaluronan synthase 2 through decreased ceramide production and activation of Akt.	Ceramides	129-137	hyaluronan synthase 2	Mus musculus	89-110
22383528-3	2012	The deficiency of NSMase2 resulted in storage of sphingomyelin (SM) and cholesterol with a 50% reduction in ceramides (Cer).	Ceramides	108-117	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	18-25
22383528-3	2012	The deficiency of NSMase2 resulted in storage of sphingomyelin (SM) and cholesterol with a 50% reduction in ceramides (Cer).	Ceramides	119-122	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	18-25
22257159-4	2012	We also found that EGCG induces aSMase translocation to the plasma membrane and PKCdelta (protein kinase Cdelta) phosphorylation at Ser664, which was necessary for aSMase/ceramide signalling via 67LR.	Ceramides	171-179	protein kinase C, delta	Mus musculus	90-111
22257159-4	2012	We also found that EGCG induces aSMase translocation to the plasma membrane and PKCdelta (protein kinase Cdelta) phosphorylation at Ser664, which was necessary for aSMase/ceramide signalling via 67LR.	Ceramides	171-179	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	164-170
22257159-4	2012	We also found that EGCG induces aSMase translocation to the plasma membrane and PKCdelta (protein kinase Cdelta) phosphorylation at Ser664, which was necessary for aSMase/ceramide signalling via 67LR.	Ceramides	171-179	ribosomal protein SA	Mus musculus	195-199
22432895-4	2012	(3S,4R,5S,6R,7R)-1-Nonylazocane-3,4,5,6,7-pentaol (6) was moderately active against rat-derived ceramide-specific glucosyltransferase, and four of the other eight-membered analogues were weakly active against rat-derived beta-glucosidase 2.	Ceramides	96-104	glucosylceramidase beta 2	Rattus norvegicus	221-239
22306364-0	2012	Ordering of ceramide formation and caspase-9 activation in CD95L-induced Jurkat leukemia T cell apoptosis.	Ceramides	12-20	Fas ligand	Homo sapiens	59-64
22306364-5	2012	Knock-down of sphingomyelin synthase 1, which metabolizes ceramide to sphingomyelin, enhanced (i) CD95L-triggered ceramide production, (ii) cytochrome c release from the mitochondria and (iii) caspase-9 activation.	Ceramides	114-122	sphingomyelin synthase 1	Homo sapiens	14-38
22428532-3	2012	LC-MS analysis of sphingolipids revealed that in human leukemia CCRF-CEM and Jurkat cells, 4-HPR induced dihydroceramide but not ceramide accumulation even at sublethal concentrations.	Ceramides	112-120	haptoglobin-related protein	Homo sapiens	93-96
22306364-1	2012	Ceramide, a biologically active sphingolipid in cell death signaling, accumulates upon CD95L treatment, concomitantly to apoptosis induction in Jurkat leukemia T cells.	Ceramides	0-8	Fas ligand	Homo sapiens	87-92
22306364-5	2012	Knock-down of sphingomyelin synthase 1, which metabolizes ceramide to sphingomyelin, enhanced (i) CD95L-triggered ceramide production, (ii) cytochrome c release from the mitochondria and (iii) caspase-9 activation.	Ceramides	114-122	Fas ligand	Homo sapiens	98-103
22306364-6	2012	Exogenous ceramide-induced caspase-3 activation and apoptosis were impaired in caspase-9-deficient Jurkat cells.	Ceramides	10-18	caspase 3	Homo sapiens	27-36
22306364-2	2012	Herein, we show that ceramide did not increase in caspase-8 and -10-doubly deficient Jurkat cells in response to CD95L, indicating that apical caspases are essential for CD95L-triggered ceramide formation.	Ceramides	186-194	Fas ligand	Homo sapiens	170-175
22306364-6	2012	Exogenous ceramide-induced caspase-3 activation and apoptosis were impaired in caspase-9-deficient Jurkat cells.	Ceramides	10-18	caspase 9	Homo sapiens	79-88
22306364-4	2012	Caspase-9-deficient Jurkat cells significantly resisted CD95L-induced apoptosis, despite ceramide accumulation.	Ceramides	89-97	caspase 9	Homo sapiens	0-9
22306364-7	2012	Conversely, caspase-9 re-expression in caspase-9-deficient Jurkat cells restored caspase-3 activation and apoptosis upon exogenous ceramide treatment.	Ceramides	131-139	caspase 9	Homo sapiens	12-21
22306364-7	2012	Conversely, caspase-9 re-expression in caspase-9-deficient Jurkat cells restored caspase-3 activation and apoptosis upon exogenous ceramide treatment.	Ceramides	131-139	caspase 9	Homo sapiens	39-48
22306364-5	2012	Knock-down of sphingomyelin synthase 1, which metabolizes ceramide to sphingomyelin, enhanced (i) CD95L-triggered ceramide production, (ii) cytochrome c release from the mitochondria and (iii) caspase-9 activation.	Ceramides	58-66	sphingomyelin synthase 1	Homo sapiens	14-38
22306364-7	2012	Conversely, caspase-9 re-expression in caspase-9-deficient Jurkat cells restored caspase-3 activation and apoptosis upon exogenous ceramide treatment.	Ceramides	131-139	caspase 3	Homo sapiens	81-90
22306364-8	2012	Collectively, our data provide genetic evidence that CD95L-triggered endogenous ceramide increase in Jurkat leukemia T cells (i) is not a mere consequence of cell death and occurs mainly in a caspase-9-independent manner, (ii) is likely involved in the pro-apoptotic mitochondrial pathway leading to caspase-9 activation.	Ceramides	80-88	Fas ligand	Homo sapiens	53-58
22306364-5	2012	Knock-down of sphingomyelin synthase 1, which metabolizes ceramide to sphingomyelin, enhanced (i) CD95L-triggered ceramide production, (ii) cytochrome c release from the mitochondria and (iii) caspase-9 activation.	Ceramides	58-66	Fas ligand	Homo sapiens	98-103
22306364-8	2012	Collectively, our data provide genetic evidence that CD95L-triggered endogenous ceramide increase in Jurkat leukemia T cells (i) is not a mere consequence of cell death and occurs mainly in a caspase-9-independent manner, (ii) is likely involved in the pro-apoptotic mitochondrial pathway leading to caspase-9 activation.	Ceramides	80-88	caspase 9	Homo sapiens	192-201
22306364-8	2012	Collectively, our data provide genetic evidence that CD95L-triggered endogenous ceramide increase in Jurkat leukemia T cells (i) is not a mere consequence of cell death and occurs mainly in a caspase-9-independent manner, (ii) is likely involved in the pro-apoptotic mitochondrial pathway leading to caspase-9 activation.	Ceramides	80-88	caspase 9	Homo sapiens	300-309
22230369-6	2012	To clarify the impact of this observation, we manipulated cellular ceramide levels by overexpressing ceramide synthases 2, 4 or 6 in MCF-7 (breast cancer) and HCT-116 (colon cancer) cells, respectively.	Ceramides	67-75	ceramide synthase 2	Homo sapiens	101-129
22467388-9	2012	Recombinant hTFF2 could also inhibit apoptosis of HCT-116 cells induced by 50 mumol/L ceramide.	Ceramides	86-94	trefoil factor 2	Homo sapiens	12-17
22176347-2	2012	We hypothesized that in NAFLD, insulin resistance dysregulates lipid metabolism, increasing production of cytotoxic lipids including ceramides, which exacerbate hepatic insulin resistance and injury.	Ceramides	133-142	insulin	Homo sapiens	31-38
22176347-7	2012	Ceramide treatment impaired Huh7 cell viability, mitochondrial function, and insulin signaling.	Ceramides	0-8	insulin	Homo sapiens	77-84
22176347-8	2012	CONCLUSIONS:   Increased hepatic ceramide generation and release may mediate both hepatic and peripheral insulin resistance in NAFLD.	Ceramides	33-41	insulin	Homo sapiens	105-112
22384976-0	2012	The plant defensin RsAFP2 induces cell wall stress, septin mislocalization and accumulation of ceramides in Candida albicans.	Ceramides	95-104	defensin-like protein 2	Raphanus sativus	19-25
21773940-0	2012	Temporal expression profiles of ceramide and ceramide-related genes in wild-type and mPer1/mPer2 double knockout mice.	Ceramides	32-40	period circadian clock 1	Mus musculus	85-90
21773940-0	2012	Temporal expression profiles of ceramide and ceramide-related genes in wild-type and mPer1/mPer2 double knockout mice.	Ceramides	32-40	period circadian clock 2	Mus musculus	91-96
21773940-0	2012	Temporal expression profiles of ceramide and ceramide-related genes in wild-type and mPer1/mPer2 double knockout mice.	Ceramides	45-53	period circadian clock 1	Mus musculus	85-90
21773940-0	2012	Temporal expression profiles of ceramide and ceramide-related genes in wild-type and mPer1/mPer2 double knockout mice.	Ceramides	45-53	period circadian clock 2	Mus musculus	91-96
21773940-10	2012	Collectively, our findings suggest that both SMases and CerS2 mRNA expression are regulated by the presence of mPer1/mPer2 circadian clock genes in vivo, and imply that ceramide may play a vital role in circadian rhythms and physiology.	Ceramides	169-177	ceramide synthase 2	Mus musculus	56-61
22357614-5	2012	Correspondingly, the ASM product, ceramide, increased locally in the cell membrane.	Ceramides	34-42	sphingomyelin phosphodiesterase 1	Homo sapiens	21-24
22384976-7	2012	Therefore, ceramide levels in C. albicans membranes were analysed following RsAFP2 treatment and, as expected, increased accumulation of phytoC24-ceramides in membranes of RsAFP2-treated C. albicans cells was detected.	Ceramides	11-19	defensin-like protein 2	Raphanus sativus	76-82
22384976-7	2012	Therefore, ceramide levels in C. albicans membranes were analysed following RsAFP2 treatment and, as expected, increased accumulation of phytoC24-ceramides in membranes of RsAFP2-treated C. albicans cells was detected.	Ceramides	11-19	defensin-like protein 2	Raphanus sativus	172-178
22311981-0	2012	Protein phosphatase 1alpha mediates ceramide-induced ERM protein dephosphorylation: a novel mechanism independent of phosphatidylinositol 4, 5-biphosphate (PIP2) and myosin/ERM phosphatase.	Ceramides	36-44	protein phosphatase, Mg2+/Mn2+ dependent 1A	Homo sapiens	0-26
22101393-4	2012	PC-PLC and/or SMS inhibition will affect lipid second messengers 1,2-diacylglycerol (DAG) and/or ceramide.	Ceramides	97-105	heparan sulfate proteoglycan 2	Homo sapiens	3-6
22311981-0	2012	Protein phosphatase 1alpha mediates ceramide-induced ERM protein dephosphorylation: a novel mechanism independent of phosphatidylinositol 4, 5-biphosphate (PIP2) and myosin/ERM phosphatase.	Ceramides	36-44	myosin heavy chain 14	Homo sapiens	166-172
22311981-9	2012	Additional results showed that the ceramide mechanism of PP1alpha activation is largely independent of PIP(2) hydrolysis and MP.	Ceramides	35-43	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	57-65
22419109-4	2012	C16:0 ceramide concentrations were increased in Atgl-/- and VLDL-loaded Wt macrophages.	Ceramides	6-14	patatin like phospholipase domain containing 2	Homo sapiens	48-52
22419109-6	2012	In accordance, inhibition of ceramide synthases in Atgl-/- macrophages by fumonisin B1 (FB1) resulted in specific inhibition of C16:0 ceramide, whereas intracellular TG concentrations remained high.	Ceramides	29-37	patatin like phospholipase domain containing 2	Homo sapiens	51-55
22419109-8	2012	We conclude that C16:0 ceramide elicits apoptosis in Atgl-/- macrophages by activation of the mitochondrial apoptosis pathway.	Ceramides	23-31	patatin like phospholipase domain containing 2	Homo sapiens	53-57
22194417-3	2012	The effect of ethanol on AMP-activated protein kinase phosphorylation was reversed by imipramine, suggesting that the generation of ceramide via acid sphingomyelinase (ASMase) is stimulated by ethanol.	Ceramides	132-140	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	168-174
22424291-2	2012	Glucosylceramide synthase (GCS) which is related to multidrug resistance (MDR) can reduce the level of ceramide and can help cells escape from the ceramide-induced cell apoptosis.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
22424291-2	2012	Glucosylceramide synthase (GCS) which is related to multidrug resistance (MDR) can reduce the level of ceramide and can help cells escape from the ceramide-induced cell apoptosis.	Ceramides	103-111	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
22424291-2	2012	Glucosylceramide synthase (GCS) which is related to multidrug resistance (MDR) can reduce the level of ceramide and can help cells escape from the ceramide-induced cell apoptosis.	Ceramides	103-111	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
22385956-4	2012	Ultimately, these cellular changes may converge to promote the accumulation of specific lipid metabolites (diacylglycerols and/or ceramides) in liver and skeletal muscle, a common final pathway leading to impaired insulin signaling and insulin resistance.	Ceramides	130-139	insulin	Homo sapiens	214-221
22399588-7	2012	CerS6 knockdown was associated with selective decreases in ceramides and dihydroceramides, markedly of C18-dihydroceramide, post-PDT.	Ceramides	59-68	ceramide synthase 6	Homo sapiens	0-5
22129459-2	2012	Furthermore, trans-Golgi membranes come in close apposition with ER (endoplasmic reticulum) membranes to form ER-trans-Golgi contact sites, which may facilitate transfer of newly synthesized ceramide from the ER to SM (sphingomyelin) synthase at the trans-Golgi via CERT (ceramide transfer protein).	Ceramides	191-199	ceramide transporter 1	Homo sapiens	266-270
22129459-2	2012	Furthermore, trans-Golgi membranes come in close apposition with ER (endoplasmic reticulum) membranes to form ER-trans-Golgi contact sites, which may facilitate transfer of newly synthesized ceramide from the ER to SM (sphingomyelin) synthase at the trans-Golgi via CERT (ceramide transfer protein).	Ceramides	191-199	ceramide transporter 1	Homo sapiens	272-297
22129459-8	2012	Thus it is likely that during cellular stress, disassembly of Golgi structure together with inactivation of CERT by caspases causes a reduction in ceramide trafficking and SM synthesis, and could contribute to the cellular response to pro-apoptotic stress.	Ceramides	147-155	ceramide transporter 1	Homo sapiens	108-112
22129459-8	2012	Thus it is likely that during cellular stress, disassembly of Golgi structure together with inactivation of CERT by caspases causes a reduction in ceramide trafficking and SM synthesis, and could contribute to the cellular response to pro-apoptotic stress.	Ceramides	147-155	caspase 2	Homo sapiens	116-124
22718629-4	2012	Full structural characterization of Stx receptors using electrospray ionization (ESI) mass spectrometry revealed Gb3Cer and Gb4Cer lipoforms with ceramide moieties mainly composed of C24:0/C24:1 or C16:0 fatty acid and sphingosine (d18:1) in GMVECs comparable to those previously found in HBMECs.	Ceramides	146-154	ST8 alpha-N-acetyl-neuraminide alpha-2,8-sialyltransferase 2	Homo sapiens	36-39
22101012-0	2012	Cell surface ceramide controls translocation of transferrin receptor to clathrin-coated pits.	Ceramides	13-21	transferrin	Homo sapiens	48-59
22101012-2	2012	We found that binding of transferrin to the receptor induced rapid generation of cell surface ceramide which correlated with activation of acid, but not neutral, sphingomyelinase.	Ceramides	94-102	transferrin	Homo sapiens	25-36
22101012-3	2012	At the onset of transferrin internalization both ceramide level and acid sphingomyelinase activity returned to their basic levels.	Ceramides	49-57	transferrin	Homo sapiens	16-27
22101012-8	2012	The data suggest that lack of cell surface ceramide, generated in physiological conditions by acid sphingomyelinase during transferrin binding, enables internalization of transferrin/transferrin receptor complex by clathrin-independent pathway.	Ceramides	43-51	transferrin	Homo sapiens	123-134
22101012-8	2012	The data suggest that lack of cell surface ceramide, generated in physiological conditions by acid sphingomyelinase during transferrin binding, enables internalization of transferrin/transferrin receptor complex by clathrin-independent pathway.	Ceramides	43-51	transferrin	Homo sapiens	171-182
22560558-4	2012	NOS2 and NOS3 knockout (KO) MRL/lpr mice had higher plasma levels of triglycerides (23% and 35%, respectively), ceramide (45% and 21%, respectively), and sphingosine 1-phosphate (S1P) (21%) compared to counterpart MRL/lpr controls.	Ceramides	112-120	nitric oxide synthase 2, inducible	Mus musculus	0-4
22101012-8	2012	The data suggest that lack of cell surface ceramide, generated in physiological conditions by acid sphingomyelinase during transferrin binding, enables internalization of transferrin/transferrin receptor complex by clathrin-independent pathway.	Ceramides	43-51	transferrin	Homo sapiens	171-182
22560558-4	2012	NOS2 and NOS3 knockout (KO) MRL/lpr mice had higher plasma levels of triglycerides (23% and 35%, respectively), ceramide (45% and 21%, respectively), and sphingosine 1-phosphate (S1P) (21%) compared to counterpart MRL/lpr controls.	Ceramides	112-120	nitric oxide synthase 3, endothelial cell	Mus musculus	9-13
22210926-3	2012	Here, we show that activation of the unfolded protein response (UPR) can restore normal ceramide levels and viability in yeast cells with a conditional defect in LCB1.	Ceramides	88-96	serine C-palmitoyltransferase LCB1	Saccharomyces cerevisiae S288C	162-166
22560558-8	2012	The findings suggest that advanced vascular disease in NOS2 and NOS3 KO MRL/lpr mice maybe mediated by increased plasma triglycerides, ceramide and S1P; decreased plasma IL-10; and accumulation of oxLDL-IC in the vessel wall.	Ceramides	135-143	nitric oxide synthase 2, inducible	Mus musculus	55-59
22560558-8	2012	The findings suggest that advanced vascular disease in NOS2 and NOS3 KO MRL/lpr mice maybe mediated by increased plasma triglycerides, ceramide and S1P; decreased plasma IL-10; and accumulation of oxLDL-IC in the vessel wall.	Ceramides	135-143	nitric oxide synthase 3, endothelial cell	Mus musculus	64-68
22320914-5	2012	Chronic alcohol consumption produces steatohepatitis, which also promotes hepatic insulin resistance, oxidative stress and injury, with the attendant increased generation of "toxic lipids" such as ceramides that increase insulin resistance.	Ceramides	197-206	insulin	Homo sapiens	221-228
22320914-6	2012	The PI3K/Akt signaling cascade is altered by direct interaction with ceramides as well as through PTEN upregulation as a downstream target gene of enhanced p53 transcriptional activity.	Ceramides	69-78	AKT serine/threonine kinase 1	Homo sapiens	9-12
22320914-8	2012	We postulate that the neurotoxic and neurodegenerative effects of liver-derived ceramides activate pro-inflammatory cytokines and increase lipid adducts and insulin resistance in the brain to impair cognitive and motor function.	Ceramides	80-89	insulin	Homo sapiens	157-164
22349696-5	2012	Furthermore, the translocation of acid sphingomyelinase (ASMase) to membrane raft clusters, whereby local ASMase activation and ceramide production--an important step that mediates membrane raft clustering--was attenuated.	Ceramides	128-136	ASM	Bos taurus	34-55
22349696-5	2012	Furthermore, the translocation of acid sphingomyelinase (ASMase) to membrane raft clusters, whereby local ASMase activation and ceramide production--an important step that mediates membrane raft clustering--was attenuated.	Ceramides	128-136	ASM	Bos taurus	57-63
22236408-5	2012	Pharmacological SPHK1 inhibitors SKI-I but not SKI-II decreased S-1-P content, elevated ceramide levels, caused a G2-M block and induced apoptotic cell death in melanomas.	Ceramides	88-96	sphingosine kinase 1	Homo sapiens	16-21
21765468-4	2012	In this study, we demonstrate that the enzyme sphingosine kinase 1 (SK1), a critical enzyme in the regulation of the key bioactive sphingolipids ceramide, sphingosine and sphingosine-1-phosphate (S1P), serves as a key downstream target for p53 action.	Ceramides	145-153	sphingosine kinase 1	Mus musculus	46-66
21765468-4	2012	In this study, we demonstrate that the enzyme sphingosine kinase 1 (SK1), a critical enzyme in the regulation of the key bioactive sphingolipids ceramide, sphingosine and sphingosine-1-phosphate (S1P), serves as a key downstream target for p53 action.	Ceramides	145-153	sphingosine kinase 1	Mus musculus	68-71
21765468-4	2012	In this study, we demonstrate that the enzyme sphingosine kinase 1 (SK1), a critical enzyme in the regulation of the key bioactive sphingolipids ceramide, sphingosine and sphingosine-1-phosphate (S1P), serves as a key downstream target for p53 action.	Ceramides	145-153	transformation related protein 53, pseudogene	Mus musculus	240-243
21765468-9	2012	The mechanism of p53 tumor suppression by loss of SK1 is mediated by elevations of sphingosine and ceramide, which in turn were accompanied by increased expression of cell cycle inhibitors and tumor cell senescence.	Ceramides	99-107	transformation related protein 53, pseudogene	Mus musculus	17-20
21765468-9	2012	The mechanism of p53 tumor suppression by loss of SK1 is mediated by elevations of sphingosine and ceramide, which in turn were accompanied by increased expression of cell cycle inhibitors and tumor cell senescence.	Ceramides	99-107	sphingosine kinase 1	Mus musculus	50-53
21945810-1	2012	Ceramide synthases (CerSs) are key enzymes in the biosynthesis of ceramides and display a group of at least six different isoenzymes (CerS1-6).	Ceramides	66-75	ceramide synthase 1	Homo sapiens	134-139
22194610-7	2012	Thapsigargin-induced beta-cell apoptosis and ceramide generation are also prevented by the p38 MAPK inhibitor PD169316.	Ceramides	45-53	mitogen-activated protein kinase 14	Mus musculus	91-99
24319543-0	2012	C-6 Ceramide Induces p53 Dependent Apoptosis in Human Astrocytoma Grade4 (Glioblastoma Multiforme) Cells.	Ceramides	4-12	complement C6	Homo sapiens	0-3
22180294-2	2012	Repression of ceramide synthase 1 (CerS1), altering C(18) -ceramide generation, was linked to drug resistance and metastasis.	Ceramides	14-22	ceramide synthase 1	Homo sapiens	35-40
22180294-6	2012	Interference with HDAC1 and miR-574-5p reconstituted CerS1-2 expression and C(18) -ceramide generation in multiple human cancer cell lines, which subsequently inhibited proliferation and anchorage-independent growth.	Ceramides	83-91	histone deacetylase 1	Homo sapiens	18-23
22180294-8	2012	Thus, these data suggest that the HDAC1/miR-574-5p axis might provide a novel therapeutic target to reconstitute tumour suppressor CerS1/ceramide signalling.	Ceramides	137-145	histone deacetylase 1	Homo sapiens	34-39
22180294-8	2012	Thus, these data suggest that the HDAC1/miR-574-5p axis might provide a novel therapeutic target to reconstitute tumour suppressor CerS1/ceramide signalling.	Ceramides	137-145	ceramide synthase 1	Homo sapiens	131-136
24319543-0	2012	C-6 Ceramide Induces p53 Dependent Apoptosis in Human Astrocytoma Grade4 (Glioblastoma Multiforme) Cells.	Ceramides	4-12	tumor protein p53	Homo sapiens	21-24
21437908-1	2012	Ceramide is involved in development of insulin resistance.	Ceramides	0-8	insulin	Homo sapiens	39-46
22139871-1	2012	Dihydroceramide Delta4-desaturase 1 (DES1) catalyzes the last step of the de novo ceramide biosynthesis, which consists of the introduction of a trans Delta4-double bond in the carbon chain of the dihydroceramide.	Ceramides	7-15	delta like canonical Notch ligand 4	Rattus norvegicus	22-35
22261821-3	2012	Acid ceramidase (ASAH1) directly regulates the intracellular balance of Cer, SPH, and SPH-1-phosphate by catalyzing the hydrolysis of Cer into SPH.	Ceramides	72-75	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
22261821-1	2012	In H295R human adrenocortical cells, ACTH rapidly activates ceramide (Cer) and sphingosine (SPH) turnover with a concomitant increase in SPH-1-phosphate secretion.	Ceramides	60-68	proopiomelanocortin	Homo sapiens	37-41
22261821-3	2012	Acid ceramidase (ASAH1) directly regulates the intracellular balance of Cer, SPH, and SPH-1-phosphate by catalyzing the hydrolysis of Cer into SPH.	Ceramides	72-75	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-22
22261821-1	2012	In H295R human adrenocortical cells, ACTH rapidly activates ceramide (Cer) and sphingosine (SPH) turnover with a concomitant increase in SPH-1-phosphate secretion.	Ceramides	70-73	proopiomelanocortin	Homo sapiens	37-41
22261821-3	2012	Acid ceramidase (ASAH1) directly regulates the intracellular balance of Cer, SPH, and SPH-1-phosphate by catalyzing the hydrolysis of Cer into SPH.	Ceramides	134-137	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
22261821-3	2012	Acid ceramidase (ASAH1) directly regulates the intracellular balance of Cer, SPH, and SPH-1-phosphate by catalyzing the hydrolysis of Cer into SPH.	Ceramides	134-137	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-22
22261821-3	2012	Acid ceramidase (ASAH1) directly regulates the intracellular balance of Cer, SPH, and SPH-1-phosphate by catalyzing the hydrolysis of Cer into SPH.	Ceramides	134-137	ankyrin 1	Homo sapiens	86-91
22211636-1	2012	Lag1p and Lac1p catalyse ceramide synthesis in Saccharomyces cerevisiae.	Ceramides	25-33	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	0-5
22211636-1	2012	Lag1p and Lac1p catalyse ceramide synthesis in Saccharomyces cerevisiae.	Ceramides	25-33	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	10-15
22561428-1	2012	Acid sphingomyelinase (ASM) is one enzyme responsible for the production of ceramide via the hydrolysis of sphingomyelin.	Ceramides	76-84	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
22561428-4	2012	ASM activation, in turn, may create excess or abnormally distributed ceramides, which could lead to tissue and organ injuries, including to the pulmonary, liver, kidney, and nervous systems.	Ceramides	69-78	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
22561428-1	2012	Acid sphingomyelinase (ASM) is one enzyme responsible for the production of ceramide via the hydrolysis of sphingomyelin.	Ceramides	76-84	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
22561428-2	2012	Recent findings have revealed the important role of ASM in the initiation of ceramide-induced cell apoptosis, as well as in the pathophysiology of many common diseases (e.g. cardiovascular diseases, diabetes, pulmonary diseases, and neurological diseases).	Ceramides	77-85	sphingomyelin phosphodiesterase 1	Homo sapiens	52-55
22257771-4	2012	Myotube atrophy induced by TNF-alpha was accompanied by a substantial increase in cell ceramide levels, and could be mimicked by the addition of exogenous ceramides.	Ceramides	87-95	tumor necrosis factor	Homo sapiens	27-36
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Ceramides	103-112	caspase 1	Homo sapiens	130-139
22832107-2	2012	Here we show that age-related increase in "lipotoxic danger signals" such as free cholesterol (FC) and ceramides, leads to thymic caspase-1 activation via the Nlrp3 inflammasome.	Ceramides	103-112	NLR family pyrin domain containing 3	Homo sapiens	159-164
22257771-4	2012	Myotube atrophy induced by TNF-alpha was accompanied by a substantial increase in cell ceramide levels, and could be mimicked by the addition of exogenous ceramides.	Ceramides	155-164	tumor necrosis factor	Homo sapiens	27-36
22257771-6	2012	In the presence of TNF-alpha, ceramide-synthesis inhibitors significantly increased protein synthesis and decreased proteolysis.	Ceramides	30-38	tumor necrosis factor	Homo sapiens	19-28
22257771-11	2012	CONCLUSIONS: Ceramide accumulation induced by TNF-alpha or tumor development participates in the mechanism of muscle-cell atrophy, and sphingolipid metabolism is a logical target for pharmacological or nutritional interventions aiming at preserving muscle mass in pathological situations.	Ceramides	13-21	tumor necrosis factor	Homo sapiens	46-55
22166213-3	2012	Aur1p is an enzyme catalyzing the formation of inositol phosphorylceramide in the yeast, and the defect leads to strong growth inhibition due to accumulation of ceramide and reductions in complex sphingolipid levels.	Ceramides	66-74	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	0-5
22166213-5	2012	Under AUR1-repressive conditions, SCS7 and SUR2 mutants showed reductions in the complex sphingolipid levels and the accumulation of ceramide, like wild-type cells.	Ceramides	133-141	fatty acid alpha-hydroxylase	Saccharomyces cerevisiae S288C	34-38
22166213-8	2012	Therefore, it is suggested that the deletion of sphingolipid hydroxylases changes the toxicity of ceramide under AUR1-repressive conditions.	Ceramides	98-106	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	113-117
22166213-5	2012	Under AUR1-repressive conditions, SCS7 and SUR2 mutants showed reductions in the complex sphingolipid levels and the accumulation of ceramide, like wild-type cells.	Ceramides	133-141	sphingosine hydroxylase	Saccharomyces cerevisiae S288C	43-47
22074919-1	2012	We previously presented that the neutral sphingomyelinase 2 (nSMase2) is the only SMase activated in human airway epithelial (HAE) cells following exposure to oxidative stress (ox-stress), yielding ceramide accumulation and thereby inducing apoptosis.	Ceramides	198-206	sphingomyelin phosphodiesterase 3	Homo sapiens	33-59
22074919-1	2012	We previously presented that the neutral sphingomyelinase 2 (nSMase2) is the only SMase activated in human airway epithelial (HAE) cells following exposure to oxidative stress (ox-stress), yielding ceramide accumulation and thereby inducing apoptosis.	Ceramides	198-206	sphingomyelin phosphodiesterase 3	Homo sapiens	61-68
22313761-7	2012	The novel ceramide was named actinidiamide, and was found significantly to inhibit nitric oxide (NO) production (30.6% inhibition at 1 microg/mL) in lipopolysaccaride (LPS)-stimulated RAW 264.7 cells and beta-hexosaminidase release (91.8% inhibition at 1 microg/mL) in IgE-sensitized RBL-2H3 cells.	Ceramides	10-18	O-GlcNAcase	Mus musculus	204-223
21984552-4	2012	However, inhibition of the synthesis and release of ceramide by either FB1 or SCY attenuated, markedly , the generation of ceramide, release of the cytokines/chemokines, and activation of NF-kappaB (as measured by activated p65 and cRel).	Ceramides	52-60	nuclear factor kappa B subunit 1	Homo sapiens	188-197
21984552-4	2012	However, inhibition of the synthesis and release of ceramide by either FB1 or SCY attenuated, markedly , the generation of ceramide, release of the cytokines/chemokines, and activation of NF-kappaB (as measured by activated p65 and cRel).	Ceramides	52-60	RELA proto-oncogene, NF-kB subunit	Homo sapiens	224-227
21984552-4	2012	However, inhibition of the synthesis and release of ceramide by either FB1 or SCY attenuated, markedly , the generation of ceramide, release of the cytokines/chemokines, and activation of NF-kappaB (as measured by activated p65 and cRel).	Ceramides	52-60	REL proto-oncogene, NF-kB subunit	Homo sapiens	232-236
22033380-10	2012	CONCLUSION AND GENERAL SIGNIFICANCE: Ceramide generation was a critical component of Fas receptor-induced apoptosis, since inhibition of acid sphingomyelinase (aSMase) interfered with Fas-induced apoptosis during Pb(2+) exposure.	Ceramides	37-45	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	137-158
22033380-10	2012	CONCLUSION AND GENERAL SIGNIFICANCE: Ceramide generation was a critical component of Fas receptor-induced apoptosis, since inhibition of acid sphingomyelinase (aSMase) interfered with Fas-induced apoptosis during Pb(2+) exposure.	Ceramides	37-45	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	160-166
22785465-3	2012	We also investigated its effect on the expression of the ceramide kinase (CERK) involved in calcium-dependent degranulation, and on ceramide activation by multiple cytokines.	Ceramides	57-65	ceramide kinase	Mus musculus	74-78
22336588-0	2012	Increased apoptosis in cancer cells in vitro and in vivo by ceramides in transferrin-modified liposomes.	Ceramides	60-69	transferrin	Mus musculus	73-84
22336588-2	2012	We hypothesized that with the modification of the ceramide-loaded liposomes with transferrin (Tf), we would achieve both tumor targeting and increased delivery of lysosome-destabilizing agents, such as ceramides to lysosomes, to initiate LMP-induced apoptosis.	Ceramides	50-58	transferrin	Mus musculus	81-92
22336588-2	2012	We hypothesized that with the modification of the ceramide-loaded liposomes with transferrin (Tf), we would achieve both tumor targeting and increased delivery of lysosome-destabilizing agents, such as ceramides to lysosomes, to initiate LMP-induced apoptosis.	Ceramides	50-58	transferrin	Mus musculus	94-96
22336588-2	2012	We hypothesized that with the modification of the ceramide-loaded liposomes with transferrin (Tf), we would achieve both tumor targeting and increased delivery of lysosome-destabilizing agents, such as ceramides to lysosomes, to initiate LMP-induced apoptosis.	Ceramides	202-211	transferrin	Mus musculus	81-92
22336588-2	2012	We hypothesized that with the modification of the ceramide-loaded liposomes with transferrin (Tf), we would achieve both tumor targeting and increased delivery of lysosome-destabilizing agents, such as ceramides to lysosomes, to initiate LMP-induced apoptosis.	Ceramides	202-211	transferrin	Mus musculus	94-96
22336588-8	2012	Ceramide-loaded Tf-liposomes significantly increased apoptosis compared with ceramide-free and ceramide-loaded non-modified liposomes.	Ceramides	0-8	transferrin	Mus musculus	16-18
22336588-11	2012	The lysosomal accumulation of ceramides delivered by Tf-liposomes initiates the permeabilization of the lysosomal membranes required for the release of lysosomal cathepsins into the cytoplasm and initiation of the cancer cell apoptosis both in vitro and in vivo.	Ceramides	30-39	transferrin	Mus musculus	53-55
22890197-1	2012	Recent studies demonstrate that rapid translocation of the acid sphingomyelinase (ASM), a lysosomal hydrolase, to the outer leaflet of the cell membrane and concomitant release of ceramide constitute a common cellular signaling cascade to various stimuli including CD95 ligation, UV-irradiation, bacterial and viral infections.	Ceramides	180-188	sphingomyelin phosphodiesterase 1	Homo sapiens	59-80
22890197-1	2012	Recent studies demonstrate that rapid translocation of the acid sphingomyelinase (ASM), a lysosomal hydrolase, to the outer leaflet of the cell membrane and concomitant release of ceramide constitute a common cellular signaling cascade to various stimuli including CD95 ligation, UV-irradiation, bacterial and viral infections.	Ceramides	180-188	sphingomyelin phosphodiesterase 1	Homo sapiens	82-85
23052231-10	2012	CONCLUSION: Based on these data we conclude that ceramide-induced Nox2-mediated oxidative stress couples mitochondrial dysfunction to loss in cell viability in the pancreatic beta-cell.	Ceramides	49-57	cytochrome b-245 beta chain	Rattus norvegicus	66-70
22890197-1	2012	Recent studies demonstrate that rapid translocation of the acid sphingomyelinase (ASM), a lysosomal hydrolase, to the outer leaflet of the cell membrane and concomitant release of ceramide constitute a common cellular signaling cascade to various stimuli including CD95 ligation, UV-irradiation, bacterial and viral infections.	Ceramides	180-188	Fas cell surface death receptor	Homo sapiens	265-269
22890197-4	2012	Here, by confocal microscopy and flow cytometry analysis, we demonstrate that hydrogen peroxide (H(2)O(2)), a primary form of ROS in mammalian cells, induces very rapid translocation of ASM and formation of ceramide-enriched membrane platforms in the plasma membrane of Jurkat T cells.	Ceramides	207-215	sphingomyelin phosphodiesterase 1	Homo sapiens	186-189
22590738-2	2012	As the ASM is a key enzyme of the sphingolipid exchange, in the present study we have investigated the effect of an ASM inhibitor imipramine on the ceramide and sphingomyelin content in the tissues of old rats.	Ceramides	148-156	H19, imprinted maternally expressed transcript (non-protein coding)	Rattus norvegicus	7-10
22474427-11	2012	Ceramide, a mediator of cytokine-induced injury, reduced the active phosphorylated form of Akt and downregulated the promoter activity of the antiapoptotic gene bcl-2.	Ceramides	0-8	thymoma viral proto-oncogene 1	Mus musculus	91-94
22474427-11	2012	Ceramide, a mediator of cytokine-induced injury, reduced the active phosphorylated form of Akt and downregulated the promoter activity of the antiapoptotic gene bcl-2.	Ceramides	0-8	B cell leukemia/lymphoma 2	Mus musculus	161-166
22590738-2	2012	As the ASM is a key enzyme of the sphingolipid exchange, in the present study we have investigated the effect of an ASM inhibitor imipramine on the ceramide and sphingomyelin content in the tissues of old rats.	Ceramides	148-156	H19, imprinted maternally expressed transcript (non-protein coding)	Rattus norvegicus	116-119
21932365-2	2012	The proinflammatory cytokine tumor necrosis factor-alpha (TNFalpha) elicits the formation of the bioactive ceramide by stimulating the hydrolysis of the membrane lipid sphingomyelin by sphingomyelinase activities.	Ceramides	107-115	tumor necrosis factor	Homo sapiens	29-56
22297646-4	2012	The rationale is that insulin resistance dysregulates lipid metabolism and promotes ceramide accumulation, and thereby increases inflammation and stress.	Ceramides	84-92	insulin	Homo sapiens	22-29
22337830-1	2012	Ceramides are lipid signaling molecules that cause cytotoxicity and cell death mediated by insulin resistance, inflammation, and endoplasmic reticulum (ER) stress.	Ceramides	0-9	insulin	Homo sapiens	91-98
22337830-2	2012	However, insulin resistance dysregulates lipid metabolism, which promotes ceramide accumulation with attendant inflammation and ER stress.	Ceramides	74-82	insulin	Homo sapiens	9-16
22337830-5	2012	Mechanistically, we propose that toxic ceramides generated in extra-CNS tissues (e.g., liver) get released into peripheral blood, and subsequently transit across the blood-brain barrier into the brain where they induce brain insulin resistance, inflammation, and cell death (extrinsic pathway).	Ceramides	39-48	insulin	Homo sapiens	225-232
22337830-7	2012	The end result is increased ER stress and ceramide generation, which exacerbate brain insulin resistance, cell death, myelin degeneration, and neuroinflammation.	Ceramides	42-50	insulin	Homo sapiens	86-93
22942738-11	2012	Altogether, our data strongly indicate that the inhibition of ceramide conversion to complex sphingolipids by D609 is accompanied by an enhancement of FasL-induced caspase-dependent and -independent cell death in T lymphocytes.	Ceramides	62-70	Fas ligand	Homo sapiens	151-155
22258513-7	2012	To explore the mechanisms underlying this dysregulation, we evaluated the expression of four genes connected to ceramide metabolism: ASMase, NSMase 2, GALC, and UGCG.	Ceramides	112-120	sphingomyelin phosphodiesterase 1	Homo sapiens	133-139
22258513-7	2012	To explore the mechanisms underlying this dysregulation, we evaluated the expression of four genes connected to ceramide metabolism: ASMase, NSMase 2, GALC, and UGCG.	Ceramides	112-120	sphingomyelin phosphodiesterase 3	Homo sapiens	141-149
22258513-7	2012	To explore the mechanisms underlying this dysregulation, we evaluated the expression of four genes connected to ceramide metabolism: ASMase, NSMase 2, GALC, and UGCG.	Ceramides	112-120	UDP-glucose ceramide glucosyltransferase	Homo sapiens	161-165
21932365-2	2012	The proinflammatory cytokine tumor necrosis factor-alpha (TNFalpha) elicits the formation of the bioactive ceramide by stimulating the hydrolysis of the membrane lipid sphingomyelin by sphingomyelinase activities.	Ceramides	107-115	tumor necrosis factor	Homo sapiens	58-66
21932365-4	2012	We demonstrated in SH-SY5Y human neuroblastoma cells and primary cortical neurons that TNFalpha is a potent stimulator of Mg(2+) -dependent neutral sphingomyelinase (Mg(2+) -nSMase) activity, and sphingomyelin hydrolysis, rather than de novo synthesis, was the predominant source of ceramide increases.	Ceramides	283-291	tumor necrosis factor	Homo sapiens	87-95
21932365-6	2012	Notably, TNFalpha provoked an NOX-dependent oxidative damage to sphingosine kinase-1, which generates sphingosine-1-phosphate, a ceramide metabolite associated with neurite outgrowth.	Ceramides	129-137	tumor necrosis factor	Homo sapiens	9-17
21932365-6	2012	Notably, TNFalpha provoked an NOX-dependent oxidative damage to sphingosine kinase-1, which generates sphingosine-1-phosphate, a ceramide metabolite associated with neurite outgrowth.	Ceramides	129-137	sphingosine kinase 1	Homo sapiens	64-84
21932365-8	2012	Blunting ceramide and ROS formation both rescued sphingosine kinase-1 activity and neurite outgrowth.	Ceramides	9-17	sphingosine kinase 1	Homo sapiens	49-69
21932365-9	2012	Our studies suggest that TNFalpha-mediated activation of Mg(2+) -nSMase and NOX in neuronal cells not only produced the neurotoxic intermediates ceramide and ROS but also directly antagonized neuronal survival mechanisms, thus accelerating neurodegeneration.	Ceramides	145-153	tumor necrosis factor	Homo sapiens	25-33
22325600-2	2012	One well-defined inter-organelle lipid movement is the transport of ceramide by ceramide transport protein (CERT).	Ceramides	68-76	ceramide transporter 1	Homo sapiens	80-106
23038012-0	2012	Effects of Hsp90 inhibitors, geldanamycin and its analog, on ceramide metabolism and cytotoxicity in PC12 cells.	Ceramides	61-69	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	11-16
22325600-2	2012	One well-defined inter-organelle lipid movement is the transport of ceramide by ceramide transport protein (CERT).	Ceramides	68-76	ceramide transporter 1	Homo sapiens	108-112
22325600-4	2012	CERT delivers ceramide from the ER to the Golgi apparatus in a non-vesicular and ATP-dependent manner.	Ceramides	14-22	ceramide transporter 1	Homo sapiens	0-4
22325600-5	2012	This chapter describes a reconstitution assay system for ceramide transport with semi-intact cells, which is useful for the study of the CERT-mediated inter-organelle transport of ceramide.	Ceramides	57-65	ceramide transporter 1	Homo sapiens	137-141
22325600-5	2012	This chapter describes a reconstitution assay system for ceramide transport with semi-intact cells, which is useful for the study of the CERT-mediated inter-organelle transport of ceramide.	Ceramides	180-188	ceramide transporter 1	Homo sapiens	137-141
22348006-11	2012	CONCLUSIONS: Stx1 binds primarily to the glycan, but Stx2 binding is influenced by residues in the ceramide portion of Gb3 and the lipid environment.	Ceramides	99-107	syntaxin-2	Chlorocebus sabaeus	53-57
22577490-7	2012	Given the role of ceramides as mediators of ER stress and insulin resistance, treatment with ceramide enzyme inhibitors may help reverse or halt progression of chronic ALD.	Ceramides	18-27	insulin	Homo sapiens	58-65
23226203-7	2012	These results suggest that ceramide production contributes to cell death induced by acetic acid, especially through hydrolysis of complex sphingolipids catalyzed by Isc1p and de novo synthesis catalyzed by Lag1p, and provide the first in vivo indication of its involvement in mitochondrial outer membrane permeabilization in yeast.	Ceramides	27-35	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	206-211
23133636-1	2012	INTRODUCTION: Glucosylceramide synthase (GCS) is one enzyme that provides a major route for ceramide clearance.	Ceramides	22-30	UDP-glucose ceramide glucosyltransferase	Homo sapiens	41-44
23049887-2	2012	In mammals, acid sphingomyelinase (ASM) is an enzyme that hydrolyzes sphingomyelin to produce ceramide.	Ceramides	94-102	sphingomyelin phosphodiesterase 1	Homo sapiens	35-38
22970244-7	2012	The SK2-selective inhibitor ABC294640 demonstrated the most pronounced effects on SK1 and SK2 mRNA expression, decrease of S1P levels, elevation of ceramide levels, cell cycle arrest, and inhibition of proliferation, migration and invasion.	Ceramides	148-156	sphingosine kinase 2	Homo sapiens	4-7
23284920-6	2012	We observed that survival of Atrx-null cells were similar to wild type cells in response to serum withdrawal, anti-Fas antibody, C2 ceramide or dexamethasone treatment but were more sensitive to 5-fluorouracil (5-FU).	Ceramides	132-140	ATRX, chromatin remodeler	Mus musculus	29-33
23226203-7	2012	These results suggest that ceramide production contributes to cell death induced by acetic acid, especially through hydrolysis of complex sphingolipids catalyzed by Isc1p and de novo synthesis catalyzed by Lag1p, and provide the first in vivo indication of its involvement in mitochondrial outer membrane permeabilization in yeast.	Ceramides	27-35	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	165-170
23110086-3	2012	Broadly, increased amounts of sphingomyelins, dihydrosphingomyelins and ceramides were found in aged CD4(+) T cells.	Ceramides	72-81	CD4 antigen	Mus musculus	101-104
23110086-6	2012	In vitro, the direct or enzymatic enhancement of ceramide levels decreased CD4(+) T cell proliferation without regard for the age of the responding T cells.	Ceramides	49-57	CD4 antigen	Mus musculus	75-78
23024785-7	2012	Cbs(+/-/)Asm(+/+) mice had significantly increased renal Asm activity, ceramide production and O(2.	Ceramides	71-79	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	9-12
23024785-8	2012	)(-) level compared to Cbs(+/+)/Asm(+/+), while Cbs(+/-/)Asm(-/-) mice showed significantly reduced renal Asm activity, ceramide production and O(2.	Ceramides	120-128	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	57-60
23024785-8	2012	)(-) level compared to Cbs(+/+)/Asm(+/+), while Cbs(+/-/)Asm(-/-) mice showed significantly reduced renal Asm activity, ceramide production and O(2.	Ceramides	120-128	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	57-60
23024785-10	2012	Confocal microscopy demonstrated that colocalization of podocin with ceramide was much lower in Cbs(+/-/)Asm(-/-) mice compared to Cbs(+/-/)Asm(+/+) mice, which was accompanied by a reduced glomerular damage index, albuminuria and proteinuria in Cbs(+/-/)Asm(-/-) mice.	Ceramides	69-77	nephrosis 2, podocin	Mus musculus	56-63
22558155-1	2012	BACKGROUND: Acid sphingomyelinase (ASM) hydrolyses sphingomyelin and generates the lipid messenger ceramide, which mediates a variety of stress-related cellular processes.	Ceramides	99-107	sphingomyelin phosphodiesterase 1	Homo sapiens	12-33
22558155-1	2012	BACKGROUND: Acid sphingomyelinase (ASM) hydrolyses sphingomyelin and generates the lipid messenger ceramide, which mediates a variety of stress-related cellular processes.	Ceramides	99-107	sphingomyelin phosphodiesterase 1	Homo sapiens	35-38
22558155-6	2012	The newly identified ASM splice variants were catalytically inactive in biochemical in vitro assays, but they decreased the relative cellular ceramide content in overexpression studies and exerted a dominant-negative effect on ASM activity in physiological cell models.	Ceramides	142-150	sphingomyelin phosphodiesterase 1	Homo sapiens	21-24
22413010-8	2012	Of importance, SCD1 substantially inhibited SFA-induced caspase 3 activation, ceramide synthesis, diacylglycerol synthesis, apoptotic cell death, and mitochondrial reactive oxygen species (ROS) generation.	Ceramides	78-86	stearoyl-CoA desaturase	Rattus norvegicus	15-19
22348006-11	2012	CONCLUSIONS: Stx1 binds primarily to the glycan, but Stx2 binding is influenced by residues in the ceramide portion of Gb3 and the lipid environment.	Ceramides	99-107	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	119-122
23229749-5	2012	Our second finding is "the ceramide-trafficking protein (CERT)" working as the specific transfer protein of ceramide from the ER to the Golgi apparatus, during the SM biosynthesis (by K. Hanada).	Ceramides	27-35	ceramide transporter 1	Homo sapiens	57-61
22065582-3	2011	Ceramide is a bioactive sphingolipid that has been suggested to regulate TLR4-induced NF-kappaB signaling, although reports on the role of ceramide in TLR4 activation conflict.	Ceramides	0-8	toll like receptor 4	Homo sapiens	73-77
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	86-94	insulin like growth factor 1	Homo sapiens	23-27
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	86-94	X-linked inhibitor of apoptosis	Homo sapiens	65-69
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	86-94	TNF superfamily member 10	Homo sapiens	168-173
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	86-94	TNF superfamily member 10	Homo sapiens	174-179
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	96-99	insulin like growth factor 1	Homo sapiens	23-27
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	96-99	X-linked inhibitor of apoptosis	Homo sapiens	65-69
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	96-99	TNF superfamily member 10	Homo sapiens	168-173
23091403-6	2012	In contrast, long-term IGF1 incubation resulted in repression of XIAP protein through ceramide (Cer) formation derived from de novo synthesis which was associated with Apo2L/TRAIL sensitization.	Ceramides	96-99	TNF superfamily member 10	Homo sapiens	174-179
22120643-3	2012	Research during the last two decades has provided evidence for a role of lipid intermediates like diacylglycerol and ceramide in the induction of lipid-induced insulin resistance.	Ceramides	117-125	insulin	Homo sapiens	160-167
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.	Ceramides	267-276	megakaryocyte-associated tyrosine kinase	Homo sapiens	158-161
22065582-3	2011	Ceramide is a bioactive sphingolipid that has been suggested to regulate TLR4-induced NF-kappaB signaling, although reports on the role of ceramide in TLR4 activation conflict.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	86-95
22065582-3	2011	Ceramide is a bioactive sphingolipid that has been suggested to regulate TLR4-induced NF-kappaB signaling, although reports on the role of ceramide in TLR4 activation conflict.	Ceramides	139-147	toll like receptor 4	Homo sapiens	151-155
21883234-8	2011	These data suggest that spontaneous cell death in the loh1 line is triggered either by the accumulation of free trihydroxy sphingoid bases or ceramide species with C(16) fatty acid.	Ceramides	142-150	RNA-binding CRS1 / YhbY (CRM) domain protein	Arabidopsis thaliana	54-58
22052905-12	2011	Elevation of ceramide in turn stimulated calpain; conversely, inhibiting ceramide formation suppressed Atg5 cleavage and apoptosis.	Ceramides	73-81	autophagy related 5	Homo sapiens	103-107
22013072-2	2011	Recent data suggest that ceramide synthase1-6 (CerS1-6)-generated ceramides, containing different fatty acid chain lengths, might exhibit distinct and opposing functions, such as apoptosis versus survival in a context-dependent manner.	Ceramides	66-75	ceramide synthase 1	Homo sapiens	25-45
22013072-2	2011	Recent data suggest that ceramide synthase1-6 (CerS1-6)-generated ceramides, containing different fatty acid chain lengths, might exhibit distinct and opposing functions, such as apoptosis versus survival in a context-dependent manner.	Ceramides	66-75	ceramide synthase 1	Homo sapiens	47-54
22013072-5	2011	Down-regulation of CerS6/C(16)-ceramide, and not its further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).	Ceramides	31-39	ceramide synthase 6	Homo sapiens	19-24
22013072-5	2011	Down-regulation of CerS6/C(16)-ceramide, and not its further metabolism to glucosylceramide or sphingomyelin, activated ATF-6 upon treatment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).	Ceramides	31-39	activating transcription factor 6	Homo sapiens	120-125
22013072-7	2011	Mechanistically, ATF-6 activation was regulated by a concerted two-step process involving the release of Ca(2+) from the ER stores ([Ca(2+)](ER)), which resulted in the fragmentation of Golgi membranes in response to CerS6/C(16)-ceramide alteration.	Ceramides	229-237	activating transcription factor 6	Homo sapiens	17-22
22013072-10	2011	Overall, these data suggest a novel mechanism of how CerS6/C(16)-ceramide alteration activates ATF6 and induces ER-stress-mediated apoptosis in squamous cell carcinomas.	Ceramides	65-73	ceramide synthase 6	Homo sapiens	53-58
22013072-10	2011	Overall, these data suggest a novel mechanism of how CerS6/C(16)-ceramide alteration activates ATF6 and induces ER-stress-mediated apoptosis in squamous cell carcinomas.	Ceramides	65-73	activating transcription factor 6	Homo sapiens	95-99
21964280-5	2011	Certain sphingosines and ceramides inhibited cathepsin D in the submicromolar range, and structural requirements for this inhibitory effect were evaluated.	Ceramides	25-34	cathepsin D	Homo sapiens	45-56
21933146-4	2011	Cholesterol accumulation and its trafficking to mitochondria sensitizes fatty liver to subsequent hits including inflammatory cytokines, such as TNF/Fas, in a pathway involving ceramide generation by acidic sphingomyelinase (ASMase).	Ceramides	177-185	tumor necrosis factor	Homo sapiens	145-148
21933146-4	2011	Cholesterol accumulation and its trafficking to mitochondria sensitizes fatty liver to subsequent hits including inflammatory cytokines, such as TNF/Fas, in a pathway involving ceramide generation by acidic sphingomyelinase (ASMase).	Ceramides	177-185	sphingomyelin phosphodiesterase 1	Homo sapiens	200-223
21933146-4	2011	Cholesterol accumulation and its trafficking to mitochondria sensitizes fatty liver to subsequent hits including inflammatory cytokines, such as TNF/Fas, in a pathway involving ceramide generation by acidic sphingomyelinase (ASMase).	Ceramides	177-185	sphingomyelin phosphodiesterase 1	Homo sapiens	225-231
21069478-3	2011	Natural glycosphingolipid, globotriaosylceramide (Gal alpha1-4, Gal beta1-4, Glc beta1-1, ceramide), is also called CD77 and its expression was previously associated with proliferating centroblasts undergoing somatic hypermutation, but it has been demonstrate that globotriaosylceramide is not a reliable marker to discriminate human centroblasts from centrocytes.	Ceramides	40-48	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	68-75
21069478-3	2011	Natural glycosphingolipid, globotriaosylceramide (Gal alpha1-4, Gal beta1-4, Glc beta1-1, ceramide), is also called CD77 and its expression was previously associated with proliferating centroblasts undergoing somatic hypermutation, but it has been demonstrate that globotriaosylceramide is not a reliable marker to discriminate human centroblasts from centrocytes.	Ceramides	40-48	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	81-88
21069478-3	2011	Natural glycosphingolipid, globotriaosylceramide (Gal alpha1-4, Gal beta1-4, Glc beta1-1, ceramide), is also called CD77 and its expression was previously associated with proliferating centroblasts undergoing somatic hypermutation, but it has been demonstrate that globotriaosylceramide is not a reliable marker to discriminate human centroblasts from centrocytes.	Ceramides	40-48	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	116-120
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.	Ceramides	168-177	glucosylceramidase beta	Homo sapiens	0-23
22177013-1	2011	BACKGROUND: Nucleotide pyrophosphatase/phosphodiesterase 7 (NPP7) is the only member of the mammalian NPP enzyme family that has been confirmed to act as a sphingomyelinase, hydrolyzing sphingomyelin (SM) to form phosphocholine and ceramide.	Ceramides	232-240	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	12-58
22177013-1	2011	BACKGROUND: Nucleotide pyrophosphatase/phosphodiesterase 7 (NPP7) is the only member of the mammalian NPP enzyme family that has been confirmed to act as a sphingomyelinase, hydrolyzing sphingomyelin (SM) to form phosphocholine and ceramide.	Ceramides	232-240	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	60-64
22359481-1	2011	B13 analogues are being considered as therapeutic agents for cancer cells, since B13 is a ceramide analogue and inhibits ceramidase to promote apoptosis in cancer cells.	Ceramides	90-98	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	0-3
22359481-1	2011	B13 analogues are being considered as therapeutic agents for cancer cells, since B13 is a ceramide analogue and inhibits ceramidase to promote apoptosis in cancer cells.	Ceramides	90-98	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	81-84
21914808-4	2011	We demonstrate that a DHC-based response to hypoxia occurs in a hypoxia-inducible factor-independent fashion and is catalyzed by the DHC desaturase (DEGS) in the de novo ceramide pathway.	Ceramides	170-178	delta 4-desaturase, sphingolipid 1	Homo sapiens	149-153
22061047-2	2011	Ceramide and, more recently, other sphingolipid species (e.g., dihydroceramide and dihydrosphingosine) have been implicated in 4-HPR-mediated tumor cell death.	Ceramides	0-8	haptoglobin-related protein	Homo sapiens	129-132
22048168-2	2011	Agonists to CB1 and CB2 promote ceramide de novo synthesis, p38-mitogen-activated protein kinase-dependent activation of caspase-3 and apoptotic cell death in most MCLs.	Ceramides	32-40	cannabinoid receptor 1	Homo sapiens	12-15
22048168-2	2011	Agonists to CB1 and CB2 promote ceramide de novo synthesis, p38-mitogen-activated protein kinase-dependent activation of caspase-3 and apoptotic cell death in most MCLs.	Ceramides	32-40	cannabinoid receptor 2	Homo sapiens	20-23
21562314-12	2011	The decreased expression of Cav-1 was associated with the activation of the Smad2/3, Stat, and a-SMase/ceramide pathways, and with the increased expression of HO-1.	Ceramides	103-111	caveolin-1	Ovis aries	28-33
21893018-2	2011	The present study was performed to determine whether acid sphingomyelinase (Asm), a ceramide-producing enzyme, is implicated in the development of hHcys-induced glomerular oxidative stress and injury.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	53-74
21893018-2	2011	The present study was performed to determine whether acid sphingomyelinase (Asm), a ceramide-producing enzyme, is implicated in the development of hHcys-induced glomerular oxidative stress and injury.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	76-79
21862613-3	2011	Our previous studies demonstrated that the ceramides activate the Nod-like receptor family, pyrin domain containing 3 (Nlrp3) inflammasome to cause the generation of mature IL-1beta and ablation of the Nlrp3 inflammasome in diet-induced obesity improves insulin signaling.	Ceramides	43-52	NLR family pyrin domain containing 3	Homo sapiens	119-124
21455605-3	2011	Sphingosine-1-phosphate (S1P) and glucosyleceramide, converted from ceramides by sphingosine kinase-1 (SK-1) and glucosyleceramide synthase (GCS) enzymes, respectively, inhibit apoptosis and develop resistance to chemotherapeutic drugs.	Ceramides	68-77	sphingosine kinase 1	Homo sapiens	81-107
21549856-4	2011	The ceramide variability caused by the diversity of the long-chain amino alcohol and the fatty acid, which both may vary in chain length, degree of unsaturation, and type and number of substituents, further contributes to the increasing number of possible GSL species.	Ceramides	4-12	cathepsin A	Homo sapiens	256-259
21707482-6	2011	In this review, we have focused on ceramide transfer protein (CERT) as a major regulator of ceramide flux in the cell.	Ceramides	35-43	ceramide transporter 1	Homo sapiens	62-66
21707483-8	2011	This review is intended to bring together those aspects of glycosphingolipid metabolism that might be leveraged to enhance the therapeutic performance of ceramide and to discuss how ABC transporters like P-gp might be targeted to potentiate and magnify ceramide-driven proapoptotic cascades.	Ceramides	154-162	ATP binding cassette subfamily B member 1	Homo sapiens	204-208
21707483-8	2011	This review is intended to bring together those aspects of glycosphingolipid metabolism that might be leveraged to enhance the therapeutic performance of ceramide and to discuss how ABC transporters like P-gp might be targeted to potentiate and magnify ceramide-driven proapoptotic cascades.	Ceramides	253-261	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	182-185
21707483-8	2011	This review is intended to bring together those aspects of glycosphingolipid metabolism that might be leveraged to enhance the therapeutic performance of ceramide and to discuss how ABC transporters like P-gp might be targeted to potentiate and magnify ceramide-driven proapoptotic cascades.	Ceramides	253-261	ATP binding cassette subfamily B member 1	Homo sapiens	204-208
21835161-3	2011	We now examine the properties of ceramide with different acyl chains including long chain (C16- and C18-), very long chain (C24-) and unsaturated (C18:1- and C24:1-) ceramides, in phosphatidylcholine model membranes.	Ceramides	33-41	Bardet-Biedl syndrome 9	Homo sapiens	100-103
21835161-3	2011	We now examine the properties of ceramide with different acyl chains including long chain (C16- and C18-), very long chain (C24-) and unsaturated (C18:1- and C24:1-) ceramides, in phosphatidylcholine model membranes.	Ceramides	33-41	Bardet-Biedl syndrome 9	Homo sapiens	147-150
21862613-3	2011	Our previous studies demonstrated that the ceramides activate the Nod-like receptor family, pyrin domain containing 3 (Nlrp3) inflammasome to cause the generation of mature IL-1beta and ablation of the Nlrp3 inflammasome in diet-induced obesity improves insulin signaling.	Ceramides	43-52	interleukin 1 beta	Homo sapiens	173-181
21862613-3	2011	Our previous studies demonstrated that the ceramides activate the Nod-like receptor family, pyrin domain containing 3 (Nlrp3) inflammasome to cause the generation of mature IL-1beta and ablation of the Nlrp3 inflammasome in diet-induced obesity improves insulin signaling.	Ceramides	43-52	NLR family pyrin domain containing 3	Homo sapiens	202-207
21972148-0	2011	Resuscitating wild-type p53 expression by disrupting ceramide glycosylation: a novel approach to target mutant p53 tumors.	Ceramides	53-61	tumor protein p53	Homo sapiens	24-27
21896638-4	2011	Ablation of SK1 did not affect mRNA or protein levels of SK2 and reduced intracellular levels of S1P while elevating ceramide levels.	Ceramides	117-125	sphingosine kinase 1	Homo sapiens	12-15
21546935-10	2011	At 6 months, the improvement in insulin sensitivity correlated with the change in total ceramide levels (r = -0.68, P = 0.02), and with plasma tumor necrosis factor-alpha (TNF-alpha) (r = -0.62, P = 0.04).	Ceramides	88-96	insulin	Homo sapiens	32-39
21546935-11	2011	We conclude that there is a potential role for ceramide lipids as mediators of the proinflammatory state and improved insulin sensitivity after gastric bypass surgery.	Ceramides	47-62	insulin	Homo sapiens	118-125
21972148-0	2011	Resuscitating wild-type p53 expression by disrupting ceramide glycosylation: a novel approach to target mutant p53 tumors.	Ceramides	53-61	tumor protein p53	Homo sapiens	111-114
21972148-3	2011	Recent evidence indicates that disrupting ceramide glycosylation can resuscitate wild-type p53 expression and p53-dependent apoptosis in mutant p53 tumors.	Ceramides	42-50	tumor protein p53	Homo sapiens	91-94
21972148-3	2011	Recent evidence indicates that disrupting ceramide glycosylation can resuscitate wild-type p53 expression and p53-dependent apoptosis in mutant p53 tumors.	Ceramides	42-50	tumor protein p53	Homo sapiens	110-113
21972148-3	2011	Recent evidence indicates that disrupting ceramide glycosylation can resuscitate wild-type p53 expression and p53-dependent apoptosis in mutant p53 tumors.	Ceramides	42-50	tumor protein p53	Homo sapiens	110-113
21595704-1	2011	BACKGROUND: Acid sphingomyelinase (ASM, EC 3.1.4.12) hydrolyzes sphingomyelin to ceramide and represents a major regulator of sphingolipid metabolism.	Ceramides	81-89	sphingomyelin phosphodiesterase 1	Homo sapiens	12-33
21595704-1	2011	BACKGROUND: Acid sphingomyelinase (ASM, EC 3.1.4.12) hydrolyzes sphingomyelin to ceramide and represents a major regulator of sphingolipid metabolism.	Ceramides	81-89	sphingomyelin phosphodiesterase 1	Homo sapiens	35-38
22331716-9	2011	CONCLUSION: These results show for the first time that these agents induce apoptosis in MCF-7 cells by downregulating the antiapoptotic SK-1 and GCS genes that may result in accumulation of apoptotic ceramides.	Ceramides	200-209	sphingosine kinase 1	Homo sapiens	136-140
21873552-0	2011	Skeletal muscle triglycerides, diacylglycerols, and ceramides in insulin resistance: another paradox in endurance-trained athletes?	Ceramides	52-61	insulin	Homo sapiens	65-72
21873552-9	2011	Ceramide content was higher in insulin-resistant obese muscle.	Ceramides	0-8	insulin	Homo sapiens	31-38
21873552-12	2011	Our data also provide additional evidence in humans linking ceramides to insulin resistance.	Ceramides	60-69	insulin	Homo sapiens	73-80
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.	Ceramides	14-22	UDP-glucose ceramide glucosyltransferase	Homo sapiens	117-120
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.	Ceramides	78-86	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-115
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.	Ceramides	78-86	UDP-glucose ceramide glucosyltransferase	Homo sapiens	117-120
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.	Ceramides	78-86	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-115
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.	Ceramides	78-86	UDP-glucose ceramide glucosyltransferase	Homo sapiens	117-120
21833718-3	2011	In this study, we investigated the role of ceramide metabolism by GCS in the regulation of imatinib-induced apoptosis in drug-sensitive and drug-resistant K562 and K562/IMA-0.2 and K562/IMA-1 human CML cells, which exhibit about 2.3- and 19-fold imatinib resistance, respectively.	Ceramides	43-51	UDP-glucose ceramide glucosyltransferase	Homo sapiens	66-69
21833718-11	2011	In reciprocal experiments, targeting GCS using its known inhibitor, PDMP, enhanced ceramide accumulation and increased cell death in response to imatinib in K562/IMA cells.	Ceramides	83-91	UDP-glucose ceramide glucosyltransferase	Homo sapiens	37-40
21833718-12	2011	CONCLUSION: Our data suggest the involvement of GCS in resistance to imatinib-induced apoptosis, and that targeting GCS by PDMP increased imatinib-induced cell death in drug-sensitive and drug-resistant K562 cells via enhancing ceramide accumulation.	Ceramides	228-236	UDP-glucose ceramide glucosyltransferase	Homo sapiens	116-119
21846728-3	2011	Expression of cysSA also inhibited endogenous AC activity in cells and increased ceramide.	Ceramides	81-89	cystatin SA	Homo sapiens	14-19
21846728-4	2011	Conversely, cysSA siRNA expression led to elevated AC activity and reduction in ceramide.	Ceramides	80-88	cystatin SA	Homo sapiens	12-17
21533981-3	2011	Recent studies have highlighted that acid sphingomyelinase (ASMase), which generates ceramide from sphingomyelin, is involved in modulation of membrane structures and signal transduction in addition to its metabolic role in the lysosome.	Ceramides	85-93	sphingomyelin phosphodiesterase 1	Homo sapiens	37-58
21533981-3	2011	Recent studies have highlighted that acid sphingomyelinase (ASMase), which generates ceramide from sphingomyelin, is involved in modulation of membrane structures and signal transduction in addition to its metabolic role in the lysosome.	Ceramides	85-93	sphingomyelin phosphodiesterase 1	Homo sapiens	60-66
21705667-8	2011	To reactivate GSK-3, we used glucosylceramide synthase (GCS) inhibitor PDMP to accumulate endogenous ceramide, a tumor-suppressor sphingolipid and a potent GSK-3 activator.	Ceramides	37-45	UDP-glucose ceramide glucosyltransferase	Homo sapiens	56-59
21705667-12	2011	The synergistic efficacy was Bcr-Abl restricted and correlated to increased intracellular ceramide levels and acted through GSK-3-mediated apoptosis.	Ceramides	90-98	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	29-36
22331716-9	2011	CONCLUSION: These results show for the first time that these agents induce apoptosis in MCF-7 cells by downregulating the antiapoptotic SK-1 and GCS genes that may result in accumulation of apoptotic ceramides.	Ceramides	200-209	UDP-glucose ceramide glucosyltransferase	Homo sapiens	145-148
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.	Ceramides	76-84	UDP-glucose ceramide glucosyltransferase	Homo sapiens	95-98
21840863-2	2011	We find that the sphingolipid pathway gene ISC1, the product of which catalyzes the generation of bioactive ceramides from complex sphingolipids, plays a novel role in determining cellular morphology following HU/MMS treatment.	Ceramides	108-117	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	43-47
21757428-5	2011	Inclusion of additional marker and exome sequence data in the analysis refined the linkage signal on chromosome 19 and implicated coding variation in LASS4, a gene regulated by leptin that is involved in ceramide synthesis.	Ceramides	204-212	ceramide synthase 4	Homo sapiens	150-155
21943220-0	2011	c-Jun NH2-terminal kinase activation is essential for up-regulation of LC3 during ceramide-induced autophagy in human nasopharyngeal carcinoma cells.	Ceramides	82-90	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
21844222-8	2011	Sms2 deficiency increased cell membrane ceramide but decreased SM levels.	Ceramides	40-48	sphingomyelin synthase 2	Mus musculus	0-4
21943220-0	2011	c-Jun NH2-terminal kinase activation is essential for up-regulation of LC3 during ceramide-induced autophagy in human nasopharyngeal carcinoma cells.	Ceramides	82-90	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	71-74
21943220-3	2011	METHODS: Ceramide-induced autophagy was determined by detecting LC3 expression with Western blotting and confocal microscopy in human nasopharyngeal carcinoma cell lines CNE2 and SUNE1.	Ceramides	9-17	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	64-67
21943220-7	2011	RESULTS: Ceramide-treated cells exhibited the characteristics of autophagy and JNK pathway activation.	Ceramides	9-17	mitogen-activated protein kinase 8	Homo sapiens	79-82
21943220-8	2011	Inhibition of JNK pathway could block the ceramide-induced autophagy and the up-regulation of LC3 expression.	Ceramides	42-50	mitogen-activated protein kinase 8	Homo sapiens	14-17
21943220-9	2011	Transcription factor c-Jun was involved in LC3 transcription regulation in response to ceramide treatment.	Ceramides	87-95	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	21-26
21943220-9	2011	Transcription factor c-Jun was involved in LC3 transcription regulation in response to ceramide treatment.	Ceramides	87-95	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	43-46
21943220-10	2011	CONCLUSIONS: Ceramide could induce autophagy in human nasopharyngeal carcinoma cells, and activation of JNK pathway was involved in ceramide-induced autophagy and LC3 expression.	Ceramides	132-140	mitogen-activated protein kinase 8	Homo sapiens	104-107
21943220-10	2011	CONCLUSIONS: Ceramide could induce autophagy in human nasopharyngeal carcinoma cells, and activation of JNK pathway was involved in ceramide-induced autophagy and LC3 expression.	Ceramides	132-140	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	163-166
21791630-8	2011	Remarkably, serum sphingolipid analysis revealed significant differences in patterns of C18-ceramide elevation in patients with CR/PR/SD in comparison with patients with PD, indicating the reconstitution of tumor suppressor ceramide generation by GEM/DOX treatment.	Ceramides	92-100	Bardet-Biedl syndrome 9	Homo sapiens	88-91
21708940-7	2011	The mechanisms of PP2A activation by IL-1beta involved neutral sphingomyelinase-2 (NSMase-2) and an accumulation of ceramide.	Ceramides	116-124	protein phosphatase 2 phosphatase activator	Homo sapiens	18-22
21708940-7	2011	The mechanisms of PP2A activation by IL-1beta involved neutral sphingomyelinase-2 (NSMase-2) and an accumulation of ceramide.	Ceramides	116-124	interleukin 1 beta	Homo sapiens	37-45
21708940-9	2011	The addition of sphingomyelinase, ceramide, or a proteasome inhibitor all led to retention of IRAK-1 at the cell membrane and to increased JNK phosphorylation.	Ceramides	34-42	interleukin 1 receptor associated kinase 1	Homo sapiens	94-100
21708940-9	2011	The addition of sphingomyelinase, ceramide, or a proteasome inhibitor all led to retention of IRAK-1 at the cell membrane and to increased JNK phosphorylation.	Ceramides	34-42	mitogen-activated protein kinase 8	Homo sapiens	139-142
21259059-8	2011	Although ceramide induced release of cytochrome c from mitochondria and activation of caspase-3, the ceramide-induced cell death was partially prevented by caspase inhibitors.	Ceramides	9-17	cytochrome c, somatic	Homo sapiens	37-49
21259059-8	2011	Although ceramide induced release of cytochrome c from mitochondria and activation of caspase-3, the ceramide-induced cell death was partially prevented by caspase inhibitors.	Ceramides	9-17	caspase 3	Homo sapiens	86-95
21610321-2	2011	In a recent study, we document that Ad.mda-7-induced ER stress and ceramide production leads to early autophagy that subsequently switches to apoptosis in human prostate cancer cells.	Ceramides	67-75	interleukin 24	Homo sapiens	39-44
21259059-8	2011	Although ceramide induced release of cytochrome c from mitochondria and activation of caspase-3, the ceramide-induced cell death was partially prevented by caspase inhibitors.	Ceramides	101-109	caspase 3	Homo sapiens	86-95
21136155-3	2011	Our new studies suggest that ceramide and its derivative, sphingosine-1-phosphate (S1P), act synergistically on embryonic stem (ES) cell differentiation.	Ceramides	29-37	sphingosine-1-phosphate receptor 1	Mus musculus	83-86
21737602-12	2011	Toxicity of accumulating lipid metabolites such as ceramides may be responsible for the fasting-induced impairment of cardiac function observed in the LCAD KO mouse.	Ceramides	51-60	acyl-Coenzyme A dehydrogenase, long-chain	Mus musculus	151-155
21771974-9	2011	Treatment of HREC with docosahexaenoic acid (DHA) specifically reduces expression of the caveolae-associated ASM, prevents a tumor necrosis factor-alpha-induced increase in the ceramide-to-sphingomyelin ratio in the caveolae, and inhibits cytokine-induced inflammatory signaling.	Ceramides	177-185	tumor necrosis factor	Homo sapiens	125-152
21719579-0	2011	Different fatty acids inhibit apoB100 secretion by different pathways: unique roles for ER stress, ceramide, and autophagy.	Ceramides	99-107	apolipoprotein B	Rattus norvegicus	30-37
21737602-10	2011	Myocardial ceramide content was higher in fasted LCAD KO mice compared with fasted WT mice (P<0.05).	Ceramides	11-19	acyl-Coenzyme A dehydrogenase, long-chain	Mus musculus	49-53
21635197-3	2011	EXPERT OPINION: Ceramide participates in beta-cell dysfunction and apoptosis after exposure to TNFalpha, IL-1beta and IFN-gamma, excessive amyloid and islet amyloid polypeptide or non-esterified fatty acids (lipotoxicity).	Ceramides	16-24	tumor necrosis factor	Homo sapiens	95-103
21635197-3	2011	EXPERT OPINION: Ceramide participates in beta-cell dysfunction and apoptosis after exposure to TNFalpha, IL-1beta and IFN-gamma, excessive amyloid and islet amyloid polypeptide or non-esterified fatty acids (lipotoxicity).	Ceramides	16-24	interleukin 1 beta	Homo sapiens	105-113
21635197-3	2011	EXPERT OPINION: Ceramide participates in beta-cell dysfunction and apoptosis after exposure to TNFalpha, IL-1beta and IFN-gamma, excessive amyloid and islet amyloid polypeptide or non-esterified fatty acids (lipotoxicity).	Ceramides	16-24	interferon gamma	Homo sapiens	118-127
21635197-4	2011	Knockout of sphingomyelin synthase 1, which converts ceramide to sphingomyelin, leads to impairment of insulin secretion.	Ceramides	53-61	sphingomyelin synthase 1	Homo sapiens	12-36
21635197-6	2011	Ceramide contributes to endoplasmatic reticulum (ER) stress, decreased mitochondrial membrane potential in insulin-secreting cells and mitochondrial release of cytochrome c into the cytosol, which are all triggers of apoptotic cell death.	Ceramides	0-8	insulin	Homo sapiens	107-114
21635197-7	2011	Ceramide-dependent signaling involves activation of extracellularly regulated kinases 1 and 2 (ERK1/2), downregulation of Period (Per)-aryl hydrocarbon receptor nuclear translocator (Arnt)-single-minded (Sim) kinase (PASK), activation of okadaic-acid-sensitive protein phosphatase 2A (PP2A) and stimulation of NADPH-oxidase with generation of superoxides and lipid peroxides.	Ceramides	0-8	mitogen-activated protein kinase 3	Homo sapiens	95-101
21635197-7	2011	Ceramide-dependent signaling involves activation of extracellularly regulated kinases 1 and 2 (ERK1/2), downregulation of Period (Per)-aryl hydrocarbon receptor nuclear translocator (Arnt)-single-minded (Sim) kinase (PASK), activation of okadaic-acid-sensitive protein phosphatase 2A (PP2A) and stimulation of NADPH-oxidase with generation of superoxides and lipid peroxides.	Ceramides	0-8	aryl hydrocarbon receptor nuclear translocator	Homo sapiens	183-187
21635197-7	2011	Ceramide-dependent signaling involves activation of extracellularly regulated kinases 1 and 2 (ERK1/2), downregulation of Period (Per)-aryl hydrocarbon receptor nuclear translocator (Arnt)-single-minded (Sim) kinase (PASK), activation of okadaic-acid-sensitive protein phosphatase 2A (PP2A) and stimulation of NADPH-oxidase with generation of superoxides and lipid peroxides.	Ceramides	0-8	PAS domain containing serine/threonine kinase	Homo sapiens	217-221
21635197-7	2011	Ceramide-dependent signaling involves activation of extracellularly regulated kinases 1 and 2 (ERK1/2), downregulation of Period (Per)-aryl hydrocarbon receptor nuclear translocator (Arnt)-single-minded (Sim) kinase (PASK), activation of okadaic-acid-sensitive protein phosphatase 2A (PP2A) and stimulation of NADPH-oxidase with generation of superoxides and lipid peroxides.	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	285-289
21635197-8	2011	Ceramide reduces the activity of voltage gated potassium (Kv)-channels in insulin-secreting cells.	Ceramides	0-8	insulin	Homo sapiens	74-81
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.	Ceramides	114-122	UDP-glucose ceramide glucosyltransferase	Homo sapiens	144-150
21336841-4	2011	However, they provide a source for the generation of harmful lipid metabolites such as diacylglycerol and ceramide, which are implicated in insulin resistance by perturbing insulin signaling pathways.	Ceramides	106-114	insulin	Homo sapiens	140-147
21336841-4	2011	However, they provide a source for the generation of harmful lipid metabolites such as diacylglycerol and ceramide, which are implicated in insulin resistance by perturbing insulin signaling pathways.	Ceramides	106-114	insulin	Homo sapiens	173-180
21873248-4	2011	Alteration of this compartmentalization, either by genetic targeting or ceramide-induced recruitment of PTEN to rafts, abolishes the activity of the entire pathway.	Ceramides	72-80	phosphatase and tensin homolog	Homo sapiens	104-108
21762071-4	2011	Sphingomyelin synthases (SMS) 1 and 2 convert ceramide to sphingomyelin (SM), a ubiquitous phospholipid in mammals.	Ceramides	46-54	sphingomyelin synthase 1	Homo sapiens	0-37
21763324-0	2011	Prohibitin (PHB) acts as a potent survival factor against ceramide induced apoptosis in rat granulosa cells.	Ceramides	58-66	prohibitin 1	Rattus norvegicus	0-10
21763324-0	2011	Prohibitin (PHB) acts as a potent survival factor against ceramide induced apoptosis in rat granulosa cells.	Ceramides	58-66	prohibitin 1	Rattus norvegicus	12-15
21763324-4	2011	MAIN METHODS: In the present study, we have examined the functional effects of loss-/gain-of-function of PHB using adenoviral technology in delaying apoptosis induced by the physiological ligand ceramide in rat GCs.	Ceramides	195-203	prohibitin 1	Rattus norvegicus	105-108
21763324-7	2011	In contrast, adenovirus (Ad) directed overexpression of PHB in GCs resulted in increased PHB content in mitochondria and delayed the onset of ceramide induced apoptosis in the infected GCs.	Ceramides	142-150	prohibitin 1	Rattus norvegicus	56-59
21763324-8	2011	SIGNIFICANCE: Taken together, these results provide novel evidences that a critical level of PHB expression within the mitochondria plays a key intra-molecular role in GC fate by mediating the inhibition of apoptosis and may therefore, contribute significantly to ceramide induced follicular atresia.	Ceramides	264-272	prohibitin 1	Rattus norvegicus	93-96
21592087-0	2011	Ceramide synthase 4 and de novo production of ceramides with specific N-acyl chain lengths are involved in glucolipotoxicity-induced apoptosis of INS-1 beta-cells.	Ceramides	46-55	insulin 1	Rattus norvegicus	146-151
21592087-8	2011	Moreover, overexpression of CerS4 amplified ceramide production and apoptosis induced by palmitate with 30 mM glucose, whereas down-regulation of CerS4 by siRNA (short interfering RNA) reduced apoptosis.	Ceramides	44-52	ceramide synthase 4	Rattus norvegicus	28-33
21592087-9	2011	CerS4 also potentiates ceramide accumulation and apoptosis induced by another saturated fatty acid: stearate.	Ceramides	23-31	ceramide synthase 4	Rattus norvegicus	0-5
21732532-11	2011	CONCLUSION: Our study suggests that HF diets reduce ceramide and lipid synthesis in the skin by reducing levels of SPT and HMG-CoA reductase through lowered adiponectin and PPAR-alpha activity.	Ceramides	52-60	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	115-118
21860602-16	2011	We found that only in human milk gangliosides was the ceramide carbon always even numbered, which is consistent with the notion that differences in the oligosaccharide and the ceramide moieties confer to their physiological distinctions.	Ceramides	54-62	Weaning weight-maternal milk	Bos taurus	28-32
21624361-1	2011	Ceramide 1-phosphate (C1P) is a novel bioactive sphingolipid formed by ceramide kinase (CERK)-catalyzed phosphorylation of ceramide.	Ceramides	71-79	ceramide kinase	Rattus norvegicus	88-92
21700700-3	2011	Among ceramidases, the enzymes that catabolize ceramide, acid ceramidase (aCDase) has been implicated in cancer progression.	Ceramides	47-55	N-acylsphingosine amidohydrolase 1	Homo sapiens	57-72
21860602-16	2011	We found that only in human milk gangliosides was the ceramide carbon always even numbered, which is consistent with the notion that differences in the oligosaccharide and the ceramide moieties confer to their physiological distinctions.	Ceramides	176-184	Weaning weight-maternal milk	Bos taurus	28-32
21735505-2	2011	Excess accumulation of intracellular LCACoA, diacylglycerols (DAGs) and ceramides may create insulin resistance with respect to glucose metabolism.	Ceramides	72-81	insulin	Homo sapiens	93-100
21669879-9	2011	Here, we established new cell lines, in which we can completely distinguish SMS2 activity from SMS1 activity, and we demonstrated that SMS2 could convert ceramide produced in the outer leaflet of the plasma membrane into SM.	Ceramides	154-162	sphingomyelin synthase 2	Mus musculus	135-139
21700700-3	2011	Among ceramidases, the enzymes that catabolize ceramide, acid ceramidase (aCDase) has been implicated in cancer progression.	Ceramides	47-55	N-acylsphingosine amidohydrolase 1	Homo sapiens	74-80
21700700-9	2011	In conclusion, we report that increased levels of ceramide, due to enhanced degradation of aCDase, are in part responsible for the cell death effects of DTIC.	Ceramides	50-58	N-acylsphingosine amidohydrolase 1	Homo sapiens	91-97
21621503-5	2011	Expression of hCERK in CHO cells caused cell rounding and lactate dehydrogenase (LDH) leakage, and co-addition of ceramide enhanced these responses.	Ceramides	114-122	ceramide kinase	Homo sapiens	14-19
21571040-5	2011	GENERAL SIGNIFICANCE: The findings help to explain why increased NADH levels resulting from ENOX2 inhibition result in decreased prosurvival sphingosine-1-phosphate and increased proapoptotic ceramide, both of which may be important to initiation of the ENOX2 inhibitor-induced apoptotic cascade.	Ceramides	192-200	ecto-NOX disulfide-thiol exchanger 2	Homo sapiens	92-97
21556947-5	2011	Application of the platform is demonstrated toward kinetic studies of ceramide, a biologically important lipid known to self-assemble into transmembrane ion channels, in response to dynamic treatments of small ions (La(3+)) and proteins (Bcl-x(L) mutant).	Ceramides	70-78	BCL2 like 1	Homo sapiens	238-246
21072519-4	2011	RESULTS: At the measured IC(50) of 10 muM, 4-HPR led to a 44-68% reduction in [(3)H]thymidine incorporation, a >3-fold increase in de novo ceramide levels, a 2.7-fold increase in ROS, and minor increases in markers of apoptosis.	Ceramides	142-150	haptoglobin-related protein	Homo sapiens	45-48
21551240-8	2011	Our findings not only provide mechanistic insight into the signaling pathways engaged by ceramide in the development of hyperalgesia, but also provide a potential pharmacological basis for developing inhibitors targeting the ceramide metabolic-to-COX-2 pathway as novel analgesics.	Ceramides	89-97	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	247-252
21551240-8	2011	Our findings not only provide mechanistic insight into the signaling pathways engaged by ceramide in the development of hyperalgesia, but also provide a potential pharmacological basis for developing inhibitors targeting the ceramide metabolic-to-COX-2 pathway as novel analgesics.	Ceramides	225-233	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	247-252
21551240-0	2011	Intraplantar-injected ceramide in rats induces hyperalgesia through an NF-kappaB- and p38 kinase-dependent cyclooxygenase 2/prostaglandin E2 pathway.	Ceramides	22-30	mitogen activated protein kinase 14	Rattus norvegicus	86-89
21615407-0	2011	Phosphorylation of Ser45 and Ser59 of alphaB-crystallin and p38/extracellular regulated kinase activity determine alphaB-crystallin-mediated protection of rat brain astrocytes from C2-ceramide- and staurosporine-induced cell death.	Ceramides	184-192	crystallin, alpha B	Rattus norvegicus	114-131
21551240-3	2011	We now demonstrate that, in addition to mechanical hyperalgesia, intraplantar injection of ceramide (10 mug) led to the development of thermal hyperalgesia that was dependent on induction of the inducible cyclooxygenase (COX-2) and subsequent increase of prostaglandin E(2) (PGE(2)).	Ceramides	91-99	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	221-226
21551240-5	2011	The importance of the COX-2 to PGE(2) pathway in ceramide signaling was underscored by the findings that intraplantar injection of a monoclonal PGE(2) antibody (4 mug) blocked the development of hyperalgesia.	Ceramides	49-57	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	22-27
21794038-2	2011	Ceramides and other toxic sphingolipids promote inflammation, lipotoxicity and insulin resistance; however, the role of ceramides in the pathogenesis of NASH has not been determined.	Ceramides	0-9	insulin	Homo sapiens	79-86
21549185-2	2011	The primary structure of the peptide that we predicted coincided completely with the amino acid sequence of the later identified sphingomyelin synthase 1 protein (SMS1), which catalyses the transfer of a phosphorylcholine moiety from phosphatidylcholine to ceramide, producing sphingomyelin and diacylglycerol (Huitema et al., 2004; Yamaoka et al., 2004).	Ceramides	257-265	sphingomyelin synthase 1	Homo sapiens	129-161
21549185-2	2011	The primary structure of the peptide that we predicted coincided completely with the amino acid sequence of the later identified sphingomyelin synthase 1 protein (SMS1), which catalyses the transfer of a phosphorylcholine moiety from phosphatidylcholine to ceramide, producing sphingomyelin and diacylglycerol (Huitema et al., 2004; Yamaoka et al., 2004).	Ceramides	257-265	sphingomyelin synthase 1	Homo sapiens	163-167
21613224-0	2011	Novel pathway of ceramide production in mitochondria: thioesterase and neutral ceramidase produce ceramide from sphingosine and acyl-CoA.	Ceramides	17-25	N-acylsphingosine amidohydrolase 2	Mus musculus	71-89
21653685-3	2011	Previously, we synthesized isoglobotrihexosylceramide (iGb3) analogues by introducing a hydroxyl group at C4 on the ceramide portion of iGb3 to produce 4-HO-iGb3 or to further deoxylation on the terminal galactose to produce 4"""-dh-iGb3.	Ceramides	45-53	alpha 1,3-galactosyltransferase 2 (isoglobotriaosylceramide synthase)	Mus musculus	55-59
21653685-3	2011	Previously, we synthesized isoglobotrihexosylceramide (iGb3) analogues by introducing a hydroxyl group at C4 on the ceramide portion of iGb3 to produce 4-HO-iGb3 or to further deoxylation on the terminal galactose to produce 4"""-dh-iGb3.	Ceramides	45-53	alpha 1,3-galactosyltransferase 2 (isoglobotriaosylceramide synthase)	Mus musculus	136-140
21653685-3	2011	Previously, we synthesized isoglobotrihexosylceramide (iGb3) analogues by introducing a hydroxyl group at C4 on the ceramide portion of iGb3 to produce 4-HO-iGb3 or to further deoxylation on the terminal galactose to produce 4"""-dh-iGb3.	Ceramides	45-53	alpha 1,3-galactosyltransferase 2 (isoglobotriaosylceramide synthase)	Mus musculus	136-140
21653685-3	2011	Previously, we synthesized isoglobotrihexosylceramide (iGb3) analogues by introducing a hydroxyl group at C4 on the ceramide portion of iGb3 to produce 4-HO-iGb3 or to further deoxylation on the terminal galactose to produce 4"""-dh-iGb3.	Ceramides	45-53	alpha 1,3-galactosyltransferase 2 (isoglobotriaosylceramide synthase)	Mus musculus	136-140
21396934-0	2011	P-glycoprotein antagonists confer synergistic sensitivity to short-chain ceramide in human multidrug-resistant cancer cells.	Ceramides	73-81	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
21396934-1	2011	P-glycoprotein (P-gp) antagonists inhibit ceramide metabolism at the juncture of glycosylation.	Ceramides	42-50	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
21396934-1	2011	P-glycoprotein (P-gp) antagonists inhibit ceramide metabolism at the juncture of glycosylation.	Ceramides	42-50	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
21613224-0	2011	Novel pathway of ceramide production in mitochondria: thioesterase and neutral ceramidase produce ceramide from sphingosine and acyl-CoA.	Ceramides	98-106	N-acylsphingosine amidohydrolase 2	Mus musculus	71-89
21613224-4	2011	Moreover, the levels of ceramide were dissimilar in liver mitochondria of WT and NCDase KO mice.	Ceramides	24-32	N-acylsphingosine amidohydrolase 2	Mus musculus	81-87
21613224-5	2011	These results suggest that NCDase is a key participant of ceramide formation in liver mitochondria.	Ceramides	58-66	N-acylsphingosine amidohydrolase 2	Homo sapiens	27-33
21389273-4	2011	Ceramide, a hydrolysis product of sphingomyelin, was also found colocalized with Duox1 or p47(phox) upon stimulation.	Ceramides	0-8	dual oxidase 1	Homo sapiens	81-86
21605625-2	2011	Once generated, ceramide is converted by sphingosine kinase (SphK) 1 and/or 2 to one of its active metabolite sphingosine-1-phosphate (S1P), which in turn signals through G-protein coupled S1P receptors.	Ceramides	16-24	sphingosine kinase 1	Rattus norvegicus	41-68
21605625-4	2011	Our results show that intraplantar injection of ceramide in rats led to a time-dependent development of thermal hyperalgesia that was associated with an increase in tumor necrosis factor-alpha (TNF-alpha) in paw tissues.	Ceramides	48-56	tumor necrosis factor	Rattus norvegicus	165-192
21605625-9	2011	Collectively, these results provide mechanistic evidence implicating the S1P-to-S1PR(1) pathway as a downstream signaling pathway in ceramide-induced hyperalgesia.	Ceramides	133-141	sphingosine-1-phosphate receptor 1	Rattus norvegicus	80-87
21605625-4	2011	Our results show that intraplantar injection of ceramide in rats led to a time-dependent development of thermal hyperalgesia that was associated with an increase in tumor necrosis factor-alpha (TNF-alpha) in paw tissues.	Ceramides	48-56	tumor necrosis factor	Rattus norvegicus	194-203
21558561-5	2011	12R-LOX forms 9R-hydroperoxy-linoleoyl-omega-hydroxyceramide, further converted by eLOX3 to specific epoxyalcohol (9R,10R-trans-epoxy-11E-13R-hydroxy) and 9-keto-10E,12Z esters of the ceramide; an epoxy-ketone derivative (9R,10R-trans-epoxy-11E-13-keto) is the most prominent oxidized ceramide in mouse skin.	Ceramides	52-60	arachidonate 12-lipoxygenase, 12R type	Mus musculus	0-7
21558561-5	2011	12R-LOX forms 9R-hydroperoxy-linoleoyl-omega-hydroxyceramide, further converted by eLOX3 to specific epoxyalcohol (9R,10R-trans-epoxy-11E-13R-hydroxy) and 9-keto-10E,12Z esters of the ceramide; an epoxy-ketone derivative (9R,10R-trans-epoxy-11E-13-keto) is the most prominent oxidized ceramide in mouse skin.	Ceramides	52-60	arachidonate lipoxygenase 3	Mus musculus	83-88
21558561-5	2011	12R-LOX forms 9R-hydroperoxy-linoleoyl-omega-hydroxyceramide, further converted by eLOX3 to specific epoxyalcohol (9R,10R-trans-epoxy-11E-13R-hydroxy) and 9-keto-10E,12Z esters of the ceramide; an epoxy-ketone derivative (9R,10R-trans-epoxy-11E-13-keto) is the most prominent oxidized ceramide in mouse skin.	Ceramides	184-192	arachidonate 12-lipoxygenase, 12R type	Mus musculus	0-7
21558561-5	2011	12R-LOX forms 9R-hydroperoxy-linoleoyl-omega-hydroxyceramide, further converted by eLOX3 to specific epoxyalcohol (9R,10R-trans-epoxy-11E-13R-hydroxy) and 9-keto-10E,12Z esters of the ceramide; an epoxy-ketone derivative (9R,10R-trans-epoxy-11E-13-keto) is the most prominent oxidized ceramide in mouse skin.	Ceramides	184-192	arachidonate lipoxygenase 3	Mus musculus	83-88
21389273-7	2011	Our results for the first time demonstrate that Duox1-mediated redox signaling in bronchial epithelial cells is associated with LR clustering dependent on the production of ceramide through ASMase.	Ceramides	173-181	dual oxidase 1	Homo sapiens	48-53
21389273-7	2011	Our results for the first time demonstrate that Duox1-mediated redox signaling in bronchial epithelial cells is associated with LR clustering dependent on the production of ceramide through ASMase.	Ceramides	173-181	sphingomyelin phosphodiesterase 1	Homo sapiens	190-196
21389273-4	2011	Ceramide, a hydrolysis product of sphingomyelin, was also found colocalized with Duox1 or p47(phox) upon stimulation.	Ceramides	0-8	pleckstrin	Homo sapiens	90-93
21530485-3	2011	Growth factor induction of neutral CDase (nCDase) has been shown to have a cytoprotective effect against cytokine-induced increases in ceramide levels.	Ceramides	135-143	N-acylsphingosine amidohydrolase 2	Homo sapiens	27-40
21530485-3	2011	Growth factor induction of neutral CDase (nCDase) has been shown to have a cytoprotective effect against cytokine-induced increases in ceramide levels.	Ceramides	135-143	N-acylsphingosine amidohydrolase 2	Homo sapiens	42-48
21530485-7	2011	RNA interference-mediated knockdown of the AP-1 subunit, c-Jun, inhibited the activity of the human nCDase proximal promoter, whereas, c-Jun overexpression increased promoter activity, which directly correlated with human nCDase mRNA transcription, decreased ceramide mass, and protection against caspase 3/7-dependent apoptosis.	Ceramides	259-267	N-acylsphingosine amidohydrolase 2	Homo sapiens	100-106
21530485-7	2011	RNA interference-mediated knockdown of the AP-1 subunit, c-Jun, inhibited the activity of the human nCDase proximal promoter, whereas, c-Jun overexpression increased promoter activity, which directly correlated with human nCDase mRNA transcription, decreased ceramide mass, and protection against caspase 3/7-dependent apoptosis.	Ceramides	259-267	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	135-140
21707788-2	2011	A lipidomic analysis revealed specific changes in sphingolipids that accompanied the premature ageing of Isc1p-deficient cells under severe calorie restriction conditions, including a decrease of dihydrosphingosine levels and an increase of dihydro-C(26) -ceramide and phyto-C(26) -ceramide levels, the latter raising the possibility of activation of ceramide-dependent protein phosphatases.	Ceramides	256-264	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	105-110
21570480-5	2011	PA-induced insulin resistance was ameliorated by inhibiting the de novo synthesis of ceramide, IkappaBalpha degradation or mTOR activation.	Ceramides	85-93	insulin	Homo sapiens	11-18
21570480-10	2011	CONCLUSIONS: PA-induced insulin resistance in skeletal muscle involves inflammatory (nuclear factor kappa B/mTOR) and nutrient (ceramide) pathways.	Ceramides	128-136	insulin	Homo sapiens	24-31
21490312-1	2011	Neutral sphingomyelinase (nSMase)-derived ceramide has been proposed as a mediator of hypoxic pulmonary vasoconstriction (HPV), a specific response of the pulmonary circulation.	Ceramides	42-50	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
21490312-1	2011	Neutral sphingomyelinase (nSMase)-derived ceramide has been proposed as a mediator of hypoxic pulmonary vasoconstriction (HPV), a specific response of the pulmonary circulation.	Ceramides	42-50	sphingomyelin phosphodiesterase 2	Homo sapiens	26-32
21490312-8	2011	Accordingly, ceramide inhibited K(v)1.5 and K(v)2.1 channels expressed in Ltk(-) cells.	Ceramides	13-21	leukocyte receptor tyrosine kinase	Homo sapiens	74-77
21490312-10	2011	The nSMase inhibitor GW4869 reduced the thromboxane-endoperoxide receptor agonist U46619-induced, but not endothelin-1-induced pulmonary vasoconstriction that was partly restored after addition of exogenous ceramide.	Ceramides	207-215	sphingomyelin phosphodiesterase 2	Homo sapiens	4-10
21707788-2	2011	A lipidomic analysis revealed specific changes in sphingolipids that accompanied the premature ageing of Isc1p-deficient cells under severe calorie restriction conditions, including a decrease of dihydrosphingosine levels and an increase of dihydro-C(26) -ceramide and phyto-C(26) -ceramide levels, the latter raising the possibility of activation of ceramide-dependent protein phosphatases.	Ceramides	282-290	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	105-110
21536668-5	2011	Importantly, pretreatment with nSMase2 siRNA significantly inhibited ATRA effects on ceramide levels and growth arrest.	Ceramides	85-93	sphingomyelin phosphodiesterase 3	Homo sapiens	31-38
21557271-1	2011	BACKGROUND: The purpose of this study was to determine whether the therapeutic efficacy of fenretinide (4-HPR), a ceramide-generating anticancer agent, could be enhanced in prostate cancer cells by inclusion of a novel synthetic acid ceramidase (AC) inhibitor, DM102, a pivaloylamide of a 2-substituted aminoethanol.	Ceramides	114-122	haptoglobin-related protein	Homo sapiens	106-109
21557271-1	2011	BACKGROUND: The purpose of this study was to determine whether the therapeutic efficacy of fenretinide (4-HPR), a ceramide-generating anticancer agent, could be enhanced in prostate cancer cells by inclusion of a novel synthetic acid ceramidase (AC) inhibitor, DM102, a pivaloylamide of a 2-substituted aminoethanol.	Ceramides	114-122	N-acylsphingosine amidohydrolase 1	Homo sapiens	1-3
21536668-6	2011	In contrast, nSMase2 overexpression was sufficient to increase ceramide levels and induce G(0)/G(1) growth arrest of asynchronous MCF-7 cells.	Ceramides	63-71	sphingomyelin phosphodiesterase 3	Homo sapiens	13-20
21593415-10	2011	Leptin treatment decreases Arc ceramide levels, with the decrease being important in leptin-induced anorectic actions and down-regulations of NPY and Bsx.	Ceramides	31-39	neuropeptide Y	Rattus norvegicus	142-145
21545791-2	2011	Treatment of SCCVII mouse squamous carcinoma cells using the silicone phthalocyanine Pc 4 for PDT induced increases in the prodeath global ceramides/dihydroceramides (DHceramides), and no changes in the prosurvival sphingosine-1-phosphate (S1P).	Ceramides	139-148	SUB1 homolog, transcriptional regulator	Mus musculus	85-89
21593415-10	2011	Leptin treatment decreases Arc ceramide levels, with the decrease being important in leptin-induced anorectic actions and down-regulations of NPY and Bsx.	Ceramides	31-39	brain specific homeobox	Rattus norvegicus	150-153
21593415-11	2011	Of interest, our data indicate that leptin impacts ceramide metabolism through malonyl-CoA and CPT-1c, and ceramide de novo biosynthesis acts downstream of both malonyl-CoA and CPT-1c in mediating their effects on feeding and expressions of NPY and Bsx.	Ceramides	107-115	carnitine palmitoyltransferase 1c	Rattus norvegicus	177-183
21593415-11	2011	Of interest, our data indicate that leptin impacts ceramide metabolism through malonyl-CoA and CPT-1c, and ceramide de novo biosynthesis acts downstream of both malonyl-CoA and CPT-1c in mediating their effects on feeding and expressions of NPY and Bsx.	Ceramides	107-115	neuropeptide Y	Rattus norvegicus	241-244
21593415-11	2011	Of interest, our data indicate that leptin impacts ceramide metabolism through malonyl-CoA and CPT-1c, and ceramide de novo biosynthesis acts downstream of both malonyl-CoA and CPT-1c in mediating their effects on feeding and expressions of NPY and Bsx.	Ceramides	107-115	brain specific homeobox	Rattus norvegicus	249-252
21378025-6	2011	Our data suggest that membrane CFTR regulates ceramide-enriched lipid raft signaling platforms required for the induction of Fas-mediated apoptotic signaling.	Ceramides	46-54	cystic fibrosis transmembrane conductance regulator	Mus musculus	31-35
21493710-3	2011	Acid ceramidase (ASAH1) plays a pivotal role in regulating the intracellular concentration of these two metabolites by hydrolyzing Cer into SPH, which is rapidly phosphorylated to form S1P.	Ceramides	131-134	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
21493710-3	2011	Acid ceramidase (ASAH1) plays a pivotal role in regulating the intracellular concentration of these two metabolites by hydrolyzing Cer into SPH, which is rapidly phosphorylated to form S1P.	Ceramides	131-134	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-22
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.	Ceramides	83-91	glucosylceramidase beta	Homo sapiens	15-38
21111813-2	2011	Many studies have shown that C1P is important for membrane biology and for the regulation of membrane-bound proteins, and the CERK enzyme has appeared to be tightly regulated in order to control both ceramide levels and production of C1P.	Ceramides	200-208	ceramide kinase	Homo sapiens	126-130
21431854-1	2011	Based on the "lipotoxic" hypothesis, the free fatty acid flux from the excessive amount of adipose tissue toward the peripheral tissues would induce the development of insulin resistance especially when the triglyceride storage or the concentration of intermediate fat metabolites (diacylglycerides, ceramides) within the cytoplasm of these cells become excessive.	Ceramides	300-309	insulin	Homo sapiens	168-175
21378025-2	2011	We have recently established a direct correlation between decreased lipid raft CFTR expression and emphysema progression through increased ceramide accumulation.	Ceramides	139-147	cystic fibrosis transmembrane conductance regulator	Mus musculus	79-83
21436125-8	2011	Moreover, in ABCB1-MDCK cells, Cd(2+)-induced ceramide formation, determined by a diacylglycerol kinase assay, was abolished and increased extrusion of nitro-2-1,3-benzoxadiazol-4-yl (NBD)-C(6)-ceramide, and NBD-C(6)-glucosylceramide was observed compared with MDCK cells.	Ceramides	46-54	ATP binding cassette subfamily B member 1	Canis lupus familiaris	13-18
21498783-7	2011	We next showed that adenovirus-mediated ATGL overexpression in human primary myotubes induced DAG and ceramide accumulation.	Ceramides	102-110	patatin like phospholipase domain containing 2	Homo sapiens	40-44
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.	Ceramides	126-134	UDP-glucose ceramide glucosyltransferase	Mus musculus	30-34
21674735-1	2011	BACKGROUND: The secretory form of acid sphingomyelinase (ASM) is postulated to play a key role in the retention and aggregation of lipoproteins in the subendothelial space of the arterial wall by converting sphingomyelin in lipoproteins into ceramide.	Ceramides	242-250	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	34-55
21674735-1	2011	BACKGROUND: The secretory form of acid sphingomyelinase (ASM) is postulated to play a key role in the retention and aggregation of lipoproteins in the subendothelial space of the arterial wall by converting sphingomyelin in lipoproteins into ceramide.	Ceramides	242-250	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	57-60
21436125-0	2011	ABCB1 protects kidney proximal tubule cells against cadmium-induced apoptosis: roles of cadmium and ceramide transport.	Ceramides	100-108	ATP binding cassette subfamily B member 1	Canis lupus familiaris	0-5
21436125-3	2011	Our aim was to investigate the role of ABCB1 in Cd(2+) transport and ceramide apoptosis.	Ceramides	69-77	ATP binding cassette subfamily B member 1	Canis lupus familiaris	39-44
22654794-0	2011	Intrinsic, Pro-Apoptotic Effects of IGFBP-3 on Breast Cancer Cells are Reversible: Involvement of PKA, Rho, and Ceramide.	Ceramides	112-120	insulin like growth factor binding protein 3	Homo sapiens	36-43
22654794-5	2011	We found on inhibiting protein kinase A (PKA), Rho associated kinase (ROCK), and ceramide, the accentuating effects of IGFBP-3 on apoptotic triggers were reversed, such that IGFBP-3 then conferred cell survival.	Ceramides	81-89	insulin like growth factor binding protein 3	Homo sapiens	119-126
22654794-5	2011	We found on inhibiting protein kinase A (PKA), Rho associated kinase (ROCK), and ceramide, the accentuating effects of IGFBP-3 on apoptotic triggers were reversed, such that IGFBP-3 then conferred cell survival.	Ceramides	81-89	insulin like growth factor binding protein 3	Homo sapiens	174-181
21388949-6	2011	Late ceramide generation was also found to be regulated by Bcl-xL, Bak, and caspases.	Ceramides	5-13	BCL2 like 1	Homo sapiens	59-65
21388949-6	2011	Late ceramide generation was also found to be regulated by Bcl-xL, Bak, and caspases.	Ceramides	5-13	BCL2 antagonist/killer 1	Homo sapiens	67-70
21388949-9	2011	Attempting to identify the CerS responsible for this effect, we found that combined knockdown of CerS5 and CerS6 was able to decrease long-chain ceramide accumulation and plasma membrane permeabilization.	Ceramides	145-153	ceramide synthase 5	Homo sapiens	97-102
21388949-9	2011	Attempting to identify the CerS responsible for this effect, we found that combined knockdown of CerS5 and CerS6 was able to decrease long-chain ceramide accumulation and plasma membrane permeabilization.	Ceramides	145-153	ceramide synthase 6	Homo sapiens	107-112
21252258-8	2011	We demonstrated that the AtCLB protein was capable of binding to the membrane lipid ceramide.	Ceramides	84-92	Calcium-dependent lipid-binding (CaLB domain) family protein	Arabidopsis thaliana	25-30
21333695-2	2011	De novo ceramide generation was responsible for the drug-induced apoptosis through a caspase-3-dependent pathway and a decrease of thrombospondin-1 expression in human thyroid carcinoma FTC-133 cells.	Ceramides	8-16	caspase 3	Homo sapiens	85-94
21333695-2	2011	De novo ceramide generation was responsible for the drug-induced apoptosis through a caspase-3-dependent pathway and a decrease of thrombospondin-1 expression in human thyroid carcinoma FTC-133 cells.	Ceramides	8-16	thrombospondin 1	Homo sapiens	131-147
21333695-4	2011	The set of our data established that camptothecin- and doxorubicin-induced activation of Jun N-terminal kinase/activating transcription factor 2 pathway via de novo ceramide synthesis down-regulates thrombospondin-1 expression and apoptosis in human thyroid carcinoma FTC-133 cells.	Ceramides	165-173	thrombospondin 1	Homo sapiens	199-215
21490391-0	2011	Lipid-induced insulin resistance mediated by the proinflammatory receptor TLR4 requires saturated fatty acid-induced ceramide biosynthesis in mice.	Ceramides	117-125	toll-like receptor 4	Mus musculus	74-78
21490391-3	2011	Using in vitro and in vivo systems to model lipid induction of TLR4-dependent inflammatory events in rodents, we show here that TLR4 is an upstream signaling component required for saturated fatty acid-induced ceramide biosynthesis.	Ceramides	210-218	toll-like receptor 4	Mus musculus	63-67
21490391-3	2011	Using in vitro and in vivo systems to model lipid induction of TLR4-dependent inflammatory events in rodents, we show here that TLR4 is an upstream signaling component required for saturated fatty acid-induced ceramide biosynthesis.	Ceramides	210-218	toll-like receptor 4	Mus musculus	128-132
21454530-4	2011	Our data demonstrate a novel role for palmitate in increasing mRNA encoding DES1, which is the enzyme responsible for generating ceramide from its precursor dihydroceramide and thus controls synthesis of the bioactive lipid ceramide.	Ceramides	129-137	delta 4-desaturase, sphingolipid 1	Homo sapiens	76-80
21454530-4	2011	Our data demonstrate a novel role for palmitate in increasing mRNA encoding DES1, which is the enzyme responsible for generating ceramide from its precursor dihydroceramide and thus controls synthesis of the bioactive lipid ceramide.	Ceramides	164-172	delta 4-desaturase, sphingolipid 1	Homo sapiens	76-80
21454530-5	2011	Moreover, co-treatment with oleate prevented the increase in ceramide, and this occurred through attenuation of the increase in message and activity of DES1.	Ceramides	61-69	delta 4-desaturase, sphingolipid 1	Homo sapiens	152-156
21327867-1	2011	AIMS/HYPOTHESIS: Intramyocellular lipids, including diacylglycerol (DAG) and ceramides, have been linked to insulin resistance.	Ceramides	77-86	insulin	Homo sapiens	108-115
21393425-9	2011	These observations are supported by the effect of ceramide, a PP2A activator, on androgen-independent C4-2 cells.	Ceramides	50-58	protein phosphatase 2 phosphatase activator	Homo sapiens	62-66
21393425-10	2011	Ceramide inhibited the growth of C4-2 cells on androgen deprivation, an effect that could be abrogated by PP2A downregulation.	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	106-110
21540829-12	2011	We have also used this method for the reconstitution of a ceramide-associated complex of recombinant aPKC with the cell polarity-related proteins Par6 and Cdc42.	Ceramides	58-66	Prader Willi/Angelman region RNA 6	Homo sapiens	146-150
20727556-5	2011	Induction of CRP protein was mimicked by ceramide, whereas bromopalmitate and other common free fatty acids such as oleate or linoleate were ineffective.	Ceramides	41-49	C-reactive protein	Homo sapiens	13-16
21303347-5	2011	Moreover, only overexpression of nSMase2, but not nSMase1 or nSMase3, had significant effects on cellular sphingolipid levels, increasing ceramide and decreasing sphingomyelin.	Ceramides	138-146	sphingomyelin phosphodiesterase 3	Homo sapiens	33-40
21487040-7	2011	Restoration of IRF8 expression repressed A-CDase expression, resulting in C16 ceramide accumulation and increased sensitivity of CML cells to FasL-induced apoptosis.	Ceramides	78-86	interferon regulatory factor 8	Homo sapiens	15-19
21487040-10	2011	At the functional level, inhibition of A-CDase activity, silencing A-CDase expression, or application of exogenous C16 ceramide sensitized CML cells to FasL-induced apoptosis, whereas overexpression of A-CDase decreased CML cells" sensitivity to FasL-induced apoptosis.	Ceramides	119-127	Fas ligand	Homo sapiens	152-156
21490391-4	2011	This increase in ceramide production was associated with the upregulation of genes driving ceramide biosynthesis, an event dependent of the activity of the proinflammatory kinase IKKbeta.	Ceramides	17-25	inhibitor of kappaB kinase beta	Mus musculus	179-186
21490391-4	2011	This increase in ceramide production was associated with the upregulation of genes driving ceramide biosynthesis, an event dependent of the activity of the proinflammatory kinase IKKbeta.	Ceramides	91-99	inhibitor of kappaB kinase beta	Mus musculus	179-186
21677348-4	2011	Accumulation of intracellular lipids such as diacylglycerols (DAG) and ceramides (CER) was found to interfere directly with the insulin signaling cascade, inducing hepatic IR.	Ceramides	71-80	insulin	Homo sapiens	128-135
21677348-4	2011	Accumulation of intracellular lipids such as diacylglycerols (DAG) and ceramides (CER) was found to interfere directly with the insulin signaling cascade, inducing hepatic IR.	Ceramides	82-85	insulin	Homo sapiens	128-135
21335555-1	2011	Acid sphingomyelinase (aSMase) generates the bioactive lipid ceramide (Cer) from hydrolysis of sphingomyelin (SM).	Ceramides	61-69	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
21335555-1	2011	Acid sphingomyelinase (aSMase) generates the bioactive lipid ceramide (Cer) from hydrolysis of sphingomyelin (SM).	Ceramides	61-69	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
21335555-1	2011	Acid sphingomyelinase (aSMase) generates the bioactive lipid ceramide (Cer) from hydrolysis of sphingomyelin (SM).	Ceramides	71-74	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
21335555-1	2011	Acid sphingomyelinase (aSMase) generates the bioactive lipid ceramide (Cer) from hydrolysis of sphingomyelin (SM).	Ceramides	71-74	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
21540829-12	2011	We have also used this method for the reconstitution of a ceramide-associated complex of recombinant aPKC with the cell polarity-related proteins Par6 and Cdc42.	Ceramides	58-66	cell division cycle 42	Homo sapiens	155-160
21355583-7	2011	On the other hand, in the more asymmetric C12:0 and C10:0 ceramides, liquid expanded states and liquid expanded-condensed transitions occurred.	Ceramides	58-67	chromosome 12 open reading frame 57	Homo sapiens	52-55
21355583-3	2011	In this work, films of ceramides N-acylated with the saturated fatty acids C10, C12, C14, and C16 were studied at the air-aqueous interface.	Ceramides	23-32	chromosome 12 open reading frame 57	Homo sapiens	75-78
21355583-9	2011	C12:0 ceramide domains were larger and more densely branched than those of C10:0 ceramide.	Ceramides	81-89	chromosome 12 open reading frame 57	Homo sapiens	75-78
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.	Ceramides	139-147	aspartyl protease BAR1	Saccharomyces cerevisiae S288C	87-92
21278133-3	2011	We investigated whether GLP-1 inhibits apoptosis in HL-1 cardiomyocytes stimulated with staurosporine, palmitate, and ceramide.	Ceramides	118-126	glucagon	Homo sapiens	24-29
21278133-12	2011	Furthermore, GLP-1 inhibited palmitate- and ceramide-induced phosphatidylserine exposure and DNA fragmentation.	Ceramides	44-52	glucagon	Homo sapiens	13-18
21163859-1	2011	Acid sphingomyelinase (ASM) regulates the homeostasis of sphingolipids, including ceramides and sphingosine-1-phosphate (S1P).	Ceramides	82-91	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
21163859-1	2011	Acid sphingomyelinase (ASM) regulates the homeostasis of sphingolipids, including ceramides and sphingosine-1-phosphate (S1P).	Ceramides	82-91	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
21695021-10	2011	Recently, studies have shown that ceramides by increasing PPAR delta also increase the expression of ABCA12, which would facilitate the formation of lamellar bodies.	Ceramides	34-43	peroxisome proliferator activated receptor delta	Homo sapiens	58-68
21695021-10	2011	Recently, studies have shown that ceramides by increasing PPAR delta also increase the expression of ABCA12, which would facilitate the formation of lamellar bodies.	Ceramides	34-43	ATP binding cassette subfamily A member 12	Homo sapiens	101-107
21177474-1	2011	Alkaline sphingomyelinase (alk-SMase) hydrolyses sphingomyelin (SM) to ceramide in the gut.	Ceramides	71-79	ectonucleotide pyrophosphatase/phosphodiesterase 7	Mus musculus	0-36
21351771-0	2011	Expedient and practical synthesis of CERT-dependent ceramide trafficking inhibitor HPA-12 and its analogues.	Ceramides	52-60	ceramide transporter 1	Homo sapiens	37-41
21351771-2	2011	This led to the revision of the reported stereochemistry of the first inhibitor of CERT-dependent ceramide trafficking HPA-12 from (R,R)-anti- to the (R,S)-syn-enantiomer.	Ceramides	98-106	ceramide transporter 1	Homo sapiens	83-87
21351771-2	2011	This led to the revision of the reported stereochemistry of the first inhibitor of CERT-dependent ceramide trafficking HPA-12 from (R,R)-anti- to the (R,S)-syn-enantiomer.	Ceramides	98-106	synemin	Homo sapiens	156-159
21040745-7	2011	Importantly, PCERA-1 and ceramide-1-phosphate (C1P) stimulated the enzymatic activity of cPLA(2)alpha in an in vitro assay, whereas CERA-1 and ceramide inhibited both basal and C1P-stimulated cPLA(2)alpha activity.	Ceramides	25-33	phospholipase A2 group IVA	Homo sapiens	89-101
21236359-0	2011	Ceramide induces serotonin release from RBL-2H3 mast cells through calcium mediated activation of phospholipase A2.	Ceramides	0-8	phospholipase A2 group IB	Rattus norvegicus	98-114
21236359-9	2011	Taken together, these results suggest that ceramide is involved in mast cell degranulation via the calcium-mediated activation of PLA(2).	Ceramides	43-51	phospholipase A2 group IB	Rattus norvegicus	130-136
21040745-7	2011	Importantly, PCERA-1 and ceramide-1-phosphate (C1P) stimulated the enzymatic activity of cPLA(2)alpha in an in vitro assay, whereas CERA-1 and ceramide inhibited both basal and C1P-stimulated cPLA(2)alpha activity.	Ceramides	25-33	phospholipase A2 group IVA	Homo sapiens	192-204
21384831-1	2011	Glucocerebrosidase (GCase, acid beta-Glucosidase) hydrolyzes the sphingolipid glucosylceramide into glucose and ceramide.	Ceramides	86-94	glucosylceramidase beta	Homo sapiens	27-48
21483866-0	2011	Mitochondrial dysfunction links ceramide activated HRK expression and cell death.	Ceramides	32-40	harakiri, BCL2 interacting protein	Homo sapiens	51-54
21483866-11	2011	Ceramide induced the expression of the harikari gene(HRK) and up-regulated JNK phosphorylation.	Ceramides	0-8	harakiri, BCL2 interacting protein	Homo sapiens	53-56
21483866-12	2011	In ceramide treated cells HRK was translocated to mitochondria, where it was found to interact with mitochondrial protein p32.	Ceramides	3-11	harakiri, BCL2 interacting protein	Homo sapiens	26-29
21483866-12	2011	In ceramide treated cells HRK was translocated to mitochondria, where it was found to interact with mitochondrial protein p32.	Ceramides	3-11	inhibitor of growth family member 2	Homo sapiens	122-125
21483866-14	2011	Ceramide-induced expression of HRK, mitochondrial dysfunction and cell death were reduced by HRK knockdown with HRK siRNA.	Ceramides	0-8	harakiri, BCL2 interacting protein	Homo sapiens	31-34
21483866-14	2011	Ceramide-induced expression of HRK, mitochondrial dysfunction and cell death were reduced by HRK knockdown with HRK siRNA.	Ceramides	0-8	harakiri, BCL2 interacting protein	Homo sapiens	93-96
21483866-14	2011	Ceramide-induced expression of HRK, mitochondrial dysfunction and cell death were reduced by HRK knockdown with HRK siRNA.	Ceramides	0-8	harakiri, BCL2 interacting protein	Homo sapiens	93-96
21483866-15	2011	CONCLUSION: Our data document that ceramide is capable of inducing death of corneal stromal fibroblasts through the induction of HRK mediated mitochondria dysfunction.	Ceramides	35-43	harakiri, BCL2 interacting protein	Homo sapiens	129-132
21251901-0	2011	A new intranasal influenza vaccine based on a novel polycationic lipid-ceramide carbamoyl-spermine (CCS).	Ceramides	71-79	copper chaperone for superoxide dismutase	Mustela putorius furo	100-103
21278235-4	2011	Here, we report an alternative approach that involves suppression of glucosylceramide synthase (GCS), an enzyme that glycosylates ceramide and blunts its proapoptotic activity in cancer cells.	Ceramides	77-85	UDP-glucose ceramide glucosyltransferase	Homo sapiens	96-99
21278235-10	2011	Our findings indicate that restoring active ceramide to cells can resuscitate wild-type p53 function in p53-mutant cells, offering preclinical support for a novel type of mechanism-based therapy in the many human cancers harboring p53 mutations.	Ceramides	44-52	tumor protein p53	Homo sapiens	88-91
21278235-10	2011	Our findings indicate that restoring active ceramide to cells can resuscitate wild-type p53 function in p53-mutant cells, offering preclinical support for a novel type of mechanism-based therapy in the many human cancers harboring p53 mutations.	Ceramides	44-52	tumor protein p53	Homo sapiens	104-107
21278235-10	2011	Our findings indicate that restoring active ceramide to cells can resuscitate wild-type p53 function in p53-mutant cells, offering preclinical support for a novel type of mechanism-based therapy in the many human cancers harboring p53 mutations.	Ceramides	44-52	tumor protein p53	Homo sapiens	104-107
21186402-1	2011	Glucosylceramide synthase (GCS) is a key enzyme engaged in the biosynthesis of glycosphingolipids and in regulating ceramide metabolism.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
20448054-3	2011	Recently, we discovered that CS-induced ceramide generation and apoptosis in pulmonary cells is governed by neutral sphingomyelinase (nSMase) 2.	Ceramides	40-48	sphingomyelin phosphodiesterase 3	Homo sapiens	108-143
20448054-4	2011	In the current experiments, we expanded our studies to investigate whether nSMase2 governs ceramide generation and apoptosis in vivo using rodent and human models of CS-induced lung injury.	Ceramides	91-99	sphingomyelin phosphodiesterase 3	Homo sapiens	75-82
20448054-7	2011	We further showed that mice that are heterozygous for nSMase2 demonstrate significant decrease in ceramide generation after CS exposure, whereas acidic sphingomyelinase (aSMase) knockout mice maintain wild-type ceramide levels, confirming our previous findings (in human airway epithelial cells) that only nSMase2, and not aSMase, is activated by CS exposure.	Ceramides	98-106	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	54-61
20448054-9	2011	Taken together, these data establish the central in vivo role of nSMase2 in ceramide generation, aberrant apoptosis, and lung injury under CS exposure, underscoring its promise as a novel target for the prevention of CS-induced airspace destruction.	Ceramides	76-84	sphingomyelin phosphodiesterase 3	Homo sapiens	65-72
21186402-3	2011	The chemosensitizing effect of inhibitors of GCS (e.g. PDMP and selected analogues) has been observed with a variety of tumor cells leading to the proposal that the sensitizing activity of GCS inhibitors is primarily through increases in intracellular ceramide leading to induction of apoptosis.	Ceramides	252-260	UDP-glucose ceramide glucosyltransferase	Homo sapiens	45-48
21186402-3	2011	The chemosensitizing effect of inhibitors of GCS (e.g. PDMP and selected analogues) has been observed with a variety of tumor cells leading to the proposal that the sensitizing activity of GCS inhibitors is primarily through increases in intracellular ceramide leading to induction of apoptosis.	Ceramides	252-260	UDP-glucose ceramide glucosyltransferase	Homo sapiens	189-192
21177823-3	2011	The MAM, which serves as a site for lipid transfer and calcium signaling to mitochondria, is enriched in detergent-resistant membrane (DRM)-forming lipids, including cholesterol and ceramide, which are found in lower concentrations in the bulk ER.	Ceramides	182-190	sarcoglycan gamma	Homo sapiens	4-7
21217100-7	2011	CME-1 reduced H(2)O(2) treatment-elevated C16- and C18-ceramide levels measured by LC/MS/MS in RAW264.7 cells.	Ceramides	55-63	Bardet-Biedl syndrome 9	Homo sapiens	51-54
21217100-8	2011	Results suggest that CME-1 protects RAW264.7 cells against oxidative stress through inhibition of SMase activity and reduction of C16- and C18-ceramide levels.	Ceramides	143-151	Bardet-Biedl syndrome 9	Homo sapiens	139-142
21119025-6	2011	Ad.5/3-mda-7 increased ceramide levels in a PERK-dependent fashion that were responsible for elevated cytosolic Ca(2+) levels that promoted ROS generation; 17AAG did not further enhance cytokine-induced ceramide generation.	Ceramides	23-31	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	44-48
21119025-0	2011	A serotype 5/3 adenovirus expressing MDA-7/IL-24 infects renal carcinoma cells and promotes toxicity of agents that increase ROS and ceramide levels.	Ceramides	133-141	interleukin 24	Homo sapiens	37-42
21119025-8	2011	Our data indicate that in RCCs, Ad.5/3-mda-7-induced ceramide generation plays a central role in tumor cell killing and inhibition of multiple signaling pathways may have utility in promoting MDA-7/IL-24 lethality in renal cancer.	Ceramides	53-61	interleukin 24	Homo sapiens	39-44
21119025-0	2011	A serotype 5/3 adenovirus expressing MDA-7/IL-24 infects renal carcinoma cells and promotes toxicity of agents that increase ROS and ceramide levels.	Ceramides	133-141	interleukin 24	Homo sapiens	43-48
21116286-2	2011	The consequence of AC overexpression is the ability to convert ceramide, which is often produced as a proapoptotic response to stress, to sphingosine, which can then be converted to the prosurvival molecule sphingosine-1-phosphate.	Ceramides	63-71	N-acylsphingosine amidohydrolase 1	Homo sapiens	19-21
21119025-5	2011	Inhibition of ROS generation, elevated cytosolic Ca(2+), or de novo ceramide synthesis blocked Ad.5/3-mda-7 +- agent-induced CD95 activation and the enhancement of apoptosis.	Ceramides	68-76	interleukin 24	Homo sapiens	102-107
21119025-5	2011	Inhibition of ROS generation, elevated cytosolic Ca(2+), or de novo ceramide synthesis blocked Ad.5/3-mda-7 +- agent-induced CD95 activation and the enhancement of apoptosis.	Ceramides	68-76	Fas cell surface death receptor	Homo sapiens	125-129
21119025-6	2011	Ad.5/3-mda-7 increased ceramide levels in a PERK-dependent fashion that were responsible for elevated cytosolic Ca(2+) levels that promoted ROS generation; 17AAG did not further enhance cytokine-induced ceramide generation.	Ceramides	23-31	interleukin 24	Homo sapiens	7-12
21116286-3	2011	In addition to their ability to metabolize ceramide produced in response to stress, we show here that prostate cancer cell lines overexpressing AC also have increased lysosomal density and increased levels of autophagy.	Ceramides	43-51	N-acylsphingosine amidohydrolase 1	Homo sapiens	144-146
21368890-3	2011	Concomitantly and independent of DNA damage, IR activates acid sphingomyelinase (ASMase), which generates ceramide, thereby promoting radiation-induced apoptosis.	Ceramides	106-114	sphingomyelin phosphodiesterase 1	Homo sapiens	81-87
21148554-1	2011	Ceramides, which are membrane sphingolipids and key mediators of cell-stress responses, are generated by a family of (dihydro) ceramide synthases (Lass1-6/CerS1-6).	Ceramides	0-9	dynein axonemal intermediate chain 7	Homo sapiens	147-154
21148554-1	2011	Ceramides, which are membrane sphingolipids and key mediators of cell-stress responses, are generated by a family of (dihydro) ceramide synthases (Lass1-6/CerS1-6).	Ceramides	0-9	ceramide synthase 1	Homo sapiens	155-160
21148554-3	2011	In contrast, C(16:0)-ceramide was gradually reduced and CerS6 was down-regulated in mitochondria, thereby implicating CerS6 as a primary ceramide synthase generating C(16:0)-ceramide.	Ceramides	21-29	ceramide synthase 6	Homo sapiens	118-123
21148554-3	2011	In contrast, C(16:0)-ceramide was gradually reduced and CerS6 was down-regulated in mitochondria, thereby implicating CerS6 as a primary ceramide synthase generating C(16:0)-ceramide.	Ceramides	137-145	ceramide synthase 6	Homo sapiens	118-123
21148554-4	2011	Investigations into the role of CerS6 in mitochondria revealed that ceramide synthase down-regulation is associated with dramatically decreased mitochondrial Ca(2+)-loading capacity, which could be rescued by addition of ceramide.	Ceramides	68-76	ceramide synthase 6	Homo sapiens	32-37
21148554-6	2011	This suggests that CerS6-generated ceramide could prevent mitochondrial permeability transition pore opening, leading to increased Ca(2+) accumulation in the mitochondrial matrix.	Ceramides	35-43	ceramide synthase 6	Homo sapiens	19-24
21368890-8	2011	SPL acts through a novel feedback mechanism that amplifies stress-induced ceramide accumulation, and downregulation/inhibition of either SPL or ASMase prevents premature cell cycle progression and mitotic death.	Ceramides	74-82	sphingosine-1-phosphate lyase 1	Homo sapiens	0-3
20823276-5	2011	Lysosomal fluorescent dye (FM1-43) quenching and de-quenching revealed that visfatin induced the fusion of lysosomes to cell membranes and incorporation of acid sphingomyelinase and its product, ceramide, in such MR-NOX signalling platforms.	Ceramides	195-203	nicotinamide phosphoribosyltransferase	Bos taurus	76-84
21115496-1	2011	Sphingomyelin synthase 1 (SMS1) catalyzes the conversion of ceramide to sphingomyelin.	Ceramides	60-68	sphingomyelin synthase 1	Mus musculus	0-24
21115496-1	2011	Sphingomyelin synthase 1 (SMS1) catalyzes the conversion of ceramide to sphingomyelin.	Ceramides	60-68	sphingomyelin synthase 1	Mus musculus	26-30
21145358-6	2011	Given that the function of dUTPase is to decrease the levels of dUTP, our results strongly support an emerging role for dUTP as a pro-apoptotic second messenger in the same vein as ROS and ceramide.	Ceramides	189-197	Deoxyuridine triphosphatase	Drosophila melanogaster	27-34
21098024-1	2011	Acid sphingomyelinase (aSMase) catalyzes the hydrolysis of sphingomyelin (SM) to form the bioactive lipid ceramide (Cer).	Ceramides	106-114	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
21098024-1	2011	Acid sphingomyelinase (aSMase) catalyzes the hydrolysis of sphingomyelin (SM) to form the bioactive lipid ceramide (Cer).	Ceramides	106-114	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
21098024-1	2011	Acid sphingomyelinase (aSMase) catalyzes the hydrolysis of sphingomyelin (SM) to form the bioactive lipid ceramide (Cer).	Ceramides	116-119	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
21098024-1	2011	Acid sphingomyelinase (aSMase) catalyzes the hydrolysis of sphingomyelin (SM) to form the bioactive lipid ceramide (Cer).	Ceramides	116-119	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
20378749-3	2011	This study examined the role in PMN chemotaxis of neutral sphingomyelinase (N-SMase), a plasma membrane-associated enzyme that converts sphingomyelin to ceramide.	Ceramides	153-161	sphingomyelin phosphodiesterase 2	Homo sapiens	50-74
20378749-3	2011	This study examined the role in PMN chemotaxis of neutral sphingomyelinase (N-SMase), a plasma membrane-associated enzyme that converts sphingomyelin to ceramide.	Ceramides	153-161	sphingomyelin phosphodiesterase 2	Homo sapiens	76-83
21380806-5	2011	Further, the two phytosphingosines specifically inhibited the ceramide generation regulated by nSMase2.	Ceramides	62-70	sphingomyelin phosphodiesterase 3	Homo sapiens	95-102
20823276-7	2011	CONCLUSION: These results suggest that lysosome-associated molecular trafficking and consequent ceramide accumulation in cell membrane may mediate the assembly of NOX subunits and their activation in response to adipokine visfatin in CAECs, thereby producing endothelial dysfunction in coronary circulation.	Ceramides	96-104	nicotinamide phosphoribosyltransferase	Bos taurus	222-230
21174057-5	2011	PKC-delta translocation to lysosomes is associated with lysosomal acidic sphingomyelinase (ASM) phosphorylation and activation, which in turn leads to an increase in ceramide (CER) content in lysosomes.	Ceramides	166-174	protein kinase C delta	Homo sapiens	0-9
21421913-4	2011	CERT mediated transport of ceramide to the TGN, we suggest, is used for increasing the local production and concentration of DAG.	Ceramides	27-35	ceramide transporter 1	Homo sapiens	0-4
21174057-5	2011	PKC-delta translocation to lysosomes is associated with lysosomal acidic sphingomyelinase (ASM) phosphorylation and activation, which in turn leads to an increase in ceramide (CER) content in lysosomes.	Ceramides	166-174	sphingomyelin phosphodiesterase 1	Homo sapiens	91-94
21174057-5	2011	PKC-delta translocation to lysosomes is associated with lysosomal acidic sphingomyelinase (ASM) phosphorylation and activation, which in turn leads to an increase in ceramide (CER) content in lysosomes.	Ceramides	176-179	protein kinase C delta	Homo sapiens	0-9
21174057-5	2011	PKC-delta translocation to lysosomes is associated with lysosomal acidic sphingomyelinase (ASM) phosphorylation and activation, which in turn leads to an increase in ceramide (CER) content in lysosomes.	Ceramides	176-179	sphingomyelin phosphodiesterase 1	Homo sapiens	91-94
21910087-8	2011	Ceramide decreases SREBP by inhibiting sphingolipid synthesis.	Ceramides	0-8	Sterol regulatory element binding protein	Drosophila melanogaster	19-24
21217695-4	2011	We further found that the Nlrp3 inflammasome senses lipotoxicity-associated increases in intracellular ceramide to induce caspase-1 cleavage in macrophages and adipose tissue.	Ceramides	103-111	NLR family, pyrin domain containing 3	Mus musculus	26-31
21217695-4	2011	We further found that the Nlrp3 inflammasome senses lipotoxicity-associated increases in intracellular ceramide to induce caspase-1 cleavage in macrophages and adipose tissue.	Ceramides	103-111	caspase 1	Mus musculus	122-131
21167294-4	2011	SPT activation by LPS elevated cellular levels of ceramides and sphingomyelin (SM).	Ceramides	50-59	toll-like receptor 4	Mus musculus	18-21
21167294-5	2011	Pharmacological inhibition of nuclear factor kappa B (NFkappaB) prevented LPS-induced upregulation of Sptlc2 while transfection of p65 subunit of NFkappaB upregulated Sptlc2 and increased cellular ceramide levels.	Ceramides	197-205	toll-like receptor 4	Mus musculus	74-77
21167294-5	2011	Pharmacological inhibition of nuclear factor kappa B (NFkappaB) prevented LPS-induced upregulation of Sptlc2 while transfection of p65 subunit of NFkappaB upregulated Sptlc2 and increased cellular ceramide levels.	Ceramides	197-205	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	131-134
21167294-5	2011	Pharmacological inhibition of nuclear factor kappa B (NFkappaB) prevented LPS-induced upregulation of Sptlc2 while transfection of p65 subunit of NFkappaB upregulated Sptlc2 and increased cellular ceramide levels.	Ceramides	197-205	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	146-154
21176778-5	2011	Understanding how DAG- and ceramide-activated PKCs impair insulin signalling would help to develop treatments to fight insulin resistance.	Ceramides	27-35	insulin	Homo sapiens	58-65
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	tumor necrosis factor	Homo sapiens	32-54
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	tumor necrosis factor	Homo sapiens	56-59
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	sphingomyelin phosphodiesterase 1	Homo sapiens	102-123
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	sphingomyelin phosphodiesterase 1	Homo sapiens	125-132
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	cathepsin D	Homo sapiens	184-195
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	BH3 interacting domain death agonist	Homo sapiens	212-215
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	caspase 9	Homo sapiens	230-239
21157428-1	2011	We previously demonstrated that tumour necrosis factor (TNF)-induced ceramide production by endosomal acid sphingomyelinase (A-SMase) couples to apoptosis signalling via activation of cathepsin D and cleavage of Bid, resulting in caspase-9 and caspase-3 activation.	Ceramides	69-77	caspase 3	Homo sapiens	244-253
20974858-10	2011	Ceramide treatment partially blocked promoter activity decreases induced by Sp1/Sp3 knockdown.	Ceramides	0-8	Sp3 transcription factor	Homo sapiens	80-83
20974858-11	2011	Ceramide treatment also altered the in vivo binding affinity of Sp1 and Sp3 for the GLTP promoter and decreased Sp3 acetylation.	Ceramides	0-8	Sp3 transcription factor	Homo sapiens	72-75
20974858-11	2011	Ceramide treatment also altered the in vivo binding affinity of Sp1 and Sp3 for the GLTP promoter and decreased Sp3 acetylation.	Ceramides	0-8	glycolipid transfer protein	Homo sapiens	84-88
20974858-11	2011	Ceramide treatment also altered the in vivo binding affinity of Sp1 and Sp3 for the GLTP promoter and decreased Sp3 acetylation.	Ceramides	0-8	Sp3 transcription factor	Homo sapiens	112-115
20974858-12	2011	This study represents the first characterization of any Gltp gene promoter and links human GLTP expression to sphingolipid homeostasis through ceramide.	Ceramides	143-151	glycolipid transfer protein	Homo sapiens	56-60
20974858-12	2011	This study represents the first characterization of any Gltp gene promoter and links human GLTP expression to sphingolipid homeostasis through ceramide.	Ceramides	143-151	glycolipid transfer protein	Homo sapiens	91-95
21035490-2	2011	Whereas some investigations have suggested that ceramide and more complex sphingolipids function upstream of p53 or in a p53-independent manner, other studies propose that p53-dependent alterations in these sphingolipids can also contribute to apoptosis.	Ceramides	48-56	tumor protein p53	Homo sapiens	109-112
21035490-4	2011	However, whereas various components of the sphingolipid and p53 pathways may simultaneously function to elicit apoptosis and/or growth inhibition, SMase and SK1 may undergo explicit regulation by p53 that could contribute to ceramide-induced senescence in cells.	Ceramides	225-233	sphingosine kinase 1	Homo sapiens	157-160
21035490-4	2011	However, whereas various components of the sphingolipid and p53 pathways may simultaneously function to elicit apoptosis and/or growth inhibition, SMase and SK1 may undergo explicit regulation by p53 that could contribute to ceramide-induced senescence in cells.	Ceramides	225-233	tumor protein p53	Homo sapiens	196-199
21379338-7	2011	Thus, DC-SIGN ligation initiates SMase-dependent formation of ceramide-enriched membrane microdomains which promote vertical segregation of CD150 from intracellular storage compartments along with ASM.	Ceramides	62-70	signaling lymphocytic activation molecule family member 1	Homo sapiens	140-145
21379338-7	2011	Thus, DC-SIGN ligation initiates SMase-dependent formation of ceramide-enriched membrane microdomains which promote vertical segregation of CD150 from intracellular storage compartments along with ASM.	Ceramides	62-70	sphingomyelin phosphodiesterase 1	Homo sapiens	197-200
21271550-3	2011	Furthermore, the aberrant interaction of glycoprotein gp120 with the CXCR4 chemokine receptor causes caspase-3-dependent apoptosis (ceramide is also released) activating apoptotic proteins (p53 and retinoblastoma), which are part of the neurotoxic mechanisms associated to neuronal dysfunction in neuroAIDS.	Ceramides	132-140	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	54-59
21271550-3	2011	Furthermore, the aberrant interaction of glycoprotein gp120 with the CXCR4 chemokine receptor causes caspase-3-dependent apoptosis (ceramide is also released) activating apoptotic proteins (p53 and retinoblastoma), which are part of the neurotoxic mechanisms associated to neuronal dysfunction in neuroAIDS.	Ceramides	132-140	C-X-C motif chemokine receptor 4	Homo sapiens	69-74
21271550-3	2011	Furthermore, the aberrant interaction of glycoprotein gp120 with the CXCR4 chemokine receptor causes caspase-3-dependent apoptosis (ceramide is also released) activating apoptotic proteins (p53 and retinoblastoma), which are part of the neurotoxic mechanisms associated to neuronal dysfunction in neuroAIDS.	Ceramides	132-140	caspase 3	Homo sapiens	101-110
20561942-7	2011	It is not yet clear, however whether ceramides or glycosphingolipids are involved as both have been implicated to be inhibitors of the insulin signaling cascade.	Ceramides	37-46	insulin	Homo sapiens	135-142
21489413-1	2011	The antibody 13B8.2, which is directed against the CDR3-like loop on the D1 domain of CD4, induces CD4/ZAP-70 reorganization and ceramide release in membrane rafts.	Ceramides	129-137	CD4 molecule	Homo sapiens	86-89
20875392-8	2011	From this study we conclude that the membrane matrix surrounding ceramide, that is ceramide miscibility, is largely affecting the transfer activity of CERT.	Ceramides	65-73	ceramide transporter 1	Homo sapiens	151-155
20875392-8	2011	From this study we conclude that the membrane matrix surrounding ceramide, that is ceramide miscibility, is largely affecting the transfer activity of CERT.	Ceramides	83-91	ceramide transporter 1	Homo sapiens	151-155
21904434-1	2011	The neutral sphingomyelinase (N-SMase) is considered a major candidate for mediating the stress-induced production of ceramide, and it plays an important role in cell-cycle arrest, apoptosis, inflammation, and eukaryotic stress responses.	Ceramides	118-126	sphingomyelin phosphodiesterase 2	Homo sapiens	4-28
21904434-1	2011	The neutral sphingomyelinase (N-SMase) is considered a major candidate for mediating the stress-induced production of ceramide, and it plays an important role in cell-cycle arrest, apoptosis, inflammation, and eukaryotic stress responses.	Ceramides	118-126	sphingomyelin phosphodiesterase 2	Homo sapiens	30-37
21904434-7	2011	Inhibition of N-SMase may lead to reduction of ceramide levels and hence may provide a novel therapeutic strategy for inflammation and autoimmune diseases.	Ceramides	47-55	sphingomyelin phosphodiesterase 2	Homo sapiens	14-21
21597176-3	2011	The mucin box-fused sphingomyelinase hydrolyzed cellular sphingomyelin efficiently to generate ceramide.	Ceramides	95-103	solute carrier family 13 member 2	Rattus norvegicus	4-9
20875392-0	2011	The intermembrane ceramide transport catalyzed by CERT is sensitive to the lipid environment.	Ceramides	18-26	ceramide transporter 1	Homo sapiens	50-54
20875392-2	2011	CERT is responsible for the in vivo non-vesicular trafficking of ceramide between the endoplasmic reticulum and Golgi.	Ceramides	65-73	ceramide transporter 1	Homo sapiens	0-4
20875392-5	2011	We found that if ceramide is in a tightly packed environment such as in sphingomyelin or dipalmitoylphosphatidylcholine containing membranes, the CERT transfer activity is markedly reduced.	Ceramides	17-25	ceramide transporter 1	Homo sapiens	146-150
20875392-6	2011	Ceramide in fluid membranes on the other hand are available for CERT mediated transfer.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	64-68
20842343-8	2011	ATGL adenovirus administration in obese mice increased the production of hepatic ATGL protein and reduced triacylglycerol, diacylglycerol and ceramide content in the liver.	Ceramides	142-150	patatin-like phospholipase domain containing 2	Mus musculus	0-4
21647331-3	2011	The aim of this study was to potentiate the effect of ceramide as anti-angiogenic compound that can regulate tumor induced angiogenesis.C6-ceramide inhibited vascular endothelial growth factor (VEGF)-induced human umbilical vein endothelial cells (HUVEC) tube formation in a dose-dependent manner within 24 hours.	Ceramides	54-62	vascular endothelial growth factor A	Homo sapiens	158-192
21576963-1	2011	BACKGROUND/AIMS: The non-lysosomal glucosylceramidase, beta-glucosidase (Gba2), hydrolyzes glucosylceramide to glucose and ceramide (Cer).	Ceramides	99-107	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).	Ceramides	99-107	glucosidase beta 2	Mus musculus	73-77
21576963-1	2011	BACKGROUND/AIMS: The non-lysosomal glucosylceramidase, beta-glucosidase (Gba2), hydrolyzes glucosylceramide to glucose and ceramide (Cer).	Ceramides	133-136	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).	Ceramides	133-136	glucosidase beta 2	Mus musculus	73-77
21076125-2	2011	Digestive breakdown of sphingomyelin results in ceramide, recently suggested to be involved in activation of cathepsin D as a novel mediator of apoptosis.	Ceramides	48-56	cathepsin D	Mus musculus	109-120
21647331-3	2011	The aim of this study was to potentiate the effect of ceramide as anti-angiogenic compound that can regulate tumor induced angiogenesis.C6-ceramide inhibited vascular endothelial growth factor (VEGF)-induced human umbilical vein endothelial cells (HUVEC) tube formation in a dose-dependent manner within 24 hours.	Ceramides	54-62	vascular endothelial growth factor A	Homo sapiens	194-198
21647331-4	2011	Ceramide at concentrations between 12.5 and 25 muM inhibited the viability of MCF-7 cells and reduced VEGF-induced cell migration in 24 hours.	Ceramides	0-8	vascular endothelial growth factor A	Homo sapiens	102-106
21647331-5	2011	At 50 muM, ceramide induced MCF-7 cell death via autophagy as demonstrated by accumulation of MDC in ceramide-treated MCF-7 vacuoles.	Ceramides	11-19	C-C motif chemokine ligand 22	Homo sapiens	94-97
22187669-4	2011	Thus, several sphingolipid-metabolizing enzymes were found to be associated with mitochondria, including neutral ceramidase, novel neutral sphingomyelinase, and (dihydro) ceramide synthase, an important ceramide-generating enzyme in de novo ceramide synthesis and recycling pathway.	Ceramides	203-211	N-acylsphingosine amidohydrolase 2	Homo sapiens	105-123
21647331-5	2011	At 50 muM, ceramide induced MCF-7 cell death via autophagy as demonstrated by accumulation of MDC in ceramide-treated MCF-7 vacuoles.	Ceramides	101-109	C-C motif chemokine ligand 22	Homo sapiens	94-97
21647331-7	2011	In vivo, 50 muM ceramide caused a 40% reduction of new vessel formation in the CAM assay within 24 hours.	Ceramides	16-24	calmodulin 3	Homo sapiens	79-82
22078959-6	2011	However, MAM might be also involved in the interorganelle transport of cholesterol, ceramides, ATP, and proteins as well as in proteasomal protein degradation and lipid droplet formation.	Ceramides	84-93	sarcoglycan gamma	Homo sapiens	9-12
21496387-1	2011	Previously, K6PC-5, a synthetic derivative of ceramide, was demonstrated to activate sphingosine kinase (SK)-1 in keratinocytes.	Ceramides	46-54	sphingosine kinase 1	Mus musculus	85-110
21135173-8	2011	Our results indicate that inhibition of de novo ceramide synthesis may be effective in disease states with low CFTR expression like emphysema and chronic lung injury but not in complete absence of lipid-raft CFTR as in DeltaF508-cystic fibrosis.	Ceramides	48-56	cystic fibrosis transmembrane conductance regulator	Mus musculus	111-115
21135173-10	2011	Our data demonstrate the critical role of membrane-localized CFTR in regulating ceramide accumulation and inflammatory signaling in lung injury and emphysema.	Ceramides	80-88	cystic fibrosis transmembrane conductance regulator	Mus musculus	61-65
21135173-0	2011	Critical modifier role of membrane-cystic fibrosis transmembrane conductance regulator-dependent ceramide signaling in lung injury and emphysema.	Ceramides	97-105	cystic fibrosis transmembrane conductance regulator	Mus musculus	35-86
21135173-2	2011	Although an association between lack of cystic fibrosis transmembrane conductance regulator (CFTR) and ceramide accumulation has been described, it is unclear how membrane-CFTR may modulate ceramide signaling in lung injury and emphysema.	Ceramides	103-111	cystic fibrosis transmembrane conductance regulator	Mus musculus	93-97
21490809-4	2011	Using SCCVII mouse squamous carcinoma cells, and the silicone phthalocyanine Pc 4 for PDT, we showed that combining PDT with LCL30 (PDT/LCL30) was more effective than individual treatments in raising global ceramide levels, as well as in reducing dihydrosphingosine levels.	Ceramides	207-215	proprotein convertase subtilisin/kexin type 4	Mus musculus	77-81
21135173-3	2011	Cftr(+/+) and Cftr(-/-) mice and cells were used to evaluate the CFTR-dependent ceramide signaling in lung injury.	Ceramides	80-88	cystic fibrosis transmembrane conductance regulator	Mus musculus	65-69
21135173-4	2011	Lung tissue from control and chronic obstructive pulmonary disease patients was used to verify the role of CFTR-dependent ceramide signaling in pathogenesis of chronic emphysema.	Ceramides	122-130	CF transmembrane conductance regulator	Homo sapiens	107-111
21135173-5	2011	Our data reveal that CFTR expression inversely correlates with severity of emphysema and ceramide accumulation in chronic obstructive pulmonary disease subjects compared with control subjects.	Ceramides	89-97	cystic fibrosis transmembrane conductance regulator	Mus musculus	21-25
21135173-6	2011	We found that chemical inhibition of de novo ceramide synthesis controls Pseudomonas aeruginosa-LPS-induced lung injury in Cftr(+/+) mice, whereas its efficacy was significantly lower in Cftr(-/-) mice, indicating that membrane-CFTR is required for controlling lipid-raft ceramide levels.	Ceramides	45-53	cystic fibrosis transmembrane conductance regulator	Mus musculus	123-127
21135173-6	2011	We found that chemical inhibition of de novo ceramide synthesis controls Pseudomonas aeruginosa-LPS-induced lung injury in Cftr(+/+) mice, whereas its efficacy was significantly lower in Cftr(-/-) mice, indicating that membrane-CFTR is required for controlling lipid-raft ceramide levels.	Ceramides	45-53	cystic fibrosis transmembrane conductance regulator	Mus musculus	228-232
21135173-7	2011	Inhibition of membrane-ceramide release showed enhanced protective effect in controlling P. aeruginosa-LPS-induced lung injury in Cftr(-/-) mice compared with that in Cftr(+/+) mice, confirming our observation that CFTR regulates lipid-raft ceramide levels and signaling.	Ceramides	23-31	cystic fibrosis transmembrane conductance regulator	Mus musculus	130-134
21135173-7	2011	Inhibition of membrane-ceramide release showed enhanced protective effect in controlling P. aeruginosa-LPS-induced lung injury in Cftr(-/-) mice compared with that in Cftr(+/+) mice, confirming our observation that CFTR regulates lipid-raft ceramide levels and signaling.	Ceramides	23-31	cystic fibrosis transmembrane conductance regulator	Mus musculus	167-171
21135173-7	2011	Inhibition of membrane-ceramide release showed enhanced protective effect in controlling P. aeruginosa-LPS-induced lung injury in Cftr(-/-) mice compared with that in Cftr(+/+) mice, confirming our observation that CFTR regulates lipid-raft ceramide levels and signaling.	Ceramides	23-31	cystic fibrosis transmembrane conductance regulator	Mus musculus	215-219
20940143-1	2011	Mammalian ceramide synthases 1 to 6 (CerS1-6) generate Cer in an acyl-CoA-dependent manner, and expression of individual CerS has been shown to enhance the synthesis of ceramides with particular acyl chain lengths.	Ceramides	169-178	ceramide synthase 1	Homo sapiens	10-35
20940143-1	2011	Mammalian ceramide synthases 1 to 6 (CerS1-6) generate Cer in an acyl-CoA-dependent manner, and expression of individual CerS has been shown to enhance the synthesis of ceramides with particular acyl chain lengths.	Ceramides	169-178	ceramide synthase 1	Homo sapiens	37-44
21490813-2	2011	Inhibition of the lysosomal acid ceramidase can increase cellular ceramide levels and thus induce apoptosis.	Ceramides	66-74	N-acylsphingosine amidohydrolase 1	Homo sapiens	28-43
21148295-11	2011	Bwa exhibits strong genetic interaction with other genes coding for ceramide-metabolizing enzymes.	Ceramides	68-76	brain washing	Drosophila melanogaster	0-3
21186369-3	2011	Here, we show that adiponectin potently stimulates a ceramidase activity associated with its two receptors, AdipoR1 and AdipoR2, and enhances ceramide catabolism and formation of its antiapoptotic metabolite--sphingosine-1-phosphate (S1P)--independently of AMP-dependent kinase (AMPK).	Ceramides	142-150	adiponectin, C1Q and collagen domain containing	Homo sapiens	19-30
21186369-5	2011	Ceramidase activity is impaired in cells lacking both adiponectin receptor isoforms, leading to elevated ceramide levels and enhanced susceptibility to palmitate-induced cell death.	Ceramides	105-113	adiponectin, C1Q and collagen domain containing	Homo sapiens	54-65
21935356-2	2011	Ceramide is a sphingolipid and localizes to caveolae, which are lined in the inner membrane leaflet by caveolin proteins.	Ceramides	0-8	caveolin 3	Mus musculus	103-111
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.	Ceramides	84-93	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.	Ceramides	84-93	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.	Ceramides	84-93	sphingosine kinase 1	Homo sapiens	36-62
21500096-5	2011	C8:ceramide, an important cell-permeable analogue of natural ceramides, increases intracellular ceramide levels significantly, while 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) and SK-1 inhibitor increase accumulation of ceramides by inhibiting GCS and SK-1, respectively.	Ceramides	3-11	sphingosine kinase 1	Homo sapiens	193-197
21500096-5	2011	C8:ceramide, an important cell-permeable analogue of natural ceramides, increases intracellular ceramide levels significantly, while 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) and SK-1 inhibitor increase accumulation of ceramides by inhibiting GCS and SK-1, respectively.	Ceramides	3-11	UDP-glucose ceramide glucosyltransferase	Homo sapiens	257-260
21500096-5	2011	C8:ceramide, an important cell-permeable analogue of natural ceramides, increases intracellular ceramide levels significantly, while 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) and SK-1 inhibitor increase accumulation of ceramides by inhibiting GCS and SK-1, respectively.	Ceramides	3-11	sphingosine kinase 1	Homo sapiens	265-269
22195025-2	2011	Pharmacological elevation of ceramide in isolated carotid arteries of SHR leads to vasoconstriction via a calcium-independent phospholipase A(2), cyclooxygenase-1 and thromboxane synthase-dependent release of thromboxane A(2).	Ceramides	29-37	prostaglandin-endoperoxide synthase 1	Rattus norvegicus	146-162
20802518-0	2010	Exogenous cell-permeable C6 ceramide sensitizes multiple cancer cell lines to Doxorubicin-induced apoptosis by promoting AMPK activation and mTORC1 inhibition.	Ceramides	28-36	CREB regulated transcription coactivator 1	Mus musculus	141-147
21886813-5	2011	We have previously established annexin A1--a member of a family of Ca(2+) and membrane-binding proteins--to be a marker of ceramide platforms.	Ceramides	123-131	annexin A1	Homo sapiens	31-41
21886813-6	2011	Using fluorescently tagged annexin A1, we show that, upon its generation within the plasma membrane, ceramide self-associates into platforms that subsequently invaginate and fuse with mitochondria.	Ceramides	101-109	annexin A1	Homo sapiens	27-37
21886813-6	2011	Using fluorescently tagged annexin A1, we show that, upon its generation within the plasma membrane, ceramide self-associates into platforms that subsequently invaginate and fuse with mitochondria.	Ceramides	101-109	Polykaryocytosis inducer	Homo sapiens	174-178
21695182-0	2011	Mitochondrial ceramide-rich macrodomains functionalize Bax upon irradiation.	Ceramides	14-22	BCL2 associated X, apoptosis regulator	Homo sapiens	55-58
21695182-2	2011	Here we show mitochondrial ceramide elevation facilitates MOMP-mediated cytochrome c release in HeLa cells by generating a previously-unrecognized mitochondrial ceramide-rich macrodomain (MCRM), which we visualize and isolate, into which Bax integrates.	Ceramides	27-35	cytochrome c, somatic	Homo sapiens	72-84
21695182-2	2011	Here we show mitochondrial ceramide elevation facilitates MOMP-mediated cytochrome c release in HeLa cells by generating a previously-unrecognized mitochondrial ceramide-rich macrodomain (MCRM), which we visualize and isolate, into which Bax integrates.	Ceramides	27-35	BCL2 associated X, apoptosis regulator	Homo sapiens	238-241
21695182-2	2011	Here we show mitochondrial ceramide elevation facilitates MOMP-mediated cytochrome c release in HeLa cells by generating a previously-unrecognized mitochondrial ceramide-rich macrodomain (MCRM), which we visualize and isolate, into which Bax integrates.	Ceramides	161-169	cytochrome c, somatic	Homo sapiens	72-84
21695182-2	2011	Here we show mitochondrial ceramide elevation facilitates MOMP-mediated cytochrome c release in HeLa cells by generating a previously-unrecognized mitochondrial ceramide-rich macrodomain (MCRM), which we visualize and isolate, into which Bax integrates.	Ceramides	161-169	BCL2 associated X, apoptosis regulator	Homo sapiens	238-241
21695182-5	2011	Inhibiting ceramide generation using a well-defined natural ceramide synthase inhibitor, Fumonisin B1, prevented radiation-induced Bax insertion, oligomerization and MOMP.	Ceramides	11-19	BCL2 associated X, apoptosis regulator	Homo sapiens	131-134
21695182-10	2011	Here we demonstrate that ceramide, generated in the mitochondrial outer membrane of mammalian cells upon irradiation, forms a platform into which Bax inserts, oligomerizes and functionalizes as a pore.	Ceramides	25-33	BCL2 associated X, apoptosis regulator	Homo sapiens	146-149
21695182-11	2011	We posit conceptualization of ceramide as a membrane-based stress calibrator, driving membrane macrodomain organization, which in mitochondria regulates intensity of Bax-induced MOMP, and is pharmacologically tractable in vitro and in vivo.	Ceramides	30-38	BCL2 associated X, apoptosis regulator	Homo sapiens	166-169
21234372-2	2010	We previously reported a strong elevation of ceramide levels in the brain of the APP(SL)/PS1Ki mouse model of AD, preceding the neuronal death.	Ceramides	45-53	presenilin 1	Mus musculus	89-92
20956540-8	2010	The effect of ceramide on efferocytosis was associated with decreased membrane ruffle formation and attenuated Rac1 plasma membrane recruitment.	Ceramides	14-22	Rac family small GTPase 1	Homo sapiens	111-115
20956540-9	2010	Constitutively active Rac1 overexpression rescued AM efferocytosis against the effects of ceramide.	Ceramides	90-98	Rac family small GTPase 1	Homo sapiens	22-26
20956540-10	2010	CS exposure significantly increased AM ceramides and recapitulated the effect of ceramides on Rac1 membrane recruitment in a sphingosine-dependent manner.	Ceramides	81-90	Rac family small GTPase 1	Homo sapiens	94-98
20850412-0	2010	Ceramide-induced activation of cytosolic NADH/cytochrome c electron transport pathway: An additional source of energy for apoptosis.	Ceramides	0-8	cytochrome c, somatic	Homo sapiens	46-58
20850412-1	2010	We have investigated whether increase in the oxidation rate of exogenous cytochrome c (cyto-c), induced by long-chain ceramides, might be due to an increased rate of cytosolic NADH/cyto-c electron transport pathway.	Ceramides	118-127	cytochrome c, somatic	Homo sapiens	73-85
20850412-1	2010	We have investigated whether increase in the oxidation rate of exogenous cytochrome c (cyto-c), induced by long-chain ceramides, might be due to an increased rate of cytosolic NADH/cyto-c electron transport pathway.	Ceramides	118-127	cytochrome c, somatic	Homo sapiens	87-93
20850412-1	2010	We have investigated whether increase in the oxidation rate of exogenous cytochrome c (cyto-c), induced by long-chain ceramides, might be due to an increased rate of cytosolic NADH/cyto-c electron transport pathway.	Ceramides	118-127	cytochrome c, somatic	Homo sapiens	181-187
20850412-3	2010	Data from highly specific test of sulfite oxidase prove that exogenous cyto-c both in the absence and presence of ceramide cannot permeate through the mitochondrial outer membrane.	Ceramides	114-122	cytochrome c, somatic	Homo sapiens	71-77
22096531-8	2011	Furthermore, Sphk1/2 double mutants displayed an overall reduction in other sphingolipids as well as an imbalance of S1P/sphingosine and S1P/ceramide ratio, thereby favoring cell death and reducing cell growth.	Ceramides	141-149	sphingosine kinase 1	Mus musculus	13-18
21853092-9	2011	We propose that ceramide increase under ox-stress disrupts cholesterol-enriched rafts leading to EGFR re-localization into the rigid, ceramide-enriched rafts.	Ceramides	16-24	epidermal growth factor receptor	Homo sapiens	97-101
21853092-9	2011	We propose that ceramide increase under ox-stress disrupts cholesterol-enriched rafts leading to EGFR re-localization into the rigid, ceramide-enriched rafts.	Ceramides	134-142	epidermal growth factor receptor	Homo sapiens	97-101
21853092-10	2011	This increase in ceramide also supports EGFR aberrant trafficking to a peri-nuclear region.	Ceramides	17-25	epidermal growth factor receptor	Homo sapiens	40-44
21047787-7	2010	Endogenous ceramide levels were 3-fold higher in ldlC cells than in WT cells, indicating that Golgi misorganization caused by Cog2 deficiency affects the delivery of ceramide to sites of SM synthesis by SMS1.	Ceramides	166-174	conserved oligomeric Golgi complex subunit 2	Cricetulus griseus	126-130
20850412-4	2010	However, the oxidation of added NADH, mediated by exogenous cyto-c and coupled to the generation of a membrane potential supporting the ATP synthesis, can also be stimulated by ceramide.	Ceramides	177-185	cytochrome c, somatic	Homo sapiens	60-66
20876532-6	2010	Indeed, de novo biosynthesis of sphingolipids performs an essential structural and/or signaling function in autophagy because autophagosome formation was eliminated by ISP1 in KLA-stimulated RAW264.7 cells (and mutation of serine palmitoyltransferase in CHO-LYB cells); furthermore, an anti-ceramide antibody co-localizes with autophagosomes in activated RAW264.7 cells versus the Golgi in unstimulated or ISP1-inhibited cells.	Ceramides	291-299	protease, serine 28	Mus musculus	168-172
20926375-2	2010	We demonstrate here that the SK1 inhibitor, SKi (2-(p-hydroxyanilino)-4-(p-chlorophenyl)thiazole) induces the proteasomal degradation of SK1 in human pulmonary artery smooth muscle cells, androgen-sensitive LNCaP prostate cancer cells, MCF-7 and MCF-7 HER2 breast cancer cells and that this is likely mediated by ceramide as a consequence of catalytic inhibition of SK1 by SKi.	Ceramides	313-321	sphingosine kinase 1	Homo sapiens	29-32
20926375-2	2010	We demonstrate here that the SK1 inhibitor, SKi (2-(p-hydroxyanilino)-4-(p-chlorophenyl)thiazole) induces the proteasomal degradation of SK1 in human pulmonary artery smooth muscle cells, androgen-sensitive LNCaP prostate cancer cells, MCF-7 and MCF-7 HER2 breast cancer cells and that this is likely mediated by ceramide as a consequence of catalytic inhibition of SK1 by SKi.	Ceramides	313-321	SKI proto-oncogene	Homo sapiens	44-47
20926375-2	2010	We demonstrate here that the SK1 inhibitor, SKi (2-(p-hydroxyanilino)-4-(p-chlorophenyl)thiazole) induces the proteasomal degradation of SK1 in human pulmonary artery smooth muscle cells, androgen-sensitive LNCaP prostate cancer cells, MCF-7 and MCF-7 HER2 breast cancer cells and that this is likely mediated by ceramide as a consequence of catalytic inhibition of SK1 by SKi.	Ceramides	313-321	sphingosine kinase 1	Homo sapiens	137-140
20926375-2	2010	We demonstrate here that the SK1 inhibitor, SKi (2-(p-hydroxyanilino)-4-(p-chlorophenyl)thiazole) induces the proteasomal degradation of SK1 in human pulmonary artery smooth muscle cells, androgen-sensitive LNCaP prostate cancer cells, MCF-7 and MCF-7 HER2 breast cancer cells and that this is likely mediated by ceramide as a consequence of catalytic inhibition of SK1 by SKi.	Ceramides	313-321	sphingosine kinase 1	Homo sapiens	137-140
20926375-2	2010	We demonstrate here that the SK1 inhibitor, SKi (2-(p-hydroxyanilino)-4-(p-chlorophenyl)thiazole) induces the proteasomal degradation of SK1 in human pulmonary artery smooth muscle cells, androgen-sensitive LNCaP prostate cancer cells, MCF-7 and MCF-7 HER2 breast cancer cells and that this is likely mediated by ceramide as a consequence of catalytic inhibition of SK1 by SKi.	Ceramides	313-321	SKI proto-oncogene	Homo sapiens	373-376
20713176-1	2010	The activation of neutral sphingomyelinase-2 (nSMase2) and consequent ceramide production are implicated in many stress-induced signaling pathways.	Ceramides	70-78	sphingomyelin phosphodiesterase 3	Homo sapiens	18-44
20935146-4	2010	In addition, the data indicated that inhibition of either SMS, p53, SPT, or CS in VSMCs exposed to low [Mg(2+)](o) resulted in marked reductions in the de novo synthesis of ceramide.	Ceramides	173-181	spermine synthase	Rattus norvegicus	58-61
20935146-4	2010	In addition, the data indicated that inhibition of either SMS, p53, SPT, or CS in VSMCs exposed to low [Mg(2+)](o) resulted in marked reductions in the de novo synthesis of ceramide.	Ceramides	173-181	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	63-66
20876761-4	2010	Blocking de novo synthesis of ceramide abolished the effects of palmitate on mtROS production, viability, and insulin signaling.	Ceramides	30-38	insulin	Homo sapiens	110-117
20713176-1	2010	The activation of neutral sphingomyelinase-2 (nSMase2) and consequent ceramide production are implicated in many stress-induced signaling pathways.	Ceramides	70-78	sphingomyelin phosphodiesterase 3	Homo sapiens	46-53
20713176-9	2010	Finally, inhibition of nSMase2 endocytosis by K+depletion reduced the intracellular pool of nSMase2 and increased nSMase2 activity resulting in elevated ceramide levels.	Ceramides	153-161	sphingomyelin phosphodiesterase 3	Homo sapiens	23-30
20935456-2	2010	Many anticancer chemotherapeutics (anthracyclines, Vinca alkaloids, paclitaxel, and fenretinide), as well as physiological stimuli such as tumor necrosis factor alpha (TNFalpha), stimulate ceramide accumulation and increase oxidative stress in malignant cells.	Ceramides	189-197	tumor necrosis factor	Homo sapiens	139-166
20858552-3	2010	The present study was performed to determine whether acid sphingomyelinase (ASM)-ceramide associated lipid raft (LR) clustering is involved in local oxidative stress in glomerular endothelial cells (GECs) induced by adipokines such as visfatin and adiponectin.	Ceramides	81-89	sphingomyelin phosphodiesterase 1	Homo sapiens	53-74
20858552-3	2010	The present study was performed to determine whether acid sphingomyelinase (ASM)-ceramide associated lipid raft (LR) clustering is involved in local oxidative stress in glomerular endothelial cells (GECs) induced by adipokines such as visfatin and adiponectin.	Ceramides	81-89	sphingomyelin phosphodiesterase 1	Homo sapiens	76-79
21118968-1	2010	A previous in vitro study showed that sphingosine-1-phosphate (S1P), a ceramide antagonist, preserved endothelial cells in culture from radiation-induced apoptosis.	Ceramides	71-79	sphingosine-1-phosphate receptor 1	Mus musculus	63-66
20935456-2	2010	Many anticancer chemotherapeutics (anthracyclines, Vinca alkaloids, paclitaxel, and fenretinide), as well as physiological stimuli such as tumor necrosis factor alpha (TNFalpha), stimulate ceramide accumulation and increase oxidative stress in malignant cells.	Ceramides	189-197	tumor necrosis factor	Homo sapiens	168-176
20935456-3	2010	Consequently, ceramide metabolism in malignant cells and, in particular the up-regulation of glucosylceramide synthase (GCS), has gained considerable interest in contributing to chemoresistance.	Ceramides	14-22	UDP-glucose ceramide glucosyltransferase	Homo sapiens	93-118
20935456-3	2010	Consequently, ceramide metabolism in malignant cells and, in particular the up-regulation of glucosylceramide synthase (GCS), has gained considerable interest in contributing to chemoresistance.	Ceramides	14-22	UDP-glucose ceramide glucosyltransferase	Homo sapiens	120-123
20393874-3	2010	In the intestinal tract, SM is mainly hydrolyzed by alkaline sphingomyelinase (alk-SMase) to ceramide.Aims We investigated the influence of SM and its hydrolytic products ceramide and sphingosine on cholesterol uptake in intestinal Caco-2 cells.Methods Micelles containing bile salt, monoolein, and (14)C-cholesterol were prepared with or without SM, ceramide,or sphingosine.	Ceramides	93-101	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	79-88
20393874-7	2010	Alk-SMase enhances SM-induced inhibition of cholesterol uptake by generating ceramide in the intestinal lumen.	Ceramides	77-85	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	0-9
21042729-0	2010	Expression of P-glycoprotein in HeLa cells confers resistance to ceramide cytotoxicity.	Ceramides	65-73	ATP binding cassette subfamily B member 1	Homo sapiens	14-28
20871013-1	2010	Acid ceramidase (aCDase) is one of several enzymes responsible for ceramide degradation within mammalian cells.	Ceramides	67-75	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
21042729-1	2010	The role of glucosylceramide synthase (GCS) in regulating ceramide-induced apoptosis has been widely studied.	Ceramides	20-28	UDP-glucose ceramide glucosyltransferase	Homo sapiens	39-42
21042729-2	2010	The purpose of this investigation was to evaluate the role of P-glycoprotein (P-gp) in regulating ceramide cytotoxicity by using C6-ceramide.	Ceramides	98-106	ATP binding cassette subfamily B member 1	Homo sapiens	62-76
21042729-2	2010	The purpose of this investigation was to evaluate the role of P-glycoprotein (P-gp) in regulating ceramide cytotoxicity by using C6-ceramide.	Ceramides	98-106	ATP binding cassette subfamily B member 1	Homo sapiens	78-82
21042729-10	2010	Experiments in another cervical cancer model showed that multidrug-resistant P-gp-rich KB-V1 cells synthesized 3-fold more C6-GC from C6-ceramide than the parental, P-gp-poor KB-3-1 cells, and whereas tamoxifen had no effect on the C6-GC synthesis in the KB-3-1 cells, it inhibited synthesis by 70% in the KB-V1 cells.	Ceramides	136-145	ATP binding cassette subfamily B member 1	Homo sapiens	77-81
21042729-12	2010	We propose that P-gp can be an effective target for enhancing short-chain ceramide cytotoxicity in the treatment of drug-resistant cancer.	Ceramides	74-82	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
20803549-4	2010	The Asah2 gene encodes neutral ceramidase, which is a hydrolytic brush border enzyme involved in ceramide digestion.	Ceramides	97-105	N-acylsphingosine amidohydrolase 2	Homo sapiens	4-9
20803549-4	2010	The Asah2 gene encodes neutral ceramidase, which is a hydrolytic brush border enzyme involved in ceramide digestion.	Ceramides	97-105	N-acylsphingosine amidohydrolase 2	Homo sapiens	23-41
21041721-6	2010	Exposure of J774 cells to bacterial sphingomyelinase or interference with ceramide hydrolysis using inhibitors of ceramidases also lowered the LPS-induced TNF-alpha production.	Ceramides	74-82	tumor necrosis factor	Mus musculus	155-164
21041721-7	2010	The latter result indicates that ceramide rather than sphingosine suppresses TNF-alpha and MIP-2 production.	Ceramides	33-41	tumor necrosis factor	Mus musculus	77-86
21041721-7	2010	The latter result indicates that ceramide rather than sphingosine suppresses TNF-alpha and MIP-2 production.	Ceramides	33-41	chemokine (C-X-C motif) ligand 2	Mus musculus	91-96
21041721-0	2010	Ceramide and ceramide 1-phosphate are negative regulators of TNF-alpha production induced by lipopolysaccharide.	Ceramides	0-8	tumor necrosis factor	Mus musculus	61-70
20871013-1	2010	Acid ceramidase (aCDase) is one of several enzymes responsible for ceramide degradation within mammalian cells.	Ceramides	67-75	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-23
21041721-10	2010	Together the data indicate that ceramide negatively regulates production of TNF-alpha and MIP-2 in response to LPS with the former being sensitive to ceramide 1-phosphate as well.	Ceramides	32-40	tumor necrosis factor	Mus musculus	76-85
21041721-10	2010	Together the data indicate that ceramide negatively regulates production of TNF-alpha and MIP-2 in response to LPS with the former being sensitive to ceramide 1-phosphate as well.	Ceramides	32-40	chemokine (C-X-C motif) ligand 2	Mus musculus	90-95
20871013-2	2010	As such, aCDase regulates the intracellular levels of the bioactive lipid ceramide.	Ceramides	74-82	N-acylsphingosine amidohydrolase 1	Homo sapiens	9-15
20871013-3	2010	An inherited deficiency of aCDase activity results in Farber disease (FD), also called lipogranulomatosis, which is characterized by ceramide accumulation in the tissues of patients.	Ceramides	133-141	N-acylsphingosine amidohydrolase 1	Homo sapiens	27-33
21311687-1	2010	B13, a ceramide analogue, is a ceramidase inhibitor and induces apoptosis to give potent anticancer activity.	Ceramides	7-15	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	0-3
20696185-6	2010	NT3 and IGF-1 increased survival at early time points, but only IGF-1 is capable to attenuate C(2)-ceramide-mediated neuronal death, and this neuroprotection is associated to strong and permanent activation of AKT and inhibition of GSK3beta.	Ceramides	99-107	insulin like growth factor 1	Homo sapiens	64-69
20837491-5	2010	Furthermore, similar to preincubation with oleate, CPT1mt expression protected muscle cells from palmitate-induced apoptosis and insulin resistance by decreasing the content of deleterious palmitate derivates (i.e. diacylglycerols and ceramides).	Ceramides	235-244	carnitine palmitoyltransferase 1A	Homo sapiens	51-55
20826817-3	2010	PHS has been shown to cause toxicity in tryptophan auxotrophic strains of yeast because this bioactive ceramide precursor causes diversion of the high affinity tryptophan permease Tat2 to the vacuole rather than the plasma membrane.	Ceramides	103-111	aromatic amino acid transmembrane transporter TAT2	Saccharomyces cerevisiae S288C	180-184
20807762-0	2010	Regulated secretion of acid sphingomyelinase: implications for selectivity of ceramide formation.	Ceramides	78-86	sphingomyelin phosphodiesterase 1	Homo sapiens	23-44
20807762-4	2010	Interleukin-1beta and tumor necrosis factor-alpha induced a time- and dose-dependent increase in S-SMase secretion and activity, coincident with selective elevations in cellular C(16)-ceramide.	Ceramides	184-192	interleukin 1 beta	Homo sapiens	0-49
20807762-6	2010	MCF7 expressing V5-aSMase(WT) exhibited increased S-SMase and L-SMase activity, as well as elevated cellular levels of specific long-chain and very long-chain ceramide species relative to vector control MCF7.	Ceramides	159-167	sphingomyelin phosphodiesterase 1	Homo sapiens	19-25
20807762-7	2010	Interestingly, elevated levels of only certain very long-chain ceramides were evident in V5-aSMase(S508A) MCF7.	Ceramides	63-72	sphingomyelin phosphodiesterase 1	Homo sapiens	92-98
20709688-5	2010	Under the AUR1-repressive conditions, the ELO3 mutant showed reduction in the complex sphingolipid levels and the accumulation of ceramide, like wild-type cells.	Ceramides	130-138	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	42-46
20853438-4	2010	METHODS: Using autozygosity mapping and candidate gene sequencing, we identified mutations in the fatty acid hydroxylase gene FA2H, newly implicating abnormalities of ceramide metabolism in the pathogenesis of NBIA.	Ceramides	167-175	fatty acid 2-hydroxylase	Homo sapiens	126-130
20814016-8	2010	The Sms2 KO/Apoe KO brachiocephalic artery contained significantly less SM, ceramide, free cholesterol, and cholesteryl ester (35%, 32%, 58%, and 60%, respectively; P<0.01) than that of the Apoe KO brachiocephalic artery.	Ceramides	76-84	apolipoprotein E	Mus musculus	12-16
20568228-9	2010	Elevated ceramide content in the SAT diet group could be a result of increased SPT activity and simultaneously decreased activity of nCDase.	Ceramides	9-17	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	133-139
20709688-7	2010	Therefore, it is suggested that the ELO3 mutant shows resistance as to accumulation of ceramides, implying that the chain lengths of fatty acids in ceramide are a critical factor for the ceramide-induced growth defect under AUR1-repressive conditions.	Ceramides	87-96	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	36-40
20709688-7	2010	Therefore, it is suggested that the ELO3 mutant shows resistance as to accumulation of ceramides, implying that the chain lengths of fatty acids in ceramide are a critical factor for the ceramide-induced growth defect under AUR1-repressive conditions.	Ceramides	87-96	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	224-228
20709688-7	2010	Therefore, it is suggested that the ELO3 mutant shows resistance as to accumulation of ceramides, implying that the chain lengths of fatty acids in ceramide are a critical factor for the ceramide-induced growth defect under AUR1-repressive conditions.	Ceramides	87-95	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	36-40
20709688-7	2010	Therefore, it is suggested that the ELO3 mutant shows resistance as to accumulation of ceramides, implying that the chain lengths of fatty acids in ceramide are a critical factor for the ceramide-induced growth defect under AUR1-repressive conditions.	Ceramides	148-156	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	36-40
20709688-7	2010	Therefore, it is suggested that the ELO3 mutant shows resistance as to accumulation of ceramides, implying that the chain lengths of fatty acids in ceramide are a critical factor for the ceramide-induced growth defect under AUR1-repressive conditions.	Ceramides	148-156	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	224-228
20974006-3	2010	RESULTS: In this study, we demonstrate that alpha-TEA induces the accumulation of cell surface membrane ceramide, leading to co-localization with Fas, DR5, and FADD, followed by activation of caspases-8 and -9 and apoptosis in human MDA-MB-231 breast cancer cells.	Ceramides	104-112	TNF receptor superfamily member 10b	Homo sapiens	151-154
20732354-4	2010	In addition, MDA-7/IL-24 has been noted to radiosensitize tumor cells which in part is due to the generation of reactive oxygen species (ROS) and ceramide that cause endoplasmic reticulum stress and suppress protein translation.	Ceramides	146-154	interleukin 24	Homo sapiens	13-18
20732354-4	2010	In addition, MDA-7/IL-24 has been noted to radiosensitize tumor cells which in part is due to the generation of reactive oxygen species (ROS) and ceramide that cause endoplasmic reticulum stress and suppress protein translation.	Ceramides	146-154	interleukin 24	Homo sapiens	19-24
20659502-7	2010	Besides CD4/ZAP-70 modulation in membrane rafts, the 13B8.2-induced activation of the acid sphingomyelinase/ceramide pathway is an important event for structuring raft platforms and transducing CD4-related intracellular signals, which can further fine-tune antibody-triggered tumoral effects.	Ceramides	108-116	CD4 molecule	Homo sapiens	194-197
20678580-1	2010	Ceramide kinase (CerK) catalyzes the conversion of ceramide to ceramide 1-phosphate (C1P).	Ceramides	51-59	ceramide kinase	Mus musculus	0-15
20678580-1	2010	Ceramide kinase (CerK) catalyzes the conversion of ceramide to ceramide 1-phosphate (C1P).	Ceramides	51-59	ceramide kinase	Mus musculus	17-21
20937879-4	2010	Retinal ceramide levels increased in rd10 mice during the period of maximum photoreceptor death.	Ceramides	8-16	phosphodiesterase 6B, cGMP, rod receptor, beta polypeptide	Mus musculus	37-41
20974006-3	2010	RESULTS: In this study, we demonstrate that alpha-TEA induces the accumulation of cell surface membrane ceramide, leading to co-localization with Fas, DR5, and FADD, followed by activation of caspases-8 and -9 and apoptosis in human MDA-MB-231 breast cancer cells.	Ceramides	104-112	Fas associated via death domain	Homo sapiens	160-164
20974006-5	2010	Functional knockdown of ASMase with either the chemical inhibitor, desipramine, or siRNA markedly reduces alpha-TEA-induced cell surface membrane accumulation of ceramide and its co-localization with Fas, DR5, and FADD, cleavage of caspases-8 and -9 and apoptosis, suggesting an early and critical role for ASMase in alpha-TEA-induced apoptosis.	Ceramides	162-170	sphingomyelin phosphodiesterase 1	Homo sapiens	24-30
20620184-0	2010	Cationic cell-penetrating peptides induce ceramide formation via acid sphingomyelinase: implications for uptake.	Ceramides	42-50	sphingomyelin phosphodiesterase 1	Homo sapiens	65-86
20620184-4	2010	Here, we demonstrate that the direct translocation of cationic CPP depends on a CPP-induced translocation of acid sphingomyelinase (ASMase) to the outer leaflet of the plasma membrane and ceramide formation.	Ceramides	188-196	sphingomyelin phosphodiesterase 1	Homo sapiens	109-130
20620184-4	2010	Here, we demonstrate that the direct translocation of cationic CPP depends on a CPP-induced translocation of acid sphingomyelinase (ASMase) to the outer leaflet of the plasma membrane and ceramide formation.	Ceramides	188-196	sphingomyelin phosphodiesterase 1	Homo sapiens	132-138
20620184-7	2010	In conclusion, we show that a previously poorly understood mechanism of cationic CPP import depends on the ASMase-dependent formation of ceramide on the outer leaflet of the plasma membrane.	Ceramides	137-145	sphingomyelin phosphodiesterase 1	Homo sapiens	107-113
20567904-6	2010	Ceramide formation was assessed with anti-ceramide antibodies in FACS and immunohistochemical analysis, sub-G1 cell population by FACS analysis, break down of phosphatidylserine asymmetry by annexin V binding, cell death by propidium iodide incorporation, metabolic cell activity by MTT assay, ROS production from dichlorofluorescein fluorescence and activation of MAPKs by Western blotting.	Ceramides	0-8	acyl-CoA synthetase long-chain family member 1	Mus musculus	65-69
20816935-7	2010	However, only the full-length of Bm-TFF2, but not its single-domain truncations, can inhibit ceramide-induced apoptosis in AGS cells.	Ceramides	93-101	trefoil factor 2	Homo sapiens	36-40
20876726-0	2010	Targeting ceramide synthesis to reverse insulin resistance.	Ceramides	10-18	insulin	Homo sapiens	40-47
20522596-9	2010	CONCLUSIONS: Our results demonstrate that the intramyocellular accumulation of ceramide correlates strongly with the development of insulin resistance, and suggests that inhibition of SPT1 is a potentially promising target for the treatment of insulin resistance.	Ceramides	79-87	serine palmitoyltransferase, long chain base subunit 1	Mus musculus	184-188
20890432-3	2010	The disialoganglioside GD3 involves ceramide-, Fas- and TNF-alpha-mediated apoptosis in lymphoid cells and hepatocytes.	Ceramides	36-44	GRDX	Homo sapiens	23-26
20566755-1	2010	Carboxyl ester lipase (CEL) is an enzyme that hydrolyzes a wide variety of lipid substrates, including ceramides, which are known to show inhibitory regulation of pituitary hormone secretion in experimental models.	Ceramides	103-112	carboxyl ester lipase	Homo sapiens	0-21
20566755-1	2010	Carboxyl ester lipase (CEL) is an enzyme that hydrolyzes a wide variety of lipid substrates, including ceramides, which are known to show inhibitory regulation of pituitary hormone secretion in experimental models.	Ceramides	103-112	carboxyl ester lipase	Homo sapiens	23-26
20566755-7	2010	Considering that CEL hydrolyzes ceramides, inactivating their inhibitory function on pituitary hormone secretion, our findings suggest a possible role of CEL in the regulation of hormone secretion in both normal and adenomatous pituitary cells.	Ceramides	32-41	carboxyl ester lipase	Homo sapiens	17-20
20566755-7	2010	Considering that CEL hydrolyzes ceramides, inactivating their inhibitory function on pituitary hormone secretion, our findings suggest a possible role of CEL in the regulation of hormone secretion in both normal and adenomatous pituitary cells.	Ceramides	32-41	carboxyl ester lipase	Homo sapiens	154-157
21029305-6	2010	Our work revealed a novel mechanism, involving ceramide generation and triggering of mitochondrial abnormalities, by which iPLA(2)beta participates in the beta-cell apoptosis process.	Ceramides	47-55	phospholipase A2 group VI	Homo sapiens	123-134
20493824-0	2010	Tiam1/Rac1 signaling pathway mediates palmitate-induced, ceramide-sensitive generation of superoxides and lipid peroxides and the loss of mitochondrial membrane potential in pancreatic beta-cells.	Ceramides	57-65	TIAM Rac1 associated GEF 1	Rattus norvegicus	0-5
20629193-3	2010	We recently demonstrated that a rapid generation of ceramide by neutral sphingomyelinase-2 (nSMase2; also known as "sphingomyelin phosphodiesterase-3") played a key role in modulating excitatory postsynaptic currents by controlling the insertion and clustering of NMDA receptors (Wheeler et al.	Ceramides	52-60	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	64-90
20629193-3	2010	We recently demonstrated that a rapid generation of ceramide by neutral sphingomyelinase-2 (nSMase2; also known as "sphingomyelin phosphodiesterase-3") played a key role in modulating excitatory postsynaptic currents by controlling the insertion and clustering of NMDA receptors (Wheeler et al.	Ceramides	52-60	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	92-99
20629193-3	2010	We recently demonstrated that a rapid generation of ceramide by neutral sphingomyelinase-2 (nSMase2; also known as "sphingomyelin phosphodiesterase-3") played a key role in modulating excitatory postsynaptic currents by controlling the insertion and clustering of NMDA receptors (Wheeler et al.	Ceramides	52-60	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	116-149
20629193-8	2010	At the molecular level, inhibition of nSMase2 decreased ceramide, increased PSD-95, increased the number of AMPA receptors, and altered the subunit composition of NMDA receptors.	Ceramides	56-64	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	38-45
20941382-4	2010	METHODOLOGY/PRINCIPAL FINDINGS: Genetic data indicate an acute wave of ceramide-mediated endothelial apoptosis, initiated by acid sphingomyelinase (ASMase), regulates tumor stem cell response to single dose radiotherapy, obligatory for tumor cure.	Ceramides	71-79	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	125-146
20941382-4	2010	METHODOLOGY/PRINCIPAL FINDINGS: Genetic data indicate an acute wave of ceramide-mediated endothelial apoptosis, initiated by acid sphingomyelinase (ASMase), regulates tumor stem cell response to single dose radiotherapy, obligatory for tumor cure.	Ceramides	71-79	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	148-154
20941382-6	2010	Anti-VEGFR2 acts conversely, enhancing ceramide generation and apoptosis.	Ceramides	39-47	kinase insert domain protein receptor	Mus musculus	5-11
20629193-9	2010	Our study identifies nSMase2 as an important component for efficient memory formation and underscores the importance of ceramide in regulating synaptic events related to learning and memory.	Ceramides	120-128	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	21-28
20886096-5	2010	TLR4 signaling was initiated after ceramide release from glycosphingolipid receptors, through TRAM, CREB, Fos and Jun phosphorylation and p38 MAPK-dependent mechanisms, resulting in nuclear translocation of IRF3 and activation of IRF3/IFNbeta-dependent antibacterial effector mechanisms.	Ceramides	35-43	toll like receptor 4	Homo sapiens	0-4
20886096-5	2010	TLR4 signaling was initiated after ceramide release from glycosphingolipid receptors, through TRAM, CREB, Fos and Jun phosphorylation and p38 MAPK-dependent mechanisms, resulting in nuclear translocation of IRF3 and activation of IRF3/IFNbeta-dependent antibacterial effector mechanisms.	Ceramides	35-43	translocation associated membrane protein 1	Homo sapiens	94-98
20886096-5	2010	TLR4 signaling was initiated after ceramide release from glycosphingolipid receptors, through TRAM, CREB, Fos and Jun phosphorylation and p38 MAPK-dependent mechanisms, resulting in nuclear translocation of IRF3 and activation of IRF3/IFNbeta-dependent antibacterial effector mechanisms.	Ceramides	35-43	cAMP responsive element binding protein 1	Homo sapiens	100-104
20886096-5	2010	TLR4 signaling was initiated after ceramide release from glycosphingolipid receptors, through TRAM, CREB, Fos and Jun phosphorylation and p38 MAPK-dependent mechanisms, resulting in nuclear translocation of IRF3 and activation of IRF3/IFNbeta-dependent antibacterial effector mechanisms.	Ceramides	35-43	interferon regulatory factor 3	Homo sapiens	207-211
20886096-6	2010	This TLR4/IRF3 pathway of pathogen discrimination was activated by ceramide and by P-fimbriated E. coli, which use ceramide-anchored glycosphingolipid receptors.	Ceramides	67-75	toll like receptor 4	Homo sapiens	5-9
20886096-6	2010	This TLR4/IRF3 pathway of pathogen discrimination was activated by ceramide and by P-fimbriated E. coli, which use ceramide-anchored glycosphingolipid receptors.	Ceramides	67-75	interferon regulatory factor 3	Mus musculus	10-14
20886096-6	2010	This TLR4/IRF3 pathway of pathogen discrimination was activated by ceramide and by P-fimbriated E. coli, which use ceramide-anchored glycosphingolipid receptors.	Ceramides	115-123	toll like receptor 4	Homo sapiens	5-9
20886096-6	2010	This TLR4/IRF3 pathway of pathogen discrimination was activated by ceramide and by P-fimbriated E. coli, which use ceramide-anchored glycosphingolipid receptors.	Ceramides	115-123	interferon regulatory factor 3	Mus musculus	10-14
20511539-4	2010	Indeed, we show that both insufficient and supraphysiologic GALC activity-by inherited genetic deficiency or forced gene expression in patients" cells and in the disease model-induce alterations of the intracellular content of the bioactive GALC downstream products ceramide and sphingosine, and thus affect HSPC survival and function and the functionality of the stem cell niche.	Ceramides	266-274	galactosylceramidase	Homo sapiens	60-64
20511539-4	2010	Indeed, we show that both insufficient and supraphysiologic GALC activity-by inherited genetic deficiency or forced gene expression in patients" cells and in the disease model-induce alterations of the intracellular content of the bioactive GALC downstream products ceramide and sphingosine, and thus affect HSPC survival and function and the functionality of the stem cell niche.	Ceramides	266-274	galactosylceramidase	Homo sapiens	241-245
20493824-0	2010	Tiam1/Rac1 signaling pathway mediates palmitate-induced, ceramide-sensitive generation of superoxides and lipid peroxides and the loss of mitochondrial membrane potential in pancreatic beta-cells.	Ceramides	57-65	Rac family small GTPase 1	Rattus norvegicus	6-10
20435159-5	2010	Promoting intracellular accumulation of free fatty acids (FFAs) in 3T3-L1 adipocytes increased expression of inflammatory cytokines, whereas inhibiting ceramide synthesis partly blocked PAI-1 expression, but not IL-6.	Ceramides	152-160	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	186-191
20836852-10	2010	Dissecting the cause of ceramide production, we found activation of neutral sphingomyelinase and showed neutral-sphingomyelinase 2 (N-SMase 2) is a critical mediator of WithaD-induced apoptosis.	Ceramides	24-32	sphingomyelin phosphodiesterase 3	Homo sapiens	104-130
20836852-10	2010	Dissecting the cause of ceramide production, we found activation of neutral sphingomyelinase and showed neutral-sphingomyelinase 2 (N-SMase 2) is a critical mediator of WithaD-induced apoptosis.	Ceramides	24-32	sphingomyelin phosphodiesterase 3	Homo sapiens	132-141
20836852-11	2010	Knockdown of N-SMase 2 by siRNA and inhibitor of N-SMase (GW4869) significantly reduced WithaD-induced ceramide generation and phosphorylation of MKK4 and MKK3/6, whereas phosphorylation of MKK7 was moderately regulated in leukemic cells.	Ceramides	103-111	sphingomyelin phosphodiesterase 2	Homo sapiens	13-20
20836852-11	2010	Knockdown of N-SMase 2 by siRNA and inhibitor of N-SMase (GW4869) significantly reduced WithaD-induced ceramide generation and phosphorylation of MKK4 and MKK3/6, whereas phosphorylation of MKK7 was moderately regulated in leukemic cells.	Ceramides	103-111	sphingomyelin phosphodiesterase 2	Homo sapiens	49-56
20836852-14	2010	CONCLUSION: Our results demonstrate that WithaD enhance the ceramide accumulation by activating N-SMase 2, modulate phosphorylation of the JNK and p38MAPK and induced apoptosis in both myeloid and lymphoid cells along with primary cells derived from leukemia patients.	Ceramides	60-68	sphingomyelin phosphodiesterase 3	Homo sapiens	96-105
20628055-4	2010	Treatment with 4-HPR induced the accumulation of dihydroceramides (DHCs) in tumor cells by inhibiting dihydroceramide desaturase (DES) activity, which catalyzes the conversion of DHCs to ceramides.	Ceramides	56-65	haptoglobin-related protein	Homo sapiens	17-20
20613485-4	2010	In addition, MDA-7/IL-24 has been noted to be a radiosensitizing cytokine, which is partly because of the generation of reactive oxygen species and ceramide that cause endoplasmic reticulum stress.	Ceramides	148-156	interleukin 24	Homo sapiens	13-18
20613485-4	2010	In addition, MDA-7/IL-24 has been noted to be a radiosensitizing cytokine, which is partly because of the generation of reactive oxygen species and ceramide that cause endoplasmic reticulum stress.	Ceramides	148-156	interleukin 24	Homo sapiens	19-24
20519553-0	2010	Selective inhibition of carbonic anhydrase IX decreases cell proliferation and induces ceramide-mediated apoptosis in human cancer cells.	Ceramides	87-95	carbonic anhydrase 9	Homo sapiens	24-45
20631069-0	2010	Vorinostat and sorafenib increase CD95 activation in gastrointestinal tumor cells through a Ca(2+)-de novo ceramide-PP2A-reactive oxygen species-dependent signaling pathway.	Ceramides	107-115	Fas cell surface death receptor	Homo sapiens	34-38
20543095-3	2010	Treatment of mice with the acid sphingomyelinase (ASMase) inhibitor amitriptyline significantly attenuated the HFD-induced plasma ceramide levels.	Ceramides	130-138	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	27-48
20543095-3	2010	Treatment of mice with the acid sphingomyelinase (ASMase) inhibitor amitriptyline significantly attenuated the HFD-induced plasma ceramide levels.	Ceramides	130-138	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	50-56
20543095-4	2010	Corresponding to increase in plasma ceramide, the HFD significantly increased the body weight gain, plasma leptin concentration, urinary total protein and albumin excretion, glomerular damage index, and adipose tissue ASMase activity compared with the LFD-fed mice.	Ceramides	36-44	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	218-224
20637730-1	2010	Ceramide kinase (CERK) produces the bioactive lipid ceramide 1-phosphate (C1P) and is, together with glucosylceramide synthase (GCS) and sphingomyelin synthases (SMS-1 and -2), a key regulator of ceramide metabolism.	Ceramides	52-60	ceramide kinase	Mus musculus	0-15
20637730-1	2010	Ceramide kinase (CERK) produces the bioactive lipid ceramide 1-phosphate (C1P) and is, together with glucosylceramide synthase (GCS) and sphingomyelin synthases (SMS-1 and -2), a key regulator of ceramide metabolism.	Ceramides	52-60	ceramide kinase	Mus musculus	17-21
20637730-3	2010	Elicitation of peritoneal macrophages as well as differentiation of bone marrow-derived monocytes into macrophages led to "ceramide anabolic switching" by re-directing ceramide anabolism towards C1P synthesis by CERK.	Ceramides	123-131	ceramide kinase	Mus musculus	212-216
20637730-4	2010	In contrast, macrophage activation by lipopolysaccharide (LPS) evoked a "ceramide anabolic switch" going in the opposite direction, i.e. featuring up-regulation of GCS and SMS and down-regulation of CERK.	Ceramides	73-81	UDP-glucose ceramide glucosyltransferase	Mus musculus	164-167
20637730-4	2010	In contrast, macrophage activation by lipopolysaccharide (LPS) evoked a "ceramide anabolic switch" going in the opposite direction, i.e. featuring up-regulation of GCS and SMS and down-regulation of CERK.	Ceramides	73-81	ceramide kinase	Mus musculus	199-203
20386061-4	2010	Expression of untargeted or ER-targeted SK1, but surprisingly not PM-targeted SK1, results in a dramatic increase in the phosphorylation of dihydrosphingosine, a metabolic precursor in de novo ceramide synthesis.	Ceramides	193-201	sphingosine kinase 1	Homo sapiens	40-43
20808818-4	2010	METHODOLOGY/PRINCIPAL FINDINGS: Genetic data indicate an acute wave of ceramide-mediated endothelial apoptosis, initiated by acid sphingomyelinase (ASMase), regulates tumor stem cell response to single dose radiotherapy, obligatory for tumor cure.	Ceramides	71-79	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	125-146
20808818-4	2010	METHODOLOGY/PRINCIPAL FINDINGS: Genetic data indicate an acute wave of ceramide-mediated endothelial apoptosis, initiated by acid sphingomyelinase (ASMase), regulates tumor stem cell response to single dose radiotherapy, obligatory for tumor cure.	Ceramides	71-79	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	148-154
20808818-6	2010	Anti-VEGFR2 acts conversely, enhancing ceramide generation and apoptosis.	Ceramides	39-47	kinase insert domain protein receptor	Mus musculus	5-11
20395562-1	2010	RATIONALE: Ceramide accumulates in the airway epithelium of mice deficient in cystic fibrosis transmembrane conductance regulator, resulting in susceptibility to Pseudomonas aeruginosa infection and inflammation.	Ceramides	11-19	cystic fibrosis transmembrane conductance regulator	Mus musculus	78-129
20395562-7	2010	The number of neutrophil elastase- and myeloperoxidase-positive cells in the airway was positively correlated with the percentage of epithelium staining for ceramide (P = 0.001).	Ceramides	157-165	elastase, neutrophil expressed	Homo sapiens	14-33
20395562-7	2010	The number of neutrophil elastase- and myeloperoxidase-positive cells in the airway was positively correlated with the percentage of epithelium staining for ceramide (P = 0.001).	Ceramides	157-165	myeloperoxidase	Homo sapiens	39-54
20434430-11	2010	Ceramide-induced expression of PGPS in Hela cells or in CHO cells did not alter expression of Mfn-2 indicating that Mfn-2 expression is independent of altered CL synthesis mediated by elevated PGPS.	Ceramides	0-8	mitofusin-2	Cricetulus griseus	116-121
20631069-0	2010	Vorinostat and sorafenib increase CD95 activation in gastrointestinal tumor cells through a Ca(2+)-de novo ceramide-PP2A-reactive oxygen species-dependent signaling pathway.	Ceramides	107-115	protein phosphatase 2 phosphatase activator	Homo sapiens	116-120
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.	Ceramides	13-21	UDP-glucose ceramide glucosyltransferase	Homo sapiens	55-80
20466846-11	2010	The ability of ceramide (5 x 10(-5) M) to induce apoptosis was prevented by the inhibitors of PP1 and PKC delta, whilst the general PKC and PI3K inhibitors had no effect on it.	Ceramides	15-23	protein kinase C, delta	Mus musculus	102-105
20654784-9	2010	RESULTS: C10 significantly inhibited secretion of both fluorescent ceramide and LEKTI in cultured normal human epidermal keratinocytes and a reconstructed human epidermis.	Ceramides	67-75	homeobox C10	Homo sapiens	9-12
20654784-10	2010	C10 also disturbed the polarized localization of fluorescent ceramide and LEKTI in the reconstructed epidermis.	Ceramides	61-69	homeobox C10	Homo sapiens	0-3
20599756-10	2010	Bm-TFF2 could also inhibit cell apoptosis induced by ceramide and sodium butyrate.	Ceramides	53-61	trefoil factor 2	Homo sapiens	3-7
20466846-9	2010	The ability of ceramide (5 x 10(-8) M) to promote osteoblast survival was prevented by a general protein kinase C (PKC) inhibitor and by a PKC zeta inhibitor, whilst osteoblast survival was enhanced in the presence of a protein phosphatase 1 (PP1) inhibitor.	Ceramides	15-23	protein kinase C, delta	Mus musculus	115-118
20466846-9	2010	The ability of ceramide (5 x 10(-8) M) to promote osteoblast survival was prevented by a general protein kinase C (PKC) inhibitor and by a PKC zeta inhibitor, whilst osteoblast survival was enhanced in the presence of a protein phosphatase 1 (PP1) inhibitor.	Ceramides	15-23	protein phosphatase 1 catalytic subunit gamma	Mus musculus	220-241
20466846-9	2010	The ability of ceramide (5 x 10(-8) M) to promote osteoblast survival was prevented by a general protein kinase C (PKC) inhibitor and by a PKC zeta inhibitor, whilst osteoblast survival was enhanced in the presence of a protein phosphatase 1 (PP1) inhibitor.	Ceramides	15-23	protein phosphatase 1 catalytic subunit gamma	Mus musculus	243-246
20466846-11	2010	The ability of ceramide (5 x 10(-5) M) to induce apoptosis was prevented by the inhibitors of PP1 and PKC delta, whilst the general PKC and PI3K inhibitors had no effect on it.	Ceramides	15-23	protein phosphatase 1 catalytic subunit gamma	Mus musculus	94-97
20466846-11	2010	The ability of ceramide (5 x 10(-5) M) to induce apoptosis was prevented by the inhibitors of PP1 and PKC delta, whilst the general PKC and PI3K inhibitors had no effect on it.	Ceramides	15-23	protein kinase C, delta	Mus musculus	102-111
20375276-0	2010	Ceramide modulates HERG potassium channel gating by translocation into lipid rafts.	Ceramides	0-8	potassium voltage-gated channel subfamily H member 2	Homo sapiens	19-23
20236926-0	2010	Studies on the role of acid sphingomyelinase and ceramide in the regulation of tumor necrosis factor alpha (TNFalpha)-converting enzyme activity and TNFalpha secretion in macrophages.	Ceramides	49-57	tumor necrosis factor	Mus musculus	79-106
20236926-0	2010	Studies on the role of acid sphingomyelinase and ceramide in the regulation of tumor necrosis factor alpha (TNFalpha)-converting enzyme activity and TNFalpha secretion in macrophages.	Ceramides	49-57	tumor necrosis factor	Mus musculus	108-116
20236926-0	2010	Studies on the role of acid sphingomyelinase and ceramide in the regulation of tumor necrosis factor alpha (TNFalpha)-converting enzyme activity and TNFalpha secretion in macrophages.	Ceramides	49-57	tumor necrosis factor	Mus musculus	149-157
20236926-8	2010	TACE activity was 2-3-fold higher in asm(-/-) macrophages as compared with asm(+/+) macrophages and was suppressed when cells were treated with exogenous ceramide and sphingomyelinase.	Ceramides	154-162	a disintegrin and metallopeptidase domain 17	Mus musculus	0-4
20375276-4	2010	Yet the acute effects of ceramide on HERG potassium channels are not known.	Ceramides	25-33	potassium voltage-gated channel subfamily H member 2	Homo sapiens	37-41
20375276-8	2010	Mechanistically, ceramide recruited HERG channels within caveolin-enriched lipid rafts.	Ceramides	17-25	potassium voltage-gated channel subfamily H member 2	Homo sapiens	36-40
20382204-0	2010	Importance of cytochrome c redox state for ceramide-induced apoptosis of human mammary adenocarcinoma cells.	Ceramides	43-51	cytochrome c, somatic	Homo sapiens	14-26
20489143-4	2010	Abca12(-/-) neonatal epidermis showed significantly reduced total ceramide amounts and aberrant ceramide composition.	Ceramides	66-74	ATP-binding cassette, sub-family A (ABC1), member 12	Mus musculus	0-6
20489143-4	2010	Abca12(-/-) neonatal epidermis showed significantly reduced total ceramide amounts and aberrant ceramide composition.	Ceramides	96-104	ATP-binding cassette, sub-family A (ABC1), member 12	Mus musculus	0-6
20489143-8	2010	Ten-passage sub-cultured Abca12(-/-) keratinocytes showed restoration of intact ceramide distribution, differentiation-specific protein expression and profilaggrin/filaggrin conversion, which were defective in primary-cultures.	Ceramides	80-88	ATP-binding cassette, sub-family A (ABC1), member 12	Mus musculus	25-31
20382204-4	2010	The present study delineates importance of the redox state of cytochrome c for release of cytochrome c and apoptosis of human mammary adenocarcinoma MCF-7 and MDA-MB-231 cells induced by ceramides.	Ceramides	187-196	cytochrome c, somatic	Homo sapiens	62-74
20382204-4	2010	The present study delineates importance of the redox state of cytochrome c for release of cytochrome c and apoptosis of human mammary adenocarcinoma MCF-7 and MDA-MB-231 cells induced by ceramides.	Ceramides	187-196	cytochrome c, somatic	Homo sapiens	90-102
20382204-7	2010	RESULTS: We show that ceramides induce mitochondrial oxidative stress and release of cytochrome c from the mitochondria of these cells.	Ceramides	22-31	cytochrome c, somatic	Homo sapiens	85-97
20382204-8	2010	Our findings show that ceramides react with oxidized cytochrome c whereas reduced cytochrome c does not react with ceramides.	Ceramides	23-32	cytochrome c, somatic	Homo sapiens	53-65
20382204-9	2010	We also show that oxidized cytochrome c reacted with ceramides exerts lower reducibility and function to support mitochondrial respiration.	Ceramides	53-62	cytochrome c, somatic	Homo sapiens	27-39
20237147-10	2010	In isotonic solutions, both ceramide (20 microM) and Ca(2+) ionophore ionomycin (0.5 microM) increased annexin V-binding, effects again significantly blunted by 500 mM urea.	Ceramides	28-36	annexin A5	Homo sapiens	103-112
20382204-10	2010	Furthermore, our data show that glutathione protects cytochrome c of reacting with ceramides by increasing the reduced state of cytochrome c.	Ceramides	83-92	cytochrome c, somatic	Homo sapiens	53-65
20382204-10	2010	Furthermore, our data show that glutathione protects cytochrome c of reacting with ceramides by increasing the reduced state of cytochrome c.	Ceramides	83-92	cytochrome c, somatic	Homo sapiens	128-140
20382204-11	2010	CONCLUSIONS: Ceramides induce oxidative stress and apoptosis in human mammary adenocarcinoma cells by interacting with oxidized cytochrome c leading to the release of cytochrome c from the mitochondria.	Ceramides	13-22	cytochrome c, somatic	Homo sapiens	128-140
20382204-11	2010	CONCLUSIONS: Ceramides induce oxidative stress and apoptosis in human mammary adenocarcinoma cells by interacting with oxidized cytochrome c leading to the release of cytochrome c from the mitochondria.	Ceramides	13-22	cytochrome c, somatic	Homo sapiens	167-179
20382204-13	2010	GENERAL SIGNIFICANCE: Our study suggests that the redox state of cytochrome c is important in oxidative stress and apoptosis induced by ceramides.	Ceramides	136-145	cytochrome c, somatic	Homo sapiens	65-77
20540705-0	2010	The acid sphingomyelinase/ceramide pathway: biomedical significance and mechanisms of regulation.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
20591223-2	2010	The inhibitory function of TMSG-1 in tumor cells may be related to vacuolar H+-ATPase and ceramide, but the underlying mechanism remains unknown.	Ceramides	90-98	ceramide synthase 2	Homo sapiens	27-33
20540705-2	2010	In a phospholipase C reaction, ASMase catalyzes the cleavage of the phosphocholine head group of sphingomyelin to generate ceramide.	Ceramides	123-131	sphingomyelin phosphodiesterase 1	Homo sapiens	31-37
20540705-4	2010	Activation of the ASMase/ceramide pathway is a shared response to an ever-growing list of receptor and non-receptor mediated forms of cellular stress including: death ligands (TNFalpha, TRAIL, Fas ligand), cytokines (IL-1, IFNgamma), radiation, pathogenic infections, cytotoxic agents and others.	Ceramides	25-33	sphingomyelin phosphodiesterase 1	Homo sapiens	18-24
20540705-4	2010	Activation of the ASMase/ceramide pathway is a shared response to an ever-growing list of receptor and non-receptor mediated forms of cellular stress including: death ligands (TNFalpha, TRAIL, Fas ligand), cytokines (IL-1, IFNgamma), radiation, pathogenic infections, cytotoxic agents and others.	Ceramides	25-33	tumor necrosis factor	Homo sapiens	176-184
20540705-4	2010	Activation of the ASMase/ceramide pathway is a shared response to an ever-growing list of receptor and non-receptor mediated forms of cellular stress including: death ligands (TNFalpha, TRAIL, Fas ligand), cytokines (IL-1, IFNgamma), radiation, pathogenic infections, cytotoxic agents and others.	Ceramides	25-33	TNF superfamily member 10	Homo sapiens	186-191
20540705-4	2010	Activation of the ASMase/ceramide pathway is a shared response to an ever-growing list of receptor and non-receptor mediated forms of cellular stress including: death ligands (TNFalpha, TRAIL, Fas ligand), cytokines (IL-1, IFNgamma), radiation, pathogenic infections, cytotoxic agents and others.	Ceramides	25-33	Fas ligand	Homo sapiens	193-203
20540705-4	2010	Activation of the ASMase/ceramide pathway is a shared response to an ever-growing list of receptor and non-receptor mediated forms of cellular stress including: death ligands (TNFalpha, TRAIL, Fas ligand), cytokines (IL-1, IFNgamma), radiation, pathogenic infections, cytotoxic agents and others.	Ceramides	25-33	interleukin 1 alpha	Homo sapiens	217-221
20540705-4	2010	Activation of the ASMase/ceramide pathway is a shared response to an ever-growing list of receptor and non-receptor mediated forms of cellular stress including: death ligands (TNFalpha, TRAIL, Fas ligand), cytokines (IL-1, IFNgamma), radiation, pathogenic infections, cytotoxic agents and others.	Ceramides	25-33	interferon gamma	Homo sapiens	223-231
20540705-6	2010	In this article, we review the translational role of the ASMase/ceramide pathway and recent advances on its mechanisms of regulation.	Ceramides	64-72	sphingomyelin phosphodiesterase 1	Homo sapiens	57-63
20540746-5	2010	GCS converts ceramide to glucosylceramide, reducing the impact of ceramide-induced apoptosis and increasing glycosphingolipid (GSL) synthesis.	Ceramides	13-21	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
20361178-6	2010	Accumulation of toxic lipid metabolites (fatty acyl CoA, diacylglycerol, ceramide) in muscle, liver, adipocytes, beta cells and arterial tissues contributes to insulin resistance, beta cell dysfunction and accelerated atherosclerosis, respectively, in type 2 diabetes.	Ceramides	73-81	insulin	Homo sapiens	160-167
20194109-2	2010	Our results indicated that treatment with both 4-HPR and 4-oxo-4-HPR led to a marked increase in dihydroceramide species, while only 4-oxo-4-HPR led to a minor increase of ceramide species.	Ceramides	104-112	haptoglobin-related protein	Homo sapiens	49-52
20194109-2	2010	Our results indicated that treatment with both 4-HPR and 4-oxo-4-HPR led to a marked increase in dihydroceramide species, while only 4-oxo-4-HPR led to a minor increase of ceramide species.	Ceramides	104-112	haptoglobin-related protein	Homo sapiens	65-68
20194109-2	2010	Our results indicated that treatment with both 4-HPR and 4-oxo-4-HPR led to a marked increase in dihydroceramide species, while only 4-oxo-4-HPR led to a minor increase of ceramide species.	Ceramides	104-112	haptoglobin-related protein	Homo sapiens	65-68
20444975-3	2010	PKD is recruited and activated at the Golgi through interaction with diacylglycerol, a pool of which is generated as a by-product of sphingomyelin synthesis from ceramide.	Ceramides	162-170	protein kinase D1	Homo sapiens	0-3
20514393-0	2010	Inhibition of p53 sensitizes MCF-7 cells to ceramide treatment.	Ceramides	44-52	tumor protein p53	Homo sapiens	14-17
20514393-3	2010	Ceramide induced a selective arrest of MCF-7 cells in the G1-phase, which was associated with a decreased expression of cyclins D and E and increased expression of p53 and p21.	Ceramides	0-8	tumor protein p53	Homo sapiens	164-167
20514393-3	2010	Ceramide induced a selective arrest of MCF-7 cells in the G1-phase, which was associated with a decreased expression of cyclins D and E and increased expression of p53 and p21.	Ceramides	0-8	H3 histone pseudogene 16	Homo sapiens	172-175
20514393-4	2010	Interestingly, inhibition of p53 using pifithrin alpha or RNAi sensitized MCF-7 cells to ceramide-induced cell death.	Ceramides	89-97	tumor protein p53	Homo sapiens	29-32
20514393-6	2010	The increased sensitivity to ceramide, in the context of p53 inhibition, may be due to decreased expression of p21, as siRNA targeted to p21 also sensitized MCF-7 cells to ceramide-induced death.	Ceramides	29-37	tumor protein p53	Homo sapiens	57-60
20514393-6	2010	The increased sensitivity to ceramide, in the context of p53 inhibition, may be due to decreased expression of p21, as siRNA targeted to p21 also sensitized MCF-7 cells to ceramide-induced death.	Ceramides	29-37	H3 histone pseudogene 16	Homo sapiens	111-114
20514393-6	2010	The increased sensitivity to ceramide, in the context of p53 inhibition, may be due to decreased expression of p21, as siRNA targeted to p21 also sensitized MCF-7 cells to ceramide-induced death.	Ceramides	29-37	H3 histone pseudogene 16	Homo sapiens	137-140
20514393-7	2010	These data demonstrate that in tumors with inactivating mutations of p53, ceramide-based therapies might provide a novel and effective treatment option.	Ceramides	74-82	tumor protein p53	Homo sapiens	69-72
20456020-2	2010	Sphingomyelin in the plasma membrane can be cleaved by neutral sphingomyelinases (nSMase) to generate ceramides and sphingosine-1-phosphate (S1P) which have been shown to play a variety of roles in cellular signaling processes.	Ceramides	102-111	sphingomyelin phosphodiesterase 2	Homo sapiens	55-80
20456020-2	2010	Sphingomyelin in the plasma membrane can be cleaved by neutral sphingomyelinases (nSMase) to generate ceramides and sphingosine-1-phosphate (S1P) which have been shown to play a variety of roles in cellular signaling processes.	Ceramides	102-111	sphingomyelin phosphodiesterase 2	Homo sapiens	82-88
20456020-6	2010	Mass spectrometry-based measurements demonstrated that nSMase activity induces a rapid increase in the levels of ceramides and S1P in cells in hippocampal slices.	Ceramides	113-122	sphingomyelin phosphodiesterase 2	Homo sapiens	55-61
20456020-7	2010	The ability of nSMase to increase CA1 neuron excitability was blocked by an inhibitor of sphingosine kinase, the enzyme that converts ceramide to S1P.	Ceramides	134-142	sphingomyelin phosphodiesterase 2	Homo sapiens	15-21
20456020-7	2010	The ability of nSMase to increase CA1 neuron excitability was blocked by an inhibitor of sphingosine kinase, the enzyme that converts ceramide to S1P.	Ceramides	134-142	carbonic anhydrase 1	Homo sapiens	34-37
20174962-4	2010	Furthermore, we investigated whether the ceramide formation is related to the activity of either neutral sphingomyelinase (N-SMase) or acidic sphingomyelinase (A-SMase).	Ceramides	41-49	sphingomyelin phosphodiesterase 2	Rattus norvegicus	97-121
20530211-6	2010	Exogenously added recombinant human ASM restores endocytosis and resealing in ASM-depleted cells, suggesting that conversion of plasma membrane sphingomyelin to ceramide by this lysosomal enzyme promotes lesion internalization.	Ceramides	161-169	sphingomyelin phosphodiesterase 1	Homo sapiens	36-39
20530211-6	2010	Exogenously added recombinant human ASM restores endocytosis and resealing in ASM-depleted cells, suggesting that conversion of plasma membrane sphingomyelin to ceramide by this lysosomal enzyme promotes lesion internalization.	Ceramides	161-169	sphingomyelin phosphodiesterase 1	Homo sapiens	78-81
20540746-5	2010	GCS converts ceramide to glucosylceramide, reducing the impact of ceramide-induced apoptosis and increasing glycosphingolipid (GSL) synthesis.	Ceramides	33-41	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
20353945-4	2010	Ceramide, whose biosynthesis is regulated by neutral sphingomyelinase 2 (nSMase2), triggers secretion of small membrane vesicles called exosomes.	Ceramides	0-8	sphingomyelin phosphodiesterase 3	Homo sapiens	45-71
20378533-3	2010	Neutral SMase (N-SMase) isoforms, which catalyze hydrolysis of sphingomyelin (SM) to ceramide and phosphocholine, have been found in the mitochondria of yeast and zebrafish, yet their existence in mammalian mitochondria remains unknown.	Ceramides	85-93	sphingomyelin phosphodiesterase 2	Homo sapiens	8-13
20378533-3	2010	Neutral SMase (N-SMase) isoforms, which catalyze hydrolysis of sphingomyelin (SM) to ceramide and phosphocholine, have been found in the mitochondria of yeast and zebrafish, yet their existence in mammalian mitochondria remains unknown.	Ceramides	85-93	sphingomyelin phosphodiesterase 2	Homo sapiens	15-22
20353945-4	2010	Ceramide, whose biosynthesis is regulated by neutral sphingomyelinase 2 (nSMase2), triggers secretion of small membrane vesicles called exosomes.	Ceramides	0-8	sphingomyelin phosphodiesterase 3	Homo sapiens	73-80
20224005-2	2010	This study shows that the inhibitory effect of ethanol on AMPK phosphorylation is exerted through the inhibition of the phosphorylation of upstream kinases and the activation of protein phosphatase 2A (PP2A).Inhibition of AMPK phosphorylation by palmitate was attributed to ceramide-dependent PP2A activation.	Ceramides	274-282	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	202-206
20378533-9	2010	Importantly, overexpression of MA-nSMase in HEK293 cells significantly increased in vitro N-SMase activity and also modulated the levels of SM and ceramide, indicating that the identified cDNA encodes a functional SMase.	Ceramides	147-155	sphingomyelin phosphodiesterase 5 (pseudogene)	Homo sapiens	31-40
20378533-9	2010	Importantly, overexpression of MA-nSMase in HEK293 cells significantly increased in vitro N-SMase activity and also modulated the levels of SM and ceramide, indicating that the identified cDNA encodes a functional SMase.	Ceramides	147-155	sphingomyelin phosphodiesterase 2	Homo sapiens	35-40
19635928-0	2010	Acid sphingomyelinase inhibitors normalize pulmonary ceramide and inflammation in cystic fibrosis.	Ceramides	53-61	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
19635928-4	2010	We tested whether inhalation of different acid sphingomyelinase inhibitors does reduce Asm activity and ceramide accumulation in lungs of CF mice.	Ceramides	104-112	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	42-63
19635928-9	2010	Inhalation of the Asm inhibitors amitriptyline, trimipramine, desipramine, chlorprothixene, fluoxetine, amlodipine, or sertraline restored normal ceramide concentrations in murine bronchial epithelial cells, reduced inflammation in the lung of CF mice and prevented infection with Pseudomonas aeruginosa.	Ceramides	146-154	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	18-21
19635928-12	2010	These findings employing several structurally different Asm inhibitors identify Asm as primary target in the lung to reduce ceramide concentrations.	Ceramides	124-132	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	56-59
19635928-12	2010	These findings employing several structurally different Asm inhibitors identify Asm as primary target in the lung to reduce ceramide concentrations.	Ceramides	124-132	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	80-83
20224005-7	2010	Ethanol treatment significantly increased cellular ceramide content and PP2A activity by approximately 18-23%, when the cells were treated with ethanol for between 4 and 12 h. These changes in intracellular ceramide concentrations and PP2A activity correlated with the time course over which ethanol inhibited AMPK phosphorylation.	Ceramides	207-215	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	72-76
20302564-4	2010	Sphingosine kinase-1 is a crucial regulator of this two-pan balance, because its produces the pro-survival and pro-angiogenic sphingosine 1-phosphate and decreases the amount of both ceramide and sphingosine, the pro-apoptotic sphingolipids.	Ceramides	183-191	sphingosine kinase 1	Homo sapiens	0-20
20393162-1	2010	The molecular mechanisms of obesity-associated insulin resistance are becoming increasingly clear, and the effects of various lipid molecules, such as diacylglycerol and ceramide, on the insulin signal are being actively explored.	Ceramides	170-178	insulin	Homo sapiens	187-194
20388485-2	2010	We showed that ceramide (Cer) modulates protein kinase A (PKA) and protein kinase C (PKC), which are involved in regulating ion transporters.	Ceramides	15-23	protein kinase C zeta	Homo sapiens	85-88
20388485-2	2010	We showed that ceramide (Cer) modulates protein kinase A (PKA) and protein kinase C (PKC), which are involved in regulating ion transporters.	Ceramides	25-28	protein kinase C zeta	Homo sapiens	85-88
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.	Ceramides	131-139	heat shock 70 kDa protein 1	Canis lupus familiaris	39-44
20083151-5	2010	This pathway involves iPLA(2)beta dependent induction of neutral sphingomyelinase, production of ceramide, and activation of the intrinsic pathway of apoptosis.	Ceramides	97-105	phospholipase A2, group VI	Mus musculus	22-33
20456488-6	2010	MATERIAL AND METHODS: Annexin V-binding was utilised to disclose PS exposure, forward scatter to analyse cell volume, Fluo 3 fluorescence to estimate cytosolic Ca(2+) activity, binding of fluorescent antibodies to determine ceramide abundance and a luciferin/luciferase-based assay to measure the cytosolic ATP concentration.	Ceramides	224-232	annexin A5	Homo sapiens	22-31
19799649-7	2010	Furthermore, we found that this effect is dependent on serine-5 phosphorylation of L-plastin and that non-conventional protein kinase C isoforms and the ceramide pathway may regulate its phosphorylation state.	Ceramides	153-161	lymphocyte cytosolic protein 1	Homo sapiens	83-92
20071681-4	2010	Acid sphingomyelinase (ASMase) and neutral sphingomyelinase (NSMase) are key regulatory enzymes of sphingolipid metabolism, promoting sphingomyelin hydrolysis to proinflammatory ceramide.	Ceramides	178-186	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
20071681-4	2010	Acid sphingomyelinase (ASMase) and neutral sphingomyelinase (NSMase) are key regulatory enzymes of sphingolipid metabolism, promoting sphingomyelin hydrolysis to proinflammatory ceramide.	Ceramides	178-186	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
20071681-4	2010	Acid sphingomyelinase (ASMase) and neutral sphingomyelinase (NSMase) are key regulatory enzymes of sphingolipid metabolism, promoting sphingomyelin hydrolysis to proinflammatory ceramide.	Ceramides	178-186	sphingomyelin phosphodiesterase 2	Homo sapiens	35-59
20071681-4	2010	Acid sphingomyelinase (ASMase) and neutral sphingomyelinase (NSMase) are key regulatory enzymes of sphingolipid metabolism, promoting sphingomyelin hydrolysis to proinflammatory ceramide.	Ceramides	178-186	sphingomyelin phosphodiesterase 2	Homo sapiens	61-67
20236389-3	2010	Subsequently, a splice variant lacking a serine-rich domain of 26 amino acids (GPBPDelta26) was found to mediate the cytosolic transport of ceramide and was therefore (re)named CERT.	Ceramides	140-148	ceramide transporter 1	Homo sapiens	177-181
20236389-7	2010	Because both mitochondria and ceramide play an important role in many biological events that regulate neuronal differentiation, cellular senescence, proliferation and cell death, we propose that GPBP and CERT are pivotal in neurodegenerative processes.	Ceramides	30-38	ceramide transporter 1	Mus musculus	195-199
20236389-8	2010	In this review, we discuss the current state of knowledge on GPBP and CERT, including the molecular and biochemical characterization of GPBP in the field of autoimmunity as well as the fundamental research on CERT in ceramide transport, biosynthesis, localization, metabolism and cell homeostasis.	Ceramides	217-225	ceramide transporter 1	Mus musculus	61-65
20236389-8	2010	In this review, we discuss the current state of knowledge on GPBP and CERT, including the molecular and biochemical characterization of GPBP in the field of autoimmunity as well as the fundamental research on CERT in ceramide transport, biosynthesis, localization, metabolism and cell homeostasis.	Ceramides	217-225	ceramide transporter 1	Mus musculus	209-213
21364652-5	2010	Apoptosis is reduced by incubation with CDP-choline (citicoline), a precursor for the conversion of ceramide to sphingomyelin.	Ceramides	100-108	cut-like homeobox 1	Mus musculus	40-43
20148315-3	2010	Ceramide can induce cell-cycle arrest by up-regulation of cyclin-dependent kinase (Cdk) inhibitors p21 and p27 through activation of protein phosphatase 2A (PP2A).	Ceramides	0-8	KRAS proto-oncogene, GTPase	Rattus norvegicus	99-102
20148315-3	2010	Ceramide can induce cell-cycle arrest by up-regulation of cyclin-dependent kinase (Cdk) inhibitors p21 and p27 through activation of protein phosphatase 2A (PP2A).	Ceramides	0-8	cyclin-dependent kinase inhibitor 1B	Rattus norvegicus	107-110
20148315-6	2010	Others have suggested bFGF-induced astrocyte proliferation is attenuated by D609 due to an increase in ceramide by SMS inhibition.	Ceramides	103-111	fibroblast growth factor 2	Rattus norvegicus	22-26
20544530-0	2010	Study of apoptosis induction and deoxycytidine kinase/cytidine deaminase modulation in the synergistic interaction of a novel ceramide analog and gemcitabine in pancreatic cancer cells.	Ceramides	126-134	deoxycytidine kinase	Homo sapiens	33-53
20544530-0	2010	Study of apoptosis induction and deoxycytidine kinase/cytidine deaminase modulation in the synergistic interaction of a novel ceramide analog and gemcitabine in pancreatic cancer cells.	Ceramides	126-134	cytidine deaminase	Homo sapiens	54-72
20127733-6	2010	RESULTS: We found that fibronectin, but not laminin or vitronectin activated a survival pathway that protected DU145 but not LNCaP prostate cancer cells against ceramide and docetaxel-induced apoptosis but not that induced by radiotherapy.	Ceramides	161-169	fibronectin 1	Homo sapiens	23-34
21364652-7	2010	Ethanol also increases the protein level of prostate apoptosis response 4 (PAR-4), a sensitizer to ceramide-induced apoptosis.	Ceramides	99-107	PRKC, apoptosis, WT1, regulator	Mus musculus	44-73
21364652-7	2010	Ethanol also increases the protein level of prostate apoptosis response 4 (PAR-4), a sensitizer to ceramide-induced apoptosis.	Ceramides	99-107	PRKC, apoptosis, WT1, regulator	Mus musculus	75-80
20178791-2	2010	The focus of this review will be to discuss the mechanism by which acid sphingomyelinase (ASMase)-generated ceramide initiates transmembrane signaling in the plasma membrane exoplasmic leaflet.	Ceramides	108-116	sphingomyelin phosphodiesterase 1	Homo sapiens	67-88
19944693-1	2010	Acid sphingomyelinase (ASM) plays an important role in normal membrane turnover through the hydrolysis of sphingomyelin, and is one of the key enzymes responsible for the production of ceramide.	Ceramides	185-193	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
19944693-1	2010	Acid sphingomyelinase (ASM) plays an important role in normal membrane turnover through the hydrolysis of sphingomyelin, and is one of the key enzymes responsible for the production of ceramide.	Ceramides	185-193	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
19944693-3	2010	ASM knockout (ASMKO) mice were originally constructed to study this disorder, and numerous defects in ceramide-related signaling have been shown.	Ceramides	102-110	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-3
19948172-1	2010	The glycosphingolipid globotriaosyl ceramide, (Galalpha1-4Galss1-4 glucosyl ceramide-Gb(3)) also known as CD77 and the P(k) blood group antigen, is bound by both verotoxins and by the HIV adhesin, gp120.	Ceramides	36-44	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	106-110
19948172-1	2010	The glycosphingolipid globotriaosyl ceramide, (Galalpha1-4Galss1-4 glucosyl ceramide-Gb(3)) also known as CD77 and the P(k) blood group antigen, is bound by both verotoxins and by the HIV adhesin, gp120.	Ceramides	36-44	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	197-202
20178791-2	2010	The focus of this review will be to discuss the mechanism by which acid sphingomyelinase (ASMase)-generated ceramide initiates transmembrane signaling in the plasma membrane exoplasmic leaflet.	Ceramides	108-116	sphingomyelin phosphodiesterase 1	Homo sapiens	90-96
20347403-1	2010	BACKGROUND: In infected lungs of the cystic fibrosis (CF) patients, opportunistic pathogens and mutated cystic fibrosis transmembrane conductance regulator protein (CFTR) contribute to chronic airway inflammation that is characterized by neutrophil/macrophage infiltration, cytokine release and ceramide accumulation.	Ceramides	295-303	CF transmembrane conductance regulator	Homo sapiens	104-155
20406981-2	2010	Adenoviral-mediated delivery by Ad.mda-7 invokes an endoplasmic reticulum (ER) stress response that is associated with ceramide production and autophagy in some cancer cells.	Ceramides	119-127	interleukin 24	Homo sapiens	35-40
20406981-3	2010	Here, we report that Ad.mda-7-induced ER stress and ceramide production trigger autophagy in human prostate cancer cells, but not in normal prostate epithelial cells, through a canonical signaling pathway that involves Beclin-1, atg5, and hVps34.	Ceramides	52-60	interleukin 24	Homo sapiens	24-29
20096352-3	2010	nSMase2 siRNA-transfected PC12 cells showed lower levels of nSMase activity and ceramide than scramble siRNA-transfected and control cells.	Ceramides	80-88	sphingomyelin phosphodiesterase 3	Rattus norvegicus	0-7
20096352-8	2010	Taken together, these data suggest that nSMase2 may increase DA uptake through inducing ceramide production and thereby decreasing intracellular calcium levels.	Ceramides	88-96	sphingomyelin phosphodiesterase 3	Rattus norvegicus	40-47
20112046-6	2010	An inactivation of Dacer by insertional mutagenesis increases the levels of ceramides in both Drosophila pupae and adult flies.	Ceramides	76-85	brain washing	Drosophila melanogaster	19-24
20112046-8	2010	Collectively, these results suggest that Dacer plays an important role in the Drosophila development and longevity by controlling the metabolism of ceramides.	Ceramides	148-157	brain washing	Drosophila melanogaster	41-46
20347403-1	2010	BACKGROUND: In infected lungs of the cystic fibrosis (CF) patients, opportunistic pathogens and mutated cystic fibrosis transmembrane conductance regulator protein (CFTR) contribute to chronic airway inflammation that is characterized by neutrophil/macrophage infiltration, cytokine release and ceramide accumulation.	Ceramides	295-303	CF transmembrane conductance regulator	Homo sapiens	165-169
20442308-0	2010	17-allylamino-17-demethoxygeldanamycin and MEK1/2 inhibitors kill GI tumor cells via Ca2+-dependent suppression of GRP78/BiP and induction of ceramide and reactive oxygen species.	Ceramides	142-150	mitogen-activated protein kinase kinase 1	Homo sapiens	43-49
20063116-6	2010	In addition, we observed that ceramide accumulation induced by NOE leads to a significant decrease in the levels of activated extracellular signal-regulated kinase (ERK); the inactivation of the ERK cascade in response to palmitate stimuli is induced by protein phosphatase 2A (PP2A) activity.	Ceramides	30-38	Eph receptor B1	Rattus norvegicus	126-163
20063116-6	2010	In addition, we observed that ceramide accumulation induced by NOE leads to a significant decrease in the levels of activated extracellular signal-regulated kinase (ERK); the inactivation of the ERK cascade in response to palmitate stimuli is induced by protein phosphatase 2A (PP2A) activity.	Ceramides	30-38	Eph receptor B1	Rattus norvegicus	165-168
20063116-6	2010	In addition, we observed that ceramide accumulation induced by NOE leads to a significant decrease in the levels of activated extracellular signal-regulated kinase (ERK); the inactivation of the ERK cascade in response to palmitate stimuli is induced by protein phosphatase 2A (PP2A) activity.	Ceramides	30-38	Eph receptor B1	Rattus norvegicus	195-198
20063116-7	2010	Based on these findings, we suggest that the aberrant accumulation of ceramide was caused by the inhibition of ceramide metabolism, which in turn leads to the inhibition of proinsulin gene expression; the inhibition of ERK cascades by PP2A serves as an important factor in the inhibitory effects of ceramide.	Ceramides	70-78	Eph receptor B1	Rattus norvegicus	219-222
20442308-10	2010	Thus, treatment of tumor cells with MEK1/2 inhibitor and 17AAG induces cytosolic Ca(2+) and loss of GRP78/BiP function, leading to de novo ceramide synthesis pathway activation that plays a key role in ROS generation and CD95 activation.	Ceramides	139-147	mitogen-activated protein kinase kinase 1	Homo sapiens	36-42
20442308-10	2010	Thus, treatment of tumor cells with MEK1/2 inhibitor and 17AAG induces cytosolic Ca(2+) and loss of GRP78/BiP function, leading to de novo ceramide synthesis pathway activation that plays a key role in ROS generation and CD95 activation.	Ceramides	139-147	heat shock protein family A (Hsp70) member 5	Homo sapiens	100-105
20442308-6	2010	MEK1/2 inhibitor and 17AAG treatment activated CD95 and inhibition of ceramide synthesis; ROS or Ca(2+) quenching blocked CD95 activation.	Ceramides	70-78	mitogen-activated protein kinase kinase 1	Homo sapiens	0-6
20442308-10	2010	Thus, treatment of tumor cells with MEK1/2 inhibitor and 17AAG induces cytosolic Ca(2+) and loss of GRP78/BiP function, leading to de novo ceramide synthesis pathway activation that plays a key role in ROS generation and CD95 activation.	Ceramides	139-147	heat shock protein family A (Hsp70) member 5	Homo sapiens	106-109
20442308-10	2010	Thus, treatment of tumor cells with MEK1/2 inhibitor and 17AAG induces cytosolic Ca(2+) and loss of GRP78/BiP function, leading to de novo ceramide synthesis pathway activation that plays a key role in ROS generation and CD95 activation.	Ceramides	139-147	Fas cell surface death receptor	Homo sapiens	221-225
20220139-8	2010	Finally, activation of DAPK by PP2A was found to be required for ceramide-induced anoikis.	Ceramides	65-73	death associated protein kinase 1	Homo sapiens	23-27
20351190-0	2010	Alterations in ceramide concentration and pH determine the release of reactive oxygen species by Cftr-deficient macrophages on infection.	Ceramides	15-23	cystic fibrosis transmembrane conductance regulator	Mus musculus	97-101
20351190-1	2010	We recently demonstrated that the accumulation of ceramide in Cftr-deficient epithelial cells is important for the pathophysiology of CF.	Ceramides	50-58	cystic fibrosis transmembrane conductance regulator	Mus musculus	62-66
20351190-6	2010	Alkalinization of these vesicles in Cftr-deficient macrophages correlates with a failure of the macrophages to respond to infection with various Pseudomonas aeruginosa strains by acutely activating acid sphingomyelinase, releasing ceramide, forming ceramide-enriched membrane platforms that serve to cluster gp91(phox), and, most importantly, releasing reactive oxygen species (ROS).	Ceramides	231-239	cystic fibrosis transmembrane conductance regulator	Mus musculus	36-40
20351190-6	2010	Alkalinization of these vesicles in Cftr-deficient macrophages correlates with a failure of the macrophages to respond to infection with various Pseudomonas aeruginosa strains by acutely activating acid sphingomyelinase, releasing ceramide, forming ceramide-enriched membrane platforms that serve to cluster gp91(phox), and, most importantly, releasing reactive oxygen species (ROS).	Ceramides	249-257	cystic fibrosis transmembrane conductance regulator	Mus musculus	36-40
20220139-0	2010	Protein phosphatase 2A (PP2A) holoenzymes regulate death-associated protein kinase (DAPK) in ceramide-induced anoikis.	Ceramides	93-101	protein phosphatase 2 phosphatase activator	Homo sapiens	24-28
20220139-8	2010	Finally, activation of DAPK by PP2A was found to be required for ceramide-induced anoikis.	Ceramides	65-73	protein phosphatase 2 phosphatase activator	Homo sapiens	31-35
20220139-0	2010	Protein phosphatase 2A (PP2A) holoenzymes regulate death-associated protein kinase (DAPK) in ceramide-induced anoikis.	Ceramides	93-101	death associated protein kinase 1	Homo sapiens	51-82
20442775-5	2010	Consequently, Sec24D-deficient cells accumulate proteins in the distended ER, although a subset of ER compartments and Golgi complexes as visualized by electron microscopy and NBD C(6)-ceramide staining appear functional.	Ceramides	185-193	SEC24 homolog D, COPII coat complex component	Danio rerio	14-20
20220139-0	2010	Protein phosphatase 2A (PP2A) holoenzymes regulate death-associated protein kinase (DAPK) in ceramide-induced anoikis.	Ceramides	93-101	death associated protein kinase 1	Homo sapiens	84-88
20172858-0	2010	The BCL-2 protein BAK is required for long-chain ceramide generation during apoptosis.	Ceramides	49-57	B cell leukemia/lymphoma 2	Mus musculus	4-9
20036206-3	2010	In this study, we found that ceramide extraction mediated by a ceramide trafficking protein (CERT) could be detected as decreasing the response of surface plasmon resonance (SPR).	Ceramides	29-37	ceramide transporter 1	Homo sapiens	63-91
20036206-3	2010	In this study, we found that ceramide extraction mediated by a ceramide trafficking protein (CERT) could be detected as decreasing the response of surface plasmon resonance (SPR).	Ceramides	29-37	ceramide transporter 1	Homo sapiens	93-97
20036206-4	2010	Based on this finding, we developed a novel real-time assay method that enables quantitative evaluation of the ceramide extraction activity of CERT, using the SPR technique.	Ceramides	111-119	ceramide transporter 1	Homo sapiens	143-147
20036206-6	2010	Furthermore, mutagenesis experiments of CERT using this SPR-based assay clearly elucidated whether an amino acid residue plays a role in the ceramide uptake process or the lipid bilayer binding process.	Ceramides	141-149	ceramide transporter 1	Homo sapiens	40-44
20172858-0	2010	The BCL-2 protein BAK is required for long-chain ceramide generation during apoptosis.	Ceramides	49-57	BCL2-antagonist/killer 1	Mus musculus	18-21
20172858-2	2010	Here we identify a MOMP-independent function of BAK as a required factor for long-chain ceramide production in response to pro-apoptotic stress.	Ceramides	88-96	BCL2-antagonist/killer 1	Mus musculus	48-51
20172858-6	2010	Importantly, long-chain ceramide generation was dependent on the presence of BAK, but not BAX.	Ceramides	24-32	BCL2-antagonist/killer 1	Mus musculus	77-80
20172858-8	2010	Finally, enzymatic assays identified ceramide synthase as the mechanism by which BAK regulates ceramide metabolism.	Ceramides	37-45	BCL2-antagonist/killer 1	Mus musculus	81-84
20172858-11	2010	The data presented indicate that ceramide-induced apoptosis is dependent upon BAK and identify a novel role for BAK during apoptosis.	Ceramides	33-41	BCL2-antagonist/killer 1	Mus musculus	78-81
20172858-11	2010	The data presented indicate that ceramide-induced apoptosis is dependent upon BAK and identify a novel role for BAK during apoptosis.	Ceramides	33-41	BCL2-antagonist/killer 1	Mus musculus	112-115
20172858-12	2010	By establishing a unique role for BAK in long-chain ceramide metabolism, these studies further demonstrate that the seemingly redundant proteins BAK and BAX have distinct mechanisms of action during apoptosis induction.	Ceramides	52-60	BCL2-antagonist/killer 1	Mus musculus	34-37
20172858-12	2010	By establishing a unique role for BAK in long-chain ceramide metabolism, these studies further demonstrate that the seemingly redundant proteins BAK and BAX have distinct mechanisms of action during apoptosis induction.	Ceramides	52-60	BCL2-antagonist/killer 1	Mus musculus	145-148
20172858-12	2010	By establishing a unique role for BAK in long-chain ceramide metabolism, these studies further demonstrate that the seemingly redundant proteins BAK and BAX have distinct mechanisms of action during apoptosis induction.	Ceramides	52-60	BCL2-associated X protein	Mus musculus	153-156
20110363-4	2010	Ceramide and downstream sphingolipids were devoid of very long (C22-C24) acyl chains, consistent with the substrate specificity of CerS2 toward acyl-CoAs.	Ceramides	0-8	ceramide synthase 2	Mus musculus	131-136
20213680-4	2010	The GSL structure is characterized by two entities: a hydrophilic glycan and a hydrophobic ceramide moiety.	Ceramides	91-99	cathepsin A	Homo sapiens	4-7
20220086-6	2010	Moreover, in DN32.D3 TIM4-knockdown NKT hybridoma cells, TIM1 engagement by rTIM1 or TIM4 enhanced IL-4 production while inhibiting IFN-gamma production in the presence of alpha-galactosyl ceramide stimulation.	Ceramides	189-197	thymoma insertional mutation	Mus musculus	57-61
20220086-6	2010	Moreover, in DN32.D3 TIM4-knockdown NKT hybridoma cells, TIM1 engagement by rTIM1 or TIM4 enhanced IL-4 production while inhibiting IFN-gamma production in the presence of alpha-galactosyl ceramide stimulation.	Ceramides	189-197	Rho guanine nucleotide exchange factor 5	Rattus norvegicus	76-81
20460737-3	2010	We investigated the inhibitory effect of C(2)-ceramide, a short-chain ceramide analog, on the PGE(2)-stimulated accumulation of cAMP in human gingival fibroblasts.	Ceramides	46-54	cathelicidin antimicrobial peptide	Homo sapiens	128-132
20106976-1	2010	We previously reported that exposure of human airway epithelial cells to oxidative stress increased ceramide generation via specific activation of neutral sphingomyelinase2 (nSMase2).	Ceramides	100-108	sphingomyelin phosphodiesterase 3	Homo sapiens	147-172
20106976-1	2010	We previously reported that exposure of human airway epithelial cells to oxidative stress increased ceramide generation via specific activation of neutral sphingomyelinase2 (nSMase2).	Ceramides	100-108	sphingomyelin phosphodiesterase 3	Homo sapiens	174-181
20110572-7	2010	Both SFA and ceramide activated PKC-zeta and the mitogen-activated protein kinases Erk, JNK, and p38.	Ceramides	13-21	protein kinase C zeta	Homo sapiens	32-40
20110572-7	2010	Both SFA and ceramide activated PKC-zeta and the mitogen-activated protein kinases Erk, JNK, and p38.	Ceramides	13-21	mitogen-activated protein kinase 8	Homo sapiens	88-91
20110572-7	2010	Both SFA and ceramide activated PKC-zeta and the mitogen-activated protein kinases Erk, JNK, and p38.	Ceramides	13-21	mitogen-activated protein kinase 14	Homo sapiens	97-100
20007509-2	2010	Herein, we show that the ceramide-metabolizing enzyme, acid ceramidase (AC), is expressed in human cumulus cells and follicular fluid, essential components of this environment, and that the levels of this enzyme are positively correlated with the quality of human embryos formed in vitro.	Ceramides	25-33	N-acylsphingosine amidohydrolase 1	Homo sapiens	55-70
19932170-0	2010	Hypoxia-induced neuronal apoptosis is mediated by de novo synthesis of ceramide through activation of serine palmitoyltransferase.	Ceramides	71-79	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	102-129
19932170-6	2010	Hypoxia increased the activity and protein levels of SPT2, suggesting that the hypoxia-induced increase in ceramide is due to the transcriptional up-regulation of SPT2.	Ceramides	107-115	SPT2 chromatin protein domain containing 1	Homo sapiens	53-57
19932170-6	2010	Hypoxia increased the activity and protein levels of SPT2, suggesting that the hypoxia-induced increase in ceramide is due to the transcriptional up-regulation of SPT2.	Ceramides	107-115	SPT2 chromatin protein domain containing 1	Homo sapiens	163-167
19932170-7	2010	Specific siRNA of SPT2 prevented hypoxia-induced cell death and ceramide production.	Ceramides	64-72	SPT2 chromatin protein domain containing 1	Homo sapiens	18-22
19932170-10	2010	Together, the current results suggest that both SPT and GCS may regulate the cellular level of ceramide, and thus may be critical enzymes for deciding the fate of the cells exposed to hypoxia.	Ceramides	95-103	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	48-51
19932170-10	2010	Together, the current results suggest that both SPT and GCS may regulate the cellular level of ceramide, and thus may be critical enzymes for deciding the fate of the cells exposed to hypoxia.	Ceramides	95-103	UDP-glucose ceramide glucosyltransferase	Homo sapiens	56-59
19779494-1	2010	Ceramide can be converted into sphingomyelin by sphingomyelin synthases (SMS) 1 and 2.	Ceramides	0-8	sphingomyelin synthase 1	Homo sapiens	48-85
19779494-9	2010	FasL-induced ceramide production and cell death were enhanced in cells stably expressing an siRNA against SMS1.	Ceramides	13-21	Fas ligand	Homo sapiens	0-4
19779494-9	2010	FasL-induced ceramide production and cell death were enhanced in cells stably expressing an siRNA against SMS1.	Ceramides	13-21	sphingomyelin synthase 1	Homo sapiens	106-110
19779494-10	2010	Conversely, in cells stably overexpressing SMS1, FasL neither increased ceramide generation nor efficiently induced cell death.	Ceramides	72-80	sphingomyelin synthase 1	Homo sapiens	43-47
20216312-3	2010	RECENT FINDINGS: Who: ceramides and glucosylceramides are likely to be independent antagonists of insulin action.	Ceramides	22-31	insulin	Homo sapiens	98-105
20216312-4	2010	Where: recent data suggest that ceramides may inhibit insulin action in skeletal muscle, whereas glucosylceramides may be more efficacious in adipose tissue.	Ceramides	32-41	insulin	Homo sapiens	54-61
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.	Ceramides	6-15	insulin	Homo sapiens	56-63
20176723-9	2010	HGF-overexpressing islets also show significantly decreased AMP-activated protein kinase-alpha and acetyl-coenzyme A carboxylase phosphorylation, diminished fatty acid oxidation, increased serine palmitoyltransferase expression, and enhanced ceramide formation compared with normal islets.	Ceramides	242-250	hepatocyte growth factor	Mus musculus	0-3
20176723-11	2010	Treatment of both mouse and human islet cells with the de novo ceramide synthesis inhibitors myriocin and fumonisin B1 abrogates beta-cell apoptosis induced by HGF and palmitate.	Ceramides	63-71	hepatocyte growth factor	Homo sapiens	160-163
20007509-2	2010	Herein, we show that the ceramide-metabolizing enzyme, acid ceramidase (AC), is expressed in human cumulus cells and follicular fluid, essential components of this environment, and that the levels of this enzyme are positively correlated with the quality of human embryos formed in vitro.	Ceramides	25-33	N-acylsphingosine amidohydrolase 1	Homo sapiens	72-74
19856145-0	2010	Phospholipase D modulation by ceramide in senescence.	Ceramides	30-38	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	0-15
20061445-2	2010	Many growth factors and inflammatory cytokines promote the cleavage of sphingomyelin and ceramide leading to rapid elevation of S1P levels through the action of sphingosine kinases (SK1 and SK2).	Ceramides	89-97	sphingosine-1-phosphate receptor 1	Mus musculus	128-131
20061445-2	2010	Many growth factors and inflammatory cytokines promote the cleavage of sphingomyelin and ceramide leading to rapid elevation of S1P levels through the action of sphingosine kinases (SK1 and SK2).	Ceramides	89-97	skin antigen 1	Mus musculus	182-185
20061445-2	2010	Many growth factors and inflammatory cytokines promote the cleavage of sphingomyelin and ceramide leading to rapid elevation of S1P levels through the action of sphingosine kinases (SK1 and SK2).	Ceramides	89-97	skin antigen 2	Mus musculus	190-193
19576658-0	2010	Cell-permeable ceramides act as novel regulators of U937 cell-cell adhesion mediated by CD29, CD98, and CD147.	Ceramides	15-24	integrin subunit beta 1	Homo sapiens	88-92
19576658-0	2010	Cell-permeable ceramides act as novel regulators of U937 cell-cell adhesion mediated by CD29, CD98, and CD147.	Ceramides	15-24	solute carrier family 3 member 2	Homo sapiens	94-98
19576658-0	2010	Cell-permeable ceramides act as novel regulators of U937 cell-cell adhesion mediated by CD29, CD98, and CD147.	Ceramides	15-24	basigin (Ok blood group)	Homo sapiens	104-109
19576658-2	2010	In this study, we report novel modulatory effects of ceramides on the functional activation of beta1 integrins (CD29) and their associated molecules, such as CD98 and CD147, using U937 cell-cell or cell-fibronectin (FN) adhesion events.	Ceramides	53-62	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	95-100
19576658-2	2010	In this study, we report novel modulatory effects of ceramides on the functional activation of beta1 integrins (CD29) and their associated molecules, such as CD98 and CD147, using U937 cell-cell or cell-fibronectin (FN) adhesion events.	Ceramides	53-62	integrin subunit beta 1	Homo sapiens	112-116
19576658-2	2010	In this study, we report novel modulatory effects of ceramides on the functional activation of beta1 integrins (CD29) and their associated molecules, such as CD98 and CD147, using U937 cell-cell or cell-fibronectin (FN) adhesion events.	Ceramides	53-62	solute carrier family 3 member 2	Homo sapiens	158-162
19576658-2	2010	In this study, we report novel modulatory effects of ceramides on the functional activation of beta1 integrins (CD29) and their associated molecules, such as CD98 and CD147, using U937 cell-cell or cell-fibronectin (FN) adhesion events.	Ceramides	53-62	basigin (Ok blood group)	Homo sapiens	167-172
19576658-2	2010	In this study, we report novel modulatory effects of ceramides on the functional activation of beta1 integrins (CD29) and their associated molecules, such as CD98 and CD147, using U937 cell-cell or cell-fibronectin (FN) adhesion events.	Ceramides	53-62	fibronectin 1	Homo sapiens	203-214
19576658-3	2010	Cell-permeable ceramides (C2- or C6-ceramides) effectively blocked monocytic cell-cell adhesion, mediated by CD29, CD98, and CD147, and cell-FN adhesion in a dose-dependent manner.	Ceramides	15-24	integrin subunit beta 1	Homo sapiens	109-113
19576658-3	2010	Cell-permeable ceramides (C2- or C6-ceramides) effectively blocked monocytic cell-cell adhesion, mediated by CD29, CD98, and CD147, and cell-FN adhesion in a dose-dependent manner.	Ceramides	15-24	solute carrier family 3 member 2	Homo sapiens	115-119
19576658-3	2010	Cell-permeable ceramides (C2- or C6-ceramides) effectively blocked monocytic cell-cell adhesion, mediated by CD29, CD98, and CD147, and cell-FN adhesion in a dose-dependent manner.	Ceramides	15-24	basigin (Ok blood group)	Homo sapiens	125-130
19576658-3	2010	Cell-permeable ceramides (C2- or C6-ceramides) effectively blocked monocytic cell-cell adhesion, mediated by CD29, CD98, and CD147, and cell-FN adhesion in a dose-dependent manner.	Ceramides	36-45	integrin subunit beta 1	Homo sapiens	109-113
19576658-3	2010	Cell-permeable ceramides (C2- or C6-ceramides) effectively blocked monocytic cell-cell adhesion, mediated by CD29, CD98, and CD147, and cell-FN adhesion in a dose-dependent manner.	Ceramides	36-45	solute carrier family 3 member 2	Homo sapiens	115-119
19576658-3	2010	Cell-permeable ceramides (C2- or C6-ceramides) effectively blocked monocytic cell-cell adhesion, mediated by CD29, CD98, and CD147, and cell-FN adhesion in a dose-dependent manner.	Ceramides	36-45	basigin (Ok blood group)	Homo sapiens	125-130
19576658-5	2010	Ceramides displayed a distinct inhibitory profile on cell-cell and cell-FN adhesions compared with other inhibitors such as PD98059 (an extracellular signal-related kinase (ERK) inhibitor), SB203580 (a p38 inhibitor), rottlerin (a PKCdelta inhibitor), and cytochalasin B (an actin cytoskeleton disruptor).	Ceramides	0-9	mitogen-activated protein kinase 14	Homo sapiens	202-205
19576658-5	2010	Ceramides displayed a distinct inhibitory profile on cell-cell and cell-FN adhesions compared with other inhibitors such as PD98059 (an extracellular signal-related kinase (ERK) inhibitor), SB203580 (a p38 inhibitor), rottlerin (a PKCdelta inhibitor), and cytochalasin B (an actin cytoskeleton disruptor).	Ceramides	0-9	protein kinase C delta	Homo sapiens	231-239
19576658-7	2010	Since there are no reports showing that ceramides act as negative regulators of the functional activation of CD29, our results therefore suggest a novel possibility that ceramides can be used as a therapeutic drug regarding CD29-mediated pathological events, including tumor metastasis, inflammatory states, granuloma formation, and blood vessel occlusion.	Ceramides	40-49	integrin subunit beta 1	Homo sapiens	109-113
19576658-7	2010	Since there are no reports showing that ceramides act as negative regulators of the functional activation of CD29, our results therefore suggest a novel possibility that ceramides can be used as a therapeutic drug regarding CD29-mediated pathological events, including tumor metastasis, inflammatory states, granuloma formation, and blood vessel occlusion.	Ceramides	170-179	integrin subunit beta 1	Homo sapiens	109-113
19576658-7	2010	Since there are no reports showing that ceramides act as negative regulators of the functional activation of CD29, our results therefore suggest a novel possibility that ceramides can be used as a therapeutic drug regarding CD29-mediated pathological events, including tumor metastasis, inflammatory states, granuloma formation, and blood vessel occlusion.	Ceramides	170-179	integrin subunit beta 1	Homo sapiens	224-228
19826105-0	2010	Direct quantitative determination of ceramide glycosylation in vivo: a new approach to evaluate cellular enzyme activity of glucosylceramide synthase.	Ceramides	37-45	UDP-glucose ceramide glucosyltransferase	Homo sapiens	124-149
19826105-1	2010	Glucosylceramide synthase (GCS or GlcT-1), converting ceramide to glucosylceramide, is a key enzyme for the synthesis of glycosphingolipids.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	34-40
19427778-0	2010	Docosahexaenoic acid down-regulates phenobarbital-induced cytochrome P450 2B1 gene expression in rat primary hepatocytes via the sphingomyelinase/ceramide pathway.	Ceramides	146-154	cytochrome P450 2B1	Rattus norvegicus	58-77
19856145-7	2010	Treatment with ceramide resulted in a decrease in PLD activity, implicating ceramide as the mediator of the inhibition.	Ceramides	15-23	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	50-53
19856145-7	2010	Treatment with ceramide resulted in a decrease in PLD activity, implicating ceramide as the mediator of the inhibition.	Ceramides	76-84	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	50-53
20053954-6	2010	The MAM, which is highly capable of accumulating ceramides, is enriched with both cholesterol and simple sphingolipids, thus forming Triton X-114-resistant DRMs.	Ceramides	49-58	sarcoglycan gamma	Homo sapiens	4-7
19765607-10	2010	Over-expression of SphK1 promoted cell proliferation and protected ARPE-19 cells from ceramide-induced apoptosis.	Ceramides	86-94	sphingosine kinase 1	Homo sapiens	19-24
20053954-9	2010	Disrupting DRMs by lowering cholesterol or inhibiting de novo synthesis of ceramides at the ER largely decreases Sig-1R at DRMs and causes translocation of Sig-1R from the MAM to ER cisternae.	Ceramides	75-84	sigma non-opioid intracellular receptor 1	Homo sapiens	113-119
20053954-9	2010	Disrupting DRMs by lowering cholesterol or inhibiting de novo synthesis of ceramides at the ER largely decreases Sig-1R at DRMs and causes translocation of Sig-1R from the MAM to ER cisternae.	Ceramides	75-84	sigma non-opioid intracellular receptor 1	Homo sapiens	156-162
20053954-9	2010	Disrupting DRMs by lowering cholesterol or inhibiting de novo synthesis of ceramides at the ER largely decreases Sig-1R at DRMs and causes translocation of Sig-1R from the MAM to ER cisternae.	Ceramides	75-84	sarcoglycan gamma	Homo sapiens	172-175
20053954-10	2010	These findings suggest that the MAM, bearing cholesterol and ceramide-enriched microdomains at the ER, may use the microdomains to anchor Sig-1Rs to the location; thus, it serves to stage Sig-1R at ER-mitochondria junctions.	Ceramides	61-69	sarcoglycan gamma	Homo sapiens	32-35
20053954-10	2010	These findings suggest that the MAM, bearing cholesterol and ceramide-enriched microdomains at the ER, may use the microdomains to anchor Sig-1Rs to the location; thus, it serves to stage Sig-1R at ER-mitochondria junctions.	Ceramides	61-69	sigma non-opioid intracellular receptor 1	Homo sapiens	138-144
20117234-6	2010	In the context of an oxidative stress such as IR, the best example is the translocation of the enzyme acid sphingomyelinase (ASMase) from lysosomes to the outer layer of cell membrane, which then induces sphingomyelin hydrolysis and ceramide formation.	Ceramides	233-241	sphingomyelin phosphodiesterase 1	Homo sapiens	125-131
20117234-7	2010	Ceramide coalescence with cholesterol forms lipids microdomains in the plasma membrane, enhancing clustering of signaling receptors (death receptors like FAS, TNF, CD40, TRAIL or G protein-coupled receptors).	Ceramides	0-8	tumor necrosis factor	Homo sapiens	159-162
20117234-7	2010	Ceramide coalescence with cholesterol forms lipids microdomains in the plasma membrane, enhancing clustering of signaling receptors (death receptors like FAS, TNF, CD40, TRAIL or G protein-coupled receptors).	Ceramides	0-8	CD40 molecule	Homo sapiens	164-168
20117234-7	2010	Ceramide coalescence with cholesterol forms lipids microdomains in the plasma membrane, enhancing clustering of signaling receptors (death receptors like FAS, TNF, CD40, TRAIL or G protein-coupled receptors).	Ceramides	0-8	TNF superfamily member 10	Homo sapiens	170-175
19765607-13	2010	Over-expression of SMPD3 may increase cellular ceramide levels, leading to enhanced cell death and arrested cell proliferation.	Ceramides	47-55	sphingomyelin phosphodiesterase 3	Homo sapiens	19-24
19765607-15	2010	SphK1 over-expression increased cellular S1P, which promoted cell proliferation and protected RPE from ceramide-induced apoptosis.	Ceramides	103-111	sphingosine kinase 1	Homo sapiens	0-5
20089856-1	2010	Human alkaline ceramidase 2 (ACER2) plays an important role in cellular responses by regulating the hydrolysis of ceramides in cells.	Ceramides	114-123	alkaline ceramidase 2	Homo sapiens	6-27
20556203-2	2010	Recent studies demonstrate that ceramide plays an important role in the pathogenesis of cystic fibrosis, a hereditary metabolic disorder caused by mutations of the Cystic Fibrosis Transmembrane Conductance Regulator.	Ceramides	32-40	CF transmembrane conductance regulator	Homo sapiens	164-215
20089856-1	2010	Human alkaline ceramidase 2 (ACER2) plays an important role in cellular responses by regulating the hydrolysis of ceramides in cells.	Ceramides	114-123	alkaline ceramidase 2	Homo sapiens	29-34
20089856-4	2010	ACER2 catalyzed the hydrolysis of various ceramides and followed Michaelis-Menten kinetics.	Ceramides	42-51	alkaline ceramidase 2	Homo sapiens	0-5
19958841-2	2010	Prominent among these so-called lipotoxic mediators are signaling molecules such as long chain acyl-CoAs, ceramides and diacyglycerols; each of which is thought to engage serine kinases that disrupt the insulin signaling cascade, thereby causing insulin resistance.	Ceramides	106-115	insulin	Homo sapiens	203-210
20068046-4	2010	In cells, ACER3 overexpression decreased C(18:1)- and C(20:1)-ceramides and dihydroceramides, whereas ACER3 knockdown by RNA interference had the opposite effect, suggesting that ACER3 controls the catabolism of ULC ceramides and dihydroceramides.	Ceramides	83-92	alkaline ceramidase 3	Homo sapiens	10-15
20068046-8	2010	ACER3 knockdown up-regulated the expression of the alkaline ceramidase 2 (ACER2), and the ACER2 up-regulation decreased non-ULC ceramide species while increasing both sphingosine and its phosphate.	Ceramides	128-136	alkaline ceramidase 3	Homo sapiens	0-5
20068046-8	2010	ACER3 knockdown up-regulated the expression of the alkaline ceramidase 2 (ACER2), and the ACER2 up-regulation decreased non-ULC ceramide species while increasing both sphingosine and its phosphate.	Ceramides	128-136	alkaline ceramidase 2	Homo sapiens	90-95
20068046-9	2010	Collectively, these data suggest that ACER3 catalyzes the hydrolysis of ULC ceramides and dihydroceramides and that ACER3 coordinates with ACER2 to regulate cell proliferation and survival.	Ceramides	76-85	alkaline ceramidase 3	Homo sapiens	38-43
20068046-9	2010	Collectively, these data suggest that ACER3 catalyzes the hydrolysis of ULC ceramides and dihydroceramides and that ACER3 coordinates with ACER2 to regulate cell proliferation and survival.	Ceramides	76-85	alkaline ceramidase 2	Homo sapiens	139-144
19698762-4	2010	Ceramide then activates protein phosphatase 2A (PP2A), a member in the ceramide-activated protein phosphatase (CAPP) family.	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	48-52
20068046-2	2010	Here, we demonstrate that our previously cloned human alkaline ceramidase 3 (ACER3) specifically controls the hydrolysis of ceramides carrying unsaturated long acyl chains, unsaturated long-chain (ULC) ceramides.	Ceramides	124-133	alkaline ceramidase 3	Homo sapiens	54-75
20068046-2	2010	Here, we demonstrate that our previously cloned human alkaline ceramidase 3 (ACER3) specifically controls the hydrolysis of ceramides carrying unsaturated long acyl chains, unsaturated long-chain (ULC) ceramides.	Ceramides	124-133	alkaline ceramidase 3	Homo sapiens	77-82
20068046-2	2010	Here, we demonstrate that our previously cloned human alkaline ceramidase 3 (ACER3) specifically controls the hydrolysis of ceramides carrying unsaturated long acyl chains, unsaturated long-chain (ULC) ceramides.	Ceramides	202-211	alkaline ceramidase 3	Homo sapiens	54-75
20068046-2	2010	Here, we demonstrate that our previously cloned human alkaline ceramidase 3 (ACER3) specifically controls the hydrolysis of ceramides carrying unsaturated long acyl chains, unsaturated long-chain (ULC) ceramides.	Ceramides	202-211	alkaline ceramidase 3	Homo sapiens	77-82
20068046-3	2010	In vitro, ACER3 only hydrolyzed C(18:1)-, C(20:1)-, C(20:4)-ceramides, dihydroceramides, and phytoceramides.	Ceramides	60-69	alkaline ceramidase 3	Homo sapiens	10-15
20068046-4	2010	In cells, ACER3 overexpression decreased C(18:1)- and C(20:1)-ceramides and dihydroceramides, whereas ACER3 knockdown by RNA interference had the opposite effect, suggesting that ACER3 controls the catabolism of ULC ceramides and dihydroceramides.	Ceramides	62-71	alkaline ceramidase 3	Homo sapiens	10-15
19958841-2	2010	Prominent among these so-called lipotoxic mediators are signaling molecules such as long chain acyl-CoAs, ceramides and diacyglycerols; each of which is thought to engage serine kinases that disrupt the insulin signaling cascade, thereby causing insulin resistance.	Ceramides	106-115	insulin	Homo sapiens	246-253
19937735-0	2010	Ceramide plays a prominent role in MDA-7/IL-24-induced cancer-specific apoptosis.	Ceramides	0-8	interleukin 24	Homo sapiens	35-40
19959757-1	2010	OBJECTIVE: Ceramide is now recognized as a negative regulator of insulin signaling by impairing protein kinase B (PKB)/Akt activation.	Ceramides	11-19	AKT serine/threonine kinase 1	Homo sapiens	114-117
19959757-1	2010	OBJECTIVE: Ceramide is now recognized as a negative regulator of insulin signaling by impairing protein kinase B (PKB)/Akt activation.	Ceramides	11-19	AKT serine/threonine kinase 1	Homo sapiens	119-122
19959757-2	2010	In different cells, two distinct mechanisms have been proposed to mediate ceramide inhibition of PKB/Akt: one involving atypical protein kinase C zeta (PKCzeta) and the other the protein phosphatase-2 (PP2A).	Ceramides	74-82	AKT serine/threonine kinase 1	Homo sapiens	97-100
19959757-2	2010	In different cells, two distinct mechanisms have been proposed to mediate ceramide inhibition of PKB/Akt: one involving atypical protein kinase C zeta (PKCzeta) and the other the protein phosphatase-2 (PP2A).	Ceramides	74-82	AKT serine/threonine kinase 1	Homo sapiens	101-104
19959757-2	2010	In different cells, two distinct mechanisms have been proposed to mediate ceramide inhibition of PKB/Akt: one involving atypical protein kinase C zeta (PKCzeta) and the other the protein phosphatase-2 (PP2A).	Ceramides	74-82	protein kinase C zeta	Homo sapiens	152-159
19959757-2	2010	In different cells, two distinct mechanisms have been proposed to mediate ceramide inhibition of PKB/Akt: one involving atypical protein kinase C zeta (PKCzeta) and the other the protein phosphatase-2 (PP2A).	Ceramides	74-82	protein phosphatase 2 phosphatase activator	Homo sapiens	202-206
19959757-3	2010	We hypothesized that ceramide action through PKCzeta or PP2A might depend on plasma membrane (PM) structural organization and especially on caveolin-enriched domain (CEM) abundance.	Ceramides	21-29	protein kinase C zeta	Homo sapiens	45-52
19959757-3	2010	We hypothesized that ceramide action through PKCzeta or PP2A might depend on plasma membrane (PM) structural organization and especially on caveolin-enriched domain (CEM) abundance.	Ceramides	21-29	protein phosphatase 2 phosphatase activator	Homo sapiens	56-60
19959757-4	2010	RESEARCH DESIGN AND METHODS: We have used different PKCzeta mutant constructs or the PP2A inhibitor, okadaic acid (OKA), to selectively inhibit PKCzeta- and PP2A-dependent pathways in cells expressing different caveolin-1 levels and evaluated the impact of insulin and ceramide on PKB/Akt activity in different PM subdomains.	Ceramides	269-277	protein kinase C zeta	Homo sapiens	144-151
19959757-4	2010	RESEARCH DESIGN AND METHODS: We have used different PKCzeta mutant constructs or the PP2A inhibitor, okadaic acid (OKA), to selectively inhibit PKCzeta- and PP2A-dependent pathways in cells expressing different caveolin-1 levels and evaluated the impact of insulin and ceramide on PKB/Akt activity in different PM subdomains.	Ceramides	269-277	protein phosphatase 2 phosphatase activator	Homo sapiens	157-161
19959757-5	2010	RESULTS: Although the PKCzeta-mediated negative effect of ceramide on insulin-stimulated PKB/Akt was dominant in adipocytes, a ceramide action through PP2A outside CEMs, prevented by OKA, was also unraveled.	Ceramides	58-66	protein kinase C zeta	Homo sapiens	22-29
19959757-5	2010	RESULTS: Although the PKCzeta-mediated negative effect of ceramide on insulin-stimulated PKB/Akt was dominant in adipocytes, a ceramide action through PP2A outside CEMs, prevented by OKA, was also unraveled.	Ceramides	58-66	AKT serine/threonine kinase 1	Homo sapiens	70-96
19959757-5	2010	RESULTS: Although the PKCzeta-mediated negative effect of ceramide on insulin-stimulated PKB/Akt was dominant in adipocytes, a ceramide action through PP2A outside CEMs, prevented by OKA, was also unraveled.	Ceramides	127-135	protein kinase C zeta	Homo sapiens	22-29
19959757-5	2010	RESULTS: Although the PKCzeta-mediated negative effect of ceramide on insulin-stimulated PKB/Akt was dominant in adipocytes, a ceramide action through PP2A outside CEMs, prevented by OKA, was also unraveled.	Ceramides	127-135	protein phosphatase 2 phosphatase activator	Homo sapiens	151-155
19959757-6	2010	To test the importance of CEM to direct ceramide action through the PKCzeta pathway, we treated 3T3-L1 preadipocytes devoid of CEMs with ceramide and we saw a shift of the lipid-negative action on PKB/Akt to a PP2A-mediated mechanism.	Ceramides	40-48	protein kinase C zeta	Homo sapiens	68-75
19959757-6	2010	To test the importance of CEM to direct ceramide action through the PKCzeta pathway, we treated 3T3-L1 preadipocytes devoid of CEMs with ceramide and we saw a shift of the lipid-negative action on PKB/Akt to a PP2A-mediated mechanism.	Ceramides	137-145	protein kinase C zeta	Homo sapiens	68-75
19959757-7	2010	In fibroblasts with low CEM abundance, the ceramide-activated PP2A pathway dominated, but could be shifted to a ceramide-activated PKCzeta pathway after caveolin-1 overexpression.	Ceramides	43-51	protein phosphatase 2 phosphatase activator	Homo sapiens	62-66
19959757-7	2010	In fibroblasts with low CEM abundance, the ceramide-activated PP2A pathway dominated, but could be shifted to a ceramide-activated PKCzeta pathway after caveolin-1 overexpression.	Ceramides	112-120	protein kinase C zeta	Homo sapiens	131-138
19959757-8	2010	CONCLUSIONS: Our results show that ceramide can switch from a PKCzeta-dependent mechanism to a PP2A pathway, acting negatively on PKB/Akt, and hence revealing a critical role of CEMs of the PM in this process.	Ceramides	35-43	protein kinase C zeta	Homo sapiens	62-69
19959757-8	2010	CONCLUSIONS: Our results show that ceramide can switch from a PKCzeta-dependent mechanism to a PP2A pathway, acting negatively on PKB/Akt, and hence revealing a critical role of CEMs of the PM in this process.	Ceramides	35-43	protein phosphatase 2 phosphatase activator	Homo sapiens	95-99
19959757-8	2010	CONCLUSIONS: Our results show that ceramide can switch from a PKCzeta-dependent mechanism to a PP2A pathway, acting negatively on PKB/Akt, and hence revealing a critical role of CEMs of the PM in this process.	Ceramides	35-43	AKT serine/threonine kinase 1	Homo sapiens	130-133
19959757-8	2010	CONCLUSIONS: Our results show that ceramide can switch from a PKCzeta-dependent mechanism to a PP2A pathway, acting negatively on PKB/Akt, and hence revealing a critical role of CEMs of the PM in this process.	Ceramides	35-43	AKT serine/threonine kinase 1	Homo sapiens	134-137
19937735-10	2010	Pretreatment of cells with FB1 or ISP-1 abolished the induction of ER stress markers (BiP/GRP78, GADD153 and pospho-eIF2alpha) triggered by Ad.mda-7 infection indicating that ceramide mediates ER stress induction by Ad.mda-7.	Ceramides	175-183	interleukin 24	Homo sapiens	219-224
19937735-11	2010	Additionally, recombinant MDA-7/IL-24 protein induced cancer-specific production of ceramide.	Ceramides	84-92	interleukin 24	Homo sapiens	26-31
19937735-11	2010	Additionally, recombinant MDA-7/IL-24 protein induced cancer-specific production of ceramide.	Ceramides	84-92	interleukin 24	Homo sapiens	32-37
19937735-12	2010	These studies define ceramide as a key mediator of an ER stress pathway that may underlie mda-7/IL-24 induction of cancer-specific killing.	Ceramides	21-29	interleukin 24	Homo sapiens	90-95
19937735-12	2010	These studies define ceramide as a key mediator of an ER stress pathway that may underlie mda-7/IL-24 induction of cancer-specific killing.	Ceramides	21-29	interleukin 24	Homo sapiens	96-101
19959757-0	2010	Plasma membrane subdomain compartmentalization contributes to distinct mechanisms of ceramide action on insulin signaling.	Ceramides	85-93	insulin	Homo sapiens	104-111
19959757-1	2010	OBJECTIVE: Ceramide is now recognized as a negative regulator of insulin signaling by impairing protein kinase B (PKB)/Akt activation.	Ceramides	11-19	insulin	Homo sapiens	65-72
23554623-0	2010	Ceramide from sphingomyelin hydrolysis differentially mediates mitogen-activated protein kinases (MAPKs) activation following cerebral ischemia in rat hippocampal CA1 subregion.	Ceramides	0-8	carbonic anhydrase 1	Rattus norvegicus	163-166
23554623-7	2010	CONCLUSION: The ceramide signaling pathway is up-regulated through sphingomyelin hydrolysis in brain ischemia, promoting JNK activation and suppressing ERK activation, culminating in the ischemic lesion.	Ceramides	16-24	mitogen-activated protein kinase 8	Rattus norvegicus	121-124
23554623-7	2010	CONCLUSION: The ceramide signaling pathway is up-regulated through sphingomyelin hydrolysis in brain ischemia, promoting JNK activation and suppressing ERK activation, culminating in the ischemic lesion.	Ceramides	16-24	Eph receptor B1	Rattus norvegicus	152-155
19937735-0	2010	Ceramide plays a prominent role in MDA-7/IL-24-induced cancer-specific apoptosis.	Ceramides	0-8	interleukin 24	Homo sapiens	41-46
19937735-2	2010	We hypothesize that ceramide, a promoter of apoptosis, might contribute to mda-7/IL-24 induction of apoptosis.	Ceramides	20-28	interleukin 24	Homo sapiens	75-80
19937735-2	2010	We hypothesize that ceramide, a promoter of apoptosis, might contribute to mda-7/IL-24 induction of apoptosis.	Ceramides	20-28	interleukin 24	Homo sapiens	81-86
19937735-3	2010	Ad.mda-7-infected tumor cells, but not normal cells, showed increased ceramide accumulation.	Ceramides	70-78	interleukin 24	Homo sapiens	3-8
19937735-4	2010	Infection with Ad.mda-7 induced a marked increase in various ceramides (C16, C24, C24:1) selectively in prostate cancer cells.	Ceramides	61-70	interleukin 24	Homo sapiens	18-23
19937735-6	2010	Fumonisin B1 (FB1) elevated ceramide formation as well as apoptosis induced by Ad.mda-7, suggesting that ceramide formation may also occur through the salvage pathway.	Ceramides	105-113	interleukin 24	Homo sapiens	82-87
19937735-8	2010	ASMase silencing by RNA interference inhibited the decreased cell viability and ceramide formation after Ad.mda-7 infection.	Ceramides	80-88	sphingomyelin phosphodiesterase 1	Homo sapiens	0-6
19937735-9	2010	Ad.mda-7 activated protein phosphatase 2A (PP2A) and promoted dephosphorylation of the anti-apoptotic molecule BCL-2, a downstream ceramide-mediated pathway of mda-7/IL-24 action.	Ceramides	131-139	interleukin 24	Homo sapiens	3-8
19937735-9	2010	Ad.mda-7 activated protein phosphatase 2A (PP2A) and promoted dephosphorylation of the anti-apoptotic molecule BCL-2, a downstream ceramide-mediated pathway of mda-7/IL-24 action.	Ceramides	131-139	BCL2 apoptosis regulator	Homo sapiens	111-116
19937735-9	2010	Ad.mda-7 activated protein phosphatase 2A (PP2A) and promoted dephosphorylation of the anti-apoptotic molecule BCL-2, a downstream ceramide-mediated pathway of mda-7/IL-24 action.	Ceramides	131-139	interleukin 24	Homo sapiens	160-165
19937735-9	2010	Ad.mda-7 activated protein phosphatase 2A (PP2A) and promoted dephosphorylation of the anti-apoptotic molecule BCL-2, a downstream ceramide-mediated pathway of mda-7/IL-24 action.	Ceramides	131-139	interleukin 24	Homo sapiens	166-171
18547682-3	2010	We found a pattern of elevated acid sphingomyelinase (ASM) and acid ceramidase (AC) expression in AD, leading to a reduction in sphingomyelin and elevation of ceramide.	Ceramides	159-167	sphingomyelin phosphodiesterase 1	Homo sapiens	54-57
18547682-3	2010	We found a pattern of elevated acid sphingomyelinase (ASM) and acid ceramidase (AC) expression in AD, leading to a reduction in sphingomyelin and elevation of ceramide.	Ceramides	159-167	sphingomyelin phosphodiesterase 1	Homo sapiens	31-52
18547682-6	2010	Based on these findings, neuronal cell cultures were treated with Abeta oligomers, which were found to activate ASM, increase ceramide, and induce apoptosis.	Ceramides	126-134	amyloid beta precursor protein	Homo sapiens	66-71
18547682-9	2010	The downstream consequences of ASM activation are elevated ceramide, activation of ceramidases, and production of sphingosine.	Ceramides	59-67	sphingomyelin phosphodiesterase 1	Homo sapiens	31-34
20060598-5	2010	Within 24h Abeta(1-42) and IAPP triggered ceramide formation, caspase 8 and caspase 3 activation, DNA fragmentation and annexin V binding in DCs obtained from wild type mice, whereas in DCs from sphingomyelinase deficient (asm(-/-)) mice and in wild type DCs treated with sphingomyelinase inhibitor amitriptyline all these effects were strongly impaired.	Ceramides	42-50	islet amyloid polypeptide	Mus musculus	27-31
20215587-7	2010	Furthermore, mips1 mutants exhibited elevated levels of ceramides, sphingolipid precursors associated with cell death, and were complemented by a MIPS1-green fluorescent protein (GFP) fusion construct.	Ceramides	56-65	myo-inositol-1-phosphate synthase 1	Arabidopsis thaliana	13-18
20032468-1	2010	Our recent studies indicate that endoplasmic reticulum (ER) stress causes INS-1 cell apoptosis by a Ca(2+)-independent phospholipase A(2) (iPLA(2)beta)-mediated mechanism that promotes ceramide generation via sphingomyelin hydrolysis and subsequent activation of the intrinsic pathway.	Ceramides	185-193	phospholipase A2 group VI	Rattus norvegicus	139-150
20215587-9	2010	Thus, MIPS1 has a significant impact on myo-inositol levels that is critical for maintaining levels of ascorbic acid, phosphatidylinositol, and ceramides that regulate growth, development, and cell death.	Ceramides	144-153	myo-inositol-1-phosphate synthase 1	Arabidopsis thaliana	6-11
20060598-6	2010	Moreover, ceramide formation was also reduced in wild type DCs in which acid sphingomyelinase (Asm) was silenced with Asm-targeted siRNA.	Ceramides	10-18	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	72-93
20060598-6	2010	Moreover, ceramide formation was also reduced in wild type DCs in which acid sphingomyelinase (Asm) was silenced with Asm-targeted siRNA.	Ceramides	10-18	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	95-98
20060598-6	2010	Moreover, ceramide formation was also reduced in wild type DCs in which acid sphingomyelinase (Asm) was silenced with Asm-targeted siRNA.	Ceramides	10-18	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	118-121
20036255-0	2010	Crystal structures of the CERT START domain with inhibitors provide insights into the mechanism of ceramide transfer.	Ceramides	99-107	ceramide transporter 1	Homo sapiens	26-30
20060598-8	2010	In conclusion, amyloid peptides induce DC apoptosis presumably through activation of acid sphingomyelinase resulting in production of ceramide.	Ceramides	134-142	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	85-106
20179888-8	2010	Among the activators of intracellular signaling transduction pathways, mitogen-activated protein kinases kinase (MAPKK/MEK) activators C(6) ceramide (1 micromol/L) abolished completely the inhibitory effect of activin.	Ceramides	140-148	inhibin subunit beta E	Homo sapiens	210-217
20036255-10	2010	These results provide insights into not only the molecular mechanism of inhibition by HPAs but also possible mechanisms by which CERT interacts with ceramide.	Ceramides	149-157	ceramide transporter 1	Homo sapiens	129-133
20036255-1	2010	The cytosolic protein CERT transfers ceramide from the endoplasmic reticulum to the Golgi apparatus where ceramide is converted to SM.	Ceramides	37-45	ceramide transporter 1	Homo sapiens	22-26
20036255-1	2010	The cytosolic protein CERT transfers ceramide from the endoplasmic reticulum to the Golgi apparatus where ceramide is converted to SM.	Ceramides	106-114	ceramide transporter 1	Homo sapiens	22-26
20036255-2	2010	The C-terminal START (steroidogenic acute regulatory protein-related lipid transfer) domain of CERT binds one ceramide molecule in its central amphiphilic cavity.	Ceramides	110-118	ceramide transporter 1	Homo sapiens	95-99
20036255-3	2010	(1R,3R)-N-(3-Hydroxy-1-hydroxymethyl-3-phenylpropyl)alkanamide (HPA), a synthesized analogue of ceramide, inhibits ceramide transfer by CERT.	Ceramides	96-104	ceramide transporter 1	Homo sapiens	136-140
20036255-3	2010	(1R,3R)-N-(3-Hydroxy-1-hydroxymethyl-3-phenylpropyl)alkanamide (HPA), a synthesized analogue of ceramide, inhibits ceramide transfer by CERT.	Ceramides	115-123	ceramide transporter 1	Homo sapiens	136-140
19965780-6	2010	Adenoviral overexpression of PGC-1alpha prevented linoleic acid-induced increases in reactive oxygen species generation and cell apoptosis in human aortic endothelial cells by increasing fatty acid oxidation, decreasing diacylglycerol and ceramide, and increasing ATP/ADP translocase activity.	Ceramides	239-247	PPARG coactivator 1 alpha	Homo sapiens	29-39
19944062-0	2010	Increased ceramide accumulation correlates with downregulation of the autophagy protein ATG-7 in MCF-7 cells sensitized to photodamage.	Ceramides	10-18	autophagy related 7	Homo sapiens	88-93
19944062-4	2010	PDT evoked an early (2h) greater global increase in ceramides in ATG-7 defective cells compared to Scr cells.	Ceramides	52-61	autophagy related 7	Homo sapiens	65-70
19944062-7	2010	The data imply that ceramide might be a marker of ATG-7 deficiency in cells sensitized to PDT.	Ceramides	20-28	autophagy related 7	Homo sapiens	50-55
19965812-2	2010	The effects of increased endogenous ceramides could be offset by sphingosine 1-phosphate (S1P), a prosurvival by-product of ceramide metabolism.	Ceramides	36-45	sphingosine-1-phosphate receptor 1	Mus musculus	90-93
19965812-2	2010	The effects of increased endogenous ceramides could be offset by sphingosine 1-phosphate (S1P), a prosurvival by-product of ceramide metabolism.	Ceramides	36-44	sphingosine-1-phosphate receptor 1	Mus musculus	90-93
20132547-3	2010	PSAP is the lysosomal precursor of saposins, which serve as activators for lysosomal hydrolases involved in the degradation of ceramide (Cer) and other sphingolipids.	Ceramides	127-135	prosaposin	Homo sapiens	0-4
20132547-3	2010	PSAP is the lysosomal precursor of saposins, which serve as activators for lysosomal hydrolases involved in the degradation of ceramide (Cer) and other sphingolipids.	Ceramides	137-140	prosaposin	Homo sapiens	0-4
20030721-1	2010	We demonstrated that a yeast deletion mutant in IPT1 and SKN1, encoding proteins involved in the biosynthesis of mannosyldiinositolphosphoryl ceramides, is characterized by increased autophagy and DNA fragmentation upon nitrogen (N) starvation as compared with the single deletion mutants or wild type (WT).	Ceramides	142-151	inositolphosphotransferase	Saccharomyces cerevisiae S288C	48-52
20103619-5	2010	PERK inhibition blocked ceramide or dihydroceramide generation, which were critical for Ca(++) induction and subsequent ROS formation.	Ceramides	24-32	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	0-4
20103619-8	2010	Our findings indicate that mda-7/IL-24 induces an endoplasmic reticulum stress response that triggers production of ceramide, Ca(2+), and ROS, which in turn promote glioma cell autophagy and cell death.	Ceramides	116-124	interleukin 24	Homo sapiens	27-32
20103619-8	2010	Our findings indicate that mda-7/IL-24 induces an endoplasmic reticulum stress response that triggers production of ceramide, Ca(2+), and ROS, which in turn promote glioma cell autophagy and cell death.	Ceramides	116-124	interleukin 24	Homo sapiens	33-38
20425071-4	2010	Ceramide has been implicated in the pathogenesis of insulin resistance and has many proinflammatory properties.	Ceramides	0-8	insulin	Homo sapiens	52-59
20030721-1	2010	We demonstrated that a yeast deletion mutant in IPT1 and SKN1, encoding proteins involved in the biosynthesis of mannosyldiinositolphosphoryl ceramides, is characterized by increased autophagy and DNA fragmentation upon nitrogen (N) starvation as compared with the single deletion mutants or wild type (WT).	Ceramides	142-151	beta-glucan synthesis-associated protein SKN1	Saccharomyces cerevisiae S288C	57-61
19860808-1	2010	BACKGROUND: Acid sphingomyelinase (ASM; EC 3.1.4.12) hydrolyses membrane sphingomyelin into the bioactive lipid ceramide and is thus involved in different cellular processes such as differentiation, immunity, or cell death.	Ceramides	112-120	sphingomyelin phosphodiesterase 1	Homo sapiens	12-33
19968763-7	2010	Ceramide generation was dependent upon the calcium ionophore A23187 and was observed in nSMase2-over-expressing COS-7 cells.	Ceramides	0-8	sphingomyelin phosphodiesterase 3	Bos taurus	88-95
20208441-6	2010	In this study, we investigated the effect of the genes involved in the synthesis of ceramide, lcb1, lcb2, tsc10, lac1, lag1, and sur2 on ceramide production levels.	Ceramides	137-145	serine C-palmitoyltransferase LCB1	Saccharomyces cerevisiae S288C	94-98
20208441-6	2010	In this study, we investigated the effect of the genes involved in the synthesis of ceramide, lcb1, lcb2, tsc10, lac1, lag1, and sur2 on ceramide production levels.	Ceramides	137-145	serine C-palmitoyltransferase LCB2	Saccharomyces cerevisiae S288C	100-104
20208441-6	2010	In this study, we investigated the effect of the genes involved in the synthesis of ceramide, lcb1, lcb2, tsc10, lac1, lag1, and sur2 on ceramide production levels.	Ceramides	137-145	3-dehydrosphinganine reductase	Saccharomyces cerevisiae S288C	106-111
20208441-6	2010	In this study, we investigated the effect of the genes involved in the synthesis of ceramide, lcb1, lcb2, tsc10, lac1, lag1, and sur2 on ceramide production levels.	Ceramides	137-145	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	113-117
20208441-6	2010	In this study, we investigated the effect of the genes involved in the synthesis of ceramide, lcb1, lcb2, tsc10, lac1, lag1, and sur2 on ceramide production levels.	Ceramides	137-145	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	119-123
20208441-6	2010	In this study, we investigated the effect of the genes involved in the synthesis of ceramide, lcb1, lcb2, tsc10, lac1, lag1, and sur2 on ceramide production levels.	Ceramides	137-145	sphingosine hydroxylase	Saccharomyces cerevisiae S288C	129-133
20208441-10	2010	The maximum production of ceramide (9.8 mg ceramide/g cell) was obtained when the tsc10 gene was amplified by the pYES2 vector.	Ceramides	26-34	3-dehydrosphinganine reductase	Saccharomyces cerevisiae S288C	82-87
20208441-10	2010	The maximum production of ceramide (9.8 mg ceramide/g cell) was obtained when the tsc10 gene was amplified by the pYES2 vector.	Ceramides	43-51	3-dehydrosphinganine reductase	Saccharomyces cerevisiae S288C	82-87
20208441-11	2010	Real time PCR analysis showed that the increase in ceramide content was proportional to the increase in the tsc10 gene expression level, which was 4.56 times higher than that of the control strain.	Ceramides	51-59	3-dehydrosphinganine reductase	Saccharomyces cerevisiae S288C	108-113
19588508-4	2010	Induced overexpression of Neu3 in the ALL-cell line, MOLT-4, led to a significant increase of ceramide (+66%) and to a parallel decrease of lactosylceramide (-55%).	Ceramides	94-102	neuraminidase 3	Homo sapiens	26-30
19588508-6	2010	Therefore, the reduced expression of Neu3 in ALL could help lymphoblasts to survive, maintaining the cellular content of ceramide below a critical level.	Ceramides	121-129	neuraminidase 3	Homo sapiens	37-41
20919648-1	2010	Evidence has consistently indicated that activation of sphingomyelinases and/or ceramide synthases and the resulting accumulation of ceramide mediate cellular responses to stressors such as lipopolysaccharide, interleukin 1beta, tumor necrosis factor alpha, serum deprivation, irradiation and various antitumor treatments.	Ceramides	80-88	interleukin 1 beta	Homo sapiens	210-256
20919648-5	2010	The latter summarizes the mechanisms by which ceramide activate its direct targets, PKCzeta, PP2A and cathepsin D.	Ceramides	46-54	protein kinase C zeta	Homo sapiens	84-91
20919648-5	2010	The latter summarizes the mechanisms by which ceramide activate its direct targets, PKCzeta, PP2A and cathepsin D.	Ceramides	46-54	protein phosphatase 2 phosphatase activator	Homo sapiens	93-97
20919648-5	2010	The latter summarizes the mechanisms by which ceramide activate its direct targets, PKCzeta, PP2A and cathepsin D.	Ceramides	46-54	cathepsin D	Homo sapiens	102-113
20919650-4	2010	C1P is formed from ceramide by the action of a specific ceramide kinase (CerK), which is distinct from the sphingosine kinases that synthesize sphingosine-1-phosphate.	Ceramides	19-27	ceramide kinase	Homo sapiens	56-71
20919650-4	2010	C1P is formed from ceramide by the action of a specific ceramide kinase (CerK), which is distinct from the sphingosine kinases that synthesize sphingosine-1-phosphate.	Ceramides	19-27	ceramide kinase	Homo sapiens	73-77
20919650-5	2010	CerK is specific for natural ceramides with the erythro configuration in the base component and esterified to long-chain fatty acids.	Ceramides	29-38	ceramide kinase	Homo sapiens	0-4
20919651-5	2010	C1P is a bioactive sphingolipid formed by the phosphorylation of ceramide catalyzed by ceramide kinase (CERK).	Ceramides	65-73	ceramide kinase	Homo sapiens	104-108
19860808-1	2010	BACKGROUND: Acid sphingomyelinase (ASM; EC 3.1.4.12) hydrolyses membrane sphingomyelin into the bioactive lipid ceramide and is thus involved in different cellular processes such as differentiation, immunity, or cell death.	Ceramides	112-120	sphingomyelin phosphodiesterase 1	Homo sapiens	35-38
19782765-5	2010	Accumulation of fatty acids and lipid metabolites (such as long chain acyl CoA, diacylglycerol, triacylglycerol, and/or ceramide) can lead to alterations in this insulin signaling pathway.	Ceramides	120-128	insulin	Homo sapiens	162-169
19165630-2	2010	TNF-alpha triggers ceramide synthesis through binding of TNF-alpha to its p55 receptor.	Ceramides	19-27	tumor necrosis factor	Mus musculus	0-9
19165630-2	2010	TNF-alpha triggers ceramide synthesis through binding of TNF-alpha to its p55 receptor.	Ceramides	19-27	tumor necrosis factor	Mus musculus	57-66
19165630-3	2010	Therefore, ceramide is implicated in many of the multiple signaling pathways initiated by TNF-alpha.	Ceramides	11-19	tumor necrosis factor	Mus musculus	90-99
19165630-5	2010	We hypothesized that stem cell adipogenesis could be retained in TNF-alpha-treated preadipocytes in which ceramide synthesis was blocked and that exogenous ceramide could inhibit adipocyte differentiation.	Ceramides	106-114	tumor necrosis factor	Mus musculus	65-74
19165630-16	2010	Our results suggest that ceramide synthase inhibitor retains the adipogenic potential of TNF-alpha-treated mesenchymal stem cells, while exogenous ceramide at lower concentrations inhibit the adipogenesis of mesenchymal stem cells.	Ceramides	25-33	tumor necrosis factor	Mus musculus	89-98
21364631-3	2010	Inhibition of JNK activation with sphingomyelinase inhibitors (20 muM desipramine, 20 muM imipramine), with the protein kinase C-delta (PKCdelta) inhibitor rottlerin (10 muM), and with the specific PKCtheta pseudosubstrate inhibitor (30 muM) indicates that ceramide and phosphorylation by PKCdelta and PKCtheta mediate gal-1-induced JNK activation.	Ceramides	257-265	mitogen-activated protein kinase 8	Homo sapiens	14-17
20502000-1	2010	Acid sphingomyelinase (ASM) is an important lipid-metabolizing enzyme cleaving sphingomyelin to ceramide, mainly within lysosomes.	Ceramides	96-104	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
20502000-1	2010	Acid sphingomyelinase (ASM) is an important lipid-metabolizing enzyme cleaving sphingomyelin to ceramide, mainly within lysosomes.	Ceramides	96-104	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
20502000-2	2010	Acid ceramidase (AC) further degrades ceramide to sphingosine which can then be phosphorylated to sphingosine-1-phosphate.	Ceramides	38-46	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
20502002-3	2010	Ostensibly, the PAF-induced signaling pathways in endothelial cells utilize similar structures and molecules including acid sphingomyelinase, ceramide, caveolae, endothelial nitric oxide synthase, and nitric oxide, in pulmonary and systemic microvessels.	Ceramides	142-150	PCNA clamp associated factor	Homo sapiens	16-19
20166926-8	2010	Factor Associated with Neutral sphingomyelinase (FAN) regulates ceramide signaling.	Ceramides	64-72	neutral sphingomyelinase activation associated factor	Homo sapiens	49-52
20954073-4	2010	Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-Calpha siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation, and prevented Skp2 downregulation.	Ceramides	92-100	protein phosphatase 2 phosphatase activator	Homo sapiens	28-32
20954073-4	2010	Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-Calpha siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation, and prevented Skp2 downregulation.	Ceramides	92-100	protein phosphatase 2 phosphatase activator	Homo sapiens	64-68
20954073-4	2010	Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-Calpha siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation, and prevented Skp2 downregulation.	Ceramides	92-100	interferon alpha inducible protein 27	Homo sapiens	118-121
20954073-4	2010	Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-Calpha siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation, and prevented Skp2 downregulation.	Ceramides	92-100	cyclin dependent kinase inhibitor 1B	Homo sapiens	122-126
20954073-4	2010	Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-Calpha siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation, and prevented Skp2 downregulation.	Ceramides	92-100	AKT serine/threonine kinase 1	Homo sapiens	151-154
20954073-4	2010	Treatment of cells with the PP2A inhibitor okadaic acid or with PP2A-Calpha siRNA inhibited ceramide-induced enhanced p27(kip1) protein expression and Akt dephosphorylation, and prevented Skp2 downregulation.	Ceramides	92-100	S-phase kinase associated protein 2	Homo sapiens	188-192
20954073-5	2010	Overexpression of constitutively active Akt attenuated ceramide-induced Skp2 downregulation and p27(kip1) upregulation.	Ceramides	55-63	AKT serine/threonine kinase 1	Homo sapiens	40-43
20954073-5	2010	Overexpression of constitutively active Akt attenuated ceramide-induced Skp2 downregulation and p27(kip1) upregulation.	Ceramides	55-63	S-phase kinase associated protein 2	Homo sapiens	72-76
20954073-5	2010	Overexpression of constitutively active Akt attenuated ceramide-induced Skp2 downregulation and p27(kip1) upregulation.	Ceramides	55-63	cyclin dependent kinase inhibitor 1B	Homo sapiens	100-104
20954073-6	2010	In addition, ceramide stimulated binding of the PP2A catalytic subunit PP2A-Calphabeta to Akt as assessed by immunoprecipitation experiments, indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway.	Ceramides	13-21	protein phosphatase 2 phosphatase activator	Homo sapiens	48-52
20954073-6	2010	In addition, ceramide stimulated binding of the PP2A catalytic subunit PP2A-Calphabeta to Akt as assessed by immunoprecipitation experiments, indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway.	Ceramides	13-21	protein phosphatase 2 phosphatase activator	Homo sapiens	71-75
20954073-6	2010	In addition, ceramide stimulated binding of the PP2A catalytic subunit PP2A-Calphabeta to Akt as assessed by immunoprecipitation experiments, indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway.	Ceramides	13-21	AKT serine/threonine kinase 1	Homo sapiens	90-93
20954073-6	2010	In addition, ceramide stimulated binding of the PP2A catalytic subunit PP2A-Calphabeta to Akt as assessed by immunoprecipitation experiments, indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway.	Ceramides	13-21	protein phosphatase 2 phosphatase activator	Homo sapiens	71-75
20954073-6	2010	In addition, ceramide stimulated binding of the PP2A catalytic subunit PP2A-Calphabeta to Akt as assessed by immunoprecipitation experiments, indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway.	Ceramides	13-21	interferon alpha inducible protein 27	Homo sapiens	195-198
20954073-6	2010	In addition, ceramide stimulated binding of the PP2A catalytic subunit PP2A-Calphabeta to Akt as assessed by immunoprecipitation experiments, indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway.	Ceramides	13-21	cyclin dependent kinase inhibitor 1B	Homo sapiens	199-203
20954073-6	2010	In addition, ceramide stimulated binding of the PP2A catalytic subunit PP2A-Calphabeta to Akt as assessed by immunoprecipitation experiments, indicating that PP2A is involved in the induction of p27(kip1) via inhibition of Akt pathway.	Ceramides	13-21	AKT serine/threonine kinase 1	Homo sapiens	223-226
20954073-9	2010	These data reveal that PP2A is a regulator of ceramide-induced p27(kip1) expression via Akt-dependent and Akt-independent pathways.	Ceramides	46-54	protein phosphatase 2 phosphatase activator	Homo sapiens	23-27
20954073-9	2010	These data reveal that PP2A is a regulator of ceramide-induced p27(kip1) expression via Akt-dependent and Akt-independent pathways.	Ceramides	46-54	interferon alpha inducible protein 27	Homo sapiens	63-66
20954073-9	2010	These data reveal that PP2A is a regulator of ceramide-induced p27(kip1) expression via Akt-dependent and Akt-independent pathways.	Ceramides	46-54	cyclin dependent kinase inhibitor 1B	Homo sapiens	67-71
20954073-9	2010	These data reveal that PP2A is a regulator of ceramide-induced p27(kip1) expression via Akt-dependent and Akt-independent pathways.	Ceramides	46-54	AKT serine/threonine kinase 1	Homo sapiens	88-91
20954073-9	2010	These data reveal that PP2A is a regulator of ceramide-induced p27(kip1) expression via Akt-dependent and Akt-independent pathways.	Ceramides	46-54	AKT serine/threonine kinase 1	Homo sapiens	106-109
19949935-14	2010	Finally, CSA and PSC833 have been shown also to modulate the ceramide metabolism which stands as second messenger of anticancer agent-induced apoptosis.	Ceramides	61-69	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	9-12
19949935-15	2010	In fact, CSA and PSC833 are also able to respectively inhibit ceramide glycosylation and stimulate de novo ceramide synthesis.	Ceramides	62-70	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	9-12
19949935-15	2010	In fact, CSA and PSC833 are also able to respectively inhibit ceramide glycosylation and stimulate de novo ceramide synthesis.	Ceramides	107-115	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	9-12
20431265-0	2010	Intracellular trafficking of ceramide by ceramide transfer protein.	Ceramides	29-37	ceramide transporter 1	Homo sapiens	41-66
20431265-3	2010	Ceramide transfer protein (CERT) mediates the ER-to-Golgi trafficking of ceramide.	Ceramides	73-81	ceramide transporter 1	Homo sapiens	0-25
20431265-3	2010	Ceramide transfer protein (CERT) mediates the ER-to-Golgi trafficking of ceramide.	Ceramides	73-81	ceramide transporter 1	Homo sapiens	27-31
20431265-4	2010	It has been suggested that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that efficient CERT-mediated trafficking of ceramide occurs at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	41-49	ceramide transporter 1	Homo sapiens	27-31
20431265-4	2010	It has been suggested that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that efficient CERT-mediated trafficking of ceramide occurs at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	174-182	ceramide transporter 1	Homo sapiens	27-31
20431265-4	2010	It has been suggested that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that efficient CERT-mediated trafficking of ceramide occurs at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	174-182	ceramide transporter 1	Homo sapiens	145-149
19778901-4	2009	Transgenic overexpression of DGAT1 in the heart using the cardiomyocyte- specific alpha-myosin heavy chain (MHC) promoter led to approximately a doubling of DGAT activity and TG content and reductions of approximately 35% in cardiac ceramide, 26% in DAG, and 20% in free fatty acid levels.	Ceramides	233-241	diacylglycerol O-acyltransferase 1	Mus musculus	29-34
19778901-4	2009	Transgenic overexpression of DGAT1 in the heart using the cardiomyocyte- specific alpha-myosin heavy chain (MHC) promoter led to approximately a doubling of DGAT activity and TG content and reductions of approximately 35% in cardiac ceramide, 26% in DAG, and 20% in free fatty acid levels.	Ceramides	233-241	diacylglycerol O-acyltransferase 1	Mus musculus	29-33
19834458-4	2009	We demonstrate that schlank is involved in the de novo synthesis of a broad range of ceramides, the key metabolites of sphingolipid biosynthesis.	Ceramides	85-94	schlank	Drosophila melanogaster	20-27
19366370-5	2009	Concomitant changes in mRNA expression included: (i) reduction, followed by induction, of ceramide-generating beta-glucocerebrosidase, (ii) increase on day 1 of two other enzymes for ceramide biosynthesis and (iii) persistent reduction of acetyl-CoA carboxylase-B, a key enzyme in fatty acid synthesis.	Ceramides	90-98	glucosylceramidase beta	Homo sapiens	110-133
19874262-3	2009	We previously observed that the ceramide metabolizing enzyme, acid ceramidase (AC) is upregulated in tumor tissues.	Ceramides	32-40	N-acylsphingosine amidohydrolase 1	Homo sapiens	62-77
19874262-3	2009	We previously observed that the ceramide metabolizing enzyme, acid ceramidase (AC) is upregulated in tumor tissues.	Ceramides	32-40	N-acylsphingosine amidohydrolase 1	Homo sapiens	79-81
19528633-0	2009	AMPK inhibitor Compound C stimulates ceramide production and promotes Bax redistribution and apoptosis in MCF7 breast carcinoma cells.	Ceramides	37-45	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	0-4
19528633-5	2009	Analyses by quantitative PCR and ceramide synthase activity assay suggest that ceramide synthase 5 (LASS/CerS 5) is involved in Compound C-induced ceramide upregulation.	Ceramides	33-41	ceramide synthase 5	Homo sapiens	79-98
19528633-5	2009	Analyses by quantitative PCR and ceramide synthase activity assay suggest that ceramide synthase 5 (LASS/CerS 5) is involved in Compound C-induced ceramide upregulation.	Ceramides	33-41	ceramide synthase 5	Homo sapiens	105-111
19528633-6	2009	Downregulation of LASS/CerS 5 was found to attenuate Compound C-mediated ceramide production, Bax redistribution, and cell death.	Ceramides	73-81	ceramide synthase 5	Homo sapiens	23-29
19828684-5	2009	The ceramide concentration was also lower in hearts of rats and ob/ob mice that were fed soy protein in association with lower serine palmitoyl transferase (SPT)-1 and tumor necrosis factor-alpha mRNA concentrations.	Ceramides	4-12	mucin-like 2	Mus musculus	157-195
18378044-1	2009	The aging program mediated by IGF1-R is responsible for a naturally occurring TrkA to p75(NTR) switch that leads to activation of the second messenger ceramide and increased production of the Alzheimer"s disease amyloid beta-peptide.	Ceramides	151-159	insulin like growth factor 1 receptor	Homo sapiens	30-36
18378044-1	2009	The aging program mediated by IGF1-R is responsible for a naturally occurring TrkA to p75(NTR) switch that leads to activation of the second messenger ceramide and increased production of the Alzheimer"s disease amyloid beta-peptide.	Ceramides	151-159	neurotrophic receptor tyrosine kinase 1	Homo sapiens	78-82
18378044-1	2009	The aging program mediated by IGF1-R is responsible for a naturally occurring TrkA to p75(NTR) switch that leads to activation of the second messenger ceramide and increased production of the Alzheimer"s disease amyloid beta-peptide.	Ceramides	151-159	PC4 and SFRS1 interacting protein 1	Homo sapiens	86-89
18378044-1	2009	The aging program mediated by IGF1-R is responsible for a naturally occurring TrkA to p75(NTR) switch that leads to activation of the second messenger ceramide and increased production of the Alzheimer"s disease amyloid beta-peptide.	Ceramides	151-159	neurotensin receptor 1	Homo sapiens	90-93
19892737-5	2009	Furthermore, we show that a significant increase in ceramide, resulting from lack of ceramide kinase, perturbs the membrane microenvironment of phosphatidylinositol 4, 5, bisphosphate (PIP(2)), altering its distribution.	Ceramides	52-60	Ceramide kinase	Drosophila melanogaster	85-100
19892737-7	2009	Thus ceramide kinase-mediated maintenance of ceramide level is important for the local regulation of PIP(2) and PLC during phototransduction.	Ceramides	5-13	no receptor potential A	Drosophila melanogaster	112-115
19728861-0	2009	Disruption of ceramide synthesis by CerS2 down-regulation leads to autophagy and the unfolded protein response.	Ceramides	14-22	ceramide synthase 2	Homo sapiens	36-41
19728861-2	2009	CerS2 (ceramide synthase 2) is one of the six mammalian isoforms of ceramide synthase and is responsible for the synthesis of VLC (very-long-chain) ceramides, e.g. C24, C24:1.	Ceramides	148-157	ceramide synthase 2	Homo sapiens	0-5
19728861-2	2009	CerS2 (ceramide synthase 2) is one of the six mammalian isoforms of ceramide synthase and is responsible for the synthesis of VLC (very-long-chain) ceramides, e.g. C24, C24:1.	Ceramides	148-157	ceramide synthase 2	Homo sapiens	7-26
19728861-4	2009	CerS2 down-regulation had a broad effect on ceramide homoeostasis, not just on VLC ceramides.	Ceramides	44-52	ceramide synthase 2	Homo sapiens	0-5
19728861-4	2009	CerS2 down-regulation had a broad effect on ceramide homoeostasis, not just on VLC ceramides.	Ceramides	83-92	ceramide synthase 2	Homo sapiens	0-5
19728861-5	2009	Surprisingly, CerS2 down-regulation resulted in significantly increased LC (long-chain) ceramides, e.g. C14, C16, and our results suggested that the increase was due to a ceramide synthase-independent mechanism.	Ceramides	88-97	ceramide synthase 2	Homo sapiens	14-19
19728861-6	2009	CerS2-down-regulation-induced LC ceramide accumulation resulted in growth arrest which was not accompanied by apoptotic cell death.	Ceramides	33-41	ceramide synthase 2	Homo sapiens	0-5
19731037-4	2009	Moreover, we show that Dox-CPPs, used alone, induce the clustering of TRAIL receptors into ceramide-enriched membrane lipid rafts, a property not shared by unconjugated Dox and that this process is due to the generation of ceramide during Dox-CPPs treatment.	Ceramides	91-99	TNF superfamily member 10	Homo sapiens	70-75
19731037-4	2009	Moreover, we show that Dox-CPPs, used alone, induce the clustering of TRAIL receptors into ceramide-enriched membrane lipid rafts, a property not shared by unconjugated Dox and that this process is due to the generation of ceramide during Dox-CPPs treatment.	Ceramides	223-231	TNF superfamily member 10	Homo sapiens	70-75
19800228-1	2009	Sphingosine kinase 1 (SK1) is an important enzyme that regulates the balance between ceramide and sphingosine-1-phosphate (S1P).	Ceramides	85-93	sphingosine kinase 1	Homo sapiens	0-20
19800228-1	2009	Sphingosine kinase 1 (SK1) is an important enzyme that regulates the balance between ceramide and sphingosine-1-phosphate (S1P).	Ceramides	85-93	sphingosine kinase 1	Homo sapiens	22-25
19937821-8	2009	The strongest effect on permeability was caused by the ceramide analogue CTR(C12-C16).	Ceramides	55-63	calcitonin receptor	Homo sapiens	73-76
20053284-1	2010	Ceramide kinase (CERK) produces the bioactive lipid ceramide-1-phosphate (C1P) and is a key regulator of ceramide and dihydroceramide levels.	Ceramides	52-60	ceramide kinase	Mus musculus	0-15
20053284-1	2010	Ceramide kinase (CERK) produces the bioactive lipid ceramide-1-phosphate (C1P) and is a key regulator of ceramide and dihydroceramide levels.	Ceramides	52-60	ceramide kinase	Mus musculus	17-21
20606403-1	2010	Sphingosine kinase-1 (SPHK1) modulates the proliferation, apoptosis and differentiation of keratinocytes through the regulation of ceramide and sphingosine-1-phosphate levels.	Ceramides	131-139	sphingosine kinase 1	Homo sapiens	0-20
20606403-1	2010	Sphingosine kinase-1 (SPHK1) modulates the proliferation, apoptosis and differentiation of keratinocytes through the regulation of ceramide and sphingosine-1-phosphate levels.	Ceramides	131-139	sphingosine kinase 1	Homo sapiens	22-27
21063109-5	2010	Intracellular accumulation of ceramide was associated with reduction of PDX-1 nuclear localization and MafA protein levels and stimulation of CCAAT/enhancer binding protein beta (C/EBP beta) expression.	Ceramides	30-38	pancreatic and duodenal homeobox 1	Rattus norvegicus	72-77
21063109-5	2010	Intracellular accumulation of ceramide was associated with reduction of PDX-1 nuclear localization and MafA protein levels and stimulation of CCAAT/enhancer binding protein beta (C/EBP beta) expression.	Ceramides	30-38	MAF bZIP transcription factor A	Rattus norvegicus	103-107
21063109-5	2010	Intracellular accumulation of ceramide was associated with reduction of PDX-1 nuclear localization and MafA protein levels and stimulation of CCAAT/enhancer binding protein beta (C/EBP beta) expression.	Ceramides	30-38	CCAAT/enhancer binding protein beta	Rattus norvegicus	142-177
21063109-5	2010	Intracellular accumulation of ceramide was associated with reduction of PDX-1 nuclear localization and MafA protein levels and stimulation of CCAAT/enhancer binding protein beta (C/EBP beta) expression.	Ceramides	30-38	CCAAT/enhancer binding protein beta	Rattus norvegicus	179-189
21063109-7	2010	Furthermore, down-regulation of C/EBP beta could block ceramide impairment of proinsulin gene expression.	Ceramides	55-63	CCAAT/enhancer binding protein beta	Rattus norvegicus	32-42
21063112-9	2010	CONCLUSIONS: These data demonstrate that the sphingomyelin/ceramide signaling pathway is involved in the pathogenesis of bleomycin-induced pulmonary fibrosis, and suggest that inhibition of ASM may potentially slow the fibrotic process in the lung.	Ceramides	59-67	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	190-193
19833891-0	2010	Insulin resistance is associated with higher intramyocellular triglycerides in type I but not type II myocytes concomitant with higher ceramide content.	Ceramides	135-143	insulin	Homo sapiens	0-7
19723703-3	2010	Unexpectedly, knockdown of CerS6/C(16)-ceramide using small interfering RNA induced endoplasmic reticulum (ER)-stress-mediated apoptosis.	Ceramides	39-47	ceramide synthase 6	Homo sapiens	27-32
19723703-6	2010	Mechanistically, regulation of ER-stress-induced apoptosis by CerS6/C(16)-ceramide was linked to the activation of a specific arm, ATF6/CHOP, of the unfolded protein response pathway.	Ceramides	74-82	ceramide synthase 6	Homo sapiens	62-67
19723703-6	2010	Mechanistically, regulation of ER-stress-induced apoptosis by CerS6/C(16)-ceramide was linked to the activation of a specific arm, ATF6/CHOP, of the unfolded protein response pathway.	Ceramides	74-82	activating transcription factor 6	Homo sapiens	131-135
19723703-6	2010	Mechanistically, regulation of ER-stress-induced apoptosis by CerS6/C(16)-ceramide was linked to the activation of a specific arm, ATF6/CHOP, of the unfolded protein response pathway.	Ceramides	74-82	DNA damage inducible transcript 3	Homo sapiens	136-140
19723703-8	2010	Thus, these data reveal an unexpected and novel prosurvival role of CerS6/C(16)-ceramide involved in the protection against ER-stress-induced apoptosis and induction of HNSCC tumor growth.	Ceramides	80-88	ceramide synthase 6	Homo sapiens	68-73
19617631-8	2010	Interestingly, the mRNA level of enzymes involved in synthesis and degradation of ceramide including serine palmitoyltransferase, sphingosine kinase 1, neutral sphingomyelinase, and ceramidases was markedly higher in the myocardium of OWT and T2D-OWT patients compared with lean subjects.	Ceramides	82-90	sphingosine kinase 1	Homo sapiens	130-150
19617631-8	2010	Interestingly, the mRNA level of enzymes involved in synthesis and degradation of ceramide including serine palmitoyltransferase, sphingosine kinase 1, neutral sphingomyelinase, and ceramidases was markedly higher in the myocardium of OWT and T2D-OWT patients compared with lean subjects.	Ceramides	82-90	sphingomyelin phosphodiesterase 2	Homo sapiens	152-176
19899769-1	2010	Ceramide kinase (CERK) is essential for production of ceramide-1-phosphate (C1P), a bioactive lipid whose formation critically modulates ceramide levels.	Ceramides	54-62	ceramide kinase	Homo sapiens	0-15
19899769-1	2010	Ceramide kinase (CERK) is essential for production of ceramide-1-phosphate (C1P), a bioactive lipid whose formation critically modulates ceramide levels.	Ceramides	54-62	ceramide kinase	Homo sapiens	17-21
20954073-0	2010	Ceramide produces apoptosis through induction of p27(kip1) by protein phosphatase 2A-dependent Akt dephosphorylation in PC-3 prostate cancer cells.	Ceramides	0-8	interferon alpha inducible protein 27	Homo sapiens	49-52
20954073-0	2010	Ceramide produces apoptosis through induction of p27(kip1) by protein phosphatase 2A-dependent Akt dephosphorylation in PC-3 prostate cancer cells.	Ceramides	0-8	cyclin dependent kinase inhibitor 1B	Homo sapiens	53-57
20954073-0	2010	Ceramide produces apoptosis through induction of p27(kip1) by protein phosphatase 2A-dependent Akt dephosphorylation in PC-3 prostate cancer cells.	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	70-84
20954073-0	2010	Ceramide produces apoptosis through induction of p27(kip1) by protein phosphatase 2A-dependent Akt dephosphorylation in PC-3 prostate cancer cells.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	95-98
20954073-1	2010	Ceramide induces cell cycle arrest and apoptotic cell death associated with increased levels of p27(kip1).	Ceramides	0-8	interferon alpha inducible protein 27	Homo sapiens	96-99
20954073-1	2010	Ceramide induces cell cycle arrest and apoptotic cell death associated with increased levels of p27(kip1).	Ceramides	0-8	cyclin dependent kinase inhibitor 1B	Homo sapiens	100-104
20954073-2	2010	The aim of this study was to examine the effects of ceramide on p27(kip1) protein levels as a measure of cell cycle arrest and apoptosis.	Ceramides	52-60	cyclin dependent kinase inhibitor 1B	Homo sapiens	64-72
20954073-3	2010	Results showed that ceramide increased p27(kip1) protein levels through activation of protein phosphatase 2A (PP2A) in PC-3 prostate cancer cells.	Ceramides	20-28	interferon alpha inducible protein 27	Homo sapiens	39-42
20954073-3	2010	Results showed that ceramide increased p27(kip1) protein levels through activation of protein phosphatase 2A (PP2A) in PC-3 prostate cancer cells.	Ceramides	20-28	cyclin dependent kinase inhibitor 1B	Homo sapiens	43-47
20954073-3	2010	Results showed that ceramide increased p27(kip1) protein levels through activation of protein phosphatase 2A (PP2A) in PC-3 prostate cancer cells.	Ceramides	20-28	protein phosphatase 2 phosphatase activator	Homo sapiens	94-108
20954073-3	2010	Results showed that ceramide increased p27(kip1) protein levels through activation of protein phosphatase 2A (PP2A) in PC-3 prostate cancer cells.	Ceramides	20-28	protein phosphatase 2 phosphatase activator	Homo sapiens	110-114
20358476-5	2010	Curcumin-treated PC3 cells showed apoptosis-inducing cellular ceramide accumulation and activation of p38 mitogen-activated protein kinase (MAPK) and c-jun N-terminal kinase (JNK).	Ceramides	62-70	chromobox 8	Homo sapiens	17-20
19921818-13	2009	EPA has more potential to elevate mitochondrial biogenesis through enhanced PGC-1alpha, and Tfam transcriptional activities may provide partial protection against ceramide cytotoxicity.	Ceramides	163-171	transcription factor A, mitochondrial	Rattus norvegicus	92-96
19891536-0	2009	Sphingomyelinase-induced ceramide production stimulate calcium-independent JNK and PP2A activation following cerebral ischemia.	Ceramides	25-33	mitogen-activated protein kinase 8	Rattus norvegicus	75-78
19891536-8	2009	CONCLUSIONS: Cerebral ischemia up-regulates the sphingomyelin-ceramide pathway, which involves calcium-independent JNK and PP2A activation in hippocampal glia; this may play a significant role in cerebral lesions post-ischemia.	Ceramides	62-70	mitogen-activated protein kinase 8	Rattus norvegicus	115-118
19669729-0	2009	Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease.	Ceramides	20-29	insulin	Homo sapiens	48-55
19669729-0	2009	Link between plasma ceramides, inflammation and insulin resistance: association with serum IL-6 concentration in patients with coronary heart disease.	Ceramides	20-29	interleukin 6	Homo sapiens	91-95
19669729-2	2009	We sought to assess the associations of circulating levels of IL-6, TNF-alpha and high-sensitivity C reactive protein (hsCRP), which are inflammatory markers related to insulin resistance (IR), with the plasma lipid metabolites ceramides and diacylglycerols (DAG) in patients with CHD.	Ceramides	228-237	interleukin 6	Homo sapiens	62-66
19669729-5	2009	RESULTS: Serum circulating levels of IL-6 were strongly correlated with plasma ceramide concentrations (r = 0.59, p < 0.001).	Ceramides	79-87	interleukin 6	Homo sapiens	37-41
19669729-8	2009	In a linear regression model, circulating levels of both ceramides and TNF-alpha had a significant independent influence on circulating levels of IL-6, altogether accounting for 41% of its variation (p < 0.001).	Ceramides	57-66	interleukin 6	Homo sapiens	146-150
19669729-9	2009	CONCLUSIONS/INTERPRETATION: Our results strongly suggest that the link between ceramides, IR and inflammation is related to the inflammatory marker IL-6.	Ceramides	79-88	interleukin 6	Homo sapiens	148-152
19908944-4	2009	Pre-incubation of cells with the cannabinoid receptor CB2 antagonist SR 144528 (SR2), but not the CB1 antagonist Rimonabant or the TRPV1 antagonist capsazepine, partially prevented the anti-proliferative effect, the ceramide accumulation, and the IL-6-induced secretion, suggesting a CB2 receptor-dependent mechanism.	Ceramides	216-224	cannabinoid receptor 2	Homo sapiens	54-57
19908944-7	2009	These results suggest that MET regulates ceramide metabolism in prostate PC3 cells which is involved in cell death as well as in IL-6 secretion.	Ceramides	41-49	interleukin 6	Homo sapiens	129-133
19828684-6	2009	These results indicate that dietary soy protein can reduce the heart ceramide concentration by reducing the expression of SPT-1, a key enzyme in the formation of this sphingolipid in the heart of obese rodents, and by reducing lipid accumulation.	Ceramides	69-77	salivary protein 1	Rattus norvegicus	122-127
19876679-3	2009	The lysosomal lipid metabolizing enzyme acid sphingomyelinase (ASM) cleaves sphingomyelin into ceramide and phosphorylcholine.	Ceramides	95-103	sphingomyelin phosphodiesterase 1	Homo sapiens	40-61
18521091-5	2009	The CERKL protein is thought to be part of the ceramide pathway, which regulates currents conducted by various potassium channels, including the hERG channel.	Ceramides	47-55	ceramide kinase like	Homo sapiens	4-9
19876679-3	2009	The lysosomal lipid metabolizing enzyme acid sphingomyelinase (ASM) cleaves sphingomyelin into ceramide and phosphorylcholine.	Ceramides	95-103	sphingomyelin phosphodiesterase 1	Homo sapiens	63-66
19876679-6	2009	The ASM/ceramide pathway might be a missing link unifying independent findings in neurobiology and the treatment of MDD such as therapeutic latency, oxidative stress, immune activation and increased risk of cardiovascular disease.	Ceramides	8-16	sphingomyelin phosphodiesterase 1	Homo sapiens	4-7
19556298-10	2009	This was associated with increased ceramide production, and use of the ceramide inhibitors myriocin and fumonisin B1 partially recovered the insulin sensitivity.	Ceramides	71-79	insulin	Homo sapiens	141-148
18521091-5	2009	The CERKL protein is thought to be part of the ceramide pathway, which regulates currents conducted by various potassium channels, including the hERG channel.	Ceramides	47-55	ETS transcription factor ERG	Homo sapiens	145-149
19777393-3	2009	T2DM/NASH has been demonstrated to be associated with increased ceramide generation, suggesting a mechanistic link between peripheral insulin resistance and neurodegeneration because ceramides mediate insulin resistance and can cross the blood-brain barrier (BBB).	Ceramides	64-72	insulin	Homo sapiens	134-141
19666872-2	2009	As GVHD progression involves tumor necrosis factor superfamily receptor activation, and as apoptotic signaling for some tumor necrosis factor superfamily receptors might involve acid sphingomyelinase (ASMase)-mediated ceramide generation, we hypothesized that ASMase deletion would ameliorate GVHD.	Ceramides	218-226	sphingomyelin phosphodiesterase 1	Homo sapiens	201-207
19632221-6	2009	Furthermore, IL-15-/- BMMCs constitutively generate more A-SMase-derived ceramide than WT controls and display a decreased expression of pro-survival sphingosin-1-phosphate (SPP) both in cytosol and membrane cell fractions.	Ceramides	73-81	interleukin 15	Mus musculus	13-18
19632221-6	2009	Furthermore, IL-15-/- BMMCs constitutively generate more A-SMase-derived ceramide than WT controls and display a decreased expression of pro-survival sphingosin-1-phosphate (SPP) both in cytosol and membrane cell fractions.	Ceramides	73-81	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	57-64
19763526-1	2009	Acid sphingomyelinase-induced ceramide release has been shown by many studies to induce apoptosis in response to various stimuli.	Ceramides	30-38	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
19762684-6	2009	IGFBP-3 also reduced the retinal ceramide/sphingomyelin ratio that was increased following laser injury.	Ceramides	33-41	insulin-like growth factor binding protein 3	Mus musculus	0-7
19818125-0	2009	Differential protection by wildtype vs. organelle-specific Bcl-2 suggests a combined requirement of both the ER and mitochondria in ceramide-mediated caspase-independent programmed cell death.	Ceramides	132-140	BCL2 apoptosis regulator	Homo sapiens	59-64
19818125-7	2009	RESULTS: Only wildtype Bcl-2 had the ability to efficiently protect from ceramide-mediated ciPCD, whereas expression of Bcl-2 solely at mitochondria, the ER, or the cytosol/nucleus did not prevent ceramide-mediated ciPCD.	Ceramides	73-81	BCL2 apoptosis regulator	Homo sapiens	23-28
19777393-3	2009	T2DM/NASH has been demonstrated to be associated with increased ceramide generation, suggesting a mechanistic link between peripheral insulin resistance and neurodegeneration because ceramides mediate insulin resistance and can cross the blood-brain barrier (BBB).	Ceramides	183-192	insulin	Homo sapiens	134-141
19777393-3	2009	T2DM/NASH has been demonstrated to be associated with increased ceramide generation, suggesting a mechanistic link between peripheral insulin resistance and neurodegeneration because ceramides mediate insulin resistance and can cross the blood-brain barrier (BBB).	Ceramides	183-192	insulin	Homo sapiens	201-208
19777393-4	2009	Peripheral insulin resistance diseases may potentially cause brain insulin resistance via a liver-brain axis of neurodegeneration as a result of the trafficking of ceramides across the BBB.	Ceramides	164-173	insulin	Homo sapiens	11-18
19777393-4	2009	Peripheral insulin resistance diseases may potentially cause brain insulin resistance via a liver-brain axis of neurodegeneration as a result of the trafficking of ceramides across the BBB.	Ceramides	164-173	insulin	Homo sapiens	67-74
19372594-4	2009	Inhibition of ceramide biosynthesis with Fumonisin B1 prevented codistribution of aPKC and Cdc42 in the centrosomal/pericentriolar compartment and severely impaired ciliogenesis.	Ceramides	14-22	cell division control protein 42 homolog	Canis lupus familiaris	91-96
19694802-0	2009	Bax distribution into mitochondrial detergent-resistant microdomains is related to ceramide and cholesterol content in postischemic hearts.	Ceramides	83-91	BCL2 associated X, apoptosis regulator	Rattus norvegicus	0-3
19694802-9	2009	Our results suggest that membrane microenvironments enriched in cholesterol and ceramide in mitochondria favor Bax translocation to this organelle, fostering propagation of the apoptotic cascade.	Ceramides	80-88	BCL2 associated X, apoptosis regulator	Rattus norvegicus	111-114
19372594-5	2009	Cilium formation and codistribution of aPKC and Cdc42 were restored by incubation with N-acetyl or N-palmitoyl sphingosine (C2 or C16 ceramide), or the ceramide analog N-oleoyl serinol (S18).	Ceramides	134-142	cell division control protein 42 homolog	Canis lupus familiaris	48-53
19372594-5	2009	Cilium formation and codistribution of aPKC and Cdc42 were restored by incubation with N-acetyl or N-palmitoyl sphingosine (C2 or C16 ceramide), or the ceramide analog N-oleoyl serinol (S18).	Ceramides	152-160	cell division control protein 42 homolog	Canis lupus familiaris	48-53
19658121-0	2009	Top-down glycolipidomics: fragmentation analysis of ganglioside oligosaccharide core and ceramide moiety by chip-nanoelectrospray collision-induced dissociation MS2-MS6.	Ceramides	89-97	MS2	Homo sapiens	161-164
19372594-6	2009	Cilium formation was also restored by the glycogen synthase kinase-3beta (GSK-3beta) inhibitor indirubin-3-monoxime, suggesting that regulation of ciliogenesis depends on the inhibition of GSK-3beta by ceramide-activated aPKC.	Ceramides	202-210	glycogen synthase kinase 3 beta	Canis lupus familiaris	42-72
19658121-3	2009	Screening of the fraction in the MS1 mode indicated the occurrence of six [M-2H]2- ions which, according to calculation, support 13 GT1 variants differing in their relative molecular mass due to dissimilar ceramide (Cer) constitutions.	Ceramides	206-214	MS	Homo sapiens	33-36
19658121-3	2009	Screening of the fraction in the MS1 mode indicated the occurrence of six [M-2H]2- ions which, according to calculation, support 13 GT1 variants differing in their relative molecular mass due to dissimilar ceramide (Cer) constitutions.	Ceramides	206-214	beta-1,4-galactosyltransferase 1	Homo sapiens	132-135
19748984-9	2009	We conclude that increased ceramide levels in the thymus of SGPL1(-/-) mice abrogate thymic development postnatally by enhanced thymocyte apoptosis and depletion of thymic ETP.	Ceramides	27-35	sphingosine phosphate lyase 1	Mus musculus	60-65
19372594-6	2009	Cilium formation was also restored by the glycogen synthase kinase-3beta (GSK-3beta) inhibitor indirubin-3-monoxime, suggesting that regulation of ciliogenesis depends on the inhibition of GSK-3beta by ceramide-activated aPKC.	Ceramides	202-210	glycogen synthase kinase 3 beta	Canis lupus familiaris	74-83
19748984-10	2009	Our findings indicate that potentially therapeutic immunosuppression by SGPL1 inhibition should benefit from monitoring ceramides to prevent their increase to apoptosis- inducing levels.	Ceramides	120-129	sphingosine phosphate lyase 1	Mus musculus	72-77
19658121-3	2009	Screening of the fraction in the MS1 mode indicated the occurrence of six [M-2H]2- ions which, according to calculation, support 13 GT1 variants differing in their relative molecular mass due to dissimilar ceramide (Cer) constitutions.	Ceramides	216-219	MS	Homo sapiens	33-36
19658121-3	2009	Screening of the fraction in the MS1 mode indicated the occurrence of six [M-2H]2- ions which, according to calculation, support 13 GT1 variants differing in their relative molecular mass due to dissimilar ceramide (Cer) constitutions.	Ceramides	216-219	beta-1,4-galactosyltransferase 1	Homo sapiens	132-135
19372594-6	2009	Cilium formation was also restored by the glycogen synthase kinase-3beta (GSK-3beta) inhibitor indirubin-3-monoxime, suggesting that regulation of ciliogenesis depends on the inhibition of GSK-3beta by ceramide-activated aPKC.	Ceramides	202-210	glycogen synthase kinase 3 beta	Canis lupus familiaris	189-198
19834551-2	2009	By promoting formation of membrane microdomains essential for clustering of receptors and signalling platforms in the plasma membrane, ceramides accumulating as a result of membrane sphingomyelin breakdown are not only essential for assembly of signalling complexes and pathogen entry, but also act as signalling modulators, e. g. by regulating relay of phosphatidyl-inositol-3-kinase (PI3K) signalling.	Ceramides	135-144	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	354-384
19787068-10	2009	Generation of ceramide by exogenous SMase increased MMP-1-protein production of Caco-2-IEC up to 7-fold.	Ceramides	14-22	matrix metallopeptidase 13	Mus musculus	52-57
19787068-13	2009	One aspect of ceramide generation is an increase of MMP-1.	Ceramides	14-22	matrix metallopeptidase 13	Mus musculus	52-57
19705920-0	2009	The proapoptotic C16-ceramide-dependent pathway requires the death-promoting factor Btf in colon adenocarcinoma cells.	Ceramides	21-29	BCL2 associated transcription factor 1	Homo sapiens	84-87
19705920-7	2009	Among them, the cell death-promoting factor Btf was found to be implicated in the apoptotic signal triggered by ceramide.	Ceramides	112-120	BCL2 associated transcription factor 1	Homo sapiens	44-47
19705920-8	2009	In adenocarcinoma cells, Btf regulates apoptosis related proteins such as Mdm2, p53, BAX and pBcl-2 and thus plays an important role in the ceramide mediated cell death.	Ceramides	140-148	BCL2 associated transcription factor 1	Homo sapiens	25-28
19834551-5	2009	Ceramides induced by MV, but also bacterial sphingomyelinase, efficiently interfered with formation of membrane protrusions and T cell spreading and front/rear polarisation in response to beta1 integrin ligation or alphaCD3/CD28 activation, and this was rescued upon pharmacological or genetic ablation of ASM/NSM activity.	Ceramides	0-9	CD28 molecule	Homo sapiens	224-228
19834551-5	2009	Ceramides induced by MV, but also bacterial sphingomyelinase, efficiently interfered with formation of membrane protrusions and T cell spreading and front/rear polarisation in response to beta1 integrin ligation or alphaCD3/CD28 activation, and this was rescued upon pharmacological or genetic ablation of ASM/NSM activity.	Ceramides	0-9	H19 imprinted maternally expressed transcript	Homo sapiens	306-309
19834551-6	2009	Moreover, membrane ceramide accumulation downmodulated chemokine-induced T cell motility on fibronectin.	Ceramides	19-27	fibronectin 1	Homo sapiens	92-103
19635817-10	2009	Our results support a model in which ceramide accumulation during early stages of retinopathy inhibits hBest1 function, leading to abnormal fluid transport across the retina, and enhanced inflammation.	Ceramides	37-45	bestrophin 1	Homo sapiens	103-109
19635817-4	2009	Here we show that hBest1 chloride channel activity is regulated by ceramide and phosphorylation.	Ceramides	67-75	bestrophin 1	Homo sapiens	18-24
19742320-1	2009	Enhanced ceramide glycosylation catalyzed by glucosylceramide synthase (GCS) limits therapeutic efficiencies of antineoplastic agents including doxorubicin in drug-resistant cancer cells.	Ceramides	9-17	UDP-glucose ceramide glucosyltransferase	Mus musculus	45-70
19742320-1	2009	Enhanced ceramide glycosylation catalyzed by glucosylceramide synthase (GCS) limits therapeutic efficiencies of antineoplastic agents including doxorubicin in drug-resistant cancer cells.	Ceramides	9-17	UDP-glucose ceramide glucosyltransferase	Mus musculus	72-75
19635817-0	2009	Dysregulation of human bestrophin-1 by ceramide-induced dephosphorylation.	Ceramides	39-47	bestrophin 1	Homo sapiens	23-35
19592499-6	2009	The physiologic existence of the SPTLC1/2-Par3 complex was detected in mouse liver and macrophages, and short interfering RNA inhibition of Par3 in human THP-1 monocytes significantly reduced SPT activity and de novo ceramide synthesis by nearly 40%.	Ceramides	217-225	serine palmitoyltransferase, long chain base subunit 1	Mus musculus	33-39
19592499-6	2009	The physiologic existence of the SPTLC1/2-Par3 complex was detected in mouse liver and macrophages, and short interfering RNA inhibition of Par3 in human THP-1 monocytes significantly reduced SPT activity and de novo ceramide synthesis by nearly 40%.	Ceramides	217-225	par-3 family cell polarity regulator	Homo sapiens	42-46
19592499-6	2009	The physiologic existence of the SPTLC1/2-Par3 complex was detected in mouse liver and macrophages, and short interfering RNA inhibition of Par3 in human THP-1 monocytes significantly reduced SPT activity and de novo ceramide synthesis by nearly 40%.	Ceramides	217-225	par-3 family cell polarity regulator	Homo sapiens	140-144
19592499-8	2009	Knockdown of Par3 significantly reduced MCP1-induced chemotaxis of THP-1 monocytes, as did knockdown of SPTLC1, and this Par3 effect depended upon SPT activity and was blunted by ceramide treatment.	Ceramides	179-187	par-3 family cell polarity regulator	Homo sapiens	13-17
19592499-8	2009	Knockdown of Par3 significantly reduced MCP1-induced chemotaxis of THP-1 monocytes, as did knockdown of SPTLC1, and this Par3 effect depended upon SPT activity and was blunted by ceramide treatment.	Ceramides	179-187	C-C motif chemokine ligand 2	Homo sapiens	40-44
19592499-8	2009	Knockdown of Par3 significantly reduced MCP1-induced chemotaxis of THP-1 monocytes, as did knockdown of SPTLC1, and this Par3 effect depended upon SPT activity and was blunted by ceramide treatment.	Ceramides	179-187	GLI family zinc finger 2	Homo sapiens	67-72
19592499-8	2009	Knockdown of Par3 significantly reduced MCP1-induced chemotaxis of THP-1 monocytes, as did knockdown of SPTLC1, and this Par3 effect depended upon SPT activity and was blunted by ceramide treatment.	Ceramides	179-187	par-3 family cell polarity regulator	Homo sapiens	121-125
19742320-7	2009	The sensitization effects of MBO-asGCS relied on the decreases of gene expression and enzyme activity of GCS, and on the increases of C(18)-ceramide and of caspase-executed apoptosis.	Ceramides	140-148	UDP-glucose ceramide glucosyltransferase	Mus musculus	35-38
19721393-0	2009	Ceramide mediates inhibition of the AKT/eNOS signaling pathway by palmitate in human vascular endothelial cells.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	36-39
19168701-2	2009	Activation of ASMase generates ceramide, which is important for innate immune response to eliminate infected pathogens.	Ceramides	31-39	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	14-20
19168702-0	2009	CFTR regulation of intracellular pH and ceramides is required for lung endothelial cell apoptosis.	Ceramides	40-49	CF transmembrane conductance regulator	Homo sapiens	0-4
19168702-5	2009	CFTR(inh)-172 treatment prevented the increases in the ceramide:sphingosine-1 phosphate ratio induced by H(2)O(2) in lung endothelial cells.	Ceramides	55-63	CF transmembrane conductance regulator	Homo sapiens	0-4
19168702-6	2009	Replenishing endogenous ceramides via sphingomyelinase supplementation restored the susceptibility of CFTR-inhibited lung endothelial cells to H(2)O(2)-induced apoptosis.	Ceramides	24-33	CF transmembrane conductance regulator	Homo sapiens	102-106
19168702-9	2009	In conclusion, CFTR function is required for stress-induced apoptosis in lung endothelial cells by maintaining adequate intracellular acidification and ceramide activation.	Ceramides	152-160	CF transmembrane conductance regulator	Homo sapiens	15-19
19631607-3	2009	On search for a physiological molecule that could mimic the effect of ethanol, we have previously demonstrated that some sphingolipids containing free "hydroxyl" groups, like ceramide, are able to stimulate the PMCA.	Ceramides	175-183	ATPase plasma membrane Ca2+ transporting 2	Homo sapiens	211-215
19631607-4	2009	Since diacylglycerol (DAG) structurally shares some characteristics with ceramide, we evaluate its effect on the PMCA.	Ceramides	73-81	ATPase plasma membrane Ca2+ transporting 2	Homo sapiens	113-117
19502418-8	2009	Inhibition of ERK1/2, but not of PKB, partially prevented the inhibition of insulin gene expression in the presence of palmitate or ceramide.	Ceramides	132-140	mitogen activated protein kinase 3	Rattus norvegicus	14-20
19367376-4	2009	A cell-permeable analog of ceramide (CER) also mimicked the effects of palmitate in significantly reducing the expression of nm23-H1 and nm23-H2 and NDP kinase activity in these cells.	Ceramides	27-35	cytidine/uridine monophosphate kinase 1	Rattus norvegicus	149-159
19520907-8	2009	Silencing of Nrp1 in A549 cells did not alter cell survival after vehicle treatment but significantly augmented apoptosis after exposure to cigarette smoke extract or ceramide.	Ceramides	167-175	neuropilin 1	Mus musculus	13-17
19545281-6	2009	Activation of NSMase occurred within 1 h, was blocked by inhibitors of caspase 8, increased mainly C18 and C24:1 ceramides, and appeared to be concentrated in detergent-resistant microdomains (Rafts).	Ceramides	113-122	sphingomyelin phosphodiesterase 2	Rattus norvegicus	14-20
19367376-4	2009	A cell-permeable analog of ceramide (CER) also mimicked the effects of palmitate in significantly reducing the expression of nm23-H1 and nm23-H2 and NDP kinase activity in these cells.	Ceramides	37-40	cytidine/uridine monophosphate kinase 1	Rattus norvegicus	149-159
19721393-0	2009	Ceramide mediates inhibition of the AKT/eNOS signaling pathway by palmitate in human vascular endothelial cells.	Ceramides	0-8	nitric oxide synthase 3	Homo sapiens	40-44
19721393-7	2009	Preventing de novo ceramide synthesis abolished the antagonistic effect of palmitate toward the Akt/ eNOS pathway.	Ceramides	19-27	AKT serine/threonine kinase 1	Homo sapiens	96-99
19721393-7	2009	Preventing de novo ceramide synthesis abolished the antagonistic effect of palmitate toward the Akt/ eNOS pathway.	Ceramides	19-27	nitric oxide synthase 3	Homo sapiens	101-105
19721393-9	2009	CONCLUSIONS: Taken together, we have demonstrated that palmitic acid induces accumulation of ceramide, which appears to mediate palmitic acid"s inhibitory effects on the Akt/eNOS pathway, leading to a significant decrease in NO generation.	Ceramides	93-101	AKT serine/threonine kinase 1	Homo sapiens	170-173
19721393-9	2009	CONCLUSIONS: Taken together, we have demonstrated that palmitic acid induces accumulation of ceramide, which appears to mediate palmitic acid"s inhibitory effects on the Akt/eNOS pathway, leading to a significant decrease in NO generation.	Ceramides	93-101	nitric oxide synthase 3	Homo sapiens	174-178
19721393-10	2009	Therefore, ceramide is a necessary and sufficient intermediate mediating the inhibition of the AKT/eNOS signaling pathway by palmitate in endothelial cells.	Ceramides	11-19	AKT serine/threonine kinase 1	Homo sapiens	95-98
19721393-10	2009	Therefore, ceramide is a necessary and sufficient intermediate mediating the inhibition of the AKT/eNOS signaling pathway by palmitate in endothelial cells.	Ceramides	11-19	nitric oxide synthase 3	Homo sapiens	99-103
19712582-5	2009	Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death.	Ceramides	193-202	insulin	Homo sapiens	97-104
20137294-8	2009	When FL cells were incubated with ceramide following the imipramine pretreatment for 30 min, EGFR clustering induced by 50-Hz MF exposure could be recovered.	Ceramides	34-42	epidermal growth factor receptor	Homo sapiens	93-97
20137294-9	2009	CONCLUSION: EGFR clustering induced by 50-Hz MF depends on A-SMase activity, and ceramide, as the hydrolyzate from A-SMase might participate in the process of EGFR clustering.	Ceramides	81-89	epidermal growth factor receptor	Homo sapiens	12-16
20137294-9	2009	CONCLUSION: EGFR clustering induced by 50-Hz MF depends on A-SMase activity, and ceramide, as the hydrolyzate from A-SMase might participate in the process of EGFR clustering.	Ceramides	81-89	sphingomyelin phosphodiesterase 1	Homo sapiens	115-122
20137294-9	2009	CONCLUSION: EGFR clustering induced by 50-Hz MF depends on A-SMase activity, and ceramide, as the hydrolyzate from A-SMase might participate in the process of EGFR clustering.	Ceramides	81-89	epidermal growth factor receptor	Homo sapiens	159-163
19712582-5	2009	Human and experimental animal studies revealed that neurodegeneration associated with peripheral insulin resistance is likely effectuated via a liver-brain axis whereby toxic lipids, including ceramides, cross the blood brain barrier and cause brain insulin resistance, oxidative stress, neuro-inflammation, and cell death.	Ceramides	193-202	insulin	Homo sapiens	250-257
19712582-6	2009	In essence, there are dual mechanisms of brain insulin resistance leading to AD-type neurodegeneration: one mediated by endogenous, CNS factors; and the other, peripheral insulin resistance with excess cytotoxic ceramide production.	Ceramides	212-220	insulin	Homo sapiens	47-54
19298866-1	2009	Acid ceramidase (encoded by ASAH1) is a lipid hydrolase that catalyzes the conversion of ceramide (cer) into sphingosine (SPH) and a free fatty acid.	Ceramides	89-97	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
19693275-0	2009	Involvement of VDAC, Bax and ceramides in the efflux of AIF from mitochondria during curcumin-induced apoptosis.	Ceramides	29-38	apoptosis inducing factor mitochondria associated 1	Homo sapiens	56-59
19693275-14	2009	Surprisingly, this process could also be blocked by DIDS, suggesting the concerted action of Bax, VDAC and ceramide in the efflux of AIF from the mitochondrion.	Ceramides	107-115	apoptosis inducing factor mitochondria associated 1	Homo sapiens	133-136
19693275-15	2009	CONCLUSIONS: Curcumin-induced fibroblast apoptosis is totally caspase-independent and relies on the mitochondrial formation of ROS and the subsequent nuclear translocation of AIF, which is released from a mitochondrial pore that involves VDAC, Bax and possibly ceramides.	Ceramides	261-270	apoptosis inducing factor mitochondria associated 1	Homo sapiens	175-178
19691145-6	2009	Sphingosine (50 microM) or ceramide (100 microM) increase PA metabolism by the pathway that involves LPP/DAGL/MAGL action in aged membranes.	Ceramides	27-35	monoglyceride lipase	Rattus norvegicus	110-114
19426719-4	2009	ABC transporters can also modulate cellular sensitivity to extrinsic pro-apoptotic signals through regulation of sphingomyelin-ceramide biosynthesis and metabolism.	Ceramides	127-135	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	0-3
19298866-1	2009	Acid ceramidase (encoded by ASAH1) is a lipid hydrolase that catalyzes the conversion of ceramide (cer) into sphingosine (SPH) and a free fatty acid.	Ceramides	89-97	N-acylsphingosine amidohydrolase 1	Homo sapiens	28-33
19345744-7	2009	Interestingly, NCDase siRNA transfection was sufficient to induce a cell cycle arrest at G(0)/G(1) and an increase in total ceramide levels, with significant elevation in very long chain ceramides (C(24:1) and C(24:0)).	Ceramides	124-132	N-acylsphingosine amidohydrolase 2	Mus musculus	15-21
19298866-1	2009	Acid ceramidase (encoded by ASAH1) is a lipid hydrolase that catalyzes the conversion of ceramide (cer) into sphingosine (SPH) and a free fatty acid.	Ceramides	5-8	N-acylsphingosine amidohydrolase 1	Homo sapiens	28-33
19345744-7	2009	Interestingly, NCDase siRNA transfection was sufficient to induce a cell cycle arrest at G(0)/G(1) and an increase in total ceramide levels, with significant elevation in very long chain ceramides (C(24:1) and C(24:0)).	Ceramides	187-196	N-acylsphingosine amidohydrolase 2	Mus musculus	15-21
19735173-7	2009	However, epidermal levels of hydration and ceramides in group H1.0 did not differ from those in group UV, in which ceramidase, an enzyme involved in ceramide degradation, was highly expressed.	Ceramides	43-51	histocompatibility 10	Mus musculus	62-66
19345744-9	2009	These data provide evidence for a novel mechanism of action for GMZ and highlight downregulation of NCDase as a critical step in GMZ-mediated ceramide elevation and cell cycle arrest.	Ceramides	142-150	N-acylsphingosine amidohydrolase 2	Mus musculus	100-106
19723203-5	2009	Furthermore, the changes of total ceramide and glycosaminoglycan in skin were recovered significantly by JC and JCH.	Ceramides	34-42	immunoglobulin joining chain	Mus musculus	112-115
19458474-1	2009	We unveiled novel p65/RelA consensus sites in the promoter of the beclin 1 gene and demonstrate that p65/RelA positively modulates canonical autophagy in various human cell lines both under basal conditions and upon induction by ceramide.	Ceramides	229-237	RELA proto-oncogene, NF-kB subunit	Homo sapiens	18-21
19458474-1	2009	We unveiled novel p65/RelA consensus sites in the promoter of the beclin 1 gene and demonstrate that p65/RelA positively modulates canonical autophagy in various human cell lines both under basal conditions and upon induction by ceramide.	Ceramides	229-237	RELA proto-oncogene, NF-kB subunit	Homo sapiens	22-26
19458474-1	2009	We unveiled novel p65/RelA consensus sites in the promoter of the beclin 1 gene and demonstrate that p65/RelA positively modulates canonical autophagy in various human cell lines both under basal conditions and upon induction by ceramide.	Ceramides	229-237	beclin 1	Homo sapiens	66-74
19458474-1	2009	We unveiled novel p65/RelA consensus sites in the promoter of the beclin 1 gene and demonstrate that p65/RelA positively modulates canonical autophagy in various human cell lines both under basal conditions and upon induction by ceramide.	Ceramides	229-237	RELA proto-oncogene, NF-kB subunit	Homo sapiens	101-104
19458474-1	2009	We unveiled novel p65/RelA consensus sites in the promoter of the beclin 1 gene and demonstrate that p65/RelA positively modulates canonical autophagy in various human cell lines both under basal conditions and upon induction by ceramide.	Ceramides	229-237	RELA proto-oncogene, NF-kB subunit	Homo sapiens	105-109
19735173-7	2009	However, epidermal levels of hydration and ceramides in group H1.0 did not differ from those in group UV, in which ceramidase, an enzyme involved in ceramide degradation, was highly expressed.	Ceramides	43-52	histocompatibility 10	Mus musculus	62-66
19531467-0	2009	Peptidoglycan induces cyclooxygenase-2 expression in macrophages by activating the neutral sphingomyelinase-ceramide pathway.	Ceramides	108-116	prostaglandin-endoperoxide synthase 2	Homo sapiens	22-38
19483104-11	2009	Our data demonstrate that treatment of colon cancer cells with sorafenib + vorinostat activates CD95 via de novo ceramide synthesis that promotes viability via autophagy or degrades survival via either the extrinsic or intrinsic pathways.	Ceramides	113-121	Fas cell surface death receptor	Homo sapiens	96-100
19698269-3	2009	Prostaglandin E(2) (PGE(2)) activates nonselective cation channels that increase cytosolic Ca(2+) activity and platelet-activating factor (PAF) activates a sphingomyelinase which lead to formation of ceramide.	Ceramides	200-208	PCNA clamp associated factor	Homo sapiens	111-137
19698269-3	2009	Prostaglandin E(2) (PGE(2)) activates nonselective cation channels that increase cytosolic Ca(2+) activity and platelet-activating factor (PAF) activates a sphingomyelinase which lead to formation of ceramide.	Ceramides	200-208	PCNA clamp associated factor	Homo sapiens	139-142
19630917-4	2009	Bet v 1 proteins may also be able to bind and transport more complex amphiphilic molecules like ceramides and sphingomyelins known to be enriched on caveolae/lipid rafts.	Ceramides	96-105	delta/notch like EGF repeat containing	Homo sapiens	0-3
19689937-5	2009	In apoptosis, the defects in CLN3 result in ceramide accumulation and upstream of mitochondrial membrane per-meabilization, which eventually induce caspase-dependent and caspase-independent cell death.	Ceramides	44-52	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	29-33
19559025-0	2009	Elastin peptides antagonize ceramide-induced apoptosis.	Ceramides	28-36	elastin	Homo sapiens	0-7
19559025-4	2009	We show that ceramide-induced apoptosis could be blocked by elastin peptides.	Ceramides	13-21	elastin	Homo sapiens	60-67
19531467-0	2009	Peptidoglycan induces cyclooxygenase-2 expression in macrophages by activating the neutral sphingomyelinase-ceramide pathway.	Ceramides	108-116	sphingomyelin phosphodiesterase 2	Homo sapiens	83-107
19531467-5	2009	PGN activated nSMase, but not acidic SMase, resulting in increased ceramide generation.	Ceramides	67-75	sphingomyelin phosphodiesterase 2	Homo sapiens	14-20
19531467-12	2009	Our data demonstrate for the first time that PGN activates the nSMase/ceramide pathway to induce MKK3/6/p38 MAPK activation, which in turn initiates NF-kappaB activation and ultimately induces COX-2 expression in macrophages.	Ceramides	70-78	sphingomyelin phosphodiesterase 2	Homo sapiens	63-69
19531467-12	2009	Our data demonstrate for the first time that PGN activates the nSMase/ceramide pathway to induce MKK3/6/p38 MAPK activation, which in turn initiates NF-kappaB activation and ultimately induces COX-2 expression in macrophages.	Ceramides	70-78	mitogen-activated protein kinase kinase 3	Homo sapiens	97-103
19429679-0	2009	Ceramide stimulates ABCA12 expression via peroxisome proliferator-activated receptor {delta} in human keratinocytes.	Ceramides	0-8	ATP binding cassette subfamily A member 12	Homo sapiens	20-26
19429679-0	2009	Ceramide stimulates ABCA12 expression via peroxisome proliferator-activated receptor {delta} in human keratinocytes.	Ceramides	0-8	peroxisome proliferator activated receptor delta	Homo sapiens	42-91
19531467-12	2009	Our data demonstrate for the first time that PGN activates the nSMase/ceramide pathway to induce MKK3/6/p38 MAPK activation, which in turn initiates NF-kappaB activation and ultimately induces COX-2 expression in macrophages.	Ceramides	70-78	mitogen-activated protein kinase 1	Homo sapiens	104-107
19429679-5	2009	Here we demonstrate that ceramide (C(2)-Cer and C(6)-Cer), but not C(8)-glucosylceramides, sphingosine, or ceramide 1-phosphate, increases ABCA12 mRNA expression in a dose- and time-dependent manner.	Ceramides	25-33	ATP binding cassette subfamily A member 12	Homo sapiens	139-145
19429679-7	2009	Moreover, simultaneous treatment with C(6)-Cer and each of these same inhibitors additively increased ABCA12 expression, indicating that ceramide is an important inducer of ABCA12 expression and that the conversion of ceramide to other sphingolipids or metabolites is not required.	Ceramides	137-145	ATP binding cassette subfamily A member 12	Homo sapiens	102-108
19531467-12	2009	Our data demonstrate for the first time that PGN activates the nSMase/ceramide pathway to induce MKK3/6/p38 MAPK activation, which in turn initiates NF-kappaB activation and ultimately induces COX-2 expression in macrophages.	Ceramides	70-78	mitogen-activated protein kinase 3	Homo sapiens	108-112
19429679-7	2009	Moreover, simultaneous treatment with C(6)-Cer and each of these same inhibitors additively increased ABCA12 expression, indicating that ceramide is an important inducer of ABCA12 expression and that the conversion of ceramide to other sphingolipids or metabolites is not required.	Ceramides	137-145	ATP binding cassette subfamily A member 12	Homo sapiens	173-179
19429679-7	2009	Moreover, simultaneous treatment with C(6)-Cer and each of these same inhibitors additively increased ABCA12 expression, indicating that ceramide is an important inducer of ABCA12 expression and that the conversion of ceramide to other sphingolipids or metabolites is not required.	Ceramides	218-226	ATP binding cassette subfamily A member 12	Homo sapiens	102-108
19531467-12	2009	Our data demonstrate for the first time that PGN activates the nSMase/ceramide pathway to induce MKK3/6/p38 MAPK activation, which in turn initiates NF-kappaB activation and ultimately induces COX-2 expression in macrophages.	Ceramides	70-78	prostaglandin-endoperoxide synthase 2	Homo sapiens	193-198
19429679-8	2009	Finally, both exogenous and endogenous ceramides preferentially stimulate PPARdelta expression (but not other PPARs or liver X receptors), whereas PPARdelta knockdown by siRNA transfection specifically diminished the ceramide-induced increase in ABCA12 mRNA levels, indicating that PPARdelta is a mediator of the ceramide effect.	Ceramides	39-48	peroxisome proliferator activated receptor delta	Homo sapiens	74-83
19429679-8	2009	Finally, both exogenous and endogenous ceramides preferentially stimulate PPARdelta expression (but not other PPARs or liver X receptors), whereas PPARdelta knockdown by siRNA transfection specifically diminished the ceramide-induced increase in ABCA12 mRNA levels, indicating that PPARdelta is a mediator of the ceramide effect.	Ceramides	39-47	peroxisome proliferator activated receptor delta	Homo sapiens	74-83
19531467-13	2009	The nSMase/ceramide pathway is required but might not be sufficient for COX-2 expression induced by PGN.	Ceramides	11-19	sphingomyelin phosphodiesterase 2	Homo sapiens	4-10
19429679-8	2009	Finally, both exogenous and endogenous ceramides preferentially stimulate PPARdelta expression (but not other PPARs or liver X receptors), whereas PPARdelta knockdown by siRNA transfection specifically diminished the ceramide-induced increase in ABCA12 mRNA levels, indicating that PPARdelta is a mediator of the ceramide effect.	Ceramides	217-225	peroxisome proliferator activated receptor delta	Homo sapiens	147-156
19435851-6	2009	Inhibition of de novo ceramide biosynthesis decreased adipose expression of suppressor of cytokine signaling-3 (SOCS-3) and induced adipose uncoupling protein-3 (UCP3).	Ceramides	22-30	suppressor of cytokine signaling 3	Mus musculus	76-110
19429679-8	2009	Finally, both exogenous and endogenous ceramides preferentially stimulate PPARdelta expression (but not other PPARs or liver X receptors), whereas PPARdelta knockdown by siRNA transfection specifically diminished the ceramide-induced increase in ABCA12 mRNA levels, indicating that PPARdelta is a mediator of the ceramide effect.	Ceramides	217-225	ATP binding cassette subfamily A member 12	Homo sapiens	246-252
19429679-8	2009	Finally, both exogenous and endogenous ceramides preferentially stimulate PPARdelta expression (but not other PPARs or liver X receptors), whereas PPARdelta knockdown by siRNA transfection specifically diminished the ceramide-induced increase in ABCA12 mRNA levels, indicating that PPARdelta is a mediator of the ceramide effect.	Ceramides	217-225	peroxisome proliferator activated receptor delta	Homo sapiens	147-156
19429679-9	2009	Together, these results show that ceramide, an important lipid component of epidermis, up-regulates ABCA12 expression via the PPARdelta-mediated signaling pathway, providing a substrate-driven, feed-forward mechanism for regulating this key lipid transporter.	Ceramides	34-42	ATP binding cassette subfamily A member 12	Homo sapiens	100-106
19429679-9	2009	Together, these results show that ceramide, an important lipid component of epidermis, up-regulates ABCA12 expression via the PPARdelta-mediated signaling pathway, providing a substrate-driven, feed-forward mechanism for regulating this key lipid transporter.	Ceramides	34-42	peroxisome proliferator activated receptor delta	Homo sapiens	126-135
19488858-3	2009	The purpose of the present study was to elucidate the dependence of amyloid peptides Abeta(1-42) and islet amyloid polypeptide (IAPP)-induced cell death on ceramide formation and ion channel activity in murine pancreatic islet cells.	Ceramides	156-164	islet amyloid polypeptide	Mus musculus	128-132
19328214-6	2009	Moreover, Bcl-x(L) silencing precluded dexamethasone-induced protection against ceramide and, by itself, induced massive death, demonstrating the strict dependence of HTC cells on Bcl-x(L) for survival also under standard culture conditions.	Ceramides	80-88	Bcl2-like 1	Rattus norvegicus	10-18
19393694-9	2009	This study reveals a novel and highly specific mechanism by which CerS1 protein levels are regulated and which directly impacts ceramide homeostasis.	Ceramides	128-136	ceramide synthase 1	Homo sapiens	66-71
19416656-0	2009	CERT-mediated trafficking of ceramide.	Ceramides	29-37	ceramide transporter 1	Homo sapiens	0-4
19416656-3	2009	CERT mediates the ER-to-Golgi trafficking of ceramide.	Ceramides	45-53	ceramide transporter 1	Homo sapiens	0-4
19416656-4	2009	CERT contains several functional domains and motifs including i) a START domain capable of catalyzing inter-membrane transfer of ceramide, ii) a pleckstrin homology domain, which serves to target the Golgi apparatus, iii) a FFAT motif which interacts with the ER-resident membrane protein VAP, and iv) a serine-repeat motif, of which hyperphosphorylation down-regulates CERT activity.	Ceramides	129-137	ceramide transporter 1	Homo sapiens	0-4
19416656-5	2009	It has been suggested that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that efficient CERT-mediated trafficking of ceramide occurs at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	41-49	ceramide transporter 1	Homo sapiens	27-31
19416656-5	2009	It has been suggested that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that efficient CERT-mediated trafficking of ceramide occurs at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	174-182	ceramide transporter 1	Homo sapiens	27-31
19416656-5	2009	It has been suggested that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that efficient CERT-mediated trafficking of ceramide occurs at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	174-182	ceramide transporter 1	Homo sapiens	145-149
19395669-0	2009	Neutral sphingomyelinase 2 is activated by cigarette smoke to augment ceramide-induced apoptosis in lung cell death.	Ceramides	70-78	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
19395669-2	2009	Using loss-of-function and overexpression analyses, we show that neutral sphingomyelinase 2 (nSMase2) is required for CS-mediated ceramide generation and apoptosis.	Ceramides	130-138	sphingomyelin phosphodiesterase 3	Homo sapiens	65-91
19395669-2	2009	Using loss-of-function and overexpression analyses, we show that neutral sphingomyelinase 2 (nSMase2) is required for CS-mediated ceramide generation and apoptosis.	Ceramides	130-138	sphingomyelin phosphodiesterase 3	Homo sapiens	93-100
19395669-4	2009	We found that the exposure to CS, as with exposure to H(2)O(2), results in increased nSMase2 activation leading to ceramide generation and therefore increased apoptosis.	Ceramides	115-123	sphingomyelin phosphodiesterase 3	Homo sapiens	85-92
19395669-7	2009	Our data support a model where CS induces nSMase2 activation thereby increasing membrane-sphingomyelin hydrolysis to ceramide.	Ceramides	117-125	sphingomyelin phosphodiesterase 3	Homo sapiens	42-49
19328214-5	2009	However, Bcl-2 transfection and Bcl-x(L) upregulation by dexamethasone significantly diminished the apoptogenic effect of ceramide but not that of TNF, suggesting that ceramide is not directly involved in TNF toxicity.	Ceramides	122-130	BCL2, apoptosis regulator	Rattus norvegicus	9-14
19328214-5	2009	However, Bcl-2 transfection and Bcl-x(L) upregulation by dexamethasone significantly diminished the apoptogenic effect of ceramide but not that of TNF, suggesting that ceramide is not directly involved in TNF toxicity.	Ceramides	122-130	Bcl2-like 1	Rattus norvegicus	32-37
19328214-5	2009	However, Bcl-2 transfection and Bcl-x(L) upregulation by dexamethasone significantly diminished the apoptogenic effect of ceramide but not that of TNF, suggesting that ceramide is not directly involved in TNF toxicity.	Ceramides	168-176	BCL2, apoptosis regulator	Rattus norvegicus	9-14
19435851-6	2009	Inhibition of de novo ceramide biosynthesis decreased adipose expression of suppressor of cytokine signaling-3 (SOCS-3) and induced adipose uncoupling protein-3 (UCP3).	Ceramides	22-30	suppressor of cytokine signaling 3	Mus musculus	112-118
19435851-6	2009	Inhibition of de novo ceramide biosynthesis decreased adipose expression of suppressor of cytokine signaling-3 (SOCS-3) and induced adipose uncoupling protein-3 (UCP3).	Ceramides	22-30	uncoupling protein 3 (mitochondrial, proton carrier)	Mus musculus	162-166
19435851-7	2009	Moreover, ceramide directly induced SOCS-3 and inhibited UCP3 mRNA in cultured adipocytes suggesting a direct role for ceramide in regulation of metabolism and energy expenditure.	Ceramides	10-18	suppressor of cytokine signaling 3	Mus musculus	36-42
19435851-7	2009	Moreover, ceramide directly induced SOCS-3 and inhibited UCP3 mRNA in cultured adipocytes suggesting a direct role for ceramide in regulation of metabolism and energy expenditure.	Ceramides	10-18	uncoupling protein 3 (mitochondrial, proton carrier)	Mus musculus	57-61
19435851-8	2009	Inhibition of de novo ceramide synthesis had no effect on adipose tumor necrosis factor-alpha (TNF-alpha) expression but dramatically reduced adipose plasminogen activator inhibitor-1 (PAI-1) and monocyte chemoattactant protein-1 (MCP-1).	Ceramides	22-30	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	185-190
19435851-8	2009	Inhibition of de novo ceramide synthesis had no effect on adipose tumor necrosis factor-alpha (TNF-alpha) expression but dramatically reduced adipose plasminogen activator inhibitor-1 (PAI-1) and monocyte chemoattactant protein-1 (MCP-1).	Ceramides	22-30	chemokine (C-C motif) ligand 2	Mus musculus	196-229
19329756-9	2009	Furthermore, this caspase 8 activation was dependent on ceramide generation by acidic sphingomyelinase.	Ceramides	56-64	caspase 8	Homo sapiens	18-27
19609004-2	2009	Here, we investigated the pathways of ceramide accumulation in the MCL cell line Rec-1 using the stable endocannabinoid analogue R(+)-methanandamide (R-MA).	Ceramides	38-46	RAD1 checkpoint DNA exonuclease	Homo sapiens	81-86
19742171-2	2009	Alcohol-induced steatohepatitis promotes synthesis and accumulation of ceramides and other toxic lipids that cause insulin resistance.	Ceramides	71-80	insulin	Homo sapiens	115-122
19742171-3	2009	Ceramides can readily cross the blood-brain barrier, and ceramide exposure causes neurodegeneration with insulin resistance and oxidative stress, similar to the effects of alcohol.	Ceramides	57-65	insulin	Homo sapiens	105-112
19609004-11	2009	Our findings suggest that R-MA induces cell death in MCL via CB1-mediated up-regulation of the de novo ceramide synthesis pathway.	Ceramides	103-111	cannabinoid receptor 1	Homo sapiens	61-64
19295452-11	2009	CONCLUSIONS: Our results suggest that short-term changes of mitogen-activated protein kinase and AKT signaling pathways and c-fos and c-jun expressions caused by glucose are abolished by palmitate through phosphatidylinositol 3-kinase inhibition via ceramide synthesis.	Ceramides	250-258	AKT serine/threonine kinase 1	Rattus norvegicus	97-100
19295452-11	2009	CONCLUSIONS: Our results suggest that short-term changes of mitogen-activated protein kinase and AKT signaling pathways and c-fos and c-jun expressions caused by glucose are abolished by palmitate through phosphatidylinositol 3-kinase inhibition via ceramide synthesis.	Ceramides	250-258	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	124-129
19385042-1	2009	Acid sphingomyelinase occupies a prominent position in sphingolipid catabolism, catalyzing the hydrolysis of sphingomyelin to ceramide and phosphorylcholine.	Ceramides	126-134	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
19394401-0	2009	Neutral sphingomyelinase-induced ceramide accumulation by oxidative stress during carbon tetrachloride intoxication.	Ceramides	33-41	sphingomyelin phosphodiesterase 2	Rattus norvegicus	0-24
19394401-2	2009	In this study, we examined the effect of CCl4 on the ceramide metabolism and indicators of oxidative stress.	Ceramides	53-61	C-C motif chemokine ligand 4	Rattus norvegicus	41-45
19394401-6	2009	The total ceramide in the liver significantly increased as early as 2h after CCl4 administration.	Ceramides	10-18	C-C motif chemokine ligand 4	Rattus norvegicus	77-81
19394401-11	2009	Thus, the activation of neutral SMase via oxidative stress induced the increase of ceramide during CCl4 intoxication in not only the liver but also other tissues.	Ceramides	83-91	C-C motif chemokine ligand 4	Rattus norvegicus	99-103
19506037-0	2009	Sphingomyelin synthase-related protein SMSr controls ceramide homeostasis in the ER.	Ceramides	53-61	sterile alpha motif domain containing 8	Homo sapiens	0-30
19506037-0	2009	Sphingomyelin synthase-related protein SMSr controls ceramide homeostasis in the ER.	Ceramides	53-61	sterile alpha motif domain containing 8	Homo sapiens	39-43
19506037-3	2009	In this study, we report the identification of an SMS1-related (SMSr) enzyme, which catalyses the synthesis of the SM analogue ceramide phosphoethanolamine (CPE) in the ER lumen.	Ceramides	127-135	sterile alpha motif domain containing 8	Homo sapiens	50-62
19506037-3	2009	In this study, we report the identification of an SMS1-related (SMSr) enzyme, which catalyses the synthesis of the SM analogue ceramide phosphoethanolamine (CPE) in the ER lumen.	Ceramides	127-135	sterile alpha motif domain containing 8	Homo sapiens	64-68
19506037-7	2009	Our results establish SMSr as a key regulator of ceramide homeostasis that seems to operate as a sensor rather than a converter of ceramides in the ER.	Ceramides	49-57	sterile alpha motif domain containing 8	Homo sapiens	22-26
19506037-7	2009	Our results establish SMSr as a key regulator of ceramide homeostasis that seems to operate as a sensor rather than a converter of ceramides in the ER.	Ceramides	131-140	sterile alpha motif domain containing 8	Homo sapiens	22-26
19385042-3	2009	Over the past decade interest in the role of acid sphingomyelinase has moved beyond its "housekeeping" function in constitutive turnover of sphingomyelin in the lysosome to include study of regulated ceramide generation.	Ceramides	200-208	sphingomyelin phosphodiesterase 1	Homo sapiens	45-66
19171550-2	2009	In many cell types, a fraction of sphingolipids contain 2-hydroxy fatty acids, produced by fatty acid 2-hydroxylase (FA2H), as the N-acyl chain of ceramide [hydroxyl fatty acid (hFA)-sphingolipids].	Ceramides	147-155	fatty acid 2-hydroxylase	Rattus norvegicus	91-115
19144995-3	2009	Here, we report that expression of defective CFTR (DeltaF508CFTR or decreased CFTR) in human lung epithelial cell lines increases sphingolipid synthesis and mass of sphinganine, sphingosine, four long-chain saturated ceramide species, C16 dihydroceramide, C22, C24, C26-ceramide, and sphingomyelin, and decreases mass of C18 and unsaturated C18:1 ceramide species.	Ceramides	217-225	CF transmembrane conductance regulator	Homo sapiens	45-49
19144995-3	2009	Here, we report that expression of defective CFTR (DeltaF508CFTR or decreased CFTR) in human lung epithelial cell lines increases sphingolipid synthesis and mass of sphinganine, sphingosine, four long-chain saturated ceramide species, C16 dihydroceramide, C22, C24, C26-ceramide, and sphingomyelin, and decreases mass of C18 and unsaturated C18:1 ceramide species.	Ceramides	246-254	CF transmembrane conductance regulator	Homo sapiens	45-49
19502811-2	2009	Besides overexpression of MDR1, the member of the ABC transporter family, glucosylceramide synthase (GCS) which allows cellular escape from ceramide-induced cellular apoptosis by mediating ceramide glycosylation was considered to be related with multidrug resistance (MDR) in breast cancer.	Ceramides	82-90	ATP binding cassette subfamily B member 1	Homo sapiens	26-30
19502811-2	2009	Besides overexpression of MDR1, the member of the ABC transporter family, glucosylceramide synthase (GCS) which allows cellular escape from ceramide-induced cellular apoptosis by mediating ceramide glycosylation was considered to be related with multidrug resistance (MDR) in breast cancer.	Ceramides	82-90	UDP-glucose ceramide glucosyltransferase	Homo sapiens	101-104
19502811-2	2009	Besides overexpression of MDR1, the member of the ABC transporter family, glucosylceramide synthase (GCS) which allows cellular escape from ceramide-induced cellular apoptosis by mediating ceramide glycosylation was considered to be related with multidrug resistance (MDR) in breast cancer.	Ceramides	140-148	ATP binding cassette subfamily B member 1	Homo sapiens	26-30
19502811-2	2009	Besides overexpression of MDR1, the member of the ABC transporter family, glucosylceramide synthase (GCS) which allows cellular escape from ceramide-induced cellular apoptosis by mediating ceramide glycosylation was considered to be related with multidrug resistance (MDR) in breast cancer.	Ceramides	140-148	UDP-glucose ceramide glucosyltransferase	Homo sapiens	74-99
19502811-2	2009	Besides overexpression of MDR1, the member of the ABC transporter family, glucosylceramide synthase (GCS) which allows cellular escape from ceramide-induced cellular apoptosis by mediating ceramide glycosylation was considered to be related with multidrug resistance (MDR) in breast cancer.	Ceramides	140-148	UDP-glucose ceramide glucosyltransferase	Homo sapiens	101-104
19454701-6	2009	We also show that ceramide synthesis is strongly induced by XBP-1 (X box-binding protein-1).	Ceramides	18-26	X-box binding protein 1	Homo sapiens	60-65
19454701-6	2009	We also show that ceramide synthesis is strongly induced by XBP-1 (X box-binding protein-1).	Ceramides	18-26	X-box binding protein 1	Homo sapiens	67-90
19476542-4	2009	TNFalpha initiated a rapid increase in ceramide that was associated with increased surface localization of NMDA receptor NR1 subunits and a specific clustering of NR1 phosphorylated on serines 896 and 897 into lipid rafts.	Ceramides	39-47	tumor necrosis factor	Homo sapiens	0-8
19476542-4	2009	TNFalpha initiated a rapid increase in ceramide that was associated with increased surface localization of NMDA receptor NR1 subunits and a specific clustering of NR1 phosphorylated on serines 896 and 897 into lipid rafts.	Ceramides	39-47	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	121-124
19476542-4	2009	TNFalpha initiated a rapid increase in ceramide that was associated with increased surface localization of NMDA receptor NR1 subunits and a specific clustering of NR1 phosphorylated on serines 896 and 897 into lipid rafts.	Ceramides	39-47	glutamate ionotropic receptor NMDA type subunit 1	Homo sapiens	163-166
19476542-6	2009	Pharmacological inhibition or genetic mutation of neutral sphingomyelinase-2 prevented TNFalpha-induced generation of ceramide, phosphorylation of NR1 subunits, clustering of NR1, enhancement of NMDA-evoked calcium flux and excitatory post-synaptic currents.	Ceramides	118-126	sphingomyelin phosphodiesterase 3	Homo sapiens	50-76
19476542-6	2009	Pharmacological inhibition or genetic mutation of neutral sphingomyelinase-2 prevented TNFalpha-induced generation of ceramide, phosphorylation of NR1 subunits, clustering of NR1, enhancement of NMDA-evoked calcium flux and excitatory post-synaptic currents.	Ceramides	118-126	tumor necrosis factor	Homo sapiens	87-95
19171550-2	2009	In many cell types, a fraction of sphingolipids contain 2-hydroxy fatty acids, produced by fatty acid 2-hydroxylase (FA2H), as the N-acyl chain of ceramide [hydroxyl fatty acid (hFA)-sphingolipids].	Ceramides	147-155	fatty acid 2-hydroxylase	Rattus norvegicus	117-121
19171550-7	2009	Partial silencing of FA2H in D6P2T cells resulted in 60-70% reduction of hFA-dihydroceramide and hFA-ceramide, with no effect on nonhydroxy dihydroceramide and ceramide.	Ceramides	84-92	fatty acid 2-hydroxylase	Rattus norvegicus	21-25
19171550-7	2009	Partial silencing of FA2H in D6P2T cells resulted in 60-70% reduction of hFA-dihydroceramide and hFA-ceramide, with no effect on nonhydroxy dihydroceramide and ceramide.	Ceramides	101-109	fatty acid 2-hydroxylase	Rattus norvegicus	21-25
19279008-4	2009	Similarly, knockdown of GBA1 by small interfering RNAs or pharmacological inhibition of GBA1 promoted further activation of p38 after PMA treatment, implicating the GBA1-ceramide pathway in the termination of p38 activation.	Ceramides	170-178	glucosylceramidase beta	Homo sapiens	88-92
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.	Ceramides	100-108	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.	Ceramides	100-108	proline rich transmembrane protein 2	Homo sapiens	32-35
19279008-4	2009	Similarly, knockdown of GBA1 by small interfering RNAs or pharmacological inhibition of GBA1 promoted further activation of p38 after PMA treatment, implicating the GBA1-ceramide pathway in the termination of p38 activation.	Ceramides	170-178	mitogen-activated protein kinase 14	Homo sapiens	209-212
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.	Ceramides	100-108	glucosylceramidase beta	Homo sapiens	192-196
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.	Ceramides	221-229	proline rich transmembrane protein 2	Homo sapiens	14-30
19279008-6	2009	On the other hand, increasing cellular ceramide with cell-permeable ceramide treatment resulted in attenuation of the IL-6 response.	Ceramides	39-47	interleukin 6	Homo sapiens	118-122
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.	Ceramides	221-229	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.	Ceramides	221-229	glucosylceramidase beta	Homo sapiens	192-196
19279008-6	2009	On the other hand, increasing cellular ceramide with cell-permeable ceramide treatment resulted in attenuation of the IL-6 response.	Ceramides	68-76	interleukin 6	Homo sapiens	118-122
19279008-2	2009	Here, we examine the role of the GBA1-ceramide pathway, in regulating a pro-inflammatory pathway initiated by PKC and leading to activation of p38 and induction of interleukin 6 (IL-6).	Ceramides	38-46	glucosylceramidase beta	Homo sapiens	33-37
19279008-9	2009	Thus, the GBA1-ceramide pathway is suggested to play an important role in terminating p38delta activation responsible for IL-6 biosynthesis.	Ceramides	15-23	glucosylceramidase beta	Homo sapiens	10-14
19279008-2	2009	Here, we examine the role of the GBA1-ceramide pathway, in regulating a pro-inflammatory pathway initiated by PKC and leading to activation of p38 and induction of interleukin 6 (IL-6).	Ceramides	38-46	proline rich transmembrane protein 2	Homo sapiens	110-113
19279008-2	2009	Here, we examine the role of the GBA1-ceramide pathway, in regulating a pro-inflammatory pathway initiated by PKC and leading to activation of p38 and induction of interleukin 6 (IL-6).	Ceramides	38-46	mitogen-activated protein kinase 14	Homo sapiens	143-146
19279008-2	2009	Here, we examine the role of the GBA1-ceramide pathway, in regulating a pro-inflammatory pathway initiated by PKC and leading to activation of p38 and induction of interleukin 6 (IL-6).	Ceramides	38-46	interleukin 6	Homo sapiens	164-177
19279008-9	2009	Thus, the GBA1-ceramide pathway is suggested to play an important role in terminating p38delta activation responsible for IL-6 biosynthesis.	Ceramides	15-23	mitogen-activated protein kinase 13	Homo sapiens	86-94
19279008-2	2009	Here, we examine the role of the GBA1-ceramide pathway, in regulating a pro-inflammatory pathway initiated by PKC and leading to activation of p38 and induction of interleukin 6 (IL-6).	Ceramides	38-46	interleukin 6	Homo sapiens	179-183
19279008-3	2009	Inhibition of ceramide formation by fumonisin B1 or down-regulation of PKCdelta potentiated PMA-induced activation of p38 in human breast cancer MCF-7 cells.	Ceramides	14-22	mitogen-activated protein kinase 14	Homo sapiens	118-121
19279008-9	2009	Thus, the GBA1-ceramide pathway is suggested to play an important role in terminating p38delta activation responsible for IL-6 biosynthesis.	Ceramides	15-23	interleukin 6	Homo sapiens	122-126
19279008-4	2009	Similarly, knockdown of GBA1 by small interfering RNAs or pharmacological inhibition of GBA1 promoted further activation of p38 after PMA treatment, implicating the GBA1-ceramide pathway in the termination of p38 activation.	Ceramides	170-178	glucosylceramidase beta	Homo sapiens	24-28
19279008-10	2009	Furthermore, the p38delta isoform was identified as a novel and predominant target of ceramide signaling as well as a regulator of IL-6 biosynthesis.	Ceramides	86-94	mitogen-activated protein kinase 13	Homo sapiens	17-25
19279008-4	2009	Similarly, knockdown of GBA1 by small interfering RNAs or pharmacological inhibition of GBA1 promoted further activation of p38 after PMA treatment, implicating the GBA1-ceramide pathway in the termination of p38 activation.	Ceramides	170-178	glucosylceramidase beta	Homo sapiens	88-92
19279008-4	2009	Similarly, knockdown of GBA1 by small interfering RNAs or pharmacological inhibition of GBA1 promoted further activation of p38 after PMA treatment, implicating the GBA1-ceramide pathway in the termination of p38 activation.	Ceramides	170-178	mitogen-activated protein kinase 14	Homo sapiens	124-127
19279011-1	2009	Activation of protein kinase C (PKC) promotes the salvage pathway of ceramide formation, and acid sphingomyelinase has been implicated, in part, in providing substrate for this pathway (Zeidan, Y. H., and Hannun, Y.	Ceramides	69-77	protein kinase C delta	Homo sapiens	32-35
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.	Ceramides	99-107	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.	Ceramides	99-107	protein kinase C delta	Homo sapiens	152-155
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.	Ceramides	126-134	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.	Ceramides	126-134	protein kinase C delta	Homo sapiens	152-155
19279011-8	2009	Silencing GBA1 by small interfering RNAs significantly attenuated acid glucocerebrosidase activity and decreased PMA-induced formation of ceramide by 50%.	Ceramides	138-146	glucosylceramidase beta	Homo sapiens	10-14
19279011-9	2009	Silencing GBA1 blocked PMA-induced degradation of glucosylceramide and generation of sphingosine, the source for ceramide biosynthesis.	Ceramides	58-66	glucosylceramidase beta	Homo sapiens	10-14
19279011-10	2009	Reciprocally, forced expression of GBA1 increased ceramide levels.	Ceramides	50-58	glucosylceramidase beta	Homo sapiens	35-39
19279011-11	2009	These observations indicate that GBA1 activation can generate the source (sphingosine) for PMA-induced formation of ceramide through the salvage pathway.	Ceramides	116-124	glucosylceramidase beta	Homo sapiens	33-37
19279011-12	2009	Next, the role of PKCdelta, a direct effector of PMA, in the formation of ceramide was determined.	Ceramides	74-82	protein kinase C delta	Homo sapiens	18-26
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.	Ceramides	102-110	protein kinase C delta	Homo sapiens	6-14
19279011-15	2009	Collectively, GBA1 is identified as a novel source of regulated formation of ceramide, and PKCdelta is an upstream regulator of this pathway.	Ceramides	77-85	glucosylceramidase beta	Homo sapiens	14-18
19286927-0	2009	Ceramide-dependent PP2A regulation of TNFalpha-induced IL-8 production in respiratory epithelial cells.	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	19-23
19286927-0	2009	Ceramide-dependent PP2A regulation of TNFalpha-induced IL-8 production in respiratory epithelial cells.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	38-46
19286927-8	2009	Inhibition of the immediate sphingomyelinase-dependent pathway as well as the de novo synthesis pathway of ceramide production reduced serine/threonine phosphatase activity and augmented IL-8 production.	Ceramides	107-115	C-X-C motif chemokine ligand 8	Homo sapiens	187-191
19286927-0	2009	Ceramide-dependent PP2A regulation of TNFalpha-induced IL-8 production in respiratory epithelial cells.	Ceramides	0-8	C-X-C motif chemokine ligand 8	Homo sapiens	55-59
19286927-9	2009	These data suggest that ceramide plays a role in activating PP2A to terminate ongoing IL-8 production.	Ceramides	24-32	protein phosphatase 2 phosphatase activator	Homo sapiens	60-64
19286927-7	2009	Because TNFalpha had been shown to activate ceramide accumulation, and separate studies had linked ceramide with activation of PP2A, we hypothesized the pathway of TNFalpha-inducing ceramide to activate PP2A comprised an endogenous regulatory pathway.	Ceramides	44-52	tumor necrosis factor	Homo sapiens	8-16
19286927-9	2009	These data suggest that ceramide plays a role in activating PP2A to terminate ongoing IL-8 production.	Ceramides	24-32	C-X-C motif chemokine ligand 8	Homo sapiens	86-90
19286927-7	2009	Because TNFalpha had been shown to activate ceramide accumulation, and separate studies had linked ceramide with activation of PP2A, we hypothesized the pathway of TNFalpha-inducing ceramide to activate PP2A comprised an endogenous regulatory pathway.	Ceramides	44-52	tumor necrosis factor	Homo sapiens	164-172
19286927-10	2009	In summary, our data suggest that in respiratory epithelium, TNFalpha induces ceramide accumulation, resulting in subsequent activation of PP2A, which targets those kinases responsible for transcriptional activation of IL-8.	Ceramides	78-86	tumor necrosis factor	Homo sapiens	61-69
19286927-10	2009	In summary, our data suggest that in respiratory epithelium, TNFalpha induces ceramide accumulation, resulting in subsequent activation of PP2A, which targets those kinases responsible for transcriptional activation of IL-8.	Ceramides	78-86	protein phosphatase 2 phosphatase activator	Homo sapiens	139-143
19286927-7	2009	Because TNFalpha had been shown to activate ceramide accumulation, and separate studies had linked ceramide with activation of PP2A, we hypothesized the pathway of TNFalpha-inducing ceramide to activate PP2A comprised an endogenous regulatory pathway.	Ceramides	99-107	protein phosphatase 2 phosphatase activator	Homo sapiens	127-131
19286927-10	2009	In summary, our data suggest that in respiratory epithelium, TNFalpha induces ceramide accumulation, resulting in subsequent activation of PP2A, which targets those kinases responsible for transcriptional activation of IL-8.	Ceramides	78-86	C-X-C motif chemokine ligand 8	Homo sapiens	219-223
19286927-7	2009	Because TNFalpha had been shown to activate ceramide accumulation, and separate studies had linked ceramide with activation of PP2A, we hypothesized the pathway of TNFalpha-inducing ceramide to activate PP2A comprised an endogenous regulatory pathway.	Ceramides	99-107	tumor necrosis factor	Homo sapiens	164-172
19286927-7	2009	Because TNFalpha had been shown to activate ceramide accumulation, and separate studies had linked ceramide with activation of PP2A, we hypothesized the pathway of TNFalpha-inducing ceramide to activate PP2A comprised an endogenous regulatory pathway.	Ceramides	99-107	protein phosphatase 2 phosphatase activator	Homo sapiens	127-131
19286927-7	2009	Because TNFalpha had been shown to activate ceramide accumulation, and separate studies had linked ceramide with activation of PP2A, we hypothesized the pathway of TNFalpha-inducing ceramide to activate PP2A comprised an endogenous regulatory pathway.	Ceramides	99-107	tumor necrosis factor	Homo sapiens	164-172
19323974-6	2009	Moreover, CerK ablation increased serum ceramide levels at the expense of dihydroceramide levels without affecting sphingosine, dihydrosphingosine, sphingosine-1-phosphate or dihydrosphingosine-1-phosphate levels.	Ceramides	40-48	ceramide kinase	Mus musculus	10-14
19337026-2	2009	Like amino acid starvation, ceramide triggers autophagy by interfering with the mTOR-signaling pathway, and by dissociating the Beclin 1:Bcl-2 complex in a c-Jun N-terminal kinase 1 (JNK1)-mediated Bcl-2 phosphorylation-dependent manner.	Ceramides	28-36	mechanistic target of rapamycin kinase	Homo sapiens	80-84
19337026-2	2009	Like amino acid starvation, ceramide triggers autophagy by interfering with the mTOR-signaling pathway, and by dissociating the Beclin 1:Bcl-2 complex in a c-Jun N-terminal kinase 1 (JNK1)-mediated Bcl-2 phosphorylation-dependent manner.	Ceramides	28-36	beclin 1	Homo sapiens	128-136
19337026-2	2009	Like amino acid starvation, ceramide triggers autophagy by interfering with the mTOR-signaling pathway, and by dissociating the Beclin 1:Bcl-2 complex in a c-Jun N-terminal kinase 1 (JNK1)-mediated Bcl-2 phosphorylation-dependent manner.	Ceramides	28-36	BCL2 apoptosis regulator	Homo sapiens	137-142
19337026-2	2009	Like amino acid starvation, ceramide triggers autophagy by interfering with the mTOR-signaling pathway, and by dissociating the Beclin 1:Bcl-2 complex in a c-Jun N-terminal kinase 1 (JNK1)-mediated Bcl-2 phosphorylation-dependent manner.	Ceramides	28-36	mitogen-activated protein kinase 8	Homo sapiens	156-181
19337026-2	2009	Like amino acid starvation, ceramide triggers autophagy by interfering with the mTOR-signaling pathway, and by dissociating the Beclin 1:Bcl-2 complex in a c-Jun N-terminal kinase 1 (JNK1)-mediated Bcl-2 phosphorylation-dependent manner.	Ceramides	28-36	mitogen-activated protein kinase 8	Homo sapiens	183-187
19337026-2	2009	Like amino acid starvation, ceramide triggers autophagy by interfering with the mTOR-signaling pathway, and by dissociating the Beclin 1:Bcl-2 complex in a c-Jun N-terminal kinase 1 (JNK1)-mediated Bcl-2 phosphorylation-dependent manner.	Ceramides	28-36	BCL2 apoptosis regulator	Homo sapiens	198-203
19337026-3	2009	Dissociation of the Beclin 1:Bcl-2 complex, and the subsequent stimulation of autophagy have been observed in various contexts in which the cellular level of long-chain ceramides was increased.	Ceramides	169-178	beclin 1	Homo sapiens	20-28
19337026-3	2009	Dissociation of the Beclin 1:Bcl-2 complex, and the subsequent stimulation of autophagy have been observed in various contexts in which the cellular level of long-chain ceramides was increased.	Ceramides	169-178	BCL2 apoptosis regulator	Homo sapiens	29-34
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.	Ceramides	146-154	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.	Ceramides	146-154	BCL2 apoptosis regulator	Homo sapiens	33-38
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.	Ceramides	235-244	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.	Ceramides	235-244	BCL2 apoptosis regulator	Homo sapiens	33-38
19337026-7	2009	Whether this autophagy that is unchecked by forced dissociation of the Beclin 1:Bcl-2 complex is related to the ability of ceramide to trigger cell death remains an open question.	Ceramides	123-131	beclin 1	Homo sapiens	71-79
19337026-7	2009	Whether this autophagy that is unchecked by forced dissociation of the Beclin 1:Bcl-2 complex is related to the ability of ceramide to trigger cell death remains an open question.	Ceramides	123-131	BCL2 apoptosis regulator	Homo sapiens	80-85
19088082-7	2009	We found that hypoxia increased ceramide content in PASMC which was abrogated by inhibition of nSMase, but not acid sphingomyelinase (aSMase).	Ceramides	32-40	sphingomyelin phosphodiesterase 2	Rattus norvegicus	95-101
19088082-13	2009	CONCLUSION: nSMase-derived ceramide production and the activation of PKCzeta are early and necessary events in the signalling cascade of acute HPV.	Ceramides	27-35	sphingomyelin phosphodiesterase 2	Rattus norvegicus	12-18
19027085-6	2009	Interestingly, de novo ceramide generation was responsible for the drug-induced malignant cell apoptosis through a caspase-3-dependent pathway and a decrease of thrombospondin amount.	Ceramides	23-31	caspase 3	Homo sapiens	115-124
19027085-7	2009	Furthermore, blocking ceramide metabolism by inhibiting glucosylceramide synthase strengthened the camptothecin and doxorubicin-dependent effects.	Ceramides	22-30	UDP-glucose ceramide glucosyltransferase	Homo sapiens	56-81
19417161-0	2009	MDA-7/IL-24-induced cell killing in malignant renal carcinoma cells occurs by a ceramide/CD95/PERK-dependent mechanism.	Ceramides	80-88	interleukin 24	Homo sapiens	0-5
19417161-0	2009	MDA-7/IL-24-induced cell killing in malignant renal carcinoma cells occurs by a ceramide/CD95/PERK-dependent mechanism.	Ceramides	80-88	interleukin 24	Homo sapiens	6-11
19417161-11	2009	Our data show that in kidney cancer cells GST-MDA-7 induces ceramide-dependent activation of CD95, which is causal in promoting an endoplasmic reticulum stress response that activates multiple proapoptotic pathways to decrease survival.	Ceramides	60-68	glutathione S-transferase kappa 1	Homo sapiens	42-45
19417161-11	2009	Our data show that in kidney cancer cells GST-MDA-7 induces ceramide-dependent activation of CD95, which is causal in promoting an endoplasmic reticulum stress response that activates multiple proapoptotic pathways to decrease survival.	Ceramides	60-68	interleukin 24	Homo sapiens	46-51
19417161-11	2009	Our data show that in kidney cancer cells GST-MDA-7 induces ceramide-dependent activation of CD95, which is causal in promoting an endoplasmic reticulum stress response that activates multiple proapoptotic pathways to decrease survival.	Ceramides	60-68	Fas cell surface death receptor	Homo sapiens	93-97
19279183-6	2009	The augmentation of the various ceramides could be assigned to an increase of the messenger RNA levels of ceramide synthases (CerS) LASS2 (longevity assurance), LASS4 and LASS6.	Ceramides	32-41	ceramide synthase 2	Homo sapiens	132-137
19279183-6	2009	The augmentation of the various ceramides could be assigned to an increase of the messenger RNA levels of ceramide synthases (CerS) LASS2 (longevity assurance), LASS4 and LASS6.	Ceramides	32-41	ceramide synthase 4	Homo sapiens	161-166
19279183-6	2009	The augmentation of the various ceramides could be assigned to an increase of the messenger RNA levels of ceramide synthases (CerS) LASS2 (longevity assurance), LASS4 and LASS6.	Ceramides	32-41	ceramide synthase 6	Homo sapiens	171-176
19179362-6	2009	In contrast, the expression level of ceramide, an inducer of cell apoptosis, was increased in the lungs of Fut8(-/-) mice.	Ceramides	37-45	fucosyltransferase 8	Mus musculus	107-111
19179362-9	2009	It is well known that, in emphysema, ceramide expression can be greatly enhanced by blockade of the VEGFR-2.	Ceramides	37-45	kinase insert domain protein receptor	Mus musculus	100-107
19303901-3	2009	Ceramide, the most simple sphingolipid, directly inhibits phosphorylation of the insulin signaling mediator Akt/Protein Kinase B.	Ceramides	0-8	insulin	Homo sapiens	81-88
19435815-0	2009	Nanoliposomal short-chain ceramide inhibits agonist-dependent translocation of neurotensin receptor 1 to structured membrane microdomains in breast cancer cells.	Ceramides	26-34	neurotensin receptor 1	Homo sapiens	79-101
19435815-4	2009	Thus, understanding the biochemical and biophysical regulation of NTSR1 by ceramide can help further define NTSR1 as a novel target in breast cancer.	Ceramides	75-83	neurotensin receptor 1	Homo sapiens	66-71
19435815-4	2009	Thus, understanding the biochemical and biophysical regulation of NTSR1 by ceramide can help further define NTSR1 as a novel target in breast cancer.	Ceramides	75-83	neurotensin receptor 1	Homo sapiens	108-113
19435815-5	2009	Our results show that nanoliposomal formulations of ceramide inhibit NTSR1-mediated MDA-MB-231 breast cancer progression (mitogenesis, migration, and matrix metalloproteinase-9 activity).	Ceramides	52-60	neurotensin receptor 1	Homo sapiens	69-74
19435815-5	2009	Our results show that nanoliposomal formulations of ceramide inhibit NTSR1-mediated MDA-MB-231 breast cancer progression (mitogenesis, migration, and matrix metalloproteinase-9 activity).	Ceramides	52-60	matrix metallopeptidase 9	Homo sapiens	150-176
19435815-6	2009	In addition, liposomal ceramide inhibited NTSR1-mediated, but not phorbol 12-myristate 13-acetate-mediated, activation of the mitogen-activated protein kinase pathway.	Ceramides	23-31	neurotensin receptor 1	Homo sapiens	42-47
19435815-7	2009	Mechanistically, nanoliposomal short-chain ceramide reduces NTSR1 interaction with Galphaq/11 subunits within structured membrane microdomains, consistent with diminished NTS-induced translocation of NTSR1 into membrane microdomains.	Ceramides	43-51	neurotensin receptor 1	Homo sapiens	60-65
19435815-7	2009	Mechanistically, nanoliposomal short-chain ceramide reduces NTSR1 interaction with Galphaq/11 subunits within structured membrane microdomains, consistent with diminished NTS-induced translocation of NTSR1 into membrane microdomains.	Ceramides	43-51	G protein subunit alpha q	Homo sapiens	83-90
19435815-7	2009	Mechanistically, nanoliposomal short-chain ceramide reduces NTSR1 interaction with Galphaq/11 subunits within structured membrane microdomains, consistent with diminished NTS-induced translocation of NTSR1 into membrane microdomains.	Ceramides	43-51	neurotensin receptor 1	Homo sapiens	200-205
19303901-3	2009	Ceramide, the most simple sphingolipid, directly inhibits phosphorylation of the insulin signaling mediator Akt/Protein Kinase B.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	112-128
19372430-6	2009	C. elegans has two ceramide synthases, hyl-1 and hyl-2, that participate in ceramide biogenesis and affect its ability to survive anoxic conditions.	Ceramides	19-27	Ceramide synthase hyl-1;TLC domain-containing protein	Caenorhabditis elegans	39-44
19240026-0	2009	Sphingosine kinase isoforms regulate oxaliplatin sensitivity of human colon cancer cells through ceramide accumulation and Akt activation.	Ceramides	97-105	sphingosine kinase 1	Homo sapiens	0-18
19240026-6	2009	In contrast, in l-OHP-resistant RKO cells, treatment with an SPHK inhibitor or SPHK1 and SPHK2 silencing by RNA interference suppressed cell viability and increased caspase activity and cellular ceramide formation after l-OHP treatment.	Ceramides	195-203	sphingosine kinase 1	Homo sapiens	61-65
19240026-6	2009	In contrast, in l-OHP-resistant RKO cells, treatment with an SPHK inhibitor or SPHK1 and SPHK2 silencing by RNA interference suppressed cell viability and increased caspase activity and cellular ceramide formation after l-OHP treatment.	Ceramides	195-203	sphingosine kinase 1	Homo sapiens	79-84
19240026-6	2009	In contrast, in l-OHP-resistant RKO cells, treatment with an SPHK inhibitor or SPHK1 and SPHK2 silencing by RNA interference suppressed cell viability and increased caspase activity and cellular ceramide formation after l-OHP treatment.	Ceramides	195-203	sphingosine kinase 2	Homo sapiens	89-94
19240026-7	2009	The elevated ceramide formation induced by SPHK inhibition and l-OHP was inhibited by fumonisin B1 but not myriocin, suggesting that ceramide formation was through the salvage pathway.	Ceramides	13-21	sphingosine kinase 1	Homo sapiens	43-47
19240026-7	2009	The elevated ceramide formation induced by SPHK inhibition and l-OHP was inhibited by fumonisin B1 but not myriocin, suggesting that ceramide formation was through the salvage pathway.	Ceramides	133-141	sphingosine kinase 1	Homo sapiens	43-47
19240026-10	2009	These findings indicate that SPHK isoforms and neutral sphingomyelinase contribute to the regulation of chemosensitivity by controlling ceramide formation and the downstream Akt pathway in human colon cancer cells.	Ceramides	136-144	sphingosine kinase 1	Homo sapiens	29-33
19372430-6	2009	C. elegans has two ceramide synthases, hyl-1 and hyl-2, that participate in ceramide biogenesis and affect its ability to survive anoxic conditions.	Ceramides	19-27	Ceramide synthase hyl-2	Caenorhabditis elegans	49-54
19372430-9	2009	These data indicate that specific ceramides produced by HYL-2 confer resistance to anoxia.	Ceramides	34-43	Ceramide synthase hyl-2	Caenorhabditis elegans	56-61
19202357-7	2009	Consistent with this idea, AMPK-deficient cells that are less able to deal with bioenergetic stress are also more sensitive to ceramide than wild-type cells.	Ceramides	127-135	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	27-31
19204004-5	2009	P2X(7) transfectants survived and even proliferated in serum-free conditions and were resistant to apoptosis triggered by ceramide, staurosporin, or intracellular Zn(2+) chelation.	Ceramides	122-130	purinergic receptor P2X 7	Homo sapiens	0-6
19088069-0	2009	Mechanistic insights into the hydrolysis and synthesis of ceramide by neutral ceramidase.	Ceramides	58-66	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	70-88
19193939-6	2009	This impairment of glucose transport induced by resistin plus palmitate could be pharmacologically rescued by the inclusion of aimidazole carboxamide ribonucleotide, a stimulator of AMP-activated protein kinase and FA oxidation, as well as inhibitors of ceramide synthesis (myriocin, fumonisin).	Ceramides	254-262	resistin	Rattus norvegicus	48-56
19193939-7	2009	However, to our surprise, resistin actually blunted the palmitate-induced increase in muscle ceramide content; as expected, ceramide content was significantly lowered by fumonisin.	Ceramides	93-101	resistin	Rattus norvegicus	26-34
19193939-8	2009	In summary, the acute impairment of insulin response by resistin was manifested only in the presence of high palmitate and was alleviated when FA metabolism was manipulated (increased oxidation, inhibited ceramide synthesis).	Ceramides	205-213	resistin	Rattus norvegicus	56-64
19193939-9	2009	Resistin"s acute impairment of insulin response does not appear to require an absolute increase in ceramide content; however, reducing ceramide content alleviated the impairment in glucose transport and insulin signaling.	Ceramides	135-143	resistin	Rattus norvegicus	0-8
19416641-1	2009	We previously reported that incubation of bone-marrow derived macrophages in the absence of macrophage-colony stimulating factor (M-CSF), a cytokine that is essential for their growth and survival, resulted in stimulation of acid sphingomyelinase, accumulation of ceramides, and induction of apoptosis [A. Gomez-Munoz et al.	Ceramides	264-273	colony stimulating factor 1	Homo sapiens	130-135
19252929-2	2009	alpha-4GT1 encodes an alpha-1,4-glycosyltransferase, known to catalyze the fifth step in a series of ceramide glycosylation events.	Ceramides	101-109	alpha1,4-galactosyltransferase 1	Drosophila melanogaster	0-10
19252929-3	2009	As reported for other enzymes involved in the glycosylation of ceramide, alpha-4GT1 is strongly expressed during oogenesis and is deposited maternally in the egg.	Ceramides	63-71	alpha1,4-galactosyltransferase 1	Drosophila melanogaster	73-83
19252929-8	2009	Thus, alpha-4GT1 appears to be an inhibitor of apoptosis, as has previously been observed for other ceramide glycosylating enzymes, suggesting that it likewise contributes to ceramide anchoring in the membrane.	Ceramides	100-108	alpha1,4-galactosyltransferase 1	Drosophila melanogaster	6-16
19136654-12	2009	CNTF-stimulated glucose uptake is impaired in obesity-induced insulin resistance and by ceramide.	Ceramides	88-96	ciliary neurotrophic factor	Mus musculus	0-4
19121379-6	2009	The evidence suggests that activation of caspase 3 was mediated by an Abeta-induced increase in sphingomyelinase, with the subsequent production of ceramide which is known to have a detrimental effect on neuronal function.	Ceramides	148-156	caspase 3	Rattus norvegicus	41-50
19121379-6	2009	The evidence suggests that activation of caspase 3 was mediated by an Abeta-induced increase in sphingomyelinase, with the subsequent production of ceramide which is known to have a detrimental effect on neuronal function.	Ceramides	148-156	amyloid beta precursor protein	Rattus norvegicus	70-75
19139096-5	2009	In contrast, sac1Delta dramatically reduced inositol phosphosphingolipids, which result from the addition of a PtdIns-derived phosphoinositol head group to ceramides through Aur1p.	Ceramides	156-165	phosphatidylinositol-3-phosphatase SAC1	Saccharomyces cerevisiae S288C	13-17
19066337-5	2009	Receptors in the PAQR family share sequence similarity with enzymes involved in ceramide metabolism, which led to the hypothesis that sphingolipids are involved in Izh2p-dependent signaling.	Ceramides	80-88	PAQR-type receptor	Saccharomyces cerevisiae S288C	164-169
19074137-1	2009	Acid sphingomyelinase plays important roles in ceramide homeostasis, which has been proposed to be linked to insulin resistance.	Ceramides	47-55	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
19372554-6	2009	A low level of the ceramide/S1P ratio, associated with a high SphK1 activity, correlates with a robust intrinsic pancreatic cancer cell chemoresistance toward gemcitabine.	Ceramides	19-27	sphingosine kinase 1	Homo sapiens	62-67
19372554-7	2009	Strikingly, increasing the ceramide/S1P ratio, by using pharmacologic (SphK1 inhibitor or ceramide analogue) or small interfering RNA-based approaches to up-regulate intracellular ceramide levels or reduce SphK1 activity, sensitized pancreatic cancer cells to gemcitabine.	Ceramides	27-35	sphingosine kinase 1	Homo sapiens	71-76
19372554-7	2009	Strikingly, increasing the ceramide/S1P ratio, by using pharmacologic (SphK1 inhibitor or ceramide analogue) or small interfering RNA-based approaches to up-regulate intracellular ceramide levels or reduce SphK1 activity, sensitized pancreatic cancer cells to gemcitabine.	Ceramides	27-35	sphingosine kinase 1	Homo sapiens	206-211
19372554-8	2009	Conversely, decreasing the ceramide/S1P ratio, by up-regulating SphK1 activity, promoted gemcitabine resistance in these cells.	Ceramides	27-35	sphingosine kinase 1	Homo sapiens	64-69
19132419-2	2009	Four missense mutations (C133W, C133Y, V144D and G387A) in SPTLC1 were reported to cause HSAN I. SPT catalyses the condensation of Serine and Palmitoyl-CoA, which is the first and rate-limiting step in the de novo synthesis of ceramides.	Ceramides	227-236	serine palmitoyltransferase 1	Cricetulus griseus	59-65
19136560-11	2009	that lysosomal acidification is CFTR-dependent, impaired in CF, or responsible for ceramide accumulation.	Ceramides	83-91	CF transmembrane conductance regulator	Homo sapiens	32-36
19139096-5	2009	In contrast, sac1Delta dramatically reduced inositol phosphosphingolipids, which result from the addition of a PtdIns-derived phosphoinositol head group to ceramides through Aur1p.	Ceramides	156-165	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	174-179
18996148-4	2009	The early inhibition of the neuronal survival pathway regulated by phosphatidil-inositol-3-kinase/protein kinase B or AKT mediated by ceramide may be a relevant early event in the decision of neuronal survival/death.	Ceramides	134-142	protein tyrosine kinase 2 beta	Homo sapiens	98-114
19289047-1	2009	Ceramide-1-phosphate, the phosphorylated form of ceramide, gained attention recently due to its diverse intracellular roles, in particular in inflammation mediated by cPLA(2)alpha.	Ceramides	49-57	phospholipase A2 group IVA	Homo sapiens	167-179
18996148-4	2009	The early inhibition of the neuronal survival pathway regulated by phosphatidil-inositol-3-kinase/protein kinase B or AKT mediated by ceramide may be a relevant early event in the decision of neuronal survival/death.	Ceramides	134-142	AKT serine/threonine kinase 1	Homo sapiens	118-121
18996148-8	2009	Subtle and early metabolic alterations caused by inhibition of the PI3K/AKT pathway mediated by ceramide may potentially work with genes associated with neurodegenerative diseases such as Parkinson"s and Alzheimer"s disease.	Ceramides	96-104	AKT serine/threonine kinase 1	Homo sapiens	72-75
19209467-7	2009	Novel is the recognition that CFTR modulates ceramide mass and uptake of sphingosine-1- phosphate.	Ceramides	45-53	cystic fibrosis transmembrane conductance regulator	Mus musculus	30-34
19101626-1	2009	Ceramide and the metabolites including ceramide-1-phosphate (C1P) and sphingosine are reported to regulate the release of arachidonic acid (AA) and/or phospholipase A(2) (PLA(2)) activity in many cell types including lymphocytes.	Ceramides	0-8	phospholipase A2 group IB	Homo sapiens	151-169
19101626-1	2009	Ceramide and the metabolites including ceramide-1-phosphate (C1P) and sphingosine are reported to regulate the release of arachidonic acid (AA) and/or phospholipase A(2) (PLA(2)) activity in many cell types including lymphocytes.	Ceramides	0-8	phospholipase A2 group IB	Homo sapiens	171-177
19129476-2	2009	OSBP partitions between the endoplasmic reticulum (ER) and Golgi apparatus where it imparts sterol-dependent regulation of ceramide transport and sphingomyelin synthesis.	Ceramides	123-131	oxysterol binding protein	Homo sapiens	0-4
18996115-0	2009	Regulation of thioredoxin by ceramide in retinal pigment epithelial cells.	Ceramides	29-37	thioredoxin	Homo sapiens	14-25
18996115-6	2009	Furthermore, the gene and protein expression of thioredoxin interacting protein (Txnip) increased with ceramide treatment and was significantly (p<0.001) elevated with HGF preincubation vs. untreated controls.	Ceramides	103-111	thioredoxin interacting protein	Homo sapiens	48-79
18996115-6	2009	Furthermore, the gene and protein expression of thioredoxin interacting protein (Txnip) increased with ceramide treatment and was significantly (p<0.001) elevated with HGF preincubation vs. untreated controls.	Ceramides	103-111	thioredoxin interacting protein	Homo sapiens	81-86
18996115-11	2009	Ceramide treatment results in translocation of Trx1 to the nucleus, and upregulation of Txnip expression; exogenous rTrx1 protects from ceramide-induced cell death.	Ceramides	0-8	thioredoxin	Homo sapiens	47-51
18996115-11	2009	Ceramide treatment results in translocation of Trx1 to the nucleus, and upregulation of Txnip expression; exogenous rTrx1 protects from ceramide-induced cell death.	Ceramides	0-8	thioredoxin interacting protein	Homo sapiens	88-93
18996115-12	2009	These results suggest that Trx1 and Txnip play an important role in the response of RPE to ceramide toxicity.	Ceramides	91-99	thioredoxin	Homo sapiens	27-31
18996115-12	2009	These results suggest that Trx1 and Txnip play an important role in the response of RPE to ceramide toxicity.	Ceramides	91-99	thioredoxin interacting protein	Homo sapiens	36-41
19276615-1	2009	Sphingolipid metabolites including ceramide, sphingosine, and their phosphorylated products [sphingosine-1-phosphate (S1P) and ceramide-1-phosphate] regulate cell functions including arachidonic acid (AA) metabolism and cell death.	Ceramides	35-43	sphingosine-1-phosphate receptor 1	Mus musculus	118-121
19028839-1	2009	In this study, the inhibitor 2 of protein phosphatase 2A (I2PP2A) was identified in vitro and in situ as a ceramide-binding protein, which exhibits stereoisomer specificity and fatty acid chain length preference.	Ceramides	107-115	SET nuclear proto-oncogene	Homo sapiens	19-56
19028839-1	2009	In this study, the inhibitor 2 of protein phosphatase 2A (I2PP2A) was identified in vitro and in situ as a ceramide-binding protein, which exhibits stereoisomer specificity and fatty acid chain length preference.	Ceramides	107-115	SET nuclear proto-oncogene	Homo sapiens	58-64
19028839-2	2009	Site- directed mutagenesis coupled with structural details of I2PP2A suggested that VIK 207-209 residues localized on helix 7 are important for ceramide binding and single mutation of K209D altered this interaction.	Ceramides	144-152	SET nuclear proto-oncogene	Homo sapiens	62-68
19028839-2	2009	Site- directed mutagenesis coupled with structural details of I2PP2A suggested that VIK 207-209 residues localized on helix 7 are important for ceramide binding and single mutation of K209D altered this interaction.	Ceramides	144-152	zinc finger protein 655	Homo sapiens	84-87
19028839-4	2009	In addition, studies in A549 human lung cancer cells revealed that ceramide mediates c-Myc degradation via its PP2A-dependent dephosphorylation at S62, and treatment with okadaic acid and expression of c-Myc mutants with S62A or S62D conversions resulted in resistance to ceramide-mediated degradation.	Ceramides	67-75	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	85-90
19028839-4	2009	In addition, studies in A549 human lung cancer cells revealed that ceramide mediates c-Myc degradation via its PP2A-dependent dephosphorylation at S62, and treatment with okadaic acid and expression of c-Myc mutants with S62A or S62D conversions resulted in resistance to ceramide-mediated degradation.	Ceramides	67-75	protein phosphatase 2 phosphatase activator	Homo sapiens	111-115
19028839-4	2009	In addition, studies in A549 human lung cancer cells revealed that ceramide mediates c-Myc degradation via its PP2A-dependent dephosphorylation at S62, and treatment with okadaic acid and expression of c-Myc mutants with S62A or S62D conversions resulted in resistance to ceramide-mediated degradation.	Ceramides	67-75	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	202-207
19028839-4	2009	In addition, studies in A549 human lung cancer cells revealed that ceramide mediates c-Myc degradation via its PP2A-dependent dephosphorylation at S62, and treatment with okadaic acid and expression of c-Myc mutants with S62A or S62D conversions resulted in resistance to ceramide-mediated degradation.	Ceramides	272-280	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	202-207
19028839-5	2009	Importantly, whereas down-regulation of I2PP2A enhanced PP2A-mediated c-Myc degradation in response to ceramide, ectopic expression of wild-type I2PP2A but not of its K209D mutant protected this degradation in A549 cells.	Ceramides	103-111	SET nuclear proto-oncogene	Homo sapiens	40-46
19028839-5	2009	Importantly, whereas down-regulation of I2PP2A enhanced PP2A-mediated c-Myc degradation in response to ceramide, ectopic expression of wild-type I2PP2A but not of its K209D mutant protected this degradation in A549 cells.	Ceramides	103-111	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	70-75
19028839-6	2009	Moreover, expression of wild-type I2PP2A prevented the growth-inhibitory effects of ceramide both against A549 cells and xenograft-driven tumors in situ and in vivo compared with that in controls.	Ceramides	84-92	SET nuclear proto-oncogene	Homo sapiens	34-40
19028839-7	2009	Thus, these results suggest that direct interaction of I2PP2A with ceramide plays important biological roles via the regulation of PP2A activity and signaling, which in turn control ceramide-mediated degradation of c-Myc and antiproliferation.	Ceramides	67-75	SET nuclear proto-oncogene	Homo sapiens	55-61
19028839-7	2009	Thus, these results suggest that direct interaction of I2PP2A with ceramide plays important biological roles via the regulation of PP2A activity and signaling, which in turn control ceramide-mediated degradation of c-Myc and antiproliferation.	Ceramides	67-75	protein phosphatase 2 phosphatase activator	Homo sapiens	57-61
19028839-7	2009	Thus, these results suggest that direct interaction of I2PP2A with ceramide plays important biological roles via the regulation of PP2A activity and signaling, which in turn control ceramide-mediated degradation of c-Myc and antiproliferation.	Ceramides	67-75	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	215-220
19028839-7	2009	Thus, these results suggest that direct interaction of I2PP2A with ceramide plays important biological roles via the regulation of PP2A activity and signaling, which in turn control ceramide-mediated degradation of c-Myc and antiproliferation.	Ceramides	182-190	SET nuclear proto-oncogene	Homo sapiens	55-61
19028839-7	2009	Thus, these results suggest that direct interaction of I2PP2A with ceramide plays important biological roles via the regulation of PP2A activity and signaling, which in turn control ceramide-mediated degradation of c-Myc and antiproliferation.	Ceramides	182-190	protein phosphatase 2 phosphatase activator	Homo sapiens	57-61
19028839-7	2009	Thus, these results suggest that direct interaction of I2PP2A with ceramide plays important biological roles via the regulation of PP2A activity and signaling, which in turn control ceramide-mediated degradation of c-Myc and antiproliferation.	Ceramides	182-190	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	215-220
19210614-2	2009	Here we analysed the lipid profile of lag1Delta lac1Delta mutants lacking acyl-CoA-dependent ceramide synthesis, which require the reverse ceramidase activity of overexpressed Ydc1p for sphingolipid biosynthesis and viability.	Ceramides	93-101	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	176-181
19210614-4	2009	Like wild-type cells, 2Delta.YDC1 cells stop growing when exposed to Aureobasidin A (AbA), an inhibitor of the inositolphosphorylceramide synthase AUR1, yet their ceramide levels remain very low.	Ceramides	129-137	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	29-33
19060920-10	2009	Chromatin immunoprecipitation and luciferase reporter analysis revealed that c-Jun was involved in the regulation of beclin 1 transcription in response to ceramide treatment.	Ceramides	155-163	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	77-82
19137010-2	2009	Resistance in SW620 cells was overcome by exogenous ceramide, leading us to propose that defective ceramide signaling contributes to TRAIL resistance.	Ceramides	52-60	TNF superfamily member 10	Homo sapiens	133-138
19137010-2	2009	Resistance in SW620 cells was overcome by exogenous ceramide, leading us to propose that defective ceramide signaling contributes to TRAIL resistance.	Ceramides	99-107	TNF superfamily member 10	Homo sapiens	133-138
19060920-5	2009	In this study, we used human cancer cell lines CNE2 and Hep3B to investigate the role of JNK-mediated Beclin 1 expression in ceramide-induced autophagic cell death.	Ceramides	125-133	mitogen-activated protein kinase 8	Homo sapiens	89-92
19060920-5	2009	In this study, we used human cancer cell lines CNE2 and Hep3B to investigate the role of JNK-mediated Beclin 1 expression in ceramide-induced autophagic cell death.	Ceramides	125-133	beclin 1	Homo sapiens	102-110
19060920-7	2009	JNK was activated in these two cell lines exposed to ceramide and the phosphorylation of c-Jun also increased.	Ceramides	53-61	mitogen-activated protein kinase 8	Homo sapiens	0-3
19225619-8	2009	The deletion mutant of the IFA38 encoding gene is known for the accumulation of ceramides.	Ceramides	80-89	ketoreductase	Saccharomyces cerevisiae S288C	27-32
19103588-0	2009	Phosphatidylinositol 3-kinase/AKT pathway regulates the endoplasmic reticulum to golgi traffic of ceramide in glioma cells: a link between lipid signaling pathways involved in the control of cell survival.	Ceramides	98-106	AKT serine/threonine kinase 1	Homo sapiens	30-33
19103588-3	2009	A reciprocal control between PI3K/Akt and ceramide signaling in glioma cell survival/death is suggested by data demonstrating a protective role of PI3K/Akt on ceramide-induced cell death in glial cells.	Ceramides	42-50	AKT serine/threonine kinase 1	Homo sapiens	152-155
19103588-3	2009	A reciprocal control between PI3K/Akt and ceramide signaling in glioma cell survival/death is suggested by data demonstrating a protective role of PI3K/Akt on ceramide-induced cell death in glial cells.	Ceramides	159-167	AKT serine/threonine kinase 1	Homo sapiens	34-37
19103588-3	2009	A reciprocal control between PI3K/Akt and ceramide signaling in glioma cell survival/death is suggested by data demonstrating a protective role of PI3K/Akt on ceramide-induced cell death in glial cells.	Ceramides	159-167	AKT serine/threonine kinase 1	Homo sapiens	152-155
19103588-4	2009	In this study we investigated the role of the PI3K/Akt pathway in the regulation of the ceramide metabolism in C6 glioma cells, a cell line in which the PI3K/Akt pathway is constitutively activated.	Ceramides	88-96	AKT serine/threonine kinase 1	Homo sapiens	51-54
19103588-5	2009	Metabolic experiments performed with different radioactive metabolic precursors of sphingolipids and microscopy studies with fluorescent ceramides demonstrated that the chemical inhibition of PI3K and the transfection with a dominant negative Akt strongly inhibited ceramide utilization for the biosynthesis of complex sphingolipids by controlling the endoplasmic reticulum (ER) to Golgi vesicular transport of ceramide.	Ceramides	137-146	AKT serine/threonine kinase 1	Homo sapiens	243-246
19103588-5	2009	Metabolic experiments performed with different radioactive metabolic precursors of sphingolipids and microscopy studies with fluorescent ceramides demonstrated that the chemical inhibition of PI3K and the transfection with a dominant negative Akt strongly inhibited ceramide utilization for the biosynthesis of complex sphingolipids by controlling the endoplasmic reticulum (ER) to Golgi vesicular transport of ceramide.	Ceramides	137-145	AKT serine/threonine kinase 1	Homo sapiens	243-246
19103588-5	2009	Metabolic experiments performed with different radioactive metabolic precursors of sphingolipids and microscopy studies with fluorescent ceramides demonstrated that the chemical inhibition of PI3K and the transfection with a dominant negative Akt strongly inhibited ceramide utilization for the biosynthesis of complex sphingolipids by controlling the endoplasmic reticulum (ER) to Golgi vesicular transport of ceramide.	Ceramides	266-274	AKT serine/threonine kinase 1	Homo sapiens	243-246
19103588-6	2009	These findings constitute the first evidence for a PI3K/Akt-dependent regulation of vesicle-mediated movements of ceramide in the ER-Golgi district.	Ceramides	114-122	AKT serine/threonine kinase 1	Homo sapiens	56-59
19103588-7	2009	Moreover, the findings also suggest the activation of the PI3K/Akt pathway as crucial to coordinate the biosynthesis of membrane complex sphingolipids with cell proliferation and growth and/or to maintain low ceramide levels, especially as concerns those treatments that promote ceramide biosynthesis in the ER.	Ceramides	209-217	AKT serine/threonine kinase 1	Homo sapiens	63-66
19103588-7	2009	Moreover, the findings also suggest the activation of the PI3K/Akt pathway as crucial to coordinate the biosynthesis of membrane complex sphingolipids with cell proliferation and growth and/or to maintain low ceramide levels, especially as concerns those treatments that promote ceramide biosynthesis in the ER.	Ceramides	279-287	AKT serine/threonine kinase 1	Homo sapiens	63-66
19217411-4	2009	Using genetic, biochemical, pharmacological, and functional approaches, we here show that ceramide and staurosporine target PP2A and protein kinases A and C, respectively, in a mitochondria-associated signaling complex to induce dephosphorylation of the BH3-only protein Bad.	Ceramides	90-98	protein phosphatase 2 phosphatase activator	Homo sapiens	124-128
19060920-7	2009	JNK was activated in these two cell lines exposed to ceramide and the phosphorylation of c-Jun also increased.	Ceramides	53-61	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	89-94
19060920-8	2009	In the meantime, we found that ceramide upregulated Beclin 1 expression in cancer cells.	Ceramides	31-39	beclin 1	Homo sapiens	52-60
19060920-10	2009	Chromatin immunoprecipitation and luciferase reporter analysis revealed that c-Jun was involved in the regulation of beclin 1 transcription in response to ceramide treatment.	Ceramides	155-163	beclin 1	Homo sapiens	117-125
19060920-11	2009	In addition, inhibition of JNK activity by SP600125 could inhibit autophagy induction by ceramide.	Ceramides	89-97	mitogen-activated protein kinase 8	Homo sapiens	27-30
19060920-12	2009	Furthermore, Beclin 1 knockdown by siRNA also inhibited ceramide-mediated autophagic cell death.	Ceramides	56-64	beclin 1	Homo sapiens	13-21
19462692-4	2009	Rather than caspase inhibitor, Inhibitor of p38 MAP kinase blocked cell death induced by a short-time treatment with ceramide (<12 h).	Ceramides	117-125	mitogen-activated protein kinase 14	Homo sapiens	44-47
18922131-1	2009	Saturated fatty acids, such as palmitate, promote accumulation of ceramide, which impairs activation and signalling of PKB (protein kinase B; also known as Akt) to important end points such as glucose transport.	Ceramides	66-74	AKT serine/threonine kinase 1	Rattus norvegicus	119-122
18922131-1	2009	Saturated fatty acids, such as palmitate, promote accumulation of ceramide, which impairs activation and signalling of PKB (protein kinase B; also known as Akt) to important end points such as glucose transport.	Ceramides	66-74	AKT serine/threonine kinase 1	Rattus norvegicus	156-159
18922131-2	2009	SPT (serine palmitoyl transferase) is a key enzyme regulating ceramide synthesis from palmitate and represents a potential molecular target in curbing lipid-induced insulin resistance.	Ceramides	62-70	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	0-3
18922131-6	2009	Silencing SPT expression (approximately 90%) by shRNA or chronic cell incubation with myriocin (for 7 days) markedly suppressed SPT activity and palmitate-driven ceramide synthesis; however, challenging these muscle cells with palmitate still inhibited the hormonal activation of PKB.	Ceramides	162-170	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	10-13
18932216-1	2009	In the present study, the roles of telomerase and prostaglandin E(2) (PGE(2)) in platelet-derived growth factor (PDGF"s) and fibroblast growth factor-2 (FGF-2"s) effects against C(2)-ceramide-induced cell death were investigated.	Ceramides	183-191	fibroblast growth factor 2	Mus musculus	125-151
19008343-0	2009	Plasma ceramides are elevated in obese subjects with type 2 diabetes and correlate with the severity of insulin resistance.	Ceramides	7-16	insulin	Homo sapiens	104-111
19008343-2	2009	Ceramides are a putative mediator of insulin resistance and lipotoxicity, and accumulation of ceramides within tissues in obese and diabetic subjects has been well described.	Ceramides	0-9	insulin	Homo sapiens	37-44
19008343-8	2009	Insulin sensitivity was inversely correlated with C18:0, C20:0, C24:1, C24:0, and total ceramide (all P < 0.01).	Ceramides	88-96	insulin	Homo sapiens	0-7
19008343-9	2009	Plasma TNF-alpha concentration was increased (P < 0.05) in type 2 diabetic subjects and correlated with increased C18:1 and C18:0 ceramide subspecies.	Ceramides	133-141	tumor necrosis factor	Homo sapiens	7-16
19008343-10	2009	CONCLUSIONS: Plasma ceramide levels are elevated in type 2 diabetic subjects and may contribute to insulin resistance through activation of inflammatory mediators, such as TNF-alpha.	Ceramides	20-28	insulin	Homo sapiens	99-106
19008343-10	2009	CONCLUSIONS: Plasma ceramide levels are elevated in type 2 diabetic subjects and may contribute to insulin resistance through activation of inflammatory mediators, such as TNF-alpha.	Ceramides	20-28	tumor necrosis factor	Homo sapiens	172-181
18716795-3	2009	NGF treatment of breast cancer cells activates NF-kappaB resulting in the inhibition of ceramide-induced apoptosis.	Ceramides	88-96	nerve growth factor	Homo sapiens	0-3
18932216-1	2009	In the present study, the roles of telomerase and prostaglandin E(2) (PGE(2)) in platelet-derived growth factor (PDGF"s) and fibroblast growth factor-2 (FGF-2"s) effects against C(2)-ceramide-induced cell death were investigated.	Ceramides	183-191	fibroblast growth factor 2	Mus musculus	153-158
18932216-10	2009	The involvement of COX-2/PGE(2)-mediated telomerase activation by PDGF and FGF-2 against C(2)-ceramide-induced cell death is first demonstrated herein.	Ceramides	94-102	prostaglandin-endoperoxide synthase 2	Mus musculus	19-24
18932216-10	2009	The involvement of COX-2/PGE(2)-mediated telomerase activation by PDGF and FGF-2 against C(2)-ceramide-induced cell death is first demonstrated herein.	Ceramides	94-102	fibroblast growth factor 2	Mus musculus	75-80
19139267-1	2009	Ceramide transfer protein (CERT) functions in the transfer of ceramide from the endoplasmic reticulum (ER) to the Golgi.	Ceramides	62-70	ceramide transporter 1	Mus musculus	0-25
19239851-6	2009	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3-6, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	steroidogenic acute regulatory protein	Homo sapiens	112-118
19239851-6	2009	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3-6, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 3	Homo sapiens	119-127
19239851-6	2009	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3-6, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 5	Homo sapiens	129-135
19239851-6	2009	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3-6, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	phosphatidylcholine transfer protein	Homo sapiens	137-143
19239851-6	2009	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3-6, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 10	Homo sapiens	144-151
19239851-6	2009	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3-6, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 10	Homo sapiens	153-160
19239851-6	2009	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3-6, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	ceramide transporter 1	Homo sapiens	165-172
19029119-0	2009	Role of JNK1-dependent Bcl-2 phosphorylation in ceramide-induced macroautophagy.	Ceramides	48-56	mitogen-activated protein kinase 8	Homo sapiens	8-12
19029119-0	2009	Role of JNK1-dependent Bcl-2 phosphorylation in ceramide-induced macroautophagy.	Ceramides	48-56	BCL2 apoptosis regulator	Homo sapiens	23-28
19029119-3	2009	Here we show that short-chain ceramides (C(2)-ceramide and C(6)-ceramide) and stimulation of the de novo ceramide synthesis by tamoxifen induce the dissociation of the complex formed between the autophagy protein Beclin 1 and the anti-apoptotic protein Bcl-2.	Ceramides	30-39	beclin 1	Homo sapiens	213-221
19029119-3	2009	Here we show that short-chain ceramides (C(2)-ceramide and C(6)-ceramide) and stimulation of the de novo ceramide synthesis by tamoxifen induce the dissociation of the complex formed between the autophagy protein Beclin 1 and the anti-apoptotic protein Bcl-2.	Ceramides	30-39	BCL2 apoptosis regulator	Homo sapiens	253-258
19029119-3	2009	Here we show that short-chain ceramides (C(2)-ceramide and C(6)-ceramide) and stimulation of the de novo ceramide synthesis by tamoxifen induce the dissociation of the complex formed between the autophagy protein Beclin 1 and the anti-apoptotic protein Bcl-2.	Ceramides	30-38	beclin 1	Homo sapiens	213-221
19029119-3	2009	Here we show that short-chain ceramides (C(2)-ceramide and C(6)-ceramide) and stimulation of the de novo ceramide synthesis by tamoxifen induce the dissociation of the complex formed between the autophagy protein Beclin 1 and the anti-apoptotic protein Bcl-2.	Ceramides	30-38	BCL2 apoptosis regulator	Homo sapiens	253-258
19029119-6	2009	We further show that activation of c-Jun N-terminal protein kinase 1 by ceramide is required both to phosphorylate Bcl-2 and to stimulate macroautophagy.	Ceramides	72-80	BCL2 apoptosis regulator	Homo sapiens	115-120
19139267-1	2009	Ceramide transfer protein (CERT) functions in the transfer of ceramide from the endoplasmic reticulum (ER) to the Golgi.	Ceramides	62-70	ceramide transporter 1	Mus musculus	27-31
19139267-3	2009	CERT mutant embryos accumulate ceramide in the ER but also mislocalize ceramide to the mitochondria, compromising their function.	Ceramides	31-39	ceramide transporter 1	Mus musculus	0-4
19139267-3	2009	CERT mutant embryos accumulate ceramide in the ER but also mislocalize ceramide to the mitochondria, compromising their function.	Ceramides	71-79	ceramide transporter 1	Mus musculus	0-4
19139267-9	2009	Thus, global compromise of ER and mitochondrial integrity caused by ceramide accumulation in CERT mutant mice primarily affects organogenesis rather than causing cell death via apoptotic pathways.	Ceramides	68-76	ceramide transporter 1	Mus musculus	93-97
19029835-8	2009	These findings support a model in which activation of PKCalpha downregulates ATM, thus relieving CS repression by ATM and enhancing apoptosis via ceramide generation.	Ceramides	146-154	protein kinase C alpha	Homo sapiens	54-62
18831956-0	2009	A secondary assay for ceramide kinase inhibitors based on cell growth inhibition by short-chain ceramides.	Ceramides	96-105	ceramide kinase	Homo sapiens	22-37
18831956-1	2009	We recently reported that ectopic expression of ceramide kinase (CerK) in various cell lines increases their sensitivity to cell death induced by the exogenous addition of short-chain (e.g., C2) ceramides (Cer).	Ceramides	195-204	ceramide kinase	Homo sapiens	48-63
18831956-1	2009	We recently reported that ectopic expression of ceramide kinase (CerK) in various cell lines increases their sensitivity to cell death induced by the exogenous addition of short-chain (e.g., C2) ceramides (Cer).	Ceramides	195-204	ceramide kinase	Homo sapiens	65-69
19029835-8	2009	These findings support a model in which activation of PKCalpha downregulates ATM, thus relieving CS repression by ATM and enhancing apoptosis via ceramide generation.	Ceramides	146-154	ATM serine/threonine kinase	Homo sapiens	77-80
18986321-9	2009	Stable overexpression of the triglyceride lipase adipose triglyceride lipase (ATGL) reduced IMTG content in myotubes, but resulted in a concomitant increase in diacylglycerol (DAG) and ceramide and caused insulin resistance.	Ceramides	185-193	patatin-like phospholipase domain containing 2	Mus musculus	78-82
19127120-0	2009	Ceramide-mediated apoptosis following ionizing radiation in human prostate cancer cells: PKCalpha joins the fray.	Ceramides	0-8	protein kinase C alpha	Homo sapiens	89-97
18986321-11	2009	Conversely, overexpression of DGAT2 in glycolytic muscle resulted in accumulation of TG and ceramide and insulin resistance in these tissues.	Ceramides	92-100	diacylglycerol O-acyltransferase 2	Mus musculus	30-35
18801905-7	2009	Concomitant with these results, leptin decreased the mRNA levels of enzymes involved in de novo ceramide synthesis (SPT-1, LASS2, LASS4) and ceramide production from sphingomyelin (SMPD-1/2).	Ceramides	96-104	salivary protein 1	Rattus norvegicus	116-121
19037882-10	2009	Glucocorticoids, cAMP and TGF-beta (transforming growth factor-beta) have stimulatory effects on TTF-1 expression, whereas TNF-alpha (tumour necrosis factor-alpha) and ceramide have inhibitory effects on TTF-1 DNA-binding activity in lung cells.	Ceramides	168-176	transcription termination factor 1	Homo sapiens	204-209
18801905-7	2009	Concomitant with these results, leptin decreased the mRNA levels of enzymes involved in de novo ceramide synthesis (SPT-1, LASS2, LASS4) and ceramide production from sphingomyelin (SMPD-1/2).	Ceramides	96-104	ceramide synthase 4	Rattus norvegicus	130-135
18801905-8	2009	The mRNA levels of enzymes of ceramide degradation (Asah1/2) and utilization (sphingomyelin synthase, ceramide kinase, glycosyl-ceramide synthase, GM3 synthase) were also down-regulated.	Ceramides	30-38	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	52-59
18820034-0	2009	Ceramide activates JNK to inhibit a cAMP-gated K+ conductance and Cl- secretion in intestinal epithelia.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	19-22
19571611-6	2009	Ceramide was quantified as a potential target of THP action.	Ceramides	0-8	uromodulin	Rattus norvegicus	49-52
19529829-0	2009	HOS3, an ELO-like gene, inhibits effects of ABA and implicates a S-1-P/ceramide control system for abiotic stress responses in Arabidopsis thaliana.	Ceramides	71-79	histone deacetylase	Saccharomyces cerevisiae S288C	0-4
18820034-7	2009	Thus, conversion of sphingomyelin to ceramide in basolateral membranes of intestinal cells rapidly activates JNK to inhibit a cAMP-gated K(+) conductance and thereby attenuates Cl(-) secretion.	Ceramides	37-45	mitogen-activated protein kinase 8	Homo sapiens	109-112
19387107-4	2009	Since ceramides are neurotoxic and cause insulin resistance, we directly investigated the role of ceramides as mediators of neurodegeneration using an in vitro culture model.	Ceramides	6-15	insulin	Homo sapiens	41-48
19005213-2	2009	For the synthesis of sphingomyelin, ceramide is transported from the endoplasmic reticulum to the Golgi apparatus by the ceramide transfer protein CERT.	Ceramides	36-44	ceramide transporter 1	Homo sapiens	147-151
19005213-6	2009	In a transformant stably expressing CKIgamma2, CERT was hyperphosphorylated, and the intracellular trafficking of ceramide was retarded, thereby reducing de novo sphingomyelin synthesis.	Ceramides	114-122	casein kinase 1 gamma 2	Homo sapiens	36-45
19276645-4	2009	The purpose of this study was to determine the effects of c2-ceramide (ceramide) on the cell viability and expression of TGF-beta, MMP-1 and elastin in cultured keratinocytes and fibroblasts.	Ceramides	61-69	matrix metallopeptidase 1	Homo sapiens	131-136
18393629-2	2009	Here, we report that ceramide, a bioactive sphingolipid, selectively eliminates hES cells differentially expressing nestin and Tuj1.	Ceramides	21-29	ribosome binding protein 1	Homo sapiens	80-83
18393629-4	2009	Ceramide-resistant hES cells express higher levels of the messenger RNA for ceramide-metabolizing enzymes that convert ceramide into pro-mitogenic metabolites.	Ceramides	0-8	ribosome binding protein 1	Homo sapiens	19-22
18393629-4	2009	Ceramide-resistant hES cells express higher levels of the messenger RNA for ceramide-metabolizing enzymes that convert ceramide into pro-mitogenic metabolites.	Ceramides	76-84	ribosome binding protein 1	Homo sapiens	19-22
18393629-4	2009	Ceramide-resistant hES cells express higher levels of the messenger RNA for ceramide-metabolizing enzymes that convert ceramide into pro-mitogenic metabolites.	Ceramides	119-127	ribosome binding protein 1	Homo sapiens	19-22
18393629-5	2009	Based on these findings, we conducted long-term studies to determine whether liposomal ceramide can be used to maintain undifferentiated hES cells free of feeder cells.	Ceramides	87-95	ribosome binding protein 1	Homo sapiens	137-140
18393629-6	2009	We continuously cultured hES cells on matrigel for 4 months with liposomal ceramide in a feeder cell-free system.	Ceramides	75-83	ribosome binding protein 1	Homo sapiens	25-28
18393629-7	2009	Human ES cells treated with liposomal ceramide maintained their pluripotent state as determined by in vivo and in vitro differentiation studies and contained no chromosomal abnormalities.	Ceramides	38-46	ribosome binding protein 1	Homo sapiens	6-8
18393629-8	2009	In conclusion, our findings suggest that exposure to ceramide provides a viable strategy to prevent premature hES cell differentiation and to maintain pluripotent stem cell populations in the absence of feeder cells.	Ceramides	53-61	ribosome binding protein 1	Homo sapiens	110-113
19276645-4	2009	The purpose of this study was to determine the effects of c2-ceramide (ceramide) on the cell viability and expression of TGF-beta, MMP-1 and elastin in cultured keratinocytes and fibroblasts.	Ceramides	61-69	transforming growth factor beta 1	Homo sapiens	121-129
19276645-4	2009	The purpose of this study was to determine the effects of c2-ceramide (ceramide) on the cell viability and expression of TGF-beta, MMP-1 and elastin in cultured keratinocytes and fibroblasts.	Ceramides	61-69	elastin	Homo sapiens	141-148
19276645-5	2009	Ceramide inhibited keratinocyte cell viability by apoptosis and stimulated expression of elastin, MMP-1 and TGF-beta, suggesting improved epidermal functioning by a TGF-beta mechanism.	Ceramides	0-8	elastin	Homo sapiens	89-96
19276645-5	2009	Ceramide inhibited keratinocyte cell viability by apoptosis and stimulated expression of elastin, MMP-1 and TGF-beta, suggesting improved epidermal functioning by a TGF-beta mechanism.	Ceramides	0-8	matrix metallopeptidase 1	Homo sapiens	98-103
19276645-5	2009	Ceramide inhibited keratinocyte cell viability by apoptosis and stimulated expression of elastin, MMP-1 and TGF-beta, suggesting improved epidermal functioning by a TGF-beta mechanism.	Ceramides	0-8	transforming growth factor beta 1	Homo sapiens	108-116
19276645-5	2009	Ceramide inhibited keratinocyte cell viability by apoptosis and stimulated expression of elastin, MMP-1 and TGF-beta, suggesting improved epidermal functioning by a TGF-beta mechanism.	Ceramides	0-8	transforming growth factor beta 1	Homo sapiens	165-173
19276645-6	2009	Conversely, ceramide stimulated fibroblast cell growth at the lower concentrations and inhibited the expression of MMP-1, elastin and TGF-beta, which indicates a predominantly beneficial effect in the prevention of photoaging-associated dermal alterationby TGF-beta and non-TGF-beta mechanisms.	Ceramides	12-20	matrix metallopeptidase 1	Homo sapiens	115-120
19276645-6	2009	Conversely, ceramide stimulated fibroblast cell growth at the lower concentrations and inhibited the expression of MMP-1, elastin and TGF-beta, which indicates a predominantly beneficial effect in the prevention of photoaging-associated dermal alterationby TGF-beta and non-TGF-beta mechanisms.	Ceramides	12-20	elastin	Homo sapiens	122-129
19276645-6	2009	Conversely, ceramide stimulated fibroblast cell growth at the lower concentrations and inhibited the expression of MMP-1, elastin and TGF-beta, which indicates a predominantly beneficial effect in the prevention of photoaging-associated dermal alterationby TGF-beta and non-TGF-beta mechanisms.	Ceramides	12-20	transforming growth factor beta 1	Homo sapiens	134-142
19276645-6	2009	Conversely, ceramide stimulated fibroblast cell growth at the lower concentrations and inhibited the expression of MMP-1, elastin and TGF-beta, which indicates a predominantly beneficial effect in the prevention of photoaging-associated dermal alterationby TGF-beta and non-TGF-beta mechanisms.	Ceramides	12-20	transforming growth factor beta 1	Homo sapiens	257-265
19276645-6	2009	Conversely, ceramide stimulated fibroblast cell growth at the lower concentrations and inhibited the expression of MMP-1, elastin and TGF-beta, which indicates a predominantly beneficial effect in the prevention of photoaging-associated dermal alterationby TGF-beta and non-TGF-beta mechanisms.	Ceramides	12-20	transforming growth factor beta 1	Homo sapiens	257-265
19276645-7	2009	The regulation of MMP-1 expression by ceramide was transcriptionally mediated and via the activator protein-1 sequence in both keratinocytes and fibroblasts.	Ceramides	38-46	matrix metallopeptidase 1	Homo sapiens	18-23
19356099-1	2008	We studied endogenous substrates for P-glycoprotein (P-gp) in an oxidative reaction mixture of ceramides, phospholipids, sphingolipids, or GM1-gangliosides (GM1-G).	Ceramides	95-104	ATP binding cassette subfamily B member 1	Homo sapiens	37-51
18722999-7	2008	The competition between ceramide and cholesterol for interaction with sphingomyelin is discussed in terms of control of lipid-mediated signaling pathways by sphingomyelinase and phospholipase A2.	Ceramides	24-32	phospholipase A2 group IB	Homo sapiens	178-194
18952671-4	2008	We show here that EEG seizures induced by intrahippocampal injection of kainic acid in C57BL6 adult mice were increased by 2-fold on average by pre-exposure to IL-1beta and this effect was blocked by 3-O-methylsphingomyelin (3-O-MS), a selective inhibitor of the ceramide-producing enzyme sphingomyelinase.	Ceramides	263-271	interleukin 1 beta	Mus musculus	160-168
18952671-5	2008	C2-ceramide, a cell permeable analog of ceramide, mimicked IL-1beta action suggesting that ceramide may be the second messenger of the proconvulsive effect of IL-1beta.	Ceramides	3-11	interleukin 1 beta	Homo sapiens	59-67
18952671-5	2008	C2-ceramide, a cell permeable analog of ceramide, mimicked IL-1beta action suggesting that ceramide may be the second messenger of the proconvulsive effect of IL-1beta.	Ceramides	3-11	interleukin 1 beta	Homo sapiens	159-167
18952671-5	2008	C2-ceramide, a cell permeable analog of ceramide, mimicked IL-1beta action suggesting that ceramide may be the second messenger of the proconvulsive effect of IL-1beta.	Ceramides	40-48	interleukin 1 beta	Homo sapiens	59-67
18952671-5	2008	C2-ceramide, a cell permeable analog of ceramide, mimicked IL-1beta action suggesting that ceramide may be the second messenger of the proconvulsive effect of IL-1beta.	Ceramides	40-48	interleukin 1 beta	Homo sapiens	159-167
18936091-0	2008	Calcium-independent phospholipase A2 (iPLA2 beta)-mediated ceramide generation plays a key role in the cross-talk between the endoplasmic reticulum (ER) and mitochondria during ER stress-induced insulin-secreting cell apoptosis.	Ceramides	59-67	phospholipase A2 group VI	Rattus norvegicus	38-48
18936091-1	2008	Endoplasmic reticulum (ER) stress induces INS-1 cell apoptosis by a pathway involving Ca(2+)-independent phospholipase A(2) (iPLA(2)beta)-mediated ceramide generation, but the mechanism by which iPLA(2)beta and ceramides contribute to apoptosis is not well understood.	Ceramides	147-155	phospholipase A2 group VI	Rattus norvegicus	125-136
18936091-8	2008	ER stress-induced mitochondrial dysfunction and apoptosis are also inhibited by forskolin, as well as by inactivation of iPLA(2)beta or NSMase, suggesting that iPLA(2)beta-mediated generation of ceramides via sphingomyelin hydrolysis during ER stress affect the mitochondria.	Ceramides	195-204	sphingomyelin phosphodiesterase 2	Rattus norvegicus	136-142
18936091-8	2008	ER stress-induced mitochondrial dysfunction and apoptosis are also inhibited by forskolin, as well as by inactivation of iPLA(2)beta or NSMase, suggesting that iPLA(2)beta-mediated generation of ceramides via sphingomyelin hydrolysis during ER stress affect the mitochondria.	Ceramides	195-204	phospholipase A2 group VI	Rattus norvegicus	160-171
18936091-10	2008	Collectively, our findings indicate that the iPLA(2)beta-ceramide axis plays a critical role in activating the mitochondrial apoptotic pathway in insulin-secreting cells during ER stress.	Ceramides	57-65	phospholipase A2 group VI	Rattus norvegicus	45-56
19019774-3	2008	Less well studied is the role of the follicular lymphoma variant translocation 1 (FVT1) gene, which was identified through its involvement in an atypical follicular lymphoma translocation and which encodes an enzyme in the synthetic pathway of ceramide.	Ceramides	244-252	3-ketodihydrosphingosine reductase	Homo sapiens	37-80
19019774-3	2008	Less well studied is the role of the follicular lymphoma variant translocation 1 (FVT1) gene, which was identified through its involvement in an atypical follicular lymphoma translocation and which encodes an enzyme in the synthetic pathway of ceramide.	Ceramides	244-252	3-ketodihydrosphingosine reductase	Homo sapiens	82-86
19047095-0	2008	Cannabinoid receptor activation induces apoptosis through tumor necrosis factor alpha-mediated ceramide de novo synthesis in colon cancer cells.	Ceramides	95-103	tumor necrosis factor	Homo sapiens	58-85
19047095-7	2008	The activation of the CB1 and, more efficiently, of the CB2 receptors induced apoptosis and increased ceramide levels in the DLD-1 and HT29 cells.	Ceramides	102-110	cannabinoid receptor 1	Homo sapiens	22-25
19047095-7	2008	The activation of the CB1 and, more efficiently, of the CB2 receptors induced apoptosis and increased ceramide levels in the DLD-1 and HT29 cells.	Ceramides	102-110	cannabinoid receptor 2	Homo sapiens	56-59
19047095-10	2008	The knockdown of TNF-alpha mRNA abrogated the ceramide increase and, therefore, the apoptotic effect induced by cannabinoid receptor activation.	Ceramides	46-54	tumor necrosis factor	Homo sapiens	17-26
19047095-11	2008	CONCLUSIONS: The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells.	Ceramides	106-114	cannabinoid receptor 1	Homo sapiens	49-52
19047095-11	2008	CONCLUSIONS: The present study shows that either CB1 or CB2 receptor activation induces apoptosis through ceramide de novo synthesis in colon cancer cells.	Ceramides	106-114	cannabinoid receptor 2	Homo sapiens	56-59
19047095-12	2008	Our data unveiled, for the first time, that TNF-alpha acts as a link between cannabinoid receptor activation and ceramide production.	Ceramides	113-121	tumor necrosis factor	Homo sapiens	44-53
19356099-1	2008	We studied endogenous substrates for P-glycoprotein (P-gp) in an oxidative reaction mixture of ceramides, phospholipids, sphingolipids, or GM1-gangliosides (GM1-G).	Ceramides	95-104	ATP binding cassette subfamily B member 1	Homo sapiens	53-57
18721197-0	2008	Inhibition of atopic dermatitis-like skin lesions by topical application of a novel ceramide derivative, K6PC-9p, in NC/Nga mice.	Ceramides	84-92	reticulon 4	Mus musculus	120-123
18664717-0	2008	Ceramide accelerates ultraviolet-induced MMP-1 expression through JAK1/STAT-1 pathway in cultured human dermal fibroblasts.	Ceramides	0-8	matrix metallopeptidase 1	Homo sapiens	41-46
18664717-0	2008	Ceramide accelerates ultraviolet-induced MMP-1 expression through JAK1/STAT-1 pathway in cultured human dermal fibroblasts.	Ceramides	0-8	Janus kinase 1	Homo sapiens	66-70
18664717-0	2008	Ceramide accelerates ultraviolet-induced MMP-1 expression through JAK1/STAT-1 pathway in cultured human dermal fibroblasts.	Ceramides	0-8	signal transducer and activator of transcription 1	Homo sapiens	71-77
18664717-2	2008	Here, we investigated the effects of ceramide on UV-induced matrix metalloproteinase-1 (MMP-1) expression in human dermal fibroblasts.	Ceramides	37-45	matrix metallopeptidase 1	Homo sapiens	60-86
18664717-2	2008	Here, we investigated the effects of ceramide on UV-induced matrix metalloproteinase-1 (MMP-1) expression in human dermal fibroblasts.	Ceramides	37-45	matrix metallopeptidase 1	Homo sapiens	88-93
18664717-5	2008	On the other hand, basal and UV-induced MMP-1 expression was increased through induction of intracellular ceramide by D-MAPP, a ceramidase inhibitor.	Ceramides	106-114	matrix metallopeptidase 1	Homo sapiens	40-45
18664717-6	2008	Our results also showed that MMP-1 protein expression was dose-dependently increased by C(2)-ceramide or SMase treatment.	Ceramides	93-101	matrix metallopeptidase 1	Homo sapiens	29-34
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	18-26	signal transducer and activator of transcription 1	Homo sapiens	80-131
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	18-26	signal transducer and activator of transcription 1	Homo sapiens	133-139
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	18-26	matrix metallopeptidase 1	Homo sapiens	167-172
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	18-26	Janus kinase 1	Homo sapiens	237-241
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	18-26	Janus kinase 3	Homo sapiens	291-295
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	18-26	Janus kinase 2	Homo sapiens	315-320
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	43-51	signal transducer and activator of transcription 1	Homo sapiens	80-131
18664717-7	2008	The activation of ceramide pathway by C(2)-ceramide enhanced phosphorylation of signal transducer and activators of transcription-1 (STAT-1), whereas ceramide-induced MMP-1 expression was potently prevented by piceatannol; Janus kinase (JAK1) inhibtor; and WHI-P131, a specific inhibitor of JAK3; but not by AG490, JAK 2 inhbitor, in human dermal fibroblasts.	Ceramides	43-51	signal transducer and activator of transcription 1	Homo sapiens	133-139
18664717-9	2008	Overall, we demonstrate that induction of intracellular ceramide by UV may activate MMP-1 gene expression via JAK1/STAT-1 pathway.	Ceramides	56-64	matrix metallopeptidase 1	Homo sapiens	84-89
18664717-9	2008	Overall, we demonstrate that induction of intracellular ceramide by UV may activate MMP-1 gene expression via JAK1/STAT-1 pathway.	Ceramides	56-64	Janus kinase 1	Homo sapiens	110-114
18664717-9	2008	Overall, we demonstrate that induction of intracellular ceramide by UV may activate MMP-1 gene expression via JAK1/STAT-1 pathway.	Ceramides	56-64	signal transducer and activator of transcription 1	Homo sapiens	115-121
18680775-7	2008	However, ceramide upregulated expression of cytosolic phospholipase-A(2) (cPLA(2)) and cyclooxygenase-2 (COX-2).	Ceramides	9-17	phospholipase A2 group IVA	Rattus norvegicus	44-72
18680775-7	2008	However, ceramide upregulated expression of cytosolic phospholipase-A(2) (cPLA(2)) and cyclooxygenase-2 (COX-2).	Ceramides	9-17	phospholipase A2 group IVA	Rattus norvegicus	74-81
18680775-7	2008	However, ceramide upregulated expression of cytosolic phospholipase-A(2) (cPLA(2)) and cyclooxygenase-2 (COX-2).	Ceramides	9-17	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	87-103
18680775-7	2008	However, ceramide upregulated expression of cytosolic phospholipase-A(2) (cPLA(2)) and cyclooxygenase-2 (COX-2).	Ceramides	9-17	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	105-110
18948750-0	2008	Ceramide promotes apoptosis in chronic myelogenous leukemia-derived K562 cells by a mechanism involving caspase-8 and JNK.	Ceramides	0-8	caspase 8	Homo sapiens	104-113
18948750-0	2008	Ceramide promotes apoptosis in chronic myelogenous leukemia-derived K562 cells by a mechanism involving caspase-8 and JNK.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	118-121
18948750-1	2008	Ceramide is a sphingolipid that activates stress kinases such as p38 and c-JUN N-Terminal Kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 14	Homo sapiens	65-68
18948750-1	2008	Ceramide is a sphingolipid that activates stress kinases such as p38 and c-JUN N-Terminal Kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	73-96
18948750-1	2008	Ceramide is a sphingolipid that activates stress kinases such as p38 and c-JUN N-Terminal Kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	98-101
18948750-4	2008	The sphingolipid killed CML derived KBM5 cells and, to a lesser extent, imatinib-resistant KBM5-STI cells suggesting that BCR-ABL can not completely block C6-ceramide-induced apoptosis but the kinase may regulate the process.	Ceramides	158-166	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	122-129
18664717-10	2008	Therefore, we suggest that targeted modulation of the ceramide signaling pathway may offer a novel therapeutic approach for inhibiting MMP-1 expression, which is a causing gene of skin aging.	Ceramides	54-62	matrix metallopeptidase 1	Homo sapiens	135-140
18772496-4	2008	Further studies demonstrated that these ceramide molecules in LR platforms were colocalized with ASMase, a ceramide producing enzyme.	Ceramides	40-48	sphingomyelin phosphodiesterase 1	Homo sapiens	97-103
18772496-4	2008	Further studies demonstrated that these ceramide molecules in LR platforms were colocalized with ASMase, a ceramide producing enzyme.	Ceramides	107-115	sphingomyelin phosphodiesterase 1	Homo sapiens	97-103
18785922-2	2008	These contacts may be the site of ceramide transfer from its site of synthesis (ER) to sphingomyelin (SM) synthase through ceramide transfer protein (CERT).	Ceramides	34-42	sphingomyelin synthase 2	Homo sapiens	87-114
18574733-6	2008	Ceramides, which production can be induced by death factors such as FasL or TNFalpha, are involved in the control of cell survival during brain development through activation of caspase-dependent mechanisms.	Ceramides	0-9	Fas ligand	Homo sapiens	68-72
18574733-6	2008	Ceramides, which production can be induced by death factors such as FasL or TNFalpha, are involved in the control of cell survival during brain development through activation of caspase-dependent mechanisms.	Ceramides	0-9	tumor necrosis factor	Homo sapiens	76-84
18805722-5	2008	Transduction of Farber patient fibroblasts and B cells with these vectors resulted in overexpression of AC and led to a 90% and 50% reduction in the accumulation of ceramide, respectively.	Ceramides	165-173	N-acylsphingosine amidohydrolase 1	Homo sapiens	104-106
18753406-5	2008	The data link TGN/endosomal dynamics with ceramide homeostasis, UPR activity, and TOR signaling in yeast, and they identify the Sit4 protein phosphatase as a primary conduit through which ceramides link to the UPR.	Ceramides	188-197	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	128-132
18787039-6	2008	Furthermore, a synthetic LXR ligand induces the expression of differentiation markers, ceramide biosynthesis enzymes, and lipid synthesis and transport genes in keratinocytes.	Ceramides	87-95	nuclear receptor subfamily 1, group H, member 3	Mus musculus	25-28
18785922-2	2008	These contacts may be the site of ceramide transfer from its site of synthesis (ER) to sphingomyelin (SM) synthase through ceramide transfer protein (CERT).	Ceramides	34-42	ceramide transporter 1	Homo sapiens	123-148
18785922-2	2008	These contacts may be the site of ceramide transfer from its site of synthesis (ER) to sphingomyelin (SM) synthase through ceramide transfer protein (CERT).	Ceramides	34-42	ceramide transporter 1	Homo sapiens	150-154
18785922-3	2008	CERT extracts ceramide from the ER and transfers it to Golgi membranes but the role of overall Golgi structure in this process is unknown.	Ceramides	14-22	ceramide transporter 1	Homo sapiens	0-4
18785922-8	2008	We propose that some Golgi structural perturbations interfere with efficient ceramide trafficking through CERT, and thus SM synthesis.	Ceramides	77-85	ceramide transporter 1	Homo sapiens	106-110
18785922-9	2008	The organization of the mammalian Golgi ribbon together with CERT may promote specific ER-Golgi interactions for efficient delivery of ceramide for SM synthesis.	Ceramides	135-143	ceramide transporter 1	Homo sapiens	61-65
18832646-4	2008	Radiation-induced increase in the concentration of ceramide localized to mitochondria and was required for BH3-domain protein EGL-1-mediated displacement of CED-4 (an APAF-1-like protein) from the CED-9 (a Bcl-2 family member)/CED-4 complex, an obligate step in activation of the CED-3 caspase.	Ceramides	51-59	Programmed cell death activator egl-1	Caenorhabditis elegans	126-131
19001565-5	2008	Sequence analysis suggests that ERH1 may encode the long-sought Arabidopsis functional homolog of yeast and protozoan inositolphosphorylceramide synthase (IPCS), which converts ceramide to inositolphosphorylceramide.	Ceramides	136-144	Inositol phosphorylceramide synthase 2	Arabidopsis thaliana	32-36
19001565-5	2008	Sequence analysis suggests that ERH1 may encode the long-sought Arabidopsis functional homolog of yeast and protozoan inositolphosphorylceramide synthase (IPCS), which converts ceramide to inositolphosphorylceramide.	Ceramides	136-144	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	155-159
19001565-7	2008	Consistent with its biochemical function, the erh1 mutation causes ceramide accumulation in plants expressing RPW8.	Ceramides	67-75	Inositol phosphorylceramide synthase 2	Arabidopsis thaliana	46-50
18772132-3	2008	Various studies have questioned these findings and proposed that GPBP serves as transporter of ceramide between the endoplasmic reticulum and the Golgi apparatus.	Ceramides	95-103	ceramide transporter 1	Homo sapiens	65-69
18682390-4	2008	Both in OLs and in the mouse brain, Lyn selectively associates with alpha(v)beta(3) integrin, not with alpha(v)beta(5) integrin, leading to suppression of acid sphingomyelinase activity and preventing ceramide-mediated apoptosis.	Ceramides	201-209	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	36-39
18832646-4	2008	Radiation-induced increase in the concentration of ceramide localized to mitochondria and was required for BH3-domain protein EGL-1-mediated displacement of CED-4 (an APAF-1-like protein) from the CED-9 (a Bcl-2 family member)/CED-4 complex, an obligate step in activation of the CED-3 caspase.	Ceramides	51-59	Cell death protein 4	Caenorhabditis elegans	157-162
18832646-4	2008	Radiation-induced increase in the concentration of ceramide localized to mitochondria and was required for BH3-domain protein EGL-1-mediated displacement of CED-4 (an APAF-1-like protein) from the CED-9 (a Bcl-2 family member)/CED-4 complex, an obligate step in activation of the CED-3 caspase.	Ceramides	51-59	Apoptosis regulator ced-9	Caenorhabditis elegans	197-202
18832646-4	2008	Radiation-induced increase in the concentration of ceramide localized to mitochondria and was required for BH3-domain protein EGL-1-mediated displacement of CED-4 (an APAF-1-like protein) from the CED-9 (a Bcl-2 family member)/CED-4 complex, an obligate step in activation of the CED-3 caspase.	Ceramides	51-59	Cell death protein 4	Caenorhabditis elegans	227-232
18832646-5	2008	These studies define CEP-1 (the worm homolog of the tumor suppressor p53)-mediated accumulation of EGL-1 and ceramide synthase-mediated generation of ceramide through parallel pathways that integrate at mitochondrial membranes to regulate stress-induced apoptosis.	Ceramides	109-117	Transcription factor cep-1	Caenorhabditis elegans	21-26
18694848-1	2008	Sphingomyelin synthase (SMS) sits at the crossroads of sphingomyelin (SM), ceramide, diacylglycerol (DAG) metabolism.	Ceramides	75-83	spermine synthase	Homo sapiens	0-22
18723763-3	2008	By confocal microscopic analysis, oxotremorine (Oxo), an M(1) receptor agonist, was found to increase LR clustering on the membrane with the formation of a complex of CD38 and LR components such as GM(1), acid sphingomyelinase (ASMase), and ceramide, a typical ceramide-enriched macrodomain.	Ceramides	261-269	CD38 molecule	Bos taurus	167-171
18723763-10	2008	These results provide the first evidence that the formation of ceramide-enriched lipid macrodomains is crucial for Oxo-induced activation of CD38 to produce cADPR in CAMs, and these lipid macrodomains mediate transmembrane signaling of M(1) receptor activation to produce second messenger cADPR.	Ceramides	63-71	CD38 molecule	Bos taurus	141-145
18598724-0	2008	Ceramide inhibition of MMP-2 expression and human cancer bronchial cell invasiveness involve decreased histone acetylation.	Ceramides	0-8	matrix metallopeptidase 2	Homo sapiens	23-28
18598724-4	2008	A SuperArray(R) analysis showed that ceramides modulate gene expression after 2 h. Among deregulated genes, we observed an inhibition of the transcript coding for the pro-metastatic enzyme MMP-2.	Ceramides	37-46	matrix metallopeptidase 2	Homo sapiens	189-194
18723763-0	2008	Formation and function of ceramide-enriched membrane platforms with CD38 during M1-receptor stimulation in bovine coronary arterial myocytes.	Ceramides	26-34	CD38 molecule	Bos taurus	68-72
18723763-2	2008	The present study tested a hypothesis that a special lipid-raft (LR) form, ceramide-enriched lipid platform, contributes to CD38 activation to produce cADPR in response to muscarinic type 1 (M(1)) receptor stimulation in bovine coronary arterial myocytes (CAMs).	Ceramides	75-83	CD38 molecule	Bos taurus	124-128
18723763-3	2008	By confocal microscopic analysis, oxotremorine (Oxo), an M(1) receptor agonist, was found to increase LR clustering on the membrane with the formation of a complex of CD38 and LR components such as GM(1), acid sphingomyelinase (ASMase), and ceramide, a typical ceramide-enriched macrodomain.	Ceramides	241-249	CD38 molecule	Bos taurus	167-171
18669882-2	2008	Acid sphingomyelinase (acid SMase), an enzyme present extracellularly within the arterial wall, strongly enhances lipoprotein retention in model systems in vitro, and retained lipoproteins in human plaques are enriched in ceramide, a product of SMase.	Ceramides	222-230	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
18719356-0	2008	Regulation of autophagy by ceramide-CD95-PERK signaling.	Ceramides	27-35	Fas cell surface death receptor	Homo sapiens	36-40
18694848-1	2008	Sphingomyelin synthase (SMS) sits at the crossroads of sphingomyelin (SM), ceramide, diacylglycerol (DAG) metabolism.	Ceramides	75-83	spermine synthase	Homo sapiens	24-27
18719356-0	2008	Regulation of autophagy by ceramide-CD95-PERK signaling.	Ceramides	27-35	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	41-45
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	autophagy related 5	Homo sapiens	275-279
18719356-4	2008	In both cell systems we discovered that the toxicity of sorafenib and vorinostat or bile acid+MEK1/2 inhibitor exposure depended on the generation of ceramide and the ligand-independent activation of the CD95 death receptor, with subsequent activation of pro-caspase 8.	Ceramides	150-158	mitogen-activated protein kinase kinase 1	Homo sapiens	94-100
18719356-7	2008	Thus ceramide-CD95 signaling promoted cell death via activation of pro-caspase 8 and cell survival via autophagy.	Ceramides	5-13	Fas cell surface death receptor	Homo sapiens	14-18
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	38-46	Fas cell surface death receptor	Homo sapiens	57-61
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-0	2008	Vorinostat and sorafenib increase ER stress, autophagy and apoptosis via ceramide-dependent CD95 and PERK activation.	Ceramides	73-81	Fas cell surface death receptor	Homo sapiens	92-96
18787411-0	2008	Vorinostat and sorafenib increase ER stress, autophagy and apoptosis via ceramide-dependent CD95 and PERK activation.	Ceramides	73-81	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	101-105
18612076-0	2008	Targeting ceramide metabolism with a potent and specific ceramide kinase inhibitor.	Ceramides	10-18	ceramide kinase	Homo sapiens	57-72
18603412-6	2008	These data suggest that, in this model, Bax is activated early in the process and that its increase is sustained till 12h after kainic acid injection which is the time of first appearance of caspase-3 activation and TUNEL positivity, and that SMases contribute to increases in ceramide levels during and after status epilepticus.	Ceramides	277-285	BCL2 associated X, apoptosis regulator	Homo sapiens	40-43
18596135-10	2008	Increased PGE(2) production in old Mphi is a result of increased cyclooxygenase 2 (COX-2) expression, leading to higher COX enzyme activity, which in turn, is associated with the ceramide-induced up-regulation of NF-kappaB.	Ceramides	179-187	prostaglandin-endoperoxide synthase 2	Mus musculus	65-81
18596135-10	2008	Increased PGE(2) production in old Mphi is a result of increased cyclooxygenase 2 (COX-2) expression, leading to higher COX enzyme activity, which in turn, is associated with the ceramide-induced up-regulation of NF-kappaB.	Ceramides	179-187	prostaglandin-endoperoxide synthase 2	Mus musculus	83-88
18596135-10	2008	Increased PGE(2) production in old Mphi is a result of increased cyclooxygenase 2 (COX-2) expression, leading to higher COX enzyme activity, which in turn, is associated with the ceramide-induced up-regulation of NF-kappaB.	Ceramides	179-187	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	213-222
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	161-165
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas associated via death domain	Homo sapiens	166-170
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	caspase 8	Homo sapiens	175-184
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	208-212
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2A	Homo sapiens	213-222
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	208-212
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	autophagy related 5	Homo sapiens	275-279
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	161-165
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas associated via death domain	Homo sapiens	166-170
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	caspase 8	Homo sapiens	175-184
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	208-212
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2A	Homo sapiens	213-222
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	208-212
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	autophagy related 5	Homo sapiens	275-279
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	161-165
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas associated via death domain	Homo sapiens	166-170
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	caspase 8	Homo sapiens	175-184
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	208-212
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2A	Homo sapiens	213-222
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	Fas cell surface death receptor	Homo sapiens	156-160
18787411-11	2008	Thus sorafenib and vorinostat promote ceramide-dependent CD95 activation followed by induction of multiple downstream survival regulatory signals: ceramide-CD95-PERK-FADD-pro-caspase 8 (death); ceramide-CD95-PERK-eIF2alpha- downward arrowc-FLIP-s (death); ceramide-CD95-PERK-ATG5-autophagy (survival).	Ceramides	147-155	eukaryotic translation initiation factor 2 alpha kinase 3	Homo sapiens	208-212
18612076-1	2008	Ceramide kinase (CerK) produces the bioactive lipid ceramide-1-phosphate (C1P) and appears as a key enzyme for controlling ceramide levels.	Ceramides	52-60	ceramide kinase	Homo sapiens	0-15
18612076-1	2008	Ceramide kinase (CerK) produces the bioactive lipid ceramide-1-phosphate (C1P) and appears as a key enzyme for controlling ceramide levels.	Ceramides	52-60	ceramide kinase	Homo sapiens	17-21
18612076-2	2008	In this study, we discovered and characterized adamantane-1-carboxylic acid (2-benzoylamino-benzothiazol-6-yl)amide (NVP-231), a potent, specific, and reversible CerK inhibitor that competitively inhibits binding of ceramide to CerK.	Ceramides	216-224	ceramide kinase	Homo sapiens	162-166
18612076-5	2008	Therefore, NVP-231 represents a novel and promising compound for controlling ceramide metabolism that may provide insight into CerK physiological function.	Ceramides	77-85	ceramide kinase	Homo sapiens	127-131
18800170-6	2008	Gangliosides in the CNS are characterized by the structure of the long-chain base (LCB) in the ceramide moiety.	Ceramides	95-103	clathrin, light polypeptide (Lcb)	Mus musculus	66-81
18515784-5	2008	Inhibition of SPT, a rate-limiting enzyme in ceramide biosynthesis, reduced fatty acid and increased glucose oxidation in isolated perfused LpL(GPI) hearts, improved systolic function, and prolonged survival rates.	Ceramides	45-53	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	14-17
18676372-6	2008	Overall, we have demonstrated that ceramide up-regulation following H/R is pertinent to Bax activation to promote cell death.	Ceramides	35-43	BCL2 associated X, apoptosis regulator	Homo sapiens	88-91
18676372-0	2008	Ceramide generated by sphingomyelin hydrolysis and the salvage pathway is involved in hypoxia/reoxygenation-induced Bax redistribution to mitochondria in NT-2 cells.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	116-119
18676372-3	2008	This elevation in ceramide was primarily due to the actions of acid sphingomyelinase and ceramide synthase LASS 5, demonstrating the action of the salvage pathway.	Ceramides	18-26	ceramide synthase 5	Homo sapiens	107-113
18676372-5	2008	Down-regulation of either acid sphingomyelinase or LASS 5-attenuated ceramide accumulation and H/R-induced Bax translocation to mitochondria.	Ceramides	69-77	ceramide synthase 5	Homo sapiens	51-57
18800170-6	2008	Gangliosides in the CNS are characterized by the structure of the long-chain base (LCB) in the ceramide moiety.	Ceramides	95-103	clathrin, light polypeptide (Lcb)	Mus musculus	83-86
18623086-9	2008	Inhibiting ceramide formation by blockage of the ceramide synthase or acid sphingomyelinase activity resulted in significant reduction of ERK phosphorylation and cell migration.	Ceramides	11-19	mitogen-activated protein kinase 1	Homo sapiens	138-141
18623086-10	2008	In summary, caspase-3 induces ERK activation through a ceramide-dependant, protease activity-independent mechanism, which represents a novel role of caspase-3 in tumor metastasis.	Ceramides	55-63	caspase 3	Homo sapiens	12-21
18623086-10	2008	In summary, caspase-3 induces ERK activation through a ceramide-dependant, protease activity-independent mechanism, which represents a novel role of caspase-3 in tumor metastasis.	Ceramides	55-63	mitogen-activated protein kinase 1	Homo sapiens	30-33
18623086-10	2008	In summary, caspase-3 induces ERK activation through a ceramide-dependant, protease activity-independent mechanism, which represents a novel role of caspase-3 in tumor metastasis.	Ceramides	55-63	caspase 3	Homo sapiens	149-158
18215418-8	2008	Rather Bcl-2 itself caused a significant amount of spontaneous cell death, and sensitised the cells to apoptotic agents such as staurosporine or ceramide.	Ceramides	145-153	BCL2 apoptosis regulator	Homo sapiens	7-12
18346153-4	2008	Confocal microscopic analysis showed an altered intracellular distribution of CD1d following the inhibition topoisomerase I or by an increase in intracellular ceramide levels, that was prevented by p38 and caspase inhibitors.	Ceramides	159-167	mitogen-activated protein kinase 14	Homo sapiens	198-201
18625703-7	2008	Knockdown of sphingosine kinase-1 expression also induced an accumulation of de novo synthesized ceramide, provoking a slight reduction in cell number and viability similar to that induced by a low concentration of the sphingosine kinase inhibitor.	Ceramides	97-105	sphingosine kinase 1	Canis lupus familiaris	13-33
18346153-2	2008	In the current study, we report that the induction of apoptosis by topoisomerase I inhibition or elevation of intracellular ceramide levels substantially impairs CD1d-mediated antigen presentation.	Ceramides	124-132	CD1d molecule	Homo sapiens	162-166
18346153-4	2008	Confocal microscopic analysis showed an altered intracellular distribution of CD1d following the inhibition topoisomerase I or by an increase in intracellular ceramide levels, that was prevented by p38 and caspase inhibitors.	Ceramides	159-167	CD1d molecule	Homo sapiens	78-82
18628757-1	2008	Exposure of cells or animals to stress frequently induces acid sphingomyelinase (ASM)-mediated ceramide production that leads to cell death.	Ceramides	95-103	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	58-79
18515909-8	2008	Even though the blockade of VLDL secretion caused hepatic steatosis accompanied by increased ceramides and diacylglycerols in the liver, the mice exhibited normal glucose tolerance and were sensitive to insulin at the whole-body level, as judged by hyperinsulinemic euglycemic clamp studies.	Ceramides	93-102	CD320 antigen	Mus musculus	28-32
18478546-9	2008	These data indicate that PP2A plays a significant role in blocking the protective effect induced by the ERK kinase pathway and that fast inactivation of ERK is the result of cross talk between calcium/calmodulin-dependent, positively regulated signal cascades and a ceramide-dependent negative signaling pathway.	Ceramides	266-274	Eph receptor B1	Rattus norvegicus	104-107
18478546-9	2008	These data indicate that PP2A plays a significant role in blocking the protective effect induced by the ERK kinase pathway and that fast inactivation of ERK is the result of cross talk between calcium/calmodulin-dependent, positively regulated signal cascades and a ceramide-dependent negative signaling pathway.	Ceramides	266-274	Eph receptor B1	Rattus norvegicus	153-156
18628757-1	2008	Exposure of cells or animals to stress frequently induces acid sphingomyelinase (ASM)-mediated ceramide production that leads to cell death.	Ceramides	95-103	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	81-84
18566297-7	2008	SMS2 deficiency decreased the relative amounts of SM and diacylglycerol (DAG) and increased ceramide, suggesting multiple mechanisms for the decrease in NFkappaB activation.	Ceramides	92-100	sphingomyelin synthase 2	Homo sapiens	0-4
17467122-7	2008	Indeed, IL-1 beta suppressed the activation of the respective scaffolding proteins IRS-1 and Shc; this effect might involve ceramide generation.	Ceramides	124-132	interleukin 1 beta	Homo sapiens	8-17
17467122-7	2008	Indeed, IL-1 beta suppressed the activation of the respective scaffolding proteins IRS-1 and Shc; this effect might involve ceramide generation.	Ceramides	124-132	insulin receptor substrate 1	Homo sapiens	83-88
17467122-7	2008	Indeed, IL-1 beta suppressed the activation of the respective scaffolding proteins IRS-1 and Shc; this effect might involve ceramide generation.	Ceramides	124-132	SHC adaptor protein 1	Homo sapiens	93-96
17467122-8	2008	IL-1-induced interference with BDNF neuroprotection and signal transduction was corrected, in part, by ceramide production inhibitors and mimicked by the cell-permeable C2-ceramide.	Ceramides	103-111	brain derived neurotrophic factor	Homo sapiens	31-35
17467122-9	2008	These results suggest that IL-1 beta places neurons at risk by interfering with BDNF signaling involving a ceramide-associated mechanism.	Ceramides	107-115	interleukin 1 beta	Homo sapiens	27-36
17467122-9	2008	These results suggest that IL-1 beta places neurons at risk by interfering with BDNF signaling involving a ceramide-associated mechanism.	Ceramides	107-115	brain derived neurotrophic factor	Homo sapiens	80-84
18694456-0	2008	Fluorescent annexin A1 reveals dynamics of ceramide platforms in living cells.	Ceramides	43-51	annexin A1	Homo sapiens	12-22
18694456-3	2008	Here, we show that ceramide increases affinity of annexin A1-membrane interaction.	Ceramides	19-27	annexin A1	Homo sapiens	50-60
18694456-5	2008	In fixed cells, using a ceramide-specific antibody, we establish a direct interaction of annexin A1 with areas of the plasma membrane enriched in ceramide (ceramide platforms).	Ceramides	24-32	annexin A1	Homo sapiens	89-99
18694456-5	2008	In fixed cells, using a ceramide-specific antibody, we establish a direct interaction of annexin A1 with areas of the plasma membrane enriched in ceramide (ceramide platforms).	Ceramides	146-154	annexin A1	Homo sapiens	89-99
18694456-5	2008	In fixed cells, using a ceramide-specific antibody, we establish a direct interaction of annexin A1 with areas of the plasma membrane enriched in ceramide (ceramide platforms).	Ceramides	146-154	annexin A1	Homo sapiens	89-99
18694456-6	2008	In living cells, the intracellular dynamics of annexin A1 match those of plasmalemmal ceramide.	Ceramides	86-94	annexin A1	Homo sapiens	47-57
18694456-7	2008	Among proteins of the annexin family, the interaction with ceramide platforms is restricted to annexin A1 and is conveyed by its unique N-terminal domain.	Ceramides	59-67	annexin A1	Homo sapiens	95-105
18694456-9	2008	Using fluorescently tagged annexin A1 as a reporter for ceramide platforms and annexin A6 as a non-selective membrane marker, we visualize ceramide platforms for the first time in living cells and provide evidence for a ceramide-driven segregation and internalization of membrane-associated proteins.	Ceramides	139-147	annexin A1	Homo sapiens	27-37
18694456-9	2008	Using fluorescently tagged annexin A1 as a reporter for ceramide platforms and annexin A6 as a non-selective membrane marker, we visualize ceramide platforms for the first time in living cells and provide evidence for a ceramide-driven segregation and internalization of membrane-associated proteins.	Ceramides	139-147	annexin A6	Homo sapiens	79-89
18694456-9	2008	Using fluorescently tagged annexin A1 as a reporter for ceramide platforms and annexin A6 as a non-selective membrane marker, we visualize ceramide platforms for the first time in living cells and provide evidence for a ceramide-driven segregation and internalization of membrane-associated proteins.	Ceramides	139-147	annexin A1	Homo sapiens	27-37
18694456-9	2008	Using fluorescently tagged annexin A1 as a reporter for ceramide platforms and annexin A6 as a non-selective membrane marker, we visualize ceramide platforms for the first time in living cells and provide evidence for a ceramide-driven segregation and internalization of membrane-associated proteins.	Ceramides	139-147	annexin A6	Homo sapiens	79-89
18511810-7	2008	SK1-I not only decreased S1P levels but concomitantly increased levels of its proapoptotic precursor ceramide.	Ceramides	101-109	sphingosine kinase 1	Homo sapiens	0-3
18555012-0	2008	Wild-type levels of ceramide and ceramide-1-phosphate in the retina of ceramide kinase-like-deficient mice.	Ceramides	20-28	ceramide kinase-like	Mus musculus	71-91
18690848-3	2008	An increase in NUPR1 expression has been seen with serum starvation and in response to compounds such as cycloheximide, ceramide, and staurosporine.	Ceramides	120-128	nuclear protein 1, transcriptional regulator	Homo sapiens	15-20
18691012-3	2008	Owing to its ability to regulate two bioactive sphingolipids, ceramide and sphingosine-1-phosphate, acid ceramidase (AC) emerges as an attractive target for drug development within the sphingolipid metabolic pathway.	Ceramides	62-70	N-acylsphingosine amidohydrolase 1	Homo sapiens	100-115
18613813-2	2008	In type I cells CD95L (CD95 ligand) binding to CD95 results in a ceramide-dependent formation of the DISC (death-inducing signalling complex) and caspase 8-dependent CD95 clustering in the plasma membrane, followed by an internalization of these multimeric-receptor-DISC complexes.	Ceramides	65-73	Fas ligand	Homo sapiens	16-21
18613813-2	2008	In type I cells CD95L (CD95 ligand) binding to CD95 results in a ceramide-dependent formation of the DISC (death-inducing signalling complex) and caspase 8-dependent CD95 clustering in the plasma membrane, followed by an internalization of these multimeric-receptor-DISC complexes.	Ceramides	65-73	Fas cell surface death receptor	Homo sapiens	16-20
18613813-2	2008	In type I cells CD95L (CD95 ligand) binding to CD95 results in a ceramide-dependent formation of the DISC (death-inducing signalling complex) and caspase 8-dependent CD95 clustering in the plasma membrane, followed by an internalization of these multimeric-receptor-DISC complexes.	Ceramides	65-73	Fas cell surface death receptor	Homo sapiens	23-27
18613813-2	2008	In type I cells CD95L (CD95 ligand) binding to CD95 results in a ceramide-dependent formation of the DISC (death-inducing signalling complex) and caspase 8-dependent CD95 clustering in the plasma membrane, followed by an internalization of these multimeric-receptor-DISC complexes.	Ceramides	65-73	Fas cell surface death receptor	Homo sapiens	23-27
18613813-4	2008	However, their activation by CD95L is sufficient to trigger a caspase 8-dependent endosomal acidification and a ceramide-dependent trafficking of intracellularly stored CD95 to the plasma membrane, thereby amplifying CD95 activation.	Ceramides	112-120	Fas ligand	Homo sapiens	29-34
18613813-4	2008	However, their activation by CD95L is sufficient to trigger a caspase 8-dependent endosomal acidification and a ceramide-dependent trafficking of intracellularly stored CD95 to the plasma membrane, thereby amplifying CD95 activation.	Ceramides	112-120	Fas cell surface death receptor	Homo sapiens	29-33
18613813-4	2008	However, their activation by CD95L is sufficient to trigger a caspase 8-dependent endosomal acidification and a ceramide-dependent trafficking of intracellularly stored CD95 to the plasma membrane, thereby amplifying CD95 activation.	Ceramides	112-120	Fas cell surface death receptor	Homo sapiens	169-173
18613813-5	2008	Thus, in both type I and type II cells, ceramide and CD95 receptor endo- and exo-cytosis are involved in CD95-mediated apoptosis, but apparently in different ways.	Ceramides	40-48	Fas cell surface death receptor	Homo sapiens	105-109
18565104-2	2008	Recently, ceramide kinase (CerK) was identified as an enzyme that converts Cer to ceramide 1-phosphate (C1P).	Ceramides	27-30	ceramide kinase	Mus musculus	10-25
18459163-2	2008	CERT transfers ceramide from the endoplasmic reticulum (ER) to the Golgi apparatus, a step crucial for sphingomyelin (SM) synthesis.	Ceramides	15-23	ceramide transporter 1	Homo sapiens	0-4
18459163-3	2008	The pleckstrin homology (PH) domain and the FFAT motif of CERT restrict the direction of transfer and destination of ceramide through binding to phosphatidylinositol 4-monophosphate (PI4P) at the Golgi and the ER resident proteins, VAPs, respectively.	Ceramides	117-125	ceramide transporter 1	Homo sapiens	58-62
18535786-7	2008	Prior exposure of myocytes to leptin blocked IL-1beta-induced cardiosuppression in conjunction with a blunting of IL-1beta stimulated ceramide accumulation.	Ceramides	134-142	leptin	Rattus norvegicus	30-36
18534987-2	2008	The pro-apoptotic Bcl-x(S) variant is up-regulated by ceramide and down-regulated by protein kinase C through specific cis-acting exonic elements, one of which is bound by SAP155.	Ceramides	54-62	BCL2 like 1	Homo sapiens	18-23
18534987-2	2008	The pro-apoptotic Bcl-x(S) variant is up-regulated by ceramide and down-regulated by protein kinase C through specific cis-acting exonic elements, one of which is bound by SAP155.	Ceramides	54-62	splicing factor 3b subunit 1	Homo sapiens	172-178
18535786-7	2008	Prior exposure of myocytes to leptin blocked IL-1beta-induced cardiosuppression in conjunction with a blunting of IL-1beta stimulated ceramide accumulation.	Ceramides	134-142	interleukin 1 beta	Rattus norvegicus	114-122
18667621-0	2008	Ceramide is responsible for the failure of compensatory nerve sprouting in apolipoprotein E knock-out mice.	Ceramides	0-8	apolipoprotein E	Mus musculus	75-91
18667621-6	2008	However, sprouting was restored in apoE KO mice (although not in aged mice) by fumonisin B1, an inhibitor of ceramide synthesis.	Ceramides	109-117	apolipoprotein E	Mus musculus	35-39
18667621-7	2008	A shotgun analysis revealed a wide array of changes in individual ceramide species in DRG neurons of apoE KO mice, and the changes for ceramide species OH_N15:0 made it a candidate inhibitor of sprouting (increased in apoE KO mice and normalized by fumonisin B1).	Ceramides	135-143	apolipoprotein E	Mus musculus	218-222
18667621-9	2008	We suggest that absence of apoE expression alters the balance among ceramide species to one that collectively inhibits compensatory sprouting, whereas fumonisin B1 establishes a new balance that allows sprouting.	Ceramides	68-76	apolipoprotein E	Mus musculus	27-31
18441093-2	2008	Oxidative stress upregulates ceramides, proapoptotic signaling sphingolipids that trigger further oxidative stress and alveolar space enlargement, as shown in an experimental model of emphysema due to VEGF blockade.	Ceramides	29-38	vascular endothelial growth factor A	Mus musculus	201-205
18441093-6	2008	Ceramide augmentation shown to mimic levels found in human emphysema lungs increased oxidative stress, and decreased, independently of caspase activation, the lung superoxide dismutase activity at 48 h. In contrast to their wild-type littermates, transgenic mice overexpressing human Cu/Zn SOD were significantly protected from ceramide-induced superoxide production, apoptosis, and air space enlargement.	Ceramides	0-8	superoxide dismutase 1, soluble	Mus musculus	284-293
18441093-7	2008	Activation of lung acid sphingomyelinase in response to ceramide treatment was abolished in the Cu/Zn SOD transgenic mice.	Ceramides	56-64	superoxide dismutase 1, soluble	Mus musculus	96-105
18441093-8	2008	Since cigarette smoke-induced emphysema in mice is similarly ameliorated by the Cu/Zn SOD overexpression, we hypothesized that cigarette smoke may induce ceramides in the mouse lung.	Ceramides	154-163	superoxide dismutase 1, soluble	Mus musculus	80-89
18423390-0	2008	C18 ceramide analysis in mammalian cells employing reversed-phase high-performance liquid chromatography tandem mass spectrometry.	Ceramides	4-12	Bardet-Biedl syndrome 9	Homo sapiens	0-3
18458870-0	2008	Ceramide: a contributor to insulin resistance or an innocent bystander?	Ceramides	0-8	insulin	Homo sapiens	27-34
18458871-1	2008	AIMS/HYPOTHESIS: In skeletal muscle, ceramides may be involved in the pathogenesis of insulin resistance through an attenuation of insulin signalling.	Ceramides	37-46	insulin	Homo sapiens	86-93
18458871-1	2008	AIMS/HYPOTHESIS: In skeletal muscle, ceramides may be involved in the pathogenesis of insulin resistance through an attenuation of insulin signalling.	Ceramides	37-46	insulin	Homo sapiens	131-138
18458871-9	2008	Interestingly, a positive correlation (r=0.42, p<0.05) was present between muscle ceramide content at baseline and insulin sensitivity.	Ceramides	85-93	insulin	Homo sapiens	118-125
18397976-2	2008	Intramyocellular sphingolipids (i.e. ceramide) have been suggested to induce insulin resistance by interfering with the insulin signaling cascade in obesity.	Ceramides	37-45	insulin	Homo sapiens	77-84
18397976-2	2008	Intramyocellular sphingolipids (i.e. ceramide) have been suggested to induce insulin resistance by interfering with the insulin signaling cascade in obesity.	Ceramides	37-45	insulin	Homo sapiens	120-127
18397976-12	2008	Whether the decrease in AKT can be attributed to the trend to higher muscle ceramide remains unanswered.	Ceramides	76-84	AKT serine/threonine kinase 1	Homo sapiens	24-27
18466329-6	2008	In membrane processes, ceramide is co-distributed with its binding partner atypical protein kinase C zeta/lambda (aPKC), and Cdc42, alpha/beta-tubulin, and beta-catenin, three proteins involved in aPKC-dependent regulation of cell polarity and motility.	Ceramides	23-31	cell division cycle 42	Mus musculus	125-130
18245173-3	2008	Here, for the first time, we show that ceramide contributes to cellular resistance to doxorubicin through up-regulating the gene expression of glucosylceramide synthase (GCS).	Ceramides	39-47	UDP-glucose ceramide glucosyltransferase	Homo sapiens	143-168
18245173-3	2008	Here, for the first time, we show that ceramide contributes to cellular resistance to doxorubicin through up-regulating the gene expression of glucosylceramide synthase (GCS).	Ceramides	39-47	UDP-glucose ceramide glucosyltransferase	Homo sapiens	170-173
18245173-5	2008	GCS catalyzes ceramide glycosylation, converting ceramide to glucosylceramide; this process hastens ceramide clearance and limits ceramide-induced apoptosis.	Ceramides	14-22	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
18245173-5	2008	GCS catalyzes ceramide glycosylation, converting ceramide to glucosylceramide; this process hastens ceramide clearance and limits ceramide-induced apoptosis.	Ceramides	49-57	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
18245173-5	2008	GCS catalyzes ceramide glycosylation, converting ceramide to glucosylceramide; this process hastens ceramide clearance and limits ceramide-induced apoptosis.	Ceramides	49-57	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
18245173-5	2008	GCS catalyzes ceramide glycosylation, converting ceramide to glucosylceramide; this process hastens ceramide clearance and limits ceramide-induced apoptosis.	Ceramides	49-57	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-3
18245173-10	2008	Fumonisin B(1), an inhibitor of ceramide synthesis, significantly suppressed doxorubicin-up-regulated GCS expression.	Ceramides	32-40	UDP-glucose ceramide glucosyltransferase	Homo sapiens	102-105
18245173-11	2008	Promoter truncation, point mutation, gel-shift, and protein-DNA ELISA analysis showed that transcription factor Sp1 was essential for ceramide-induced GCS up-regulation.	Ceramides	134-142	UDP-glucose ceramide glucosyltransferase	Homo sapiens	151-154
18245173-12	2008	These data indicate that ceramide-governed GCS gene expression drives cellular resistance to doxorubicin.	Ceramides	25-33	UDP-glucose ceramide glucosyltransferase	Homo sapiens	43-46
18466329-7	2008	Sphingolipid depletion by myriocin prevents membrane translocation of aPKC and Cdc42, which is restored by ceramide or S18.	Ceramides	107-115	cell division cycle 42	Mus musculus	79-84
18466329-8	2008	These results suggest that ceramide-mediated membrane association of aPKC/Cdc42 is important for NP motility.	Ceramides	27-35	cell division cycle 42	Mus musculus	74-79
18390550-9	2008	Because worm ceramides exclusively contain a monomethyl branched chain sphingoid base, we also investigated ceramides in let-767 (RNAi).	Ceramides	108-117	Very-long-chain 3-oxooacyl-coA reductase let-767	Caenorhabditis elegans	121-128
18611440-5	2008	Myriocin-treated apoE KO mice had significant reductions in plasma total cholesterol, triglycerides, VLDL-cholesterol, ceramide, sphinganine and sphingomyelin (SM) compared to 24- and 36-week-old control mice.	Ceramides	119-127	apolipoprotein E	Mus musculus	17-21
18591870-5	2008	Moreover, we found that CM caused an increase in ceramide content in renal tubular cells, which leads to apoptosis by inhibiting the phosphorylation of Akt and cAMP responsive element binding protein (CREB) and the subsequent reduction in Bcl-2 expression.	Ceramides	49-57	thymoma viral proto-oncogene 1	Mus musculus	152-155
18591870-5	2008	Moreover, we found that CM caused an increase in ceramide content in renal tubular cells, which leads to apoptosis by inhibiting the phosphorylation of Akt and cAMP responsive element binding protein (CREB) and the subsequent reduction in Bcl-2 expression.	Ceramides	49-57	cAMP responsive element binding protein 1	Mus musculus	160-199
18591870-5	2008	Moreover, we found that CM caused an increase in ceramide content in renal tubular cells, which leads to apoptosis by inhibiting the phosphorylation of Akt and cAMP responsive element binding protein (CREB) and the subsequent reduction in Bcl-2 expression.	Ceramides	49-57	cAMP responsive element binding protein 1	Mus musculus	201-205
18591870-5	2008	Moreover, we found that CM caused an increase in ceramide content in renal tubular cells, which leads to apoptosis by inhibiting the phosphorylation of Akt and cAMP responsive element binding protein (CREB) and the subsequent reduction in Bcl-2 expression.	Ceramides	49-57	B cell leukemia/lymphoma 2	Mus musculus	239-244
18364460-4	2008	In addition, insulin-resistant skeletal muscle cells exhibit enhanced production of reactive oxygen species and ceramide as well as a downregulation of myogenic transcription factors such as myogenin and MyoD.	Ceramides	112-120	insulin	Homo sapiens	13-20
18411267-6	2008	Ceramide binding activity was decreased in recombinant CERT proteins containing the UVB-induced homotrimer.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	55-59
18411267-8	2008	Finally like UVB-treated keratinocytes, HPA-12 blockade of CERT function increased keratinocyte apoptosis, decreased sphingomyelin synthesis, and led to accumulation of ceramide.	Ceramides	169-177	ceramide transporter 1	Homo sapiens	59-63
18411267-9	2008	Thus, UVB-induced CERT homotrimer formation accounts, at least in part, for apoptosis and failed up-regulation of sphingomyelin synthesis following UVB irradiation, revealing that inactive CERT can attenuate a key metabolic protective mechanism against ceramide-induced apoptosis in keratinocytes.	Ceramides	253-261	ceramide transporter 1	Homo sapiens	18-22
18411267-9	2008	Thus, UVB-induced CERT homotrimer formation accounts, at least in part, for apoptosis and failed up-regulation of sphingomyelin synthesis following UVB irradiation, revealing that inactive CERT can attenuate a key metabolic protective mechanism against ceramide-induced apoptosis in keratinocytes.	Ceramides	253-261	ceramide transporter 1	Homo sapiens	189-193
18310483-9	2008	In the mouse model at 48 hours, a-SMase-deficient mice showed reduced pulmonary ceramide levels and attenuated leukocyte influx into the alveolar space.	Ceramides	80-88	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	32-39
18353542-4	2008	Stimuli that trigger a release of ceramide to mediate apoptosis include CD95, TNF-receptor, DR5, gamma-irradiation, cytotoxic drugs, UV-light, bacteria, viruses, some forms of developmental death, anti-CD20 and disruption of the cell"s contact with its matrix, to name a few.	Ceramides	34-42	Fas cell surface death receptor	Homo sapiens	72-76
18353542-4	2008	Stimuli that trigger a release of ceramide to mediate apoptosis include CD95, TNF-receptor, DR5, gamma-irradiation, cytotoxic drugs, UV-light, bacteria, viruses, some forms of developmental death, anti-CD20 and disruption of the cell"s contact with its matrix, to name a few.	Ceramides	34-42	keratin 20	Homo sapiens	202-206
18192502-4	2008	Intermediate-chain length (C(8:0)) extracellular ceramides, used as a surrogate of paracellular ceramides, triggered caspase-3 activation in primary mouse lung endothelial cells, similar to TNF-alpha-generated endogenous ceramides.	Ceramides	49-58	caspase 3	Mus musculus	117-126
18192502-6	2008	Tandem mass spectrometry analysis detected increases in both relative and absolute levels of C(16:0) ceramide in response to C(8:0) and TNF-alpha treatments.	Ceramides	101-109	tumor necrosis factor	Mus musculus	136-145
18192502-7	2008	These results implicate the de novo pathway of ceramide synthesis in the apoptotic effects of both paracellular ceramides and TNF-alpha-stimulated intracellular ceramides in primary lung endothelial cells.	Ceramides	47-55	tumor necrosis factor	Mus musculus	126-135
18192502-7	2008	These results implicate the de novo pathway of ceramide synthesis in the apoptotic effects of both paracellular ceramides and TNF-alpha-stimulated intracellular ceramides in primary lung endothelial cells.	Ceramides	161-170	tumor necrosis factor	Mus musculus	126-135
18395507-5	2008	Treatment with exogenous ceramides, or increasing the endogenous ceramide levels also inhibited HMGCR by 60-80%.	Ceramides	25-34	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	96-101
18395507-5	2008	Treatment with exogenous ceramides, or increasing the endogenous ceramide levels also inhibited HMGCR by 60-80%.	Ceramides	25-33	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	96-101
18395507-6	2008	Phosphorylation of HMGCR was stimulated by SMase C or exogenous ceramide.	Ceramides	64-72	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	19-24
18451260-6	2008	Herein we will review the role of ceramide and other sphingolipid metabolites in insulin resistance, beta-cell failure, cardiomyopathy, and vascular dysfunction, focusing on these in vivo studies that identify enzymes controlling sphingolipid metabolism as therapeutic targets for combating metabolic disease.	Ceramides	34-42	insulin	Homo sapiens	81-88
18323863-3	2008	Using a culture of cerebellar neuronal precursors, we have previously demonstrated protective effect of the neuropeptide PACAP, which suppresses ceramide-induced apoptosis by blockade of the mitochondrial apoptotic pathway.	Ceramides	145-153	adenylate cyclase activating polypeptide 1	Homo sapiens	121-126
18500447-1	2008	Saccharomyces cerevisiae dihydroceramidase Ydc1p hydrolyzes ceramide, resulting in accumulation of free long-chain bases and their phosphates.	Ceramides	60-68	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	43-48
18500447-9	2008	Exogenous addition of ceramide to YDC1-overexpressing cultures increased chronological lifespan and restored organelle function.	Ceramides	22-30	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	34-38
18460913-4	2008	RECENT FINDINGS: Muscle lipid metabolites such as long chain fatty acid coenzyme As, diacylglycerol and ceramides may impair insulin signalling directly.	Ceramides	104-113	insulin	Homo sapiens	125-132
18649016-0	2008	Ceramide inhibits CCN2 expression in fibroblasts.	Ceramides	0-8	cellular communication network factor 2	Homo sapiens	18-22
18270209-8	2008	Increased levels of cholesterol, ceramide and polyunsaturated fatty acids were also detected in the lungs and spleen of Neu4(-/-) mice by high-resolution NMR spectroscopy.	Ceramides	33-41	sialidase 4	Mus musculus	120-124
18649016-3	2008	C2 ceramide reduced the ability of TGFbeta to induce the generic Smad responsive promoter/reporter construct SBE-luciferase.	Ceramides	3-11	transforming growth factor beta 1	Homo sapiens	35-42
18649016-4	2008	These results suggest that C2 ceramide reduces the action of TGFbeta in fibroblasts via Smad antagonism.	Ceramides	30-38	transforming growth factor beta 1	Homo sapiens	61-68
18400537-0	2008	De novo N-palmitoylsphingosine synthesis is the major biochemical mechanism of ceramide accumulation following p53 up-regulation.	Ceramides	79-87	tumor protein p53	Homo sapiens	111-114
18400537-10	2008	These studies indicate that p53 specifically drives de novo ceramide synthesis by activation of a ceramide synthase that favors the synthesis of N-palmitoylsphingosine.	Ceramides	60-68	tumor protein p53	Homo sapiens	28-31
18311838-7	2008	The involvement of caspases-9, -3, and -2 in ceramide-mediated apoptotic death of CGC was further supported by the use of specific inhibitors.	Ceramides	45-53	caspase 9	Homo sapiens	19-41
18317235-11	2008	CLN1/CLN2/CLN6 proteins bind to lysophosphatidic acid/sulfatide, CLN6/CLN8 proteins to GalCer, and CLN8 protein to ceramide.	Ceramides	115-123	palmitoyl-protein thioesterase 1	Homo sapiens	0-4
18317235-11	2008	CLN1/CLN2/CLN6 proteins bind to lysophosphatidic acid/sulfatide, CLN6/CLN8 proteins to GalCer, and CLN8 protein to ceramide.	Ceramides	115-123	tripeptidyl peptidase 1	Homo sapiens	5-9
18317235-11	2008	CLN1/CLN2/CLN6 proteins bind to lysophosphatidic acid/sulfatide, CLN6/CLN8 proteins to GalCer, and CLN8 protein to ceramide.	Ceramides	115-123	CLN6 transmembrane ER protein	Homo sapiens	65-69
18317235-11	2008	CLN1/CLN2/CLN6 proteins bind to lysophosphatidic acid/sulfatide, CLN6/CLN8 proteins to GalCer, and CLN8 protein to ceramide.	Ceramides	115-123	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	70-74
18317235-11	2008	CLN1/CLN2/CLN6 proteins bind to lysophosphatidic acid/sulfatide, CLN6/CLN8 proteins to GalCer, and CLN8 protein to ceramide.	Ceramides	115-123	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	99-103
18400537-2	2008	Previously we had shown that, in a p53-dependent model of cell death, ceramide accumulated in a p53-dependent manner [Dbaibo GS, Pushkareva MY, Rachid RA, Alter N, Smyth MJ, Obeid LM, Hannun YA.	Ceramides	70-78	tumor protein p53	Homo sapiens	35-38
18400537-2	2008	Previously we had shown that, in a p53-dependent model of cell death, ceramide accumulated in a p53-dependent manner [Dbaibo GS, Pushkareva MY, Rachid RA, Alter N, Smyth MJ, Obeid LM, Hannun YA.	Ceramides	70-78	tumor protein p53	Homo sapiens	96-99
18400537-4	2008	In the current study, we investigated the biochemical pathways by which ceramide accumulated following p53 up-regulation.	Ceramides	72-80	tumor protein p53	Homo sapiens	103-106
18400537-5	2008	In both Molt-4 LXSN leukemia cells exposed to gamma-irradiation and in EB-1 colon cancer cells treated with ZnCl(2), p53 up-regulation led to de novo ceramide synthesis with predominance of N-palmitoylsphingosine (C16-ceramide) synthesis.	Ceramides	150-158	tumor protein p53	Homo sapiens	117-120
18400537-8	2008	The SPT inhibitor ISP-1 or the ceramide synthase inhibitor fumonisin B1 led to substantial inhibition of ceramide accumulation in response to p53 up-regulation.	Ceramides	31-39	tumor protein p53	Homo sapiens	142-145
18513408-10	2008	An analysis of Swi6 suggests a possible role in lipid metabolism, and more specifically in metabolism of ceramide, a bioactive lipid currently being investigated for anti-cancer properties.	Ceramides	105-113	transcriptional regulator SWI6	Saccharomyces cerevisiae S288C	15-19
17988958-8	2008	This increase in bone volume was also related to an increased concentration of ceramide in the plasma resulting in the down regulation of phospholipid-bound AA in Cftr-KO mice.	Ceramides	79-87	cystic fibrosis transmembrane conductance regulator	Mus musculus	163-167
18388185-5	2008	In addition, genes involved in ceramide signaling (MAP2K4) and metabolism (UGCG) were found to be positively associated with liver fat content.	Ceramides	31-39	mitogen-activated protein kinase kinase 4	Homo sapiens	51-57
18388185-5	2008	In addition, genes involved in ceramide signaling (MAP2K4) and metabolism (UGCG) were found to be positively associated with liver fat content.	Ceramides	31-39	UDP-glucose ceramide glucosyltransferase	Homo sapiens	75-79
17973185-8	2008	Taken together the ceramide binding/recognition site previously proposed for the mouse ST3Gal II might represent a unique feature of mammalian ST3Gal II that is missing in the evolutionary more distant fish and tunicate species reported here.	Ceramides	19-27	ST3 beta-galactoside alpha-2,3-sialyltransferase 2	Mus musculus	87-96
17973185-8	2008	Taken together the ceramide binding/recognition site previously proposed for the mouse ST3Gal II might represent a unique feature of mammalian ST3Gal II that is missing in the evolutionary more distant fish and tunicate species reported here.	Ceramides	19-27	ST3 beta-galactoside alpha-2,3-sialyltransferase 3	Homo sapiens	143-152
18207474-5	2008	Hence it is believed that intermediates in fatty acid metabolism, such as fatty acyl-CoA, ceramides or diacylglycerol (DAG) link fat deposition in the muscle to compromised insulin signaling.	Ceramides	90-99	insulin	Homo sapiens	173-180
18359942-0	2008	Protection from high fat diet-induced increase in ceramide in mice lacking plasminogen activator inhibitor 1.	Ceramides	50-58	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	75-108
18359942-5	2008	Next, we investigated the relationship of ceramide to plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of plasminogen activation and another key player in obesity.	Ceramides	42-50	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	54-87
18359942-5	2008	Next, we investigated the relationship of ceramide to plasminogen activator inhibitor-1 (PAI-1), the primary inhibitor of plasminogen activation and another key player in obesity.	Ceramides	42-50	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	89-94
18359942-7	2008	Interestingly, the changes in ceramide were attenuated in mice lacking PAI-1.	Ceramides	30-38	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	71-76
18359942-8	2008	Mechanistically, mice lacking PAI-1 were protected from diet-induced increase in serine palmitoyltransferase, acid sphingomyelinase, and neutral sphingomyelinase mRNA, providing a mechanistic link for decreased ceramide in PAI-1-/- mice.	Ceramides	211-219	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	30-35
18359942-9	2008	The decreases in plasma free fatty acids and adipose tumor necrosis factor-alpha in PAI-1-/- mice may have additionally contributed indirectly to improvements in ceramide profile in these mice.	Ceramides	162-170	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	84-89
18359942-10	2008	This study has identified a novel link between sphingolipid metabolism and PAI-1 and also suggests that ceramide may be an intermediary molecule linking elevated PAI-1 to insulin resistance.	Ceramides	104-112	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	162-167
18346453-4	2008	Our results show that components with poor affinity toward the liquid-ordered phase, such as several fluorescent lipid analogues or the synaptic protein Synaptobrevin 2, are excluded from ceramide-rich domains.	Ceramides	188-196	vesicle associated membrane protein 2	Homo sapiens	153-168
18299447-0	2008	Mutations in the neutral sphingomyelinase gene SMPD3 implicate the ceramide pathway in human leukemias.	Ceramides	67-75	sphingomyelin phosphodiesterase 2	Homo sapiens	17-41
18299447-0	2008	Mutations in the neutral sphingomyelinase gene SMPD3 implicate the ceramide pathway in human leukemias.	Ceramides	67-75	sphingomyelin phosphodiesterase 3	Homo sapiens	47-52
18299447-2	2008	Defects in the neutral SMase (nSMase) gene Smpd3, the primary regulator of ceramide biosynthesis, are responsible for developmental defects of bone; regulation of ceramide levels have been implicated in macrophage differentiation, but this pathway has not been directly implicated in human cancer.	Ceramides	75-83	sphingomyelin phosphodiesterase 3	Homo sapiens	43-48
18299447-2	2008	Defects in the neutral SMase (nSMase) gene Smpd3, the primary regulator of ceramide biosynthesis, are responsible for developmental defects of bone; regulation of ceramide levels have been implicated in macrophage differentiation, but this pathway has not been directly implicated in human cancer.	Ceramides	163-171	sphingomyelin phosphodiesterase 3	Homo sapiens	43-48
17786164-3	2008	The emphasis is on the implication of ATP-binding cassette (ABC) multidrug efflux transporters in drug disposition and antiapoptotic factors, including epidermal growth factor receptor cascades and deregulated enzymes in ceramide metabolic pathways.	Ceramides	221-229	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	38-58
17786164-3	2008	The emphasis is on the implication of ATP-binding cassette (ABC) multidrug efflux transporters in drug disposition and antiapoptotic factors, including epidermal growth factor receptor cascades and deregulated enzymes in ceramide metabolic pathways.	Ceramides	221-229	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	60-63
17786164-3	2008	The emphasis is on the implication of ATP-binding cassette (ABC) multidrug efflux transporters in drug disposition and antiapoptotic factors, including epidermal growth factor receptor cascades and deregulated enzymes in ceramide metabolic pathways.	Ceramides	221-229	epidermal growth factor receptor	Homo sapiens	152-184
18374917-0	2008	Suppression of sphingomyelin synthase 1 by small interference RNA is associated with enhanced ceramide production and apoptosis after photodamage.	Ceramides	94-102	sphingomyelin synthase 1	Homo sapiens	15-39
18374917-1	2008	We have shown that overexpression of SMS1, an enzyme that converts de novo ceramide into sphingomyelin, is accompanied by attenuated ceramide response and apoptotic resistance after photodamage with the photosensitizer Pc 4 (photodynamic therapy; PDT).	Ceramides	75-83	sphingomyelin synthase 1	Homo sapiens	37-41
18374917-1	2008	We have shown that overexpression of SMS1, an enzyme that converts de novo ceramide into sphingomyelin, is accompanied by attenuated ceramide response and apoptotic resistance after photodamage with the photosensitizer Pc 4 (photodynamic therapy; PDT).	Ceramides	75-83	proprotein convertase subtilisin/kexin type 4	Homo sapiens	219-223
18374917-1	2008	We have shown that overexpression of SMS1, an enzyme that converts de novo ceramide into sphingomyelin, is accompanied by attenuated ceramide response and apoptotic resistance after photodamage with the photosensitizer Pc 4 (photodynamic therapy; PDT).	Ceramides	133-141	sphingomyelin synthase 1	Homo sapiens	37-41
18374917-4	2008	In SMS1 siRNA-transfected cells increases in ceramides were higher than in control siRNA-transfectants after PDT.	Ceramides	45-54	sphingomyelin synthase 1	Homo sapiens	3-7
18374917-7	2008	The data show that RNA interference-dependent downregulation of SMS1 is associated with increased accumulation of ceramide and dihydroceramide with concomitant sensitization of cells to apoptosis after photodamage.	Ceramides	114-122	sphingomyelin synthase 1	Homo sapiens	64-68
18281275-7	2008	Mutations at these three amino acids prevented AC cleavage and activity, the latter assessed using BODIPY-conjugated ceramide.	Ceramides	117-125	N-acylsphingosine amidohydrolase 1	Homo sapiens	47-49
18505924-8	2008	Overexpression of exogenous nSMase3 sensitizes cells to Adriamycin-induced cell killing, a finding consistent with the proposed proapoptotic role of nSMase enzymes and nSMase-generated ceramide.	Ceramides	185-193	sphingomyelin phosphodiesterase 4	Homo sapiens	28-35
18505924-8	2008	Overexpression of exogenous nSMase3 sensitizes cells to Adriamycin-induced cell killing, a finding consistent with the proposed proapoptotic role of nSMase enzymes and nSMase-generated ceramide.	Ceramides	185-193	sphingomyelin phosphodiesterase 2	Homo sapiens	28-34
18272525-4	2008	In fact, in this study we found that reduced Phs1 levels result in significant impairment of the conversion of ceramide to inositol phosphorylceramide.	Ceramides	111-119	enoyl-CoA hydratase PHS1	Saccharomyces cerevisiae S288C	45-49
18401414-1	2008	We examined the involvement of sphingosine kinase-1 (SphK1), which governs the ceramide/sphingosine-1-phosphate balance, in susceptibility to imatinib of either sensitive or resistant chronic myeloid leukemia cells.	Ceramides	79-87	sphingosine kinase 1	Homo sapiens	31-51
18401414-1	2008	We examined the involvement of sphingosine kinase-1 (SphK1), which governs the ceramide/sphingosine-1-phosphate balance, in susceptibility to imatinib of either sensitive or resistant chronic myeloid leukemia cells.	Ceramides	79-87	sphingosine kinase 1	Homo sapiens	53-58
18202145-7	2008	ATGL overexpression in myotubes increased the oxidation of fatty acid liberated from TG and diglyceride and ceramide contents.	Ceramides	108-116	patatin-like phospholipase domain containing 2	Rattus norvegicus	0-4
18281275-12	2008	Treatment of recombinant AC with the cysteine protease inhibitor, methyl methanethiosulfonate, inhibited both cleavage and enzymatic activity, further indicating that cysteine-mediated self-cleavage is required for ceramide hydrolysis.	Ceramides	215-223	N-acylsphingosine amidohydrolase 1	Homo sapiens	25-27
18270325-0	2008	Ceramide induces p38 MAPK and JNK activation through a mechanism involving a thioredoxin-interacting protein-mediated pathway.	Ceramides	0-8	mitogen-activated protein kinase 14	Homo sapiens	17-20
18343365-6	2008	Spisulosine also induced in both PC-3 and LNCaP cells, an activation of the atypical PKC isoform, PKCzeta, which is one of the target proteins of ceramide.	Ceramides	146-154	protein kinase C zeta	Homo sapiens	85-88
18343365-6	2008	Spisulosine also induced in both PC-3 and LNCaP cells, an activation of the atypical PKC isoform, PKCzeta, which is one of the target proteins of ceramide.	Ceramides	146-154	protein kinase C zeta	Homo sapiens	98-105
18343365-7	2008	These results indicate that the marine compound Spisulosine inhibits the growth of the prostate PC-3 and LNCaP cells through intracellular ceramide accumulation and PKCzeta activation.	Ceramides	139-147	proprotein convertase subtilisin/kexin type 1	Homo sapiens	96-100
18426979-0	2008	Remodeling of cellular cytoskeleton by the acid sphingomyelinase/ceramide pathway.	Ceramides	65-73	sphingomyelin phosphodiesterase 1	Homo sapiens	43-64
18270325-0	2008	Ceramide induces p38 MAPK and JNK activation through a mechanism involving a thioredoxin-interacting protein-mediated pathway.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	30-33
18270325-0	2008	Ceramide induces p38 MAPK and JNK activation through a mechanism involving a thioredoxin-interacting protein-mediated pathway.	Ceramides	0-8	thioredoxin interacting protein	Homo sapiens	77-108
18270325-4	2008	Using microarray analysis, we found that ceramide up-regulated a tumor suppressor gene called thioredoxin-interacting protein (Txnip).	Ceramides	41-49	thioredoxin interacting protein	Homo sapiens	94-125
18270325-4	2008	Using microarray analysis, we found that ceramide up-regulated a tumor suppressor gene called thioredoxin-interacting protein (Txnip).	Ceramides	41-49	thioredoxin interacting protein	Homo sapiens	127-132
18270325-5	2008	Similarly, the chemotherapeutic agent etoposide induced Txnip expression en route to apoptosis, which was blocked by inhibitors of ceramide production.	Ceramides	131-139	thioredoxin interacting protein	Homo sapiens	56-61
18270325-7	2008	Cells expressing ASK1 siRNA were more resistant to ceramide-induced apoptosis.	Ceramides	51-59	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	17-21
18270325-8	2008	Ceramide caused ASK1-regulated p38 mitogen-activated protein kinase (MAPK) and JNK activation, as well as activation of the endoplasmic reticulum (ER) stress cascade, and pharmacologic or siRNA-mediated inhibition of p38 MAPK or JNK partially reduced ceramide-induced mitochondria-mediated apoptosis.	Ceramides	0-8	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	16-20
18270325-8	2008	Ceramide caused ASK1-regulated p38 mitogen-activated protein kinase (MAPK) and JNK activation, as well as activation of the endoplasmic reticulum (ER) stress cascade, and pharmacologic or siRNA-mediated inhibition of p38 MAPK or JNK partially reduced ceramide-induced mitochondria-mediated apoptosis.	Ceramides	0-8	mitogen-activated protein kinase 14	Homo sapiens	31-67
18270325-8	2008	Ceramide caused ASK1-regulated p38 mitogen-activated protein kinase (MAPK) and JNK activation, as well as activation of the endoplasmic reticulum (ER) stress cascade, and pharmacologic or siRNA-mediated inhibition of p38 MAPK or JNK partially reduced ceramide-induced mitochondria-mediated apoptosis.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	79-82
18270325-8	2008	Ceramide caused ASK1-regulated p38 mitogen-activated protein kinase (MAPK) and JNK activation, as well as activation of the endoplasmic reticulum (ER) stress cascade, and pharmacologic or siRNA-mediated inhibition of p38 MAPK or JNK partially reduced ceramide-induced mitochondria-mediated apoptosis.	Ceramides	0-8	mitogen-activated protein kinase 14	Homo sapiens	31-34
18270325-8	2008	Ceramide caused ASK1-regulated p38 mitogen-activated protein kinase (MAPK) and JNK activation, as well as activation of the endoplasmic reticulum (ER) stress cascade, and pharmacologic or siRNA-mediated inhibition of p38 MAPK or JNK partially reduced ceramide-induced mitochondria-mediated apoptosis.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	229-232
18270325-8	2008	Ceramide caused ASK1-regulated p38 mitogen-activated protein kinase (MAPK) and JNK activation, as well as activation of the endoplasmic reticulum (ER) stress cascade, and pharmacologic or siRNA-mediated inhibition of p38 MAPK or JNK partially reduced ceramide-induced mitochondria-mediated apoptosis.	Ceramides	251-259	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	16-20
18270325-9	2008	Furthermore, ceramide-induced ASK1, p38, and JNK phosphorylation and cell apoptosis were inhibited by Txnip siRNA transfection.	Ceramides	13-21	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	30-34
18270325-9	2008	Furthermore, ceramide-induced ASK1, p38, and JNK phosphorylation and cell apoptosis were inhibited by Txnip siRNA transfection.	Ceramides	13-21	mitogen-activated protein kinase 14	Homo sapiens	36-39
18270325-9	2008	Furthermore, ceramide-induced ASK1, p38, and JNK phosphorylation and cell apoptosis were inhibited by Txnip siRNA transfection.	Ceramides	13-21	mitogen-activated protein kinase 8	Homo sapiens	45-48
18270325-9	2008	Furthermore, ceramide-induced ASK1, p38, and JNK phosphorylation and cell apoptosis were inhibited by Txnip siRNA transfection.	Ceramides	13-21	thioredoxin interacting protein	Homo sapiens	102-107
18270325-10	2008	Taken together, we show that ceramide exhibits a mechanism of transcriptional regulation involving up-regulation of Txnip expression, also induced by etoposide, which results in ASK1 activation, ER stress, and p38 and JNK phosphorylation, all leading to apoptosis.	Ceramides	29-37	thioredoxin interacting protein	Homo sapiens	116-121
18270325-10	2008	Taken together, we show that ceramide exhibits a mechanism of transcriptional regulation involving up-regulation of Txnip expression, also induced by etoposide, which results in ASK1 activation, ER stress, and p38 and JNK phosphorylation, all leading to apoptosis.	Ceramides	29-37	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	178-182
18270325-10	2008	Taken together, we show that ceramide exhibits a mechanism of transcriptional regulation involving up-regulation of Txnip expression, also induced by etoposide, which results in ASK1 activation, ER stress, and p38 and JNK phosphorylation, all leading to apoptosis.	Ceramides	29-37	mitogen-activated protein kinase 14	Homo sapiens	210-213
18270325-10	2008	Taken together, we show that ceramide exhibits a mechanism of transcriptional regulation involving up-regulation of Txnip expression, also induced by etoposide, which results in ASK1 activation, ER stress, and p38 and JNK phosphorylation, all leading to apoptosis.	Ceramides	29-37	mitogen-activated protein kinase 8	Homo sapiens	218-221
18166162-8	2008	One subset of raft is enriched with cholesterol-sphingomyeline-ganglioside-cav-1/Src/EGFR (hereafter, "chol-raft") that is involved in normal cell signaling, and when dysregulated promotes cell transformation and tumor progression; another subset of raft is enriched with ceramide-sphingomyeline-ganglioside-FAS/Ezrin (hereafter, "cer-raft") that generally promotes apoptosis.	Ceramides	272-280	caveolin 1	Homo sapiens	75-80
18382692-5	2008	Herein, global lipid profiling demonstrates that Hsp70 membrane-positive tumors differ from their membrane-negative counterparts by containing significantly higher amounts of globotriaoslyceramide (Gb3), but not of other lipids such as lactosylceramide (LacCer), dodecasaccharideceramide (DoCer), galactosylceramide (GalCer), ceramide (Cer), or the ganglioside GM1.	Ceramides	188-196	Heat-shock-protein-70Ab	Drosophila melanogaster	49-54
18382692-5	2008	Herein, global lipid profiling demonstrates that Hsp70 membrane-positive tumors differ from their membrane-negative counterparts by containing significantly higher amounts of globotriaoslyceramide (Gb3), but not of other lipids such as lactosylceramide (LacCer), dodecasaccharideceramide (DoCer), galactosylceramide (GalCer), ceramide (Cer), or the ganglioside GM1.	Ceramides	257-260	Heat-shock-protein-70Ab	Drosophila melanogaster	49-54
18297110-2	2008	We hypothesized that ceramide accumulation was from an age-related loss of endothelial glutathione (GSH) and subsequent activation of neutral sphingomyelinase (nSMase), an enzyme whose activity increases when GSH is limited.	Ceramides	21-29	sphingomyelin phosphodiesterase 2	Rattus norvegicus	134-158
18297110-2	2008	We hypothesized that ceramide accumulation was from an age-related loss of endothelial glutathione (GSH) and subsequent activation of neutral sphingomyelinase (nSMase), an enzyme whose activity increases when GSH is limited.	Ceramides	21-29	sphingomyelin phosphodiesterase 2	Rattus norvegicus	160-166
18166162-8	2008	One subset of raft is enriched with cholesterol-sphingomyeline-ganglioside-cav-1/Src/EGFR (hereafter, "chol-raft") that is involved in normal cell signaling, and when dysregulated promotes cell transformation and tumor progression; another subset of raft is enriched with ceramide-sphingomyeline-ganglioside-FAS/Ezrin (hereafter, "cer-raft") that generally promotes apoptosis.	Ceramides	272-280	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	81-84
18166162-8	2008	One subset of raft is enriched with cholesterol-sphingomyeline-ganglioside-cav-1/Src/EGFR (hereafter, "chol-raft") that is involved in normal cell signaling, and when dysregulated promotes cell transformation and tumor progression; another subset of raft is enriched with ceramide-sphingomyeline-ganglioside-FAS/Ezrin (hereafter, "cer-raft") that generally promotes apoptosis.	Ceramides	272-280	epidermal growth factor receptor	Homo sapiens	85-89
18548166-6	2008	In vitro data indicate that ceramide inhibits insulin signaling, mainly through inactivation of protein kinase B.	Ceramides	28-36	insulin	Homo sapiens	46-53
18228202-3	2008	Long-chain acyl-CoA derivatives, which are catalyzed by human ACSL5, are important metabolites in several biochemical pathways, including ceramide de novo synthesis.	Ceramides	138-146	acyl-CoA synthetase long chain family member 5	Homo sapiens	62-67
18548166-7	2008	In vivo data suggest that ceramide accumulation within muscle cells might be associated with the development of insulin resistance.	Ceramides	26-34	insulin	Homo sapiens	112-119
18086664-2	2008	Although C1P synthesis is thought to occur via phosphorylation of ceramide by ceramide kinase (CerK), the processes that regulate C1P formation and fate remain largely unknown.	Ceramides	66-74	ceramide kinase	Mus musculus	78-93
18376404-2	2008	Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells.	Ceramides	19-27	cystic fibrosis transmembrane conductance regulator	Mus musculus	95-99
18376404-2	2008	Here, we show that ceramide age-dependently accumulates in the respiratory tract of uninfected Cftr-deficient mice owing to an alkalinization of intracellular vesicles in Cftr-deficient cells.	Ceramides	19-27	cystic fibrosis transmembrane conductance regulator	Mus musculus	171-175
18376404-3	2008	This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide.	Ceramides	107-115	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	50-71
18376404-3	2008	This change in pH results in an imbalance between acid sphingomyelinase (Asm) cleavage of sphingomyelin to ceramide and acid ceramidase consumption of ceramide, resulting in the higher levels of ceramide.	Ceramides	107-115	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	73-76
18376404-4	2008	The accumulation of ceramide causes Cftr-deficient mice to suffer from constitutive age-dependent pulmonary inflammation, death of respiratory epithelial cells, deposits of DNA in bronchi and high susceptibility to severe Pseudomonas aeruginosa infections.	Ceramides	20-28	cystic fibrosis transmembrane conductance regulator	Mus musculus	36-40
18376404-5	2008	Partial genetic deficiency of Asm in Cftr(-/-)Smpd1(+/-) mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection.	Ceramides	170-178	cystic fibrosis transmembrane conductance regulator	Mus musculus	94-98
18376404-5	2008	Partial genetic deficiency of Asm in Cftr(-/-)Smpd1(+/-) mice or pharmacological treatment of Cftr-deficient mice with the Asm blocker amitriptyline normalizes pulmonary ceramide and prevents all pathological findings, including susceptibility to infection.	Ceramides	170-178	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	123-126
18086664-2	2008	Although C1P synthesis is thought to occur via phosphorylation of ceramide by ceramide kinase (CerK), the processes that regulate C1P formation and fate remain largely unknown.	Ceramides	66-74	ceramide kinase	Mus musculus	95-99
18086664-7	2008	We further demonstrated that ceramide must be transported to the Golgi complex to be phosphorylated by CerK.	Ceramides	29-37	ceramide kinase	Mus musculus	103-107
18086664-11	2008	Altogether, our results indicate that CerK is essential to C1P formation via phosphorylation of Cer, providing the first insights into mechanisms underlying ceramide access to CerK and C1P trafficking as well as clarifying C1P as a signaling entity.	Ceramides	157-165	ceramide kinase	Mus musculus	38-42
18086664-11	2008	Altogether, our results indicate that CerK is essential to C1P formation via phosphorylation of Cer, providing the first insights into mechanisms underlying ceramide access to CerK and C1P trafficking as well as clarifying C1P as a signaling entity.	Ceramides	157-165	ceramide kinase	Mus musculus	176-180
18255161-8	2008	Interestingly we found a substantial elevation of CD21+ T cells during both spontaneous and ceramide-induced apoptosis.	Ceramides	92-100	complement receptor 2	Mus musculus	50-54
18339876-5	2008	This cannabinoid-induced inhibition of MMP-2 expression in gliomas (a) was MMP-2-selective, as levels of other MMP family members were unaffected; (b) was mimicked by JWH-133, a CB(2) cannabinoid receptor-selective agonist that is devoid of psychoactive side effects; (c) was abrogated by fumonisin B1, a selective inhibitor of ceramide biosynthesis; and (d) was also evident in two patients with recurrent glioblastoma multiforme.	Ceramides	328-336	matrix metallopeptidase 2	Homo sapiens	39-44
18339876-5	2008	This cannabinoid-induced inhibition of MMP-2 expression in gliomas (a) was MMP-2-selective, as levels of other MMP family members were unaffected; (b) was mimicked by JWH-133, a CB(2) cannabinoid receptor-selective agonist that is devoid of psychoactive side effects; (c) was abrogated by fumonisin B1, a selective inhibitor of ceramide biosynthesis; and (d) was also evident in two patients with recurrent glioblastoma multiforme.	Ceramides	328-336	matrix metallopeptidase 2	Homo sapiens	39-42
18339876-8	2008	Cannabinoid-induced inhibition of MMP-2 expression and cell invasion was prevented by blocking ceramide biosynthesis and by knocking-down the expression of the stress protein p8.	Ceramides	95-103	matrix metallopeptidase 2	Homo sapiens	34-39
17979982-0	2008	Ceramide enrichment of the plasma membrane induces CD81 internalization and inhibits hepatitis C virus entry.	Ceramides	0-8	CD81 molecule	Homo sapiens	51-55
18245333-2	2008	ASAH1 hydrolyzes ceramides and regulates neuronal development, and its deficiency often results in mental retardation.	Ceramides	17-26	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-5
18165232-8	2008	These results suggest that CERT is a physiological substrate of PP2Cepsilon and that dephosphorylation of CERT by PP2Cepsilon may play an important role in the regulation of ceramide trafficking from the ER to the Golgi apparatus.	Ceramides	174-182	ceramide transporter 1	Homo sapiens	27-31
18165232-8	2008	These results suggest that CERT is a physiological substrate of PP2Cepsilon and that dephosphorylation of CERT by PP2Cepsilon may play an important role in the regulation of ceramide trafficking from the ER to the Golgi apparatus.	Ceramides	174-182	protein phosphatase, Mg2+/Mn2+ dependent 1L	Homo sapiens	64-75
18165232-8	2008	These results suggest that CERT is a physiological substrate of PP2Cepsilon and that dephosphorylation of CERT by PP2Cepsilon may play an important role in the regulation of ceramide trafficking from the ER to the Golgi apparatus.	Ceramides	174-182	ceramide transporter 1	Homo sapiens	106-110
18165232-8	2008	These results suggest that CERT is a physiological substrate of PP2Cepsilon and that dephosphorylation of CERT by PP2Cepsilon may play an important role in the regulation of ceramide trafficking from the ER to the Golgi apparatus.	Ceramides	174-182	protein phosphatase, Mg2+/Mn2+ dependent 1L	Homo sapiens	114-125
17983354-0	2008	Targeting of PKCzeta and PKB to caveolin-enriched microdomains represents a crucial step underpinning the disruption in PKB-directed signalling by ceramide.	Ceramides	147-155	protein kinase C, zeta	Mus musculus	13-20
17983354-0	2008	Targeting of PKCzeta and PKB to caveolin-enriched microdomains represents a crucial step underpinning the disruption in PKB-directed signalling by ceramide.	Ceramides	147-155	thymoma viral proto-oncogene 1	Mus musculus	25-28
17983354-0	2008	Targeting of PKCzeta and PKB to caveolin-enriched microdomains represents a crucial step underpinning the disruption in PKB-directed signalling by ceramide.	Ceramides	147-155	thymoma viral proto-oncogene 1	Mus musculus	120-123
17983354-1	2008	Elevated ceramide concentrations in adipocytes and skeletal muscle impair PKB (protein kinase B; also known as Akt)-directed insulin signalling to key hormonal end points.	Ceramides	9-17	thymoma viral proto-oncogene 1	Mus musculus	74-77
17983354-1	2008	Elevated ceramide concentrations in adipocytes and skeletal muscle impair PKB (protein kinase B; also known as Akt)-directed insulin signalling to key hormonal end points.	Ceramides	9-17	thymoma viral proto-oncogene 1	Mus musculus	111-114
17983354-2	2008	An important feature of this inhibition involves the ceramide-induced activation of atypical PKCzeta (protein kinase C-zeta), which associates with and negatively regulates PKB.	Ceramides	53-61	protein kinase C, zeta	Mus musculus	93-100
17983354-2	2008	An important feature of this inhibition involves the ceramide-induced activation of atypical PKCzeta (protein kinase C-zeta), which associates with and negatively regulates PKB.	Ceramides	53-61	protein kinase C, zeta	Mus musculus	102-123
17983354-2	2008	An important feature of this inhibition involves the ceramide-induced activation of atypical PKCzeta (protein kinase C-zeta), which associates with and negatively regulates PKB.	Ceramides	53-61	thymoma viral proto-oncogene 1	Mus musculus	173-176
17983354-4	2008	Ceramide also recruits PTEN (phosphatase and tensin homologue detected on chromosome 10), a 3"-phosphoinositide phosphatase, thereby creating a repressive membrane microenvironment from which PKB cannot signal.	Ceramides	0-8	phosphatase and tensin homolog	Mus musculus	23-27
17983354-4	2008	Ceramide also recruits PTEN (phosphatase and tensin homologue detected on chromosome 10), a 3"-phosphoinositide phosphatase, thereby creating a repressive membrane microenvironment from which PKB cannot signal.	Ceramides	0-8	thymoma viral proto-oncogene 1	Mus musculus	192-195
17983354-5	2008	Disrupting the structural integrity of caveolae by cholesterol depletion prevented caveolar targeting of PKCzeta and PKB and suppressed kinase-caveolin association, but, importantly, also ameliorated ceramide-induced inhibition of PKB.	Ceramides	200-208	thymoma viral proto-oncogene 1	Mus musculus	231-234
17983354-6	2008	Consistent with this, adipocytes from caveolin-1-/- mice, which lack functional caveolae, exhibit greater resistance to ceramide compared with caveolin-1+/+ adipocytes.	Ceramides	120-128	caveolin 1, caveolae protein	Mus musculus	38-48
17983354-7	2008	We conclude that the recruitment and retention of PKB within CEM contribute significantly to ceramide-induced inhibition of PKB-directed signalling.	Ceramides	93-101	thymoma viral proto-oncogene 1	Mus musculus	50-53
17983354-7	2008	We conclude that the recruitment and retention of PKB within CEM contribute significantly to ceramide-induced inhibition of PKB-directed signalling.	Ceramides	93-101	thymoma viral proto-oncogene 1	Mus musculus	124-127
18204081-6	2008	Addition of soluble ceramide to the cells induced a senescence phenotype that is blocked through PPP1CA downregulation by specific shRNA.	Ceramides	20-28	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	97-103
18204081-9	2008	We propose that oncogenic stress induced by ras causes ceramide accumulation, therefore, increasing PPP1CA activity, pRb dephosphorylation and onset of the p53-induced arrest, contributing to tumor suppression.	Ceramides	55-63	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	100-106
18204081-9	2008	We propose that oncogenic stress induced by ras causes ceramide accumulation, therefore, increasing PPP1CA activity, pRb dephosphorylation and onset of the p53-induced arrest, contributing to tumor suppression.	Ceramides	55-63	RB transcriptional corepressor 1	Homo sapiens	117-120
18204081-9	2008	We propose that oncogenic stress induced by ras causes ceramide accumulation, therefore, increasing PPP1CA activity, pRb dephosphorylation and onset of the p53-induced arrest, contributing to tumor suppression.	Ceramides	55-63	tumor protein p53	Homo sapiens	156-159
18205190-0	2008	Long-chain ceramide is elevated in presenilin 1 (PS1M146V) mouse brain and induces apoptosis in PS1 astrocytes.	Ceramides	11-19	presenilin 1	Mus musculus	35-47
18205190-0	2008	Long-chain ceramide is elevated in presenilin 1 (PS1M146V) mouse brain and induces apoptosis in PS1 astrocytes.	Ceramides	11-19	presenilin 1	Mus musculus	49-52
18205190-3	2008	We found that PS1 tissue contains 3.1 (+/-0.5)-fold more total ceramide than wild-type tissue.	Ceramides	63-71	presenilin 1	Mus musculus	14-17
18205190-5	2008	The ceramide elevation in PS1 brain is consistent with a 3.7 (+/-0.5)-fold increase of the protein level of the neurotrophin receptor p75NTR, which has been suggested to stimulate the hydrolysis of sphingomyelin to generate ceramide.	Ceramides	4-12	presenilin 1	Mus musculus	26-29
18205190-5	2008	The ceramide elevation in PS1 brain is consistent with a 3.7 (+/-0.5)-fold increase of the protein level of the neurotrophin receptor p75NTR, which has been suggested to stimulate the hydrolysis of sphingomyelin to generate ceramide.	Ceramides	4-12	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	134-140
18205190-5	2008	The ceramide elevation in PS1 brain is consistent with a 3.7 (+/-0.5)-fold increase of the protein level of the neurotrophin receptor p75NTR, which has been suggested to stimulate the hydrolysis of sphingomyelin to generate ceramide.	Ceramides	224-232	presenilin 1	Mus musculus	26-29
18205190-5	2008	The ceramide elevation in PS1 brain is consistent with a 3.7 (+/-0.5)-fold increase of the protein level of the neurotrophin receptor p75NTR, which has been suggested to stimulate the hydrolysis of sphingomyelin to generate ceramide.	Ceramides	224-232	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	134-140
18205190-6	2008	The predominance of C20 and C24 ceramide is concurrent with the elevated gene expression of lass 2 and lass 4, two isoforms of ceramide synthase that generate dihydroceramide with long-chain fatty acid.	Ceramides	32-40	ceramide synthase 4	Mus musculus	103-109
18205190-9	2008	The sensitivity of PS1 astrocytes is most likely due to the 9.5 (+/-0.4)-fold elevated expression of PAR-4 (prostate apoptosis response-4), a protein that inhibits atypical PKC zeta/lambda in the presence of ceramide.	Ceramides	208-216	presenilin 1	Mus musculus	19-22
18205190-9	2008	The sensitivity of PS1 astrocytes is most likely due to the 9.5 (+/-0.4)-fold elevated expression of PAR-4 (prostate apoptosis response-4), a protein that inhibits atypical PKC zeta/lambda in the presence of ceramide.	Ceramides	208-216	PRKC, apoptosis, WT1, regulator	Mus musculus	101-106
18205190-9	2008	The sensitivity of PS1 astrocytes is most likely due to the 9.5 (+/-0.4)-fold elevated expression of PAR-4 (prostate apoptosis response-4), a protein that inhibits atypical PKC zeta/lambda in the presence of ceramide.	Ceramides	208-216	PRKC, apoptosis, WT1, regulator	Mus musculus	108-137
18292930-0	2008	Modulation of ceramide metabolism in T-leukemia cell lines potentiates apoptosis induced by the cationic antimicrobial peptide bovine lactoferricin.	Ceramides	14-22	lactotransferrin	Homo sapiens	134-147
18292930-6	2008	Treatment with C6 ceramide, a cell-permeable, short-chain ceramide analog, also induced apoptotic nuclear morphology, PARP cleavage, and DNA fragmentation in T-leukemia cells.	Ceramides	18-26	poly(ADP-ribose) polymerase 1	Homo sapiens	118-122
18292930-8	2008	Furthermore, modulation of cellular ceramide metabolism either by inhibiting ceramidases with D-erythro-2-(N-myristoylamino)-1-phenyl-1-propanol or N-oleoylethanolamine, or by blocking glucosylceramide synthase activity with 1-phenyl-2-palmitoylamino-3-morpholino-1-propanol, enhanced the ability of LfcinB to trigger apoptosis in both Jurkat and CCRF-CEM cells.	Ceramides	36-44	UDP-glucose ceramide glucosyltransferase	Homo sapiens	185-210
17979982-7	2008	Importantly, ceramide enrichment of the plasma membrane led to a 50% decrease in cell-surface CD81, which was due to its ATP-independent internalization.	Ceramides	13-21	CD81 molecule	Homo sapiens	94-98
17979982-8	2008	Our results strongly suggest that the ceramide-induced internalization of CD81 is responsible for the inhibitory effect of ceramide on HCV entry.	Ceramides	38-46	CD81 molecule	Homo sapiens	74-78
17979982-8	2008	Our results strongly suggest that the ceramide-induced internalization of CD81 is responsible for the inhibitory effect of ceramide on HCV entry.	Ceramides	123-131	CD81 molecule	Homo sapiens	74-78
18156590-1	2008	Ceramide-1-phosphate (C1P) is a novel bioactive sphingolipid formed by the phosphorylation of ceramide catalyzed by ceramide kinase (CERK).	Ceramides	94-102	ceramide kinase	Homo sapiens	133-137
18336673-3	2008	Tumor necrosis factor alpha (TNF) has been considered a key ALD mediator with acidic sphingomyelinase (ASMase)-mediated ceramide generation playing a critical role.	Ceramides	120-128	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	78-101
18336673-3	2008	Tumor necrosis factor alpha (TNF) has been considered a key ALD mediator with acidic sphingomyelinase (ASMase)-mediated ceramide generation playing a critical role.	Ceramides	120-128	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	103-109
18292572-1	2008	In mammals, ceramide kinase (CerK)-mediated phosphorylation of ceramide is the only known pathway to ceramide-1-phosphate (C1P), a recently identified signaling sphingolipid metabolite.	Ceramides	12-20	ceramide kinase	Mus musculus	29-33
18073406-9	2008	Sufficient ceramide is transferred to permeabilize the outer membrane to cytochrome c and adenylate kinase.	Ceramides	11-19	cytochrome c, somatic	Homo sapiens	73-85
18083977-4	2008	In smooth muscle cells, exogenously supplemented ceramide inhibited classical nuclear protein import that involved the activation of cytosolic p38 mitogen-activated protein kinase (MAPK).	Ceramides	49-57	mitogen-activated protein kinase 14	Homo sapiens	143-179
18162584-0	2008	StARD13(Dlc-2) RhoGap mediates ceramide activation of phosphatidylglycerolphosphate synthase and drug response in Chinese hamster ovary cells.	Ceramides	31-39	stAR-related lipid transfer protein 13	Cricetulus griseus	0-7
18083977-7	2008	Furthermore, cell counts, nuclear cyclin A, and proliferating cell nuclear antigen expression, markers of cellular proliferation, were diminished after ceramide treatment and effectively rescued by the addition of inhibitor.	Ceramides	152-160	cyclin A2	Homo sapiens	34-42
17709137-2	2008	Glucosylceramide synthase (GCS) catalyzes glycosylation of ceramide and produces glucosylceramide.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
17709137-3	2008	Through GCS, ceramide glycosylation allows cellular escape from ceramide-induced programmed cell death.	Ceramides	13-21	UDP-glucose ceramide glucosyltransferase	Homo sapiens	8-11
17709137-3	2008	Through GCS, ceramide glycosylation allows cellular escape from ceramide-induced programmed cell death.	Ceramides	64-72	UDP-glucose ceramide glucosyltransferase	Homo sapiens	8-11
18162584-7	2008	These results suggested that intracellular ceramide signaling was defective in E91 cells due to increased levels of active GTP-bound RhoA.	Ceramides	43-51	transforming protein RhoA	Cricetulus griseus	133-137
18162584-9	2008	Expression of a dominant-negative RhoA in the E91 cell line allowed induction of PGP synthase by ceramide.	Ceramides	97-105	transforming protein RhoA	Cricetulus griseus	34-38
18165233-6	2008	CerS2 has a remarkable acyl-CoA specificity, showing no activity using C16:0-CoA and very low activity using C18:0, rather utilizing longer acyl-chain CoAs (C20-C26) for ceramide synthesis.	Ceramides	170-178	ceramide synthase 2	Homo sapiens	0-5
18226198-4	2008	In the present paper, the ceramide content and production in the CCl4- and ethanol-treated liver and hepatocytes as well as the correction of sphingolipid metabolism in the damaged liver using the mixture of German chamomile flavonoids (chamiloflan) or apigenin-7-glucoside (AP7Glu) have been investigated.	Ceramides	26-34	C-C motif chemokine ligand 4	Rattus norvegicus	65-69
18054155-0	2008	Ceramide induces p38 MAPK-dependent apoptosis and Bax translocation via inhibition of Akt in HL-60 cells.	Ceramides	0-8	mitogen-activated protein kinase 14	Homo sapiens	17-20
18054155-0	2008	Ceramide induces p38 MAPK-dependent apoptosis and Bax translocation via inhibition of Akt in HL-60 cells.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	50-53
18054155-0	2008	Ceramide induces p38 MAPK-dependent apoptosis and Bax translocation via inhibition of Akt in HL-60 cells.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	86-89
18054155-1	2008	Ceramide induces apoptosis through caspase activation, cytochrome c release, and Bax translocation in HL-60 cells.	Ceramides	0-8	cytochrome c, somatic	Homo sapiens	55-67
18054155-1	2008	Ceramide induces apoptosis through caspase activation, cytochrome c release, and Bax translocation in HL-60 cells.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	81-84
18054155-2	2008	However, the upstream signal transduction pathways that induce Bax translocation during ceramide-mediated apoptosis have not been well defined yet.	Ceramides	88-96	BCL2 associated X, apoptosis regulator	Homo sapiens	63-66
18054155-4	2008	Pharmacological inhibition of p38 MAPK with SB203580 or expression of a dominant-negative p38 MAPK attenuated DNA fragmentation, caspase-3 activation, and Bax translocation in response to ceramide.	Ceramides	188-196	mitogen-activated protein kinase 14	Homo sapiens	30-33
18054155-4	2008	Pharmacological inhibition of p38 MAPK with SB203580 or expression of a dominant-negative p38 MAPK attenuated DNA fragmentation, caspase-3 activation, and Bax translocation in response to ceramide.	Ceramides	188-196	mitogen-activated protein kinase 14	Homo sapiens	90-93
18054155-4	2008	Pharmacological inhibition of p38 MAPK with SB203580 or expression of a dominant-negative p38 MAPK attenuated DNA fragmentation, caspase-3 activation, and Bax translocation in response to ceramide.	Ceramides	188-196	caspase 3	Homo sapiens	129-138
18054155-4	2008	Pharmacological inhibition of p38 MAPK with SB203580 or expression of a dominant-negative p38 MAPK attenuated DNA fragmentation, caspase-3 activation, and Bax translocation in response to ceramide.	Ceramides	188-196	BCL2 associated X, apoptosis regulator	Homo sapiens	155-158
18054155-5	2008	Overexpression of Akt also led to suppression of Bax translocation to mitochondria during ceramide-induced apoptosis in HL-60 cells.	Ceramides	90-98	AKT serine/threonine kinase 1	Homo sapiens	18-21
18054155-5	2008	Overexpression of Akt also led to suppression of Bax translocation to mitochondria during ceramide-induced apoptosis in HL-60 cells.	Ceramides	90-98	BCL2 associated X, apoptosis regulator	Homo sapiens	49-52
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).	Ceramides	231-239	glucosylceramidase beta	Homo sapiens	145-148
18249168-0	2008	More chores for TOR: de novo ceramide synthesis.	Ceramides	29-37	RAR related orphan receptor C	Homo sapiens	16-19
18249174-6	2008	Because Ypk2 is activated independently by LCBs, the direct precursors to ceramides, our data suggest a model wherein TORC2 signaling is coupled with LCB levels to control Ypk2 activity and, ultimately, regulate ceramide formation.	Ceramides	74-83	putative protein kinase YPK2	Saccharomyces cerevisiae S288C	8-12
18249174-6	2008	Because Ypk2 is activated independently by LCBs, the direct precursors to ceramides, our data suggest a model wherein TORC2 signaling is coupled with LCB levels to control Ypk2 activity and, ultimately, regulate ceramide formation.	Ceramides	74-83	putative protein kinase YPK2	Saccharomyces cerevisiae S288C	172-176
18249174-6	2008	Because Ypk2 is activated independently by LCBs, the direct precursors to ceramides, our data suggest a model wherein TORC2 signaling is coupled with LCB levels to control Ypk2 activity and, ultimately, regulate ceramide formation.	Ceramides	74-82	putative protein kinase YPK2	Saccharomyces cerevisiae S288C	8-12
18249174-6	2008	Because Ypk2 is activated independently by LCBs, the direct precursors to ceramides, our data suggest a model wherein TORC2 signaling is coupled with LCB levels to control Ypk2 activity and, ultimately, regulate ceramide formation.	Ceramides	74-82	putative protein kinase YPK2	Saccharomyces cerevisiae S288C	172-176
17982138-1	2008	Sphingomyelin synthase (SMS), the last enzyme in the sphingomyelin (SM) biosynthetic pathway, uses ceramide and phosphatidylcholine as substrates to produce SM and diacylglycerol (DAG).	Ceramides	99-107	spermine synthase	Homo sapiens	0-22
17982138-1	2008	Sphingomyelin synthase (SMS), the last enzyme in the sphingomyelin (SM) biosynthetic pathway, uses ceramide and phosphatidylcholine as substrates to produce SM and diacylglycerol (DAG).	Ceramides	99-107	spermine synthase	Homo sapiens	24-27
18032586-1	2008	Acid sphingomyelinase (ASM) converts sphingomyelin (SM) into ceramide.	Ceramides	61-69	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
18155680-0	2008	Glucosylceramide synthase decrease in frontal cortex of Alzheimer brain correlates with abnormal increase in endogenous ceramides: consequences to morphology and viability on enzyme suppression in cultured primary neurons.	Ceramides	120-129	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-25
18045865-2	2008	This process involves an NADPH oxidase-dependent generation of reactive oxygen species (ROS) through a ceramide- and protein kinase Czeta-dependent pathway, which leads to an activating phosphorylation of p47(phox).	Ceramides	103-111	NSFL1 cofactor	Rattus norvegicus	205-208
18045865-3	2008	The mechanisms underlying CD95L-induced ceramide formation were addressed in the present study.	Ceramides	40-48	Fas ligand	Rattus norvegicus	26-31
18045865-5	2008	Bafilomycin or 4,4"-diisothiocyanostilbene-2,2"-disulfonic acid disodium salt largely abolished the CD95L-induced endosomal acidification, ceramide formation, and downstream events, such as p47(phox) phosphorylation, ROS formation, CD95 activation, and apoptosis.	Ceramides	139-147	Fas ligand	Rattus norvegicus	100-105
18045865-7	2008	Interestingly, caspase 8 inhibitors abolished these CD95L-induced signaling events, including the increase in cytosolic [Cl(-)], endosomal acidification, ceramide formation, and ROS generation as well as CD95 targeting to the plasma membrane and CD95 activation.	Ceramides	154-162	caspase 8	Rattus norvegicus	15-24
18045865-7	2008	Interestingly, caspase 8 inhibitors abolished these CD95L-induced signaling events, including the increase in cytosolic [Cl(-)], endosomal acidification, ceramide formation, and ROS generation as well as CD95 targeting to the plasma membrane and CD95 activation.	Ceramides	154-162	Fas ligand	Rattus norvegicus	52-57
18045865-8	2008	The data suggest that CD95L initiates a rapid caspase 8-dependent endosomal acidification, which triggers ceramide-dependent ROS formation as an upstream event of trafficking of intracellularly stored CD95 to the plasma membrane.	Ceramides	106-114	Fas ligand	Rattus norvegicus	22-27
18045865-8	2008	The data suggest that CD95L initiates a rapid caspase 8-dependent endosomal acidification, which triggers ceramide-dependent ROS formation as an upstream event of trafficking of intracellularly stored CD95 to the plasma membrane.	Ceramides	106-114	caspase 8	Rattus norvegicus	46-55
18226198-7	2008	Addition of the CCl4 or ethanol to isolated hepatocyte suspensions caused loss of cell viability and increased the lactate dehydrogenase release from the cells into supernatant and ceramide level in the cells.	Ceramides	181-189	C-C motif chemokine ligand 4	Rattus norvegicus	16-20
18226198-8	2008	CCl4 administration to the rats enlarged ceramide mass as well as neutral sphingomyelinase (SMase) activity and reduced ceramide degradation by the neutral ceramidase.	Ceramides	41-49	C-C motif chemokine ligand 4	Rattus norvegicus	0-4
18226198-8	2008	CCl4 administration to the rats enlarged ceramide mass as well as neutral sphingomyelinase (SMase) activity and reduced ceramide degradation by the neutral ceramidase.	Ceramides	120-128	C-C motif chemokine ligand 4	Rattus norvegicus	0-4
18184806-0	2008	Structural basis for specific lipid recognition by CERT responsible for nonvesicular trafficking of ceramide.	Ceramides	100-108	ceramide transporter 1	Homo sapiens	51-55
18184806-2	2008	Ceramide transport occurs in a nonvesicular manner and is mediated by CERT, a cytosolic 68-kDa protein with a C-terminal steroidogenic acute regulatory protein-related lipid transfer (START) domain.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	70-74
18184806-5	2008	Here we report the crystal structures of the CERT START domain in its apo-form and in complex with ceramides having different acyl chain lengths.	Ceramides	99-108	ceramide transporter 1	Homo sapiens	45-49
18184806-11	2008	Thus, the structures demonstrate the structural basis for the mechanism by which CERT can distinguish ceramide from other lipid types yet still recognize multiple species of ceramides.	Ceramides	102-110	ceramide transporter 1	Homo sapiens	81-85
18184806-11	2008	Thus, the structures demonstrate the structural basis for the mechanism by which CERT can distinguish ceramide from other lipid types yet still recognize multiple species of ceramides.	Ceramides	174-183	ceramide transporter 1	Homo sapiens	81-85
17656682-5	2008	We report that Cftr-knockout mice display diminished ceramide levels in CF-related organs (lung, pancreas, ileum, and plasma) compared with their littermate controls.	Ceramides	53-61	cystic fibrosis transmembrane conductance regulator	Mus musculus	15-19
17959603-8	2008	In contrast, the exogenous expression of p21 or the silencing of Beclin 1 and Atg5 with small interfering RNA increased the number of apoptotic cells and decreased the number of autophagic cells among C(2)-ceramide-treated p21(-/-) MEFs.	Ceramides	206-214	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	41-44
17959603-8	2008	In contrast, the exogenous expression of p21 or the silencing of Beclin 1 and Atg5 with small interfering RNA increased the number of apoptotic cells and decreased the number of autophagic cells among C(2)-ceramide-treated p21(-/-) MEFs.	Ceramides	206-214	beclin 1, autophagy related	Mus musculus	65-73
17959603-8	2008	In contrast, the exogenous expression of p21 or the silencing of Beclin 1 and Atg5 with small interfering RNA increased the number of apoptotic cells and decreased the number of autophagic cells among C(2)-ceramide-treated p21(-/-) MEFs.	Ceramides	206-214	autophagy related 5	Mus musculus	78-82
17959603-8	2008	In contrast, the exogenous expression of p21 or the silencing of Beclin 1 and Atg5 with small interfering RNA increased the number of apoptotic cells and decreased the number of autophagic cells among C(2)-ceramide-treated p21(-/-) MEFs.	Ceramides	206-214	cyclin-dependent kinase inhibitor 1A (P21)	Mus musculus	223-226
18068681-0	2008	Ceramide traffic in C6 glioma cells: evidence for CERT-dependent and independent transport from ER to the Golgi apparatus.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	50-54
18068681-2	2008	The recent identification of the ceramide specific carrier protein CERT has revealed a novel pathway for the delivery of ceramide to the Golgi apparatus for sphingomyelin biosynthesis.	Ceramides	33-41	ceramide transporter 1	Homo sapiens	67-71
18068681-2	2008	The recent identification of the ceramide specific carrier protein CERT has revealed a novel pathway for the delivery of ceramide to the Golgi apparatus for sphingomyelin biosynthesis.	Ceramides	121-129	ceramide transporter 1	Homo sapiens	67-71
18068681-5	2008	Metabolic experiments performed with different radioactive metabolic precursors of sphingolipids demonstrated that the down regulation of CERT by RNAi technology resulted in a significant but not complete reduction of ceramide metabolism to sphingomyelin, without affecting its utilization for glycosphingolipid biosynthesis.	Ceramides	218-226	ceramide transporter 1	Homo sapiens	138-142
18068681-6	2008	Since nitric oxide is an inhibitor of ceramide ER-to-Golgi traffic and metabolism in C6 glioma cells, we evaluated the possibility that the CERT-mediated transport of ceramide might represent a target for nitric oxide.	Ceramides	167-175	ceramide transporter 1	Homo sapiens	140-144
18068681-7	2008	The data obtained demonstrate that CERT down regulation does not affect the inhibitory activity of nitric oxide on Cer metabolism, and the effects of nitric oxide and CERT silencing on ceramide utilization were additive.	Ceramides	185-193	ceramide transporter 1	Homo sapiens	167-171
17913601-4	2008	Ceramide is formed from SM by the action of sphingomyelinases (SMase), however, ceramide can be very rapidly hydrolysed, by ceramidases to yield sphingosine, and sphingosine can be phosphorylated by sphingosine kinase (SphK) to yield S1P.	Ceramides	0-8	sphingosine kinase 1	Homo sapiens	199-217
17913601-4	2008	Ceramide is formed from SM by the action of sphingomyelinases (SMase), however, ceramide can be very rapidly hydrolysed, by ceramidases to yield sphingosine, and sphingosine can be phosphorylated by sphingosine kinase (SphK) to yield S1P.	Ceramides	0-8	sphingosine kinase 1	Homo sapiens	219-223
17913601-4	2008	Ceramide is formed from SM by the action of sphingomyelinases (SMase), however, ceramide can be very rapidly hydrolysed, by ceramidases to yield sphingosine, and sphingosine can be phosphorylated by sphingosine kinase (SphK) to yield S1P.	Ceramides	0-8	membrane bound transcription factor peptidase, site 1	Homo sapiens	234-237
17913601-4	2008	Ceramide is formed from SM by the action of sphingomyelinases (SMase), however, ceramide can be very rapidly hydrolysed, by ceramidases to yield sphingosine, and sphingosine can be phosphorylated by sphingosine kinase (SphK) to yield S1P.	Ceramides	80-88	sphingosine kinase 1	Homo sapiens	199-217
17913601-4	2008	Ceramide is formed from SM by the action of sphingomyelinases (SMase), however, ceramide can be very rapidly hydrolysed, by ceramidases to yield sphingosine, and sphingosine can be phosphorylated by sphingosine kinase (SphK) to yield S1P.	Ceramides	80-88	sphingosine kinase 1	Homo sapiens	219-223
17913601-4	2008	Ceramide is formed from SM by the action of sphingomyelinases (SMase), however, ceramide can be very rapidly hydrolysed, by ceramidases to yield sphingosine, and sphingosine can be phosphorylated by sphingosine kinase (SphK) to yield S1P.	Ceramides	80-88	membrane bound transcription factor peptidase, site 1	Homo sapiens	234-237
17913601-11	2008	Binding of S1P to these receptors trigger an wide range of cellular responses including proliferation, enhanced extracellular matrix assembly, stimulation of adherent junctions, formation of actin stress fibres, and inhibition of apoptosis induced by either ceramide or growth factor withdrawal.	Ceramides	258-266	membrane bound transcription factor peptidase, site 1	Homo sapiens	11-14
19087284-11	2008	The Flk-1 antagonist SU5416 obliterated the reduction of ceramide and apoptosis by DC, indicating that enhanced cell survival is due to Flk-1-induced reduction in ceramide.	Ceramides	57-65	kinase insert domain protein receptor	Mus musculus	4-9
19087284-11	2008	The Flk-1 antagonist SU5416 obliterated the reduction of ceramide and apoptosis by DC, indicating that enhanced cell survival is due to Flk-1-induced reduction in ceramide.	Ceramides	57-65	kinase insert domain protein receptor	Mus musculus	136-141
19087284-11	2008	The Flk-1 antagonist SU5416 obliterated the reduction of ceramide and apoptosis by DC, indicating that enhanced cell survival is due to Flk-1-induced reduction in ceramide.	Ceramides	163-171	kinase insert domain protein receptor	Mus musculus	4-9
19087284-11	2008	The Flk-1 antagonist SU5416 obliterated the reduction of ceramide and apoptosis by DC, indicating that enhanced cell survival is due to Flk-1-induced reduction in ceramide.	Ceramides	163-171	kinase insert domain protein receptor	Mus musculus	136-141
19087284-13	2008	Reducing the level or effect of serum DC and elevating ceramide in breast cancer progenitor cells by treatment with Z-guggulsterone and/or vascular endothelial growth factor receptor 2/Flk-1 antagonists may thus be a promising strategy to reduce breast cancer metastasis.	Ceramides	55-63	kinase insert domain protein receptor	Mus musculus	139-184
19087284-13	2008	Reducing the level or effect of serum DC and elevating ceramide in breast cancer progenitor cells by treatment with Z-guggulsterone and/or vascular endothelial growth factor receptor 2/Flk-1 antagonists may thus be a promising strategy to reduce breast cancer metastasis.	Ceramides	55-63	kinase insert domain protein receptor	Mus musculus	185-190
19088422-10	2008	However, upon infection, ceramide formation was stimulated in both, acid sphingomyelinase knockout mice (Smpd1(-/-)) and their wild type littermates (Smpd1(+/+)).	Ceramides	25-33	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	105-110
17964645-2	2008	Although in vitro tumor cell culture models have illuminated the potential therapeutic utility of a cell-permeable analog of ceramide, C(6), in vivo delivery is impeded by the extreme hydrophobicity and physical-chemical properties of this bioactive lipid.	Ceramides	125-133	complement C6	Homo sapiens	135-139
19088422-10	2008	However, upon infection, ceramide formation was stimulated in both, acid sphingomyelinase knockout mice (Smpd1(-/-)) and their wild type littermates (Smpd1(+/+)).	Ceramides	25-33	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	150-155
19058512-7	2008	It was due to stimulating enzymatic degradation of sphingosine-1-phosphate as effective regulator of iNOS, COX and GTP-cyclohydrolase in cardio-vascular system: sphingomyelin > ceramide > sphingosine > S-I-P > phosphoethanolamine > ethanolamine.	Ceramides	180-188	coproporphyrinogen oxidase	Rattus norvegicus	107-110
18406376-1	2008	Acid sphingomyelinase (ASMase) has been implemented in cellular signaling mainly because its reaction product, ceramide, has been assumed to be a mediator within signaling pathways.	Ceramides	111-119	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
17981711-3	2008	Particularly, inhibition of the ceramide metabolizing enzyme acid ceramidase, whose over-expression in cancer cells has been implicated in resistance to treatment, is proving to be an efficient and promising strategy.	Ceramides	32-40	N-acylsphingosine amidohydrolase 1	Homo sapiens	61-76
17981627-4	2008	Inflammatory response after stroke suggests that cytokines (TNF-alpha, IL-1alpha/beta, IL-6), affect the phospholipid metabolism and subsequent production of eicosanoids, ceramide, and ROS that may potentiate brain injury.	Ceramides	171-179	tumor necrosis factor	Homo sapiens	60-69
17981627-4	2008	Inflammatory response after stroke suggests that cytokines (TNF-alpha, IL-1alpha/beta, IL-6), affect the phospholipid metabolism and subsequent production of eicosanoids, ceramide, and ROS that may potentiate brain injury.	Ceramides	171-179	interleukin 1 alpha	Homo sapiens	71-80
17981627-4	2008	Inflammatory response after stroke suggests that cytokines (TNF-alpha, IL-1alpha/beta, IL-6), affect the phospholipid metabolism and subsequent production of eicosanoids, ceramide, and ROS that may potentiate brain injury.	Ceramides	171-179	interleukin 6	Homo sapiens	87-91
18406376-1	2008	Acid sphingomyelinase (ASMase) has been implemented in cellular signaling mainly because its reaction product, ceramide, has been assumed to be a mediator within signaling pathways.	Ceramides	111-119	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
18406376-4	2008	In light of the biochemical and biophysical properties of ceramide, we provide a model suggesting that ASMase regulates select vesicular fusion processes by modifying the steric conformation of cellular membranes.	Ceramides	58-66	sphingomyelin phosphodiesterase 1	Homo sapiens	103-109
17940217-4	2007	Overexpression of DGAT2, which encodes an acyl-CoA:diacylglycerol acyltransferase that catalyzes triacylglycerol (TG) synthesis, in glycolytic muscle of mice increased the content of TG, ceramides, and unsaturated long-chain fatty acyl-CoAs in young adult mice.	Ceramides	187-196	diacylglycerol O-acyltransferase 2	Mus musculus	18-23
18173730-4	2008	We also demonstrate that the saccharides must be attached to a ceramide backbone in order to inhibit SERCA as the ceramide-free ganglioside saccharides only inhibit SERCA to a minimal extent.	Ceramides	63-71	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	101-106
18173730-5	2008	Finally, we attempted to use the ceramide-free ganglioside saccharides to antagonize the effects of the gangliosides on SERCA; although some reversal was observed, the inhibitory effects of the gangliosides were not completely abolished.	Ceramides	33-41	ATPase sarcoplasmic/endoplasmic reticulum Ca2+ transporting 3	Homo sapiens	120-125
17675107-5	2008	This cannabinoid-induced inhibition of TIMP-1 expression in gliomas (i) was mimicked by JWH-133, a selective CB(2) cannabinoid receptor agonist that is devoid of psychoactive side effects, (ii) was abrogated by fumonisin B1, a selective inhibitor of ceramide synthesis de novo, and (iii) was also evident in two patients with recurrent glioblastoma multiforme (grade IV astrocytoma).	Ceramides	250-258	TIMP metallopeptidase inhibitor 1	Homo sapiens	39-45
18751914-5	2008	TNF-alpha and IL-1 alter lipid metabolism and stimulate production of eicosanoids, ceramide, and reactive oxygen species that potentiate CNS injuries and certain neurological disorders.	Ceramides	83-91	tumor necrosis factor	Homo sapiens	0-9
18751914-5	2008	TNF-alpha and IL-1 alter lipid metabolism and stimulate production of eicosanoids, ceramide, and reactive oxygen species that potentiate CNS injuries and certain neurological disorders.	Ceramides	83-91	interleukin 1 alpha	Homo sapiens	14-18
18751923-5	2008	This phenomenon is referred to as IL-1b hyperresponsiveness and is linked to abnormal regulation of various acute phase proteins during aging.Evidence has consistently indicated that activation of neutral sphingomyelinase and the resulting accumulation of ceramide mediate cellular responses to LPS, IL-1beta, and TNFalpha in young animals.	Ceramides	256-264	interleukin 1 beta	Rattus norvegicus	34-39
18751923-5	2008	This phenomenon is referred to as IL-1b hyperresponsiveness and is linked to abnormal regulation of various acute phase proteins during aging.Evidence has consistently indicated that activation of neutral sphingomyelinase and the resulting accumulation of ceramide mediate cellular responses to LPS, IL-1beta, and TNFalpha in young animals.	Ceramides	256-264	interleukin 1 beta	Rattus norvegicus	300-308
18751923-5	2008	This phenomenon is referred to as IL-1b hyperresponsiveness and is linked to abnormal regulation of various acute phase proteins during aging.Evidence has consistently indicated that activation of neutral sphingomyelinase and the resulting accumulation of ceramide mediate cellular responses to LPS, IL-1beta, and TNFalpha in young animals.	Ceramides	256-264	tumor necrosis factor	Rattus norvegicus	314-322
18052040-1	2007	The human acid sphingomyelinase (ASM, EC 3.1.4.12), a lysosomal and secretory protein coded by the sphingomyelin phosphodiesterase 1 (SMPD-1) gene, catalyzes the degradation of sphingomyelin (SM) to ceramide and phosphorylcholine.	Ceramides	199-207	sphingomyelin phosphodiesterase 1	Homo sapiens	10-31
18052040-1	2007	The human acid sphingomyelinase (ASM, EC 3.1.4.12), a lysosomal and secretory protein coded by the sphingomyelin phosphodiesterase 1 (SMPD-1) gene, catalyzes the degradation of sphingomyelin (SM) to ceramide and phosphorylcholine.	Ceramides	199-207	sphingomyelin phosphodiesterase 1	Homo sapiens	33-36
18052040-1	2007	The human acid sphingomyelinase (ASM, EC 3.1.4.12), a lysosomal and secretory protein coded by the sphingomyelin phosphodiesterase 1 (SMPD-1) gene, catalyzes the degradation of sphingomyelin (SM) to ceramide and phosphorylcholine.	Ceramides	199-207	sphingomyelin phosphodiesterase 1	Homo sapiens	99-132
18052040-1	2007	The human acid sphingomyelinase (ASM, EC 3.1.4.12), a lysosomal and secretory protein coded by the sphingomyelin phosphodiesterase 1 (SMPD-1) gene, catalyzes the degradation of sphingomyelin (SM) to ceramide and phosphorylcholine.	Ceramides	199-207	sphingomyelin phosphodiesterase 1	Homo sapiens	134-140
17915332-3	2008	Through its p75NTR receptor, NGF activates proapoptotic signalling pathways including the MAPK c-Jun N-terminal kinase (JNK), ceramides, and the small G protein Rac, but also activates pathways promoting cell survival through the transcription factor nuclear factor-kappaB (NF-kappaB).	Ceramides	126-135	nerve growth factor receptor	Homo sapiens	12-18
18176793-7	2008	Also there was expression of cleaved caspase-3 with C(2)-ceramide treatment.	Ceramides	57-65	caspase 3	Homo sapiens	37-46
18035065-0	2007	Ceramide and glucosylceramide upregulate expression of the multidrug resistance gene MDR1 in cancer cells.	Ceramides	0-8	ATP binding cassette subfamily B member 1	Homo sapiens	85-89
17996206-0	2007	Confluence induced threonine41/serine45 phospho-beta-catenin dephosphorylation via ceramide-mediated activation of PP1cgamma.	Ceramides	83-91	catenin beta 1	Homo sapiens	48-60
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.	Ceramides	87-95	ATP binding cassette subfamily B member 1	Homo sapiens	139-143
17996206-6	2007	The effect of confluence on beta-catenin dephosphorylation was prevented by down regulation of nSMase2 using siRNA; reciprocally, exogenous addition of short or very long chain ceramides induced dephosphorylation of beta-catenin.	Ceramides	177-186	catenin beta 1	Homo sapiens	28-40
17996206-6	2007	The effect of confluence on beta-catenin dephosphorylation was prevented by down regulation of nSMase2 using siRNA; reciprocally, exogenous addition of short or very long chain ceramides induced dephosphorylation of beta-catenin.	Ceramides	177-186	sphingomyelin phosphodiesterase 3	Homo sapiens	95-102
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.	Ceramides	87-95	ATP binding cassette subfamily B member 1	Homo sapiens	190-204
17996206-6	2007	The effect of confluence on beta-catenin dephosphorylation was prevented by down regulation of nSMase2 using siRNA; reciprocally, exogenous addition of short or very long chain ceramides induced dephosphorylation of beta-catenin.	Ceramides	177-186	catenin beta 1	Homo sapiens	216-228
17996206-10	2007	All together these results establish: A) a specific intracellular pathway involving the activation of PP1 to mediate the effects of confluence-induced beta-catenin dephosphorylation and B) PP1 as a lipid-regulated protein phosphatase downstream of nSMase2/ceramide.	Ceramides	256-264	inorganic pyrophosphatase 1	Homo sapiens	102-105
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.	Ceramides	87-95	ATP binding cassette subfamily B member 1	Homo sapiens	206-210
17996206-10	2007	All together these results establish: A) a specific intracellular pathway involving the activation of PP1 to mediate the effects of confluence-induced beta-catenin dephosphorylation and B) PP1 as a lipid-regulated protein phosphatase downstream of nSMase2/ceramide.	Ceramides	256-264	catenin beta 1	Homo sapiens	151-163
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.	Ceramides	87-95	ATP binding cassette subfamily B member 1	Homo sapiens	261-265
17996206-10	2007	All together these results establish: A) a specific intracellular pathway involving the activation of PP1 to mediate the effects of confluence-induced beta-catenin dephosphorylation and B) PP1 as a lipid-regulated protein phosphatase downstream of nSMase2/ceramide.	Ceramides	256-264	inorganic pyrophosphatase 1	Homo sapiens	189-192
17996206-10	2007	All together these results establish: A) a specific intracellular pathway involving the activation of PP1 to mediate the effects of confluence-induced beta-catenin dephosphorylation and B) PP1 as a lipid-regulated protein phosphatase downstream of nSMase2/ceramide.	Ceramides	256-264	sphingomyelin phosphodiesterase 3	Homo sapiens	248-255
18035065-2	2007	Acute exposure (72 h) to C8-ceramide (5 microg/ml culture medium), a cell-permeable ceramide, increased MDR1 mRNA levels by 3- and 5-fold in T47D and in MDA-MB-435 cells, respectively.	Ceramides	28-36	ATP binding cassette subfamily B member 1	Homo sapiens	104-108
18035065-8	2007	Exposing cells to the GCS inhibitor, ethylenedioxy-P4, a substituted analog of 1-phenyl-2-hexadecanoylamino-3-pyrrolidino-1-propanol, prevented ceramide"s enhancement of MDR1 expression.	Ceramides	144-152	ATP binding cassette subfamily B member 1	Homo sapiens	170-174
17888878-1	2007	The discovery of ceramide kinase (CerK), which phosphorylates ceramide (Cer) to ceramide 1-phisphate (C1P), established a new pathway for Cer metabolism.	Ceramides	17-25	ceramide kinase	Mus musculus	34-38
18020949-1	2007	Human acid ceramidase catalyzes the last step of lysosomal sphingolipid degradation, the hydrolysis of ceramide to sphingosine and free fatty acid.	Ceramides	103-111	N-acylsphingosine amidohydrolase 1	Homo sapiens	6-21
17471535-0	2007	PKB/Akt inhibits ceramide-induced apoptosis in neuroblastoma cells by blocking apoptosis-inducing factor (AIF) translocation.	Ceramides	17-25	AKT serine/threonine kinase 1	Homo sapiens	0-3
17471535-0	2007	PKB/Akt inhibits ceramide-induced apoptosis in neuroblastoma cells by blocking apoptosis-inducing factor (AIF) translocation.	Ceramides	17-25	AKT serine/threonine kinase 1	Homo sapiens	4-7
17471535-4	2007	Treatment of the human neuroblastoma cell line SH-SY5Y with ceramide induced dephosphorylation of the PKB/Akt kinase and subsequent mitochondrial dysfunction.	Ceramides	60-68	AKT serine/threonine kinase 1	Homo sapiens	102-105
17471535-4	2007	Treatment of the human neuroblastoma cell line SH-SY5Y with ceramide induced dephosphorylation of the PKB/Akt kinase and subsequent mitochondrial dysfunction.	Ceramides	60-68	AKT serine/threonine kinase 1	Homo sapiens	106-109
17471535-7	2007	Furthermore, overexpression of active PKB/Akt or Bcl-2 successfully blocked ceramide-induced neuronal cell death through inhibition of the translocation of apoptosis-inducing factor.	Ceramides	76-84	AKT serine/threonine kinase 1	Homo sapiens	38-41
17471535-7	2007	Furthermore, overexpression of active PKB/Akt or Bcl-2 successfully blocked ceramide-induced neuronal cell death through inhibition of the translocation of apoptosis-inducing factor.	Ceramides	76-84	AKT serine/threonine kinase 1	Homo sapiens	42-45
17471535-7	2007	Furthermore, overexpression of active PKB/Akt or Bcl-2 successfully blocked ceramide-induced neuronal cell death through inhibition of the translocation of apoptosis-inducing factor.	Ceramides	76-84	BCL2 apoptosis regulator	Homo sapiens	49-54
18166682-0	2007	Peroxisome proliferator-activated receptor alpha down-regulation is associated with enhanced ceramide levels in age-associated cardiac hypertrophy.	Ceramides	93-101	peroxisome proliferator activated receptor alpha	Mus musculus	0-48
18166682-5	2007	The mRNA levels of PPARalpha target genes involved in fatty acid use were strongly suppressed in SAM-P8, which was consistent with the accumulation of ceramide in SAM-P8 hearts (2.5-fold induction, p<.05).	Ceramides	151-159	peroxisome proliferator activated receptor alpha	Mus musculus	19-28
18166682-6	2007	These findings suggest that NF-kappaB activation in SAM-P8 heart prevents PPARalpha from binding to its response elements leading to changes in gene expression that may lead to ceramide accumulation in the aged heart.	Ceramides	177-185	peroxisome proliferator activated receptor alpha	Mus musculus	74-83
17854348-9	2007	The molar ratio between cholesterol, sphingomyelin and ceramide was 15 : 6 : 1 in the PrP-rich environment from control neurons, and 6 : 2 : 1 in that from apoptotic cells.	Ceramides	55-63	prion protein	Rattus norvegicus	86-89
17923691-2	2007	Bcl-x splicing is coupled to signal transduction, since ceramide, hormones, and growth factors alter the ratio of the Bcl-x isoforms in different cell lines.	Ceramides	56-64	BCL2 like 1	Homo sapiens	0-5
17923691-2	2007	Bcl-x splicing is coupled to signal transduction, since ceramide, hormones, and growth factors alter the ratio of the Bcl-x isoforms in different cell lines.	Ceramides	56-64	BCL2 like 1	Homo sapiens	118-123
17895250-1	2007	In yeast, the long-chain sphingoid base phosphate phosphohydrolase Lcb3p is required for efficient ceramide synthesis from exogenous sphingoid bases.	Ceramides	99-107	sphinganine kinase LCB3	Saccharomyces cerevisiae S288C	67-72
17895250-2	2007	Similarly, in this study, we found that incorporation of exogenous sphingosine into ceramide in mammalian cells was regulated by the homologue of Lcb3p, sphingosine-1-phosphate phosphohydrolase 1 (SPP-1), an endoplasmic reticulum resident protein.	Ceramides	84-92	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	146-151
17888878-1	2007	The discovery of ceramide kinase (CerK), which phosphorylates ceramide (Cer) to ceramide 1-phisphate (C1P), established a new pathway for Cer metabolism.	Ceramides	34-37	ceramide kinase	Mus musculus	17-32
17895250-7	2007	Sphingosine kinase 2, but not sphingosine kinase 1, acted in concert with SPP-1 to regulate recycling of sphingosine into ceramide.	Ceramides	122-130	sphingosine kinase 2	Homo sapiens	0-20
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).	Ceramides	28-36	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).	Ceramides	28-36	glucosidase beta 2	Mus musculus	153-157
17828457-7	2007	Pharmacological inhibition of JNK kinase, as well as inhibition of ROS by the reducing agent N-acetylcysteine, prevented ceramide accumulation and capsaicin-induced cell death.	Ceramides	121-129	mitogen-activated protein kinase 8	Homo sapiens	30-33
17828457-9	2007	These data reveal JNK as an upstream regulator of ceramide production.	Ceramides	50-58	mitogen-activated protein kinase 8	Homo sapiens	18-21
17425515-1	2007	The lipid second messenger ceramide regulates the rate of beta cleavage of the Alzheimer"s disease APP (amyloid precursor protein) by affecting the molecular stability of the beta secretase BACE1 (beta-site APP cleaving enzyme 1).	Ceramides	27-35	amyloid beta precursor protein	Homo sapiens	104-129
18225555-6	2007	Moreover, addition of ceramide rescued the NAC-inhibited MAPK activation and pretreatment with the ceramide synthase inhibitor, fumonisin B1, reduced cell death.	Ceramides	22-30	X-linked Kx blood group	Homo sapiens	43-46
17425515-1	2007	The lipid second messenger ceramide regulates the rate of beta cleavage of the Alzheimer"s disease APP (amyloid precursor protein) by affecting the molecular stability of the beta secretase BACE1 (beta-site APP cleaving enzyme 1).	Ceramides	27-35	beta-secretase 1	Homo sapiens	190-195
17425515-1	2007	The lipid second messenger ceramide regulates the rate of beta cleavage of the Alzheimer"s disease APP (amyloid precursor protein) by affecting the molecular stability of the beta secretase BACE1 (beta-site APP cleaving enzyme 1).	Ceramides	27-35	beta-secretase 1	Homo sapiens	197-228
17702848-0	2007	Ceramide and adenosine 5"-monophosphate-activated protein kinase are two novel regulators of 11beta-hydroxysteroid dehydrogenase type 1 expression and activity in cultured preadipocytes.	Ceramides	0-8	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	93-135
17880915-1	2007	The Saccharomyces cerevisiae inositol sphingolipid phospholipase C (Isc1p), a homolog of mammalian neutral sphingomyelinases, hydrolyzes complex sphingolipids to produce ceramide in vitro.	Ceramides	170-178	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	68-73
17880915-9	2007	These results suggest that Isc1p generates ceramide in mitochondria, and the generated ceramide contributes to the normal function of mitochondria.	Ceramides	43-51	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	27-32
18066115-6	2007	Where quantitative structure-activity relationship analysis was insufficient, biochemical assessment demonstrated that the benzoate orsellinic acid blocked downstream caspase-12 activation following ceramide challenge.	Ceramides	199-207	caspase 12	Rattus norvegicus	167-177
17702848-2	2007	As recent studies have highlighted a potential role of preadipocytes in adipose dysfunction, we tested the hypothesis that a variety of metabolic stress mediated by ceramide or AMP-activated protein kinase (AMPK) would regulate 11beta-HSD1 in preadipocytes.	Ceramides	165-173	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	228-239
17702848-6	2007	The present study provides novel evidence that ceramide- and AMPK-mediated signaling pathways augment the expression and activity of 11beta-HSD1 in preadipocytes by way of C/EBPbeta, thereby highlighting a novel, metabolic stress-related regulation of 11beta-HSD1 in a cell-specific manner.	Ceramides	47-55	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	133-144
17702848-6	2007	The present study provides novel evidence that ceramide- and AMPK-mediated signaling pathways augment the expression and activity of 11beta-HSD1 in preadipocytes by way of C/EBPbeta, thereby highlighting a novel, metabolic stress-related regulation of 11beta-HSD1 in a cell-specific manner.	Ceramides	47-55	CCAAT enhancer binding protein beta	Homo sapiens	172-181
17702848-6	2007	The present study provides novel evidence that ceramide- and AMPK-mediated signaling pathways augment the expression and activity of 11beta-HSD1 in preadipocytes by way of C/EBPbeta, thereby highlighting a novel, metabolic stress-related regulation of 11beta-HSD1 in a cell-specific manner.	Ceramides	47-55	hydroxysteroid 11-beta dehydrogenase 1	Homo sapiens	252-263
17595345-4	2007	Silencing of BCRP expression in BeWo cells significantly increased their sensitivity to apoptotic injury in response to cytokines and exogenous C6 and C8 ceramides.	Ceramides	154-163	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	13-17
17595345-5	2007	BCRP silencing also increased intracellular ceramide levels after cytokine exposure but did not affect cellular protoporphyrin IX concentrations or sensitivity to activators of the intrinsic apoptotic pathway.	Ceramides	44-52	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	0-4
17595345-7	2007	We conclude that BCRP may play a hitherto unrecognized survival role in the placenta, protecting the trophoblast against cytokine-induced apoptosis and possibly other extrinsic activators via modulation of ceramide signaling.	Ceramides	206-214	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	17-21
17627285-0	2007	Ceramide-induced G2 arrest in rhabdomyosarcoma (RMS) cells requires p21Cip1/Waf1 induction and is prevented by MDM2 overexpression.	Ceramides	0-8	cyclin dependent kinase inhibitor 1A	Homo sapiens	68-75
17724577-1	2007	AIMS/HYPOTHESIS: Intramyocellular lipids, including ceramide, a second messenger in the sphingomyelin signalling pathway, might contribute to the development of insulin resistance.	Ceramides	52-60	insulin	Homo sapiens	161-168
17724577-11	2007	Muscle ceramide was related to insulin sensitivity independently of other muscle lipid fractions.	Ceramides	7-15	insulin	Homo sapiens	31-38
17876892-8	2007	Lipid analysis showed rapid accumulation of ceramide in the membrane fractions containing occludin and claudin-4, representing TJs.	Ceramides	44-52	occludin	Homo sapiens	90-98
17876892-8	2007	Lipid analysis showed rapid accumulation of ceramide in the membrane fractions containing occludin and claudin-4, representing TJs.	Ceramides	44-52	claudin 4	Homo sapiens	103-112
17760463-9	2007	Our results show that cellular sphingolipids, ceramide and sphingomyelin, have important effects on the post-transcriptional handling of nascent apoE by macrophages.	Ceramides	46-54	apolipoprotein E	Homo sapiens	145-149
17760463-10	2007	Increased cellular ceramide reduces apoE secretion without increased cell retention, consistent with enhanced degradation of newly synthesized apoE.	Ceramides	19-27	apolipoprotein E	Homo sapiens	36-40
17760463-10	2007	Increased cellular ceramide reduces apoE secretion without increased cell retention, consistent with enhanced degradation of newly synthesized apoE.	Ceramides	19-27	apolipoprotein E	Homo sapiens	143-147
17700073-8	2007	Treatment of NRK-52E cells with ceramide suppressed PKC alpha and activated PP2A in a manner that mimicked simulated ischemia.	Ceramides	32-40	protein kinase C, alpha	Rattus norvegicus	52-61
17944019-12	2007	Inhibition of NF-[kappa]B suppressed acid sphingomyelinase activity and ceramide generation, indicating a novel proinflammatory link of NF-[kappa]B.	Ceramides	72-80	nuclear factor kappa B subunit 1	Homo sapiens	14-25
17944019-12	2007	Inhibition of NF-[kappa]B suppressed acid sphingomyelinase activity and ceramide generation, indicating a novel proinflammatory link of NF-[kappa]B.	Ceramides	72-80	nuclear factor kappa B subunit 1	Homo sapiens	136-147
17942080-0	2007	Ceramide-dependent release of ceramide kinase from cultured cells.	Ceramides	0-8	ceramide kinase	Cricetulus griseus	30-45
17942080-2	2007	When checking for intracellular effects of Cer-1-P by exposing CERK-expressing CHO cells to truncated ceramides, an unexpected decrease in CERK activity and protein level was observed.	Ceramides	102-111	cerberus	Cricetulus griseus	43-48
17942080-2	2007	When checking for intracellular effects of Cer-1-P by exposing CERK-expressing CHO cells to truncated ceramides, an unexpected decrease in CERK activity and protein level was observed.	Ceramides	102-111	ceramide kinase	Cricetulus griseus	63-67
17942080-2	2007	When checking for intracellular effects of Cer-1-P by exposing CERK-expressing CHO cells to truncated ceramides, an unexpected decrease in CERK activity and protein level was observed.	Ceramides	102-111	ceramide kinase	Cricetulus griseus	139-143
17942080-5	2007	In cells expressing CERK lacking the pleckstrin domain or an inactive CERK mutant, this ceramide effect was not observed, indicating that clustering and release of CERK may be mediated by Cer-1-P.	Ceramides	88-96	ceramide kinase	Cricetulus griseus	20-24
17942080-5	2007	In cells expressing CERK lacking the pleckstrin domain or an inactive CERK mutant, this ceramide effect was not observed, indicating that clustering and release of CERK may be mediated by Cer-1-P.	Ceramides	88-96	cerberus	Cricetulus griseus	188-193
17761529-0	2007	Saccharomyces cerevisiae CWH43 is involved in the remodeling of the lipid moiety of GPI anchors to ceramides.	Ceramides	99-108	Cwh43p	Saccharomyces cerevisiae S288C	25-30
17761529-3	2007	Here, we report that S. cerevisiae Cwh43p, whose N-terminal region contains a sequence homologous to mammalian PGAP2, is involved in the remodeling of the lipid moiety of GPI anchors to ceramides.	Ceramides	186-195	Cwh43p	Saccharomyces cerevisiae S288C	35-41
17761529-3	2007	Here, we report that S. cerevisiae Cwh43p, whose N-terminal region contains a sequence homologous to mammalian PGAP2, is involved in the remodeling of the lipid moiety of GPI anchors to ceramides.	Ceramides	186-195	post-GPI attachment to proteins 2	Homo sapiens	111-116
17761529-5	2007	Moreover, the C-terminal region of Cwh43p (Cwh43-C), which is not present in PGAP2, is essential for the ability to remodel GPI lipids to ceramides.	Ceramides	138-147	Cwh43p	Saccharomyces cerevisiae S288C	35-41
17761529-5	2007	Moreover, the C-terminal region of Cwh43p (Cwh43-C), which is not present in PGAP2, is essential for the ability to remodel GPI lipids to ceramides.	Ceramides	138-147	Cwh43p	Saccharomyces cerevisiae S288C	35-40
17761529-6	2007	The N-terminal region of Cwh43p (Cwh43-N) is associated with Cwh43-C, and it enhanced the lipid remodeling to ceramides by Cwh43-C. Our results also indicate that mouse FRAG1 and C130090K23, which are homologous to Cwh43-N and -C, respectively, share these activities.	Ceramides	110-119	Cwh43p	Saccharomyces cerevisiae S288C	25-31
17761529-6	2007	The N-terminal region of Cwh43p (Cwh43-N) is associated with Cwh43-C, and it enhanced the lipid remodeling to ceramides by Cwh43-C. Our results also indicate that mouse FRAG1 and C130090K23, which are homologous to Cwh43-N and -C, respectively, share these activities.	Ceramides	110-119	Cwh43p	Saccharomyces cerevisiae S288C	25-30
17761529-6	2007	The N-terminal region of Cwh43p (Cwh43-N) is associated with Cwh43-C, and it enhanced the lipid remodeling to ceramides by Cwh43-C. Our results also indicate that mouse FRAG1 and C130090K23, which are homologous to Cwh43-N and -C, respectively, share these activities.	Ceramides	110-119	Cwh43p	Saccharomyces cerevisiae S288C	33-38
17761529-6	2007	The N-terminal region of Cwh43p (Cwh43-N) is associated with Cwh43-C, and it enhanced the lipid remodeling to ceramides by Cwh43-C. Our results also indicate that mouse FRAG1 and C130090K23, which are homologous to Cwh43-N and -C, respectively, share these activities.	Ceramides	110-119	Cwh43p	Saccharomyces cerevisiae S288C	33-38
17761529-6	2007	The N-terminal region of Cwh43p (Cwh43-N) is associated with Cwh43-C, and it enhanced the lipid remodeling to ceramides by Cwh43-C. Our results also indicate that mouse FRAG1 and C130090K23, which are homologous to Cwh43-N and -C, respectively, share these activities.	Ceramides	110-119	post-GPI attachment to proteins 2	Mus musculus	169-174
17761529-6	2007	The N-terminal region of Cwh43p (Cwh43-N) is associated with Cwh43-C, and it enhanced the lipid remodeling to ceramides by Cwh43-C. Our results also indicate that mouse FRAG1 and C130090K23, which are homologous to Cwh43-N and -C, respectively, share these activities.	Ceramides	110-119	Cwh43p	Saccharomyces cerevisiae S288C	33-38
17618736-4	2007	Our findings indicate for the first time in Hs578T cells that caveolin-1 might play a pivotal role in regulating apoptosis as a suppressor rather than a facilitator through inhibition of neutral-sphingomyelinase, decrease of ceramide, furthermore, activation of Akt signaling pathway.	Ceramides	225-233	caveolin 1	Homo sapiens	62-72
17634398-0	2007	Ceramide mediates inhibition of the renal epithelial sodium channel by tumor necrosis factor-alpha through protein kinase C. To determine whether ceramide mediates regulation of the renal epithelial sodium channel (ENaC) by tumor necrosis factor-alpha (TNF-alpha), confocal microscopy and patch-clamp experiments were performed in A6 distal nephron cells.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	71-98
17634398-4	2007	Together with our previous finding that cytosolic PS maintains ENaC activity in A6 cells, these data suggest that ceramide mediates TNF-alpha inhibition of the renal ENaC via a pathway associated with PKC-dependent externalization of PS.	Ceramides	114-122	tumor necrosis factor	Homo sapiens	132-141
17627285-6	2007	Inhibition of p21(Cip1/Waf1) protein synthesis with cyclohexamide (CHX) or silencing of p21(Cip1/Waf1) with siRNA, prevented ceramide-mediated G(2) arrest and the late induction of apoptosis.	Ceramides	125-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	14-17
17627285-6	2007	Inhibition of p21(Cip1/Waf1) protein synthesis with cyclohexamide (CHX) or silencing of p21(Cip1/Waf1) with siRNA, prevented ceramide-mediated G(2) arrest and the late induction of apoptosis.	Ceramides	125-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	18-22
17627285-6	2007	Inhibition of p21(Cip1/Waf1) protein synthesis with cyclohexamide (CHX) or silencing of p21(Cip1/Waf1) with siRNA, prevented ceramide-mediated G(2) arrest and the late induction of apoptosis.	Ceramides	125-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	23-27
17627285-6	2007	Inhibition of p21(Cip1/Waf1) protein synthesis with cyclohexamide (CHX) or silencing of p21(Cip1/Waf1) with siRNA, prevented ceramide-mediated G(2) arrest and the late induction of apoptosis.	Ceramides	125-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	88-91
17627285-6	2007	Inhibition of p21(Cip1/Waf1) protein synthesis with cyclohexamide (CHX) or silencing of p21(Cip1/Waf1) with siRNA, prevented ceramide-mediated G(2) arrest and the late induction of apoptosis.	Ceramides	125-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	92-96
17627285-6	2007	Inhibition of p21(Cip1/Waf1) protein synthesis with cyclohexamide (CHX) or silencing of p21(Cip1/Waf1) with siRNA, prevented ceramide-mediated G(2) arrest and the late induction of apoptosis.	Ceramides	125-133	cyclin dependent kinase inhibitor 1A	Homo sapiens	97-101
17627285-7	2007	Further, adopting the recent discovery that murine double minute 2 (MDM2) controls p21(Cip1/Waf1) expression by presenting this CDK inhibitor to the proteasome for degradation, RD cells overexpressing MDM2 abrogated ceramide-mediated p21(Cip1/Waf1) induction, G(2) arrest and the late ensuing apoptosis.	Ceramides	216-224	transformed mouse 3T3 cell double minute 2	Mus musculus	68-72
17627285-7	2007	Further, adopting the recent discovery that murine double minute 2 (MDM2) controls p21(Cip1/Waf1) expression by presenting this CDK inhibitor to the proteasome for degradation, RD cells overexpressing MDM2 abrogated ceramide-mediated p21(Cip1/Waf1) induction, G(2) arrest and the late ensuing apoptosis.	Ceramides	216-224	transformed mouse 3T3 cell double minute 2	Mus musculus	201-205
17627285-9	2007	Additionally, these observations highlight MDM2 expression and proteasomal activity as key determinants of the cellular response to ceramide accumulation.	Ceramides	132-140	MDM2 proto-oncogene	Homo sapiens	43-47
17627285-0	2007	Ceramide-induced G2 arrest in rhabdomyosarcoma (RMS) cells requires p21Cip1/Waf1 induction and is prevented by MDM2 overexpression.	Ceramides	0-8	cyclin dependent kinase inhibitor 1A	Homo sapiens	76-80
17627285-0	2007	Ceramide-induced G2 arrest in rhabdomyosarcoma (RMS) cells requires p21Cip1/Waf1 induction and is prevented by MDM2 overexpression.	Ceramides	0-8	MDM2 proto-oncogene	Homo sapiens	111-115
17458900-0	2007	Ceramide inhibits LPS-induced production of IL-5, IL-10, and IL-13 from mast cells.	Ceramides	0-8	interleukin 5	Mus musculus	44-48
17548428-0	2007	Mechanisms of ceramide-mediated repression of the human telomerase reverse transcriptase promoter via deacetylation of Sp3 by histone deacetylase 1.	Ceramides	14-22	Sp3 transcription factor	Homo sapiens	119-122
17548428-0	2007	Mechanisms of ceramide-mediated repression of the human telomerase reverse transcriptase promoter via deacetylation of Sp3 by histone deacetylase 1.	Ceramides	14-22	histone deacetylase 1	Homo sapiens	126-147
17548428-3	2007	Then roles and mechanisms of action of ceramide-mediated deacetylation of Sp3 in inhibiting the hTERT promoter were determined using constitutively deacetylated or acetylated Sp3 mutants at lysine (K) 551.	Ceramides	39-47	Sp3 transcription factor	Homo sapiens	74-77
17548428-3	2007	Then roles and mechanisms of action of ceramide-mediated deacetylation of Sp3 in inhibiting the hTERT promoter were determined using constitutively deacetylated or acetylated Sp3 mutants at lysine (K) 551.	Ceramides	39-47	telomerase reverse transcriptase	Homo sapiens	96-101
17657734-8	2007	On the other hand, HuH7 cells with an overexpression of RUVBL2 grew better in soft agar (P < 0.03), had increased resistance to C2 ceramide-induced apoptosis (P < 0.001), and gave rise to significantly larger tumors when injected into immunodeficient Rag2/gammac mice (P = 0.016).	Ceramides	134-142	MIR7-3 host gene	Homo sapiens	19-23
17657734-8	2007	On the other hand, HuH7 cells with an overexpression of RUVBL2 grew better in soft agar (P < 0.03), had increased resistance to C2 ceramide-induced apoptosis (P < 0.001), and gave rise to significantly larger tumors when injected into immunodeficient Rag2/gammac mice (P = 0.016).	Ceramides	134-142	RuvB like AAA ATPase 2	Homo sapiens	56-62
17908174-5	2007	We found that palmitic acid significantly increased de-novo synthesis of ceramide in astroglia, which in turn was involved in inducing both increased production of the Abeta protein and hyperphosphorylation of the tau protein.	Ceramides	73-81	amyloid beta precursor protein	Rattus norvegicus	168-173
17458900-10	2007	Thus, ceramide appeared to down-regulate LPS-stimulated production of IL-5, IL-10, and IL-13 from mast cells by inhibiting PI3 kinase-Akt pathway in a cell type-specific manner.	Ceramides	6-14	interleukin 5	Mus musculus	70-74
17458900-10	2007	Thus, ceramide appeared to down-regulate LPS-stimulated production of IL-5, IL-10, and IL-13 from mast cells by inhibiting PI3 kinase-Akt pathway in a cell type-specific manner.	Ceramides	6-14	interleukin 10	Mus musculus	76-81
17458900-0	2007	Ceramide inhibits LPS-induced production of IL-5, IL-10, and IL-13 from mast cells.	Ceramides	0-8	interleukin 10	Mus musculus	50-55
17458900-10	2007	Thus, ceramide appeared to down-regulate LPS-stimulated production of IL-5, IL-10, and IL-13 from mast cells by inhibiting PI3 kinase-Akt pathway in a cell type-specific manner.	Ceramides	6-14	interleukin 13	Mus musculus	87-92
17458900-0	2007	Ceramide inhibits LPS-induced production of IL-5, IL-10, and IL-13 from mast cells.	Ceramides	0-8	interleukin 13	Mus musculus	61-66
17458900-10	2007	Thus, ceramide appeared to down-regulate LPS-stimulated production of IL-5, IL-10, and IL-13 from mast cells by inhibiting PI3 kinase-Akt pathway in a cell type-specific manner.	Ceramides	6-14	thymoma viral proto-oncogene 1	Mus musculus	134-137
17458900-6	2007	Consistently, LPS-stimulated production of IL-5, IL-10, and IL-13 from BMMCs is significantly enhanced in the presence of fumonisin B1, a de novo ceramide synthesis inhibitor.	Ceramides	146-154	interleukin 5	Mus musculus	43-47
17458900-6	2007	Consistently, LPS-stimulated production of IL-5, IL-10, and IL-13 from BMMCs is significantly enhanced in the presence of fumonisin B1, a de novo ceramide synthesis inhibitor.	Ceramides	146-154	interleukin 13	Mus musculus	60-65
17458900-7	2007	Interestingly, the same C8 ceramide treatment showed opposite effects on cytokine production from LPS-stimulated macrophages, reducing IL-6 and TNF-alpha while not affecting IL-10 production.	Ceramides	27-35	interleukin 6	Mus musculus	135-139
17458900-7	2007	Interestingly, the same C8 ceramide treatment showed opposite effects on cytokine production from LPS-stimulated macrophages, reducing IL-6 and TNF-alpha while not affecting IL-10 production.	Ceramides	27-35	tumor necrosis factor	Mus musculus	144-153
17458900-8	2007	C8 ceramide pretreatment significantly reduced LPS-induced Akt phosphorylation in BMMCs, but not in macrophages.	Ceramides	3-11	thymoma viral proto-oncogene 1	Mus musculus	59-62
17982236-3	2007	In this study, we investigated the protein expression of serine palmitoyltransferase (SPT) and ceramidase, two major ceramide metabolizing enzymes, in both psoriatic epidermis and non-lesional epidermis.	Ceramides	117-125	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	57-84
17626977-2	2007	LPLA2 transfers sn-1 or sn-2 acyl groups of phospholipids to the C1 hydroxyl of the short-chain ceramide N-acetylsphingosine (NAS) under acidic conditions.	Ceramides	96-104	phospholipase A2 group XV	Homo sapiens	0-5
17982236-3	2007	In this study, we investigated the protein expression of serine palmitoyltransferase (SPT) and ceramidase, two major ceramide metabolizing enzymes, in both psoriatic epidermis and non-lesional epidermis.	Ceramides	117-125	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	86-89
17982236-4	2007	The expression of SPT, the ceramide generating enzyme in the de novo synthesis in psoriatic epidermis, was significantly less than that of the non-lesional epidermis, which was inversely correlated with PASI score.	Ceramides	27-35	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	18-21
17982236-6	2007	This might suggest that decreased expression of SPT protein is one of the important causative factors for decreased ceramide levels in psoriasis.	Ceramides	116-124	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	48-51
18206046-0	2007	[Association between murine double minute 2 expression and AngII and ceramide induced endothelial cells apoptosis].	Ceramides	69-77	transformed mouse 3T3 cell double minute 2	Mus musculus	21-43
17647040-6	2007	Ceramide levels in the plasma and the liver of apoE-/- mice were intrinsically higher than those of the wild type.	Ceramides	0-8	apolipoprotein E	Mus musculus	47-51
18206046-1	2007	OBJECTIVE: To observe the relationship between murine double minute 2 (mdm2) expression and AngII and ceramide induced human umbilical endothelial cells apoptosis.	Ceramides	102-110	transformed mouse 3T3 cell double minute 2	Mus musculus	47-69
18206046-1	2007	OBJECTIVE: To observe the relationship between murine double minute 2 (mdm2) expression and AngII and ceramide induced human umbilical endothelial cells apoptosis.	Ceramides	102-110	transformed mouse 3T3 cell double minute 2	Mus musculus	71-75
18206046-7	2007	CONCLUSIONS: AngII binding with AT2 induces ECs apoptosis via ceramide.	Ceramides	62-70	angiotensinogen (serpin peptidase inhibitor, clade A, member 8)	Mus musculus	13-18
18206046-7	2007	CONCLUSIONS: AngII binding with AT2 induces ECs apoptosis via ceramide.	Ceramides	62-70	serine (or cysteine) peptidase inhibitor, clade B, member 9d	Mus musculus	32-35
18206046-8	2007	AngII and ceramide induce EC apoptosis by inhibiting mdm2.	Ceramides	10-18	transformed mouse 3T3 cell double minute 2	Mus musculus	53-57
17685585-10	2007	However, inhibition of iPLA2beta or NSMase (chemically or with siRNA) suppressed induction of NSMase message, ceramide generation, sphingomyelin hydrolysis, and apoptosis in both V and OE INS-1 cells during ER stress.	Ceramides	110-118	phospholipase A2 group VI	Rattus norvegicus	23-32
17685585-10	2007	However, inhibition of iPLA2beta or NSMase (chemically or with siRNA) suppressed induction of NSMase message, ceramide generation, sphingomyelin hydrolysis, and apoptosis in both V and OE INS-1 cells during ER stress.	Ceramides	110-118	sphingomyelin phosphodiesterase 2	Rattus norvegicus	36-42
17685585-0	2007	The group VIA calcium-independent phospholipase A2 participates in ER stress-induced INS-1 insulinoma cell apoptosis by promoting ceramide generation via hydrolysis of sphingomyelins by neutral sphingomyelinase.	Ceramides	130-138	sphingomyelin phosphodiesterase 2	Rattus norvegicus	186-210
17685585-12	2007	These findings indicate that iPLA2beta activation participates in ER stress-induced INS-1 cell apoptosis by promoting ceramide generation via NSMase-catalyzed hydrolysis of sphingomyelins, raising the possibility that this pathway contributes to beta-cell apoptosis due to ER stress.	Ceramides	118-126	phospholipase A2 group VI	Rattus norvegicus	29-38
17685585-2	2007	We previously reported that apoptosis of INS-1 insulinoma cells due to thapsigargin-induced ER stress was suppressed by inhibition of the group VIA Ca2+-independent phospholipase A2 (iPLA2beta), associated with an increased level of ceramide generation, and that the effects of ER stress were amplified in INS-1 cells in which iPLA2beta was overexpressed (OE INS-1 cells).	Ceramides	233-241	phospholipase A2 group VI	Rattus norvegicus	183-192
17685585-12	2007	These findings indicate that iPLA2beta activation participates in ER stress-induced INS-1 cell apoptosis by promoting ceramide generation via NSMase-catalyzed hydrolysis of sphingomyelins, raising the possibility that this pathway contributes to beta-cell apoptosis due to ER stress.	Ceramides	118-126	insulin 1	Rattus norvegicus	84-89
17685585-2	2007	We previously reported that apoptosis of INS-1 insulinoma cells due to thapsigargin-induced ER stress was suppressed by inhibition of the group VIA Ca2+-independent phospholipase A2 (iPLA2beta), associated with an increased level of ceramide generation, and that the effects of ER stress were amplified in INS-1 cells in which iPLA2beta was overexpressed (OE INS-1 cells).	Ceramides	233-241	insulin 1	Rattus norvegicus	41-46
17685585-3	2007	These findings suggested that iPLA2beta and ceramides participate in ER stress-induced INS-1 cell apoptosis.	Ceramides	44-53	insulin 1	Rattus norvegicus	87-92
17685585-12	2007	These findings indicate that iPLA2beta activation participates in ER stress-induced INS-1 cell apoptosis by promoting ceramide generation via NSMase-catalyzed hydrolysis of sphingomyelins, raising the possibility that this pathway contributes to beta-cell apoptosis due to ER stress.	Ceramides	118-126	sphingomyelin phosphodiesterase 2	Rattus norvegicus	142-148
17610065-0	2007	Potential roles of membrane fluidity and ceramide in hyperthermia and alcohol stimulation of TRAIL apoptosis.	Ceramides	41-49	TNF superfamily member 10	Homo sapiens	93-98
17616479-10	2007	We measured cellular lipid levels, including SM, ceramide, phosphatidylcholine, and diacylglycerol and found that SMS1 and SMS2 siRNA treatment caused a significant decrease of SM levels (20% and 11%, respectively), compared to control siRNA treatment; SMS1 but not SMS2 siRNA treatment caused a significant increase of ceramide levels (10%).	Ceramides	49-57	sphingomyelin synthase 1	Homo sapiens	114-118
17616479-10	2007	We measured cellular lipid levels, including SM, ceramide, phosphatidylcholine, and diacylglycerol and found that SMS1 and SMS2 siRNA treatment caused a significant decrease of SM levels (20% and 11%, respectively), compared to control siRNA treatment; SMS1 but not SMS2 siRNA treatment caused a significant increase of ceramide levels (10%).	Ceramides	320-328	sphingomyelin synthase 1	Homo sapiens	114-118
17616479-10	2007	We measured cellular lipid levels, including SM, ceramide, phosphatidylcholine, and diacylglycerol and found that SMS1 and SMS2 siRNA treatment caused a significant decrease of SM levels (20% and 11%, respectively), compared to control siRNA treatment; SMS1 but not SMS2 siRNA treatment caused a significant increase of ceramide levels (10%).	Ceramides	320-328	sphingomyelin synthase 2	Homo sapiens	123-127
17576160-3	2007	However, it is unknown whether overexpression of acid sphingomyelinase releasing ceramide from sphingomyelin sensitizes cells to chemotherapy and, thus, serves as a potential target to amplify chemotherapy.	Ceramides	81-89	sphingomyelin phosphodiesterase 1	Homo sapiens	49-70
17610065-3	2007	A caspase-dependent and D609-sensitive two-fold increase in ceramide level was elicited by heat shock plus TRAIL combined treatment.	Ceramides	60-68	TNF superfamily member 10	Homo sapiens	107-112
17610065-4	2007	One day after heat shock, a similar increase in ceramide was induced by TRAIL.	Ceramides	48-56	TNF superfamily member 10	Homo sapiens	72-77
17610065-9	2007	These results suggest that stress agents that trigger ceramide production and an overall increase in membrane fluidity are stimulators of TRAIL apoptosis.	Ceramides	54-62	TNF superfamily member 10	Homo sapiens	138-143
17881906-8	2007	In addition, mass spectroscopic analysis of sphingolipids indicated that long chain ceramide levels were decreased in AC-EGFP cells treated with either doxorubicin or etoposide.	Ceramides	84-92	N-acylsphingosine amidohydrolase 1	Homo sapiens	118-120
17563067-5	2007	We show that islets isolated from RIPcre(+)Casp8(fl/fl) mice were protected from Fas ligand (FasL)-and ceramide-induced cell death.	Ceramides	103-111	caspase 8	Mus musculus	43-48
17699793-1	2007	We have previously shown that cisplatin triggers an early acid sphingomyelinase (aSMase)-dependent ceramide generation concomitantly with an increase in membrane fluidity and induces apoptosis in HT29 cells.	Ceramides	99-107	sphingomyelin phosphodiesterase 1	Homo sapiens	81-87
17664132-3	2007	It is demonstrated here that gamma-irradiation of a radiosensitive human head and neck squamous carcinoma cell line (SCC61) results in the triggering of raft coalescence to larger membrane platforms associated with the externalization of an acid sphingomyelinase (A-SMase), leading to ceramide release in raft, 30 min postirradiation.	Ceramides	285-293	sphingomyelin phosphodiesterase 1	Homo sapiens	241-262
17714445-0	2007	CWH43 is required for the introduction of ceramides into GPI anchors in Saccharomyces cerevisiae.	Ceramides	42-51	Cwh43p	Saccharomyces cerevisiae S288C	0-5
17714445-0	2007	CWH43 is required for the introduction of ceramides into GPI anchors in Saccharomyces cerevisiae.	Ceramides	42-51	glucose-6-phosphate isomerase	Homo sapiens	57-60
17714445-2	2007	Furthermore the diacylglycerol moiety of the yeast GPI anchor can also be replaced by ceramides.	Ceramides	86-95	glucose-6-phosphate isomerase	Homo sapiens	51-54
17681786-3	2007	In this study, we demonstrated that various inflammatory agents, including lipopolysaccharide, 12-o-tetradecanoylphorbol-13-acetate, hydrogen peroxide, okadaic acid and ceramide, were able to induce IL-1beta and TNF-alpha productions in human lung epithelial cells (A-549), fibroblasts (HFL1), and lymphoma cells (U-937).	Ceramides	169-177	interleukin 1 beta	Homo sapiens	199-207
17681786-3	2007	In this study, we demonstrated that various inflammatory agents, including lipopolysaccharide, 12-o-tetradecanoylphorbol-13-acetate, hydrogen peroxide, okadaic acid and ceramide, were able to induce IL-1beta and TNF-alpha productions in human lung epithelial cells (A-549), fibroblasts (HFL1), and lymphoma cells (U-937).	Ceramides	169-177	tumor necrosis factor	Homo sapiens	212-221
17681786-3	2007	In this study, we demonstrated that various inflammatory agents, including lipopolysaccharide, 12-o-tetradecanoylphorbol-13-acetate, hydrogen peroxide, okadaic acid and ceramide, were able to induce IL-1beta and TNF-alpha productions in human lung epithelial cells (A-549), fibroblasts (HFL1), and lymphoma cells (U-937).	Ceramides	169-177	complement factor H related 1	Homo sapiens	287-291
17609208-7	2007	Stimulation of ceramide biosynthesis seems to be under control of JNK3 signaling: IR-induced ceramide generation and respiratory chain damage was abolished in mitochondria of JNK3-deficient mice, which exhibited reduced infarct volume after IR.	Ceramides	15-23	mitogen-activated protein kinase 10	Mus musculus	66-70
17609208-7	2007	Stimulation of ceramide biosynthesis seems to be under control of JNK3 signaling: IR-induced ceramide generation and respiratory chain damage was abolished in mitochondria of JNK3-deficient mice, which exhibited reduced infarct volume after IR.	Ceramides	93-101	mitogen-activated protein kinase 10	Mus musculus	66-70
17699793-5	2007	Early after cisplatin treatment, Na+/H+ membrane exchanger-1 (NHE1) was inhibited leading to intracellular acidification, aSMase was activated, and ceramide was detected at the cell membrane.	Ceramides	148-156	solute carrier family 9 member A1	Homo sapiens	33-60
17699793-5	2007	Early after cisplatin treatment, Na+/H+ membrane exchanger-1 (NHE1) was inhibited leading to intracellular acidification, aSMase was activated, and ceramide was detected at the cell membrane.	Ceramides	148-156	solute carrier family 9 member A1	Homo sapiens	62-66
17475390-2	2007	Although previous rodent studies including experiments on knockout mice indicate a role of neutral ceramidase in ceramide digestion, the human enzyme has never been purified and characterized in its purified form.	Ceramides	113-121	N-acylsphingosine amidohydrolase 2	Mus musculus	91-109
17666435-8	2007	These results indicate a role for GSK-3beta in ceramide-induced apoptosis, in which GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.	Ceramides	47-55	glycogen synthase kinase 3 beta	Homo sapiens	34-43
17666435-8	2007	These results indicate a role for GSK-3beta in ceramide-induced apoptosis, in which GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.	Ceramides	47-55	glycogen synthase kinase 3 beta	Homo sapiens	84-93
17666435-8	2007	These results indicate a role for GSK-3beta in ceramide-induced apoptosis, in which GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.	Ceramides	47-55	protein phosphatase 2 phosphatase activator	Homo sapiens	113-117
17666435-8	2007	These results indicate a role for GSK-3beta in ceramide-induced apoptosis, in which GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.	Ceramides	47-55	AKT serine/threonine kinase 1	Homo sapiens	138-141
17666435-8	2007	These results indicate a role for GSK-3beta in ceramide-induced apoptosis, in which GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.	Ceramides	47-55	caspase 2	Homo sapiens	167-176
17666435-8	2007	These results indicate a role for GSK-3beta in ceramide-induced apoptosis, in which GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 and caspase-8.	Ceramides	47-55	caspase 8	Homo sapiens	181-190
17666435-0	2007	GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 in ceramide-induced mitochondrial apoptosis.	Ceramides	96-104	glycogen synthase kinase 3 beta	Homo sapiens	0-9
17666435-0	2007	GSK-3beta acts downstream of PP2A and the PI 3-kinase-Akt pathway, and upstream of caspase-2 in ceramide-induced mitochondrial apoptosis.	Ceramides	96-104	caspase 2	Homo sapiens	83-92
17666435-3	2007	Here, we show the involvement of GSK-3beta in ceramide-induced mitochondrial apoptosis.	Ceramides	46-54	glycogen synthase kinase 3 beta	Homo sapiens	33-42
17666435-4	2007	Ceramide induced GSK-3beta activation via protein dephosphorylation at serine 9.	Ceramides	0-8	glycogen synthase kinase 3 beta	Homo sapiens	17-26
17666435-5	2007	We previously reported that ceramide induced caspase-2 and caspase-8 activation, Bid cleavage, mitochondrial damage, and apoptosis.	Ceramides	28-36	caspase 2	Homo sapiens	45-54
17666435-5	2007	We previously reported that ceramide induced caspase-2 and caspase-8 activation, Bid cleavage, mitochondrial damage, and apoptosis.	Ceramides	28-36	caspase 8	Homo sapiens	59-68
17666435-5	2007	We previously reported that ceramide induced caspase-2 and caspase-8 activation, Bid cleavage, mitochondrial damage, and apoptosis.	Ceramides	28-36	BH3 interacting domain death agonist	Homo sapiens	81-84
17520194-0	2007	Doxorubicin enhances TRAIL-induced cell death via ceramide-enriched membrane platforms.	Ceramides	50-58	TNF superfamily member 10	Homo sapiens	21-26
17520194-1	2007	Previous studies indicated that signalling via CD95 and DR5 is greatly enhanced by the formation of ceramide-enriched membrane platforms.	Ceramides	100-108	Fas cell surface death receptor	Homo sapiens	47-51
17520194-1	2007	Previous studies indicated that signalling via CD95 and DR5 is greatly enhanced by the formation of ceramide-enriched membrane platforms.	Ceramides	100-108	TNF receptor superfamily member 10b	Homo sapiens	56-59
17520194-2	2007	Here, we employed this concept to convert doses of subtherapeutic TRAIL that were unable to release ceramide and kill leukemic B-cells or ex vivo T lymphocytes, into a very effective apoptotic stimulus.	Ceramides	100-108	TNF superfamily member 10	Homo sapiens	66-71
17520194-3	2007	Ceramide production was induced by application of sub-toxic doses of doxorubicin that resulted in an activation of the acid sphingomyelinase (ASM), release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	119-140
17520194-3	2007	Ceramide production was induced by application of sub-toxic doses of doxorubicin that resulted in an activation of the acid sphingomyelinase (ASM), release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	142-145
17520194-5	2007	Genetic deficiency of the ASM abrogated doxorubicin-induced ceramide release, as well as clustering of DR5 and apoptosis induced by the combined treatment of doxorubicin and TRAIL.	Ceramides	60-68	sphingomyelin phosphodiesterase 1	Homo sapiens	26-29
17520194-6	2007	These data show that local release of ceramide potentiates very low, otherwise inactive doses of TRAIL that may represent a novel therapeutic concept to treat tumors.	Ceramides	38-46	TNF superfamily member 10	Homo sapiens	97-102
17475390-18	2007	Our study indicates that neutral ceramidase is expressed in human intestine, released in the intestinal lumen and plays a major role in ceramide metabolism in the human gut.	Ceramides	136-144	N-acylsphingosine amidohydrolase 2	Homo sapiens	25-43
17620421-0	2007	Adipose tissue inflammation and increased ceramide content characterize subjects with high liver fat content independent of obesity.	Ceramides	42-50	CD36 molecule	Homo sapiens	97-100
17712833-7	2007	The primary structure of NAAA exhibits 33-35% amino acid identity to that of acid ceramidase, a lysosomal enzyme hydrolyzing ceramide to fatty acid and sphingosine.	Ceramides	125-133	N-acylethanolamine acid amidase	Rattus norvegicus	25-29
17712833-7	2007	The primary structure of NAAA exhibits 33-35% amino acid identity to that of acid ceramidase, a lysosomal enzyme hydrolyzing ceramide to fatty acid and sphingosine.	Ceramides	125-133	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	77-92
17712833-8	2007	NAAA actually showed a low, but detectable ceramide-hydrolyzing activity, while acid ceramidase hydrolyzed N-lauroylethanolamine.	Ceramides	43-51	N-acylethanolamine acid amidase	Rattus norvegicus	0-4
17620421-11	2007	Ceramides or their metabolites could contribute to adverse effects of long-chain fatty acids on insulin resistance and inflammation.	Ceramides	0-9	insulin	Homo sapiens	96-103
17498692-2	2007	Previous work from our laboratory demonstrated that the reactive oxygen species (ROS), hydrogen peroxide (H(2)O(2)), specifically activates neutral sphingomyelinase 2 (nSMase2) to generate ceramide and induce apoptosis in airway epithelial cells.	Ceramides	189-197	sphingomyelin phosphodiesterase 3	Homo sapiens	140-166
17681178-6	2007	Over expression of ACSL5-fl protein is associated with a decrease of the anti-apoptotic FLIP protein in a ceramide-dependent manner and an increased cell-surface expression of the death receptor TRAIL-R1.	Ceramides	106-114	acyl-CoA synthetase long chain family member 5	Homo sapiens	19-24
17654249-4	2007	These results were similar to the profiles induced by daunorubicin, an activator of serine palmitoyl CoA transferase (SPT), suggesting that H2O2 stimulated the de novo synthetic pathway of ceramides.	Ceramides	189-198	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	84-116
17654249-4	2007	These results were similar to the profiles induced by daunorubicin, an activator of serine palmitoyl CoA transferase (SPT), suggesting that H2O2 stimulated the de novo synthetic pathway of ceramides.	Ceramides	189-198	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	118-121
17522181-1	2007	We examined the role of sphingosine kinase-1 (SphK1), a critical regulator of the ceramide/sphingosine 1-phosphate (S1P) biostat, in the regulation of death and survival of SH-SY5Y neuroblastoma cells in response to amyloid beta (Abeta) peptide (25-35).	Ceramides	82-90	sphingosine kinase 1	Homo sapiens	24-44
17522181-1	2007	We examined the role of sphingosine kinase-1 (SphK1), a critical regulator of the ceramide/sphingosine 1-phosphate (S1P) biostat, in the regulation of death and survival of SH-SY5Y neuroblastoma cells in response to amyloid beta (Abeta) peptide (25-35).	Ceramides	82-90	sphingosine kinase 1	Homo sapiens	46-51
17522181-2	2007	Upon incubation with Abeta, SH-SY5Y cells displayed a marked down-regulation of SphK1 activity coupled with an increase in the ceramide/S1P ratio followed by cell death.	Ceramides	127-135	amyloid beta precursor protein	Homo sapiens	21-26
17650308-11	2007	Meanwhile, it releases abundant fatty acid products (e.g. diacylglycerol, ceramides) that impair insulin actions via signal transduction, thereby causing MIR.	Ceramides	74-83	insulin	Homo sapiens	97-104
17634371-9	2007	Together, our data indicate that p75(NTR)-mediated motor neuron apoptosis involves ceramide-dependent increased mitochondrial superoxide production.	Ceramides	83-91	TNF receptor superfamily member 1B	Homo sapiens	33-36
17634371-9	2007	Together, our data indicate that p75(NTR)-mediated motor neuron apoptosis involves ceramide-dependent increased mitochondrial superoxide production.	Ceramides	83-91	neurotensin receptor 1	Homo sapiens	37-40
17521618-0	2007	De novo ceramide biosynthesis is associated with resveratrol-induced inhibition of ornithine decarboxylase activity.	Ceramides	8-16	ornithine decarboxylase 1	Homo sapiens	83-106
17498692-2	2007	Previous work from our laboratory demonstrated that the reactive oxygen species (ROS), hydrogen peroxide (H(2)O(2)), specifically activates neutral sphingomyelinase 2 (nSMase2) to generate ceramide and induce apoptosis in airway epithelial cells.	Ceramides	189-197	sphingomyelin phosphodiesterase 3	Homo sapiens	168-175
17521618-9	2007	Compared to controls the cell-permeable ceramide analogues C2- and C6-ceramide significantly inhibit ODC-activity (p<0.001) in colorectal cancer cells.	Ceramides	40-48	ornithine decarboxylase 1	Homo sapiens	101-104
17521618-9	2007	Compared to controls the cell-permeable ceramide analogues C2- and C6-ceramide significantly inhibit ODC-activity (p<0.001) in colorectal cancer cells.	Ceramides	70-78	ornithine decarboxylase 1	Homo sapiens	101-104
17521618-10	2007	C6-ceramide further diminished protein levels of protooncogenes c-myc (p<0.05) and ODC (p<0.01), which is strictly related to the ability of ceramides to inhibit cell growth in a time- and dose-dependent manner.	Ceramides	147-156	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	64-69
17521618-10	2007	C6-ceramide further diminished protein levels of protooncogenes c-myc (p<0.05) and ODC (p<0.01), which is strictly related to the ability of ceramides to inhibit cell growth in a time- and dose-dependent manner.	Ceramides	147-156	ornithine decarboxylase 1	Homo sapiens	86-89
17504762-3	2007	In MCF-7 human breast cancer cells, the action of the PKC activator 4beta-phorbol-12-myristate-13-acetate (PMA) evokes ceramide formation, which in turn prevents PKCalpha/betaII translocation to the pericentrion.	Ceramides	119-127	protein kinase C alpha	Homo sapiens	54-57
17521618-12	2007	These data suggest that the induction of ceramide de novo biosynthesis but not hydrolysis of sphingomyelin is involved in resveratrol-mediated inhibition of ODC.	Ceramides	41-49	ornithine decarboxylase 1	Homo sapiens	157-160
17504762-3	2007	In MCF-7 human breast cancer cells, the action of the PKC activator 4beta-phorbol-12-myristate-13-acetate (PMA) evokes ceramide formation, which in turn prevents PKCalpha/betaII translocation to the pericentrion.	Ceramides	119-127	protein kinase C alpha	Homo sapiens	162-177
17504762-0	2007	Mechanism of inhibition of sequestration of protein kinase C alpha/betaII by ceramide.	Ceramides	77-85	protein kinase C alpha	Homo sapiens	44-66
17504762-4	2007	In this study we investigated the mechanisms by which ceramide negatively regulates this translocation of PKCalpha/betaII.	Ceramides	54-62	protein kinase C alpha	Homo sapiens	106-121
17504762-6	2007	Inhibition of ceramide synthesis by fumonisin B1 overcame the defect in PKC phosphorylation and restored translocation of PKCalpha/betaII to the pericentrion.	Ceramides	14-22	protein kinase C alpha	Homo sapiens	72-75
17504762-6	2007	Inhibition of ceramide synthesis by fumonisin B1 overcame the defect in PKC phosphorylation and restored translocation of PKCalpha/betaII to the pericentrion.	Ceramides	14-22	protein kinase C alpha	Homo sapiens	122-130
17504762-10	2007	Reciprocally, a point mutation of Thr-641 to Glu, which mimics phosphorylation, in PKCbetaII overcame the inhibitory effects of ceramide on PKC translocation in PMA-stimulated MCF-7 cells.	Ceramides	128-136	protein kinase C alpha	Homo sapiens	83-86
17504762-11	2007	Therefore, the results demonstrate a novel role for carboxyl-terminal phosphorylation of PKCalpha/betaII in the translocation of PKC to the pericentrion, and they disclose specific regulation of PKC autophosphorylation by ceramide through the activation of specific isoforms of protein phosphatase 1.	Ceramides	222-230	protein kinase C alpha	Homo sapiens	89-104
17504762-11	2007	Therefore, the results demonstrate a novel role for carboxyl-terminal phosphorylation of PKCalpha/betaII in the translocation of PKC to the pericentrion, and they disclose specific regulation of PKC autophosphorylation by ceramide through the activation of specific isoforms of protein phosphatase 1.	Ceramides	222-230	protein kinase C alpha	Homo sapiens	89-92
17504762-11	2007	Therefore, the results demonstrate a novel role for carboxyl-terminal phosphorylation of PKCalpha/betaII in the translocation of PKC to the pericentrion, and they disclose specific regulation of PKC autophosphorylation by ceramide through the activation of specific isoforms of protein phosphatase 1.	Ceramides	222-230	protein kinase C alpha	Homo sapiens	129-132
17618857-3	2007	Liv-DGAT2 mice developed hepatic steatosis, with increased amounts of TG, diacylglycerol, ceramides, and unsaturated long-chain fatty acyl-CoAs in the liver.	Ceramides	90-99	diacylglycerol O-acyltransferase 2	Mus musculus	4-9
17591919-2	2007	Recruitment and activation of PKD at the TGN is mediated by the lipid diacylglycerol, a pool of which is generated by sphingomyelin synthase from ceramide and phosphatidylcholine.	Ceramides	146-154	protein kinase D1	Homo sapiens	30-33
17591919-3	2007	The nonvesicular transfer of ceramide from the endoplasmic reticulum to the Golgi complex is mediated by the lipid transfer protein CERT (ceramide transport).	Ceramides	29-37	ceramide transporter 1	Homo sapiens	132-136
17591919-3	2007	The nonvesicular transfer of ceramide from the endoplasmic reticulum to the Golgi complex is mediated by the lipid transfer protein CERT (ceramide transport).	Ceramides	138-146	ceramide transporter 1	Homo sapiens	132-136
17592126-1	2007	Ceramide transfer protein (CERT) transfers ceramide from the endoplasmic reticulum to the Golgi complex, a process critical in synthesis and maintenance of normal levels of sphingolipids in mammalian cells.	Ceramides	43-51	ceramide transporter 1	Homo sapiens	0-25
17592126-1	2007	Ceramide transfer protein (CERT) transfers ceramide from the endoplasmic reticulum to the Golgi complex, a process critical in synthesis and maintenance of normal levels of sphingolipids in mammalian cells.	Ceramides	43-51	ceramide transporter 1	Homo sapiens	27-31
17346242-0	2007	PKCzeta protects against UV-C-induced apoptosis by inhibiting acid sphingomyelinase-dependent ceramide production.	Ceramides	94-102	protein kinase C zeta	Homo sapiens	0-7
17346242-0	2007	PKCzeta protects against UV-C-induced apoptosis by inhibiting acid sphingomyelinase-dependent ceramide production.	Ceramides	94-102	sphingomyelin phosphodiesterase 1	Homo sapiens	62-83
17346242-1	2007	In a recent study, we described that UV-C irradiation resulted in redox-dependent activation and relocalization of A-SMase (acid sphingomyelinase) to the external surface of raft membrane microdomains, hydrolysis of SM (sphingomyelin) associated with the plasma membrane outer leaflet, ceramide generation and apoptosis.	Ceramides	286-294	sphingomyelin phosphodiesterase 1	Homo sapiens	115-122
17346242-1	2007	In a recent study, we described that UV-C irradiation resulted in redox-dependent activation and relocalization of A-SMase (acid sphingomyelinase) to the external surface of raft membrane microdomains, hydrolysis of SM (sphingomyelin) associated with the plasma membrane outer leaflet, ceramide generation and apoptosis.	Ceramides	286-294	sphingomyelin phosphodiesterase 1	Homo sapiens	124-145
17346242-3	2007	This study shows that PKCzeta overexpression resulted in the abrogation of UV-C-induced A-SMase translocation and activation into the raft microdomains, lack of ceramide generation and apoptosis inhibition.	Ceramides	161-169	protein kinase C zeta	Homo sapiens	22-29
17466493-0	2007	Interleukin-4 depresses levels of transcripts for acid-sphingomyelinase and glucocerebrosidase and the amount of ceramide in acetone-wounded epidermis, as demonstrated in a living skin equivalent.	Ceramides	113-121	interleukin 4	Homo sapiens	0-13
17508908-2	2007	Using small interference RNA (siRNA) of ASM, Fas ligand (FasL)-induced increase in ASM activity, production of ceramide, and LR clustering in CAECs were blocked, and clustered Fas was also substantially reduced in detergent-resistant membrane fractions of CAECs.	Ceramides	111-119	sphingomyelin phosphodiesterase 1	Homo sapiens	40-43
17508908-2	2007	Using small interference RNA (siRNA) of ASM, Fas ligand (FasL)-induced increase in ASM activity, production of ceramide, and LR clustering in CAECs were blocked, and clustered Fas was also substantially reduced in detergent-resistant membrane fractions of CAECs.	Ceramides	111-119	Fas ligand	Homo sapiens	45-55
17508908-2	2007	Using small interference RNA (siRNA) of ASM, Fas ligand (FasL)-induced increase in ASM activity, production of ceramide, and LR clustering in CAECs were blocked, and clustered Fas was also substantially reduced in detergent-resistant membrane fractions of CAECs.	Ceramides	111-119	Fas ligand	Homo sapiens	57-61
17393491-7	2007	Arachidonic acid, a product derived from glycerophospholipid catabolism by PLA(2), modulates sphingomyelinase (SMase), the enzyme that generates ceramide and phosphocholine.	Ceramides	145-153	phospholipase A2 group IB	Homo sapiens	75-81
17437539-4	2007	This function shift reflects the signaling effects of ceramide that is generated upon stimulation of p75.	Ceramides	54-62	PC4 and SFRS1 interacting protein 1	Homo sapiens	101-104
17437539-5	2007	The use of ceramide signaling by p75 may provide a key to understanding the cell-biological role of p75.	Ceramides	11-19	PC4 and SFRS1 interacting protein 1	Homo sapiens	33-36
17437539-5	2007	The use of ceramide signaling by p75 may provide a key to understanding the cell-biological role of p75.	Ceramides	11-19	PC4 and SFRS1 interacting protein 1	Homo sapiens	100-103
17426710-3	2007	Here, we study the role of the ceramide-metabolizing enzyme acid ceramidase (AC) in therapeutic responses in HNSCC.	Ceramides	31-39	N-acylsphingosine amidohydrolase 1	Homo sapiens	60-75
17426710-3	2007	Here, we study the role of the ceramide-metabolizing enzyme acid ceramidase (AC) in therapeutic responses in HNSCC.	Ceramides	31-39	N-acylsphingosine amidohydrolase 1	Homo sapiens	77-79
17573191-2	2007	Endogenous agents such as TNF-alpha, INF-gamma, IL-1beta and others stress signals activate the sphingomyelin pathway increasing ceramide levels.	Ceramides	129-137	tumor necrosis factor	Homo sapiens	26-35
17573191-2	2007	Endogenous agents such as TNF-alpha, INF-gamma, IL-1beta and others stress signals activate the sphingomyelin pathway increasing ceramide levels.	Ceramides	129-137	interleukin 1 beta	Homo sapiens	48-56
17467659-0	2007	Sphingomyelin synthase 1 suppresses ceramide production and apoptosis post-photodamage.	Ceramides	36-44	sphingomyelin synthase 1	Homo sapiens	0-24
17467659-1	2007	The role of sphingomyelin synthase 1 (SMS1), the Golgi membrane isoform of the enzyme, in ceramide metabolism and apoptosis after photodamage with the photosensitizer Pc 4 (PDT) is unclear.	Ceramides	90-98	sphingomyelin synthase 1	Homo sapiens	12-36
17467659-1	2007	The role of sphingomyelin synthase 1 (SMS1), the Golgi membrane isoform of the enzyme, in ceramide metabolism and apoptosis after photodamage with the photosensitizer Pc 4 (PDT) is unclear.	Ceramides	90-98	sphingomyelin synthase 1	Homo sapiens	38-42
17446166-3	2007	Here we show that in Fao rat hepatoma cells, the IkappaB kinase beta (IKKbeta) is an IRS-1 kinase activated by selected inducers of insulin resistance, including sphingomyelinase, ceramide, and free fatty acids.	Ceramides	180-188	inhibitor of nuclear factor kappa B kinase subunit beta	Rattus norvegicus	49-68
17467659-2	2007	In the present study, using electrospray ionization/double mass spectrometry, we show that in Jurkat cells overexpressing SMS1, increases in ceramides were lower than in empty-vector transfectants post-PDT.	Ceramides	141-150	sphingomyelin synthase 1	Homo sapiens	122-126
17446166-3	2007	Here we show that in Fao rat hepatoma cells, the IkappaB kinase beta (IKKbeta) is an IRS-1 kinase activated by selected inducers of insulin resistance, including sphingomyelinase, ceramide, and free fatty acids.	Ceramides	180-188	inhibitor of nuclear factor kappa B kinase subunit beta	Rattus norvegicus	70-77
17467659-3	2007	Similarly, the responses of dihydroceramides and dihydrosphingosine, precursors of ceramide in the de novo synthetic pathway, were attenuated in SMS1-overexpressor after photodamage, suggesting the involvement of the de novo pathway.	Ceramides	35-43	sphingomyelin synthase 1	Homo sapiens	145-149
17467659-5	2007	Concomitant with the suppressed ceramide response, PDT-induced DEVDase activation was substantially reduced in SMS1-overexpressors.	Ceramides	32-40	sphingomyelin synthase 1	Homo sapiens	111-115
17467659-6	2007	The data show that overexpression of SMS1 is associated with suppressed ceramide response and apoptotic resistance after photodamage.	Ceramides	72-80	sphingomyelin synthase 1	Homo sapiens	37-41
17449912-6	2007	RNA interference-mediated depletion of either SMS1 or SMS2 caused a substantial decrease in SM production levels, an accumulation of ceramides, and a block in cell growth.	Ceramides	133-142	sphingomyelin synthase 1	Homo sapiens	46-50
17442665-0	2007	Interorganelle trafficking of ceramide is regulated by phosphorylation-dependent cooperativity between the PH and START domains of CERT.	Ceramides	30-38	ceramide transporter 1	Homo sapiens	131-135
17442665-3	2007	Ceramide is synthesized at the endoplasmic reticulum (ER) and transported by the ceramide transfer protein CERT to the Golgi apparatus, where it is converted to sphingomyelin.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	107-111
17449912-6	2007	RNA interference-mediated depletion of either SMS1 or SMS2 caused a substantial decrease in SM production levels, an accumulation of ceramides, and a block in cell growth.	Ceramides	133-142	sphingomyelin synthase 2	Homo sapiens	54-58
17442665-3	2007	Ceramide is synthesized at the endoplasmic reticulum (ER) and transported by the ceramide transfer protein CERT to the Golgi apparatus, where it is converted to sphingomyelin.	Ceramides	81-89	ceramide transporter 1	Homo sapiens	107-111
17442665-4	2007	CERT has a phosphoinositide-binding pleckstrin homology (PH) domain for Golgi-targeting and a lipid transfer START domain for intermembrane transfer of ceramide.	Ceramides	152-160	ceramide transporter 1	Homo sapiens	0-4
17314061-3	2007	CERT has been identified as a key factor for the ER-to-Golgi trafficking of ceramide.	Ceramides	76-84	ceramide transporter 1	Homo sapiens	0-4
17442665-5	2007	We here show that CERT receives multiple phosphorylations at a serine-repeat motif, a possibe site for casein kinase I, and that the phosphorylation down-regulates the ER-to-Golgi transport of ceramide.	Ceramides	193-201	ceramide transporter 1	Homo sapiens	18-22
17442665-6	2007	In vitro assays show that the phosphorylation induces an autoinhibitory interaction between the PH and START domains and consequently inactivates both the phosphoinositide binding and ceramide transfer activities of CERT.	Ceramides	184-192	ceramide transporter 1	Homo sapiens	216-220
17442665-8	2007	The cooperative control of functionally distinct domains of CERT is a novel molecular event to regulate the intracellular trafficking of ceramide.	Ceramides	137-145	ceramide transporter 1	Homo sapiens	60-64
17283068-1	2007	The role of dihydroceramide desaturase as a key enzyme in the de novo pathway of ceramide generation was investigated in human neuroblastoma cells (SMS-KCNR).	Ceramides	19-27	Desaturase 1	Drosophila melanogaster	28-38
17314061-4	2007	CERT contains several functional domains including (i) a START domain capable of catalyzing inter-membrane transfer of ceramide, (ii) a pleckstrin homology domain, which serves to target the Golgi apparatus by recognizing phosphatidylinositol 4-monophosphate, and (iii) a short peptide motif named FFAT motif which interacts with the ER-resident membrane protein VAP.	Ceramides	119-127	ceramide transporter 1	Homo sapiens	0-4
17314061-6	2007	On the basis of these results, it has been proposed that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that a particularly efficient cycle of CERT movement for trafficking of ceramide may proceed at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	71-79	ceramide transporter 1	Homo sapiens	57-61
17314061-6	2007	On the basis of these results, it has been proposed that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that a particularly efficient cycle of CERT movement for trafficking of ceramide may proceed at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	232-240	ceramide transporter 1	Homo sapiens	57-61
17314061-6	2007	On the basis of these results, it has been proposed that CERT extracts ceramide from the ER and carries it to the Golgi apparatus in a non-vesicular manner and that a particularly efficient cycle of CERT movement for trafficking of ceramide may proceed at membrane contact sites between the ER and the Golgi apparatus.	Ceramides	232-240	ceramide transporter 1	Homo sapiens	199-203
17329567-9	2007	Finally, GM-CSF, a cytokine that delays neutrophil apoptosis, abrogated C(16)- and C(24)-ceramide accumulation totally in cultured neutrophils, whereas Fas ligation accelerated apoptosis in these cells without affecting de novo ceramide production.	Ceramides	89-97	colony stimulating factor 2	Homo sapiens	9-15
17543577-7	2007	Studies of purified SCP-2 and in cells show that SCP-2 has high affinity for and selectively transfers many lipid species involved in intracellular signaling: fatty acids, fatty acyl CoAs, lysophosphatidic acid, phosphatidylinositols, and sphingolipids (sphingomyelin, ceramide, mono-di-and multi-hexosylceramides, gangliosides).	Ceramides	269-277	sterol carrier protein 2, liver	Mus musculus	49-54
17550847-0	2007	Arsenic trioxide induces accumulation of cytotoxic levels of ceramide in acute promyelocytic leukemia and adult T-cell leukemia/lymphoma cells through de novo ceramide synthesis and inhibition of glucosylceramide synthase activity.	Ceramides	61-69	UDP-glucose ceramide glucosyltransferase	Homo sapiens	196-221
17329567-9	2007	Finally, GM-CSF, a cytokine that delays neutrophil apoptosis, abrogated C(16)- and C(24)-ceramide accumulation totally in cultured neutrophils, whereas Fas ligation accelerated apoptosis in these cells without affecting de novo ceramide production.	Ceramides	228-236	colony stimulating factor 2	Homo sapiens	9-15
17223929-0	2007	Ceramide as a TLR4 agonist; a putative signalling intermediate between sphingolipid receptors for microbial ligands and TLR4.	Ceramides	0-8	toll like receptor 4	Homo sapiens	14-18
17392267-2	2007	In this study, mass spectrometry analysis disclosed that the main forms of C1P in cells were C(16:0) C1P and C(18:0) C1P, suggesting that CERK uses ceramide transported to the trans-Golgi apparatus by ceramide transport protein (CERT).	Ceramides	148-156	ceramide kinase	Homo sapiens	138-142
17392267-2	2007	In this study, mass spectrometry analysis disclosed that the main forms of C1P in cells were C(16:0) C1P and C(18:0) C1P, suggesting that CERK uses ceramide transported to the trans-Golgi apparatus by ceramide transport protein (CERT).	Ceramides	148-156	ceramide transporter 1	Homo sapiens	201-227
17392267-2	2007	In this study, mass spectrometry analysis disclosed that the main forms of C1P in cells were C(16:0) C1P and C(18:0) C1P, suggesting that CERK uses ceramide transported to the trans-Golgi apparatus by ceramide transport protein (CERT).	Ceramides	148-156	ceramide transporter 1	Homo sapiens	229-233
17392267-5	2007	In conclusion, these results demonstrate that CERK localizes to areas of eicosanoid synthesis and uses a ceramide "pool" transported in an active manner via CERT.	Ceramides	105-113	ceramide kinase	Homo sapiens	46-50
17392267-5	2007	In conclusion, these results demonstrate that CERK localizes to areas of eicosanoid synthesis and uses a ceramide "pool" transported in an active manner via CERT.	Ceramides	105-113	ceramide transporter 1	Homo sapiens	157-161
17396235-7	2007	SK2-S promoter activity was also induced by the cell-permeable ceramide analog, N-acetylsphingosine (C2-ceramide).	Ceramides	63-71	potassium calcium-activated channel subfamily N member 2	Rattus norvegicus	0-3
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.	Ceramides	19-27	UDP-glucose ceramide glucosyltransferase	Homo sapiens	38-41
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.	Ceramides	72-80	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.	Ceramides	72-80	fatty acid 2-hydroxylase	Homo sapiens	194-198
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.	Ceramides	229-238	fatty acid 2-hydroxylase	Homo sapiens	194-198
17300923-16	2007	Interestingly, the levels of hexose-ceramide (glucosyl- and galactosylceramide, principal myelin cerebrosides) were decreased in Aldh5a1(-/-) brain tissue (one-tailed t test, p=0.0449).	Ceramides	36-44	aldhehyde dehydrogenase family 5, subfamily A1	Mus musculus	129-136
17392267-0	2007	Ceramide kinase uses ceramide provided by ceramide transport protein: localization to organelles of eicosanoid synthesis.	Ceramides	21-29	ceramide kinase	Homo sapiens	0-15
17392267-0	2007	Ceramide kinase uses ceramide provided by ceramide transport protein: localization to organelles of eicosanoid synthesis.	Ceramides	21-29	ceramide transporter 1	Homo sapiens	42-68
17428472-8	2007	In ceramide-inducing apoptosis, CD55(hi) cells showed high tolerance.	Ceramides	3-11	CD55 molecule (Cromer blood group)	Homo sapiens	32-36
17428472-8	2007	In ceramide-inducing apoptosis, CD55(hi) cells showed high tolerance.	Ceramides	3-11	CD55 molecule (Cromer blood group)	Homo sapiens	37-39
17360714-9	2007	H(2)O(2) and ceramide, two naturally occurring PKCalpha agonists that promote growth arrest in intestinal cells, activate 4E-BP1 in PKC/PKCalpha-dependent manner, supporting the physiological significance of the findings.	Ceramides	13-21	protein kinase C, alpha	Rattus norvegicus	47-55
17360714-9	2007	H(2)O(2) and ceramide, two naturally occurring PKCalpha agonists that promote growth arrest in intestinal cells, activate 4E-BP1 in PKC/PKCalpha-dependent manner, supporting the physiological significance of the findings.	Ceramides	13-21	eukaryotic translation initiation factor 4E binding protein 1	Rattus norvegicus	122-128
17360714-9	2007	H(2)O(2) and ceramide, two naturally occurring PKCalpha agonists that promote growth arrest in intestinal cells, activate 4E-BP1 in PKC/PKCalpha-dependent manner, supporting the physiological significance of the findings.	Ceramides	13-21	protein kinase C, gamma	Rattus norvegicus	47-50
17360714-9	2007	H(2)O(2) and ceramide, two naturally occurring PKCalpha agonists that promote growth arrest in intestinal cells, activate 4E-BP1 in PKC/PKCalpha-dependent manner, supporting the physiological significance of the findings.	Ceramides	13-21	protein kinase C, alpha	Rattus norvegicus	136-144
17487280-5	2007	Using large collections of publicly accessible genome-wide gene expression, we identify small, common sets of pathways - Trka Receptor, Apoptosis response to DNA Damage, Ceramide, Telomerase, CD40L and Calcineurin - whose differences robustly distinguish diverse tumor types from corresponding normal samples, predict tumor grade, and distinguish phenotypes such as estrogen receptor status and p53 mutation state.	Ceramides	170-178	neurotrophic receptor tyrosine kinase 1	Homo sapiens	121-125
17223929-0	2007	Ceramide as a TLR4 agonist; a putative signalling intermediate between sphingolipid receptors for microbial ligands and TLR4.	Ceramides	0-8	toll like receptor 4	Homo sapiens	120-124
17223929-4	2007	In this study, ceramide was identified as a TLR4 agonist and as a putative signalling intermediate between the glycosphingolipid recognition receptors and TLR4.	Ceramides	15-23	toll like receptor 4	Homo sapiens	44-48
17223929-4	2007	In this study, ceramide was identified as a TLR4 agonist and as a putative signalling intermediate between the glycosphingolipid recognition receptors and TLR4.	Ceramides	15-23	toll like receptor 4	Homo sapiens	155-159
17223929-5	2007	Exogenous ceramide activated a TLR4-dependent epithelial cell response, as shown by exposing stably transfected TLR4-positive or -negative human embryonal kidney cells to C2 and C6 ceramide.	Ceramides	10-18	toll like receptor 4	Homo sapiens	31-35
17223929-5	2007	Exogenous ceramide activated a TLR4-dependent epithelial cell response, as shown by exposing stably transfected TLR4-positive or -negative human embryonal kidney cells to C2 and C6 ceramide.	Ceramides	10-18	toll like receptor 4	Homo sapiens	112-116
17223929-5	2007	Exogenous ceramide activated a TLR4-dependent epithelial cell response, as shown by exposing stably transfected TLR4-positive or -negative human embryonal kidney cells to C2 and C6 ceramide.	Ceramides	181-189	toll like receptor 4	Homo sapiens	31-35
17223929-6	2007	A similar, TLR4-dependent response occurred after deliberate release of endogenous long-chained ceramide with sphingomyelinase.	Ceramides	96-104	toll like receptor 4	Homo sapiens	11-15
17223929-8	2007	The results show that ceramide activates TLR4 signalling and suggest that this mechanism might allow pathogens to elicit mucosal TLR4 responses by perturbing sphingolipid receptors for virulence ligands like P fimbriae.	Ceramides	22-30	toll like receptor 4	Homo sapiens	41-45
17223929-8	2007	The results show that ceramide activates TLR4 signalling and suggest that this mechanism might allow pathogens to elicit mucosal TLR4 responses by perturbing sphingolipid receptors for virulence ligands like P fimbriae.	Ceramides	22-30	toll like receptor 4	Homo sapiens	129-133
17264167-3	2007	Acid ceramidase (AC) is a key regulatory enzyme involved in ceramide metabolism, and mutations in the AC gene (Asah1) result in Farber Lipogranulomatosis, a fatal human genetic disorder.	Ceramides	60-68	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
17287460-4	2007	When administered to mice and rats, AMP-DNM significantly reduced glycosphingolipid but not ceramide concentrations in various tissues.	Ceramides	92-100	dynamin 1	Mus musculus	40-43
17264167-3	2007	Acid ceramidase (AC) is a key regulatory enzyme involved in ceramide metabolism, and mutations in the AC gene (Asah1) result in Farber Lipogranulomatosis, a fatal human genetic disorder.	Ceramides	60-68	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
17264167-3	2007	Acid ceramidase (AC) is a key regulatory enzyme involved in ceramide metabolism, and mutations in the AC gene (Asah1) result in Farber Lipogranulomatosis, a fatal human genetic disorder.	Ceramides	60-68	N-acylsphingosine amidohydrolase 1	Homo sapiens	111-116
17264167-10	2007	Based on these observations, we suggest that AC is an essential factor required for embryo survival that functions by removing ceramide from the newly formed embryos, thus inhibiting the default apoptosis pathway.	Ceramides	127-135	N-acylsphingosine amidohydrolase 1	Homo sapiens	45-47
17220321-0	2007	Leishmania donovani-induced ceramide as the key mediator of Akt dephosphorylation in murine macrophages: role of protein kinase Czeta and phosphatase.	Ceramides	28-36	thymoma viral proto-oncogene 1	Mus musculus	60-63
17454142-2	2007	Here, we have analyzed at greater depth the 4-HPR-triggered molecular events, demonstrating that 4-HPR induces an early (15 min) increase in ceramide levels by sphingomyelin hydrolysis and later (from 1 h) by de novo synthesis.	Ceramides	141-149	haptoglobin-related protein	Homo sapiens	99-102
17454142-3	2007	Using specific inhibitors of both pathways, we demonstrate that ceramide accumulation is responsible for early ROS generation, which act as apoptotic signalling intermediates leading to conformational activation of Bak and Bax, loss of mitochondrial membrane potential (DeltaPsim), mitochondrial membrane permeabilization (MMP) and cell death.	Ceramides	64-72	BCL2 antagonist/killer 1	Homo sapiens	215-218
17454142-3	2007	Using specific inhibitors of both pathways, we demonstrate that ceramide accumulation is responsible for early ROS generation, which act as apoptotic signalling intermediates leading to conformational activation of Bak and Bax, loss of mitochondrial membrane potential (DeltaPsim), mitochondrial membrane permeabilization (MMP) and cell death.	Ceramides	64-72	BCL2 associated X, apoptosis regulator	Homo sapiens	223-226
17454142-5	2007	In conclusion, our study delineates for the fist time the sequence and timing of the principal events induced by 4-HPR in leukemia cells and points to the potential use of modulators of ceramide metabolism as enhancers in 4-HPR-based therapies.	Ceramides	186-194	haptoglobin-related protein	Homo sapiens	115-118
17454142-0	2007	4-HPR-mediated leukemia cell cytotoxicity is triggered by ceramide-induced mitochondrial oxidative stress and is regulated downstream by Bcl-2.	Ceramides	58-66	haptoglobin-related protein	Homo sapiens	2-5
17454142-2	2007	Here, we have analyzed at greater depth the 4-HPR-triggered molecular events, demonstrating that 4-HPR induces an early (15 min) increase in ceramide levels by sphingomyelin hydrolysis and later (from 1 h) by de novo synthesis.	Ceramides	141-149	haptoglobin-related protein	Homo sapiens	46-49
17220321-3	2007	We observed that the endogenous ceramide generated during leishmanial infection led to the dephosphorylation of protein kinase B (PKB) (Akt) in infected cells.	Ceramides	32-40	thymoma viral proto-oncogene 1	Mus musculus	130-133
17013545-5	2007	In contrast to synthesis and turn-over of glycerolipids, the levels of very-long-chain fatty acids, long-chain bases and ceramide are severely affected by Acb1p depletion, suggesting that Acb1p, rather than playing a general role, serves specific roles in cellular lipid metabolism.	Ceramides	121-129	long-chain fatty acid transporter ACB1	Saccharomyces cerevisiae S288C	155-160
17220321-3	2007	We observed that the endogenous ceramide generated during leishmanial infection led to the dephosphorylation of protein kinase B (PKB) (Akt) in infected cells.	Ceramides	32-40	thymoma viral proto-oncogene 1	Mus musculus	136-139
17220321-4	2007	The study of ceramide-mediated Akt phosphorylation revealed that Akt was dephosphorylated at both Thr308 and Ser473 sites in infected cells.	Ceramides	13-21	thymoma viral proto-oncogene 1	Mus musculus	31-34
17220321-4	2007	The study of ceramide-mediated Akt phosphorylation revealed that Akt was dephosphorylated at both Thr308 and Ser473 sites in infected cells.	Ceramides	13-21	thymoma viral proto-oncogene 1	Mus musculus	65-68
17220321-6	2007	We found that Akt dephosphorylation was mediated by ceramide-induced PKCzeta-Akt association and PP2A activation.	Ceramides	52-60	thymoma viral proto-oncogene 1	Mus musculus	14-17
17220321-6	2007	We found that Akt dephosphorylation was mediated by ceramide-induced PKCzeta-Akt association and PP2A activation.	Ceramides	52-60	thymoma viral proto-oncogene 1	Mus musculus	77-80
17329257-8	2007	Finally we demonstrated that anandamide and ceramide treatment of cholangiocarcinoma cells recruited Fas and Fas ligand into the lipid rafts, subsequently activating death receptor pathways.	Ceramides	44-52	Fas ligand	Homo sapiens	109-119
17337731-0	2007	Key role for ceramides in mediating insulin resistance in human muscle cells.	Ceramides	13-22	insulin	Homo sapiens	36-43
17308302-2	2007	Furthermore, ceramide selectively and directly activated protein kinase C zeta (PKC zeta) to suppress Akt-dependent mitogenesis.	Ceramides	13-21	AKT serine/threonine kinase 1	Rattus norvegicus	102-105
17337731-1	2007	Elevated non-esterified fatty acids, triglyceride, diacylglycerol, and ceramide have all been associated with insulin resistance in muscle.	Ceramides	71-79	insulin	Homo sapiens	110-117
17303574-5	2007	In reciprocal experiments, overexpression of hLASS1, and not hLASS6, in drug-resistant cells caused a marked increase in imatinib-induced C18-ceramide generation, and enhanced apoptosis.	Ceramides	142-150	ceramide synthase 1	Homo sapiens	45-51
17337731-8	2007	Insulin resistance was also caused by cell-permeable analogues of ceramide, and palmitate-induced resistance was blocked in the presence of inhibitors of de novo ceramide synthesis.	Ceramides	66-74	insulin	Homo sapiens	0-7
17337731-8	2007	Insulin resistance was also caused by cell-permeable analogues of ceramide, and palmitate-induced resistance was blocked in the presence of inhibitors of de novo ceramide synthesis.	Ceramides	162-170	insulin	Homo sapiens	0-7
17337731-10	2007	Our data are consistent with ceramide being the agent responsible for insulin resistance caused by palmitate exposure.	Ceramides	29-37	insulin	Homo sapiens	70-77
17308302-6	2007	Pharmacological disruption of highly structured lipid microdomains resulted in abrogation of ceramide-activated, PKC zeta-dependent Akt inactivation, whereas molecular strategies suggest that ceramide-dependent PKC zeta phosphorylation of Akt3 at Ser(34) was necessary for ceramide-induced vascular smooth muscle cell growth arrest.	Ceramides	93-101	AKT serine/threonine kinase 1	Rattus norvegicus	132-135
17308302-6	2007	Pharmacological disruption of highly structured lipid microdomains resulted in abrogation of ceramide-activated, PKC zeta-dependent Akt inactivation, whereas molecular strategies suggest that ceramide-dependent PKC zeta phosphorylation of Akt3 at Ser(34) was necessary for ceramide-induced vascular smooth muscle cell growth arrest.	Ceramides	93-101	AKT serine/threonine kinase 3	Rattus norvegicus	239-243
17308302-7	2007	Taken together, these data demonstrate that structured membrane microdomains are necessary for ceramide-induced activation of PKC zeta and resultant diminished Akt activity, leading to vascular smooth muscle cell growth arrest.	Ceramides	95-103	AKT serine/threonine kinase 1	Rattus norvegicus	160-163
17306937-3	2007	Although sphingolipids such as ceramide and sphingosine 1-phosphate (S1-P) have been shown to serve as signaling molecules in the TNF-alpha inflammatory response, their role in the TNF-alpha induction of IL-8 gene expression in lung epithelial cells is not known.	Ceramides	31-39	tumor necrosis factor	Homo sapiens	130-139
17306937-3	2007	Although sphingolipids such as ceramide and sphingosine 1-phosphate (S1-P) have been shown to serve as signaling molecules in the TNF-alpha inflammatory response, their role in the TNF-alpha induction of IL-8 gene expression in lung epithelial cells is not known.	Ceramides	31-39	tumor necrosis factor	Homo sapiens	181-190
17306937-3	2007	Although sphingolipids such as ceramide and sphingosine 1-phosphate (S1-P) have been shown to serve as signaling molecules in the TNF-alpha inflammatory response, their role in the TNF-alpha induction of IL-8 gene expression in lung epithelial cells is not known.	Ceramides	31-39	C-X-C motif chemokine ligand 8	Homo sapiens	204-208
17303574-6	2007	Interestingly, there were no defects in the levels of mRNA and enzyme activity levels of hLASS1 for ceramide generation in K562/IMA-1 cells.	Ceramides	100-108	ceramide synthase 1	Homo sapiens	89-95
17303574-9	2007	On the other hand, forced expression of SK1 in K562 cells increased the ratio between total S1P/C18-ceramide levels approximately 6-fold and prevented apoptosis significantly in response to imatinib.	Ceramides	100-108	sphingosine kinase 1	Homo sapiens	40-43
17303574-11	2007	In conclusion, these data suggest a role for endogenous C18-ceramide synthesis mainly via hLASS1 in imatinib-induced apoptosis in sensitive cells, whereas in resistant cells, alterations of the balance between the levels of ceramide and S1P by overexpression of SK1 result in resistance to imatinib-induced apoptosis.	Ceramides	60-68	ceramide synthase 1	Homo sapiens	90-96
17303575-2	2007	Previous studies showed that treatment of MCF-7 mammary carcinoma cells with the potent protein kinase C (PKC) agonist, phorbol 12-myristate 13-acetate (PMA), induces a transient drop in sphingomyelin concomitant with an increase in cellular ceramide levels (Becker, K. P., Kitatani, K., Idkowiak-Baldys, J., Bielawski, J., and Hannun, Y.	Ceramides	242-250	protein kinase C delta	Homo sapiens	106-109
17303575-7	2007	Here we show that PMA selectively activates ASMase and that ASMase accounts for the majority of PMA-induced ceramide.	Ceramides	108-116	sphingomyelin phosphodiesterase 1	Homo sapiens	60-66
17303575-14	2007	Moreover, when transiently overexpressed, ASMase(S508A) blocked the ceramide formation after PMA treatment, suggesting a dominant negative function for this mutant.	Ceramides	68-76	sphingomyelin phosphodiesterase 1	Homo sapiens	42-48
17391062-3	2007	The loss of omega-hydroxylated very long-chain fatty acids (VLCFA) and ceramides substituted with omega-hydroxylated VLCFA covalently linked to corneocyte surface proteins leads to the disruption of the epidermal lipid barrier in scd1-/- mutants.	Ceramides	71-80	stearoyl-Coenzyme A desaturase 1	Mus musculus	230-234
17349629-1	2007	Neutral sphingomyelinase 2 (nSMase2), which has two hydrophobic segments at its NH(2)-terminus, plays an important role in ceramide-mediated cell regulation.	Ceramides	123-131	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
17349629-1	2007	Neutral sphingomyelinase 2 (nSMase2), which has two hydrophobic segments at its NH(2)-terminus, plays an important role in ceramide-mediated cell regulation.	Ceramides	123-131	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
17404114-5	2007	RESULTS: We showed by DNA-binding assay that NF-kappaB activation induced by tumor necrosis factor (TNF), phorbol 12-myristate 13-acetate, lipopolysaccharide, ceramide, interleukin-1, and H(2)O(2) was suppressed by morin; the suppression was not cell type specific.	Ceramides	159-167	interleukin 1 alpha	Homo sapiens	169-182
17275084-4	2007	Suppression of ABCG2 expression by siRNA led to a marked increase in phosphatidylserine externalisation followed by accumulation of ceramides and increased apoptosis.	Ceramides	132-141	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	15-20
17241120-4	2007	Second, apoE contributes to galactosylceramide and ceramide homeostasis in mouse DRG.	Ceramides	38-46	apolipoprotein E	Mus musculus	8-12
17219404-0	2007	Fatty acid-induced defects in insulin signalling, in myotubes derived from children, are related to ceramide production from palmitate rather than the accumulation of intramyocellular lipid.	Ceramides	100-108	insulin	Homo sapiens	30-37
17219404-8	2007	In summary, palmitate appears to cause insulin resistance in children"s myotubes via its metabolism to ceramide, and this process appears unrelated to IMCL formation and is ameliorated by oleate.	Ceramides	103-111	insulin	Homo sapiens	39-46
17210985-3	2007	Our results indicate that the antibody (rabbit IgG) specifically recognizes ceramide in lipid overlay assays and detects ceramide species with different fatty acid chain lengths that include C2, C8, C16, C18, C20, and C24.	Ceramides	121-129	Bardet-Biedl syndrome 9	Homo sapiens	204-207
17255104-12	2007	Taken together, we conclude that palmitate inhibits the phosphorylation of both AMPK and endothelial nitric-oxide synthase in endothelial cells via ceramide-dependent PP2A activation.	Ceramides	148-156	nitric oxide synthase 3, endothelial cell	Mus musculus	89-122
17272284-3	2007	nSMase2, which has two hydrophobic segments near the NH(2)-terminal region, has been reported to be located at the plasma membrane and play important roles in ceramide-mediated signaling.	Ceramides	159-167	sphingomyelin phosphodiesterase 3	Homo sapiens	0-7
17255104-12	2007	Taken together, we conclude that palmitate inhibits the phosphorylation of both AMPK and endothelial nitric-oxide synthase in endothelial cells via ceramide-dependent PP2A activation.	Ceramides	148-156	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	167-171
16822514-2	2007	Novel apoptotic markers like apolipoprotein C-I have been implicated in apoptotic human vascular smooth muscle cell death via recruiting a neutral sphingomyelinase (N-SMase)-ceramide pathway.	Ceramides	174-182	apolipoprotein C1	Homo sapiens	29-47
17374154-1	2007	BACKGROUND: Sphingosine-1-phosphate (S1P), a downstream metabolite of ceramide, induces various bioactivities via two distinct pathways: as an intracellular second messenger or through receptor activation.	Ceramides	70-78	membrane bound transcription factor peptidase, site 1	Homo sapiens	37-40
16822514-2	2007	Novel apoptotic markers like apolipoprotein C-I have been implicated in apoptotic human vascular smooth muscle cell death via recruiting a neutral sphingomyelinase (N-SMase)-ceramide pathway.	Ceramides	174-182	sphingomyelin phosphodiesterase 2	Homo sapiens	139-163
16822514-2	2007	Novel apoptotic markers like apolipoprotein C-I have been implicated in apoptotic human vascular smooth muscle cell death via recruiting a neutral sphingomyelinase (N-SMase)-ceramide pathway.	Ceramides	174-182	sphingomyelin phosphodiesterase 2	Homo sapiens	165-172
17158207-8	2007	Effects of TNFalpha and C6 on insulin-stimulated phosphorylation of glycogen synthase kinase 3beta were prevented by myriocin and tautomycin, a PP1 inhibitor, further implicating a de novo ceramide-PP1 pathway.	Ceramides	189-197	tumor necrosis factor	Homo sapiens	11-19
17339023-0	2007	The path to insulin resistance: paved with ceramides?	Ceramides	43-52	insulin	Homo sapiens	12-19
17339023-3	2007	(2007) provide pharmacological and genetic evidence that ceramide plays a key role in the development of insulin resistance induced by these factors.	Ceramides	57-65	insulin	Homo sapiens	105-112
17339025-6	2007	Second, they identify enzymes required for ceramide synthesis as therapeutic targets for combating insulin resistance caused by nutrient excess or glucocorticoid therapy.	Ceramides	43-51	insulin	Homo sapiens	99-106
17158207-5	2007	TNFalpha increased serine/threonine phosphatase activity of protein phosphatase 1 (PP1) in response to C6, but not insulin, suggesting a ceramide-specific effect.	Ceramides	137-145	tumor necrosis factor	Homo sapiens	0-8
17158207-5	2007	TNFalpha increased serine/threonine phosphatase activity of protein phosphatase 1 (PP1) in response to C6, but not insulin, suggesting a ceramide-specific effect.	Ceramides	137-145	inorganic pyrophosphatase 1	Homo sapiens	60-81
17158207-5	2007	TNFalpha increased serine/threonine phosphatase activity of protein phosphatase 1 (PP1) in response to C6, but not insulin, suggesting a ceramide-specific effect.	Ceramides	137-145	inorganic pyrophosphatase 1	Homo sapiens	83-86
17158207-8	2007	Effects of TNFalpha and C6 on insulin-stimulated phosphorylation of glycogen synthase kinase 3beta were prevented by myriocin and tautomycin, a PP1 inhibitor, further implicating a de novo ceramide-PP1 pathway.	Ceramides	189-197	insulin	Homo sapiens	30-37
17158207-6	2007	Myriocin, an inhibitor of de novo ceramide synthesis, blocked stimulation of the PP1 activity.	Ceramides	34-42	inorganic pyrophosphatase 1	Homo sapiens	81-84
17158207-8	2007	Effects of TNFalpha and C6 on insulin-stimulated phosphorylation of glycogen synthase kinase 3beta were prevented by myriocin and tautomycin, a PP1 inhibitor, further implicating a de novo ceramide-PP1 pathway.	Ceramides	189-197	glycogen synthase kinase 3 beta	Homo sapiens	68-98
17158207-8	2007	Effects of TNFalpha and C6 on insulin-stimulated phosphorylation of glycogen synthase kinase 3beta were prevented by myriocin and tautomycin, a PP1 inhibitor, further implicating a de novo ceramide-PP1 pathway.	Ceramides	189-197	inorganic pyrophosphatase 1	Homo sapiens	198-201
17180345-8	2007	The effect of patient plasma on erythrocyte annexin V binding was paralleled by formation of ceramide and a significant increase of cytosolic Ca2+ activity.	Ceramides	93-101	annexin A5	Homo sapiens	44-53
17285001-4	2007	RECENT FINDINGS: Recent studies have suggested that local accumulation of fat metabolites such as ceramides, diacylglycerol or acyl-CoA, inside skeletal muscle and liver, may activate a serine kinase cascade leading to defects in insulin signalling and glucose transport.	Ceramides	98-107	insulin	Homo sapiens	230-237
17239851-0	2007	Nitric oxide-enhanced caspase-3 and acidic sphingomyelinase interaction: a novel mechanism by which airway epithelial cells escape ceramide-induced apoptosis.	Ceramides	131-139	caspase 3	Homo sapiens	22-31
17440226-0	2007	PPARalpha agonist induces the accumulation of ceramide in the heart of rats fed high-fat diet.	Ceramides	46-54	peroxisome proliferator activated receptor alpha	Rattus norvegicus	0-9
17440226-1	2007	It was shown that high-fat feeding of mice with cardiac-specific overexpression of peroxisome proliferator-activated receptor (PPAR) alpha but not wild type animals leads to the accumulation of ceramide (an important mediator of lipotoxicity) in the heart [Finck et al.	Ceramides	194-202	peroxisome proliferator activated receptor alpha	Mus musculus	83-138
17440226-3	2007	To investigate the mechanism of this phenomenon we examined the effects of PPARalpha activation on ceramide metabolism in the myocardium.	Ceramides	99-107	peroxisome proliferator activated receptor alpha	Rattus norvegicus	75-84
17440226-11	2007	Our results demonstrated that PPARalpha activation modulates myocardial ceramide metabolism and leads to the accumulation of ceramide in the heart of the high-fat fed rats due to its increased synthesis de novo.	Ceramides	72-80	peroxisome proliferator activated receptor alpha	Rattus norvegicus	30-39
17440226-11	2007	Our results demonstrated that PPARalpha activation modulates myocardial ceramide metabolism and leads to the accumulation of ceramide in the heart of the high-fat fed rats due to its increased synthesis de novo.	Ceramides	125-133	peroxisome proliferator activated receptor alpha	Rattus norvegicus	30-39
17311087-0	2007	Depletion of ceramides with very long chain fatty acids causes defective skin permeability barrier function, and neonatal lethality in ELOVL4 deficient mice.	Ceramides	13-22	elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 4	Mus musculus	135-141
17311087-9	2007	We further showed that the absence of ELOVL4 results in depletion in the epidermis of ceramides with omega-hydroxy very long chain fatty acids (> or = C28) and accumulation of ceramides with non omega-hydroxy fatty acids of C26, implicating C26 fatty acids as possible substrates of ELOVL4.	Ceramides	86-95	elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 4	Mus musculus	38-44
17311087-9	2007	We further showed that the absence of ELOVL4 results in depletion in the epidermis of ceramides with omega-hydroxy very long chain fatty acids (> or = C28) and accumulation of ceramides with non omega-hydroxy fatty acids of C26, implicating C26 fatty acids as possible substrates of ELOVL4.	Ceramides	179-188	elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 4	Mus musculus	38-44
17135264-9	2007	On the other hand, during cancer and endothelial cell interaction, t-PTER- and QUER-induced NO release from the vascular endothelium up-regulated neutral sphingomyelinase activity and ceramide generation in B16M-F10 cells.	Ceramides	184-192	phosphotriesterase related	Mus musculus	69-73
17135264-10	2007	Direct NO-induced cytotoxicity and ceramide-induced mitochondrial permeability transition and apoptosis activation can explain the increased endothelium-induced death of Bcl-2-depleted B16M-F10 cells.	Ceramides	35-43	B cell leukemia/lymphoma 2	Mus musculus	170-175
16862171-3	2007	Acid CDase silencing by small interfering RNA (siRNA) or pharmacological inhibition with N-oleoylethanolamine (NOE) enhanced the ceramide to S1P balance compared to DNR alone, sensitizing hepatoma cells (HepG2, Hep-3B, SK-Hep and Hepa1c1c7) to DNR-induced cell death.	Ceramides	129-137	N-acylsphingosine amidohydrolase 1	Mus musculus	0-10
17239851-0	2007	Nitric oxide-enhanced caspase-3 and acidic sphingomyelinase interaction: a novel mechanism by which airway epithelial cells escape ceramide-induced apoptosis.	Ceramides	131-139	sphingomyelin phosphodiesterase 1	Homo sapiens	36-59
17239851-9	2007	However, this ceramide induction does not lead to apoptosis unless aSMase is knocked down, allowing the release of caspase-3, its activation and execution of apoptosis.	Ceramides	14-22	sphingomyelin phosphodiesterase 1	Homo sapiens	67-73
17239851-9	2007	However, this ceramide induction does not lead to apoptosis unless aSMase is knocked down, allowing the release of caspase-3, its activation and execution of apoptosis.	Ceramides	14-22	caspase 3	Homo sapiens	115-124
17005604-10	2007	p38 and JNK stimulation by CML-collagen was almost entirely blocked when formation of ROS was inhibited and was partially reduced by NO and ceramide inhibitors.	Ceramides	140-148	mitogen-activated protein kinase 14	Homo sapiens	0-3
17005604-10	2007	p38 and JNK stimulation by CML-collagen was almost entirely blocked when formation of ROS was inhibited and was partially reduced by NO and ceramide inhibitors.	Ceramides	140-148	mitogen-activated protein kinase 8	Homo sapiens	8-11
17159597-4	2007	Sphingosine kinase-1 is a crucial regulator of this two-pan balance, because it produces the prosurvival sphingosine 1-phosphate, and reduces the content of both ceramide and sphingosine, the proapoptotic sphingolipids.	Ceramides	162-170	sphingosine kinase 1	Homo sapiens	0-20
17105725-6	2007	Ceramide depletion prevented plasma membrane translocation of PKCzeta/lambda, its interaction with Cdc42, and phosphorylation of GSK-3beta, a substrate of PKCzeta/lambda.	Ceramides	0-8	cell division cycle 42	Mus musculus	99-104
17105725-6	2007	Ceramide depletion prevented plasma membrane translocation of PKCzeta/lambda, its interaction with Cdc42, and phosphorylation of GSK-3beta, a substrate of PKCzeta/lambda.	Ceramides	0-8	glycogen synthase kinase 3 beta	Mus musculus	129-138
17105725-7	2007	Recombinant PKCzeta formed a complex with the polarity protein Par6 and Cdc42 when bound to ceramide containing lipid vesicles.	Ceramides	92-100	par-6 family cell polarity regulator alpha	Mus musculus	63-67
17105725-7	2007	Recombinant PKCzeta formed a complex with the polarity protein Par6 and Cdc42 when bound to ceramide containing lipid vesicles.	Ceramides	92-100	cell division cycle 42	Mus musculus	72-77
17191114-8	2007	Similarly, the pre-incubation of macrophages with PtdIns(3,5)BP prevented microparticle-induced upregulation of caspase 8, which is a major target molecule of ceramide action in the apoptosis pathway.	Ceramides	159-167	caspase 8	Homo sapiens	112-121
17240190-6	2007	Palmitate-induced caspase-3 activation was prevented by triacsin C and slightly reduced by alpha-tocopherol and by the de novo ceramide synthesis inhibitor fumonisin B(1).	Ceramides	127-135	caspase 3	Homo sapiens	18-27
17355200-2	2007	Ceramide kinase (CERK) is a lipid kinase that catalyzes the formation of ceramide-1-phosphate from ceramide, a sphingolipid that is a key mediator of cellular apoptosis.	Ceramides	73-81	ceramide kinase	Homo sapiens	0-15
17355200-2	2007	Ceramide kinase (CERK) is a lipid kinase that catalyzes the formation of ceramide-1-phosphate from ceramide, a sphingolipid that is a key mediator of cellular apoptosis.	Ceramides	73-81	ceramide kinase	Homo sapiens	17-21
17355200-4	2007	Here we describe a homogeneous chemiluminescence assay that directly measures the ceramide-dependent ATP depletion by recombinant full-length human CERK.	Ceramides	82-90	ceramide kinase	Homo sapiens	148-152
17355200-7	2007	These compounds can serve as tools to further elucidate the CERK pathway and its role in ceramide metabolism and human diseases.	Ceramides	89-97	ceramide kinase	Homo sapiens	60-64
17259384-8	2007	We propose that ceramide and oxidative stress can each affect two independent arms of insulin signaling to GLUT4 at distinct steps, Rac-GTP loading and Akt phosphorylation.	Ceramides	16-24	insulin	Homo sapiens	86-93
17259384-8	2007	We propose that ceramide and oxidative stress can each affect two independent arms of insulin signaling to GLUT4 at distinct steps, Rac-GTP loading and Akt phosphorylation.	Ceramides	16-24	solute carrier family 2 member 4	Homo sapiens	107-112
17259384-0	2007	Ceramide- and oxidant-induced insulin resistance involve loss of insulin-dependent Rac-activation and actin remodeling in muscle cells.	Ceramides	0-8	insulin	Homo sapiens	30-37
17259384-0	2007	Ceramide- and oxidant-induced insulin resistance involve loss of insulin-dependent Rac-activation and actin remodeling in muscle cells.	Ceramides	0-8	insulin	Homo sapiens	65-72
17259384-8	2007	We propose that ceramide and oxidative stress can each affect two independent arms of insulin signaling to GLUT4 at distinct steps, Rac-GTP loading and Akt phosphorylation.	Ceramides	16-24	AKT serine/threonine kinase 1	Homo sapiens	132-135
17259384-0	2007	Ceramide- and oxidant-induced insulin resistance involve loss of insulin-dependent Rac-activation and actin remodeling in muscle cells.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	83-86
17259384-8	2007	We propose that ceramide and oxidative stress can each affect two independent arms of insulin signaling to GLUT4 at distinct steps, Rac-GTP loading and Akt phosphorylation.	Ceramides	16-24	AKT serine/threonine kinase 1	Homo sapiens	152-155
17213336-6	2007	Phospholipase D (PLD), a recognized target of ceramide, is required for myogenesis, as shown by the negative effects of PLD1 isoform depletion obtained by siRNA treatment.	Ceramides	46-54	phospholipase D1	Mus musculus	120-124
17213336-8	2007	The expression of PLD1 mRNA transcripts was selectively decreased by C6-ceramide, and increased by ceramide synthesis inhibitors.	Ceramides	72-80	phospholipase D1	Mus musculus	18-22
17213336-11	2007	Ceramide might thus regulate myogenesis through downregulation of PLD1 expression and activity.	Ceramides	0-8	phospholipase D1	Mus musculus	66-70
17259995-4	2007	Cu(2+) induced the secretion of activated Asm from leukocytes, leading to ceramide release in and phosphatidylserine exposure on erythrocytes, events also prevented by inhibition of Asm.	Ceramides	74-82	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	42-45
17484380-2	2007	As a novel toxin, levels of ceramide, a well-studied lipid mediator of apoptosis, were determined by LC-MS/MS in the liver and plasma of carbon tetrachloride (CCl4)-intoxicated rats.	Ceramides	28-36	C-C motif chemokine ligand 4	Rattus norvegicus	159-163
17484380-5	2007	The total ceramide concentration in the plasma was also increased to 4.1 times that in the control 24 h after administration of CCl4.	Ceramides	10-18	C-C motif chemokine ligand 4	Rattus norvegicus	128-132
17086544-3	2007	In this study, we showed increased expression of serine palmitoyltransferase (SPT), the first enzyme in the ceramide biosynthetic pathway, in reactive astrocytes of the hippocampus after kainate injections.	Ceramides	108-116	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	49-76
17086544-3	2007	In this study, we showed increased expression of serine palmitoyltransferase (SPT), the first enzyme in the ceramide biosynthetic pathway, in reactive astrocytes of the hippocampus after kainate injections.	Ceramides	108-116	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	78-81
17086544-5	2007	In vitro studies showed that treatment of hippocampal slice cultures with SPT inhibitor ISP-1 (myriocin) or L-cycloserine modulated increases in 16:0, 18:0, and 20:0 ceramide species, and partially reduced kainate-induced cell death.	Ceramides	166-174	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	74-77
17086544-6	2007	The above findings indicate a role of SPT in ceramide increase after kainate injury, although additional effects of sphingomyelinase cannot be ruled out.	Ceramides	45-53	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	38-41
17308067-2	2007	Then, possible involvement of the human homologue of yeast longevity assurance gene 1 (LASS1)/C(18)-ceramide in chemotherapy-induced cell death in these cells was examined.	Ceramides	100-108	ceramide synthase 1	Homo sapiens	59-85
17308067-2	2007	Then, possible involvement of the human homologue of yeast longevity assurance gene 1 (LASS1)/C(18)-ceramide in chemotherapy-induced cell death in these cells was examined.	Ceramides	100-108	ceramide synthase 1	Homo sapiens	87-92
17308067-9	2007	In conclusion, these data suggest an important role for LASS1/C(18)-ceramide in gemcitabine/doxorubicin-induced cell death via the activation of caspase-9/3 in HNSCC.	Ceramides	68-76	ceramide synthase 1	Homo sapiens	56-61
17308067-9	2007	In conclusion, these data suggest an important role for LASS1/C(18)-ceramide in gemcitabine/doxorubicin-induced cell death via the activation of caspase-9/3 in HNSCC.	Ceramides	68-76	caspase 9	Homo sapiens	145-154
16942465-9	2007	Furthermore, here we demonstrate that activation of PAR-2, as well as PAR-1, rescued astrocytes from ceramide-induced apoptosis via regulating chemokine GRO/CINC-1 release.	Ceramides	101-109	F2R like trypsin receptor 1	Rattus norvegicus	52-57
17158340-9	2007	In conclusion, we show for the first time that the upregulation of ceramide/sphingosine 1-phosphate ratio is a critical event in MAO-A-mediated cardiac cell apoptosis.	Ceramides	67-75	monoamine oxidase A	Rattus norvegicus	129-134
17381401-3	2007	PURPOSE: We determined whether LPS-induced TLR4 assembly and activation are dependent on the sphingolipid metabolite ceramide, produced by acid sphingomyelinase following the initial binding of LPS to CD14.	Ceramides	117-125	toll like receptor 4	Homo sapiens	43-47
17381401-3	2007	PURPOSE: We determined whether LPS-induced TLR4 assembly and activation are dependent on the sphingolipid metabolite ceramide, produced by acid sphingomyelinase following the initial binding of LPS to CD14.	Ceramides	117-125	sphingomyelin phosphodiesterase 1	Homo sapiens	139-160
17381401-3	2007	PURPOSE: We determined whether LPS-induced TLR4 assembly and activation are dependent on the sphingolipid metabolite ceramide, produced by acid sphingomyelinase following the initial binding of LPS to CD14.	Ceramides	117-125	CD14 molecule	Homo sapiens	201-205
17381401-10	2007	CONCLUSION: Assembly and activation of the TLR4 receptor following LPS binding to CD14 requires the production of ceramide by acid sphingomyelinase.	Ceramides	114-122	toll like receptor 4	Homo sapiens	43-47
17381401-10	2007	CONCLUSION: Assembly and activation of the TLR4 receptor following LPS binding to CD14 requires the production of ceramide by acid sphingomyelinase.	Ceramides	114-122	CD14 molecule	Homo sapiens	82-86
17381401-10	2007	CONCLUSION: Assembly and activation of the TLR4 receptor following LPS binding to CD14 requires the production of ceramide by acid sphingomyelinase.	Ceramides	114-122	sphingomyelin phosphodiesterase 1	Homo sapiens	126-147
16942465-9	2007	Furthermore, here we demonstrate that activation of PAR-2, as well as PAR-1, rescued astrocytes from ceramide-induced apoptosis via regulating chemokine GRO/CINC-1 release.	Ceramides	101-109	coagulation factor II (thrombin) receptor	Rattus norvegicus	70-75
16987101-7	2007	Notwithstanding, IPCs incorporated into glycosylphosphatidylinositol anchors of 4Delta.Lass5 show normal mobility on TLC and the ceramide- and raft-dependent traffic of Gas1p (glycophospholipid-anchored surface protein) from endoplasmic reticulum to Golgi remains almost normal.	Ceramides	129-137	ceramide synthase 5	Mus musculus	87-92
16987101-2	2007	The bulk of VLCFAs and DHS are used for ceramide synthesis by the Lag1p (longevity-assurance gene 1)/Lac1p (longevity-assurance gene cognate 1)/Lip1p (Lag1p/Lac1p interacting protein) ceramide synthase.	Ceramides	40-48	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	66-71
16942465-9	2007	Furthermore, here we demonstrate that activation of PAR-2, as well as PAR-1, rescued astrocytes from ceramide-induced apoptosis via regulating chemokine GRO/CINC-1 release.	Ceramides	101-109	C-X-C motif chemokine ligand 1	Rattus norvegicus	153-156
16987101-2	2007	The bulk of VLCFAs and DHS are used for ceramide synthesis by the Lag1p (longevity-assurance gene 1)/Lac1p (longevity-assurance gene cognate 1)/Lip1p (Lag1p/Lac1p interacting protein) ceramide synthase.	Ceramides	40-48	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	101-106
16987101-7	2007	Notwithstanding, IPCs incorporated into glycosylphosphatidylinositol anchors of 4Delta.Lass5 show normal mobility on TLC and the ceramide- and raft-dependent traffic of Gas1p (glycophospholipid-anchored surface protein) from endoplasmic reticulum to Golgi remains almost normal.	Ceramides	129-137	1,3-beta-glucanosyltransferase GAS1	Saccharomyces cerevisiae S288C	169-174
16942465-9	2007	Furthermore, here we demonstrate that activation of PAR-2, as well as PAR-1, rescued astrocytes from ceramide-induced apoptosis via regulating chemokine GRO/CINC-1 release.	Ceramides	101-109	C-X-C motif chemokine ligand 1	Rattus norvegicus	157-163
17595532-6	2007	Furthermore, our studies indicate that the activation of the acid sphingomyelinase (ASM) is intrigued in the formation of ceramide- or GM1- enriched membrane platforms.	Ceramides	122-130	sphingomyelin phosphodiesterase 1	Homo sapiens	84-87
17466962-5	2007	The addition of SMA-7 suppressed neutral SMase-catalyzed ceramide production, NF-kappaB activation, and IL-8 release from HT-29 cells caused by LPS.	Ceramides	57-65	immunoglobulin mu binding protein 2	Mus musculus	16-19
16987101-2	2007	The bulk of VLCFAs and DHS are used for ceramide synthesis by the Lag1p (longevity-assurance gene 1)/Lac1p (longevity-assurance gene cognate 1)/Lip1p (Lag1p/Lac1p interacting protein) ceramide synthase.	Ceramides	40-48	sphingosine N-acyltransferase subunit LIP1	Saccharomyces cerevisiae S288C	144-149
16987101-2	2007	The bulk of VLCFAs and DHS are used for ceramide synthesis by the Lag1p (longevity-assurance gene 1)/Lac1p (longevity-assurance gene cognate 1)/Lip1p (Lag1p/Lac1p interacting protein) ceramide synthase.	Ceramides	40-48	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	151-156
16987101-2	2007	The bulk of VLCFAs and DHS are used for ceramide synthesis by the Lag1p (longevity-assurance gene 1)/Lac1p (longevity-assurance gene cognate 1)/Lip1p (Lag1p/Lac1p interacting protein) ceramide synthase.	Ceramides	40-48	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	157-162
17310111-9	2007	The effect of Abeta (1-42) (> or = 0.5 microM) on erythrocyte annexin V binding was paralleled by formation of ceramide but not by significant increase of cytosolic Ca(2+) activity.	Ceramides	114-122	annexin A5	Homo sapiens	65-74
17595532-7	2007	Inhibition of the ASM reduces the number of ceramide-enriched platforms and glycosphingolipid-enriched membrane domains.	Ceramides	44-52	sphingomyelin phosphodiesterase 1	Homo sapiens	18-21
17982273-10	2007	Furthermore, we found that Hcys induced Vav2 phosphorylation in a time-dependent manner, which could be induced by C16-Cer and blocked by inhibition of de novo ceramide synthesis.	Ceramides	160-168	vav guanine nucleotide exchange factor 2	Rattus norvegicus	40-44
17762163-6	2007	The effects of the drugs on the phosphorylation of Fc gamma RII and NTAL were prominent and correlated with a reduction of the cell surface ceramide production by imipramine and an augmentation of the ceramide generation by B13.	Ceramides	140-148	linker for activation of T cells family member 2	Homo sapiens	68-72
17762163-6	2007	The effects of the drugs on the phosphorylation of Fc gamma RII and NTAL were prominent and correlated with a reduction of the cell surface ceramide production by imipramine and an augmentation of the ceramide generation by B13.	Ceramides	201-209	linker for activation of T cells family member 2	Homo sapiens	68-72
17762170-0	2007	Sphingolipid metabolite ceramide causes metabolic perturbation contributing to HERG K+ channel dysfunction.	Ceramides	24-32	potassium voltage-gated channel subfamily H member 2	Homo sapiens	79-83
17762170-3	2007	To investigate how ceramide is involved in modulating cardiac repolarization, we performed whole-cell patch-clamp studies on HERG current (I(HERG)), a critical determinant of cardiac repolarization, expressed in HEK293 cells.	Ceramides	19-27	potassium voltage-gated channel subfamily H member 2	Homo sapiens	125-129
17762170-13	2007	We conclude that ceramide depresses I(HERG) mainly via ROS overproduction and ceramide-induced I(HERG) impairment may contribute to QT prolongation in prolonged myocardial ischemia, heart failure and diabetic cardiomyopathy.	Ceramides	17-25	potassium voltage-gated channel subfamily H member 2	Homo sapiens	38-42
17982273-11	2007	These results suggest that Vav2 importantly contributes to Hcys-induced increase in Rac1 activity and consequent activation of NADPH oxidase in RMCs via ceramide-associated tyrosine phosphorylation.	Ceramides	153-161	vav guanine nucleotide exchange factor 2	Rattus norvegicus	27-31
17982273-11	2007	These results suggest that Vav2 importantly contributes to Hcys-induced increase in Rac1 activity and consequent activation of NADPH oxidase in RMCs via ceramide-associated tyrosine phosphorylation.	Ceramides	153-161	Rac family small GTPase 1	Rattus norvegicus	84-88
17294743-10	2007	CONCLUSION: TNF-alpha can induce the ceramide increase in GMC, which is significant to effect on the kidney injury of the rats with obstructive jaundice, by the means of inducing GMC apoptosis and decreasing the activity of PC-PLD.	Ceramides	37-45	tumor necrosis factor	Rattus norvegicus	12-21
17370039-6	2007	The activity of the protein phosphatase PP-2A, which restricts motility and which can be activated by ceramide, was also diminished.	Ceramides	102-110	protein phosphatase 2 phosphatase activator	Homo sapiens	40-45
17370039-8	2007	Treatment with a membrane-permeable ceramide restored PP-2A activity and blocked migration.	Ceramides	36-44	protein phosphatase 2 phosphatase activator	Homo sapiens	54-59
17370039-9	2007	These studies show an autocrine motility-stimulatory pathway that is mediated in premalignant lesion cells by IL-10 through its reduction of ceramide levels and inhibition of PP-2A activity.	Ceramides	141-149	interleukin 10	Homo sapiens	110-115
17969452-4	2007	These mediate the response of PKR to additional indirect stimuli, including bacterial lipopolysaccharides, ceramide and polyanionic molecules.	Ceramides	107-115	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	30-33
17416967-1	2007	Ceramide is a bioactive sphingolipid that can prevent calpain activation and beta-amyloid (A beta) neurotoxicity in cortical neurons.	Ceramides	0-8	amyloid beta (A4) precursor protein	Mus musculus	77-97
17416967-4	2007	Ceramide inhibited A beta-induced calpain activation and cdk5 activity in wild-type neurons and protected against neuronal death and tau hyperphosphorylation.	Ceramides	0-8	amyloid beta (A4) precursor protein	Mus musculus	19-25
17416967-4	2007	Ceramide inhibited A beta-induced calpain activation and cdk5 activity in wild-type neurons and protected against neuronal death and tau hyperphosphorylation.	Ceramides	0-8	cyclin-dependent kinase 5	Mus musculus	57-61
17416967-6	2007	In p35 null neurons, ceramide blocked A beta-induced calpain activation but did not inhibit cdk5 activity or cell death.	Ceramides	21-29	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	3-6
17416967-6	2007	In p35 null neurons, ceramide blocked A beta-induced calpain activation but did not inhibit cdk5 activity or cell death.	Ceramides	21-29	amyloid beta (A4) precursor protein	Mus musculus	38-44
17416967-7	2007	However, ceramide blocked tau hyperphosphorylation potentially via inhibition of glycogen synthase kinase-3beta.	Ceramides	9-17	glycogen synthase kinase 3 beta	Mus musculus	81-111
17416967-8	2007	These data suggest that ceramide can regulate A beta cell toxicity in a p35/cdk5-dependent manner.	Ceramides	24-32	amyloid beta (A4) precursor protein	Mus musculus	46-52
17416967-8	2007	These data suggest that ceramide can regulate A beta cell toxicity in a p35/cdk5-dependent manner.	Ceramides	24-32	cyclin-dependent kinase 5, regulatory subunit 1 (p35)	Mus musculus	72-75
17416967-8	2007	These data suggest that ceramide can regulate A beta cell toxicity in a p35/cdk5-dependent manner.	Ceramides	24-32	cyclin-dependent kinase 5	Mus musculus	76-80
17875416-5	2007	In hepatocytes, hyperosmotic exposure induces an almost instantaneous acidification of an acidic sphingomyelinase (ASM) containing endosomal compartment, which is followed by an increase in the intracellular ceramide concentration.	Ceramides	208-216	sphingomyelin phosphodiesterase 1	Homo sapiens	90-113
17875416-5	2007	In hepatocytes, hyperosmotic exposure induces an almost instantaneous acidification of an acidic sphingomyelinase (ASM) containing endosomal compartment, which is followed by an increase in the intracellular ceramide concentration.	Ceramides	208-216	sphingomyelin phosphodiesterase 1	Homo sapiens	115-118
17044054-1	2007	The acyl-CoA binding protein (ACBP) is essential for the fatty acid metabolism, membrane structure, membrane fusion, and ceramide synthesis.	Ceramides	121-129	diazepam binding inhibitor, acyl-CoA binding protein	Homo sapiens	4-28
17044054-1	2007	The acyl-CoA binding protein (ACBP) is essential for the fatty acid metabolism, membrane structure, membrane fusion, and ceramide synthesis.	Ceramides	121-129	diazepam binding inhibitor, acyl-CoA binding protein	Homo sapiens	30-34
17013895-7	2007	These findings indicate that the combined use of inhibitors of EGF-EGFR and E2-ER-beta signaling with etoposide, which act by increasing the cellular ceramide levels and caspase activity, represents a promising strategy for a more effective treatment of metastatic PC forms.	Ceramides	150-158	epidermal growth factor receptor	Homo sapiens	67-71
17013895-7	2007	These findings indicate that the combined use of inhibitors of EGF-EGFR and E2-ER-beta signaling with etoposide, which act by increasing the cellular ceramide levels and caspase activity, represents a promising strategy for a more effective treatment of metastatic PC forms.	Ceramides	150-158	estrogen receptor 2	Homo sapiens	79-86
17210739-1	2007	Sphingomyelin synthase 2 (SMS2) is an enzyme that catalyzes the conversion of phosphatidylcholine and ceramide to sphingomyelin and diacylglycerol, and it is crucial to cellular lipid metabolism.	Ceramides	102-110	sphingomyelin synthase 2	Rattus norvegicus	0-24
17210739-1	2007	Sphingomyelin synthase 2 (SMS2) is an enzyme that catalyzes the conversion of phosphatidylcholine and ceramide to sphingomyelin and diacylglycerol, and it is crucial to cellular lipid metabolism.	Ceramides	102-110	sphingomyelin synthase 2	Rattus norvegicus	26-30
17225464-3	2006	The ceramide analog induced cell death through an apoptotic mechanism, which was demonstrated by DNA fragmentation, the cleavage of poly ADP ribose polymerase (PARP), and a loss of membrane asymmetry.	Ceramides	4-12	poly(ADP-ribose) polymerase 1	Homo sapiens	132-158
16849630-6	2006	Supporting this notion, reducing stearoyl-CoA desaturase-1 (SCD-1) protein content with short interfering RNA resulted in ceramide accumulation and was associated with increased apoptosis in the absence of palmitate.	Ceramides	122-130	stearoyl-CoA desaturase	Homo sapiens	33-58
16849630-6	2006	Supporting this notion, reducing stearoyl-CoA desaturase-1 (SCD-1) protein content with short interfering RNA resulted in ceramide accumulation and was associated with increased apoptosis in the absence of palmitate.	Ceramides	122-130	stearoyl-CoA desaturase	Homo sapiens	60-65
17097614-4	2006	Induction of transcription factor AP-2alpha by UVA had been previously shown to be mediated through the second messenger ceramide.	Ceramides	121-129	transcription factor AP-2 alpha	Homo sapiens	34-43
17097614-6	2006	Finally, forced expression of GPx-1 eliminated UVA-induced ceramide accumulation as well as AP-2alpha expression.	Ceramides	59-67	glutathione peroxidase 1	Homo sapiens	30-35
17056602-2	2006	In this study, we confirmed the existence of the alternatively spliced human DAPK-beta, and we examined the levels of DAPK autophosphorylation and DAPK catalytic activity in response to tumor necrosis factor or ceramide.	Ceramides	211-219	death associated protein kinase 1	Homo sapiens	118-122
17056602-2	2006	In this study, we confirmed the existence of the alternatively spliced human DAPK-beta, and we examined the levels of DAPK autophosphorylation and DAPK catalytic activity in response to tumor necrosis factor or ceramide.	Ceramides	211-219	death associated protein kinase 1	Homo sapiens	118-122
17056602-3	2006	It was found that DAPK is rapidly dephosphorylated in response to tumor necrosis factor or ceramide and then subsequently degraded via proteasome activity.	Ceramides	91-99	death associated protein kinase 1	Homo sapiens	18-22
17384258-4	2006	Here we show that these subapoptotic ceramide signals also inhibit the antigen-triggered Ca2+ signals in B lymphocytes or the FcepsilonRI-mediated response of mast cells to antigen, but in a differential manner.	Ceramides	37-45	Fc epsilon receptor Ia	Homo sapiens	126-137
17225464-3	2006	The ceramide analog induced cell death through an apoptotic mechanism, which was demonstrated by DNA fragmentation, the cleavage of poly ADP ribose polymerase (PARP), and a loss of membrane asymmetry.	Ceramides	4-12	poly(ADP-ribose) polymerase 1	Homo sapiens	160-164
16938269-2	2006	Ceramide formation from the hydrolysis of sphingomyelin is considered to be a major pathway of stress-induced ceramide production with magnesium-dependent neutral sphingomyelinase (N-SMase) identified as a prime candidate in this pathway.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	155-179
16938269-2	2006	Ceramide formation from the hydrolysis of sphingomyelin is considered to be a major pathway of stress-induced ceramide production with magnesium-dependent neutral sphingomyelinase (N-SMase) identified as a prime candidate in this pathway.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	181-188
17225464-4	2006	Treating the cells with ceramide analog resulted in the release of various proapoptotic mitochondrial proteins including cytochrome c and Smac/DIBLO into the cytosol, and a decrease in the mitochondrial membrane potential.	Ceramides	24-32	cytochrome c, somatic	Homo sapiens	121-133
17225464-4	2006	Treating the cells with ceramide analog resulted in the release of various proapoptotic mitochondrial proteins including cytochrome c and Smac/DIBLO into the cytosol, and a decrease in the mitochondrial membrane potential.	Ceramides	24-32	diablo IAP-binding mitochondrial protein	Homo sapiens	138-142
17225464-5	2006	In addition, the ceramide analog decreased the phospho-Akt and phospho-Bad levels.	Ceramides	17-25	AKT serine/threonine kinase 1	Homo sapiens	55-58
17033839-5	2006	RESULTS: Reducing SCD1 protein resulted in marked esterification of exogenous fatty acids into diacylglycerol (DAG) and ceramide.	Ceramides	120-128	stearoyl-CoA desaturase	Rattus norvegicus	18-22
17064658-1	2006	Acid ceramidase (N-acylsphingosine deacylase, EC 3.5.1.23; AC) is the lipid hydrolase responsible for the degradation of ceramide into sphingosine and free fatty acids within lysosomes.	Ceramides	121-129	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
16946004-2	2006	Because the transcription of both P450AROM and inhibin alpha-subunit can be suppressed in the ovary by the inducible repressor isoform of cAMP-responsive element binding modulator (ICER), we have investigated whether TNFalpha and its intracellular messenger ceramide can induce ICER expression and the mechanisms whereby the induction is accomplished.	Ceramides	258-266	cAMP responsive element modulator	Rattus norvegicus	181-185
16946004-3	2006	ICER mRNA levels were assessed by RT-PCR in granulosa cells treated with TNFalpha, the ceramide-mobilizing enzyme sphingomyelinase (SMase), or C6-cer, a cell-permeant ceramide analog.	Ceramides	87-95	cAMP responsive element modulator	Rattus norvegicus	0-4
16946004-3	2006	ICER mRNA levels were assessed by RT-PCR in granulosa cells treated with TNFalpha, the ceramide-mobilizing enzyme sphingomyelinase (SMase), or C6-cer, a cell-permeant ceramide analog.	Ceramides	167-175	cAMP responsive element modulator	Rattus norvegicus	0-4
17033839-8	2006	Overexpression of SCD1 resulted in triacylglycerol esterification but attenuated ceramide and DAG accumulation and protected myotubes from fatty acid-induced insulin resistance.	Ceramides	81-89	stearoyl-CoA desaturase	Rattus norvegicus	18-22
17095838-3	2006	OBJECTIVE: Herein, we investigated whether IL-1beta-induced nitric oxide synthetase (iNOS) expression, nitric oxide (NO) release and loss in metabolic cell viability require ceramide biosynthesis either via the activation of sphingomyelinase or ceramide synthase.	Ceramides	174-182	nitric oxide synthase 2	Rattus norvegicus	43-83
17003043-1	2006	The recently identified ceramide transfer protein, CERT, is responsible for the bulk of ceramide transport from the endoplasmic reticulum (ER) to the Golgi.	Ceramides	24-32	ceramide transporter 1	Homo sapiens	51-55
17003043-2	2006	CERT has a C-terminal START domain for ceramide binding and an N-terminal pleck-strin homology domain that binds phosphatidylinositol 4-phosphate suggesting that phosphatidylinositol (PI) 4-kinases are involved in the regulation of CERT-mediated ceramide transport.	Ceramides	39-47	ceramide transporter 1	Homo sapiens	0-4
17003043-2	2006	CERT has a C-terminal START domain for ceramide binding and an N-terminal pleck-strin homology domain that binds phosphatidylinositol 4-phosphate suggesting that phosphatidylinositol (PI) 4-kinases are involved in the regulation of CERT-mediated ceramide transport.	Ceramides	246-254	ceramide transporter 1	Homo sapiens	0-4
16980694-9	2006	We thus conclude that the essential function of sphingolipids for membrane domain formation and stable surface delivery of Pma1p is provided by the C26 fatty acid that forms part of the yeast ceramide.	Ceramides	192-200	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	123-128
17030510-8	2006	Interestingly, fumonisin B1 (FB1), an inhibitor of the salvage pathway, attenuated loss of phosphorylation of p38, suggesting a role for ceramide in p38 dephosphorylation.	Ceramides	137-145	mitogen-activated protein kinase 1	Homo sapiens	110-113
17030510-8	2006	Interestingly, fumonisin B1 (FB1), an inhibitor of the salvage pathway, attenuated loss of phosphorylation of p38, suggesting a role for ceramide in p38 dephosphorylation.	Ceramides	137-145	mitogen-activated protein kinase 1	Homo sapiens	149-152
17030510-15	2006	Taken together, these data suggest that accumulation of C(16)-ceramide in mitochondria formed from the protein kinase C-dependent salvage pathway results at least in part from the action of longevity-assurance homologue 5, and the generated ceramide modulates the p38 cascade via PP1.	Ceramides	62-70	mitogen-activated protein kinase 1	Homo sapiens	264-267
17030510-15	2006	Taken together, these data suggest that accumulation of C(16)-ceramide in mitochondria formed from the protein kinase C-dependent salvage pathway results at least in part from the action of longevity-assurance homologue 5, and the generated ceramide modulates the p38 cascade via PP1.	Ceramides	62-70	inorganic pyrophosphatase 1	Homo sapiens	280-283
17105764-7	2006	HPTLC analysis showed significant accumulation of Cer[NS] and Cer[NH] ceramide species in Arnt-null epidermis, suggesting alterations in lipid metabolism.	Ceramides	70-78	aryl hydrocarbon receptor nuclear translocator	Mus musculus	90-94
16990644-0	2006	Ceramide structural features required to stimulate ABCA1-mediated cholesterol efflux to apolipoprotein A-I.	Ceramides	0-8	ATP binding cassette subfamily A member 1	Homo sapiens	51-56
16990644-0	2006	Ceramide structural features required to stimulate ABCA1-mediated cholesterol efflux to apolipoprotein A-I.	Ceramides	0-8	apolipoprotein A1	Homo sapiens	88-106
16990644-2	2006	We recently reported that ceramide specifically increased ABCA1-mediated cholesterol efflux to apolipoprotein A-I (apoA-I), a critical process that leads to the formation of cardioprotective HDL.	Ceramides	26-34	ATP binding cassette subfamily A member 1	Homo sapiens	58-63
16990644-2	2006	We recently reported that ceramide specifically increased ABCA1-mediated cholesterol efflux to apolipoprotein A-I (apoA-I), a critical process that leads to the formation of cardioprotective HDL.	Ceramides	26-34	apolipoprotein A1	Homo sapiens	95-113
16990644-2	2006	We recently reported that ceramide specifically increased ABCA1-mediated cholesterol efflux to apolipoprotein A-I (apoA-I), a critical process that leads to the formation of cardioprotective HDL.	Ceramides	26-34	apolipoprotein A1	Homo sapiens	115-121
16990644-4	2006	C2 dihydroceramide, which contains a fully saturated acyl chain and is commonly used as a negative control for ceramide apoptotic signaling, stimulated a 2- to 5-fold increase in ABCA1-mediated cholesterol efflux to apoA-I over a 0-60 muM concentration range without the cell toxicity apparent with native C2 ceramide.	Ceramides	10-18	ATP binding cassette subfamily A member 1	Homo sapiens	179-184
16990644-4	2006	C2 dihydroceramide, which contains a fully saturated acyl chain and is commonly used as a negative control for ceramide apoptotic signaling, stimulated a 2- to 5-fold increase in ABCA1-mediated cholesterol efflux to apoA-I over a 0-60 muM concentration range without the cell toxicity apparent with native C2 ceramide.	Ceramides	10-18	apolipoprotein A1	Homo sapiens	216-222
16990644-4	2006	C2 dihydroceramide, which contains a fully saturated acyl chain and is commonly used as a negative control for ceramide apoptotic signaling, stimulated a 2- to 5-fold increase in ABCA1-mediated cholesterol efflux to apoA-I over a 0-60 muM concentration range without the cell toxicity apparent with native C2 ceramide.	Ceramides	111-119	ATP binding cassette subfamily A member 1	Homo sapiens	179-184
16990644-8	2006	These data show that the overall ceramide shape and the amide bond are critical for the cholesterol efflux effect and suggest that ceramide acts through a protein-mediated pathway to affect ABCA1 activity.	Ceramides	131-139	ATP binding cassette subfamily A member 1	Homo sapiens	190-195
16914288-5	2006	SLS and CAPB induced a concentration-dependent increase in the expression of enzymes producing cholesterol and ceramides, while transcripts of enzymes producing fatty acids were unaffected.	Ceramides	111-120	capping actin protein of muscle Z-line subunit beta	Homo sapiens	8-12
17026999-0	2006	The murine TRAIL receptor signals caspase-independent cell death through ceramide.	Ceramides	73-81	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	11-16
17026999-4	2006	Cells overexpressing acid ceramidase (AC), an enzyme that metabolizes the sphingolipid ceramide, show enhanced survival from TRAIL-induced caspase-independent PCD but not from apoptosis, implicating a function of ceramide as a key mediator in caspase-independent PCD (but not apoptosis) induced by mTRAIL-R2.	Ceramides	87-95	N-acylsphingosine amidohydrolase 1	Mus musculus	21-36
17026999-4	2006	Cells overexpressing acid ceramidase (AC), an enzyme that metabolizes the sphingolipid ceramide, show enhanced survival from TRAIL-induced caspase-independent PCD but not from apoptosis, implicating a function of ceramide as a key mediator in caspase-independent PCD (but not apoptosis) induced by mTRAIL-R2.	Ceramides	87-95	N-acylsphingosine amidohydrolase 1	Mus musculus	38-40
17026999-5	2006	In concert with the enhanced resistance of AC-overexpressing cells against caspase-independent PCD induced by TNF, our results suggest that ceramide acts as a common mediator of caspase-independent PCD caused by death receptors such as mTRAIL-R2 and TNF-R55.	Ceramides	140-148	N-acylsphingosine amidohydrolase 1	Mus musculus	43-45
17026999-5	2006	In concert with the enhanced resistance of AC-overexpressing cells against caspase-independent PCD induced by TNF, our results suggest that ceramide acts as a common mediator of caspase-independent PCD caused by death receptors such as mTRAIL-R2 and TNF-R55.	Ceramides	140-148	tumor necrosis factor receptor superfamily, member 10b	Mus musculus	236-245
17026999-5	2006	In concert with the enhanced resistance of AC-overexpressing cells against caspase-independent PCD induced by TNF, our results suggest that ceramide acts as a common mediator of caspase-independent PCD caused by death receptors such as mTRAIL-R2 and TNF-R55.	Ceramides	140-148	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	250-257
17069807-3	2006	TNFalpha/CHX induced a robust increase in ceramide levels after 16 h of treatment when cell death was maximal.	Ceramides	42-50	tumor necrosis factor	Homo sapiens	0-8
17036198-0	2006	Ceramide induces apoptosis via a peroxisome proliferator-activated receptor gamma-dependent pathway.	Ceramides	0-8	peroxisome proliferator activated receptor gamma	Homo sapiens	33-81
17036198-4	2006	Furthermore, MAP kinase pathway provided a potential modulation mechanism for PPARgamma pathway related with ceramide.	Ceramides	109-117	peroxisome proliferator activated receptor gamma	Homo sapiens	78-87
16549336-0	2006	Acid sphingomyelinase mediated release of ceramide is essential to trigger the mitochondrial pathway of apoptosis by galectin-1.	Ceramides	42-50	galectin 1	Homo sapiens	117-127
16977445-5	2006	We examine Musk T called Ethylene brassylate, Astratone or 1,4-Dioxacycloheptadecane-5,17-dione, which used as just a perfume ingredient, plays a role as PPAR-alpha ligand in vitro and stimulates skin barrier recovery, ceramide synthesis, beta-Glucocerebrosidase, involucrin expression in epidermis in vivo; and examine that Musk T stimulates HAS expression and HA synthesis in human skin fibroblast.	Ceramides	219-227	peroxisome proliferator activated receptor alpha	Homo sapiens	154-164
16549336-2	2006	Here we first show that galectin-1 initiate the acid sphingomyelinase mediated release of ceramide and this event is critical in the further steps.	Ceramides	90-98	galectin 1	Homo sapiens	24-34
16549336-4	2006	The downstream events, decrease of Bcl-2 protein amount, depolarization of the mitochondria and activation of the caspase 9 and caspase 3 depend on production of ceramide.	Ceramides	162-170	BCL2 apoptosis regulator	Homo sapiens	35-40
16549336-4	2006	The downstream events, decrease of Bcl-2 protein amount, depolarization of the mitochondria and activation of the caspase 9 and caspase 3 depend on production of ceramide.	Ceramides	162-170	caspase 9	Homo sapiens	114-123
16549336-4	2006	The downstream events, decrease of Bcl-2 protein amount, depolarization of the mitochondria and activation of the caspase 9 and caspase 3 depend on production of ceramide.	Ceramides	162-170	caspase 3	Homo sapiens	128-137
16549336-5	2006	All downstream steps, including production of ceramide, require the generation of membrane rafts and the presence of two tyrosine kinases, p56(lck) and ZAP70.	Ceramides	46-54	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	139-147
16549336-5	2006	All downstream steps, including production of ceramide, require the generation of membrane rafts and the presence of two tyrosine kinases, p56(lck) and ZAP70.	Ceramides	46-54	zeta chain of T cell receptor associated protein kinase 70	Homo sapiens	152-157
16979119-5	2006	Despite higher constitutive levels of GSH in CF cells, their intracellular ceramide content showed a greater enhancement following fenretinide and TNF-alpha treatment than non-CF cells.	Ceramides	75-83	tumor necrosis factor	Homo sapiens	147-156
16979119-7	2006	Although fenretinide treatment was associated with a higher intracellular ceramide content in the mutant DeltaF508 CFTR cells, the fenretinide-mediated decrease in IL-8 secretion was not consistently explained by changes in the intracellular content of this sphingolipid.	Ceramides	74-82	CF transmembrane conductance regulator	Homo sapiens	115-119
16979119-2	2006	CFTR-deficient lung epithelial cells may have high constitutive glutathione (GSH) levels that could decrease the intracellular content of the sphingolipid second messenger, ceramide.	Ceramides	173-181	CF transmembrane conductance regulator	Homo sapiens	0-4
16979119-3	2006	Altered ceramide levels in CF cells could, in turn, lead to their resistance to apoptosis and an immune hyper-responsiveness.	Ceramides	8-16	CF transmembrane conductance regulator	Homo sapiens	27-29
17242489-5	2006	Consistent with increased beta-oxidation, the contents of free fatty acids and long-chain acyl-CoAs are significantly decreased, which together with reduced mRNA level and activity of serine palmitoyltransferase led to reduced ceramide synthesis in oxidative muscles of SCD1-/- mice.	Ceramides	227-235	stearoyl-Coenzyme A desaturase 1	Mus musculus	270-274
17242489-3	2006	In this review, we examine data showing that SCD is an important component in the regulation of skeletal muscle metabolism, which affects insulin sensitivity, mitochondrial fatty acid oxidation and ceramide de novo synthesis in oxidative myofibers.	Ceramides	198-206	stearoyl-Coenzyme A desaturase 1	Mus musculus	45-48
17242489-6	2006	Thus, reduced contents of free fatty acids, acyl-CoAs and ceramides as well as increased AMPK phosphorylation, might contribute to increased insulin sensitivity observed in muscle of SCD1-/- mice.	Ceramides	58-67	stearoyl-Coenzyme A desaturase 1	Mus musculus	183-187
17242494-1	2006	Ceramide is involved in the pathogenesis of insulin resistance in skeletal muscles of humans and rodents.	Ceramides	0-8	insulin	Homo sapiens	44-51
17242494-2	2006	However, there are conflicting reports in the literature on the effect of thiazolidinediones (a new class of insulin sensitizing drugs) on skeletal muscle ceramide content.	Ceramides	155-163	insulin	Homo sapiens	109-116
17100636-15	2006	Its synthesis from ceramide is catalyzed by the enzyme glucosylceramide synthase.	Ceramides	19-27	UDP-glucose ceramide glucosyltransferase	Homo sapiens	55-80
16887394-6	2006	Interestingly, 10 of 15 primary prostate cancers examined by Western blotting overexpressed acid ceramidase (AC), suggesting that ceramide deacylation might serve to negate elevated levels of ceramide, creating a more antiapoptotic phenotype.	Ceramides	130-138	N-acylsphingosine amidohydrolase 1	Homo sapiens	92-107
16887394-6	2006	Interestingly, 10 of 15 primary prostate cancers examined by Western blotting overexpressed acid ceramidase (AC), suggesting that ceramide deacylation might serve to negate elevated levels of ceramide, creating a more antiapoptotic phenotype.	Ceramides	130-138	N-acylsphingosine amidohydrolase 1	Homo sapiens	109-111
16887394-6	2006	Interestingly, 10 of 15 primary prostate cancers examined by Western blotting overexpressed acid ceramidase (AC), suggesting that ceramide deacylation might serve to negate elevated levels of ceramide, creating a more antiapoptotic phenotype.	Ceramides	192-200	N-acylsphingosine amidohydrolase 1	Homo sapiens	92-107
16887394-6	2006	Interestingly, 10 of 15 primary prostate cancers examined by Western blotting overexpressed acid ceramidase (AC), suggesting that ceramide deacylation might serve to negate elevated levels of ceramide, creating a more antiapoptotic phenotype.	Ceramides	192-200	N-acylsphingosine amidohydrolase 1	Homo sapiens	109-111
16675629-7	2006	Enforced reduction of TrxR2 (small interfering RNA) in myoblasts under exposure to ceramide or TNF-alpha causes a dramatic enhancement of nucleosomal DNA cleavage, caspase 9 activation, and mitochondrial reactive oxygen species release, together with reduced cell viability, while this TrxR2 reduction is without effect in unstimulated myoblasts under basal conditions.	Ceramides	83-91	thioredoxin reductase 2	Rattus norvegicus	22-27
16936228-5	2006	Treatment with R(+)-MA and Win55 was associated with accumulation of ceramide, and pharmacological inhibition of ceramide synthesis de novo prevented both p38 activation and mitochondria depolarization assessed by binding of 3,3"-dihexyloxacarbocyanine iodide (DiOC(6)).	Ceramides	113-121	mitogen-activated protein kinase 14	Homo sapiens	155-158
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.	Ceramides	36-44	glucosidase beta 2	Mus musculus	12-16
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.	Ceramides	36-44	glucosidase, beta, acid	Mus musculus	130-134
17088406-0	2006	Ceramide inhibition of chondrocyte proliferation and bone growth is IGF-I independent.	Ceramides	0-8	insulin-like growth factor 1	Mus musculus	68-73
16895911-0	2006	Efficient trafficking of ceramide from the endoplasmic reticulum to the Golgi apparatus requires a VAMP-associated protein-interacting FFAT motif of CERT.	Ceramides	25-33	ceramide transporter 1	Homo sapiens	149-153
16895911-1	2006	Ceramide is synthesized at the endoplasmic reticulum (ER) and transported to the Golgi apparatus by CERT for its conversion to sphingomyelin in mammalian cells.	Ceramides	0-8	ceramide transporter 1	Homo sapiens	100-104
16895911-2	2006	CERT has a pleck-strin homology (PH) domain for Golgi targeting and a START domain catalyzing the intermembrane transfer of ceramide.	Ceramides	124-132	ceramide transporter 1	Homo sapiens	0-4
16895911-7	2006	By contrast, when overexpressed, both the FFAT motif and the PH domain mutants of CERT substantially supported the transport of ceramide from the ER to the site where sphingomyelin is produced.	Ceramides	128-136	ceramide transporter 1	Homo sapiens	82-86
16895911-8	2006	These results suggest that the Golgi-targeting PH domain and ER-interacting FFAT motif of CERT spatially restrict the random ceramide transfer activity of the START domain in cells.	Ceramides	125-133	ceramide transporter 1	Homo sapiens	90-94
16969513-8	2006	Furthermore, we observed that paclitaxel, ceramide, or combo-induced EGFR phosphorylation was inhibited by EGFR inhibitor, PD153035, while paclitaxel, ceramide, or combo-induced JNK and ERK phosphorylation was blocked by EGFR inhibitor, PD153035 and ERK inhibitor, U126.	Ceramides	151-159	epidermal growth factor receptor	Homo sapiens	69-73
16529909-4	2006	Stable isotope pulse-labeling experiments in conjunction with LC-MS/MS quantitation of different sphingolipids demonstrated strong interference of overexpressed SK1 with the de novo sphingolipid biosynthesis by deviating metabolic flow of newly formed sphingoid bases from ceramide formation toward the synthesis of DHS1P.	Ceramides	273-281	sphingosine kinase 1	Homo sapiens	161-164
16529909-9	2006	These findings uncover a new functional role for SK1, which can control survival/death (DHS1P-S1P/ceramides) balance by targeting sphingolipid de novo biosynthesis and selectively generating DHS1P at a metabolic step preceding ceramide formation.	Ceramides	98-107	sphingosine kinase 1	Homo sapiens	49-52
16529909-9	2006	These findings uncover a new functional role for SK1, which can control survival/death (DHS1P-S1P/ceramides) balance by targeting sphingolipid de novo biosynthesis and selectively generating DHS1P at a metabolic step preceding ceramide formation.	Ceramides	98-106	sphingosine kinase 1	Homo sapiens	49-52
16740654-7	2006	Although granulosa cell apoptosis induced by ceramide was attenuated by the presence of GDF-9, this protective effect of GDF-9 was prevented by the phosphatidylinositol 3-kinase inhibitor LY294002 and a dominant negative form of Akt.	Ceramides	45-53	growth differentiation factor 9	Homo sapiens	88-93
16969513-0	2006	Paclitaxel and ceramide synergistically induce cell death with transient activation of EGFR and ERK pathway in pancreatic cancer cells.	Ceramides	15-23	epidermal growth factor receptor	Homo sapiens	87-91
16969513-0	2006	Paclitaxel and ceramide synergistically induce cell death with transient activation of EGFR and ERK pathway in pancreatic cancer cells.	Ceramides	15-23	mitogen-activated protein kinase 1	Homo sapiens	96-99
16969513-8	2006	Furthermore, we observed that paclitaxel, ceramide, or combo-induced EGFR phosphorylation was inhibited by EGFR inhibitor, PD153035, while paclitaxel, ceramide, or combo-induced JNK and ERK phosphorylation was blocked by EGFR inhibitor, PD153035 and ERK inhibitor, U126.	Ceramides	42-50	epidermal growth factor receptor	Homo sapiens	107-111
16969513-8	2006	Furthermore, we observed that paclitaxel, ceramide, or combo-induced EGFR phosphorylation was inhibited by EGFR inhibitor, PD153035, while paclitaxel, ceramide, or combo-induced JNK and ERK phosphorylation was blocked by EGFR inhibitor, PD153035 and ERK inhibitor, U126.	Ceramides	42-50	mitogen-activated protein kinase 8	Homo sapiens	178-181
16969513-8	2006	Furthermore, we observed that paclitaxel, ceramide, or combo-induced EGFR phosphorylation was inhibited by EGFR inhibitor, PD153035, while paclitaxel, ceramide, or combo-induced JNK and ERK phosphorylation was blocked by EGFR inhibitor, PD153035 and ERK inhibitor, U126.	Ceramides	42-50	mitogen-activated protein kinase 1	Homo sapiens	186-189
16969513-8	2006	Furthermore, we observed that paclitaxel, ceramide, or combo-induced EGFR phosphorylation was inhibited by EGFR inhibitor, PD153035, while paclitaxel, ceramide, or combo-induced JNK and ERK phosphorylation was blocked by EGFR inhibitor, PD153035 and ERK inhibitor, U126.	Ceramides	42-50	epidermal growth factor receptor	Homo sapiens	107-111
17073606-1	2006	Fabry disease is caused by a deficiency of a-galactosidase A which leads to the progressive intra-lysosomal accumulation of ceramide trihexoside (CTH), also known as globotriaosylceramide (Gb3), in different cell types and body fluids.	Ceramides	124-132	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	189-192
16969513-8	2006	Furthermore, we observed that paclitaxel, ceramide, or combo-induced EGFR phosphorylation was inhibited by EGFR inhibitor, PD153035, while paclitaxel, ceramide, or combo-induced JNK and ERK phosphorylation was blocked by EGFR inhibitor, PD153035 and ERK inhibitor, U126.	Ceramides	42-50	mitogen-activated protein kinase 1	Homo sapiens	250-253
16969513-9	2006	Taken together, our results demonstrated that the combination of paclitaxel and ceramide synergistically induced pancreatic cancer cell death through differential activation of EGFR-mediated MAP kinases.	Ceramides	80-88	epidermal growth factor receptor	Homo sapiens	177-181
16969513-10	2006	EGFR and ERK inhibitors may further enhance the paclitaxel and ceramide effect.	Ceramides	63-71	epidermal growth factor receptor	Homo sapiens	0-4
16969513-10	2006	EGFR and ERK inhibitors may further enhance the paclitaxel and ceramide effect.	Ceramides	63-71	mitogen-activated protein kinase 1	Homo sapiens	9-12
17056709-8	2006	Expression of RGXT1- and RGXT2-enhanced green fluorescent protein constructs in Arabidopsis revealed that both fusion proteins were targeted to a Brefeldin A-sensitive compartment and also colocalized with the Golgi marker dye BODIPY TR ceramide, consistent with targeting to the Golgi apparatus.	Ceramides	237-245	rhamnogalacturonan xylosyltransferase 2	Arabidopsis thaliana	25-30
16636669-0	2006	TRAIL activates acid sphingomyelinase via a redox mechanism and releases ceramide to trigger apoptosis.	Ceramides	73-81	TNF superfamily member 10	Homo sapiens	0-5
16981685-1	2006	The neutral sphingomyelinases (N-SMases) are considered major candidates for mediating the stress-induced production of ceramide, and N-SMase activity has been identified, characterized, and cloned from bacteria, yeast, and mammalian cells.	Ceramides	120-128	sphingomyelin phosphodiesterase 2	Homo sapiens	31-38
16861742-4	2006	In animal cells, ceramide is a substrate for sphingomyelin (SM) production via the enzyme SM synthase.	Ceramides	17-25	sphingomyelin synthase 2	Homo sapiens	90-101
16753040-4	2006	In vivo, [3H]dihydrosphingosine labelling and electrospray-ionization MS revealed that overproduction of either LASS3 isoform results in increases in several ceramide species, with some preference toward those having middle- to long-chain-fatty acyl-CoAs.	Ceramides	158-166	ceramide synthase 3	Mus musculus	112-117
16970407-0	2006	Isolation, structure elucidation, total synthesis, and evaluation of new natural and synthetic ceramides on human SK-MEL-1 melanoma cells.	Ceramides	95-104	PR/SET domain 16	Homo sapiens	117-122
16970407-3	2006	The acetyl derivative of the natural ceramide (1a) and synthetic ceramides (24-27) showed cytotoxicity on the human melanoma cell line SK-MEL-1, which was caused by induction of apoptosis as determined by DNA fragmentation, poly(ADP-ribose) polymerase cleavage, and procaspase-9 and -8 processing.	Ceramides	37-45	PR/SET domain 16	Homo sapiens	138-143
16970407-3	2006	The acetyl derivative of the natural ceramide (1a) and synthetic ceramides (24-27) showed cytotoxicity on the human melanoma cell line SK-MEL-1, which was caused by induction of apoptosis as determined by DNA fragmentation, poly(ADP-ribose) polymerase cleavage, and procaspase-9 and -8 processing.	Ceramides	65-74	PR/SET domain 16	Homo sapiens	138-143
16636669-1	2006	We have previously shown that activation of the acid sphingomyelinase (ASM), the release of ceramide and the formation of ceramide-enriched membrane domains are central for the induction of apoptosis by CD95.	Ceramides	92-100	Fas cell surface death receptor	Homo sapiens	203-207
16636669-1	2006	We have previously shown that activation of the acid sphingomyelinase (ASM), the release of ceramide and the formation of ceramide-enriched membrane domains are central for the induction of apoptosis by CD95.	Ceramides	122-130	sphingomyelin phosphodiesterase 1	Homo sapiens	48-69
16636669-1	2006	We have previously shown that activation of the acid sphingomyelinase (ASM), the release of ceramide and the formation of ceramide-enriched membrane domains are central for the induction of apoptosis by CD95.	Ceramides	122-130	Fas cell surface death receptor	Homo sapiens	203-207
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	162-170	TNF superfamily member 10	Homo sapiens	26-81
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	162-170	TNF superfamily member 10	Homo sapiens	83-88
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	162-170	Fas cell surface death receptor	Homo sapiens	94-98
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	162-170	sphingomyelin phosphodiesterase 1	Homo sapiens	112-115
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	188-196	TNF superfamily member 10	Homo sapiens	26-81
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	188-196	TNF superfamily member 10	Homo sapiens	83-88
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	188-196	Fas cell surface death receptor	Homo sapiens	94-98
16636669-2	2006	Here, we demonstrate that tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and CD95 activate the ASM via a redox mechanism resulting in release of ceramide and formation of ceramide-enriched membrane platforms.	Ceramides	188-196	sphingomyelin phosphodiesterase 1	Homo sapiens	112-115
16636669-3	2006	Ceramide-enriched membrane platforms serve to cluster DR5 upon stimulation.	Ceramides	0-8	TNF receptor superfamily member 10b	Homo sapiens	54-57
16636669-4	2006	Antioxidants prevent TRAIL-mediated stimulation of ASM, the release of ceramide, the formation of ceramide-enriched membrane platforms and the induction of apoptosis by TRAIL.	Ceramides	71-79	TNF superfamily member 10	Homo sapiens	21-26
16636669-4	2006	Antioxidants prevent TRAIL-mediated stimulation of ASM, the release of ceramide, the formation of ceramide-enriched membrane platforms and the induction of apoptosis by TRAIL.	Ceramides	98-106	TNF superfamily member 10	Homo sapiens	21-26
16636669-6	2006	A dose-response analysis indicates that ceramide-enriched membrane platforms greatly sensitized tumor cells to TRAIL-induced apoptosis.	Ceramides	40-48	TNF superfamily member 10	Homo sapiens	111-116
16636669-7	2006	Our data indicate that ceramide-enriched membrane platforms are required for the signaling of TRAIL-DR5 complexes under physiological conditions.	Ceramides	23-31	TNF superfamily member 10	Homo sapiens	94-99
16636669-7	2006	Our data indicate that ceramide-enriched membrane platforms are required for the signaling of TRAIL-DR5 complexes under physiological conditions.	Ceramides	23-31	TNF receptor superfamily member 10b	Homo sapiens	100-103
16782799-1	2006	Ceramides are known to have a regulatory function in apoptosis, including the release of cytochrome c and other proapoptotic factors from the mitochondrial intermembrane space.	Ceramides	0-9	cytochrome c, somatic	Homo sapiens	89-101
16777343-7	2006	Ceramide, a second messenger of the IL-1R1-dependent fast signaling cascade, is produced by IL-1R1-MyD88-mediated activation of the neutral sphingomyelinase.	Ceramides	0-8	interleukin 1 receptor, type I	Mus musculus	36-42
16777343-7	2006	Ceramide, a second messenger of the IL-1R1-dependent fast signaling cascade, is produced by IL-1R1-MyD88-mediated activation of the neutral sphingomyelinase.	Ceramides	0-8	interleukin 1 receptor, type I	Mus musculus	92-98
16777343-7	2006	Ceramide, a second messenger of the IL-1R1-dependent fast signaling cascade, is produced by IL-1R1-MyD88-mediated activation of the neutral sphingomyelinase.	Ceramides	0-8	myeloid differentiation primary response gene 88	Mus musculus	99-104
16941686-4	2006	Hepatic ceramide levels transiently increased after the reperfusion phase of the ischemic liver in mice, because of an early activation of acidic sphingomyelinase (ASMase) followed by acid ceramidase stimulation.	Ceramides	8-16	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	139-162
16936207-3	2006	Expression of enzymes involved in ceramide generation (neutral sphingomyelinase [NSMase], acid sphingomyelinase [ASMase], and serine-palmitoyl-transferase [SPT]) and ceramide hydrolysis (ceramidase) are elevated in obese adipose tissues.	Ceramides	34-42	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	55-79
16940153-3	2006	Here we identify a novel human ceramidase (haCER2) that regulates the levels of both sphingosine and S1P by controlling the hydrolysis of ceramides.	Ceramides	138-147	alkaline ceramidase 2	Homo sapiens	43-49
16941686-4	2006	Hepatic ceramide levels transiently increased after the reperfusion phase of the ischemic liver in mice, because of an early activation of acidic sphingomyelinase (ASMase) followed by acid ceramidase stimulation.	Ceramides	8-16	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	164-170
16941686-5	2006	In vivo administration of an ASMase inhibitor, imipramine, or ASMase knockdown by siRNA decreased ceramide generation during I/R, and attenuated serum ALT levels, hepatocellular necrosis, cytochrome c release, and caspase-3 activation.	Ceramides	98-106	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	29-35
16941686-5	2006	In vivo administration of an ASMase inhibitor, imipramine, or ASMase knockdown by siRNA decreased ceramide generation during I/R, and attenuated serum ALT levels, hepatocellular necrosis, cytochrome c release, and caspase-3 activation.	Ceramides	98-106	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	62-68
16941686-6	2006	ASMase-induced ceramide generation activated JNK resulting in BimL phosphorylation and translocation to mitochondria, as the inhibition of ASMase by imipramine prevented these events.	Ceramides	15-23	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
16941686-6	2006	ASMase-induced ceramide generation activated JNK resulting in BimL phosphorylation and translocation to mitochondria, as the inhibition of ASMase by imipramine prevented these events.	Ceramides	15-23	mitogen-activated protein kinase 8	Mus musculus	45-48
16941686-10	2006	In conclusion, ceramide generated from ASMase plays a key role in I/R-induced liver damage, and its modulation may be of therapeutic relevance.	Ceramides	15-23	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	39-45
16923157-8	2006	Additionally, we provide evidence that ceramide also activates the endolysosomal protease cathepsin D pathway.	Ceramides	39-47	cathepsin D	Mus musculus	90-101
16775254-8	2006	We also show that cell-permeant C6 ceramide, like OxPAPC, causes the inhibition of LPS-induced IL-8 synthesis and alters caveolin distribution similar to OxPAPC.	Ceramides	35-43	C-X-C motif chemokine ligand 8	Homo sapiens	95-99
16936207-7	2006	In cultured adipocytes, ceramide, sphingosine, and S1P induced gene expression of plasminogen activator inhibitor-1, TNF-alpha, monocyte chemoattractant protein-1, interleukin-6, and keratinocyte-derived chemokine.	Ceramides	24-32	serine (or cysteine) peptidase inhibitor, clade E, member 1	Mus musculus	82-115
16936207-7	2006	In cultured adipocytes, ceramide, sphingosine, and S1P induced gene expression of plasminogen activator inhibitor-1, TNF-alpha, monocyte chemoattractant protein-1, interleukin-6, and keratinocyte-derived chemokine.	Ceramides	24-32	tumor necrosis factor	Mus musculus	117-126
16936207-7	2006	In cultured adipocytes, ceramide, sphingosine, and S1P induced gene expression of plasminogen activator inhibitor-1, TNF-alpha, monocyte chemoattractant protein-1, interleukin-6, and keratinocyte-derived chemokine.	Ceramides	24-32	chemokine (C-C motif) ligand 2	Mus musculus	128-162
16936207-7	2006	In cultured adipocytes, ceramide, sphingosine, and S1P induced gene expression of plasminogen activator inhibitor-1, TNF-alpha, monocyte chemoattractant protein-1, interleukin-6, and keratinocyte-derived chemokine.	Ceramides	24-32	interleukin 6	Mus musculus	164-177
16771830-0	2006	IL-1beta induces a MyD88-dependent and ceramide-mediated activation of Src in anterior hypothalamic neurons.	Ceramides	39-47	interleukin 1 beta	Mus musculus	0-8
16771830-0	2006	IL-1beta induces a MyD88-dependent and ceramide-mediated activation of Src in anterior hypothalamic neurons.	Ceramides	39-47	Rous sarcoma oncogene	Mus musculus	71-74
16771830-6	2006	These effects of IL-1beta were dependent on the association of the cytosolic adaptor protein, MyD88, to the IL-1 receptor, and on the activation of the neutral sphingomyelinase, leading to production of ceramide.	Ceramides	203-211	interleukin 1 beta	Mus musculus	17-25
16771830-6	2006	These effects of IL-1beta were dependent on the association of the cytosolic adaptor protein, MyD88, to the IL-1 receptor, and on the activation of the neutral sphingomyelinase, leading to production of ceramide.	Ceramides	203-211	myeloid differentiation primary response gene 88	Mus musculus	94-99
16771830-7	2006	A cell-permeable analog of ceramide mimicked the effects of IL-1beta on the cultured AH neurons.	Ceramides	27-35	interleukin 1 beta	Mus musculus	60-68
16771830-8	2006	These results suggest that ceramide may be the second messenger of the fast IL-1beta actions in AH neurons, and that this IL-1beta/ceramide pathway may underlie the fast non-transcription-dependent, electrophysiological effects of IL-1beta observed in AH neurons in vivo.	Ceramides	27-35	interleukin 1 beta	Mus musculus	76-84
16771830-8	2006	These results suggest that ceramide may be the second messenger of the fast IL-1beta actions in AH neurons, and that this IL-1beta/ceramide pathway may underlie the fast non-transcription-dependent, electrophysiological effects of IL-1beta observed in AH neurons in vivo.	Ceramides	131-139	interleukin 1 beta	Mus musculus	122-130
16771830-8	2006	These results suggest that ceramide may be the second messenger of the fast IL-1beta actions in AH neurons, and that this IL-1beta/ceramide pathway may underlie the fast non-transcription-dependent, electrophysiological effects of IL-1beta observed in AH neurons in vivo.	Ceramides	131-139	interleukin 1 beta	Mus musculus	122-130
17086696-7	2006	Meanwhile, ceramide increased the expression of Bax, Bad and Bid mRNA, and decreased the expression of Bcl-2 and Bcl-xl mRNA.	Ceramides	11-19	BCL2 associated X, apoptosis regulator	Homo sapiens	48-51
16928273-9	2006	RESULTS: We noted both qualitative and quantitative differences in the functional activity of these two anti-apoptotic proteins in cells: Bcl-2 localized to the endoplasmic reticulum inhibits apoptosis induced by ceramide and thapsigargin but not by doxorubicin or TNFalpha, while Bcl-XL at the endoplasmic reticulum is active against all four drugs.	Ceramides	213-221	BCL2 apoptosis regulator	Homo sapiens	138-143
16740613-1	2006	Our previous studies found that nerve growth factor (NGF), via ceramide, enhanced the number of action potentials (APs) evoked by a ramp of depolarizing current in capsaicin-sensitive sensory neurons.	Ceramides	63-71	nerve growth factor	Rattus norvegicus	32-51
16740613-1	2006	Our previous studies found that nerve growth factor (NGF), via ceramide, enhanced the number of action potentials (APs) evoked by a ramp of depolarizing current in capsaicin-sensitive sensory neurons.	Ceramides	63-71	nerve growth factor	Rattus norvegicus	53-56
16740613-4	2006	This raises the question as to whether the enhanced excitability produced by NGF was mediated directly by ceramide or required additional metabolism to Sph and/or S1P.	Ceramides	106-114	nerve growth factor	Rattus norvegicus	77-80
16763091-3	2006	Ceramide, mainly generated from the degradation of sphingomyelin, was hypothesized upstream above PKCdelta in (Ac)5GP-transduced apoptosis.	Ceramides	0-8	protein kinase C delta	Homo sapiens	98-106
16763091-6	2006	The NGF and p75 enhanced by (Ac)5GP was inhibited when added with GW4869, the N-SMase inhibitor, indicating NGF/p75 as the downstream signals of N-SMase/ceramide.	Ceramides	153-161	nerve growth factor	Homo sapiens	4-7
16763091-6	2006	The NGF and p75 enhanced by (Ac)5GP was inhibited when added with GW4869, the N-SMase inhibitor, indicating NGF/p75 as the downstream signals of N-SMase/ceramide.	Ceramides	153-161	TNF receptor superfamily member 1B	Homo sapiens	12-15
16763091-6	2006	The NGF and p75 enhanced by (Ac)5GP was inhibited when added with GW4869, the N-SMase inhibitor, indicating NGF/p75 as the downstream signals of N-SMase/ceramide.	Ceramides	153-161	sphingomyelin phosphodiesterase 2	Homo sapiens	78-85
16763091-6	2006	The NGF and p75 enhanced by (Ac)5GP was inhibited when added with GW4869, the N-SMase inhibitor, indicating NGF/p75 as the downstream signals of N-SMase/ceramide.	Ceramides	153-161	nerve growth factor	Homo sapiens	108-111
16763091-6	2006	The NGF and p75 enhanced by (Ac)5GP was inhibited when added with GW4869, the N-SMase inhibitor, indicating NGF/p75 as the downstream signals of N-SMase/ceramide.	Ceramides	153-161	TNF receptor superfamily member 1B	Homo sapiens	112-115
16763091-6	2006	The NGF and p75 enhanced by (Ac)5GP was inhibited when added with GW4869, the N-SMase inhibitor, indicating NGF/p75 as the downstream signals of N-SMase/ceramide.	Ceramides	153-161	sphingomyelin phosphodiesterase 2	Homo sapiens	145-152
17086696-7	2006	Meanwhile, ceramide increased the expression of Bax, Bad and Bid mRNA, and decreased the expression of Bcl-2 and Bcl-xl mRNA.	Ceramides	11-19	BH3 interacting domain death agonist	Homo sapiens	61-64
17086696-7	2006	Meanwhile, ceramide increased the expression of Bax, Bad and Bid mRNA, and decreased the expression of Bcl-2 and Bcl-xl mRNA.	Ceramides	11-19	BCL2 apoptosis regulator	Homo sapiens	103-108
17086696-7	2006	Meanwhile, ceramide increased the expression of Bax, Bad and Bid mRNA, and decreased the expression of Bcl-2 and Bcl-xl mRNA.	Ceramides	11-19	BCL2 like 1	Homo sapiens	113-119
16670104-5	2006	The major SM4s was composed of ceramides possessing d18:1 with C22 hydroxy fatty acids (C22:0 h), C23:0 h, and C24:0 h, whereas the major SM3/SM2 were composed of ceramides possessing t18:0 with C22 normal fatty acids (C22:0), C23:0, C24:0.	Ceramides	163-172	SM2	Homo sapiens	142-145
16772302-11	2006	The data suggest that hyperosmolarity induces endosomal acidification as an important upstream event for CD95 activation through stimulation of ASM-dependent ceramide formation and activation of NADPH oxidase isoforms.	Ceramides	158-166	Fas (TNF receptor superfamily member 6)	Mus musculus	105-109
16879426-3	2006	Sphingomyelin synthase 1 functions by catalyzing the conversion of ceramide and phosphatidylcholine to sphingomyelin and diacylglycerol.	Ceramides	67-75	sphingomyelin synthase 1	Mus musculus	0-24
16879426-5	2006	Consistent with its biochemical function, yeast cells expressing sphingomyelin synthase 1 have an enhanced ability to grow in media containing the cell-permeable C2-ceramide analog as well as the ceramide precursor phytosphingosine.	Ceramides	165-173	sphingomyelin synthase 1	Mus musculus	65-89
16772302-2	2006	This study shows that hyperosmotic ROS formation involves a rapid ceramide- and protein kinase Czeta (PKCzeta)-dependent serine phosphorylation of p47phox and subsequent activation of NADPH oxidase isoforms.	Ceramides	66-74	neutrophil cytosolic factor 1	Rattus norvegicus	147-154
16790528-0	2006	SAP155 Binds to ceramide-responsive RNA cis-element 1 and regulates the alternative 5" splice site selection of Bcl-x pre-mRNA.	Ceramides	16-24	splicing factor 3b subunit 1	Homo sapiens	0-6
16790528-0	2006	SAP155 Binds to ceramide-responsive RNA cis-element 1 and regulates the alternative 5" splice site selection of Bcl-x pre-mRNA.	Ceramides	16-24	BCL2 like 1	Homo sapiens	112-117
16790528-2	2006	In previous studies, our laboratory identified an RNA cis-element within exon 2 of Bcl-x pre-mRNA that is a ceramide responsive termed CRCE 1.	Ceramides	108-116	BCL2 like 1	Homo sapiens	83-88
16790528-7	2006	Specific down-regulation of SAP155 also inhibited the ability of exogenous ceramide treatment to further induce the activation of the Bcl-x(s) 5" splice site.	Ceramides	75-83	splicing factor 3b subunit 1	Homo sapiens	28-34
16790528-7	2006	Specific down-regulation of SAP155 also inhibited the ability of exogenous ceramide treatment to further induce the activation of the Bcl-x(s) 5" splice site.	Ceramides	75-83	BCL2 like 1	Homo sapiens	134-139
16790528-9	2006	Therefore, we have identified SAP155 as an RNA trans-acting factor that binds to CRCE 1, functions to regulate the alternative 5" splice site selection of Bcl-x pre-mRNA, and is required for ceramide to induce the activation of the Bcl-x(s) 5" splice site.	Ceramides	191-199	splicing factor 3b subunit 1	Homo sapiens	30-36
16790528-9	2006	Therefore, we have identified SAP155 as an RNA trans-acting factor that binds to CRCE 1, functions to regulate the alternative 5" splice site selection of Bcl-x pre-mRNA, and is required for ceramide to induce the activation of the Bcl-x(s) 5" splice site.	Ceramides	191-199	BCL2 like 1	Homo sapiens	232-237
16754725-3	2006	The purpose of this study is to determine if LPS-induced TLR4 assembly and activation are dependent on the sphingolipid metabolite ceramide produced by phosphatidylcholine-specific phospholipase C (PC-PLC) or CD14.	Ceramides	131-139	toll like receptor 4	Homo sapiens	57-61
16754725-3	2006	The purpose of this study is to determine if LPS-induced TLR4 assembly and activation are dependent on the sphingolipid metabolite ceramide produced by phosphatidylcholine-specific phospholipase C (PC-PLC) or CD14.	Ceramides	131-139	CD14 molecule	Homo sapiens	209-213
16754725-8	2006	Pretreatment with D609 or CD14 blockade was associated with attenuated LPS-induced ceramide production, TLR4 assembly on lipid rafts, and cytokine production.	Ceramides	83-91	CD14 molecule	Homo sapiens	26-30
16754725-11	2006	C2 ceramide alone induced the activation of PKC-zeta and the assembly of TLR4 but was not associated with cytokine liberation.	Ceramides	3-11	protein kinase C zeta	Homo sapiens	44-52
16754725-11	2006	C2 ceramide alone induced the activation of PKC-zeta and the assembly of TLR4 but was not associated with cytokine liberation.	Ceramides	3-11	toll like receptor 4	Homo sapiens	73-77
16754725-12	2006	This study demonstrates that TLR4 assembly and activation following LPS exposure require the production of ceramide by PC-PLC, which appears to be CD14-dependent.	Ceramides	107-115	toll like receptor 4	Homo sapiens	29-33
16754725-12	2006	This study demonstrates that TLR4 assembly and activation following LPS exposure require the production of ceramide by PC-PLC, which appears to be CD14-dependent.	Ceramides	107-115	CD14 molecule	Homo sapiens	147-151
16704983-0	2006	Ethanolaminephosphate side chain added to glycosylphosphatidylinositol (GPI) anchor by mcd4p is required for ceramide remodeling and forward transport of GPI proteins from endoplasmic reticulum to Golgi.	Ceramides	109-117	mannose-ethanolamine phosphotransferase MCD4	Saccharomyces cerevisiae S288C	87-92
16632640-1	2006	Sphingosine kinase (SK) is an oncogenic sphingolipid-metabolizing enzyme that catalyzes the formation of the mitogenic second messenger sphingosine-1-phosphate (S1P) at the expense of proapoptotic ceramide.	Ceramides	197-205	sphingosine-1-phosphate receptor 1	Mus musculus	161-164
16682503-0	2006	Lithium inhibits ceramide- and etoposide-induced protein phosphatase 2A methylation, Bcl-2 dephosphorylation, caspase-2 activation, and apoptosis.	Ceramides	17-25	protein phosphatase 2 phosphatase activator	Homo sapiens	57-71
16682503-3	2006	Here, we report a novel role of lithium on the blockage of ceramide- and etoposide-induced apoptosis via inhibition of protein phosphatase 2A (PP2A) activity.	Ceramides	59-67	protein phosphatase 2 phosphatase activator	Homo sapiens	127-141
16682503-3	2006	Here, we report a novel role of lithium on the blockage of ceramide- and etoposide-induced apoptosis via inhibition of protein phosphatase 2A (PP2A) activity.	Ceramides	59-67	protein phosphatase 2 phosphatase activator	Homo sapiens	143-147
16682503-5	2006	Lithium and OA abrogated ceramide- and etoposide-induced Bcl-2 dephosphorylation at serine 70.	Ceramides	25-33	BCL2 apoptosis regulator	Homo sapiens	57-62
16682503-6	2006	Furthermore, ceramide- and etoposide-induced PP2A activation involved methylation of PP2A C subunit, which lithium suppressed.	Ceramides	13-21	protein phosphatase 2 phosphatase activator	Homo sapiens	45-49
16682503-6	2006	Furthermore, ceramide- and etoposide-induced PP2A activation involved methylation of PP2A C subunit, which lithium suppressed.	Ceramides	13-21	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	85-91
16869980-16	2006	The early rise in Bax and ceramide appears to overcome the anti-apoptotic activity of Bcl-2.	Ceramides	26-34	BCL2, apoptosis regulator	Rattus norvegicus	86-91
16749907-8	2006	Further studies demonstrated that PAR-1 activation, as well as application of recombinant GRO/CINC-1, protected astrocytes from C(2)-ceramide-induced cell death.	Ceramides	133-141	coagulation factor II (thrombin) receptor	Rattus norvegicus	34-39
16749907-8	2006	Further studies demonstrated that PAR-1 activation, as well as application of recombinant GRO/CINC-1, protected astrocytes from C(2)-ceramide-induced cell death.	Ceramides	133-141	C-X-C motif chemokine ligand 1	Rattus norvegicus	90-93
16749907-8	2006	Further studies demonstrated that PAR-1 activation, as well as application of recombinant GRO/CINC-1, protected astrocytes from C(2)-ceramide-induced cell death.	Ceramides	133-141	C-X-C motif chemokine ligand 1	Rattus norvegicus	94-100
16571104-1	2006	Des2 (degenerative spermatocyte 2) is a bifunctional enzyme that produces phytoceramide and ceramide from dihydroceramide.	Ceramides	79-87	delta(4)-desaturase, sphingolipid 2	Mus musculus	0-4
16888176-2	2006	It has been shown that the proinflammatory cytokine second messenger ceramides and the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) play pivotal roles in the histogenesis of the cerebellum.	Ceramides	69-78	adenylate cyclase activating polypeptide 1	Homo sapiens	152-157
16888176-6	2006	These data suggest that PACAP and factors inducing ceramide production may control granule cell migration during cerebellar development.	Ceramides	51-59	adenylate cyclase activating polypeptide 1	Homo sapiens	24-29
16645158-7	2006	This effect is associated with attenuation of the anti-migratory effects of rapamycin under high glucose conditions that are not observed with paclitaxel, as well as with increased protection against ceramide-induced cytotoxicity, both of which are dependent on FOXO1 phosphorylation.	Ceramides	200-208	forkhead box O1	Homo sapiens	262-267
16837612-6	2006	Furthermore, inhibition of protein phosphatases with okadaic acid suppressed E2 inhibition of TX-elicited LHRH-induced LH secretion, while stimulation of protein phosphatases with ceramide blocked TX-induced LHRH self-priming.	Ceramides	180-188	gonadotropin releasing hormone 1	Rattus norvegicus	208-212
16624285-0	2006	The CB2 cannabinoid receptor signals apoptosis via ceramide-dependent activation of the mitochondrial intrinsic pathway.	Ceramides	51-59	cannabinoid receptor 2	Homo sapiens	4-7
16624285-5	2006	Cannabinoid treatment led to a CB2 receptor-dependent stimulation of ceramide biosynthesis and inhibition of this pathway prevented Delta9-tetrahydrocannabinol-induced mitochondrial hypopolarization and cytochrome c release, indicating that ceramide acts at a pre-mitochondrial level.	Ceramides	69-77	cannabinoid receptor 2	Homo sapiens	31-34
16624285-5	2006	Cannabinoid treatment led to a CB2 receptor-dependent stimulation of ceramide biosynthesis and inhibition of this pathway prevented Delta9-tetrahydrocannabinol-induced mitochondrial hypopolarization and cytochrome c release, indicating that ceramide acts at a pre-mitochondrial level.	Ceramides	69-77	cytochrome c, somatic	Homo sapiens	203-215
16624285-5	2006	Cannabinoid treatment led to a CB2 receptor-dependent stimulation of ceramide biosynthesis and inhibition of this pathway prevented Delta9-tetrahydrocannabinol-induced mitochondrial hypopolarization and cytochrome c release, indicating that ceramide acts at a pre-mitochondrial level.	Ceramides	241-249	cannabinoid receptor 2	Homo sapiens	31-34
16624285-6	2006	Inhibition of ceramide synthesis de novo also prevented caspase activation and apoptosis.	Ceramides	14-22	caspase 8	Homo sapiens	56-63
16624285-9	2006	In summary, results presented here show that CB2 receptor activation signals apoptosis via a ceramide-dependent stimulation of the mitochondrial intrinsic pathway.	Ceramides	93-101	cannabinoid receptor 2	Homo sapiens	45-48
16818650-10	2006	In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB(2) receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress-related genes ATF-4 and TRB3.	Ceramides	150-158	activating transcription factor 4	Homo sapiens	240-245
16818650-10	2006	In conclusion, results presented here show that cannabinoids lead to apoptosis of pancreatic tumor cells via a CB(2) receptor and de novo synthesized ceramide-dependent up-regulation of p8 and the endoplasmic reticulum stress-related genes ATF-4 and TRB3.	Ceramides	150-158	taste 2 receptor member 13	Homo sapiens	250-254
16645048-5	2006	In fact, the production of ceramide from GM3 has been observed even under experimental conditions able to block endocytosis or lysosomal activity, and the overexpression of the plasma membrane ganglioside sialidase Neu3 corresponded to a higher production of ceramide in the plasma membrane.	Ceramides	27-35	neuraminidase 3	Homo sapiens	215-219
16631623-5	2006	Moreover, nSMase2 subcellular localization is governed by oxidant exposure, which leads to its preferential trafficking to the plasma membrane, where it generates ceramide and induces apoptosis.	Ceramides	163-171	sphingomyelin phosphodiesterase 3	Homo sapiens	10-17
16626961-0	2006	Soluble oligomers of amyloid-beta peptide induce neuronal apoptosis by activating a cPLA2-dependent sphingomyelinase-ceramide pathway.	Ceramides	117-125	phospholipase A2 group IVA	Homo sapiens	84-89
16701558-1	2006	The oxidative stress induced by photodynamic therapy using the phthalocyanine Pc 4 (PDT) can lead to apoptosis, and is accompanied by photodamage to Bcl-2 and accumulation of de novo ceramide.	Ceramides	183-191	proprotein convertase subtilisin/kexin type 4	Homo sapiens	78-82
16773715-9	2006	Meanwhile, ceramide up-regulated or down-regulated the mRNA expression of Bcl-2 family gene members.	Ceramides	11-19	BCL2 apoptosis regulator	Homo sapiens	74-79
16773715-10	2006	CONCLUSION: Ceramide induces apoptosis of human colon carcinoma HT-29 cells by affecting the expression of Bcl-2 family gene members and impacting the mitochondrial function.	Ceramides	12-20	BCL2 apoptosis regulator	Homo sapiens	107-112
16645048-5	2006	In fact, the production of ceramide from GM3 has been observed even under experimental conditions able to block endocytosis or lysosomal activity, and the overexpression of the plasma membrane ganglioside sialidase Neu3 corresponded to a higher production of ceramide in the plasma membrane.	Ceramides	259-267	neuraminidase 3	Homo sapiens	215-219
16554657-6	2006	Primary alcohols, which attenuate the formation of phosphatidic acid (the product of PLD), and cell-permeable ceramides, which inhibit PLD activity, blocked S1P-stimulated aldosterone secretion.	Ceramides	110-119	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	135-138
16547352-1	2006	Previous studies have indicated a role for glucosylceramide synthase (GCS) in multidrug resistance (MDR), either related to turnover of ceramide (Cer) or generation of gangliosides, which modulate apoptosis and/or the activity of ABC transporters.	Ceramides	51-59	UDP-glucose ceramide glucosyltransferase	Homo sapiens	70-73
16740734-6	2006	We also found that the knockdown of FAS expression significantly increased ceramide level in the tumor cells, and this increase was abrogated by acetyl-CoA carboxylase inhibitor.	Ceramides	75-83	fatty acid synthase	Homo sapiens	36-39
16740734-7	2006	In addition, carnitine palmitoyltransferase-1 (CPT-1) inhibitor up-regulated the ceramide and BNIP3 levels in these cells, whereas treatment of tumor cells with FAS siRNA in the presence of a ceramide synthase inhibitor abrogated the up-regulation of BNIP3 and inhibited apoptosis.	Ceramides	81-89	carnitine palmitoyltransferase 1A	Homo sapiens	13-45
16740734-7	2006	In addition, carnitine palmitoyltransferase-1 (CPT-1) inhibitor up-regulated the ceramide and BNIP3 levels in these cells, whereas treatment of tumor cells with FAS siRNA in the presence of a ceramide synthase inhibitor abrogated the up-regulation of BNIP3 and inhibited apoptosis.	Ceramides	81-89	carnitine palmitoyltransferase 1A	Homo sapiens	47-52
16740734-10	2006	Collectively, our results indicate that inhibition of FAS in breast cancer cells causes accumulation of malonyl-CoA, which leads to inhibition of CPT-1 and up-regulation of ceramide and induction of the proapoptotic genes BNIP3, TRAIL, and DAPK2, resulting in apoptosis.	Ceramides	173-181	fatty acid synthase	Homo sapiens	54-57
16440306-12	2006	Inferring that caspase-9 was the main executioner (rather than caspase-8 and-3) in Saos2 cell death, indicates that the nSMase-induced release of ceramide, directly activated the intrinsic mitochondrial apoptotic pathway.	Ceramides	146-154	caspase 9	Homo sapiens	15-24
16440306-12	2006	Inferring that caspase-9 was the main executioner (rather than caspase-8 and-3) in Saos2 cell death, indicates that the nSMase-induced release of ceramide, directly activated the intrinsic mitochondrial apoptotic pathway.	Ceramides	146-154	sphingomyelin phosphodiesterase 2	Homo sapiens	120-126
16619032-3	2006	This TrkA-to-p75(NTR) switch is accompanied by activation of the second messenger ceramide, stabilization of beta-site amyloid precursor protein-cleaving enzyme-1 (BACE1), and increased production of amyloid beta-peptide (Abeta).	Ceramides	82-90	neurotrophic receptor tyrosine kinase 1	Homo sapiens	5-9
16601923-0	2006	Discovery of the molecular machinery CERT for endoplasmic reticulum-to-Golgi trafficking of ceramide.	Ceramides	92-100	ceramide transporter 1	Homo sapiens	37-41
16601923-3	2006	We have recently identified a key factor (named CERT) for ceramide trafficking.	Ceramides	58-66	ceramide transporter 1	Homo sapiens	48-52
16510697-1	2006	In this study, a cationic water-soluble ceramide analog L-threo-C6-pyridinium-ceramide-bromide (L-t-C6-Pyr-Cer), which exhibits high solubility and bioavailability, inhibited the growth of various human head and neck squamous cell carcinoma (HNSCC) cell lines at low IC50 concentrations, independent of their p53 status.	Ceramides	40-48	tumor protein p53	Homo sapiens	309-312
16571669-4	2006	RNA interference (RNAi) experiments in Chinese hamster ovary (CHO)-K1 cells revealed that OSBP and vesicle-associated membrane protein-associated protein (VAP) were required for stimulation of CERT-dependent ceramide transport and SM synthesis by 25-hydroxycholesterol and cholesterol depletion in response to cyclodextrin.	Ceramides	208-216	LOW QUALITY PROTEIN: oxysterol-binding protein 1	Cricetulus griseus	90-94
16571669-4	2006	RNA interference (RNAi) experiments in Chinese hamster ovary (CHO)-K1 cells revealed that OSBP and vesicle-associated membrane protein-associated protein (VAP) were required for stimulation of CERT-dependent ceramide transport and SM synthesis by 25-hydroxycholesterol and cholesterol depletion in response to cyclodextrin.	Ceramides	208-216	ceramide transfer protein	Cricetulus griseus	193-197
16571669-6	2006	Activation of ER-to-Golgi ceramide transport in CHO-K1 cells required interaction of OSBP with the ER and Golgi apparatus, OSBP-dependent Golgi translocation of CERT, and enhanced CERT-VAP interaction.	Ceramides	26-34	LOW QUALITY PROTEIN: oxysterol-binding protein 1	Cricetulus griseus	85-89
16571669-6	2006	Activation of ER-to-Golgi ceramide transport in CHO-K1 cells required interaction of OSBP with the ER and Golgi apparatus, OSBP-dependent Golgi translocation of CERT, and enhanced CERT-VAP interaction.	Ceramides	26-34	LOW QUALITY PROTEIN: oxysterol-binding protein 1	Cricetulus griseus	123-127
16571669-6	2006	Activation of ER-to-Golgi ceramide transport in CHO-K1 cells required interaction of OSBP with the ER and Golgi apparatus, OSBP-dependent Golgi translocation of CERT, and enhanced CERT-VAP interaction.	Ceramides	26-34	ceramide transfer protein	Cricetulus griseus	161-165
16571669-6	2006	Activation of ER-to-Golgi ceramide transport in CHO-K1 cells required interaction of OSBP with the ER and Golgi apparatus, OSBP-dependent Golgi translocation of CERT, and enhanced CERT-VAP interaction.	Ceramides	26-34	ceramide transfer protein	Cricetulus griseus	180-184
16571669-7	2006	Regulation of CERT by OSBP, sterols, and VAP reveals a novel mechanism for integrating sterol regulatory signals with ceramide transport and SM synthesis in the Golgi apparatus.	Ceramides	118-126	ceramide transfer protein	Cricetulus griseus	14-18
16571669-7	2006	Regulation of CERT by OSBP, sterols, and VAP reveals a novel mechanism for integrating sterol regulatory signals with ceramide transport and SM synthesis in the Golgi apparatus.	Ceramides	118-126	LOW QUALITY PROTEIN: oxysterol-binding protein 1	Cricetulus griseus	22-26
16387389-0	2006	Leptin-induced suppression of cardiomyocyte contraction is amplified by ceramide.	Ceramides	72-80	leptin	Rattus norvegicus	0-6
16387389-3	2006	The purpose of this study was to examine the effect of ceramide on leptin-elicited cardiac contractile response.	Ceramides	55-63	leptin	Rattus norvegicus	67-73
16387389-6	2006	While ceramide did not elicit any effect on cell mechanics and intracellular Ca2+ transients, it sensitized leptin-induced effects on myocyte shortening and intracellular Ca2+ transients.	Ceramides	6-14	leptin	Rattus norvegicus	108-114
16387389-8	2006	With ceramide co-incubation, 5 nM leptin depressed PS, +/-dL/dt, Delta[Ca2+] and prolonged TR90 whereas 50 nM leptin-elicited effects on PS, +/-dL/dt, Delta[Ca2+] and TR90 were significantly potentiated in addition to slowing intracellular Ca2+ decay.	Ceramides	5-13	leptin	Rattus norvegicus	34-40
16387389-9	2006	In summary, our data demonstrated that ceramide sensitizes cardiac depressive effects of leptin and may contribute to hyperleptinemia-related cardiac contractile dysfunction.	Ceramides	39-47	leptin	Rattus norvegicus	89-95
16517606-1	2006	Two genes encoding neutral sphingomyelinases-1 and -2 (sphingomyelin phosphodiesterases-2 and -3) have been recently identified that hydrolyze sphingomyelin to phosphorylcholine and ceramide.	Ceramides	182-190	sphingomyelin phosphodiesterase 3	Homo sapiens	19-53
16517606-1	2006	Two genes encoding neutral sphingomyelinases-1 and -2 (sphingomyelin phosphodiesterases-2 and -3) have been recently identified that hydrolyze sphingomyelin to phosphorylcholine and ceramide.	Ceramides	182-190	sphingomyelin phosphodiesterase 2	Homo sapiens	55-96
16734755-5	2006	On the other hand, osmotic shock activates a phospholipase A2 leading to release of platelet activating factor, which in turn activates a sphingomyelinase and thus stimulates the formation of ceramide.	Ceramides	192-200	phospholipase A2 group IB	Homo sapiens	45-61
16619032-3	2006	This TrkA-to-p75(NTR) switch is accompanied by activation of the second messenger ceramide, stabilization of beta-site amyloid precursor protein-cleaving enzyme-1 (BACE1), and increased production of amyloid beta-peptide (Abeta).	Ceramides	82-90	interleukin 2 receptor subunit beta	Homo sapiens	13-16
16339830-2	2006	Overexpression of nuclear receptor peroxisome proliferator-activated receptor-alpha (PPARalpha) increases intramyocellular ceramide and left ventricular (LV) dysfunction.	Ceramides	123-131	peroxisome proliferator activated receptor alpha	Rattus norvegicus	35-83
16339830-2	2006	Overexpression of nuclear receptor peroxisome proliferator-activated receptor-alpha (PPARalpha) increases intramyocellular ceramide and left ventricular (LV) dysfunction.	Ceramides	123-131	peroxisome proliferator activated receptor alpha	Rattus norvegicus	85-94
16339830-3	2006	We tested the hypothesis that activation of fatty acid metabolism with fat feeding or a PPARalpha agonist increases myocardial triglyceride and/or ceramide and exacerbates LV dysfunction in HF.	Ceramides	147-155	peroxisome proliferator activated receptor alpha	Rattus norvegicus	88-97
16339830-7	2006	Myocardial ceramide content was elevated in the INF group compared with sham-operated rats, with no further change in the INF + Fat or INF + Feno groups.	Ceramides	11-19	cobalamin binding intrinsic factor	Rattus norvegicus	48-51
16396984-0	2006	Ciliary neurotrophic factor prevents acute lipid-induced insulin resistance by attenuating ceramide accumulation and phosphorylation of c-Jun N-terminal kinase in peripheral tissues.	Ceramides	91-99	ciliary neurotrophic factor	Homo sapiens	0-27
16808175-1	2006	Total ceramides containing nonbranched and iso-branched C18- and C19-phytosphingosines acylated with non-hydroxylated fatty acids were isolated from a marine sponge Oceanapia sp.	Ceramides	6-15	Bardet-Biedl syndrome 9	Homo sapiens	56-59
16396984-0	2006	Ciliary neurotrophic factor prevents acute lipid-induced insulin resistance by attenuating ceramide accumulation and phosphorylation of c-Jun N-terminal kinase in peripheral tissues.	Ceramides	91-99	insulin	Homo sapiens	57-64
16691498-10	2006	In summary, our studies suggest that TNF-alpha-induced N-SMase activation and production of ceramide is required to activate the apoptosis pathway in human osteosarcoma cells.	Ceramides	92-100	tumor necrosis factor	Homo sapiens	37-46
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.	Ceramides	122-130	ATP-binding cassette, sub-family B (MDR/TAP), member 1B	Mus musculus	22-26
16505493-0	2006	SRp30a (ASF/SF2) regulates the alternative splicing of caspase-9 pre-mRNA and is required for ceramide-responsiveness.	Ceramides	94-102	serine and arginine rich splicing factor 1	Homo sapiens	0-6
16505493-0	2006	SRp30a (ASF/SF2) regulates the alternative splicing of caspase-9 pre-mRNA and is required for ceramide-responsiveness.	Ceramides	94-102	serine and arginine rich splicing factor 1	Homo sapiens	8-15
16505493-2	2006	Previous studies from our laboratory have shown that the alternative splicing of caspase-9 and the phosphorylation status of SR proteins, a conserved family of splicing factors, are regulated by chemotherapy and ceramide via the action of protein phosphatase-1.	Ceramides	212-220	caspase 9	Homo sapiens	81-90
16505493-3	2006	In this study, a link between ceramide, SR proteins, and the alternative splicing of caspase-9 was established.	Ceramides	30-38	caspase 9	Homo sapiens	85-94
16505493-5	2006	The specific downregulation of SRp30a also inhibited the ability of exogenous ceramide treatment to induce the inclusion of the exon 3, 4, 5, and 6 cassette.	Ceramides	78-86	serine and arginine rich splicing factor 1	Homo sapiens	31-37
16505493-6	2006	Therefore, we have identified SRp30a as an RNA trans-acting factor that functions as a major regulator of caspase-9 pre-mRNA processing and is required for ceramide to mediate the alternative splicing of caspase-9.	Ceramides	156-164	serine and arginine rich splicing factor 1	Homo sapiens	30-36
16505493-6	2006	Therefore, we have identified SRp30a as an RNA trans-acting factor that functions as a major regulator of caspase-9 pre-mRNA processing and is required for ceramide to mediate the alternative splicing of caspase-9.	Ceramides	156-164	caspase 9	Homo sapiens	204-213
16499950-9	2006	Of all of the pathways, neutral sphingomyelinase appears to be the most likely source of the senescence-associated ceramide.	Ceramides	115-123	sphingomyelin phosphodiesterase 2	Homo sapiens	24-48
16470810-11	2006	Ceramide, a negative regulator of astrocyte proliferation and down-regulated by bFGF (Riboni et al., 2002.	Ceramides	0-8	fibroblast growth factor 2	Homo sapiens	80-84
16524368-2	2006	We have previously reported that the amyloid beta peptide (Abeta) induces apoptosis in oligodendrocytes (OLG), via activation of neutral sphingomyelinase (nSMase) and resultant generation of ceramide.	Ceramides	191-199	amyloid beta precursor protein	Homo sapiens	59-64
16524368-3	2006	In the current study, we report that both Abeta and ceramide increased expression of the proapoptotic protein DP5/Hrk (DP5), and release of cytochrome C from mitochondria to cytoplasm in OLGs.	Ceramides	52-60	harakiri, BCL2 interacting protein	Homo sapiens	110-117
16524368-3	2006	In the current study, we report that both Abeta and ceramide increased expression of the proapoptotic protein DP5/Hrk (DP5), and release of cytochrome C from mitochondria to cytoplasm in OLGs.	Ceramides	52-60	harakiri, BCL2 interacting protein	Homo sapiens	110-113
16524368-3	2006	In the current study, we report that both Abeta and ceramide increased expression of the proapoptotic protein DP5/Hrk (DP5), and release of cytochrome C from mitochondria to cytoplasm in OLGs.	Ceramides	52-60	cytochrome c, somatic	Homo sapiens	140-152
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	mitogen-activated protein kinase 8	Homo sapiens	29-50
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	mitogen-activated protein kinase 8	Homo sapiens	52-55
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	amyloid beta precursor protein	Homo sapiens	128-133
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	mitogen-activated protein kinase 8	Homo sapiens	157-160
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	193-197
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	mitogen-activated protein kinase 8	Homo sapiens	157-160
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	240-244
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	95-103	harakiri, BCL2 interacting protein	Homo sapiens	258-261
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	mitogen-activated protein kinase 8	Homo sapiens	29-50
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	mitogen-activated protein kinase 8	Homo sapiens	52-55
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	amyloid beta precursor protein	Homo sapiens	84-89
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	mitogen-activated protein kinase 8	Homo sapiens	157-160
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	193-197
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	mitogen-activated protein kinase 8	Homo sapiens	157-160
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	240-244
16524368-4	2006	We provide evidence that the Jun N-terminal kinase (JNK) signaling pathway mediates Abeta- and ceramide-induced apoptosis: Both Abeta and ceramide activated JNK phosphorylation, and subsequent AP-1 DNA binding activity; JNK siRNA decreased AP-1 DNA binding, DP5 expression and reduced cell death.	Ceramides	138-146	harakiri, BCL2 interacting protein	Homo sapiens	258-261
16524368-6	2006	Collectively, these results suggest that Abeta-induced apoptosis involves the sequential activation of nSMase with ceramide generation, JNK activation, AP-1 DNA binding, and DP5 expression.	Ceramides	115-123	amyloid beta precursor protein	Homo sapiens	41-46
16524368-6	2006	Collectively, these results suggest that Abeta-induced apoptosis involves the sequential activation of nSMase with ceramide generation, JNK activation, AP-1 DNA binding, and DP5 expression.	Ceramides	115-123	sphingomyelin phosphodiesterase 2	Homo sapiens	103-109
16605271-0	2006	Regulation of the activity and fatty acid specificity of lecithin-cholesterol acyltransferase by sphingomyelin and its metabolites, ceramide and ceramide phosphate.	Ceramides	132-140	lecithin-cholesterol acyltransferase	Homo sapiens	57-93
16605271-2	2006	In this study, we investigated the effects of its metabolites, ceramide and ceramide phosphate, on the activity and fatty acid specificity of LCAT in vitro.	Ceramides	63-71	lecithin-cholesterol acyltransferase	Homo sapiens	142-146
16605271-4	2006	Although incorporation of ceramide into the substrate in the absence of SM activated the LCAT reaction only modestly, its co-incorporation with SM neutralized the inhibitory effect of SM.	Ceramides	26-34	lecithin-cholesterol acyltransferase	Homo sapiens	89-93
16605271-9	2006	Since the plasma ceramide levels are increased during inflammation, these results indicate that the activity and fatty acid specificity of LCAT may be altered during the inflammatory response.	Ceramides	17-25	lecithin-cholesterol acyltransferase	Homo sapiens	139-143
16596215-0	2006	Lactoferricin-induced apoptosis in estrogen-nonresponsive MDA-MB-435 breast cancer cells is enhanced by C6 ceramide or tamoxifen.	Ceramides	107-115	lactotransferrin	Homo sapiens	0-13
16467304-7	2006	Additionally, arrested LPP2 cells contained decreased lysophosphatidate concentrations and increased ceramide.	Ceramides	101-109	phospholipid phosphatase 2	Homo sapiens	23-27
16448625-3	2006	In a previous study, we demonstrated that ceramide derivatives coupled with a lauroyl group exerted strong inhibitory effects on IL-4 production in T cells.	Ceramides	42-50	interleukin 4	Mus musculus	129-133
16448625-9	2006	These results indicate that the ceramides, LES and LECS, may inhibit the production of IL-4 in the activated T cells, via the downregulation of AP-1/NF-AT activation and PKC activity.	Ceramides	32-41	interleukin 4	Mus musculus	87-91
16415050-1	2006	Ceramides have been implicated in the initiation of apoptosis by permeabilizing the mitochondrial outer membrane to small proteins, including cytochrome c.	Ceramides	0-9	cytochrome c, somatic	Homo sapiens	142-154
16415476-5	2006	ATP activated neutral sphingomyelinase (N-SMase), which provoked a decrease of the cellular content of sphingomyelin and an increase of ceramide levels in these cells and in the rafts.	Ceramides	136-144	sphingomyelin phosphodiesterase 2	Rattus norvegicus	14-38
16730193-2	2006	Sphingosine/ceramide and nitric oxide have been associated with apoptosis induced by TNF-alpha; however, signaling mechanisms of TNF-alpha-induced apoptosis in cardiac myocytes are not well defined.	Ceramides	12-20	tumor necrosis factor	Homo sapiens	85-94
16565407-11	2006	Inhibiting glucosylceramide synthase, which catalyzes ceramide glucosylation, before ceramide or paraquat treatment blocked DHA"s protective effect.	Ceramides	54-62	UDP-glucose ceramide glucosyltransferase	Homo sapiens	11-36
16415476-5	2006	ATP activated neutral sphingomyelinase (N-SMase), which provoked a decrease of the cellular content of sphingomyelin and an increase of ceramide levels in these cells and in the rafts.	Ceramides	136-144	sphingomyelin phosphodiesterase 2	Rattus norvegicus	40-47
16415476-10	2006	P2X7 receptors in the rafts are coupled to the activation of N-SMase, which increases the content of ceramides in rafts.	Ceramides	101-110	sphingomyelin phosphodiesterase 2	Rattus norvegicus	61-68
16545138-8	2006	Co culture with CD40L L cells also blocked the apoptosis induced by exogenous ceramides in breast carcinoma and non Hodgkin"s lymphoma cell lines through a caspase-3-like, 8-like and 9-like dependent pathways.	Ceramides	78-87	CD40 ligand	Homo sapiens	16-21
16545138-8	2006	Co culture with CD40L L cells also blocked the apoptosis induced by exogenous ceramides in breast carcinoma and non Hodgkin"s lymphoma cell lines through a caspase-3-like, 8-like and 9-like dependent pathways.	Ceramides	78-87	caspase 3	Homo sapiens	156-165
16545138-9	2006	CONCLUSION: These results indicate that CD40L expressed on adjacent non tumoral cells induces multidrug resistance to cytotoxic agents and ceramides in both breast carcinoma and non Hodgkin"s lymphoma cell lines, albeit through a caspase independent and dependent pathway respectively.	Ceramides	139-148	CD40 ligand	Homo sapiens	40-45
16380386-7	2006	Indeed, Asah2 null mice were deficient in the intestinal degradation of ceramide.	Ceramides	72-80	N-acylsphingosine amidohydrolase 2	Mus musculus	8-13
16261164-8	2006	Pathway analysis with the 85 genes using Gene Ontology suggested that genes involved in endocytosis, ceramide generation, Ras/ERK/Ark cascade, and JAT-STAT pathways may play roles related to ER.	Ceramides	101-109	mitogen-activated protein kinase 1	Homo sapiens	126-129
16540676-7	2006	We also showed that 4-oxo-4-HPR, similarly to 4-HPR, increased reactive oxygen species generation and ceramide levels by de novo synthesis.	Ceramides	102-110	haptoglobin-related protein	Homo sapiens	28-31
16293265-11	2006	Ceramide was also associated with a 29% and 38% increase in catalase and CuZnSOD activities, respectively, compared with control group.	Ceramides	0-8	catalase	Rattus norvegicus	60-68
16293265-11	2006	Ceramide was also associated with a 29% and 38% increase in catalase and CuZnSOD activities, respectively, compared with control group.	Ceramides	0-8	superoxide dismutase 1	Rattus norvegicus	73-80
16261164-8	2006	Pathway analysis with the 85 genes using Gene Ontology suggested that genes involved in endocytosis, ceramide generation, Ras/ERK/Ark cascade, and JAT-STAT pathways may play roles related to ER.	Ceramides	101-109	AXL receptor tyrosine kinase	Homo sapiens	130-133
16306078-4	2006	Both ACTH and Bt2cAMP decreased cellular amounts of several sphingolipids, including sphingomyelin, ceramides, and sphingosine and stimulating the activity of sphingosine kinase and increasing the release of sphingosine-1-phosphate (S1P) into the media.	Ceramides	100-109	proopiomelanocortin	Homo sapiens	5-9
16099142-5	2006	The modest ceramide stimuli strongly suppressed the calcium response and inhibited several downstream signal events (e.g. ERK1/2-, JNK-phosphorylation, CD69 expression or IL-2 production) in TH cells during both anti-CD3 induced and APC-triggered activation.	Ceramides	11-19	mitogen-activated protein kinase 3	Mus musculus	122-128
16099142-5	2006	The modest ceramide stimuli strongly suppressed the calcium response and inhibited several downstream signal events (e.g. ERK1/2-, JNK-phosphorylation, CD69 expression or IL-2 production) in TH cells during both anti-CD3 induced and APC-triggered activation.	Ceramides	11-19	mitogen-activated protein kinase 8	Mus musculus	131-134
16099142-5	2006	The modest ceramide stimuli strongly suppressed the calcium response and inhibited several downstream signal events (e.g. ERK1/2-, JNK-phosphorylation, CD69 expression or IL-2 production) in TH cells during both anti-CD3 induced and APC-triggered activation.	Ceramides	11-19	CD69 antigen	Mus musculus	152-156
16099142-5	2006	The modest ceramide stimuli strongly suppressed the calcium response and inhibited several downstream signal events (e.g. ERK1/2-, JNK-phosphorylation, CD69 expression or IL-2 production) in TH cells during both anti-CD3 induced and APC-triggered activation.	Ceramides	11-19	interleukin 2	Mus musculus	171-175
16099142-6	2006	Ceramide moderately affected the Ca2+ -release from internal stores upon antigen-specific engagement of TCR in immunological synapses, while the influx phase was remarkably reduced in both amplitude and rate, suggesting that the major target(s) of ceramide-effects are membrane-proximal.	Ceramides	0-8	T cell receptor alpha variable 6-3	Mus musculus	104-107
16099142-7	2006	Ceramide inhibited Kv1.3 potassium channels, store operated Ca2+ -entry (SOC) and depolarized the plasma membrane to which contribution of spontaneously formed ceramide channels is possible.	Ceramides	0-8	potassium voltage-gated channel, shaker-related subfamily, member 3	Mus musculus	19-24
16099142-1	2006	Sphingomyelinase (SMase)-mediated release of ceramide in the plasma membrane of T-lymphocytes induced by different stimuli such as ligation of Fas/CD95, irradiation, stress, inflammation or anticancer drugs primarily involves mitochondrial apoptosis signaling, but under specific conditions non-apoptotic Fas-signaling was also reported.	Ceramides	45-53	Fas (TNF receptor superfamily member 6)	Mus musculus	147-151
16397504-6	2006	Ceramide analogs also induced cell death in Jurkat mutants that are deficient in cell death signaling proteins, including FADD, caspase-8 and 10, and RIP.	Ceramides	0-8	Fas associated via death domain	Homo sapiens	122-126
16507765-11	2006	SK1 knockdown also induced significant increases in ceramide levels in whole cells and in mitochondria enriched fractions of cells.	Ceramides	52-60	sphingosine kinase 1	Homo sapiens	0-3
16571915-2	2006	The diacylglycerol kinase (DGK) assay showed that the intracellular concentration of ceramide increased time-dependently after X irradiation of cells, and this radiation-induced accumulation of ceramide did not occur prior to the appearance of apoptotic cells.	Ceramides	85-93	diacylglycerol kinase beta	Homo sapiens	4-25
16571915-2	2006	The diacylglycerol kinase (DGK) assay showed that the intracellular concentration of ceramide increased time-dependently after X irradiation of cells, and this radiation-induced accumulation of ceramide did not occur prior to the appearance of apoptotic cells.	Ceramides	85-93	diacylglycerol kinase beta	Homo sapiens	27-30
16571915-2	2006	The diacylglycerol kinase (DGK) assay showed that the intracellular concentration of ceramide increased time-dependently after X irradiation of cells, and this radiation-induced accumulation of ceramide did not occur prior to the appearance of apoptotic cells.	Ceramides	194-202	diacylglycerol kinase beta	Homo sapiens	27-30
16397504-6	2006	Ceramide analogs also induced cell death in Jurkat mutants that are deficient in cell death signaling proteins, including FADD, caspase-8 and 10, and RIP.	Ceramides	0-8	caspase 8	Homo sapiens	128-137
16397504-6	2006	Ceramide analogs also induced cell death in Jurkat mutants that are deficient in cell death signaling proteins, including FADD, caspase-8 and 10, and RIP.	Ceramides	0-8	receptor interacting serine/threonine kinase 1	Homo sapiens	150-153
16477014-3	2006	Here we show by radiotelemetry that the early phase of the fever response to IL-1beta is mediated by ceramide.	Ceramides	101-109	interleukin 1 beta	Homo sapiens	77-85
16477014-0	2006	Ceramide mediates the rapid phase of febrile response to IL-1beta.	Ceramides	0-8	interleukin 1 beta	Homo sapiens	57-65
16636914-6	2006	We validated the upregulation of four such genes (CHK, EIF4EBP1, GADD45A and PTPN-5) by real-time PCR after 3, 6, 9 and 12 h of ceramide treatment in cells that overexpressed parkin or not.	Ceramides	128-136	choline kinase alpha	Rattus norvegicus	50-53
16636914-6	2006	We validated the upregulation of four such genes (CHK, EIF4EBP1, GADD45A and PTPN-5) by real-time PCR after 3, 6, 9 and 12 h of ceramide treatment in cells that overexpressed parkin or not.	Ceramides	128-136	eukaryotic translation initiation factor 4E binding protein 1	Rattus norvegicus	55-63
16636914-6	2006	We validated the upregulation of four such genes (CHK, EIF4EBP1, GADD45A and PTPN-5) by real-time PCR after 3, 6, 9 and 12 h of ceramide treatment in cells that overexpressed parkin or not.	Ceramides	128-136	growth arrest and DNA-damage-inducible, alpha	Rattus norvegicus	65-72
16636914-6	2006	We validated the upregulation of four such genes (CHK, EIF4EBP1, GADD45A and PTPN-5) by real-time PCR after 3, 6, 9 and 12 h of ceramide treatment in cells that overexpressed parkin or not.	Ceramides	128-136	protein tyrosine phosphatase, non-receptor type 5	Rattus norvegicus	77-83
16477014-7	2006	IL-1beta-mediated hyperpolarization is blocked by PP2, the selective inhibitor of the protein tyrosine kinase Src, which is known to be activated by ceramide.	Ceramides	149-157	interleukin 1 beta	Homo sapiens	0-8
16477014-7	2006	IL-1beta-mediated hyperpolarization is blocked by PP2, the selective inhibitor of the protein tyrosine kinase Src, which is known to be activated by ceramide.	Ceramides	149-157	neuropeptide Y receptor Y6 (pseudogene)	Homo sapiens	50-53
16477014-7	2006	IL-1beta-mediated hyperpolarization is blocked by PP2, the selective inhibitor of the protein tyrosine kinase Src, which is known to be activated by ceramide.	Ceramides	149-157	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	110-113
16255717-1	2006	Alkaline sphingomyelinase (alk-SMase) is a new member of the NPP (nucleotide pyrophosphatase/phosphodiesterase) family that hydrolyses SM (sphingomyelin) to generate ceramide in the intestinal tract.	Ceramides	166-174	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	27-36
16216516-0	2006	C-Glycoside analogues of beta-galactosylceramide with a simple ceramide substitute: synthesis and binding to HIV-1 gp120.	Ceramides	40-48	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	115-120
16216516-1	2006	The synthesis and HIV-1 gp120 binding of C- and aza-C-glycoside analogues of beta-galactosylceramide (GalCer) that contain a simple C-17 hydrocarbon chain as a ceramide substitute are described.	Ceramides	92-100	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	24-29
16456021-0	2006	Ceramide-dependent regulation of human epidermal keratinocyte CD1d expression during terminal differentiation.	Ceramides	0-8	CD1d molecule	Homo sapiens	62-66
16456021-5	2006	Increased CD1d gene expression was dependent on ceramide synthesis, because fumonisin B1, a ceramide synthetase inhibitor, blocked the increase in CD1d gene expression during terminal differentiation.	Ceramides	48-56	CD1d molecule	Homo sapiens	10-14
16456021-5	2006	Increased CD1d gene expression was dependent on ceramide synthesis, because fumonisin B1, a ceramide synthetase inhibitor, blocked the increase in CD1d gene expression during terminal differentiation.	Ceramides	48-56	CD1d molecule	Homo sapiens	147-151
16456021-6	2006	Similarly, exogenous ceramide or the ceramidase inhibitor, B13, induced CD1d gene expression by undifferentiated, but not terminally differentiated, KC.	Ceramides	21-29	CD1d molecule	Homo sapiens	72-76
16456021-7	2006	A protein kinase C-zeta (PKC-zeta) inhibitor (a pseudosubstrate oligopeptide), but not a PKC-alphabeta inhibitor, significantly decreased CD1d gene expression by undifferentiated or ceramide-stimulated cultured, undifferentiated KC.	Ceramides	182-190	protein kinase C zeta	Homo sapiens	2-23
16456021-7	2006	A protein kinase C-zeta (PKC-zeta) inhibitor (a pseudosubstrate oligopeptide), but not a PKC-alphabeta inhibitor, significantly decreased CD1d gene expression by undifferentiated or ceramide-stimulated cultured, undifferentiated KC.	Ceramides	182-190	protein kinase C zeta	Homo sapiens	25-33
16456021-7	2006	A protein kinase C-zeta (PKC-zeta) inhibitor (a pseudosubstrate oligopeptide), but not a PKC-alphabeta inhibitor, significantly decreased CD1d gene expression by undifferentiated or ceramide-stimulated cultured, undifferentiated KC.	Ceramides	182-190	CD1d molecule	Homo sapiens	138-142
16183668-0	2006	Ceramide decreases surfactant protein B gene expression via downregulation of TTF-1 DNA binding activity.	Ceramides	0-8	surfactant protein B	Homo sapiens	19-39
16183668-10	2006	Protein kinase C inhibitor bisindolylmaleimide and the protein tyrosine kinase inhibitor genistein partially reversed ceramide inhibition, indicating that protein kinases play important roles in the ceramide inhibition of SP-B gene expression.	Ceramides	118-126	surfactant protein B	Homo sapiens	222-226
16303764-7	2006	Transfection with the yeast gene Lag1 Sc and the human homolog LASS1 increased ceramide levels and partially corrected growth and apoptosis in CLN9-deficient cells.	Ceramides	79-87	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	33-37
16303764-7	2006	Transfection with the yeast gene Lag1 Sc and the human homolog LASS1 increased ceramide levels and partially corrected growth and apoptosis in CLN9-deficient cells.	Ceramides	79-87	ceramide synthase 1	Homo sapiens	63-68
16183668-10	2006	Protein kinase C inhibitor bisindolylmaleimide and the protein tyrosine kinase inhibitor genistein partially reversed ceramide inhibition, indicating that protein kinases play important roles in the ceramide inhibition of SP-B gene expression.	Ceramides	199-207	surfactant protein B	Homo sapiens	222-226
16183668-0	2006	Ceramide decreases surfactant protein B gene expression via downregulation of TTF-1 DNA binding activity.	Ceramides	0-8	transcription termination factor 1	Homo sapiens	78-83
16183668-2	2006	Mediators of acute lung injury such as TNF-alpha, platelet-activating factor, and Fas/Apo ligand stimulate sphingomyelin hydrolysis to increase intracellular ceramide levels.	Ceramides	158-166	tumor necrosis factor	Homo sapiens	39-48
16183668-4	2006	In this study we investigated the effects of ceramide on SP-B gene expression in H441 lung epithelial cells.	Ceramides	45-53	surfactant protein B	Homo sapiens	57-61
16183668-5	2006	Ceramide decreased SP-B mRNA levels in control and dexamethasone-treated cells after 24-h incubation and inhibition of SP-B mRNA was associated with inhibition of immunoreactive SP-B.	Ceramides	0-8	surfactant protein B	Homo sapiens	19-23
16183668-6	2006	In transient transfections assays, ceramide inhibited SP-B promoter activity, indicating that the inhibitory effects are exerted at the transcriptional level.	Ceramides	35-43	surfactant protein B	Homo sapiens	54-58
16183668-7	2006	Deletion mapping experiments showed that the ceramide-responsive region is located within the -233/-80-bp region of human SP-B promoter.	Ceramides	45-53	surfactant protein B	Homo sapiens	122-126
16183668-8	2006	Electrophoretic mobility shift and reporter assays showed that ceramide reduced the DNA binding activity and transactivation capability of thyroid transcription factor 1 (TTF-1/Nkx2.1), a key factor for SP-B promoter activity.	Ceramides	63-71	NK2 homeobox 1	Homo sapiens	139-169
16183668-8	2006	Electrophoretic mobility shift and reporter assays showed that ceramide reduced the DNA binding activity and transactivation capability of thyroid transcription factor 1 (TTF-1/Nkx2.1), a key factor for SP-B promoter activity.	Ceramides	63-71	transcription termination factor 1	Homo sapiens	171-176
16183668-8	2006	Electrophoretic mobility shift and reporter assays showed that ceramide reduced the DNA binding activity and transactivation capability of thyroid transcription factor 1 (TTF-1/Nkx2.1), a key factor for SP-B promoter activity.	Ceramides	63-71	NK2 homeobox 1	Homo sapiens	177-183
16183668-8	2006	Electrophoretic mobility shift and reporter assays showed that ceramide reduced the DNA binding activity and transactivation capability of thyroid transcription factor 1 (TTF-1/Nkx2.1), a key factor for SP-B promoter activity.	Ceramides	63-71	surfactant protein B	Homo sapiens	203-207
16183668-9	2006	Collectively these data showed that ceramide inhibits SP-B gene expression by reducing the DNA biding activity of TTF-1/Nkx2.1 transcription factor.	Ceramides	36-44	surfactant protein B	Homo sapiens	54-58
16183668-9	2006	Collectively these data showed that ceramide inhibits SP-B gene expression by reducing the DNA biding activity of TTF-1/Nkx2.1 transcription factor.	Ceramides	36-44	transcription termination factor 1	Homo sapiens	114-119
16183668-9	2006	Collectively these data showed that ceramide inhibits SP-B gene expression by reducing the DNA biding activity of TTF-1/Nkx2.1 transcription factor.	Ceramides	36-44	NK2 homeobox 1	Homo sapiens	120-126
16201964-4	2006	Ceramide production was measured at normal and increased temperature in an ISC1 deletion and its parental strain (ISC1 being the gene that codes for Isc1p).	Ceramides	0-8	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	75-79
16754199-0	2006	Ceramide mediates TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	18-27
16754199-0	2006	Ceramide mediates TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes.	Ceramides	0-8	insulin	Homo sapiens	36-43
16754199-0	2006	Ceramide mediates TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes.	Ceramides	0-8	solute carrier family 2 member 4	Homo sapiens	58-63
16754199-2	2006	We have explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, since TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	102-110	tumor necrosis factor	Homo sapiens	53-62
16754199-2	2006	We have explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, since TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	102-110	tumor necrosis factor	Homo sapiens	118-127
16754199-2	2006	We have explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, since TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	164-172	tumor necrosis factor	Homo sapiens	53-62
16201964-4	2006	Ceramide production was measured at normal and increased temperature in an ISC1 deletion and its parental strain (ISC1 being the gene that codes for Isc1p).	Ceramides	0-8	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	114-118
16754199-2	2006	We have explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, since TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	164-172	tumor necrosis factor	Homo sapiens	118-127
16754199-3	2006	A short-chain ceramide analogue, C2-ceramide, precluded insulin-induced GLUT4 mRNA accumulation and GLUT4-chloramphenicol acetyltransferase (CAT) full promoter activation.	Ceramides	14-22	insulin	Homo sapiens	56-63
16201964-4	2006	Ceramide production was measured at normal and increased temperature in an ISC1 deletion and its parental strain (ISC1 being the gene that codes for Isc1p).	Ceramides	0-8	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	149-154
16754199-3	2006	A short-chain ceramide analogue, C2-ceramide, precluded insulin-induced GLUT4 mRNA accumulation and GLUT4-chloramphenicol acetyltransferase (CAT) full promoter activation.	Ceramides	14-22	solute carrier family 2 member 4	Homo sapiens	72-77
16754199-3	2006	A short-chain ceramide analogue, C2-ceramide, precluded insulin-induced GLUT4 mRNA accumulation and GLUT4-chloramphenicol acetyltransferase (CAT) full promoter activation.	Ceramides	14-22	solute carrier family 2 member 4	Homo sapiens	100-105
16337960-10	2006	Ceramide plays a crucial role in this process, because prevention of ceramide formation either by myocardial adaptation to ischemia or with desipramine results in the inhibition of eNOS association with caveolin-1 thereby reducing myocardial ischemic reperfusion injury.	Ceramides	0-8	nitric oxide synthase 3	Rattus norvegicus	181-185
16754199-4	2006	Moreover, inhibition of the ceramide biosynthesis with fumonisin B, which inhibits ceramide synthase, completely restored insulin-induced GLUT4 mRNA and protein accumulation as well as GLUT4-CAT transactivation in the presence of TNF-alpha.	Ceramides	28-36	insulin	Homo sapiens	122-129
16754199-4	2006	Moreover, inhibition of the ceramide biosynthesis with fumonisin B, which inhibits ceramide synthase, completely restored insulin-induced GLUT4 mRNA and protein accumulation as well as GLUT4-CAT transactivation in the presence of TNF-alpha.	Ceramides	28-36	solute carrier family 2 member 4	Homo sapiens	138-143
16754199-4	2006	Moreover, inhibition of the ceramide biosynthesis with fumonisin B, which inhibits ceramide synthase, completely restored insulin-induced GLUT4 mRNA and protein accumulation as well as GLUT4-CAT transactivation in the presence of TNF-alpha.	Ceramides	28-36	solute carrier family 2 member 4	Homo sapiens	185-190
16754199-4	2006	Moreover, inhibition of the ceramide biosynthesis with fumonisin B, which inhibits ceramide synthase, completely restored insulin-induced GLUT4 mRNA and protein accumulation as well as GLUT4-CAT transactivation in the presence of TNF-alpha.	Ceramides	28-36	tumor necrosis factor	Homo sapiens	230-239
16754199-8	2006	Our results indicate that de novo ceramide produced by TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes by interfering C/EBP-alpha expression, a transcription factor essential for the expression of GLUT4.	Ceramides	34-42	tumor necrosis factor	Homo sapiens	55-64
16754199-8	2006	Our results indicate that de novo ceramide produced by TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes by interfering C/EBP-alpha expression, a transcription factor essential for the expression of GLUT4.	Ceramides	34-42	insulin	Homo sapiens	73-80
16754199-8	2006	Our results indicate that de novo ceramide produced by TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes by interfering C/EBP-alpha expression, a transcription factor essential for the expression of GLUT4.	Ceramides	34-42	solute carrier family 2 member 4	Homo sapiens	95-100
16754199-8	2006	Our results indicate that de novo ceramide produced by TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes by interfering C/EBP-alpha expression, a transcription factor essential for the expression of GLUT4.	Ceramides	34-42	CCAAT enhancer binding protein alpha	Homo sapiens	152-163
16754199-8	2006	Our results indicate that de novo ceramide produced by TNF-alpha-induced insulin resistance on GLUT4 gene expression in brown adipocytes by interfering C/EBP-alpha expression, a transcription factor essential for the expression of GLUT4.	Ceramides	34-42	solute carrier family 2 member 4	Homo sapiens	231-236
16413574-10	2006	These data indicate that TNF inhibits endothelium-dependent NO-mediated dilation of coronary arterioles by ceramide-induced activation of JNK and subsequent production of superoxide via xanthine oxidase.	Ceramides	107-115	tumor necrosis factor	Homo sapiens	25-28
16413574-10	2006	These data indicate that TNF inhibits endothelium-dependent NO-mediated dilation of coronary arterioles by ceramide-induced activation of JNK and subsequent production of superoxide via xanthine oxidase.	Ceramides	107-115	mitogen-activated protein kinase 8	Homo sapiens	138-141
16337960-10	2006	Ceramide plays a crucial role in this process, because prevention of ceramide formation either by myocardial adaptation to ischemia or with desipramine results in the inhibition of eNOS association with caveolin-1 thereby reducing myocardial ischemic reperfusion injury.	Ceramides	0-8	caveolin 1	Rattus norvegicus	203-213
16337960-10	2006	Ceramide plays a crucial role in this process, because prevention of ceramide formation either by myocardial adaptation to ischemia or with desipramine results in the inhibition of eNOS association with caveolin-1 thereby reducing myocardial ischemic reperfusion injury.	Ceramides	69-77	nitric oxide synthase 3	Rattus norvegicus	181-185
16337960-10	2006	Ceramide plays a crucial role in this process, because prevention of ceramide formation either by myocardial adaptation to ischemia or with desipramine results in the inhibition of eNOS association with caveolin-1 thereby reducing myocardial ischemic reperfusion injury.	Ceramides	69-77	caveolin 1	Rattus norvegicus	203-213
16544881-10	2006	A method using a narrow-bore PVA-Sil column was used to collect ceramide fraction.	Ceramides	64-72	STIL centriolar assembly protein	Homo sapiens	33-36
16358009-0	2006	Chemoenzymatic synthesis of GM3 and GM2 gangliosides containing a truncated ceramide functionalized for glycoconjugate synthesis and solid phase applications.	Ceramides	76-84	granulocyte macrophage antigen 3	Mus musculus	28-31
16479073-0	2006	Ceramides and cell signaling molecules in psoriatic epidermis: reduced levels of ceramides, PKC-alpha, and JNK.	Ceramides	0-9	protein kinase C alpha	Homo sapiens	92-101
16479073-0	2006	Ceramides and cell signaling molecules in psoriatic epidermis: reduced levels of ceramides, PKC-alpha, and JNK.	Ceramides	0-9	mitogen-activated protein kinase 8	Homo sapiens	107-110
16479073-7	2006	The ceramide level was reduced significantly, and this was associated with the downregulation of apoptotic signaling molecules, such as PKC-alpha and JNK, in the lesional epidermis of psoriasis patients.	Ceramides	4-12	protein kinase C alpha	Homo sapiens	136-145
16479073-7	2006	The ceramide level was reduced significantly, and this was associated with the downregulation of apoptotic signaling molecules, such as PKC-alpha and JNK, in the lesional epidermis of psoriasis patients.	Ceramides	4-12	mitogen-activated protein kinase 8	Homo sapiens	150-153
16310170-2	2006	In this study, we show that interleukin-1 beta (IL-1beta) induces an early production of endogenous ceramides via N-sphingomyelinase (N-Smase) as well as an inhibition of adenylyl cyclase activity in pig thyroid cells.	Ceramides	100-109	interleukin-1 beta	Sus scrofa	28-46
16310170-2	2006	In this study, we show that interleukin-1 beta (IL-1beta) induces an early production of endogenous ceramides via N-sphingomyelinase (N-Smase) as well as an inhibition of adenylyl cyclase activity in pig thyroid cells.	Ceramides	100-109	interleukin-1 beta	Sus scrofa	48-56
16310170-8	2006	Our study shows for the first time that endogenous ceramides are important second messengers in IL-1beta-induced apoptosis in pig thyroid cells through inhibition of adenylyl cyclase and ERK1/2 activities.	Ceramides	51-60	interleukin-1 beta	Sus scrofa	96-104
16359673-0	2006	Involvement of de novo ceramide biosynthesis in macrophage death induced by activation of ATP-sensitive P2X7 receptor.	Ceramides	23-31	purinergic receptor P2X 7	Homo sapiens	104-117
16359673-3	2006	Benzoylbenzoyl-ATP, a potent P2X7 agonist, was able to mimic the effects of ATP on ceramide accumulation while oxidized ATP had the opposite effect.	Ceramides	83-91	purinergic receptor P2X 7	Homo sapiens	29-33
16359673-5	2006	Interestingly, ATP-induced caspase-3/7 activation was dependent on ceramide generation.	Ceramides	67-75	caspase 3	Homo sapiens	27-36
16201965-8	2006	Inhibition of the generation of longchain ceramide in response to C6-cer by FB1 or NAC significantly blocked the modulation of the c-Myc/Max function.	Ceramides	42-50	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	131-136
16201965-9	2006	These data demonstrate that the sphingosine-recycling pathway for the generation of endogenous long-chain ceramide in response to exogenous C6-cer is regulated by ROS, and plays an important biological role in controlling c-Myc function.	Ceramides	106-114	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	222-227
16310170-8	2006	Our study shows for the first time that endogenous ceramides are important second messengers in IL-1beta-induced apoptosis in pig thyroid cells through inhibition of adenylyl cyclase and ERK1/2 activities.	Ceramides	51-60	mitogen-activated protein kinase 3	Sus scrofa	187-193
16359673-7	2006	Our results indicate a novel role of ceramide in P2X7-regulated cell-death.	Ceramides	37-45	purinergic receptor P2X 7	Homo sapiens	49-53
16358009-0	2006	Chemoenzymatic synthesis of GM3 and GM2 gangliosides containing a truncated ceramide functionalized for glycoconjugate synthesis and solid phase applications.	Ceramides	76-84	cytochrome b5 domain containing 2	Mus musculus	36-39
16358009-1	2006	Analogues of GM3 and GM2 gangliosides were chemoenzymatically synthesized on a multifunctional ceramide-type tether designed to facilitate diverse strategies for glycoconjugate synthesis.	Ceramides	95-103	granulocyte macrophage antigen 3	Mus musculus	13-16
16358009-1	2006	Analogues of GM3 and GM2 gangliosides were chemoenzymatically synthesized on a multifunctional ceramide-type tether designed to facilitate diverse strategies for glycoconjugate synthesis.	Ceramides	95-103	cytochrome b5 domain containing 2	Mus musculus	21-24
16358009-4	2006	Inhibition experiments showed that antibodies generated by tetanus toxoid conjugates of GM3 and GM2 exhibited specificity for the carbohydrate epitope and the stereogenic centres of the ceramide.	Ceramides	186-194	granulocyte macrophage antigen 3	Mus musculus	88-91
16358009-4	2006	Inhibition experiments showed that antibodies generated by tetanus toxoid conjugates of GM3 and GM2 exhibited specificity for the carbohydrate epitope and the stereogenic centres of the ceramide.	Ceramides	186-194	cytochrome b5 domain containing 2	Mus musculus	96-99
16297852-6	2006	However, mutant p53(143ala) increased the sensitivity of MRC-5 to C(2)-ceramide-induced apoptosis by markedly downregulating Bcl-2, pointing to a role for p53.	Ceramides	71-79	tumor protein p53	Homo sapiens	16-19
16497175-7	2006	Thus, leptin and adiponectin resistance may be an initiating factor in the accumulation of intramuscular lipids, such as diacylglycerol and ceramide, and the ensuing development of insulin resistance.	Ceramides	140-148	leptin	Homo sapiens	6-12
16497175-7	2006	Thus, leptin and adiponectin resistance may be an initiating factor in the accumulation of intramuscular lipids, such as diacylglycerol and ceramide, and the ensuing development of insulin resistance.	Ceramides	140-148	adiponectin, C1Q and collagen domain containing	Homo sapiens	17-28
16497175-7	2006	Thus, leptin and adiponectin resistance may be an initiating factor in the accumulation of intramuscular lipids, such as diacylglycerol and ceramide, and the ensuing development of insulin resistance.	Ceramides	140-148	insulin	Homo sapiens	181-188
16297852-0	2006	Bcl-2 but not clusterin/apolipoprotein J protected human diploid fibroblasts and immortalized keratinocytes from ceramide-induced apoptosis: role of p53 in the ceramide response.	Ceramides	113-121	BCL2 apoptosis regulator	Homo sapiens	0-5
16297852-6	2006	However, mutant p53(143ala) increased the sensitivity of MRC-5 to C(2)-ceramide-induced apoptosis by markedly downregulating Bcl-2, pointing to a role for p53.	Ceramides	71-79	BCL2 apoptosis regulator	Homo sapiens	125-130
16297852-0	2006	Bcl-2 but not clusterin/apolipoprotein J protected human diploid fibroblasts and immortalized keratinocytes from ceramide-induced apoptosis: role of p53 in the ceramide response.	Ceramides	160-168	BCL2 apoptosis regulator	Homo sapiens	0-5
16297852-8	2006	Moreover, the ceramide-activated apoptotic pathway may be regulated by p53.	Ceramides	14-22	tumor protein p53	Homo sapiens	71-74
16787207-1	2006	Ceramide, a product of sphingolipid metabolism, is generated in response to various stress stimuli, such as tumor necrosis factor-alpha, CD95/Fas, chemotherapeutic agents, and irradiation.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	108-135
16696862-1	2006	We previously established a role for the second messenger ceramide in protein kinase R (PKR)-mediated articular cartilage degradation.	Ceramides	58-66	eukaryotic translation initiation factor 2 alpha kinase 2	Bos taurus	70-86
16696862-1	2006	We previously established a role for the second messenger ceramide in protein kinase R (PKR)-mediated articular cartilage degradation.	Ceramides	58-66	eukaryotic translation initiation factor 2 alpha kinase 2	Bos taurus	88-91
16696862-11	2006	Therefore, small increments in endogenous ceramide in chondrocytes appear to push the homeostatic balance toward extracellular matrix synthesis but at the expense of the chondrocytic phenotype, which was, in part, mediated by PKR.	Ceramides	42-50	eukaryotic translation initiation factor 2 alpha kinase 2	Bos taurus	226-229
16787207-1	2006	Ceramide, a product of sphingolipid metabolism, is generated in response to various stress stimuli, such as tumor necrosis factor-alpha, CD95/Fas, chemotherapeutic agents, and irradiation.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	137-141
16971166-0	2006	Thrombospondin-1 C-terminal-derived peptide protects thyroid cells from ceramide-induced apoptosis through the adenylyl cyclase pathway.	Ceramides	72-80	thrombospondin 1	Homo sapiens	0-16
16971166-3	2006	In this work, we examined the role of thrombospondin-1 in ceramide-induced thyroid apoptosis.	Ceramides	58-66	thrombospondin 1	Homo sapiens	38-54
16971166-8	2006	Furthermore, we demonstrated that the thrombospondin-1-derived peptide 4N1 (RFYVVMWK) abolished ceramide-induced thyroid cell death by preventing intracellular cAMP levels from dropping.	Ceramides	96-104	thrombospondin 1	Homo sapiens	38-54
16971166-9	2006	Finally, we reported that 4N1-mediated inhibition of ceramide-induced apoptosis was consistently associated with a down-regulation of the caspase-3 processing.	Ceramides	53-61	caspase 3	Homo sapiens	138-147
16277606-7	2006	In addition, the intracellular signaling intermediate from the TNFR1 receptor, ceramide, caused a similar increase in CGRP release.	Ceramides	79-87	TNF receptor superfamily member 1A	Rattus norvegicus	63-68
16424801-1	2006	We have previously demonstrated that tumor necrosis factor alpha (TNFalpha), a cytokine known to be induced by ischemia, independently promotes preconditioning in part via ceramide generation.	Ceramides	172-180	tumor necrosis factor	Homo sapiens	37-64
16424801-1	2006	We have previously demonstrated that tumor necrosis factor alpha (TNFalpha), a cytokine known to be induced by ischemia, independently promotes preconditioning in part via ceramide generation.	Ceramides	172-180	tumor necrosis factor	Homo sapiens	66-74
16424801-2	2006	As reactive oxygen species (ROS) signaling is evoked by ischemic preconditioning, by TNFalpha and by ceramide we reasoned that ceramide-induced preconditioning is ROS-mediated.	Ceramides	127-135	tumor necrosis factor	Homo sapiens	85-93
16424801-4	2006	Pretreatment with ceramide reduced lactate dehydrogenase release at the end of the simulated ischemia but this cytoprotective effect was lost in the presence of MPG.	Ceramides	18-26	N-methylpurine DNA glycosylase	Homo sapiens	161-164
16424801-6	2006	Ceramide increased ROS production after 30 minutes and this induction was decreased by MPG.	Ceramides	0-8	N-methylpurine DNA glycosylase	Homo sapiens	87-90
16424801-7	2006	Incubation of ceramide with cyclooxygenase-2 inhibitor, NS 398 (10 microM), or with a mitochondrial respiratory chain inhibitor, rotenone (10 microM) reduced the cytoprotective effect of ceramide in parallel with a partial diminution in ROS generation.	Ceramides	14-22	prostaglandin-endoperoxide synthase 2	Homo sapiens	28-44
16951918-1	2006	Farber disease is a rare lysosomal storage disorder caused by a deficiency of the acid ceramidase enzyme, leading to the accumulation of ceramide in various tissues.	Ceramides	137-145	N-acylsphingosine amidohydrolase 1	Homo sapiens	82-97
16277606-7	2006	In addition, the intracellular signaling intermediate from the TNFR1 receptor, ceramide, caused a similar increase in CGRP release.	Ceramides	79-87	calcitonin-related polypeptide alpha	Rattus norvegicus	118-122
16424801-7	2006	Incubation of ceramide with cyclooxygenase-2 inhibitor, NS 398 (10 microM), or with a mitochondrial respiratory chain inhibitor, rotenone (10 microM) reduced the cytoprotective effect of ceramide in parallel with a partial diminution in ROS generation.	Ceramides	187-195	prostaglandin-endoperoxide synthase 2	Homo sapiens	28-44
16281067-6	2006	Incubation with cell-permeable ceramide of chemoresistant cells led to a sphingosine kinase-1 inhibition and apoptosis both prevented by sphingosine kinase-1 over-expression.	Ceramides	31-39	sphingosine kinase 1	Homo sapiens	73-93
16281067-6	2006	Incubation with cell-permeable ceramide of chemoresistant cells led to a sphingosine kinase-1 inhibition and apoptosis both prevented by sphingosine kinase-1 over-expression.	Ceramides	31-39	sphingosine kinase 1	Homo sapiens	137-157
16189296-6	2006	Together, these findings indicate that LAQ824-induced lethality represents a multifactorial process in which LAQ824-mediated ROS generation is necessary but not sufficient to induce apoptosis, and that the degree of XIAP and Mcl-1 down-regulation and ceramide generation determines whether this agent engages a maturation rather than an apoptotic program.	Ceramides	251-259	X-linked inhibitor of apoptosis	Homo sapiens	216-220
16175636-4	2006	Second, treatment with either PR antagonists or a cell permeable ceramide analog consistently increases SUMO-1 expression in parallel with an increase in apoptosis as well as a decrease in cell proliferation in periovulatory granulosa cells in vitro.	Ceramides	65-73	small ubiquitin-like modifier 1	Mus musculus	104-110
16416005-1	2006	Glucosylceramide synthase (GCS), the enzyme that converts ceramide to glucosylceramide, induce multidrug resistance (MDR) in cancer cells.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
16143399-5	2006	Ceramide caused activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 1	Mus musculus	30-67
16143399-5	2006	Ceramide caused activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 1	Mus musculus	69-72
16143399-5	2006	Ceramide caused activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 8	Mus musculus	78-101
16143399-5	2006	Ceramide caused activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 8	Mus musculus	103-106
16143399-7	2006	Ceramide induced an increase in Bax expression, depolarization of mitochondrial membrane potential, and caspase activation.	Ceramides	0-8	BCL2-associated X protein	Mus musculus	32-35
16143399-9	2006	These results suggest that activation of ERK and JNK is involved in ceramide-induced apoptosis through a mitochondria-dependent pathway in astrocytes.	Ceramides	68-76	mitogen-activated protein kinase 1	Mus musculus	41-44
16143399-9	2006	These results suggest that activation of ERK and JNK is involved in ceramide-induced apoptosis through a mitochondria-dependent pathway in astrocytes.	Ceramides	68-76	mitogen-activated protein kinase 8	Mus musculus	49-52
16500425-1	2005	Acid ceramidase (AC; E.C.3.5.1.23) activity is required to hydrolyze ceramide into sphingosine.	Ceramides	69-77	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
16445986-0	2006	Ceramides in insulin resistance and lipotoxicity.	Ceramides	0-9	insulin	Homo sapiens	13-20
16445986-7	2006	In this review, I will evaluate the contribution of ceramides in the development of insulin resistance and the complications associated with metabolic diseases.	Ceramides	52-61	insulin	Homo sapiens	84-91
16500425-1	2005	Acid ceramidase (AC; E.C.3.5.1.23) activity is required to hydrolyze ceramide into sphingosine.	Ceramides	69-77	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
16357153-0	2005	Cyclooxygenase-2 inhibition sensitizes human colon carcinoma cells to TRAIL-induced apoptosis through clustering of DR5 and concentrating death-inducing signaling complex components into ceramide-enriched caveolae.	Ceramides	187-195	prostaglandin-endoperoxide synthase 2	Homo sapiens	0-16
16357178-4	2005	SphK1 overexpression in both cell lines impaired the efficacy of chemotherapy by decreasing the ceramide/S1P ratio.	Ceramides	96-104	sphingosine kinase 1	Mus musculus	0-5
16357178-5	2005	Alternatively, silencing SphK1 by RNA interference or pharmacologic inhibition induced apoptosis coupled with ceramide elevation and loss of S1P.	Ceramides	110-118	sphingosine kinase 1	Mus musculus	25-30
16263092-7	2005	However, only the ceramide-like compound PDMP inhibited the expression of activation markers and the secretion of IFN-gamma which was not seen with myriocin treatment.	Ceramides	18-26	interferon gamma	Homo sapiens	114-123
16226406-1	2005	Sphingomyelin synthase 1 (SMS1) is a recently identified 413-residue protein that plays a critical role in sphingolipid metabolism by catalyzing the conversion of ceramide and phosphatidylcholine to sphingomyelin and diacylglycerol (DAG).	Ceramides	163-171	sphingomyelin synthase 1	Mus musculus	0-24
16226406-1	2005	Sphingomyelin synthase 1 (SMS1) is a recently identified 413-residue protein that plays a critical role in sphingolipid metabolism by catalyzing the conversion of ceramide and phosphatidylcholine to sphingomyelin and diacylglycerol (DAG).	Ceramides	163-171	sphingomyelin synthase 1	Mus musculus	26-30
16357153-3	2005	We have shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistribution of the death-inducing signaling complex components (DR5, FADD, and procaspase-8) into cholesterol-rich and ceramide-rich domains known as caveolae.	Ceramides	359-367	prostaglandin-endoperoxide synthase 2	Homo sapiens	19-24
16357153-3	2005	We have shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistribution of the death-inducing signaling complex components (DR5, FADD, and procaspase-8) into cholesterol-rich and ceramide-rich domains known as caveolae.	Ceramides	359-367	TNF superfamily member 10	Homo sapiens	78-133
16357153-3	2005	We have shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistribution of the death-inducing signaling complex components (DR5, FADD, and procaspase-8) into cholesterol-rich and ceramide-rich domains known as caveolae.	Ceramides	359-367	TNF superfamily member 10	Homo sapiens	135-140
16357153-3	2005	We have shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistribution of the death-inducing signaling complex components (DR5, FADD, and procaspase-8) into cholesterol-rich and ceramide-rich domains known as caveolae.	Ceramides	359-367	TNF superfamily member 10	Homo sapiens	190-195
16357153-0	2005	Cyclooxygenase-2 inhibition sensitizes human colon carcinoma cells to TRAIL-induced apoptosis through clustering of DR5 and concentrating death-inducing signaling complex components into ceramide-enriched caveolae.	Ceramides	187-195	TNF superfamily member 10	Homo sapiens	70-75
16357153-3	2005	We have shown that COX-2 inhibition sensitizes human colon carcinoma cells to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)-induced apoptosis by inducing clustering of the TRAIL receptor DR5 at the cell surface and the redistribution of the death-inducing signaling complex components (DR5, FADD, and procaspase-8) into cholesterol-rich and ceramide-rich domains known as caveolae.	Ceramides	359-367	TNF receptor superfamily member 10b	Homo sapiens	205-208
16357153-0	2005	Cyclooxygenase-2 inhibition sensitizes human colon carcinoma cells to TRAIL-induced apoptosis through clustering of DR5 and concentrating death-inducing signaling complex components into ceramide-enriched caveolae.	Ceramides	187-195	TNF receptor superfamily member 10b	Homo sapiens	116-119
16290312-6	2005	Analysis of the signal transduction pathways revealed that IGF-I induces CREB phosphorylation via PI-3K and ERK, whereas simultaneous ceramide and IGF-I treatment decreases CREB phosphorylation.	Ceramides	134-142	cAMP responsive element binding protein 1	Homo sapiens	173-177
16290312-0	2005	IGF-I protects cortical neurons against ceramide-induced apoptosis via activation of the PI-3K/Akt and ERK pathways; is this protection independent of CREB and Bcl-2?	Ceramides	40-48	insulin like growth factor 1	Homo sapiens	0-5
16290312-0	2005	IGF-I protects cortical neurons against ceramide-induced apoptosis via activation of the PI-3K/Akt and ERK pathways; is this protection independent of CREB and Bcl-2?	Ceramides	40-48	AKT serine/threonine kinase 1	Homo sapiens	95-98
16290312-7	2005	Although an overexpression of Bcl-2 protects cortical neurons against ceramide-induced apoptosis, our data indicate that the Bcl-2 protein level is not modulated during IGF-I, ceramide and/or LY294002 treatment.	Ceramides	70-78	BCL2 apoptosis regulator	Homo sapiens	30-35
16290312-0	2005	IGF-I protects cortical neurons against ceramide-induced apoptosis via activation of the PI-3K/Akt and ERK pathways; is this protection independent of CREB and Bcl-2?	Ceramides	40-48	mitogen-activated protein kinase 1	Homo sapiens	103-106
16290312-4	2005	We show that IGF-I protects cortical neurons against ceramide-induced apoptosis.	Ceramides	53-61	insulin like growth factor 1	Homo sapiens	13-18
16162942-8	2005	These results show that SM and ceramide in the lipoproteins and the cell membranes regulate the SR-BI-mediated selective uptake of CE, possibly by interacting with the sterol ring or with SR-BI itself.	Ceramides	31-39	scavenger receptor class B member 1	Homo sapiens	96-101
16290312-5	2005	Ceramide decreases Akt phosphorylation during apoptotic process whereas a simultaneous treatment with IGF-I increases Akt phosphorylation.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	19-22
16215670-7	2005	Ectopic expression of Bcl-2 appeared to inhibit ceramide-, and Akt specific inhibitor (SH-6)-induced apoptosis by sustained Akt activation.	Ceramides	48-56	BCL2 apoptosis regulator	Homo sapiens	22-27
16274459-0	2005	The EP3 receptor stimulates ceramide and diacylglycerol release and inhibits growth of primary keratinocytes.	Ceramides	28-36	prostaglandin E receptor 3	Homo sapiens	4-7
16278342-6	2005	These results demonstrate that in endothelial cells submitted to hypoxia and glucose depletion followed by reoxygenation with glucose, the pathway implicated in mitochondrial complex III ROS production is ceramide dependent and is decreased by the antiapoptotic protein Bcl-2.	Ceramides	205-213	BCL2 apoptosis regulator	Homo sapiens	270-275
15953673-0	2005	Interleukin-1beta (IL-1beta) induces a crosstalk between cAMP and ceramide signaling pathways in thyroid epithelial cells.	Ceramides	66-74	interleukin 1 beta	Homo sapiens	0-17
15953673-0	2005	Interleukin-1beta (IL-1beta) induces a crosstalk between cAMP and ceramide signaling pathways in thyroid epithelial cells.	Ceramides	66-74	interleukin 1 beta	Homo sapiens	19-27
16018771-11	2005	The appearance of ACBP very early on in evolution points towards a fundamental role of ACBP in acyl-CoA metabolism, including ceramide synthesis and in signalling.	Ceramides	126-134	diazepam binding inhibitor, acyl-CoA binding protein	Homo sapiens	18-22
16018771-11	2005	The appearance of ACBP very early on in evolution points towards a fundamental role of ACBP in acyl-CoA metabolism, including ceramide synthesis and in signalling.	Ceramides	126-134	diazepam binding inhibitor, acyl-CoA binding protein	Homo sapiens	87-91
16274459-8	2005	These data suggest that EP3 receptors produce epidermal growth inhibition through the action of DAG and ceramide second messengers.	Ceramides	104-112	prostaglandin E receptor 3	Homo sapiens	24-27
16319138-3	2005	Under conditions where apoptosis is either not initiated or actively inhibited, TNF induces caspase-independent PCD in L929 fibrosarcoma cells, NIH3T3 fibroblasts, human leukemic Jurkat T cells, and lung fibroblasts by increasing intracellular ceramide levels prior to the onset of cell death.	Ceramides	244-252	tumor necrosis factor	Mus musculus	80-83
16319138-4	2005	Survival is significantly enhanced when ceramide accumulation is prevented, as demonstrated in fibroblasts genetically deficient for acid sphingomyelinase, in L929 cells overexpressing acid ceramidase, by pharmacological intervention, or by RNA interference.	Ceramides	40-48	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	133-154
16319138-4	2005	Survival is significantly enhanced when ceramide accumulation is prevented, as demonstrated in fibroblasts genetically deficient for acid sphingomyelinase, in L929 cells overexpressing acid ceramidase, by pharmacological intervention, or by RNA interference.	Ceramides	40-48	N-acylsphingosine amidohydrolase 1	Mus musculus	185-200
16162942-8	2005	These results show that SM and ceramide in the lipoproteins and the cell membranes regulate the SR-BI-mediated selective uptake of CE, possibly by interacting with the sterol ring or with SR-BI itself.	Ceramides	31-39	scavenger receptor class B member 1	Homo sapiens	188-193
16170208-4	2005	The results indicate that the ability of CERK to recognize ceramide as a substrate is stereospecific.	Ceramides	59-67	ceramide kinase	Homo sapiens	41-45
16170208-11	2005	Together, these results indicate a very high specificity for substrate recognition by CERK, explaining the use of ceramide and not sphingosine or diacylglycerol as substrates.	Ceramides	114-122	ceramide kinase	Homo sapiens	86-90
16166077-1	2005	Carboxyl ester lipase (CEL, also called cholesterol esterase or bile salt-dependent lipase) is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, triacylglycerols, and phospholipids in a trihydroxy bile salt-dependent manner but hydrolyzes ceramides and lysophospholipids via bile salt-independent mechanisms.	Ceramides	251-260	carboxyl ester lipase	Mus musculus	0-21
16166077-1	2005	Carboxyl ester lipase (CEL, also called cholesterol esterase or bile salt-dependent lipase) is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, triacylglycerols, and phospholipids in a trihydroxy bile salt-dependent manner but hydrolyzes ceramides and lysophospholipids via bile salt-independent mechanisms.	Ceramides	251-260	carboxyl ester lipase	Mus musculus	23-26
16166077-1	2005	Carboxyl ester lipase (CEL, also called cholesterol esterase or bile salt-dependent lipase) is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, triacylglycerols, and phospholipids in a trihydroxy bile salt-dependent manner but hydrolyzes ceramides and lysophospholipids via bile salt-independent mechanisms.	Ceramides	251-260	carboxyl ester lipase	Mus musculus	40-60
16166077-6	2005	The differences in cholesteryl ester accumulation were attributed to the lower levels of ceramide and lysophosphatidylcholine in CEL-expressing cells than in CEL-negative cells.	Ceramides	89-97	carboxyl ester lipase	Mus musculus	129-132
16166077-9	2005	These studies documented that CEL expression in macrophages is pro-atherogenic and that the mechanism is because of its hydrolysis of ceramide and lysophosphatidylcholine in promoting cholesterol esterification and decreasing cholesterol efflux.	Ceramides	134-142	carboxyl ester lipase	Mus musculus	30-33
16344602-4	2005	RESULTS: Studies in experimental animal models of the disease have provided evidence for the role of ceramide generated from acidic sphingomyelinase in the apoptotic signaling of TNF through recruitment of mitochondria.	Ceramides	101-109	tumor necrosis factor	Homo sapiens	179-182
16263765-0	2005	Downregulation of the HERG (KCNH2) K(+) channel by ceramide: evidence for ubiquitin-mediated lysosomal degradation.	Ceramides	51-59	potassium voltage-gated channel subfamily H member 2	Homo sapiens	22-26
16263765-0	2005	Downregulation of the HERG (KCNH2) K(+) channel by ceramide: evidence for ubiquitin-mediated lysosomal degradation.	Ceramides	51-59	potassium voltage-gated channel subfamily H member 2	Homo sapiens	28-33
16263765-5	2005	Here we show, using stable HERG-expressing HEK 293 cells, that ceramide evokes a time-dependent decrease in HERG current which was not attributable to a change in gating properties of the channel.	Ceramides	63-71	potassium voltage-gated channel subfamily H member 2	Homo sapiens	27-31
16263765-5	2005	Here we show, using stable HERG-expressing HEK 293 cells, that ceramide evokes a time-dependent decrease in HERG current which was not attributable to a change in gating properties of the channel.	Ceramides	63-71	potassium voltage-gated channel subfamily H member 2	Homo sapiens	108-112
16263765-6	2005	Surface expression of the HERG channel protein was reduced by ceramide as shown by biotinylation of surface proteins, western blotting and immunocytochemistry.	Ceramides	62-70	potassium voltage-gated channel subfamily H member 2	Homo sapiens	26-30
16263765-7	2005	The rapid decline in HERG protein after ceramide stimulation was due to protein ubiquitylation and its association with lysosomes.	Ceramides	40-48	potassium voltage-gated channel subfamily H member 2	Homo sapiens	21-25
16263765-8	2005	The results demonstrate that the surface expression of HERG is strictly regulated, and that ceramide modifies HERG currents and targets the protein for lysosomal degradation.	Ceramides	92-100	potassium voltage-gated channel subfamily H member 2	Homo sapiens	110-114
16118219-9	2005	Importantly, specific down-regulation of SphK2 reduced conversion of sphingosine to ceramide in the recycling pathway and conversely, down-regulation of SphK1 increased it.	Ceramides	84-92	sphingosine kinase 2	Homo sapiens	41-46
16118219-10	2005	Our results demonstrate that SphK1 and SphK2 have opposing roles in the regulation of ceramide biosynthesis and suggest that the location of sphingosine 1-phosphate production dictates its functions.	Ceramides	86-94	sphingosine kinase 1	Homo sapiens	29-34
16118219-10	2005	Our results demonstrate that SphK1 and SphK2 have opposing roles in the regulation of ceramide biosynthesis and suggest that the location of sphingosine 1-phosphate production dictates its functions.	Ceramides	86-94	sphingosine kinase 2	Homo sapiens	39-44
16126722-0	2005	Involvement of neutral ceramidase in ceramide metabolism at the plasma membrane and in extracellular milieu.	Ceramides	37-45	N-acylsphingosine amidohydrolase 2	Homo sapiens	15-33
16126722-2	2005	We found that when overexpressed in CHOP cells, neutral ceramidase hydrolyzed cell surface ceramide, which increased in amount after the treatment of cells with bacterial sphingomyelinase, leading to an increase in the cellular level of sphingosine and sphingosine 1-phosphate.	Ceramides	91-99	N-acylsphingosine amidohydrolase 2	Homo sapiens	48-66
16106045-0	2005	Ceramide- and ERK-dependent pathway for the activation of CCAAT/enhancer binding protein by interleukin-1beta in hepatocytes.	Ceramides	0-8	CCAAT enhancer binding protein alpha	Homo sapiens	58-88
16020509-6	2005	Moreover, we provide evidence that the protective effect of GM-CSF is related to its capacity to interfere with both ceramide generation and ceramide signaling.	Ceramides	117-125	colony stimulating factor 2	Homo sapiens	60-66
16020509-6	2005	Moreover, we provide evidence that the protective effect of GM-CSF is related to its capacity to interfere with both ceramide generation and ceramide signaling.	Ceramides	141-149	colony stimulating factor 2	Homo sapiens	60-66
16106045-0	2005	Ceramide- and ERK-dependent pathway for the activation of CCAAT/enhancer binding protein by interleukin-1beta in hepatocytes.	Ceramides	0-8	interleukin 1 beta	Homo sapiens	92-109
16106045-3	2005	Activation of sphingomyelinase (SMase) and the subsequent generation of ceramide are early steps in the IL-1beta signaling cascade.	Ceramides	72-80	interleukin 1 beta	Homo sapiens	104-112
16106045-4	2005	In this study, we investigate the role of ceramide in the IL-1beta regulation of C/EBP in primary hepatocytes.	Ceramides	42-50	interleukin 1 beta	Homo sapiens	58-66
16106045-4	2005	In this study, we investigate the role of ceramide in the IL-1beta regulation of C/EBP in primary hepatocytes.	Ceramides	42-50	CCAAT enhancer binding protein alpha	Homo sapiens	81-86
16106045-7	2005	Both IL-1beta and ceramide led to extracellular signal-regulated kinase 1/2 (ERK1/2) activation as early as 15 min after treatment.	Ceramides	18-26	mitogen-activated protein kinase 1	Homo sapiens	34-75
16106045-7	2005	Both IL-1beta and ceramide led to extracellular signal-regulated kinase 1/2 (ERK1/2) activation as early as 15 min after treatment.	Ceramides	18-26	mitogen-activated protein kinase 3	Homo sapiens	77-83
16106045-8	2005	Furthermore, the increase of cellular ceramide content resulted in increased phosphorylation of C/EBPbeta at serine 105 at later time points.	Ceramides	38-46	CCAAT enhancer binding protein beta	Homo sapiens	96-105
16106045-9	2005	Concurrently, the cytosolic levels of C/EBPbeta decreased, suggesting that IL-1beta and ceramide induced nuclear translocation of C/EBPbeta.	Ceramides	88-96	CCAAT enhancer binding protein beta	Homo sapiens	38-47
16245071-1	2005	Acid sphingomyelinase (A-SMase) and its reaction product ceramide may play a role in the pathophysiology of depressive disorders and in the therapeutic action of antidepressive drugs.	Ceramides	57-65	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
16106045-9	2005	Concurrently, the cytosolic levels of C/EBPbeta decreased, suggesting that IL-1beta and ceramide induced nuclear translocation of C/EBPbeta.	Ceramides	88-96	CCAAT enhancer binding protein beta	Homo sapiens	130-139
16245071-1	2005	Acid sphingomyelinase (A-SMase) and its reaction product ceramide may play a role in the pathophysiology of depressive disorders and in the therapeutic action of antidepressive drugs.	Ceramides	57-65	sphingomyelin phosphodiesterase 1	Homo sapiens	23-30
16106045-10	2005	Ceramide-induced C/EBPbeta phosphorylation, translocation, and DNA binding were suppressed by the addition of PD98059, an inhibitor of ERK1/2 phosphorylation.	Ceramides	0-8	CCAAT enhancer binding protein beta	Homo sapiens	17-26
16106045-10	2005	Ceramide-induced C/EBPbeta phosphorylation, translocation, and DNA binding were suppressed by the addition of PD98059, an inhibitor of ERK1/2 phosphorylation.	Ceramides	0-8	mitogen-activated protein kinase 3	Homo sapiens	135-141
16106045-11	2005	These results suggest that ceramide and ERK mediate a pathway in the IL-1beta signaling cascade, which results in rapid posttranslational activation of C/EBPbeta.	Ceramides	27-35	interleukin 1 beta	Homo sapiens	69-77
16106045-11	2005	These results suggest that ceramide and ERK mediate a pathway in the IL-1beta signaling cascade, which results in rapid posttranslational activation of C/EBPbeta.	Ceramides	27-35	CCAAT enhancer binding protein beta	Homo sapiens	152-161
16129666-5	2005	Next, using the luciferase reporter assay in both C. neoformans wild-type and GAL7:IPC1 strains, we investigated the role of DAG and sphingolipids in the activation of the APP1 promoter and found that treatment with 1,2-dioctanoylglycerol does increase APP1 transcription, whereas treatment with phytosphingosine or ceramides does not.	Ceramides	316-325	X-prolyl aminopeptidase 1	Homo sapiens	172-176
16231160-2	2005	The present study was designed to investigate the effects of ceramide and its key initial regulators, TNF-alpha and neutral sphingomyelinase (SMase), on vascular tone of isolated rat thoracic aortic rings and elucidate the mechanisms involved in the changes in vascular tone induced by ceramide.	Ceramides	61-69	tumor necrosis factor	Rattus norvegicus	102-111
16231160-2	2005	The present study was designed to investigate the effects of ceramide and its key initial regulators, TNF-alpha and neutral sphingomyelinase (SMase), on vascular tone of isolated rat thoracic aortic rings and elucidate the mechanisms involved in the changes in vascular tone induced by ceramide.	Ceramides	286-294	tumor necrosis factor	Rattus norvegicus	102-111
16231160-10	2005	Furthermore, inhibition of phenylephrine-induced activation of RhoA/Rho-kinase pathway as well as phenylephrine-induced elevations in [Ca2+]i are clearly a key factors in C2-ceramide-induced vasodilation.	Ceramides	174-182	ras homolog family member A	Rattus norvegicus	63-67
16042758-6	2005	In the adult and aging brain, PLD activity has antiapoptotic properties suppressing ceramide formation.	Ceramides	84-92	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	30-33
16007138-7	2005	In the subclass with better survival, genes involved in differentiated intracellular functions, such as the MAPKKK cascade, ceramide metabolism, or regulation of transcription, were upregulated.	Ceramides	124-132	mitogen-activated protein kinase kinase kinase 4	Homo sapiens	108-114
16140251-2	2005	In this article, we report a new reliable method to determine GlcT and GalT activities using the fluorescent acceptor substrates C6-4-nitrobenzo-2-oxa-1,3-diazole (NBD)-ceramide and C6-NBD-glucosylceramide, respectively, and a normal-phase high-performance liquid chromatography (HPLC).	Ceramides	169-177	UDP-glucose ceramide glucosyltransferase	Danio rerio	62-66
16140251-2	2005	In this article, we report a new reliable method to determine GlcT and GalT activities using the fluorescent acceptor substrates C6-4-nitrobenzo-2-oxa-1,3-diazole (NBD)-ceramide and C6-NBD-glucosylceramide, respectively, and a normal-phase high-performance liquid chromatography (HPLC).	Ceramides	169-177	galactose-1-phosphate uridylyltransferase	Danio rerio	71-75
16151633-3	2005	This was tested by analyzing caspase-dependent/independent pathways and autophagy, and caspase effects on ceramide and Golgi fragmentation.	Ceramides	106-114	caspase 6	Homo sapiens	87-94
16151633-13	2005	CLN3, not zVAD, prevented ceramide elevation.	Ceramides	26-34	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
16151633-14	2005	IN CONCLUSION: caspase-dependent/independent apoptosis and autophagy occur caspase-dependent pathways initiate autophagy Golgi fragmentation results from apoptosis ceramide elevation is independent of caspases, and CLN3 blocks all cell death, prevents Golgi fragmentation and elevation of ceramide in JNCL.	Ceramides	164-172	caspase 6	Homo sapiens	15-22
16151633-14	2005	IN CONCLUSION: caspase-dependent/independent apoptosis and autophagy occur caspase-dependent pathways initiate autophagy Golgi fragmentation results from apoptosis ceramide elevation is independent of caspases, and CLN3 blocks all cell death, prevents Golgi fragmentation and elevation of ceramide in JNCL.	Ceramides	164-172	caspase 6	Homo sapiens	75-82
16151633-14	2005	IN CONCLUSION: caspase-dependent/independent apoptosis and autophagy occur caspase-dependent pathways initiate autophagy Golgi fragmentation results from apoptosis ceramide elevation is independent of caspases, and CLN3 blocks all cell death, prevents Golgi fragmentation and elevation of ceramide in JNCL.	Ceramides	164-172	caspase 6	Homo sapiens	201-209
16151633-14	2005	IN CONCLUSION: caspase-dependent/independent apoptosis and autophagy occur caspase-dependent pathways initiate autophagy Golgi fragmentation results from apoptosis ceramide elevation is independent of caspases, and CLN3 blocks all cell death, prevents Golgi fragmentation and elevation of ceramide in JNCL.	Ceramides	164-172	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	215-219
16151633-14	2005	IN CONCLUSION: caspase-dependent/independent apoptosis and autophagy occur caspase-dependent pathways initiate autophagy Golgi fragmentation results from apoptosis ceramide elevation is independent of caspases, and CLN3 blocks all cell death, prevents Golgi fragmentation and elevation of ceramide in JNCL.	Ceramides	289-297	caspase 6	Homo sapiens	15-22
16151633-14	2005	IN CONCLUSION: caspase-dependent/independent apoptosis and autophagy occur caspase-dependent pathways initiate autophagy Golgi fragmentation results from apoptosis ceramide elevation is independent of caspases, and CLN3 blocks all cell death, prevents Golgi fragmentation and elevation of ceramide in JNCL.	Ceramides	289-297	caspase 6	Homo sapiens	75-82
16151633-14	2005	IN CONCLUSION: caspase-dependent/independent apoptosis and autophagy occur caspase-dependent pathways initiate autophagy Golgi fragmentation results from apoptosis ceramide elevation is independent of caspases, and CLN3 blocks all cell death, prevents Golgi fragmentation and elevation of ceramide in JNCL.	Ceramides	289-297	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	215-219
16174294-4	2005	We have earlier reported that LPS/Abeta stimulation-induced ceramide and ROS generation leads to iNOS expression and nitric oxide production in glial cells.	Ceramides	60-68	nitric oxide synthase 2	Rattus norvegicus	97-101
16225875-3	2005	We found that ceramide can induce peroxide oxidation and lead to accumulation of TNF-alpha in animal organs.	Ceramides	14-22	tumor necrosis factor	Mus musculus	81-90
15907365-2	2005	In SH-SY5Y neuroblastoma cells, evidence suggests that acid sphingomyelinase activity is essential for the induction of ceramide and apoptosis in response to fenretinide.	Ceramides	120-128	sphingomyelin phosphodiesterase 1	Homo sapiens	55-76
15966860-5	2005	The p75NTR-dependent effect requires NGF (nerve growth factor) binding and activation of the second messenger ceramide.	Ceramides	110-118	nerve growth factor receptor	Homo sapiens	4-10
15966860-8	2005	In contrast with caloric restriction, which prevents the age-associated up-regulation of p75NTR expression, nSMase inhibitors block the activation of ceramide.	Ceramides	150-158	sphingomyelin phosphodiesterase 2	Homo sapiens	108-114
15966860-9	2005	When taken together, these results indicate that the p75NTR-ceramide signalling pathway activates the rate of Abeta generation in an age-dependent fashion, and provide a new target for both the understanding and the prevention of late-onset AD.	Ceramides	60-68	nerve growth factor receptor	Homo sapiens	53-59
15966860-9	2005	When taken together, these results indicate that the p75NTR-ceramide signalling pathway activates the rate of Abeta generation in an age-dependent fashion, and provide a new target for both the understanding and the prevention of late-onset AD.	Ceramides	60-68	amyloid beta precursor protein	Homo sapiens	110-115
15978826-16	2005	CSA is able to inhibit ceramide glucosylation and modulate MDR phenotype.	Ceramides	23-31	ERCC excision repair 8, CSA ubiquitin ligase complex subunit	Homo sapiens	0-3
16180087-0	2005	Ceramide activates a mitochondrial p38 mitogen-activated protein kinase: a potential mechanism for loss of mitochondrial transmembrane potential and apoptosis.	Ceramides	0-8	adapter molecule crk	Gallus gallus	35-38
16180087-1	2005	This study examined the impact of ceramide, an intracellular mediator of apoptosis, on the mitochondria to test the hypothesis that ceramide utilized p38 MAPK in the mitochondria to alter mitochondrial potential and induce apoptosis.	Ceramides	132-140	adapter molecule crk	Gallus gallus	150-153
16180087-3	2005	p38 MAPK was identified in the mitochondrial fraction of the cell and p38 MAPK phosphorylation in this mitochondrial fraction of the cell occurred with ceramide treatment.	Ceramides	152-160	adapter molecule crk	Gallus gallus	0-3
16180087-3	2005	p38 MAPK was identified in the mitochondrial fraction of the cell and p38 MAPK phosphorylation in this mitochondrial fraction of the cell occurred with ceramide treatment.	Ceramides	152-160	adapter molecule crk	Gallus gallus	70-73
16180087-5	2005	The p38 MAPK inhibitor SB 202190 but not the MEK inhibitor PD 98059 significantly inhibited ceramide-induced apoptosis and loss of DeltaPsim.	Ceramides	92-100	adapter molecule crk	Gallus gallus	4-7
16180087-6	2005	These data suggest that p38 MAPK is present in the mitochondria and its activation by ceramide indicates local signaling more directly coupled to the mitochondrial pathway in apoptosis.	Ceramides	86-94	adapter molecule crk	Gallus gallus	24-27
15823095-0	2005	Mammalian Lass6 and its related family members regulate synthesis of specific ceramides.	Ceramides	78-87	ceramide synthase 6	Homo sapiens	10-15
16170023-0	2005	Resistance to TRAIL is associated with defects in ceramide signaling that can be overcome by exogenous C6-ceramide without requiring down-regulation of cellular FLICE inhibitory protein.	Ceramides	50-58	TNF superfamily member 10	Homo sapiens	14-19
16170023-6	2005	Mass spectrometry was used to compare ceramide content in untreated and TRAIL-treated cells.	Ceramides	38-46	TNF superfamily member 10	Homo sapiens	72-77
16170023-7	2005	Overall levels of ceramide were comparable in the cell lines but TRAIL-sensitive SW480 cells contained a higher percentage of C(16)-, and C(18)-ceramide and lower C(24)-ceramides than TRAIL-resistant SW620 cells.	Ceramides	18-26	TNF superfamily member 10	Homo sapiens	65-70
16170023-7	2005	Overall levels of ceramide were comparable in the cell lines but TRAIL-sensitive SW480 cells contained a higher percentage of C(16)-, and C(18)-ceramide and lower C(24)-ceramides than TRAIL-resistant SW620 cells.	Ceramides	144-152	TNF superfamily member 10	Homo sapiens	65-70
16170023-7	2005	Overall levels of ceramide were comparable in the cell lines but TRAIL-sensitive SW480 cells contained a higher percentage of C(16)-, and C(18)-ceramide and lower C(24)-ceramides than TRAIL-resistant SW620 cells.	Ceramides	169-178	TNF superfamily member 10	Homo sapiens	65-70
16170023-8	2005	Upon TRAIL treatment, ceramide (primarily C(16)-ceramide) increased in SW480 but not SW620 cells.	Ceramides	22-30	TNF superfamily member 10	Homo sapiens	5-10
16170023-9	2005	The increase in ceramide occurred with slow kinetics, paralleling caspase-3/7 activation.	Ceramides	16-24	caspase 3	Homo sapiens	66-75
16170023-12	2005	Exposure to TRAIL prior to ceramide was required to induce apoptosis, suggesting that ceramide plays a role in enhancing or amplifying TRAIL-mediated signaling.	Ceramides	86-94	TNF superfamily member 10	Homo sapiens	12-17
16170023-12	2005	Exposure to TRAIL prior to ceramide was required to induce apoptosis, suggesting that ceramide plays a role in enhancing or amplifying TRAIL-mediated signaling.	Ceramides	86-94	TNF superfamily member 10	Homo sapiens	135-140
16170023-13	2005	Our results suggest that ceramide plays a role in promoting TRAIL-mediated apoptosis and that TRAIL-resistant cancers may benefit from combination therapy with ceramide or agents that enhance ceramide accumulation.	Ceramides	25-33	TNF superfamily member 10	Homo sapiens	60-65
16170023-13	2005	Our results suggest that ceramide plays a role in promoting TRAIL-mediated apoptosis and that TRAIL-resistant cancers may benefit from combination therapy with ceramide or agents that enhance ceramide accumulation.	Ceramides	160-168	TNF superfamily member 10	Homo sapiens	94-99
16170023-13	2005	Our results suggest that ceramide plays a role in promoting TRAIL-mediated apoptosis and that TRAIL-resistant cancers may benefit from combination therapy with ceramide or agents that enhance ceramide accumulation.	Ceramides	160-168	TNF superfamily member 10	Homo sapiens	94-99
15856005-2	2005	Here, we demonstrate that FGF-2 is also a potent stimulator of breast cancer cell survival, as it counteracts the apoptotic activity of the C2 ceramide analogue and various chemotherapeutic agents (5-fluorouracil, camptothecin, etoposide) in MCF-7, T47-D and BT-20 cells.	Ceramides	143-151	fibroblast growth factor 2	Homo sapiens	26-31
15823095-5	2005	Overproduction of Lass1 increased C18:0-ceramide levels preferentially, and overproduction of Lass2 and Lass4 increased levels of longer ceramides such as C22:0- and C24:0-ceramides.	Ceramides	40-48	ceramide synthase 1	Homo sapiens	18-23
15823095-5	2005	Overproduction of Lass1 increased C18:0-ceramide levels preferentially, and overproduction of Lass2 and Lass4 increased levels of longer ceramides such as C22:0- and C24:0-ceramides.	Ceramides	137-146	ceramide synthase 2	Homo sapiens	94-99
15823095-5	2005	Overproduction of Lass1 increased C18:0-ceramide levels preferentially, and overproduction of Lass2 and Lass4 increased levels of longer ceramides such as C22:0- and C24:0-ceramides.	Ceramides	137-146	ceramide synthase 4	Homo sapiens	104-109
15823095-5	2005	Overproduction of Lass1 increased C18:0-ceramide levels preferentially, and overproduction of Lass2 and Lass4 increased levels of longer ceramides such as C22:0- and C24:0-ceramides.	Ceramides	172-181	ceramide synthase 2	Homo sapiens	94-99
15823095-5	2005	Overproduction of Lass1 increased C18:0-ceramide levels preferentially, and overproduction of Lass2 and Lass4 increased levels of longer ceramides such as C22:0- and C24:0-ceramides.	Ceramides	172-181	ceramide synthase 4	Homo sapiens	104-109
15823095-6	2005	Lass5 and Lass6 produced shorter ceramide species (C14:0- and C16:0-ceramides); however, their substrate preferences towards saturated/unsaturated fatty acyl-CoA differed.	Ceramides	33-41	ceramide synthase 5	Homo sapiens	0-5
15823095-6	2005	Lass5 and Lass6 produced shorter ceramide species (C14:0- and C16:0-ceramides); however, their substrate preferences towards saturated/unsaturated fatty acyl-CoA differed.	Ceramides	33-41	ceramide synthase 6	Homo sapiens	10-15
15800925-3	2005	Here we show that LPS induces cyclooxygenase (COX) 2 by activating sphingomyelinases leading to the release of ceramides, which in turn, activate the p38 mitogen-activated protein kinases (MAPK), but not the p42/44 MAPK.	Ceramides	111-120	mitogen activated protein kinase 14	Rattus norvegicus	150-153
15823095-6	2005	Lass5 and Lass6 produced shorter ceramide species (C14:0- and C16:0-ceramides); however, their substrate preferences towards saturated/unsaturated fatty acyl-CoA differed.	Ceramides	68-77	ceramide synthase 5	Homo sapiens	0-5
15800925-4	2005	We further show that exogenously added ceramide analogue (C2-ceramide) also induce PGE2 synthesis through a p38 MAPK-dependent pathway.	Ceramides	39-47	mitogen activated protein kinase 14	Rattus norvegicus	108-111
15823095-6	2005	Lass5 and Lass6 produced shorter ceramide species (C14:0- and C16:0-ceramides); however, their substrate preferences towards saturated/unsaturated fatty acyl-CoA differed.	Ceramides	68-77	ceramide synthase 6	Homo sapiens	10-15
16081073-1	2005	Ceramide kinase (CERK) converts ceramide (Cer) to ceramide-1-phosphate (C1P), a newly recognized bioactive molecule capable of regulating diverse cellular functions.	Ceramides	32-40	ceramide kinase	Homo sapiens	0-15
15968641-0	2005	Ceramide regulation of the tumor suppressor phosphatase PTEN in rafts isolated from neurotumor cell lines.	Ceramides	0-8	phosphatase and tensin homolog	Homo sapiens	56-60
15968641-2	2005	Here we present evidence that ceramide recruits the tumor suppressor PTEN (phosphatase and tensin homolog deleted from chromosome 10) into membrane microdomains (rafts), where it could act to reduce the levels of polyphosphoinositides necessary for the activation of Akt.	Ceramides	30-38	phosphatase and tensin homolog	Homo sapiens	69-73
15968641-2	2005	Here we present evidence that ceramide recruits the tumor suppressor PTEN (phosphatase and tensin homolog deleted from chromosome 10) into membrane microdomains (rafts), where it could act to reduce the levels of polyphosphoinositides necessary for the activation of Akt.	Ceramides	30-38	AKT serine/threonine kinase 1	Homo sapiens	267-270
16081073-1	2005	Ceramide kinase (CERK) converts ceramide (Cer) to ceramide-1-phosphate (C1P), a newly recognized bioactive molecule capable of regulating diverse cellular functions.	Ceramides	32-40	ceramide kinase	Homo sapiens	17-21
16081073-1	2005	Ceramide kinase (CERK) converts ceramide (Cer) to ceramide-1-phosphate (C1P), a newly recognized bioactive molecule capable of regulating diverse cellular functions.	Ceramides	0-3	ceramide kinase	Homo sapiens	17-21
15863835-0	2005	Ceramide displaces cholesterol from lipid rafts and decreases the association of the cholesterol binding protein caveolin-1.	Ceramides	0-8	caveolin 1	Homo sapiens	113-123
15951564-1	2005	In this study, the roles of Sp1/Sp3 transcription factors in the regulation of the activity of human telomerase reverse transcriptase (hTERT) promoter in response to ceramide were examined in the A549 human lung adenocarcinoma cells.	Ceramides	166-174	Sp3 transcription factor	Homo sapiens	32-35
15951564-1	2005	In this study, the roles of Sp1/Sp3 transcription factors in the regulation of the activity of human telomerase reverse transcriptase (hTERT) promoter in response to ceramide were examined in the A549 human lung adenocarcinoma cells.	Ceramides	166-174	telomerase reverse transcriptase	Homo sapiens	101-133
15951564-1	2005	In this study, the roles of Sp1/Sp3 transcription factors in the regulation of the activity of human telomerase reverse transcriptase (hTERT) promoter in response to ceramide were examined in the A549 human lung adenocarcinoma cells.	Ceramides	166-174	telomerase reverse transcriptase	Homo sapiens	135-140
15951564-2	2005	The activity of the N-terminal truncated hTERT promoter, lacking the c-Myc recognition (E-box) region but containing multiple Sp1/Sp3 sites, was also significantly inhibited by C6-ceramide, indicating a role for ceramide in the regulation of Sp1/Sp3 function.	Ceramides	180-188	telomerase reverse transcriptase	Homo sapiens	41-46
15951564-5	2005	The interaction between Sp1 and hTERT promoter DNA was significantly reduced in response to ceramide as assessed by chromatin immunoprecipitation analysis.	Ceramides	92-100	telomerase reverse transcriptase	Homo sapiens	32-37
15951564-7	2005	Furthermore, mutations of various Sp1/Sp3 recognition sequences significantly attenuated the activity of the promoter in the presence or absence of ceramide, demonstrating the importance of multiple Sp1/Sp3 recognition sites for the promoter activity.	Ceramides	148-156	Sp3 transcription factor	Homo sapiens	38-41
15951564-7	2005	Furthermore, mutations of various Sp1/Sp3 recognition sequences significantly attenuated the activity of the promoter in the presence or absence of ceramide, demonstrating the importance of multiple Sp1/Sp3 recognition sites for the promoter activity.	Ceramides	148-156	Sp3 transcription factor	Homo sapiens	203-206
15951564-9	2005	The roles of endogenous long chain ceramide generated in response to gemcitabine in the inhibition of hTERT promoter activity and the regulation of Sp3 acetylation were also demonstrated.	Ceramides	35-43	telomerase reverse transcriptase	Homo sapiens	102-107
15951564-9	2005	The roles of endogenous long chain ceramide generated in response to gemcitabine in the inhibition of hTERT promoter activity and the regulation of Sp3 acetylation were also demonstrated.	Ceramides	35-43	Sp3 transcription factor	Homo sapiens	148-151
16061638-4	2005	When Darpp-32 and t-Darpp were overexpressed in AGS and RKO gastrointestinal cells, up to a 4-fold reduction in the apoptosis rate was observed (terminal deoxynucleotidyl transferase-mediated nick-end labeling and Annexin V assays) in response to camptothecin, sodium butyrate, and ceramide.	Ceramides	282-290	protein phosphatase 1 regulatory inhibitor subunit 1B	Homo sapiens	5-13
16026583-3	2005	We recently showed that epidermal acid sphingomyelinase (A-SMase) generates ceramides with structural function in the stratum corneum lipid bilayers, which provide for the permeability barrier function of the skin.	Ceramides	76-85	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	34-55
16026583-3	2005	We recently showed that epidermal acid sphingomyelinase (A-SMase) generates ceramides with structural function in the stratum corneum lipid bilayers, which provide for the permeability barrier function of the skin.	Ceramides	76-85	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	57-64
15863835-6	2005	Ceramide-induced cholesterol depletion increased the association of 5"-nucleotidase and ATP synthase beta-subunit with the CEMs but had a minimal effect on changing the abundance of other lipid raft proteins, such as flotillin-1 and G-proteins.	Ceramides	0-8	5'-nucleotidase ecto	Homo sapiens	68-83
15863835-6	2005	Ceramide-induced cholesterol depletion increased the association of 5"-nucleotidase and ATP synthase beta-subunit with the CEMs but had a minimal effect on changing the abundance of other lipid raft proteins, such as flotillin-1 and G-proteins.	Ceramides	0-8	flotillin 1	Homo sapiens	217-228
16009715-1	2005	Engagement of the Fas receptor (CD95) initiates multiple signaling pathways that lead to apoptosis, such as the formation of death-inducing signaling complex (DISC), activation of caspase cascades, and the generation of the lipid messenger, ceramide.	Ceramides	241-249	Fas cell surface death receptor	Homo sapiens	32-36
16043028-7	2005	Part of these events is mediated by mitogen-activated protein kinases (MAPKs) and tyrosine kinases (e.g., Src) and leads to the modulation of survival and apoptotic factors [e.g., Bcl2 family members, inhibitors of apoptosis (IAPs), ceramide] as well as enzymes involved in carcinogenesis [cyclooxygenases (COXs), nitric oxide synthase (NOS), phase I and II enzymes].	Ceramides	233-241	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	106-109
16043028-7	2005	Part of these events is mediated by mitogen-activated protein kinases (MAPKs) and tyrosine kinases (e.g., Src) and leads to the modulation of survival and apoptotic factors [e.g., Bcl2 family members, inhibitors of apoptosis (IAPs), ceramide] as well as enzymes involved in carcinogenesis [cyclooxygenases (COXs), nitric oxide synthase (NOS), phase I and II enzymes].	Ceramides	233-241	nitric oxide synthase 2	Homo sapiens	314-335
15997205-1	2005	Acid sphingomyelinase (ASM) is the lysosomal enzyme responsible for the hydrolysis of sphingomyelin to ceramide and phosphocholine.	Ceramides	103-111	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
15997205-1	2005	Acid sphingomyelinase (ASM) is the lysosomal enzyme responsible for the hydrolysis of sphingomyelin to ceramide and phosphocholine.	Ceramides	103-111	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
16033420-4	2005	Abeta, TNF-alpha, or the combination of both, increased neutral sphingomyelinase (nSMase) activity, but not acidic sphingomyelinase (aSMase) activity, leading to ceramide accumulation.	Ceramides	162-170	tumor necrosis factor	Homo sapiens	7-16
16014908-6	2005	Our data indicate that p13(II)-expressing Jurkat T cells are sensitive to caspase-dependent, ceramide- and FasL-induced apoptosis.	Ceramides	93-101	H3 histone pseudogene 6	Homo sapiens	23-26
15946935-1	2005	Tumor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	Ceramides	98-106	tumor necrosis factor	Rattus norvegicus	0-33
15946935-1	2005	Tumor necrosis factor (TNF)-alpha signals cell death and simultaneously induces the generation of ceramide, which is metabolized to sphingosine and sphingosine 1-phosphate (S1P) by ceramidase (CDase) and sphingosine kinase.	Ceramides	98-106	membrane-bound transcription factor peptidase, site 1	Rattus norvegicus	173-176
15917250-5	2005	CD95L induced within 1 min ceramide formation and serine phosphorylation of p47phox, which was sensitive to inhibitors of sphingomyelinase and protein kinase Czeta (PKCzeta).	Ceramides	27-35	Fas ligand	Rattus norvegicus	0-5
15917250-6	2005	These inhibitors and p47phox protein knockdown inhibited the early CD95L-induced ROS response, suggesting that ceramide and PKCzeta are upstream events of the CD95L-induced Nox/Duox activation.	Ceramides	111-119	neutrophil cytosolic factor 1	Rattus norvegicus	21-28
15917250-6	2005	These inhibitors and p47phox protein knockdown inhibited the early CD95L-induced ROS response, suggesting that ceramide and PKCzeta are upstream events of the CD95L-induced Nox/Duox activation.	Ceramides	111-119	Fas ligand	Rattus norvegicus	67-72
15917250-6	2005	These inhibitors and p47phox protein knockdown inhibited the early CD95L-induced ROS response, suggesting that ceramide and PKCzeta are upstream events of the CD95L-induced Nox/Duox activation.	Ceramides	111-119	Fas ligand	Rattus norvegicus	159-164
16009715-6	2005	Furthermore, WR/Fas-SMS1 cells, but not WR/Fas-SM(-) cells, showed a considerable increase in ceramide generation within lipid rafts upon Fas stimulation.	Ceramides	94-102	sphingomyelin synthase 1	Homo sapiens	13-24
15849201-6	2005	Translocation of the secretory form of acid sphingomyelinase (ASMase) into microscopic rafts generates therein the ceramide that drives raft coalescence.	Ceramides	115-123	sphingomyelin phosphodiesterase 1	Homo sapiens	39-60
15901738-0	2005	Direct binding to ceramide activates protein kinase Czeta before the formation of a pro-apoptotic complex with PAR-4 in differentiating stem cells.	Ceramides	18-26	pro-apoptotic WT1 regulator	Homo sapiens	111-116
15901738-1	2005	We have reported that ceramide mediates binding of atypical protein kinase C (PKC) zeta to its inhibitor protein, PAR-4 (prostate apoptosis response-4), thereby inducing apoptosis in differentiating embryonic stem cells.	Ceramides	22-30	protein kinase C zeta	Homo sapiens	78-81
15901738-1	2005	We have reported that ceramide mediates binding of atypical protein kinase C (PKC) zeta to its inhibitor protein, PAR-4 (prostate apoptosis response-4), thereby inducing apoptosis in differentiating embryonic stem cells.	Ceramides	22-30	pro-apoptotic WT1 regulator	Homo sapiens	114-119
15901738-1	2005	We have reported that ceramide mediates binding of atypical protein kinase C (PKC) zeta to its inhibitor protein, PAR-4 (prostate apoptosis response-4), thereby inducing apoptosis in differentiating embryonic stem cells.	Ceramides	22-30	pro-apoptotic WT1 regulator	Homo sapiens	121-150
15901738-2	2005	Using a novel method of lipid vesicle-mediated affinity chromatography, we showed here that endogenous ceramide binds directly to the PKCzeta.PAR-4 complex.	Ceramides	103-111	protein kinase C zeta	Homo sapiens	134-141
15901738-2	2005	Using a novel method of lipid vesicle-mediated affinity chromatography, we showed here that endogenous ceramide binds directly to the PKCzeta.PAR-4 complex.	Ceramides	103-111	pro-apoptotic WT1 regulator	Homo sapiens	142-147
15901738-3	2005	Ceramide and its analogs activated PKCzeta prior to binding to PAR-4, as determined by increased levels of phosphorylated PKCzeta and glycogen synthase kinase-3beta and emergence of a PAR-4-to-phosphorylated PKCzeta fluorescence resonance energy transfer signal that co-localizes with ceramide.	Ceramides	0-8	protein kinase C zeta	Homo sapiens	35-42
15901738-3	2005	Ceramide and its analogs activated PKCzeta prior to binding to PAR-4, as determined by increased levels of phosphorylated PKCzeta and glycogen synthase kinase-3beta and emergence of a PAR-4-to-phosphorylated PKCzeta fluorescence resonance energy transfer signal that co-localizes with ceramide.	Ceramides	0-8	pro-apoptotic WT1 regulator	Homo sapiens	63-68
15901738-3	2005	Ceramide and its analogs activated PKCzeta prior to binding to PAR-4, as determined by increased levels of phosphorylated PKCzeta and glycogen synthase kinase-3beta and emergence of a PAR-4-to-phosphorylated PKCzeta fluorescence resonance energy transfer signal that co-localizes with ceramide.	Ceramides	0-8	protein kinase C zeta	Homo sapiens	122-129
15901738-3	2005	Ceramide and its analogs activated PKCzeta prior to binding to PAR-4, as determined by increased levels of phosphorylated PKCzeta and glycogen synthase kinase-3beta and emergence of a PAR-4-to-phosphorylated PKCzeta fluorescence resonance energy transfer signal that co-localizes with ceramide.	Ceramides	0-8	glycogen synthase kinase 3 beta	Homo sapiens	134-164
15901738-3	2005	Ceramide and its analogs activated PKCzeta prior to binding to PAR-4, as determined by increased levels of phosphorylated PKCzeta and glycogen synthase kinase-3beta and emergence of a PAR-4-to-phosphorylated PKCzeta fluorescence resonance energy transfer signal that co-localizes with ceramide.	Ceramides	0-8	pro-apoptotic WT1 regulator	Homo sapiens	184-189
15901738-3	2005	Ceramide and its analogs activated PKCzeta prior to binding to PAR-4, as determined by increased levels of phosphorylated PKCzeta and glycogen synthase kinase-3beta and emergence of a PAR-4-to-phosphorylated PKCzeta fluorescence resonance energy transfer signal that co-localizes with ceramide.	Ceramides	0-8	protein kinase C zeta	Homo sapiens	122-129
15901738-6	2005	A luciferase reporter assay showed that ceramide analogs activate nuclear factor (NF)-kappaB unless PAR-4-dependent inhibition of PKCzeta suppresses NF-kappaB activation.	Ceramides	40-48	nuclear factor kappa B subunit 1	Homo sapiens	66-92
15901738-6	2005	A luciferase reporter assay showed that ceramide analogs activate nuclear factor (NF)-kappaB unless PAR-4-dependent inhibition of PKCzeta suppresses NF-kappaB activation.	Ceramides	40-48	pro-apoptotic WT1 regulator	Homo sapiens	100-105
15901738-6	2005	A luciferase reporter assay showed that ceramide analogs activate nuclear factor (NF)-kappaB unless PAR-4-dependent inhibition of PKCzeta suppresses NF-kappaB activation.	Ceramides	40-48	protein kinase C zeta	Homo sapiens	130-137
15901738-7	2005	Taken together, our results show that direct physical association with ceramide and PAR-4 regulates the activity of PKCzeta.	Ceramides	71-79	protein kinase C zeta	Homo sapiens	116-123
15849201-6	2005	Translocation of the secretory form of acid sphingomyelinase (ASMase) into microscopic rafts generates therein the ceramide that drives raft coalescence.	Ceramides	115-123	sphingomyelin phosphodiesterase 1	Homo sapiens	62-68
15849201-7	2005	This process serves to feed forward Fas activation, with approximately 2% of full caspase 8 activation sufficient for maximal ASMase translocation, leading to death-inducing signaling complex formation within ceramide-rich platforms, and apoptosis.	Ceramides	209-217	caspase 8	Homo sapiens	82-91
15929065-3	2005	Overexpression of palmitoyl:protein thioesterase (PPT1; verified by Western blot of the V5-tagged protein and increased enzyme activity) resulted in decreased ceramide in the detergent-resistant microdomain (DRM, or raft) relative to cholesterol and sphingomyelin (SM).	Ceramides	159-167	palmitoyl-protein thioesterase 1	Homo sapiens	50-54
15849201-7	2005	This process serves to feed forward Fas activation, with approximately 2% of full caspase 8 activation sufficient for maximal ASMase translocation, leading to death-inducing signaling complex formation within ceramide-rich platforms, and apoptosis.	Ceramides	209-217	sphingomyelin phosphodiesterase 1	Homo sapiens	126-132
15929065-5	2005	In contrast, overexpression of neutral sphingomyelinase 2 (NSMase2; verified by Western blot of the FLAG-tagged protein and increased enzyme activity) resulted in increased membrane NSMase and increased ceramide in rafts relative to cholesterol and SM.	Ceramides	203-211	sphingomyelin phosphodiesterase 3	Homo sapiens	31-57
15929065-5	2005	In contrast, overexpression of neutral sphingomyelinase 2 (NSMase2; verified by Western blot of the FLAG-tagged protein and increased enzyme activity) resulted in increased membrane NSMase and increased ceramide in rafts relative to cholesterol and SM.	Ceramides	203-211	sphingomyelin phosphodiesterase 3	Homo sapiens	59-66
15929065-5	2005	In contrast, overexpression of neutral sphingomyelinase 2 (NSMase2; verified by Western blot of the FLAG-tagged protein and increased enzyme activity) resulted in increased membrane NSMase and increased ceramide in rafts relative to cholesterol and SM.	Ceramides	203-211	sphingomyelin phosphodiesterase 2	Homo sapiens	59-65
15849201-8	2005	Here we report that treatment of Jurkat T cells with UV-C also induces ASMase translocation into rafts within 1 min, catalyzing sphingomyelin hydrolysis to ceramide and raft clustering.	Ceramides	156-164	sphingomyelin phosphodiesterase 1	Homo sapiens	71-77
15978590-5	2005	Based on these and our previous observations, we propose a working model for C1P in which inhibition of acid sphingomyelinase and the subsequent decrease in ceramide levels would allow cell signaling through stimulation of the PI3-K/PKB pathway to promote cell survival.	Ceramides	157-165	AKT serine/threonine kinase 1	Homo sapiens	233-236
15894290-4	2005	In Jurkat cells overexpressing mutant MnSOD, however, DEVDase activation and ceramide formation were promoted post-Pc 4-PDT.	Ceramides	77-85	superoxide dismutase 2	Homo sapiens	38-43
15894290-5	2005	Similarly, in MnSOD-null cells, Pc 4-PDT-induced apoptosis, as well as ceramide accumulation, were enhanced compared to their normal counterparts.	Ceramides	71-79	superoxide dismutase 2	Homo sapiens	14-19
15894290-6	2005	The data show that MnSOD affects sensitivity of cells to Pc 4-PDT-initiated apoptosis, and partly ceramide accumulation, suggesting that the processes are superoxide-mediated.	Ceramides	98-106	superoxide dismutase 2	Homo sapiens	19-24
15741222-0	2005	Thalidomide-induced antiangiogenic action is mediated by ceramide through depletion of VEGF receptors, and is antagonized by sphingosine-1-phosphate.	Ceramides	57-65	vascular endothelial growth factor A	Homo sapiens	87-91
15741222-4	2005	Transient increase of ceramide content through activation of neutral sphingomyelinase (nSMase) precedes thalidomide-induced vascular defect in the embryos.	Ceramides	22-30	sphingomyelin phosphodiesterase 2	Homo sapiens	61-85
15741222-4	2005	Transient increase of ceramide content through activation of neutral sphingomyelinase (nSMase) precedes thalidomide-induced vascular defect in the embryos.	Ceramides	22-30	sphingomyelin phosphodiesterase 2	Homo sapiens	87-93
15741222-6	2005	The blockade of ceramide generation by antisense morpholino oligonucleotides for nSMase prevents thalidomide-induced ceramide generation and vascular defect.	Ceramides	16-24	sphingomyelin phosphodiesterase 2	Homo sapiens	81-87
15741222-6	2005	The blockade of ceramide generation by antisense morpholino oligonucleotides for nSMase prevents thalidomide-induced ceramide generation and vascular defect.	Ceramides	117-125	sphingomyelin phosphodiesterase 2	Homo sapiens	81-87
15741222-7	2005	In contrast to ceramide, sphingosine-1-phosphate (S1P) inhibits nSMase-dependent ceramide generation and restores thalidomide-induced embryonic vascular defect with an increase of expression of VEGF receptors.	Ceramides	81-89	sphingomyelin phosphodiesterase 2	Homo sapiens	64-70
15741222-8	2005	In human umbilical vein endothelial cells (HUVECs), thalidomide-induced inhibition of cell growth, generation of ceramide through nSMase, and depletion of VEGF receptors are restored to the control levels by pretreatment with S1P.	Ceramides	113-121	sphingomyelin phosphodiesterase 2	Homo sapiens	130-136
15942662-4	2005	On the other hand, viability of HBL-2 cells was decreased by SM treatment with neuraminidase pre-treatment after 6 and 24 h of incubation, and ceramide production on cell surfaces of SM treated cells was enhanced by neuraminidase treatment as shown by flow cytometric analysis.	Ceramides	143-151	neuraminidase 1	Homo sapiens	216-229
15942662-7	2005	Together these data suggest that alteration in susceptibility of HBL-2 cells to SM by neuraminidase treatment may precede the process of ceramide production, and that cell death through the activation of SM, which induces ceramide production, is regulated by cell surface sialylation in DLBCL.	Ceramides	137-145	neuraminidase 1	Homo sapiens	86-99
15905098-5	2005	Inhibitors of the p38 MAP kinase pathway (SB-202190 or SB-203580) and an inhibitor of the ERK1/2 pathway (U0126) reduced ceramide-induced neuronal death.	Ceramides	121-129	mitogen-activated protein kinase 14	Homo sapiens	18-32
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	steroidogenic acute regulatory protein	Homo sapiens	112-118
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 3	Homo sapiens	119-125
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 5	Homo sapiens	126-132
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 5	Homo sapiens	134-140
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	phosphatidylcholine transfer protein	Homo sapiens	142-148
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 10	Homo sapiens	149-156
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	StAR related lipid transfer domain containing 10	Homo sapiens	158-165
15976441-3	2005	Cholesterol, 25-hydroxycholesterol, phosphatidylcholine, phosphatidylethanolamine and ceramides are ligands for STARD1/STARD3/STARD5, STARD5, STARD2/STARD10, STARD10 and STARD11, respectively.	Ceramides	86-95	ceramide transporter 1	Homo sapiens	170-177
15905098-3	2005	Ceramide induced the translocation of certain, but not all, pro-apoptotic mitochondrial proteins: cytochrome c, Omi, SMAC, and AIF were released from the mitochondria, whereas Endonuclease G was not.	Ceramides	0-8	cytochrome c, somatic	Homo sapiens	98-110
15905098-3	2005	Ceramide induced the translocation of certain, but not all, pro-apoptotic mitochondrial proteins: cytochrome c, Omi, SMAC, and AIF were released from the mitochondria, whereas Endonuclease G was not.	Ceramides	0-8	diablo IAP-binding mitochondrial protein	Homo sapiens	117-121
15905098-3	2005	Ceramide induced the translocation of certain, but not all, pro-apoptotic mitochondrial proteins: cytochrome c, Omi, SMAC, and AIF were released from the mitochondria, whereas Endonuclease G was not.	Ceramides	0-8	apoptosis inducing factor mitochondria associated 1	Homo sapiens	127-130
15905098-4	2005	Ceramide also selectively altered the phosphorylation state of members of the MAPK superfamily, causing dephosphorylation of ERK1/2 and hyperphosphorylation of p38 MAP kinases, but not affecting the phosphorylation of JNK or ERK5.	Ceramides	0-8	mitogen-activated protein kinase 3	Homo sapiens	78-82
15905098-4	2005	Ceramide also selectively altered the phosphorylation state of members of the MAPK superfamily, causing dephosphorylation of ERK1/2 and hyperphosphorylation of p38 MAP kinases, but not affecting the phosphorylation of JNK or ERK5.	Ceramides	0-8	mitogen-activated protein kinase 3	Homo sapiens	125-131
15905098-4	2005	Ceramide also selectively altered the phosphorylation state of members of the MAPK superfamily, causing dephosphorylation of ERK1/2 and hyperphosphorylation of p38 MAP kinases, but not affecting the phosphorylation of JNK or ERK5.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	218-221
15905098-4	2005	Ceramide also selectively altered the phosphorylation state of members of the MAPK superfamily, causing dephosphorylation of ERK1/2 and hyperphosphorylation of p38 MAP kinases, but not affecting the phosphorylation of JNK or ERK5.	Ceramides	0-8	mitogen-activated protein kinase 7	Homo sapiens	225-229
15817701-9	2005	Exogenous addition of SMase or ceramide mimicked the effects of TNFR1 signals on Ca(2+) responses in Jurkat T cells.	Ceramides	31-39	TNF receptor superfamily member 1A	Homo sapiens	64-69
15905098-5	2005	Inhibitors of the p38 MAP kinase pathway (SB-202190 or SB-203580) and an inhibitor of the ERK1/2 pathway (U0126) reduced ceramide-induced neuronal death.	Ceramides	121-129	mitogen-activated protein kinase 3	Homo sapiens	90-96
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	48-56	mitogen-activated protein kinase 14	Homo sapiens	6-9
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	48-56	mitogen-activated protein kinase 3	Homo sapiens	14-20
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	48-56	cytochrome c, somatic	Homo sapiens	161-173
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	48-56	apoptosis inducing factor mitochondria associated 1	Homo sapiens	180-183
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	48-56	diablo IAP-binding mitochondrial protein	Homo sapiens	189-193
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	48-56	caspase 3	Homo sapiens	232-241
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	215-223	mitogen-activated protein kinase 14	Homo sapiens	6-9
15905098-6	2005	These p38 and ERK1/2 inhibitors appear to block ceramide-activated apoptotic signaling upstream of the mitochondria, as they attenuated mitochondrial release of cytochrome c, Omi, AIF, and SMAC, as well as reducing ceramide-induced caspase-3 activation.	Ceramides	215-223	mitogen-activated protein kinase 3	Homo sapiens	14-20
15817474-3	2005	We have previously shown that newly synthesized Pma1p is mistargeted to the vacuole in an elo3Delta mutant that affects the synthesis of the ceramide-bound C26 very long chain fatty acid (Eisenkolb, M., Zenzmaier, C., Leitner, E., and Schneiter, R. (2002) Mol.	Ceramides	141-149	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	48-53
16000722-2	2005	beta-Glucuronidase activity plays a major role in the generation of toxic and carcinogenic metabolites in the large intestine, as well as in the absorption and enterohepatic circulation of many aglycone residues with protective effects, such as lignans, flavonoids, ceramide and glycyrrhetinic acid, that are liberated by the hydrolysis of the corresponding glucuronides.	Ceramides	266-274	glucuronidase beta	Homo sapiens	0-18
15817479-0	2005	Bcl-2 rescues ceramide- and etoposide-induced mitochondrial apoptosis through blockage of caspase-2 activation.	Ceramides	14-22	BCL2 apoptosis regulator	Homo sapiens	0-5
15817479-0	2005	Bcl-2 rescues ceramide- and etoposide-induced mitochondrial apoptosis through blockage of caspase-2 activation.	Ceramides	14-22	caspase 2	Homo sapiens	90-99
15817479-4	2005	Stress stimuli, including ceramide and etoposide, caused caspase-2 activation, mitochondrial damage followed by downstream caspase-9 and -3 activation, and cell apoptosis in human lung epithelial cell line A549.	Ceramides	26-34	caspase 2	Homo sapiens	57-66
15817479-4	2005	Stress stimuli, including ceramide and etoposide, caused caspase-2 activation, mitochondrial damage followed by downstream caspase-9 and -3 activation, and cell apoptosis in human lung epithelial cell line A549.	Ceramides	26-34	caspase 9	Homo sapiens	123-139
15817479-6	2005	Overexpression of Bcl-2 prevented ceramide- and etoposide-induced caspase-2 activation and mitochondrial apoptosis.	Ceramides	34-42	BCL2 apoptosis regulator	Homo sapiens	18-23
15817479-6	2005	Overexpression of Bcl-2 prevented ceramide- and etoposide-induced caspase-2 activation and mitochondrial apoptosis.	Ceramides	34-42	caspase 2	Homo sapiens	66-75
15817479-10	2005	Further studies showed that Bcl-2 was dephosphorylated at serine 70 after ceramide and etoposide treatment.	Ceramides	74-82	BCL2 apoptosis regulator	Homo sapiens	28-33
15817479-12	2005	Taken together, ceramide and etoposide induced mitochondria-mediated apoptosis by initiating caspase-2 activation, which was, at least in part, regulated by Bcl-2.	Ceramides	16-24	caspase 2	Homo sapiens	93-102
15817479-12	2005	Taken together, ceramide and etoposide induced mitochondria-mediated apoptosis by initiating caspase-2 activation, which was, at least in part, regulated by Bcl-2.	Ceramides	16-24	BCL2 apoptosis regulator	Homo sapiens	157-162
15817474-7	2005	However, a block in sphingolipid synthesis or any perturbation in the synthesis of the ceramide-bound C26 very long chain fatty acid results in mistargeting of newly synthesized Pma1p to the vacuole.	Ceramides	87-95	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	178-183
15705795-4	2005	Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase), suppressed RGDfV-induced ceramide increase.	Ceramides	99-107	sphingomyelin phosphodiesterase 1	Homo sapiens	42-63
15907394-3	2005	The recent discovery of the ceramide transport protein CERT has revealed a novel pathway for the delivery of ceramide to the Golgi apparatus for sphingomyelin (SM) synthesis.	Ceramides	28-36	ceramide transporter 1	Homo sapiens	55-59
15907394-4	2005	In addition to a ceramide-binding START domain, CERT has FFAT (referring to two phenylalanines [FF] in an acidic tract) and pleckstrin homology (PH) domains that recognize the ER integral membrane protein VAMP-associated protein (VAP) and Golgi-associated PtdIns 4-phosphate, respectively.	Ceramides	17-25	ceramide transporter 1	Homo sapiens	48-52
15907394-6	2005	Similar Golgi-ER targeting motifs are also present in the oxysterol-binding protein (OSBP), which regulates ceramide transport and SM synthesis in an oxysterol-dependent manner.	Ceramides	108-116	oxysterol binding protein	Homo sapiens	58-83
15907394-6	2005	Similar Golgi-ER targeting motifs are also present in the oxysterol-binding protein (OSBP), which regulates ceramide transport and SM synthesis in an oxysterol-dependent manner.	Ceramides	108-116	oxysterol binding protein	Homo sapiens	85-89
15705795-4	2005	Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase), suppressed RGDfV-induced ceramide increase.	Ceramides	99-107	sphingomyelin phosphodiesterase 1	Homo sapiens	65-71
15815728-4	2005	Here we show that CML CD34(+) progenitors are sensitive to several apoptosis-inducing stimuli including the chemotherapeutic agents Ara-C and VP-16, radiation, arsenic trioxide, ceramide, growth factor withdrawal, and the death receptor activators TNFalpha and TRAIL.	Ceramides	178-186	CD34 molecule	Homo sapiens	22-26
15772421-6	2005	Exogenously expressed LASS5 in lung epithelia was membrane-associated, triggering increased ceramide synthesis, whereas knockdown studies using fumonisin B1 or LASS5 small, interfering RNA reduced ceramide synthase activity by 78% or 45%, respectively.	Ceramides	92-100	ceramide synthase 5	Homo sapiens	22-27
15774472-9	2005	Moreover, these FFAs stimulated the de novo synthesis of ceramide and sphingosine, two sphingolipids shown previously to inhibit insulin action.	Ceramides	57-65	insulin	Homo sapiens	129-136
15941398-9	2005	Consistent with their essential nature in yeast, the accumulation of the ceramide moiety of sphingolipids is substantially reduced and their fatty acid composition altered in gl8a and gl8b double mutant kernels relative to wild-type kernels.	Ceramides	73-81	very-long-chain 3-oxoacyl-CoA reductase 1-like	Zea mays	184-188
15774472-10	2005	To determine the contribution of either sphingolipid in FFA-dependent inhibition of insulin action, we generated C2C12 myotubes that constitutively overexpress acid ceramidase (AC), an enzyme that catalyzes the lysosomal conversion of ceramide to sphingosine.	Ceramides	235-243	N-acylsphingosine amidohydrolase 1	Homo sapiens	177-179
15774472-11	2005	AC overexpression negated the inhibitory effects of saturated FFAs on insulin signaling while blocking their stimulation of ceramide accumulation.	Ceramides	124-132	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-2
15769735-2	2005	Several studies have also described ceramide (CER), a lipid second messenger, as a major contributor in mediating UV light-induced c-Jun N-terminal kinase (JNK) activation and cell death.	Ceramides	36-44	mitogen-activated protein kinase 8	Homo sapiens	131-154
15769735-2	2005	Several studies have also described ceramide (CER), a lipid second messenger, as a major contributor in mediating UV light-induced c-Jun N-terminal kinase (JNK) activation and cell death.	Ceramides	36-44	mitogen-activated protein kinase 8	Homo sapiens	156-159
15769735-2	2005	Several studies have also described ceramide (CER), a lipid second messenger, as a major contributor in mediating UV light-induced c-Jun N-terminal kinase (JNK) activation and cell death.	Ceramides	46-49	mitogen-activated protein kinase 8	Homo sapiens	131-154
15769735-2	2005	Several studies have also described ceramide (CER), a lipid second messenger, as a major contributor in mediating UV light-induced c-Jun N-terminal kinase (JNK) activation and cell death.	Ceramides	46-49	mitogen-activated protein kinase 8	Homo sapiens	156-159
15867385-3	2005	In that study, doxorubicin promoted generation of ceramide in MCF-7-AdrR/GCS antisense cells; the present study implicates factors in addition to ceramide that augment sensitivity to chemotherapy.	Ceramides	50-58	UDP-glucose ceramide glucosyltransferase	Homo sapiens	73-76
15796901-5	2005	Acid sphingomyelinase (ASM) is responsible for hydrolyzing sphingomyelin to generate ceramide, and it was demonstrated that MNNG treatment caused ASM distribution changing from diffused state to concentrated area of cells, which colocalized with lipid rafts.	Ceramides	85-93	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
15796901-5	2005	Acid sphingomyelinase (ASM) is responsible for hydrolyzing sphingomyelin to generate ceramide, and it was demonstrated that MNNG treatment caused ASM distribution changing from diffused state to concentrated area of cells, which colocalized with lipid rafts.	Ceramides	85-93	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
15796901-7	2005	In addition, blockage of ceramide production by ASM inhibitor imipramine interrupted MNNG-induced receptor clustering.	Ceramides	25-33	sphingomyelin phosphodiesterase 1	Homo sapiens	48-51
15657896-3	2005	Galactocerebrosidase is the enzyme responsible for degrading galactosylcerebroside to ceramide.	Ceramides	86-94	galactosylceramidase	Homo sapiens	0-20
15965081-0	2005	Pravastatin attenuates ceramide-induced cytotoxicity in mouse cerebral endothelial cells with HIF-1 activation and VEGF upregulation.	Ceramides	23-31	vascular endothelial growth factor A	Mus musculus	115-119
15965081-1	2005	Ceramide is a pro-apoptotic lipid messenger that induces oxidative stress and may mediate apoptosis in cerebral endothelial cells (CECs) induced by TNF-alpha/cycloheximide, lipopolysaccharide, oxidized LDL, IL-1, and amyloid peptide.	Ceramides	0-8	tumor necrosis factor	Mus musculus	148-157
15965081-1	2005	Ceramide is a pro-apoptotic lipid messenger that induces oxidative stress and may mediate apoptosis in cerebral endothelial cells (CECs) induced by TNF-alpha/cycloheximide, lipopolysaccharide, oxidized LDL, IL-1, and amyloid peptide.	Ceramides	0-8	interleukin 1 complex	Mus musculus	207-211
15965081-7	2005	These results raise the possibility that pravastatin may protect CECs against ceramide-induced death via the HIF-VEGF cascade.	Ceramides	78-86	vascular endothelial growth factor A	Mus musculus	113-117
15867385-9	2005	This work shows that limiting GCS activity down-regulates the expression of MDR1, a phenomenon that may drive the chemosensitization associated with blocking ceramide metabolism.	Ceramides	158-166	UDP-glucose ceramide glucosyltransferase	Homo sapiens	30-33
15867385-9	2005	This work shows that limiting GCS activity down-regulates the expression of MDR1, a phenomenon that may drive the chemosensitization associated with blocking ceramide metabolism.	Ceramides	158-166	ATP binding cassette subfamily B member 1	Homo sapiens	76-80
15867385-4	2005	Although GCS antisense cells showed enhanced ceramide formation compared with MCF-7-AdrR when challenged with paclitaxel, GCS antisense cells also showed a 10-fold increase in levels of intracellular drug (paclitaxel and vinblastine).	Ceramides	45-53	UDP-glucose ceramide glucosyltransferase	Homo sapiens	9-12
15879700-5	2005	The viability of ceramide-treated chicken oviduct cells decreased in a dose-dependent manner and apoptotic cells were detected by staining with annexin V.	Ceramides	17-25	annexin A5	Gallus gallus	144-153
15933726-5	2005	Furthermore, p105 processing and activation of NF-kappaB survival genes in response to C2 ceramide is impaired in Capn4-/- mouse embryonic fibroblasts defective in calpain activity.	Ceramides	90-98	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	13-17
15933726-5	2005	Furthermore, p105 processing and activation of NF-kappaB survival genes in response to C2 ceramide is impaired in Capn4-/- mouse embryonic fibroblasts defective in calpain activity.	Ceramides	90-98	calpain, small subunit 1	Mus musculus	114-119
15879522-5	2005	kti6 membranes lack M(IP)(2)C and sphingolipid mutants that have reduced levels of M(IP)(2)C precursors, including the sphingolipid building block ceramide survive zymocin.	Ceramides	147-155	inositolphosphotransferase	Saccharomyces cerevisiae S288C	0-4
15852018-3	2005	Inhibition of enzymes controlling de novo ceramide synthesis prevented alveolar cell apoptosis, oxidative stress and emphysema caused by blockade of the vascular endothelial growth factor (VEGF) receptors in both rats and mice.	Ceramides	42-50	vascular endothelial growth factor A	Rattus norvegicus	153-187
15852018-3	2005	Inhibition of enzymes controlling de novo ceramide synthesis prevented alveolar cell apoptosis, oxidative stress and emphysema caused by blockade of the vascular endothelial growth factor (VEGF) receptors in both rats and mice.	Ceramides	42-50	vascular endothelial growth factor A	Rattus norvegicus	189-193
15695626-4	2005	Pure hydrated ceramides exhibit cooperative endothermic order-disorder transitions at 93 degrees C (Cer16), 60 degrees C (Cer6), and 54 degrees C (Cer2).	Ceramides	14-23	DAN domain BMP antagonist family member 5	Homo sapiens	147-151
15695626-11	2005	The different behavior of the long- and short-chain ceramides can be rationalized in terms of their different molecular geometries, Cer16 favoring negative curvature in the monolayers, thus inverted phases, and the opposite being true of the micelle-forming Cer2.	Ceramides	52-61	DAN domain BMP antagonist family member 5	Homo sapiens	258-262
15879700-6	2005	The expression of apoptosis-related genes was assessed by RT-PCR and bcl-2 mRNA was found to decrease after exposure to ceramide while Bcl-x mRNA increased 12 h post-treatment.	Ceramides	120-128	BCL2, apoptosis regulator	Gallus gallus	69-74
15879700-8	2005	We conclude that ceramide induces apoptosis in oviduct-derived primary cells via a caspase- and bcl-2- dependent pathway.	Ceramides	17-25	BCL2, apoptosis regulator	Gallus gallus	96-101
15794940-7	2005	These findings implicate ceramide as an important intermediate in the regulation of Akt after troglitazone treatment.	Ceramides	25-33	thymoma viral proto-oncogene 1	Mus musculus	84-87
15722351-4	2005	Accumulated, positively charged ceramides increased inner membrane permeability and triggered release of mitochondrial cytochrome c.	Ceramides	32-41	cytochrome c, somatic	Homo sapiens	119-131
15843619-10	2005	Mutation of threonine 231 to alanine, so that tau could not be phosphorylated at this site, prevented the ceramide-induced release of tau from microtubules, organelle clustering, the increase in mitochondrial-free calcium levels, and neuronal death, demonstrating the importance of the CDK5-dependent signaling cascade in this calcium-dependent cell-death mechanism.	Ceramides	106-114	cyclin-dependent kinase 5	Rattus norvegicus	286-290
15755660-0	2005	Inhibitory activity of a ceramide library on interleukin-4 production from activated T cells.	Ceramides	25-33	interleukin 4	Mus musculus	45-58
15721320-3	2005	Multiple candidate kinases have been identified that serine-phosphorylate IRS-1 in response to TNF or ceramide.	Ceramides	102-110	insulin receptor substrate 1	Homo sapiens	74-79
15794940-0	2005	Increased Akt protein expression is associated with decreased ceramide content in skeletal muscle of troglitazone-treated mice.	Ceramides	62-70	thymoma viral proto-oncogene 1	Mus musculus	10-13
15755660-3	2005	In this study we investigated the inhibitory activity of IL-4 production in activated T cells by screening ceramide derivatives prepared by solid phase combinatorial chemistry.	Ceramides	107-115	interleukin 4	Mus musculus	57-61
15721320-5	2005	Here, we identify the death domain of TNF-R55 as responsible for the inhibitory effects of TNF on tyrosine phosphorylation of IRS-1, implicating ceramide generated by A-SMase as a downstream mediator of inhibition of IR signaling.	Ceramides	145-153	TNF receptor superfamily member 1A	Homo sapiens	38-45
15721320-5	2005	Here, we identify the death domain of TNF-R55 as responsible for the inhibitory effects of TNF on tyrosine phosphorylation of IRS-1, implicating ceramide generated by A-SMase as a downstream mediator of inhibition of IR signaling.	Ceramides	145-153	tumor necrosis factor	Homo sapiens	38-41
15755660-4	2005	Many ceramide derivatives significantly inhibited IL-4 production in T cells.	Ceramides	5-13	interleukin 4	Mus musculus	50-54
15721320-5	2005	Here, we identify the death domain of TNF-R55 as responsible for the inhibitory effects of TNF on tyrosine phosphorylation of IRS-1, implicating ceramide generated by A-SMase as a downstream mediator of inhibition of IR signaling.	Ceramides	145-153	insulin receptor substrate 1	Homo sapiens	126-131
15721320-5	2005	Here, we identify the death domain of TNF-R55 as responsible for the inhibitory effects of TNF on tyrosine phosphorylation of IRS-1, implicating ceramide generated by A-SMase as a downstream mediator of inhibition of IR signaling.	Ceramides	145-153	sphingomyelin phosphodiesterase 1	Homo sapiens	167-174
15755660-5	2005	In particular, ceramide derivatives with a lauroyl group showed strong inhibitory activities on IL-4 production in both phorbol 12-myristate 13-acetate (PMA)-activated EL4 T cells and antigen-primed cells, suggesting that they can be used as compounds for the development of anti-allergic agents.	Ceramides	15-23	interleukin 4	Mus musculus	96-100
15749390-2	2005	We have previously demonstrated ceramide production secondary to Abeta-induced activation of neutral sphingomyelinase (nSMase) in cerebral endothelial cells and oligodendrocytes, which may contribute to cellular injury during progression of AD.	Ceramides	32-40	sphingomyelin phosphodiesterase 2	Homo sapiens	93-117
15816837-0	2005	Interleukin-4 suppresses the enhancement of ceramide synthesis and cutaneous permeability barrier functions induced by tumor necrosis factor-alpha and interferon-gamma in human epidermis.	Ceramides	44-52	interleukin 4	Homo sapiens	0-13
15816837-0	2005	Interleukin-4 suppresses the enhancement of ceramide synthesis and cutaneous permeability barrier functions induced by tumor necrosis factor-alpha and interferon-gamma in human epidermis.	Ceramides	44-52	tumor necrosis factor	Homo sapiens	119-146
15816837-0	2005	Interleukin-4 suppresses the enhancement of ceramide synthesis and cutaneous permeability barrier functions induced by tumor necrosis factor-alpha and interferon-gamma in human epidermis.	Ceramides	44-52	interferon gamma	Homo sapiens	151-167
15816837-3	2005	Acid-ceramidase (acid-CDase) catalyzes the hydrolysis of ceramide in the SC.	Ceramides	57-65	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
15816837-3	2005	Acid-ceramidase (acid-CDase) catalyzes the hydrolysis of ceramide in the SC.	Ceramides	57-65	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-27
15816837-5	2005	Levels of transcripts for acid-SMase and GCase and the amount of ceramide in human epidermal sheets were enhanced by tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma and these effects were inhibited in the presence of interleukin (IL)-4.	Ceramides	65-73	tumor necrosis factor	Homo sapiens	117-150
15816837-5	2005	Levels of transcripts for acid-SMase and GCase and the amount of ceramide in human epidermal sheets were enhanced by tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma and these effects were inhibited in the presence of interleukin (IL)-4.	Ceramides	65-73	interferon gamma	Homo sapiens	155-177
15816837-5	2005	Levels of transcripts for acid-SMase and GCase and the amount of ceramide in human epidermal sheets were enhanced by tumor necrosis factor (TNF)-alpha and interferon (IFN)-gamma and these effects were inhibited in the presence of interleukin (IL)-4.	Ceramides	65-73	interleukin 4	Homo sapiens	230-248
15816837-8	2005	The balance between Th1 and Th2 might affect the construction and/or the repair of the epidermal permeability barrier via regulation of the production of ceramide.	Ceramides	154-162	negative elongation factor complex member C/D	Homo sapiens	20-23
15749390-2	2005	We have previously demonstrated ceramide production secondary to Abeta-induced activation of neutral sphingomyelinase (nSMase) in cerebral endothelial cells and oligodendrocytes, which may contribute to cellular injury during progression of AD.	Ceramides	32-40	sphingomyelin phosphodiesterase 2	Homo sapiens	119-125
15749390-3	2005	In this study, we first established the "Abeta --> nSMase --> ceramide --> free radical --> cell death" pathway in primary cultures of fetal rat cortical neurons.	Ceramides	68-76	sphingomyelin phosphodiesterase 2	Rattus norvegicus	54-60
15749390-6	2005	Activation of the cGMP/PKG pathway induced expression of thioredoxin and Bcl-2 that were beneficial to cortical neurons in antagonizing Abeta/ceramide toxicity.	Ceramides	142-150	protein kinase cGMP-dependent 1	Homo sapiens	23-26
15749390-6	2005	Activation of the cGMP/PKG pathway induced expression of thioredoxin and Bcl-2 that were beneficial to cortical neurons in antagonizing Abeta/ceramide toxicity.	Ceramides	142-150	thioredoxin	Homo sapiens	57-68
15749390-6	2005	Activation of the cGMP/PKG pathway induced expression of thioredoxin and Bcl-2 that were beneficial to cortical neurons in antagonizing Abeta/ceramide toxicity.	Ceramides	142-150	BCL2 apoptosis regulator	Homo sapiens	73-78
15764706-1	2005	Neutral sphingomyelinases sphingomyelin phosphodiesterase (SMPD)2 and -3 hydrolyze sphingomyelin to phosphocholine and ceramide.	Ceramides	119-127	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	0-72
15604116-5	2005	Sphingomyelinase increases cAMP production due to the release of ceramide, a direct activator of PKCzeta.	Ceramides	65-73	protein kinase C zeta	Homo sapiens	97-104
15655246-9	2005	Most interestingly, a very low ceramide hydrolyzing activity was also detected with NAAA, and N-lauroylethanolamine hydrolyzing activity was observed with acid ceramidase.	Ceramides	31-39	N-acylethanolamine acid amidase	Homo sapiens	84-88
15655246-7	2005	Human NAAA was essentially identical to a gene product that had been noted to resemble acid ceramidase but lacked ceramide hydrolyzing activity.	Ceramides	114-122	N-acylethanolamine acid amidase	Homo sapiens	6-10
15516208-2	2005	In the present study, we investigated the role of this mitochondrial pool of ceramide in response to a receptor-mediated event, namely TNFalpha (tumour necrosis factor alpha), and the involvement of this mitochondrial pool of ceramide in Bax translocation to mitochondria, an event that precedes cytochrome c release.	Ceramides	77-85	tumor necrosis factor	Homo sapiens	135-143
15516208-2	2005	In the present study, we investigated the role of this mitochondrial pool of ceramide in response to a receptor-mediated event, namely TNFalpha (tumour necrosis factor alpha), and the involvement of this mitochondrial pool of ceramide in Bax translocation to mitochondria, an event that precedes cytochrome c release.	Ceramides	226-234	BCL2 associated X, apoptosis regulator	Homo sapiens	238-241
15516208-3	2005	Treatment of MCF7 cells with TNFalpha caused an increase in ceramide levels in the mitochondrial fraction which accompanied Bax translocation to mitochondria.	Ceramides	60-68	BCL2 associated X, apoptosis regulator	Homo sapiens	124-127
15516208-4	2005	Targeting bSMase to mitochondria specifically resulted in Bax translocation to mitochondria, suggesting that the mitochondrial ceramide pool is involved in Bax translocation.	Ceramides	127-135	BCL2 associated X, apoptosis regulator	Homo sapiens	156-159
15748701-4	2005	SNP dose-dependently decreased MC3T3-E1 osteoblast viability, increased NO production in the culture media and enhanced the release of intracellular ceramides C22 and C24.	Ceramides	149-158	Sp7 transcription factor 7	Mus musculus	159-162
15516208-3	2005	Treatment of MCF7 cells with TNFalpha caused an increase in ceramide levels in the mitochondrial fraction which accompanied Bax translocation to mitochondria.	Ceramides	60-68	tumor necrosis factor	Homo sapiens	29-37
15516208-6	2005	Collectively, these results suggest that the generation of ceramide in mitochondria in response to TNFalpha is sufficient to induce Bax translocation to mitochondria and subsequent cytochrome c release and cell death.	Ceramides	59-67	tumor necrosis factor	Homo sapiens	99-107
15516208-6	2005	Collectively, these results suggest that the generation of ceramide in mitochondria in response to TNFalpha is sufficient to induce Bax translocation to mitochondria and subsequent cytochrome c release and cell death.	Ceramides	59-67	BCL2 associated X, apoptosis regulator	Homo sapiens	132-135
15741229-0	2005	Stimulation of erythrocyte ceramide formation by platelet-activating factor.	Ceramides	27-35	PCNA clamp associated factor	Homo sapiens	49-75
15516208-6	2005	Collectively, these results suggest that the generation of ceramide in mitochondria in response to TNFalpha is sufficient to induce Bax translocation to mitochondria and subsequent cytochrome c release and cell death.	Ceramides	59-67	cytochrome c, somatic	Homo sapiens	181-193
15781658-6	2005	Enforced expression of constitutively active mitogen-activated protein kinase kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell death, suggesting that MEK/ERK and Akt inactivation play a primary role in these phenomena.	Ceramides	148-156	mitogen-activated protein kinase kinase 7	Homo sapiens	45-84
15781658-6	2005	Enforced expression of constitutively active mitogen-activated protein kinase kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell death, suggesting that MEK/ERK and Akt inactivation play a primary role in these phenomena.	Ceramides	148-156	mitogen-activated protein kinase kinase 1	Homo sapiens	86-92
15781658-6	2005	Enforced expression of constitutively active mitogen-activated protein kinase kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell death, suggesting that MEK/ERK and Akt inactivation play a primary role in these phenomena.	Ceramides	148-156	AKT serine/threonine kinase 1	Homo sapiens	110-113
15781658-6	2005	Enforced expression of constitutively active mitogen-activated protein kinase kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell death, suggesting that MEK/ERK and Akt inactivation play a primary role in these phenomena.	Ceramides	148-156	mitogen-activated protein kinase kinase 7	Homo sapiens	86-89
15781658-6	2005	Enforced expression of constitutively active mitogen-activated protein kinase kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell death, suggesting that MEK/ERK and Akt inactivation play a primary role in these phenomena.	Ceramides	148-156	mitogen-activated protein kinase 1	Homo sapiens	204-207
15781658-6	2005	Enforced expression of constitutively active mitogen-activated protein kinase kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell death, suggesting that MEK/ERK and Akt inactivation play a primary role in these phenomena.	Ceramides	148-156	AKT serine/threonine kinase 1	Homo sapiens	212-215
15741229-5	2005	The experiments further disclose the presence of PAF receptors in erythrocytes and show that PAF stimulates the breakdown of sphingomyelin and the release of ceramide from erythrocytes at isotonic conditions.	Ceramides	158-166	PCNA clamp associated factor	Homo sapiens	49-52
15741229-5	2005	The experiments further disclose the presence of PAF receptors in erythrocytes and show that PAF stimulates the breakdown of sphingomyelin and the release of ceramide from erythrocytes at isotonic conditions.	Ceramides	158-166	PCNA clamp associated factor	Homo sapiens	93-96
15741229-8	2005	In conclusion, PAF activates an erythrocyte sphingomyelinase and the then formed ceramide leads to the activation of scramblase with subsequent phosphatidylserine exposure.	Ceramides	81-89	PCNA clamp associated factor	Homo sapiens	15-18
15771622-9	2005	Etoposide, ceramide, serum depletion and confluence all led to elevated YKL-40.	Ceramides	11-19	chitinase 3 like 1	Homo sapiens	72-78
15757672-0	2005	Formation of ceramide-enriched domains in lipid particles enhances the binding of apolipoprotein E.	Ceramides	13-21	apolipoprotein E	Homo sapiens	82-98
15562249-5	2005	The mRNA levels and activity of serine palmitoyltransferase (SPT), a key enzyme in ceramide synthesis, as well as the incorporation of [14C]palmitate into ceramide were decreased by approximately 50% in red muscles of SCD1-/- mice.	Ceramides	83-91	stearoyl-Coenzyme A desaturase 1	Mus musculus	218-222
15562249-5	2005	The mRNA levels and activity of serine palmitoyltransferase (SPT), a key enzyme in ceramide synthesis, as well as the incorporation of [14C]palmitate into ceramide were decreased by approximately 50% in red muscles of SCD1-/- mice.	Ceramides	155-163	stearoyl-Coenzyme A desaturase 1	Mus musculus	218-222
15562249-8	2005	Furthermore, SCD1 deficiency increased phosphorylation of AMP-activated protein kinase (AMPK), suggesting that AMPK activation may be partially responsible for the increased fatty acid oxidation and decreased ceramide synthesis in red muscles of SCD1-/- mice.	Ceramides	209-217	stearoyl-Coenzyme A desaturase 1	Mus musculus	13-17
15881228-0	2005	Sphingosine 1-phosphate acts as a signal molecule in ceramide signal transduction of TNF-alpha-induced activator protein-1 in osteoblastic cell line MC3T3-E1 cells.	Ceramides	53-61	tumor necrosis factor	Mus musculus	85-94
15611152-5	2005	Concomitant with transporter down-regulation, ceramide diminished both intramyocellular amino acid abundance and the phosphorylation of translation regulators lying downstream of mTOR.	Ceramides	46-54	mechanistic target of rapamycin kinase	Rattus norvegicus	179-183
15881228-4	2005	DL-threo-1-phenyl-2-hexadecanoyl-amino-3-pyrrolidino-1-propanol (PPPP), which causes accumulation of intracellular ceramide, stimulated the TNF-alpha-induced expression of the c-fos and c-jun genes.	Ceramides	115-123	tumor necrosis factor	Mus musculus	140-149
15881228-6	2005	In addition, cell-permeable ceramide (N-acetylsphingosine, N-hexanoylsphingosine or N-octanoylsphingosine) stimulated expression of the c-fos and c-jun genes and nuclear protein binding to TRE.	Ceramides	28-36	FBJ osteosarcoma oncogene	Mus musculus	136-141
15881228-6	2005	In addition, cell-permeable ceramide (N-acetylsphingosine, N-hexanoylsphingosine or N-octanoylsphingosine) stimulated expression of the c-fos and c-jun genes and nuclear protein binding to TRE.	Ceramides	28-36	jun proto-oncogene	Mus musculus	146-151
15881228-11	2005	The present study thus suggests that SPP acts as a signal molecule in ceramide-dependent signal transduction in TNF-alpha-induced AP-1 in osteoblastic MC3T3-E1 cells.	Ceramides	70-78	sphingosine-1-phosphate phosphatase 1	Mus musculus	37-40
15881228-11	2005	The present study thus suggests that SPP acts as a signal molecule in ceramide-dependent signal transduction in TNF-alpha-induced AP-1 in osteoblastic MC3T3-E1 cells.	Ceramides	70-78	tumor necrosis factor	Mus musculus	112-121
15881228-0	2005	Sphingosine 1-phosphate acts as a signal molecule in ceramide signal transduction of TNF-alpha-induced activator protein-1 in osteoblastic cell line MC3T3-E1 cells.	Ceramides	53-61	jun proto-oncogene	Mus musculus	103-122
15881228-2	2005	Recent studies have shown the importance of ceramide and its metabolites as signal molecules for TNF-alpha-induced gene expression in several cell types.	Ceramides	44-52	tumor necrosis factor	Mus musculus	97-106
15611094-1	2005	Inositolsphingolipid phospholipase C (Isc1p) is the Saccharomyces cerevisiae member of the extended family of neutral sphingomyelinases that regulates the generation of bioactive ceramides.	Ceramides	179-188	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	38-43
15692566-2	2005	Although Lac1p and Lag1p have been shown recently to be involved in acyl-CoA-dependent ceramide synthesis, ceramide synthase is still poorly characterized.	Ceramides	87-95	ceramide synthase 1	Homo sapiens	19-24
15596449-0	2005	CERT mediates intermembrane transfer of various molecular species of ceramides.	Ceramides	69-78	ceramide transporter 1	Homo sapiens	0-4
15596449-2	2005	The main pathway of endoplasmic reticulum-to-Golgi transport of ceramide is mediated by CERT, a cytosolic 68-kDa protein, in a nonvesicular manner.	Ceramides	64-72	ceramide transporter 1	Homo sapiens	88-92
15596449-6	2005	The activity of CERT to transfer saturated and unsaturated diacylglycerols, which structurally resemble ceramide, was 5-10% of the activity toward C(16)-ceramide.	Ceramides	104-112	ceramide transporter 1	Homo sapiens	16-20
15596449-8	2005	CERT efficiently transferred ceramides having C(14), C(16), C(18), and C(20) chains, but not longer acyl chains, and also mediated efficient transfer of C(16)-dihydroceramide and C(16)-phyto-ceramide.	Ceramides	29-38	ceramide transporter 1	Homo sapiens	0-4
15596449-9	2005	Binding assays showed that CERT also recognizes short chain fluorescent analogs of ceramide with a stoichiometry of 1:1.	Ceramides	83-91	ceramide transporter 1	Homo sapiens	27-31
15596449-10	2005	Moreover, (1R,3R)-N-(3-hydroxy-1-hydroxymethyl-3-phenylpropyl)dodecamide, which inhibited the CERT-dependent pathway of ceramide trafficking in intact cells, was found to be an antagonist of the CERT protein.	Ceramides	120-128	ceramide transporter 1	Homo sapiens	94-98
15596449-10	2005	Moreover, (1R,3R)-N-(3-hydroxy-1-hydroxymethyl-3-phenylpropyl)dodecamide, which inhibited the CERT-dependent pathway of ceramide trafficking in intact cells, was found to be an antagonist of the CERT protein.	Ceramides	120-128	ceramide transporter 1	Homo sapiens	195-199
15596449-11	2005	These results indicate that CERT can mediate transfer of various types of ceramides that naturally exist and their close relatives.	Ceramides	74-83	ceramide transporter 1	Homo sapiens	28-32
15692566-7	2005	Lip1p is a single-span ER membrane protein that is required for ceramide synthesis in vivo and in vitro.	Ceramides	64-72	lipoic acid synthetase	Homo sapiens	0-5
15692566-8	2005	The Lip1p regions required for ceramide synthesis are localized within the ER membrane or lumen.	Ceramides	31-39	lipoic acid synthetase	Homo sapiens	4-9
15471985-5	2005	With the conversion rate of L-[3H]arginine to L-[3H]citrulline measured, endostatin had no effect on endothelial NO synthase (NOS) activity, but it stimulated ceramide by activation of sphingomyelinase (SMase), whereby O2*-.	Ceramides	159-167	collagen type XVIII alpha 1 chain	Homo sapiens	73-83
15695581-0	2005	Pituitary adenylate cyclase-activating polypeptide prevents the effects of ceramides on migration, neurite outgrowth, and cytoskeleton remodeling.	Ceramides	75-84	adenylate cyclase activating polypeptide 1	Homo sapiens	0-50
15471985-1	2005	The present study tested the hypothesis that endostatin stimulates superoxide (O2*-) production through a ceramide-mediating signaling pathway and thereby results in an uncoupling of bradykinin (BK)-induced increases in intracellular Ca2+ concentration ([Ca2+]i) from nitric oxide (NO) production in coronary endothelial cells.	Ceramides	106-114	collagen type XVIII alpha 1 chain	Homo sapiens	45-55
15708351-1	2005	Ceramide is a key player governing cell fate, and its conversion to ceramide-1-phosphate by ceramide kinase (CERK) is emerging as an important mean to regulate apoptosis and inflammatory processes.	Ceramides	0-8	ceramide kinase	Homo sapiens	92-107
15708351-1	2005	Ceramide is a key player governing cell fate, and its conversion to ceramide-1-phosphate by ceramide kinase (CERK) is emerging as an important mean to regulate apoptosis and inflammatory processes.	Ceramides	0-8	ceramide kinase	Homo sapiens	109-113
15708351-4	2005	Surprisingly, various ceramides, known substrates for CERK, were not phosphorylated by CERKL in vitro.	Ceramides	22-31	ceramide kinase	Homo sapiens	54-58
15471985-9	2005	These results indicate that endostatin increases intracellular ceramide levels, which enhances O2*-.	Ceramides	63-71	collagen type XVIII alpha 1 chain	Homo sapiens	28-38
15479855-9	2005	A specific inhibitor of ceramide synthase, fumonisin B1 (50 microM), suppressed hypoxia-reoxygenation-induced ceramide generation and provided protection against hypoxia-reoxygenation-induced EndoG release, DNA fragmentation, and cell death.	Ceramides	24-32	endonuclease G	Rattus norvegicus	192-197
15862961-0	2005	Aromatase inhibition by 15-deoxy-prostaglandin J(2) (15-dPGJ(2)) and N-(4-hydroxyphenyl)-retinamide (4HPR) is associated with enhanced ceramide production.	Ceramides	135-143	haptoglobin-related protein	Homo sapiens	102-105
15687119-0	2005	Letter regarding article by Auge et al., "Role for matrix metalloproteinase-2 in oxidized low-density lipoprotein-induced activation of the sphingomyelin/ceramide pathway and smooth muscle cell proliferation".	Ceramides	154-162	matrix metallopeptidase 2	Homo sapiens	51-77
15746654-13	2005	These data demonstrate that endogenous ceramide generation and subsequent phosphatase activation during apoptosis are key steps in the alternative splicing of caspase-2 mRNA and further suggest a link between the signal-transduction pathway and alternative splicing.	Ceramides	39-47	caspase 2	Homo sapiens	159-168
15361069-5	2005	Here, we present the first evidence of PP-1c activation by ceramide in live cells, namely NGF-deprived sympathetic neurons.	Ceramides	59-67	protein phosphatase 1 catalytic subunit gamma	Homo sapiens	39-44
15361069-9	2005	Ceramide was able to prevent pRb (retinoblastoma gene product) hyperphosphorylation by a mechanism dependent on PP-1c activation, suggesting that two consequences of NGF deprivation in sympathetic neurons are inhibition of PP-1c and subsequent hyperphosphorylation of pRb protein.	Ceramides	0-8	RB transcriptional corepressor 1	Homo sapiens	29-32
15361069-9	2005	Ceramide was able to prevent pRb (retinoblastoma gene product) hyperphosphorylation by a mechanism dependent on PP-1c activation, suggesting that two consequences of NGF deprivation in sympathetic neurons are inhibition of PP-1c and subsequent hyperphosphorylation of pRb protein.	Ceramides	0-8	protein phosphatase 1 catalytic subunit gamma	Homo sapiens	112-117
15361069-9	2005	Ceramide was able to prevent pRb (retinoblastoma gene product) hyperphosphorylation by a mechanism dependent on PP-1c activation, suggesting that two consequences of NGF deprivation in sympathetic neurons are inhibition of PP-1c and subsequent hyperphosphorylation of pRb protein.	Ceramides	0-8	protein phosphatase 1 catalytic subunit gamma	Homo sapiens	223-228
15361069-9	2005	Ceramide was able to prevent pRb (retinoblastoma gene product) hyperphosphorylation by a mechanism dependent on PP-1c activation, suggesting that two consequences of NGF deprivation in sympathetic neurons are inhibition of PP-1c and subsequent hyperphosphorylation of pRb protein.	Ceramides	0-8	RB transcriptional corepressor 1	Homo sapiens	268-271
15637591-0	2005	Sphingosine kinase activity counteracts ceramide-mediated cell death in human melanoma cells: role of Bcl-2 expression.	Ceramides	40-48	sphingosine kinase 1	Homo sapiens	0-18
15389789-9	2005	CONCLUSIONS: The simultaneous use of EGFR inhibitor and compound releasing NO(*) might lead to a synergy in the ceramide and ROS production which might cause cellular membrane damages resulting in a massive apoptotic/necrotic death of metastatic PC cells.	Ceramides	112-120	epidermal growth factor receptor	Homo sapiens	37-41
15642349-2	2005	N-SMase induced translocation of endothelial NOS (eNOS) from plasma membrane caveolae to intracellular region, eNOS phosphorylation on serine 1179, and an increase of ceramide level in endothelial cells.	Ceramides	167-175	sphingomyelin phosphodiesterase 2	Homo sapiens	0-7
15642349-3	2005	Membrane-permeable ceramide (C(8)-ceramide) mimicked the responses to N-SMase.	Ceramides	19-27	sphingomyelin phosphodiesterase 2	Homo sapiens	70-77
15642349-4	2005	We propose the involvement of N-SMase and ceramide in Ca(2+)-independent eNOS activation and NO production in endothelial cells in situ, linking to endothelium-dependent vasorelaxation.	Ceramides	42-50	nitric oxide synthase 3	Homo sapiens	73-77
15637591-4	2005	As sphingosine kinase (SphK) type 1 plays a critical role in determining the dynamic balance between the proapoptotic sphingolipid metabolite ceramide and the prosurvival S1P, we examined its role in apoptosis of melanoma cells.	Ceramides	142-150	sphingosine kinase 1	Homo sapiens	3-21
15637591-4	2005	As sphingosine kinase (SphK) type 1 plays a critical role in determining the dynamic balance between the proapoptotic sphingolipid metabolite ceramide and the prosurvival S1P, we examined its role in apoptosis of melanoma cells.	Ceramides	142-150	sphingosine kinase 1	Homo sapiens	23-27
15637591-5	2005	Increasing SphK1 expression reduced the sensitivity of A-375 melanoma cells to Fas- and ceramide-mediated apoptosis.	Ceramides	88-96	sphingosine kinase 1	Homo sapiens	11-16
15742814-0	2005	Potentiation of ceramide-induced apoptosis by p27kip1 overexpression.	Ceramides	16-24	cyclin dependent kinase inhibitor 1B	Homo sapiens	46-53
15742814-4	2005	Furthermore, overexpression of p27 accelerated DNA fragmentation, PARP cleavage and cytochrome c release induced by ceramide.	Ceramides	116-124	cytochrome c, somatic	Homo sapiens	84-96
15528474-2	2005	The goal of this study was to determine whether overexpression of CuZn superoxide dismutase (SOD) protects against ceramide-induced increases in vascular superoxide and endothelial dysfunction.	Ceramides	115-123	superoxide dismutase 1, soluble	Mus musculus	93-96
15528474-9	2005	Ceramide increased superoxide in arteries from nontransgenic vessels, and this effect was prevented by polyethyleneglycol-SOD (50 U/mL) or overexpression of CuZnSOD.	Ceramides	0-8	superoxide dismutase 1, soluble	Mus musculus	157-164
15528474-10	2005	CONCLUSIONS: These results suggest that ceramide-induced increases in superoxide impair endothelium-dependent relaxation, and that select overexpression of the CuZn isoform of SOD prevents ceramide-induced oxidative stress in vessels.	Ceramides	40-48	superoxide dismutase 1, soluble	Mus musculus	176-179
15528474-10	2005	CONCLUSIONS: These results suggest that ceramide-induced increases in superoxide impair endothelium-dependent relaxation, and that select overexpression of the CuZn isoform of SOD prevents ceramide-induced oxidative stress in vessels.	Ceramides	189-197	superoxide dismutase 1, soluble	Mus musculus	176-179
15742814-5	2005	In addition, ceramide induced Bax expression independent of p27.	Ceramides	13-21	BCL2 associated X, apoptosis regulator	Homo sapiens	30-33
15742814-2	2005	Recently, we have demonstrated that ceramide induces apoptotic cell death associated with increase in the level of p27 in HL-60 cells.	Ceramides	36-44	cyclin dependent kinase inhibitor 1B	Homo sapiens	115-118
15742814-3	2005	In the present study, we showed that overexpression of p27 increases ceramide-induced apoptotic cell death in HL-60 cells.	Ceramides	69-77	cyclin dependent kinase inhibitor 1B	Homo sapiens	55-58
15742814-4	2005	Furthermore, overexpression of p27 accelerated DNA fragmentation, PARP cleavage and cytochrome c release induced by ceramide.	Ceramides	116-124	cyclin dependent kinase inhibitor 1B	Homo sapiens	31-34
15371271-1	2005	Deficiency of acid sphingomyelinase (ASM), an enzyme responsible for producing a pro-apoptotic second messenger ceramide, has previously been shown to promote the survival of fetal mouse oocytes in vivo and to protect oocytes from chemotherapy-induced apoptosis in vitro.	Ceramides	112-120	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	37-40
15465865-4	2005	Short-chain (C6 and C2) ceramides were less active than egg ceramide, whereas dihydroceramides or dioleoylglycerol were virtually inactive in promoting flip-flop.	Ceramides	24-33	complement C6	Homo sapiens	13-22
16873929-5	2005	To relate inhibition of plasma membrane redox to increased ceramide levels and arrest of cell proliferation in G(1) and apoptosis, we show that neutral sphingomyelinase, a major contributor to plasma membrane ceramide, is inhibited by reduced glutathione and ubiquinone.	Ceramides	59-67	sphingomyelin phosphodiesterase 2	Homo sapiens	144-168
16873929-5	2005	To relate inhibition of plasma membrane redox to increased ceramide levels and arrest of cell proliferation in G(1) and apoptosis, we show that neutral sphingomyelinase, a major contributor to plasma membrane ceramide, is inhibited by reduced glutathione and ubiquinone.	Ceramides	209-217	sphingomyelin phosphodiesterase 2	Homo sapiens	144-168
15465865-4	2005	Short-chain (C6 and C2) ceramides were less active than egg ceramide, whereas dihydroceramides or dioleoylglycerol were virtually inactive in promoting flip-flop.	Ceramides	24-32	complement C6	Homo sapiens	13-22
15604870-4	2005	In addition, cells treated with ceramide or phytoceramide were stained with an antibody to cytochrome c.	Ceramides	32-40	cytochrome c	Oryctolagus cuniculus	91-103
15604870-8	2005	The specific caspase-8 inhibitor reduced the apoptotic response to ceramide type VI and phytoceramide types II and VI, whereas the specific caspase-9 inhibitor significantly reduced the apoptotic response to phytoceramide types II and VI.	Ceramides	67-75	LOW QUALITY PROTEIN: caspase-8	Oryctolagus cuniculus	13-22
15604870-9	2005	Following exposure to ceramides, corneal fibroblasts stained positively with antibody to cytochrome c.	Ceramides	22-31	cytochrome c	Oryctolagus cuniculus	89-101
16280636-9	2005	All of these compounds appear to be acting as possible modulators of AST responses to C2 ceramide.	Ceramides	89-97	solute carrier family 17 member 5	Homo sapiens	69-72
16026301-5	2005	We also show the relation of ceramide level through regulation of ceramide-related enzymes (sphingomyelinase, ceramidase, sphingomyelin synthase and glucosylceramide synthase) with diseases such as cancer, leukemia, bacterial infections, AIDS, Alzheimer"s disease, atherosclerosis, diabetes mellitus and atopic dermatitis.	Ceramides	29-37	UDP-glucose ceramide glucosyltransferase	Homo sapiens	149-174
16026301-5	2005	We also show the relation of ceramide level through regulation of ceramide-related enzymes (sphingomyelinase, ceramidase, sphingomyelin synthase and glucosylceramide synthase) with diseases such as cancer, leukemia, bacterial infections, AIDS, Alzheimer"s disease, atherosclerosis, diabetes mellitus and atopic dermatitis.	Ceramides	66-74	UDP-glucose ceramide glucosyltransferase	Homo sapiens	149-174
15593299-3	2005	Recent work from our laboratory demonstrating the involvement of ABCA7 in cellular ceramide and phosphatidylserine export suggests a role for this transporter in programmed cell death.	Ceramides	83-91	ATP binding cassette subfamily A member 7	Homo sapiens	65-70
15654844-7	2005	Our results suggest that these effects are independent of Trk receptors and mediated by the p75/ceramide signaling pathway.	Ceramides	96-104	PC4 and SFRS1 interacting protein 1	Homo sapiens	92-95
15661399-0	2005	P-glycoprotein is implicated in the inhibition of ceramide-induced apoptosis in TF-1 acute myeloid leukemia cells by modulation of the glucosylceramide synthase pathway.	Ceramides	50-58	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
15661399-0	2005	P-glycoprotein is implicated in the inhibition of ceramide-induced apoptosis in TF-1 acute myeloid leukemia cells by modulation of the glucosylceramide synthase pathway.	Ceramides	50-58	UDP-glucose ceramide glucosyltransferase	Homo sapiens	135-160
15661399-11	2005	P-gp inhibitors GF120918 and cyclosporin A enhanced ceramide-induced apoptosis in the p-gp expressing cells.	Ceramides	52-60	phosphoglycolate phosphatase	Homo sapiens	0-4
15661399-11	2005	P-gp inhibitors GF120918 and cyclosporin A enhanced ceramide-induced apoptosis in the p-gp expressing cells.	Ceramides	52-60	ATP binding cassette subfamily B member 1	Homo sapiens	86-90
15661399-2	2005	P-glycoprotein (p-gp) might augment ceramide glycosylation by translocating glucosylceramide (GC) across the Golgi membrane.	Ceramides	36-44	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
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.	Ceramides	111-119	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
15661399-2	2005	P-glycoprotein (p-gp) might augment ceramide glycosylation by translocating glucosylceramide (GC) across the Golgi membrane.	Ceramides	36-44	ATP binding cassette subfamily B member 1	Homo sapiens	16-20
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.	Ceramides	111-119	ATP binding cassette subfamily B member 1	Homo sapiens	84-88
15661399-3	2005	We aimed to show that glucosylceramide synthase (GCS) activity is linked to p-gp expression and resistance to ceramide-induced apoptosis in acute myeloid leukemia (AML).	Ceramides	30-38	UDP-glucose ceramide glucosyltransferase	Homo sapiens	49-52
15661399-3	2005	We aimed to show that glucosylceramide synthase (GCS) activity is linked to p-gp expression and resistance to ceramide-induced apoptosis in acute myeloid leukemia (AML).	Ceramides	30-38	ATP binding cassette subfamily B member 1	Homo sapiens	76-80
16415501-3	2005	Despite the fact that PAF exerts these actions within minutes, they are mediated by other lipid mediators, in particular eicosanoids generated by cyclooxygenase and lipoxygenase enzymes and sphingolipids generated by acid sphingomyelinase.We will discuss the mechanisms of the PAF-induced pressor responses that are triggered by thromboxane A(2) and leukotrienes, as well the PAF-induced increase in vascular permeability that is mediated by prostaglandin E(2) (PGE(2)) and ceramide.	Ceramides	474-482	PCNA clamp associated factor	Homo sapiens	22-25
16292752-24	2005	This decrease in CPT activity was not associated with any mutation of the CPT gene is probably mediated by accumulation of ceramides.	Ceramides	123-132	cholinephosphotransferase 1	Cavia porcellus	17-20
16292752-24	2005	This decrease in CPT activity was not associated with any mutation of the CPT gene is probably mediated by accumulation of ceramides.	Ceramides	123-132	cholinephosphotransferase 1	Cavia porcellus	74-77
16292752-25	2005	CEES induced ceramide accumulation may thus play an important role in the development of ARDS by modulating CPT enzyme.	Ceramides	13-21	cholinephosphotransferase 1	Cavia porcellus	108-111
16107015-4	2005	This signaling pathway is initiated by activation of the membrane enzyme neutral sphingomyelinase (nSMase), which catalyses the hydrolysis of membrane shingomyelin to the secondary cellular messenger ceramide.	Ceramides	200-208	sphingomyelin phosphodiesterase 2	Homo sapiens	73-97
15880667-1	2005	Globotriaosylceramide is a neutral glycolipid containing the trihexoside Gal(alpha1-4)Gal(ss1-4)Glc(ss1-1") covalently bound to N-acylsphingosine.	Ceramides	128-145	adrenoceptor alpha 1D	Homo sapiens	77-85
16107015-4	2005	This signaling pathway is initiated by activation of the membrane enzyme neutral sphingomyelinase (nSMase), which catalyses the hydrolysis of membrane shingomyelin to the secondary cellular messenger ceramide.	Ceramides	200-208	sphingomyelin phosphodiesterase 2	Homo sapiens	99-105
15653433-1	2004	Degradation of membrane-bound sphingomyelin to phosphorylcholine and ceramide is catalyzed by the water-soluble lysosomal acid sphingomyelinase (A-SMase).	Ceramides	69-77	sphingomyelin phosphodiesterase 1	Homo sapiens	122-143
15452132-7	2004	Abeta1-42-induced production of ceramide was redox-sensitive, as reactive oxygen species were involved in the activation of N-SMase but not A-SMase.	Ceramides	32-40	sphingomyelin phosphodiesterase 2	Homo sapiens	124-131
15653433-1	2004	Degradation of membrane-bound sphingomyelin to phosphorylcholine and ceramide is catalyzed by the water-soluble lysosomal acid sphingomyelinase (A-SMase).	Ceramides	69-77	sphingomyelin phosphodiesterase 1	Homo sapiens	145-152
15381257-7	2004	We conclude that TNFalpha and ceramide depolarise the RMP of thyroid FRTL-5 cells by attenuating a Ba(2+)- and acid-sensitive potassium conductance via activation of PKCzeta.	Ceramides	30-38	protein kinase C, zeta	Rattus norvegicus	166-173
15563986-7	2004	Since ceramide is known to activate atypical PKC, we also studied the role of atypical PKC on the PPARgamma reducing effect.	Ceramides	6-14	proline rich transmembrane protein 2	Homo sapiens	45-48
15381257-0	2004	Tumor necrosis factor alpha and ceramide depolarise the resting membrane potential of thyroid FRTL-5 cells via a protein kinase Czeta-dependent regulation of K+ channels.	Ceramides	32-40	protein kinase C, zeta	Rattus norvegicus	113-133
15563986-12	2004	These results indicate that the reducing effect of TNFalpha is mediated through ceramide, atypical PKC and NF-kappaB pathway.	Ceramides	80-88	tumor necrosis factor	Homo sapiens	51-59
15563986-0	2004	TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC.	Ceramides	118-126	tumor necrosis factor	Homo sapiens	0-8
15563986-0	2004	TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC.	Ceramides	118-126	peroxisome proliferator activated receptor gamma	Homo sapiens	35-83
15569266-8	2004	U0126 blocked PACAP-induced Bcl-2 expression, abrogated the inhibitory effect of PACAP on ceramide-induced caspase-9 activity, and promoted granule cell death.	Ceramides	90-98	adenylate cyclase activating polypeptide 1	Homo sapiens	81-86
15563986-0	2004	TNFalpha reduces the expression of peroxisome proliferator-activated receptor gamma (PPARgamma) via the production of ceramide and activation of atypical PKC.	Ceramides	118-126	peroxisome proliferator activated receptor gamma	Homo sapiens	85-94
15563986-2	2004	We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes.	Ceramides	27-35	tumor necrosis factor	Homo sapiens	61-69
15563986-2	2004	We evaluated the effect of ceramide, the second messenger of TNFalpha, on the expression of PPARgamma in primary cultured adipocytes.	Ceramides	27-35	peroxisome proliferator activated receptor gamma	Homo sapiens	92-101
15569266-1	2004	The sphingomyelin-derived messenger ceramides provoke neuronal apoptosis through caspase-3 activation, while the neuropeptide pituitary adenylate cyclase-activating polypeptide (PACAP) promotes neuronal survival and inhibits caspase-3 activity.	Ceramides	36-45	caspase 3	Homo sapiens	81-90
15569266-8	2004	U0126 blocked PACAP-induced Bcl-2 expression, abrogated the inhibitory effect of PACAP on ceramide-induced caspase-9 activity, and promoted granule cell death.	Ceramides	90-98	caspase 9	Homo sapiens	107-116
15504043-1	2004	Glycolipid transfer protein (GLTP) catalyzes the intermembrane transfer of lipids that have sugars beta-linked to either diacylglycerol or ceramide backbones, including simple glycosphingolipids (GSLs) and gangliosides.	Ceramides	139-147	glycolipid transfer protein	Homo sapiens	0-27
15660866-1	2004	BACKGROUND: Human alpha-galactosidase A (halphaG) is an essential lysosomal enzyme in catalyzing the hydrolysis of ceramide trihexoside in humans.	Ceramides	115-123	galactosidase alpha	Homo sapiens	18-39
15545317-2	2004	We show that in tumors formed after engraftment of EBCs into mouse brain, expression of the pluripotency marker Oct-4 colocalized with that of prostate apoptosis response-4 (PAR-4), a protein mediating ceramide-induced apoptosis during neural differentiation of ES cells.	Ceramides	202-210	POU domain, class 5, transcription factor 1, related sequence 1	Mus musculus	112-117
15545317-2	2004	We show that in tumors formed after engraftment of EBCs into mouse brain, expression of the pluripotency marker Oct-4 colocalized with that of prostate apoptosis response-4 (PAR-4), a protein mediating ceramide-induced apoptosis during neural differentiation of ES cells.	Ceramides	202-210	PRKC, apoptosis, WT1, regulator	Mus musculus	143-172
15545317-2	2004	We show that in tumors formed after engraftment of EBCs into mouse brain, expression of the pluripotency marker Oct-4 colocalized with that of prostate apoptosis response-4 (PAR-4), a protein mediating ceramide-induced apoptosis during neural differentiation of ES cells.	Ceramides	202-210	PRKC, apoptosis, WT1, regulator	Mus musculus	174-179
15545317-3	2004	We tested the ability of the novel ceramide analogue N-oleoyl serinol (S18) to eliminate mouse and human Oct-4(+)/PAR-4(+) cells and to increase the proportion of nestin(+) neuroprogenitors in EBC-derived cell cultures and grafts.	Ceramides	35-43	POU class 5 homeobox 1	Homo sapiens	105-110
15545317-3	2004	We tested the ability of the novel ceramide analogue N-oleoyl serinol (S18) to eliminate mouse and human Oct-4(+)/PAR-4(+) cells and to increase the proportion of nestin(+) neuroprogenitors in EBC-derived cell cultures and grafts.	Ceramides	35-43	pro-apoptotic WT1 regulator	Homo sapiens	114-119
15271800-0	2004	Interleukin-2-induced survival of natural killer (NK) cells involving phosphatidylinositol-3 kinase-dependent reduction of ceramide through acid sphingomyelinase, sphingomyelin synthase, and glucosylceramide synthase.	Ceramides	123-131	interleukin 2	Homo sapiens	0-13
15271800-0	2004	Interleukin-2-induced survival of natural killer (NK) cells involving phosphatidylinositol-3 kinase-dependent reduction of ceramide through acid sphingomyelinase, sphingomyelin synthase, and glucosylceramide synthase.	Ceramides	123-131	UDP-glucose ceramide glucosyltransferase	Homo sapiens	191-216
15271800-1	2004	Interleukin 2 (IL-2) rescued human natural killer (NK) KHYG-1 cells from apoptosis along with a reduction of ceramide.	Ceramides	109-117	interleukin 2	Homo sapiens	0-13
15271800-1	2004	Interleukin 2 (IL-2) rescued human natural killer (NK) KHYG-1 cells from apoptosis along with a reduction of ceramide.	Ceramides	109-117	interleukin 2	Homo sapiens	15-19
15271800-2	2004	Conversely, an increase of ceramide inhibited IL-2-rescued survival.	Ceramides	27-35	interleukin 2	Homo sapiens	46-50
15271800-5	2004	LY294002 inhibited IL-2-induced reduction of ceramide through activation of acid SMase and inhibition of GCS and SMS, suggesting the positive involvement of PI-3 kinase in ceramide reduction through enzymatic regulation.	Ceramides	45-53	interleukin 2	Homo sapiens	19-23
15271800-5	2004	LY294002 inhibited IL-2-induced reduction of ceramide through activation of acid SMase and inhibition of GCS and SMS, suggesting the positive involvement of PI-3 kinase in ceramide reduction through enzymatic regulation.	Ceramides	172-180	interleukin 2	Homo sapiens	19-23
15271800-8	2004	These results suggest that PI-3 kinase-dependent reduction of ceramide through regulation of acid SMase, GCS, and SMS plays a role in IL-2-rescued survival of NK cells.	Ceramides	62-70	UDP-glucose ceramide glucosyltransferase	Homo sapiens	105-108
15271800-8	2004	These results suggest that PI-3 kinase-dependent reduction of ceramide through regulation of acid SMase, GCS, and SMS plays a role in IL-2-rescued survival of NK cells.	Ceramides	62-70	interleukin 2	Homo sapiens	134-138
15340841-0	2004	Reduced levels of the adenomatous polyposis coli (APC) protein are associated with ceramide-induced apoptosis of colon cancer cells.	Ceramides	83-91	APC regulator of WNT signaling pathway	Homo sapiens	50-53
15557261-9	2004	His 319 in ASM is predicted to protonate the ceramide-leaving group in the catalysis of SM.	Ceramides	45-53	sphingomyelin phosphodiesterase 1	Homo sapiens	11-14
15494128-1	2004	Lysosomal acid beta-glucocerebrosidase hydrolyzes glucocerebroside to glucose ceramide.	Ceramides	78-86	glucosylceramidase beta	Homo sapiens	15-38
15474472-2	2004	The underlying mechanism was recently shown to involve increased synthesis of ceramide, which in turn leads to activation of p38 and p42/44 mitogen-activated protein kinases (MAPKs).	Ceramides	78-86	mitogen-activated protein kinase 14	Homo sapiens	125-128
15474472-2	2004	The underlying mechanism was recently shown to involve increased synthesis of ceramide, which in turn leads to activation of p38 and p42/44 mitogen-activated protein kinases (MAPKs).	Ceramides	78-86	erythrocyte membrane protein band 4.2	Homo sapiens	133-136
15504043-1	2004	Glycolipid transfer protein (GLTP) catalyzes the intermembrane transfer of lipids that have sugars beta-linked to either diacylglycerol or ceramide backbones, including simple glycosphingolipids (GSLs) and gangliosides.	Ceramides	139-147	glycolipid transfer protein	Homo sapiens	29-33
15493986-6	2004	Death receptor clustering in ceramide-rich lipid rafts is thought to be an early event in their signalling, so we investigated the role of ceramide generated by ASM (acid sphingomyelinase) in neutrophil apoptosis.	Ceramides	139-147	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	166-187
15474513-7	2004	These results suggest that the ceramide originating from basolateral sphingomyelin acts on activated CFTR from the cytosolic side, hindering anion secretion.	Ceramides	31-39	CF transmembrane conductance regulator	Homo sapiens	101-105
15493986-10	2004	Generation of ceramide was blocked by desferrioxamine, suggesting that hydroxyl radicals are important for the activation of ASM.	Ceramides	14-22	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	125-128
15520191-0	2004	Ceramide promotes apoptosis in lung cancer-derived A549 cells by a mechanism involving c-Jun NH2-terminal kinase.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	87-92
15331118-13	2004	Ceramide has been shown to induce, by itself, and also augment, LPS-stimulated COX-2 expression and PGE2 production.	Ceramides	0-8	cytochrome c oxidase II, mitochondrial	Mus musculus	79-84
15331118-14	2004	Several lines of evidence indicate that the higher ceramide levels in old Mphi are an important contributor to the age-associated up-regulation of COX-2 in Mphi.	Ceramides	51-59	cytochrome c oxidase II, mitochondrial	Mus musculus	147-152
15331118-15	2004	Ceramide up-regulates COX-2 transcription by increasing activation of transcription factor NF-kappaB.	Ceramides	0-8	cytochrome c oxidase II, mitochondrial	Mus musculus	22-27
15331118-15	2004	Ceramide up-regulates COX-2 transcription by increasing activation of transcription factor NF-kappaB.	Ceramides	0-8	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	91-100
15520191-10	2004	On the other hand, ceramide promoted phosphorylation of Bim and induced translocation of active JNK from the nucleus to the cytoplasm and mitochondrial fraction.	Ceramides	19-27	mitogen-activated protein kinase 8	Homo sapiens	96-99
15520191-11	2004	Ceramide-mediated changes in localization of JNK were consistent with the observed changes in phosphorylation status of c-Jun and Bim.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	45-48
15520191-10	2004	On the other hand, ceramide promoted phosphorylation of Bim and induced translocation of active JNK from the nucleus to the cytoplasm and mitochondrial fraction.	Ceramides	19-27	BCL2 like 11	Homo sapiens	56-59
15520191-11	2004	Ceramide-mediated changes in localization of JNK were consistent with the observed changes in phosphorylation status of c-Jun and Bim.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	120-125
15520191-2	2004	Ceramide is known to potently activate a number of stress-regulated enzymes, including the c-Jun NH(2)-terminal kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	91-118
15520191-2	2004	Ceramide is known to potently activate a number of stress-regulated enzymes, including the c-Jun NH(2)-terminal kinase (JNK).	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	120-123
15520191-11	2004	Ceramide-mediated changes in localization of JNK were consistent with the observed changes in phosphorylation status of c-Jun and Bim.	Ceramides	0-8	BCL2 like 11	Homo sapiens	130-133
15520191-12	2004	Furthermore, ceramide promoted Bim translocation to the mitochondria.	Ceramides	13-21	BCL2 like 11	Homo sapiens	31-34
15520191-4	2004	Here, we report that ceramide promotes apoptosis in A549 cells by a mechanism involving JNK.	Ceramides	21-29	mitogen-activated protein kinase 8	Homo sapiens	88-91
15520191-14	2004	These results suggest that JNK may participate in ceramide-induced apoptosis in A549 cells by a mechanism involving Bim.	Ceramides	50-58	mitogen-activated protein kinase 8	Homo sapiens	27-30
15520191-14	2004	These results suggest that JNK may participate in ceramide-induced apoptosis in A549 cells by a mechanism involving Bim.	Ceramides	50-58	BCL2 like 11	Homo sapiens	116-119
15520191-5	2004	The JNK inhibitor SP600125 proved effective at protecting cells from the lethal effects of ceramide.	Ceramides	91-99	mitogen-activated protein kinase 8	Homo sapiens	4-7
15520191-8	2004	Ceramide was found to inhibit c-Jun phosphorylation, suggesting that JNK-mediated phosphorylation of c-Jun is not likely involved in ceramide-induced apoptosis.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	30-35
15520191-8	2004	Ceramide was found to inhibit c-Jun phosphorylation, suggesting that JNK-mediated phosphorylation of c-Jun is not likely involved in ceramide-induced apoptosis.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	69-72
15520191-8	2004	Ceramide was found to inhibit c-Jun phosphorylation, suggesting that JNK-mediated phosphorylation of c-Jun is not likely involved in ceramide-induced apoptosis.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	101-106
15557813-5	2004	Ceramide/DMS-treated cells displayed several apoptotic features after gamma-irradiation, including increased sub G(1) population, TUNEL-positive fraction, and poly-(ADP-ribose) polymerase (PARP) cleavage.	Ceramides	0-8	poly (ADP-ribose) polymerase family, member 1	Mus musculus	159-187
15666826-6	2004	ACTH/cAMP rapidly decreased levels of the signaling molecules ceramide, sphingosine and sphingosine-1-phosphate (S1P).	Ceramides	62-70	proopiomelanocortin	Homo sapiens	0-4
15482479-5	2004	In the present study, small-angle X-ray diffraction was used to examine the organization in synthetic lipid mixtures of which the synthetic ceramide fraction was prepared with sphingosine-based CER1 or phytosphingosine-based CER9.	Ceramides	140-148	cerberus 1, DAN family BMP antagonist	Homo sapiens	194-198
15557813-5	2004	Ceramide/DMS-treated cells displayed several apoptotic features after gamma-irradiation, including increased sub G(1) population, TUNEL-positive fraction, and poly-(ADP-ribose) polymerase (PARP) cleavage.	Ceramides	0-8	poly (ADP-ribose) polymerase family, member 1	Mus musculus	189-193
15557813-6	2004	We also observed ceramide/ DMS induced disruption of mitochondrial membrane potential (MMP) and activation of caspase- 9 and -3 in a radiation-dose-dependent manner.	Ceramides	17-25	caspase 9	Mus musculus	110-127
15557813-7	2004	Furthermore, pretreatment of LLC cells with ceramide/DMS not only increased the protein expression level of Bax, but also decreased Bcl-2 after gamma-irradiation.	Ceramides	44-52	BCL2-associated X protein	Mus musculus	108-111
15557813-7	2004	Furthermore, pretreatment of LLC cells with ceramide/DMS not only increased the protein expression level of Bax, but also decreased Bcl-2 after gamma-irradiation.	Ceramides	44-52	B cell leukemia/lymphoma 2	Mus musculus	132-137
15509740-10	2004	These studies suggest that gp120 may induce neuronal apoptosis in the CNS of HAD patients through the CXCR4-NADPH oxidase-superoxide-NSMase-ceramide pathway.	Ceramides	140-148	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	27-32
15509740-10	2004	These studies suggest that gp120 may induce neuronal apoptosis in the CNS of HAD patients through the CXCR4-NADPH oxidase-superoxide-NSMase-ceramide pathway.	Ceramides	140-148	C-X-C motif chemokine receptor 4	Homo sapiens	102-107
15509740-4	2004	The present study underlines the importance of gp120 in inducing the production of ceramide, an important inducer of apoptosis, in human primary neurons.	Ceramides	83-91	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	47-52
15509740-10	2004	These studies suggest that gp120 may induce neuronal apoptosis in the CNS of HAD patients through the CXCR4-NADPH oxidase-superoxide-NSMase-ceramide pathway.	Ceramides	140-148	sphingomyelin phosphodiesterase 2	Homo sapiens	133-139
15509740-5	2004	gp120 induced the activation of sphingomyelinases (primarily the neutral one) and the production of ceramide in primary neurons.	Ceramides	100-108	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	0-5
15271994-12	2004	These results indicate that znCD is essential for the metabolism of ceramide and the early development of zebrafish.	Ceramides	68-76	N-acylsphingosine amidohydrolase 2	Danio rerio	28-32
15509740-8	2004	Furthermore, gp120-induced production of ceramide was redox sensitive, because reactive oxygen species were involved in the activation of NSMase but not ASMase.	Ceramides	41-49	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	13-18
15509740-8	2004	Furthermore, gp120-induced production of ceramide was redox sensitive, because reactive oxygen species were involved in the activation of NSMase but not ASMase.	Ceramides	41-49	sphingomyelin phosphodiesterase 2	Homo sapiens	138-144
15317812-0	2004	Defects in cell growth regulation by C18:0-ceramide and longevity assurance gene 1 in human head and neck squamous cell carcinomas.	Ceramides	43-51	Bardet-Biedl syndrome 9	Homo sapiens	37-40
15317812-6	2004	Liquid chromatography/mass spectroscopy analysis showed that overexpression of the mLAG1/mUOG1 resulted in increased levels of only C(18:0)-ceramide by approximately 2-fold, i.e. concentrations similar to those of normal head and neck tissues.	Ceramides	140-148	ceramide synthase 1	Mus musculus	89-94
15469822-4	2004	Consequently, in Drp-1-expressing cells the apoptotic efficacy of ceramide, which causes a Ca2+-dependent perturbation of mitochondrial structure and function, was drastically reduced.	Ceramides	66-74	dynamin 1 like	Homo sapiens	17-22
15364016-9	2004	These findings indicate that chronic cerebral ischemia induces an increased ceramide level in astroglia as a result of downregulation of GCS and an upregulation of ASMase activity.	Ceramides	76-84	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	137-140
15466700-2	2004	The activation of caspase 3 and release of PKCdelta KD are inhibited strongly by the incubation of cells with the ceramidase inhibitor D-erythro-2-tetradecanoylamino-1-phenyl-1-propanol and, to a much lesser extent, by L-cycloserine, an inhibitor of de novo ceramide synthesis.	Ceramides	258-266	caspase 3	Homo sapiens	18-27
15474071-10	2004	CONCLUSION(S): The results suggest that IL-1alpha stimulates the production of IL-8 and M-CSF by a mechanism that involves the sphingomyelin-ceramide system.	Ceramides	141-149	interleukin 1 alpha	Homo sapiens	40-49
15361788-4	2004	Some of the proapoptotic actions of ceramide are to facilitate assembly of death receptor complexes in the plasma membrane, to prevent the activation of protein kinase B/Akt, and to promote the activation of caspase 3.	Ceramides	36-44	AKT serine/threonine kinase 1	Homo sapiens	170-173
15361788-4	2004	Some of the proapoptotic actions of ceramide are to facilitate assembly of death receptor complexes in the plasma membrane, to prevent the activation of protein kinase B/Akt, and to promote the activation of caspase 3.	Ceramides	36-44	caspase 3	Homo sapiens	208-217
15256490-3	2004	Here we extend these results by showing that ceramide, a second messenger in both TNFalpha and IL-1beta receptor signaling pathways, is a key downstream sphingosine-based lipid that leads to IGF-I resistance.	Ceramides	45-53	tumor necrosis factor	Homo sapiens	82-90
15256490-3	2004	Here we extend these results by showing that ceramide, a second messenger in both TNFalpha and IL-1beta receptor signaling pathways, is a key downstream sphingosine-based lipid that leads to IGF-I resistance.	Ceramides	45-53	interleukin 1 beta	Homo sapiens	95-103
15256490-3	2004	Here we extend these results by showing that ceramide, a second messenger in both TNFalpha and IL-1beta receptor signaling pathways, is a key downstream sphingosine-based lipid that leads to IGF-I resistance.	Ceramides	45-53	insulin like growth factor 1	Homo sapiens	191-196
15256490-4	2004	A cell-permeable ceramide analog, C2-ceramide, inhibits IGF-I-induced protein synthesis by 65% and blocks the ability of IGF-I to increase expression of two key myogenic factors, myogenin and MyoD.	Ceramides	17-25	insulin like growth factor 1	Homo sapiens	56-61
15256490-4	2004	A cell-permeable ceramide analog, C2-ceramide, inhibits IGF-I-induced protein synthesis by 65% and blocks the ability of IGF-I to increase expression of two key myogenic factors, myogenin and MyoD.	Ceramides	17-25	insulin like growth factor 1	Homo sapiens	121-126
15256490-4	2004	A cell-permeable ceramide analog, C2-ceramide, inhibits IGF-I-induced protein synthesis by 65% and blocks the ability of IGF-I to increase expression of two key myogenic factors, myogenin and MyoD.	Ceramides	17-25	myogenin	Homo sapiens	179-187
15256490-4	2004	A cell-permeable ceramide analog, C2-ceramide, inhibits IGF-I-induced protein synthesis by 65% and blocks the ability of IGF-I to increase expression of two key myogenic factors, myogenin and MyoD.	Ceramides	17-25	myogenic differentiation 1	Homo sapiens	192-196
15256490-6	2004	Consistent with these data, neutral sphingomyelinase (N-SMase), an enzyme that catalyzes formation of ceramide from sphingomyelin, blocks IGF-I-induced protein synthesis and expression of both myogenin and MyoD.	Ceramides	102-110	sphingomyelin phosphodiesterase 2	Homo sapiens	28-52
15256490-6	2004	Consistent with these data, neutral sphingomyelinase (N-SMase), an enzyme that catalyzes formation of ceramide from sphingomyelin, blocks IGF-I-induced protein synthesis and expression of both myogenin and MyoD.	Ceramides	102-110	sphingomyelin phosphodiesterase 2	Homo sapiens	54-61
15256490-6	2004	Consistent with these data, neutral sphingomyelinase (N-SMase), an enzyme that catalyzes formation of ceramide from sphingomyelin, blocks IGF-I-induced protein synthesis and expression of both myogenin and MyoD.	Ceramides	102-110	insulin like growth factor 1	Homo sapiens	138-143
15256490-6	2004	Consistent with these data, neutral sphingomyelinase (N-SMase), an enzyme that catalyzes formation of ceramide from sphingomyelin, blocks IGF-I-induced protein synthesis and expression of both myogenin and MyoD.	Ceramides	102-110	myogenin	Homo sapiens	193-201
15256490-6	2004	Consistent with these data, neutral sphingomyelinase (N-SMase), an enzyme that catalyzes formation of ceramide from sphingomyelin, blocks IGF-I-induced protein synthesis and expression of both myogenin and MyoD.	Ceramides	102-110	myogenic differentiation 1	Homo sapiens	206-210
15256490-7	2004	The possibility that cytokine-induced ceramide production is required for disruption of IGF-I biologic activity was confirmed by treating C2C12 myoblasts with inhibitors of all three ceramide-generating pathways.	Ceramides	38-46	insulin like growth factor 1	Homo sapiens	88-93
15256490-7	2004	The possibility that cytokine-induced ceramide production is required for disruption of IGF-I biologic activity was confirmed by treating C2C12 myoblasts with inhibitors of all three ceramide-generating pathways.	Ceramides	183-191	insulin like growth factor 1	Homo sapiens	88-93
15256490-9	2004	Likewise, an inhibitor of de novo ceramide synthesis, FB1, causes a 50% inhibition.	Ceramides	34-42	TCF3 fusion partner	Homo sapiens	54-57
15256490-11	2004	These experiments establish that ceramide, derived both from sphingomyelin and de novo synthesis, is a key intermediate by which proinflammatory cytokines impair the ability of IGF-I to promote protein synthesis and expression of critical muscle-specific transcription factors.	Ceramides	33-41	insulin like growth factor 1	Homo sapiens	177-182
15474071-0	2004	Synergistic effect of interleukin (IL)-1alpha and ceramide analogue on the production of IL-6, IL-8, and macrophage colony-stimulating factor by endometrial stromal cells.	Ceramides	50-58	interleukin 6	Homo sapiens	89-93
15474071-0	2004	Synergistic effect of interleukin (IL)-1alpha and ceramide analogue on the production of IL-6, IL-8, and macrophage colony-stimulating factor by endometrial stromal cells.	Ceramides	50-58	C-X-C motif chemokine ligand 8	Homo sapiens	95-99
15474071-0	2004	Synergistic effect of interleukin (IL)-1alpha and ceramide analogue on the production of IL-6, IL-8, and macrophage colony-stimulating factor by endometrial stromal cells.	Ceramides	50-58	colony stimulating factor 1	Homo sapiens	105-141
15474071-1	2004	OBJECTIVE: To measure the level of interleukin 6 (IL-6), IL-8, and macrophage colony-stimulating factor (M-CSF) induced by IL-1alpha in endometrial stromal cells (ESC) following treatment with ceramide analogues.	Ceramides	193-201	interleukin 1 alpha	Homo sapiens	123-132
15448091-2	2004	Here we investigated 1) whether ceramide synthesis, which we reported to mediate fatty acid inhibition of insulin gene expression, also inhibits insulin secretion and 2) whether fatty acid inhibition of insulin secretion involves the generation of reactive oxygen species (ROS), nitric oxide (NO), or prostaglandin E(2) (PGE(2)).	Ceramides	32-40	insulin	Homo sapiens	106-113
15474071-10	2004	CONCLUSION(S): The results suggest that IL-1alpha stimulates the production of IL-8 and M-CSF by a mechanism that involves the sphingomyelin-ceramide system.	Ceramides	141-149	C-X-C motif chemokine ligand 8	Homo sapiens	79-83
15474071-10	2004	CONCLUSION(S): The results suggest that IL-1alpha stimulates the production of IL-8 and M-CSF by a mechanism that involves the sphingomyelin-ceramide system.	Ceramides	141-149	colony stimulating factor 1	Homo sapiens	88-93
15474071-11	2004	Ceramide may be important in increasing the production of IL-8 and M-CSF in the human endometrium.	Ceramides	0-8	C-X-C motif chemokine ligand 8	Homo sapiens	58-62
15474071-11	2004	Ceramide may be important in increasing the production of IL-8 and M-CSF in the human endometrium.	Ceramides	0-8	colony stimulating factor 1	Homo sapiens	67-72
15142848-1	2004	Recently, we showed that neutral sphingomyelinase (N-SMase) is concentrated at the endothelial cell surface in caveolae and is activated to produce ceramide in an acute and transient manner by increase in flow rate and pressure in rat lung vasculature (Czarny M, Liu J, Oh P, and Schnitzer JE, J Biol Chem 278: 4424-4430, 2003).	Ceramides	148-156	sphingomyelin phosphodiesterase 2	Rattus norvegicus	25-49
15625319-2	2004	Challenging [(3)H]Sph-labeled platelet suspensions with thrombin or 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in a decrease in Sph-1-P formation and an increase in sphingosine (Sph), ceramide (Cer), and sphingomyelin formation.	Ceramides	193-201	coagulation factor II, thrombin	Homo sapiens	56-64
15625319-2	2004	Challenging [(3)H]Sph-labeled platelet suspensions with thrombin or 12-O-tetradecanoylphorbol 13-acetate (TPA) resulted in a decrease in Sph-1-P formation and an increase in sphingosine (Sph), ceramide (Cer), and sphingomyelin formation.	Ceramides	203-206	coagulation factor II, thrombin	Homo sapiens	56-64
15350970-5	2004	Abeta25-35-induced synthesis of ceramide was selectively mediated by activation of neutral sphingomyelinase (nSMase), but not acidic sphingomyelinase (aSMase) or ceramide synthase.	Ceramides	32-40	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	83-107
15350970-5	2004	Abeta25-35-induced synthesis of ceramide was selectively mediated by activation of neutral sphingomyelinase (nSMase), but not acidic sphingomyelinase (aSMase) or ceramide synthase.	Ceramides	32-40	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	109-115
15350970-6	2004	Both 3-O-Me-SM and N-acetyl-L-cysteine, the selective and nonselective pharmacological inhibitors of nSMase, respectively, suppressed nSMase activation, ceramide production, and cytotoxic action induced by Abeta25-35 in CECs.	Ceramides	153-161	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	101-107
15350970-8	2004	Together, nSMase activation with subsequent ceramide production may contribute, at least partially, to Abeta25-35 cytotoxicity in cell types with cerebral endothelial and glial lineage.	Ceramides	44-52	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	10-16
15498114-1	2004	Recently, a mitochondrial ceramidase has been identified and cloned, whose mitochondrial localization strongly suggests the existence of an unexpected mitochondrial pathway of ceramide metabolism that may play a key role in mitochondrial functions, especially in the regulation of apoptosis.	Ceramides	176-184	N-acylsphingosine amidohydrolase 2	Homo sapiens	12-36
15252046-5	2004	Recombinant MuLK phosphorylates diacylglycerol, ceramide, and 1-acylglycerol but not sphingosine.	Ceramides	48-56	acylglycerol kinase	Homo sapiens	12-16
15252046-6	2004	Although its affinity for diacylglycerol and ceramide are similar, MuLK exhibits a higher V(max) toward diacylglycerol in vitro, consistent with it acting primarily as a diacylglycerol kinase.	Ceramides	45-53	acylglycerol kinase	Homo sapiens	67-71
15273737-2	2004	In the present work, we show that pretreatment with TNFalpha sensitized the cells to apoptosis induced by antineoplastic agents and ceramide.	Ceramides	132-140	tumor necrosis factor	Homo sapiens	52-60
15273737-3	2004	TNFalpha pretreatment resulted in enhanced cleavage and activity of caspase-3 upon addition of etoposide, epirubicin or ceramide.	Ceramides	120-128	tumor necrosis factor	Homo sapiens	0-8
15273737-3	2004	TNFalpha pretreatment resulted in enhanced cleavage and activity of caspase-3 upon addition of etoposide, epirubicin or ceramide.	Ceramides	120-128	caspase 3	Homo sapiens	68-77
15383576-5	2004	Apoptosis was accompanied by generation of ceramide through activation of acid sphingomyelinase (A-SMase), was prevented by inhibitors of this enzyme, and was restored by exogenous ceramide.	Ceramides	43-51	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	97-104
15262979-4	2004	Here we report a potential regulatory role of caspase-2 on caspase-8 during ceramide-induced apoptosis.	Ceramides	76-84	caspase 2	Homo sapiens	46-55
15262979-4	2004	Here we report a potential regulatory role of caspase-2 on caspase-8 during ceramide-induced apoptosis.	Ceramides	76-84	caspase 8	Homo sapiens	59-68
15262979-5	2004	Our results demonstrate the sequential events of initiator caspase-2 and caspase-8 activation, Bid cleavage and translocation, and mitochondrial damage followed by downstream caspase-9 and -3 activation and cell apoptosis after ceramide induction in T cell lines.	Ceramides	228-236	BH3 interacting domain death agonist	Homo sapiens	95-98
15262979-5	2004	Our results demonstrate the sequential events of initiator caspase-2 and caspase-8 activation, Bid cleavage and translocation, and mitochondrial damage followed by downstream caspase-9 and -3 activation and cell apoptosis after ceramide induction in T cell lines.	Ceramides	228-236	caspase 9	Homo sapiens	175-191
15262979-7	2004	Ceramide-induced caspase-8 activation, mitochondrial damage, and apoptosis were blocked in caspase-2 short interfering RNA-expressing cells.	Ceramides	0-8	caspase 8	Homo sapiens	17-26
15262979-7	2004	Ceramide-induced caspase-8 activation, mitochondrial damage, and apoptosis were blocked in caspase-2 short interfering RNA-expressing cells.	Ceramides	0-8	caspase 2	Homo sapiens	91-100
15262979-8	2004	Therefore, caspase-2 acts upstream of caspase-8 during ceramide-induced mitochondrial apoptosis.	Ceramides	55-63	caspase 2	Homo sapiens	11-20
15262979-8	2004	Therefore, caspase-2 acts upstream of caspase-8 during ceramide-induced mitochondrial apoptosis.	Ceramides	55-63	caspase 8	Homo sapiens	38-47
15262979-10	2004	These data suggest sequential initiator caspase-2 and caspase-8 activation in the mitochondrial apoptotic pathway induced by ceramide or etoposide.	Ceramides	125-133	caspase 2	Homo sapiens	40-49
15262979-10	2004	These data suggest sequential initiator caspase-2 and caspase-8 activation in the mitochondrial apoptotic pathway induced by ceramide or etoposide.	Ceramides	125-133	caspase 8	Homo sapiens	54-63
15142848-1	2004	Recently, we showed that neutral sphingomyelinase (N-SMase) is concentrated at the endothelial cell surface in caveolae and is activated to produce ceramide in an acute and transient manner by increase in flow rate and pressure in rat lung vasculature (Czarny M, Liu J, Oh P, and Schnitzer JE, J Biol Chem 278: 4424-4430, 2003).	Ceramides	148-156	sphingomyelin phosphodiesterase 2	Rattus norvegicus	51-58
15142848-7	2004	Ceramides also induced serine/threonine phosphorylation to activate the Akt/endothelial nitric oxide synthase pathway.	Ceramides	0-9	AKT serine/threonine kinase 1	Rattus norvegicus	72-75
15142848-8	2004	Thus N-SMase at the plasma membrane in caveolae may be an upstream initiating mechanosensor, which acutely triggers mechanotransduction by generation of the lipid second messenger ceramide.	Ceramides	180-188	sphingomyelin phosphodiesterase 2	Rattus norvegicus	5-12
15319326-0	2004	Ceramide, an apoptotic rheostat, inhibits CCAAT/enhancer binding protein-beta and NF-E2-related factor-2 activation: the role in glutathione S-transferase A2 gene repression.	Ceramides	0-8	CCAAT/enhancer binding protein beta	Rattus norvegicus	42-77
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.	Ceramides	98-106	UDP-glucose ceramide glucosyltransferase	Homo sapiens	117-120
15342415-3	2004	Thus, abrogation of apoptosis in HL-60/ADR cells might be involved in ceramide reduction through DOX-induced up-regulation of GCS function.	Ceramides	70-78	UDP-glucose ceramide glucosyltransferase	Homo sapiens	126-129
15342415-8	2004	Together, the results suggest that transcriptional up-regulation of GCS through DOX-induced activation of Sp1 is one potential mechanism to regulate ceramide increase and apoptosis in HL-60/ADR cells.	Ceramides	149-157	UDP-glucose ceramide glucosyltransferase	Homo sapiens	68-71
15319326-0	2004	Ceramide, an apoptotic rheostat, inhibits CCAAT/enhancer binding protein-beta and NF-E2-related factor-2 activation: the role in glutathione S-transferase A2 gene repression.	Ceramides	0-8	NFE2 like bZIP transcription factor 2	Rattus norvegicus	82-104
15319326-0	2004	Ceramide, an apoptotic rheostat, inhibits CCAAT/enhancer binding protein-beta and NF-E2-related factor-2 activation: the role in glutathione S-transferase A2 gene repression.	Ceramides	0-8	glutathione S-transferase alpha 2	Rattus norvegicus	129-157
15319326-4	2004	In the present study, we examined the effects of ceramide on C/EBPbeta or Nrf2 activation and on the inducible GSTA2 gene transactivation.	Ceramides	49-57	CCAAT/enhancer binding protein beta	Rattus norvegicus	61-70
15319326-4	2004	In the present study, we examined the effects of ceramide on C/EBPbeta or Nrf2 activation and on the inducible GSTA2 gene transactivation.	Ceramides	49-57	NFE2 like bZIP transcription factor 2	Rattus norvegicus	74-78
15319326-9	2004	In another study, we found that ceramide decreased nuclear hepatic nuclear factor-1 (HNF1), whose binding to the HNF1-response element in the GSTA2 gene was responsible for the constitutive and inducible gene expression.	Ceramides	32-40	HNF1 homeobox A	Rattus norvegicus	59-83
15319326-9	2004	In another study, we found that ceramide decreased nuclear hepatic nuclear factor-1 (HNF1), whose binding to the HNF1-response element in the GSTA2 gene was responsible for the constitutive and inducible gene expression.	Ceramides	32-40	HNF1 homeobox A	Rattus norvegicus	85-89
15319326-9	2004	In another study, we found that ceramide decreased nuclear hepatic nuclear factor-1 (HNF1), whose binding to the HNF1-response element in the GSTA2 gene was responsible for the constitutive and inducible gene expression.	Ceramides	32-40	HNF1 homeobox A	Rattus norvegicus	113-117
15319326-9	2004	In another study, we found that ceramide decreased nuclear hepatic nuclear factor-1 (HNF1), whose binding to the HNF1-response element in the GSTA2 gene was responsible for the constitutive and inducible gene expression.	Ceramides	32-40	glutathione S-transferase alpha 2	Rattus norvegicus	142-147
15319326-12	2004	Thus, ceramide inhibits C/EBPbeta or Nrf2 activation, which contributes to repression of GSTA2 gene transactivation.	Ceramides	6-14	CCAAT/enhancer binding protein beta	Rattus norvegicus	24-33
15319326-12	2004	Thus, ceramide inhibits C/EBPbeta or Nrf2 activation, which contributes to repression of GSTA2 gene transactivation.	Ceramides	6-14	NFE2 like bZIP transcription factor 2	Rattus norvegicus	37-41
15319326-12	2004	Thus, ceramide inhibits C/EBPbeta or Nrf2 activation, which contributes to repression of GSTA2 gene transactivation.	Ceramides	6-14	glutathione S-transferase alpha 2	Rattus norvegicus	89-94
15231724-0	2004	The sphingomyelin/ceramide pathway is involved in ERK1/2 phosphorylation, cell proliferation, and uPAR overexpression induced by tissue-type plasminogen activator.	Ceramides	18-26	mitogen-activated protein kinase 3	Homo sapiens	50-56
15231724-0	2004	The sphingomyelin/ceramide pathway is involved in ERK1/2 phosphorylation, cell proliferation, and uPAR overexpression induced by tissue-type plasminogen activator.	Ceramides	18-26	plasminogen activator, urokinase receptor	Homo sapiens	98-102
15247143-3	2004	Herein, we investigated the role of IGFBP-3 on apoptosis of human umbilical vein endothelial cells (HUVEC) and its relationship with ceramide levels.	Ceramides	133-141	insulin like growth factor binding protein 3	Homo sapiens	36-43
15231724-0	2004	The sphingomyelin/ceramide pathway is involved in ERK1/2 phosphorylation, cell proliferation, and uPAR overexpression induced by tissue-type plasminogen activator.	Ceramides	18-26	plasminogen activator, tissue type	Homo sapiens	129-162
15247143-5	2004	Ceramide was increased by IGFBP-3 in the presence of doxorubicin and decreased when IGFBP-3 was added alone to cells cultured in serum-free medium.	Ceramides	0-8	insulin like growth factor binding protein 3	Homo sapiens	26-33
15247143-5	2004	Ceramide was increased by IGFBP-3 in the presence of doxorubicin and decreased when IGFBP-3 was added alone to cells cultured in serum-free medium.	Ceramides	0-8	insulin like growth factor binding protein 3	Homo sapiens	84-91
15264225-5	2004	Because it has been reported that NGF binding to p75NTR leads to ceramide generation, we evaluated whether ceramide was also neuroprotective.	Ceramides	65-73	nerve growth factor receptor	Homo sapiens	49-55
15247143-6	2004	The protection exerted by the ceramide synthase inhibitor fumonisin B1 over doxorubicin-induced apoptosis was enhanced by IGFBP-3 with concomitant reduction of ceramide levels.	Ceramides	30-38	insulin like growth factor binding protein 3	Homo sapiens	122-129
15339967-2	2004	Metabolism of ceramide involves several enzymes, including glucosylceramide synthase and GD3 synthase, and results in the formation of gangliosides (GM3, GD3, and GT3), which in turn promote the generation of reactive oxygen species (ROS) and apoptosis.	Ceramides	14-22	UDP-glucose ceramide glucosyltransferase	Homo sapiens	59-84
15339967-2	2004	Metabolism of ceramide involves several enzymes, including glucosylceramide synthase and GD3 synthase, and results in the formation of gangliosides (GM3, GD3, and GT3), which in turn promote the generation of reactive oxygen species (ROS) and apoptosis.	Ceramides	14-22	GRDX	Homo sapiens	89-92
15339967-2	2004	Metabolism of ceramide involves several enzymes, including glucosylceramide synthase and GD3 synthase, and results in the formation of gangliosides (GM3, GD3, and GT3), which in turn promote the generation of reactive oxygen species (ROS) and apoptosis.	Ceramides	14-22	GRDX	Homo sapiens	154-157
15328045-1	2004	Cholesterol (CHOL), free fatty acids (FFA) and nine classes of ceramides (CER1-CER9) form the main constituents of the intercellular lipid lamellae in stratum corneum (SC), which regulate the skin barrier function.	Ceramides	63-72	cerberus 1, DAN family BMP antagonist	Bos taurus	74-83
15220355-0	2004	Regulation of insulin action by ceramide: dual mechanisms linking ceramide accumulation to the inhibition of Akt/protein kinase B.	Ceramides	32-40	AKT serine/threonine kinase 1	Homo sapiens	109-112
15220355-0	2004	Regulation of insulin action by ceramide: dual mechanisms linking ceramide accumulation to the inhibition of Akt/protein kinase B.	Ceramides	32-40	protein tyrosine kinase 2 beta	Homo sapiens	113-129
15220355-0	2004	Regulation of insulin action by ceramide: dual mechanisms linking ceramide accumulation to the inhibition of Akt/protein kinase B.	Ceramides	66-74	AKT serine/threonine kinase 1	Homo sapiens	109-112
15220355-0	2004	Regulation of insulin action by ceramide: dual mechanisms linking ceramide accumulation to the inhibition of Akt/protein kinase B.	Ceramides	66-74	protein tyrosine kinase 2 beta	Homo sapiens	113-129
15220355-3	2004	Herein we utilized deletion constructs encoding two different functional domains of Akt/PKB to identify which region of the enzyme conferred responsiveness to ceramide.	Ceramides	159-167	AKT serine/threonine kinase 1	Homo sapiens	84-91
15220355-4	2004	Surprisingly the findings obtained with these separate domains reveal that ceramide blocks insulin stimulation of Akt/PKB by two independent mechanisms.	Ceramides	75-83	AKT serine/threonine kinase 1	Homo sapiens	114-117
15131591-0	2004	Molecular mechanisms of TNF-alpha-induced ceramide formation in human glioma cells: P53-mediated oxidant stress-dependent and -independent pathways.	Ceramides	42-50	tumor necrosis factor	Homo sapiens	24-33
15131591-0	2004	Molecular mechanisms of TNF-alpha-induced ceramide formation in human glioma cells: P53-mediated oxidant stress-dependent and -independent pathways.	Ceramides	42-50	tumor protein p53	Homo sapiens	84-87
15131591-2	2004	In cells possessing wild-type p53, TNF-alpha stimulated ceramide formation via the activation of both neutral and acid sphingomyelinases (SMases), accompanied by superoxide anion (O2-*) production, and induced mitochondrial depolarization and cytochrome c release, whereas p53-deficient cells were partially resistant to TNF-alpha and lacked O2-* generation and neutral SMase activation.	Ceramides	56-64	tumor protein p53	Homo sapiens	30-33
15131591-2	2004	In cells possessing wild-type p53, TNF-alpha stimulated ceramide formation via the activation of both neutral and acid sphingomyelinases (SMases), accompanied by superoxide anion (O2-*) production, and induced mitochondrial depolarization and cytochrome c release, whereas p53-deficient cells were partially resistant to TNF-alpha and lacked O2-* generation and neutral SMase activation.	Ceramides	56-64	tumor necrosis factor	Homo sapiens	35-44
15131591-2	2004	In cells possessing wild-type p53, TNF-alpha stimulated ceramide formation via the activation of both neutral and acid sphingomyelinases (SMases), accompanied by superoxide anion (O2-*) production, and induced mitochondrial depolarization and cytochrome c release, whereas p53-deficient cells were partially resistant to TNF-alpha and lacked O2-* generation and neutral SMase activation.	Ceramides	56-64	cytochrome c, somatic	Homo sapiens	243-255
15131591-2	2004	In cells possessing wild-type p53, TNF-alpha stimulated ceramide formation via the activation of both neutral and acid sphingomyelinases (SMases), accompanied by superoxide anion (O2-*) production, and induced mitochondrial depolarization and cytochrome c release, whereas p53-deficient cells were partially resistant to TNF-alpha and lacked O2-* generation and neutral SMase activation.	Ceramides	56-64	tumor protein p53	Homo sapiens	273-276
15131591-2	2004	In cells possessing wild-type p53, TNF-alpha stimulated ceramide formation via the activation of both neutral and acid sphingomyelinases (SMases), accompanied by superoxide anion (O2-*) production, and induced mitochondrial depolarization and cytochrome c release, whereas p53-deficient cells were partially resistant to TNF-alpha and lacked O2-* generation and neutral SMase activation.	Ceramides	56-64	tumor necrosis factor	Homo sapiens	321-330
15131591-6	2004	Two separate signaling cascades, p53-mediated ROS-dependent and -independent pathways, both of which are initiated by caspase-8 activation, thus contribute to ceramide formation in TNF-alpha-induced apoptosis of human glioma cells.	Ceramides	159-167	tumor protein p53	Homo sapiens	33-36
15131591-6	2004	Two separate signaling cascades, p53-mediated ROS-dependent and -independent pathways, both of which are initiated by caspase-8 activation, thus contribute to ceramide formation in TNF-alpha-induced apoptosis of human glioma cells.	Ceramides	159-167	caspase 8	Homo sapiens	118-127
15131591-6	2004	Two separate signaling cascades, p53-mediated ROS-dependent and -independent pathways, both of which are initiated by caspase-8 activation, thus contribute to ceramide formation in TNF-alpha-induced apoptosis of human glioma cells.	Ceramides	159-167	tumor necrosis factor	Homo sapiens	181-190
15322180-0	2004	Ceramide inhibits IL-2 production by preventing protein kinase C-dependent NF-kappaB activation: possible role in protein kinase Ctheta regulation.	Ceramides	0-8	interleukin 2	Homo sapiens	18-22
15322180-0	2004	Ceramide inhibits IL-2 production by preventing protein kinase C-dependent NF-kappaB activation: possible role in protein kinase Ctheta regulation.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	75-84
15322180-1	2004	The role of the sphingolipid ceramide in modulating the immune response has been controversial, in part because of conflicting data regarding its ability to regulate the transcription factor NF-kappaB.	Ceramides	29-37	nuclear factor kappa B subunit 1	Homo sapiens	191-200
15322180-2	2004	To help clarify this role, we investigated the effects of ceramide on IL-2, a central NF-kappaB target.	Ceramides	58-66	interleukin 2	Homo sapiens	70-74
15322180-3	2004	We found that ceramide inhibited protein kinase C (PKC)-mediated activation of NF-kappaB.	Ceramides	14-22	protein kinase C alpha	Homo sapiens	51-54
15322180-3	2004	We found that ceramide inhibited protein kinase C (PKC)-mediated activation of NF-kappaB.	Ceramides	14-22	nuclear factor kappa B subunit 1	Homo sapiens	79-88
15322180-4	2004	Ceramide was found to significantly reduce the kinase activity of PKCtheta as well as PKCalpha, the critical PKC isozymes involved in TCR-induced NF-kappaB activation.	Ceramides	0-8	protein kinase C alpha	Homo sapiens	86-94
15322180-4	2004	Ceramide was found to significantly reduce the kinase activity of PKCtheta as well as PKCalpha, the critical PKC isozymes involved in TCR-induced NF-kappaB activation.	Ceramides	0-8	protein kinase C alpha	Homo sapiens	66-69
15322180-4	2004	Ceramide was found to significantly reduce the kinase activity of PKCtheta as well as PKCalpha, the critical PKC isozymes involved in TCR-induced NF-kappaB activation.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	146-155
15322180-6	2004	Exogenous sphingomyelinase, which generates ceramide at the cell membrane, also inhibited IL-2 production.	Ceramides	44-52	interleukin 2	Homo sapiens	90-94
15322180-7	2004	As expected, the repression of NF-kappaB activation by ceramide led to the reduction of transcription of the IL-2 gene in a dose-dependent manner.	Ceramides	55-63	nuclear factor kappa B subunit 1	Homo sapiens	31-40
15322180-7	2004	As expected, the repression of NF-kappaB activation by ceramide led to the reduction of transcription of the IL-2 gene in a dose-dependent manner.	Ceramides	55-63	interleukin 2	Homo sapiens	109-113
15322180-8	2004	Inhibition of IL-2 production by ceramide was partially overcome when NF-kappaB nuclear translocation was reconstituted with activation of a PKC-independent pathway by TNF-alpha or when PKCtheta was overexpressed.	Ceramides	33-41	interleukin 2	Homo sapiens	14-18
15322180-8	2004	Inhibition of IL-2 production by ceramide was partially overcome when NF-kappaB nuclear translocation was reconstituted with activation of a PKC-independent pathway by TNF-alpha or when PKCtheta was overexpressed.	Ceramides	33-41	nuclear factor kappa B subunit 1	Homo sapiens	70-79
15322180-8	2004	Inhibition of IL-2 production by ceramide was partially overcome when NF-kappaB nuclear translocation was reconstituted with activation of a PKC-independent pathway by TNF-alpha or when PKCtheta was overexpressed.	Ceramides	33-41	protein kinase C alpha	Homo sapiens	141-144
15322180-8	2004	Inhibition of IL-2 production by ceramide was partially overcome when NF-kappaB nuclear translocation was reconstituted with activation of a PKC-independent pathway by TNF-alpha or when PKCtheta was overexpressed.	Ceramides	33-41	tumor necrosis factor	Homo sapiens	168-177
15322180-10	2004	These results indicate that ceramide plays a negative regulatory role in the activation of NF-kappaB and its targets as a result of inhibition of PKC.	Ceramides	28-36	nuclear factor kappa B subunit 1	Homo sapiens	91-100
15322180-10	2004	These results indicate that ceramide plays a negative regulatory role in the activation of NF-kappaB and its targets as a result of inhibition of PKC.	Ceramides	28-36	protein kinase C alpha	Homo sapiens	146-149
15220355-4	2004	Surprisingly the findings obtained with these separate domains reveal that ceramide blocks insulin stimulation of Akt/PKB by two independent mechanisms.	Ceramides	75-83	AKT serine/threonine kinase 1	Homo sapiens	118-121
15220355-5	2004	First, using the isolated pleckstrin homology domain, we found that ceramide specifically blocks the translocation of Akt/PKB, but not its upstream activator phosphoinositide-dependent kinase-1, to the plasma membrane.	Ceramides	68-76	AKT serine/threonine kinase 1	Homo sapiens	118-125
15220355-6	2004	Second, using a construct lacking this pleckstrin homology domain, which does not require translocation for activation, we found that ceramide stimulates the dephosphorylation of Akt/PKB by protein phosphatase 2A.	Ceramides	134-142	AKT serine/threonine kinase 1	Homo sapiens	179-182
15220355-6	2004	Second, using a construct lacking this pleckstrin homology domain, which does not require translocation for activation, we found that ceramide stimulates the dephosphorylation of Akt/PKB by protein phosphatase 2A.	Ceramides	134-142	AKT serine/threonine kinase 1	Homo sapiens	183-186
15220355-8	2004	Moreover the results obtained provide a unifying theory to account for the numerous dissenting reports investigating the actions of ceramide toward Akt/PKB.	Ceramides	132-140	AKT serine/threonine kinase 1	Homo sapiens	148-155
15262207-0	2004	In vivo influence of ceramide accumulation induced by treatment with a glucosylceramide synthase inhibitor on ischemic neuronal cell death.	Ceramides	21-29	UDP-glucose ceramide glucosyltransferase	Homo sapiens	71-96
15264216-2	2004	As the most important interaction, TrkA signaling was found to inhibit p75(NTR)-mediated sphingomyelinase (SMase) stimulation, ceramide production, and apoptosis.	Ceramides	127-135	neurotrophic receptor tyrosine kinase 1	Homo sapiens	35-39
15264216-2	2004	As the most important interaction, TrkA signaling was found to inhibit p75(NTR)-mediated sphingomyelinase (SMase) stimulation, ceramide production, and apoptosis.	Ceramides	127-135	TNF receptor superfamily member 1B	Homo sapiens	71-74
15264216-2	2004	As the most important interaction, TrkA signaling was found to inhibit p75(NTR)-mediated sphingomyelinase (SMase) stimulation, ceramide production, and apoptosis.	Ceramides	127-135	neurotensin receptor 1	Homo sapiens	75-78
15264216-5	2004	In this study, we found that, in SK-N-BE cells, which selectively express p75(NTR), phorbol ester-induced PKC stimulation resulted in the abrogation of SMase stimulation and ceramide production induced by NGF.	Ceramides	174-182	TNF receptor superfamily member 1B	Homo sapiens	74-77
15264216-5	2004	In this study, we found that, in SK-N-BE cells, which selectively express p75(NTR), phorbol ester-induced PKC stimulation resulted in the abrogation of SMase stimulation and ceramide production induced by NGF.	Ceramides	174-182	neurotensin receptor 1	Homo sapiens	78-81
15264216-5	2004	In this study, we found that, in SK-N-BE cells, which selectively express p75(NTR), phorbol ester-induced PKC stimulation resulted in the abrogation of SMase stimulation and ceramide production induced by NGF.	Ceramides	174-182	proline rich transmembrane protein 2	Homo sapiens	106-109
15264216-5	2004	In this study, we found that, in SK-N-BE cells, which selectively express p75(NTR), phorbol ester-induced PKC stimulation resulted in the abrogation of SMase stimulation and ceramide production induced by NGF.	Ceramides	174-182	nerve growth factor	Homo sapiens	205-208
15264216-8	2004	However, in these cells, the inhibition of TrkA, PI3K, and PKC resulted in the restoration of NGF-induced ceramide production.	Ceramides	106-114	neurotrophic receptor tyrosine kinase 1	Homo sapiens	43-47
15264216-8	2004	However, in these cells, the inhibition of TrkA, PI3K, and PKC resulted in the restoration of NGF-induced ceramide production.	Ceramides	106-114	proline rich transmembrane protein 2	Homo sapiens	59-62
15264216-8	2004	However, in these cells, the inhibition of TrkA, PI3K, and PKC resulted in the restoration of NGF-induced ceramide production.	Ceramides	106-114	nerve growth factor	Homo sapiens	94-97
15264225-12	2004	Overall, we interpret these results as consistent with an NGF neuroprotective pathway wherein p75NTR activation leads sequentially to ceramide generation, new protein synthesis, and inhibition of calpain activation.	Ceramides	134-142	nerve growth factor receptor	Homo sapiens	94-100
15276244-7	2004	These results indicate that NGF can increase the excitability of nociceptive sensory neurons through activation of the p75 neurotrophin receptor and its consequent liberation of ceramide from neuronal sphingomyelins.	Ceramides	178-186	nerve growth factor receptor	Rattus norvegicus	119-122
15313899-5	2004	Cannabinoid-induced inhibition of VEGF production and VEGFR-2 activation was abrogated both in vitro and in vivo by pharmacological blockade of ceramide biosynthesis.	Ceramides	144-152	vascular endothelial growth factor A	Mus musculus	34-38
15313899-5	2004	Cannabinoid-induced inhibition of VEGF production and VEGFR-2 activation was abrogated both in vitro and in vivo by pharmacological blockade of ceramide biosynthesis.	Ceramides	144-152	kinase insert domain protein receptor	Mus musculus	54-61
15161907-6	2004	In addition, mangiferin inhibits TNF-induced p65 phosphorylation as well as translocation to the nucleus and also inhibits NF-kappaB activation induced by other inflammatory agents like PMA, ceramide, and SA-LPS.	Ceramides	191-199	nuclear factor kappa B subunit 1	Homo sapiens	123-132
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.	Ceramides	8-16	Glucosylceramide synthase	Drosophila melanogaster	27-33
15210713-3	2004	Recently, we have shown that GlcT-1 functions to regulate intracellular ceramide levels via glycosylation of ceramide.	Ceramides	72-80	Glucosylceramide synthase	Drosophila melanogaster	29-35
15210713-3	2004	Recently, we have shown that GlcT-1 functions to regulate intracellular ceramide levels via glycosylation of ceramide.	Ceramides	109-117	Glucosylceramide synthase	Drosophila melanogaster	29-35
15210713-9	2004	Conversely, targeted expression of GlcT-1 partially rescued cell death caused by the proapoptotic factors Reaper and Grim, suggesting that ceramide generation might be one signal pathway that executes the cell death program.	Ceramides	139-147	Glucosylceramide synthase	Drosophila melanogaster	35-41
15210713-9	2004	Conversely, targeted expression of GlcT-1 partially rescued cell death caused by the proapoptotic factors Reaper and Grim, suggesting that ceramide generation might be one signal pathway that executes the cell death program.	Ceramides	139-147	grim	Drosophila melanogaster	117-121
15320336-6	2004	GM1a injected into the gastric cavity was incorporated and then directly catabolized by EGCase to produce GM1a-oligosaccharide and ceramide, which were further degraded by exoglycosidases and ceramidase, respectively.	Ceramides	131-139	LOC101236181	Hydra vulgaris	88-94
15210713-11	2004	These results indicate that GlcT-1 might down-regulate ceramide generated in these membranes.	Ceramides	55-63	Glucosylceramide synthase	Drosophila melanogaster	28-34
15320336-1	2004	Endoglycoceramidase (EGCase; EC 3.2.1.123) is an enzyme capable of cleaving the glycosidic linkage between oligosaccharides and ceramides of various glycosphingolipids.	Ceramides	128-137	LOC101236181	Hydra vulgaris	0-19
15320336-1	2004	Endoglycoceramidase (EGCase; EC 3.2.1.123) is an enzyme capable of cleaving the glycosidic linkage between oligosaccharides and ceramides of various glycosphingolipids.	Ceramides	128-137	LOC101236181	Hydra vulgaris	21-27
15276646-9	2004	Interestingly, one inhibitor of caspase-10 and related caspases z-AEVD-fmk (50 microM) inhibited both AGE-MGX-induced apoptosis and DAG/ceramide formation in pericytes.	Ceramides	136-144	caspase-10	Bos taurus	32-42
15276646-9	2004	Interestingly, one inhibitor of caspase-10 and related caspases z-AEVD-fmk (50 microM) inhibited both AGE-MGX-induced apoptosis and DAG/ceramide formation in pericytes.	Ceramides	136-144	caspase 8	Bos taurus	55-63
15277330-0	2004	Role for matrix metalloproteinase-2 in oxidized low-density lipoprotein-induced activation of the sphingomyelin/ceramide pathway and smooth muscle cell proliferation.	Ceramides	112-120	matrix metallopeptidase 2	Homo sapiens	9-35
15277330-8	2004	MMP inhibitors (batimastat and Ro28-2653) and the blocking antibodies anti-MMP-2 and anti-membrane type 1-MMP inhibited the oxLDL-induced sphingomyelin/ceramide pathway activation and subsequent activation of ERK1/2 and DNA synthesis but did not inhibit the oxLDL-induced epidermal growth factor receptor and platelet-derived growth factor receptor activation.	Ceramides	152-160	matrix metallopeptidase 2	Homo sapiens	0-3
15277330-8	2004	MMP inhibitors (batimastat and Ro28-2653) and the blocking antibodies anti-MMP-2 and anti-membrane type 1-MMP inhibited the oxLDL-induced sphingomyelin/ceramide pathway activation and subsequent activation of ERK1/2 and DNA synthesis but did not inhibit the oxLDL-induced epidermal growth factor receptor and platelet-derived growth factor receptor activation.	Ceramides	152-160	matrix metallopeptidase 2	Homo sapiens	75-80
15217913-5	2004	Exogenous ceramide induces vWF release from endothelial cells in a dose-dependent manner.	Ceramides	10-18	von Willebrand factor	Homo sapiens	27-30
15217913-8	2004	The NO donor S-nitroso-N-acetylpenicillamine decreases ceramide-induced vWF release in a dose-dependent manner, whereas the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester increases ceramide-induced vWF release.	Ceramides	55-63	von Willebrand factor	Homo sapiens	72-75
15217913-8	2004	The NO donor S-nitroso-N-acetylpenicillamine decreases ceramide-induced vWF release in a dose-dependent manner, whereas the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester increases ceramide-induced vWF release.	Ceramides	55-63	von Willebrand factor	Homo sapiens	208-211
15276646-5	2004	Effects of peptidic inhibitors of caspases were determined on DAG/ceramide production and apoptosis.	Ceramides	66-74	caspase 8	Bos taurus	34-42
15277330-9	2004	Exogenously added activated MMP-2 or membrane type 1-MMP-1 triggered the activation of both sphingomyelin/ceramide and ERK1/2 pathways and DNA synthesis.	Ceramides	106-114	matrix metallopeptidase 2	Homo sapiens	28-33
15277330-10	2004	Conversely, suppression of MMP-2 expression in MMP-2-/- cells or in SMCs treated by small-interference RNA also blocked both sphingomyelin/ceramide signaling and DNA synthesis.	Ceramides	139-147	matrix metallopeptidase 2	Homo sapiens	27-32
15277330-10	2004	Conversely, suppression of MMP-2 expression in MMP-2-/- cells or in SMCs treated by small-interference RNA also blocked both sphingomyelin/ceramide signaling and DNA synthesis.	Ceramides	139-147	matrix metallopeptidase 2	Homo sapiens	47-52
15277330-11	2004	CONCLUSIONS: Together, these data demonstrate that MMP-2 plays a pivotal role in oxLDL-induced activation of the sphingomyelin/ceramide signaling pathway and subsequent SMC proliferation.	Ceramides	127-135	matrix metallopeptidase 2	Homo sapiens	51-56
15157676-7	2004	These results suggest that ceramide elicits up-regulation of NF-kappaB through ROS production, which, in turn, leads to stimulation of COX-2 and sPLA2 expression.	Ceramides	27-35	prostaglandin-endoperoxide synthase 2	Homo sapiens	135-140
15088070-0	2004	p53-Independent ceramide formation in human glioma cells during gamma-radiation-induced apoptosis.	Ceramides	16-24	tumor protein p53	Homo sapiens	0-3
15088070-4	2004	The formation of ceramide by acid sphingomyelinase (A-SMase), but not by neutral sphingomyelinase, was associated with p53-independent apoptosis.	Ceramides	17-25	sphingomyelin phosphodiesterase 1	Homo sapiens	29-50
15088070-4	2004	The formation of ceramide by acid sphingomyelinase (A-SMase), but not by neutral sphingomyelinase, was associated with p53-independent apoptosis.	Ceramides	17-25	sphingomyelin phosphodiesterase 1	Homo sapiens	52-59
15088070-4	2004	The formation of ceramide by acid sphingomyelinase (A-SMase), but not by neutral sphingomyelinase, was associated with p53-independent apoptosis.	Ceramides	17-25	tumor protein p53	Homo sapiens	119-122
15157676-0	2004	Ceramide-induced enhancement of secretory phospholipase A2 expression via generation of reactive oxygen species in tumor necrosis factor-alpha-stimulated mesangial cells.	Ceramides	0-8	phospholipase A2 group X	Homo sapiens	32-58
15157676-0	2004	Ceramide-induced enhancement of secretory phospholipase A2 expression via generation of reactive oxygen species in tumor necrosis factor-alpha-stimulated mesangial cells.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	115-142
15157676-7	2004	These results suggest that ceramide elicits up-regulation of NF-kappaB through ROS production, which, in turn, leads to stimulation of COX-2 and sPLA2 expression.	Ceramides	27-35	phospholipase A2 group X	Homo sapiens	145-150
15157676-1	2004	Since prostanoids such as prostaglandin E2 play a pivotal role in modulating renal function, we investigated the involvement of ceramide in expression of secretory phospholipase A2 (sPLA2) and cyclooxygenase-2 (COX-2) in tumor necrosis factor-alpha (TNF-alpha)-stimulated mesangial cells.	Ceramides	128-136	phospholipase A2 group X	Homo sapiens	154-180
15157676-1	2004	Since prostanoids such as prostaglandin E2 play a pivotal role in modulating renal function, we investigated the involvement of ceramide in expression of secretory phospholipase A2 (sPLA2) and cyclooxygenase-2 (COX-2) in tumor necrosis factor-alpha (TNF-alpha)-stimulated mesangial cells.	Ceramides	128-136	phospholipase A2 group X	Homo sapiens	182-187
15157676-2	2004	TNF-alpha stimulation increased ceramide generation in parallel with a decrease in sphingomyelin.	Ceramides	32-40	tumor necrosis factor	Homo sapiens	0-9
15088070-9	2004	Moreover, cells with functional p53 could be sensitized to gamma-radiation by N-oleoylethanolamine, which suppressed radiation-induced acid ceramidase expression and then enhanced ceramide formation.	Ceramides	180-188	tumor protein p53	Homo sapiens	32-35
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	tumor protein p53	Homo sapiens	67-70
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	tumor protein p53	Homo sapiens	164-167
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	N-acylsphingosine amidohydrolase 1	Homo sapiens	192-207
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	sphingomyelin phosphodiesterase 1	Homo sapiens	224-231
15088070-11	2004	These results indicate that ceramide may function as a mediator of p53-independent apoptosis in human glioma cells in response to gamma-radiation, and suggest that p53-dependent expression of acid ceramidase and blockage of A-SMase activation play pivotal roles in protection from gamma-radiation of cells with endogenous functional p53.	Ceramides	28-36	tumor protein p53	Homo sapiens	164-167
15289350-13	2004	We conclude the following: (a) 4-HPR was active against ESFT cell lines in vitro at concentrations achievable clinically, but activity was decreased in hypoxia; and (b) combining 4-HPR with ceramide modulators synergized 4-HPR cytotoxicity in normoxia and hypoxia.	Ceramides	190-198	haptoglobin-related protein	Homo sapiens	33-36
15289350-8	2004	4-HPR increased ceramide species in the three cell lines tested (up to 9-fold; P < 0.05).	Ceramides	16-24	haptoglobin-related protein	Homo sapiens	2-5
15123644-1	2004	Several lines of evidence suggest that neutral ceramidase is involved in the regulation of ceramide-mediated signaling.	Ceramides	91-99	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	39-57
15289350-11	2004	Hypoxia increased AC RNA expression; the AC inhibitor NOE enhanced 4-HPR-induced ceramide species increase and cytotoxicity.	Ceramides	81-89	haptoglobin-related protein	Homo sapiens	69-72
15223066-4	2004	We also observed that LPS, IFN-gamma, and A beta(25-35) treatment led to the activation of the sphingomyelin-ceramide (SM-Cer) cascade with an increase in cellular ceramide.	Ceramides	109-117	interferon gamma	Homo sapiens	27-36
15223066-4	2004	We also observed that LPS, IFN-gamma, and A beta(25-35) treatment led to the activation of the sphingomyelin-ceramide (SM-Cer) cascade with an increase in cellular ceramide.	Ceramides	109-117	amyloid beta precursor protein	Homo sapiens	42-48
15223066-4	2004	We also observed that LPS, IFN-gamma, and A beta(25-35) treatment led to the activation of the sphingomyelin-ceramide (SM-Cer) cascade with an increase in cellular ceramide.	Ceramides	164-172	interferon gamma	Homo sapiens	27-36
15223066-4	2004	We also observed that LPS, IFN-gamma, and A beta(25-35) treatment led to the activation of the sphingomyelin-ceramide (SM-Cer) cascade with an increase in cellular ceramide.	Ceramides	164-172	amyloid beta precursor protein	Homo sapiens	42-48
15223066-6	2004	Hence, these findings suggest a role for ceramide in iNOS induction and NO production in Abeta-induced AD pathobiology and provide a possible explanation for the beneficial effects of vitamin E therapy.	Ceramides	41-49	nitric oxide synthase 2	Homo sapiens	53-57
15203188-0	2004	Ceramide-induced apoptosis: role of catalase and hepatocyte growth factor.	Ceramides	0-8	catalase	Homo sapiens	36-44
15203188-0	2004	Ceramide-induced apoptosis: role of catalase and hepatocyte growth factor.	Ceramides	0-8	hepatocyte growth factor	Homo sapiens	49-73
15203188-1	2004	The aim of this study was to elucidate cellular mechanisms involved in ceramide-induced apoptosis and its attenuation by hepatocyte growth factor (HGF).	Ceramides	71-79	hepatocyte growth factor	Homo sapiens	121-145
15203188-1	2004	The aim of this study was to elucidate cellular mechanisms involved in ceramide-induced apoptosis and its attenuation by hepatocyte growth factor (HGF).	Ceramides	71-79	hepatocyte growth factor	Homo sapiens	147-150
15203188-3	2004	Ceramide-treated cells showed increased caspase-3 activation and an increase in mitochondrial membrane permeability transition (MPT).	Ceramides	0-8	caspase 3	Homo sapiens	40-49
15203188-5	2004	Furthermore, ceramide treatment significantly decreased catalase enzymatic activity and protein expression.	Ceramides	13-21	catalase	Homo sapiens	56-64
15203188-6	2004	HGF pretreatment (20 ng/ml) significantly inhibited ceramide-induced apoptosis and reduced the accumulation of ROS, the activation of caspase-3, and the increase in MPT and prevented the reduction in catalase activity and expression.	Ceramides	52-60	hepatocyte growth factor	Homo sapiens	0-3
15203188-7	2004	Together, the data suggest that ceramide induces apoptosis in RPE cells by increasing ROS production, MPT, and caspase-3 activation.	Ceramides	32-40	caspase 3	Homo sapiens	111-120
15203188-8	2004	The ceramide effect is potentiated by H2O2 and associated with a reduction in catalase activity, suggesting that catalase plays a central role in regulating this apoptotic response.	Ceramides	4-12	catalase	Homo sapiens	78-86
15203188-8	2004	The ceramide effect is potentiated by H2O2 and associated with a reduction in catalase activity, suggesting that catalase plays a central role in regulating this apoptotic response.	Ceramides	4-12	catalase	Homo sapiens	113-121
15102832-2	2004	The proapoptotic effects of tumor necrosis factor-alpha, hypoxia, and chemotherapeutic drugs were attributed to increased ceramide formation.	Ceramides	122-130	tumor necrosis factor	Bos taurus	28-55
15453638-8	2004	Interestingly, EGF-induced tyrosine phosphorylation of the EGF receptor was strongly attenuated by 1O2 but unimpaired by C2-ceramide, implying that, although ceramide formation may mediate the above attenuation of ERK and Akt phosphorylation induced by 1O2, mechanisms beyond ceramide formation exist that mediate impairment of growth factor signaling by singlet oxygen.	Ceramides	158-166	epidermal growth factor receptor	Homo sapiens	59-71
15236759-6	2004	The two multicopy suppressors YBR183w (YPC1) and YPL087w (YDC1) encode ceramidases unrelated to Lag1p and Lac1p, which were previously found to support the reverse reaction of ceramide synthesis.	Ceramides	176-184	phytoceramidase	Saccharomyces cerevisiae S288C	39-43
15236759-6	2004	The two multicopy suppressors YBR183w (YPC1) and YPL087w (YDC1) encode ceramidases unrelated to Lag1p and Lac1p, which were previously found to support the reverse reaction of ceramide synthesis.	Ceramides	176-184	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	58-62
15236759-6	2004	The two multicopy suppressors YBR183w (YPC1) and YPL087w (YDC1) encode ceramidases unrelated to Lag1p and Lac1p, which were previously found to support the reverse reaction of ceramide synthesis.	Ceramides	176-184	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	96-101
15236759-6	2004	The two multicopy suppressors YBR183w (YPC1) and YPL087w (YDC1) encode ceramidases unrelated to Lag1p and Lac1p, which were previously found to support the reverse reaction of ceramide synthesis.	Ceramides	176-184	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	106-111
15236759-13	2004	Homologues of Lag1p have been identified in higher eukaryotes, including human, raising the possibility that ceramide and other sphingolipid metabolites play a wider role in biological aging.	Ceramides	109-117	ceramide synthase 1	Homo sapiens	14-19
15255262-5	2004	CONCLUSIONS: Ceramide resistance was found to arise from the inhibition of caspase-7 induced by IAPs, especially X chromosome-linked IAP (XIAP).	Ceramides	13-21	caspase 7	Homo sapiens	75-84
15239106-12	2004	Induction of Bcl-x(S) by ceramide in HepG2 cells also resulted in apoptosis.	Ceramides	25-33	BCL2 like 1	Homo sapiens	13-18
15255262-5	2004	CONCLUSIONS: Ceramide resistance was found to arise from the inhibition of caspase-7 induced by IAPs, especially X chromosome-linked IAP (XIAP).	Ceramides	13-21	X-linked inhibitor of apoptosis	Homo sapiens	113-136
15255262-5	2004	CONCLUSIONS: Ceramide resistance was found to arise from the inhibition of caspase-7 induced by IAPs, especially X chromosome-linked IAP (XIAP).	Ceramides	13-21	X-linked inhibitor of apoptosis	Homo sapiens	138-142
15255262-6	2004	Small interfering RNA (siRNA) on XIAP quenched that resistance in ceramide-resistant human glioma cells (U251SP, T98G, SKAO2, U251MG), indicating that a siRNA for XIAP may be a useful tool for overcoming the resistance to ceramide in human glioma cells.	Ceramides	66-74	X-linked inhibitor of apoptosis	Homo sapiens	33-37
15255262-6	2004	Small interfering RNA (siRNA) on XIAP quenched that resistance in ceramide-resistant human glioma cells (U251SP, T98G, SKAO2, U251MG), indicating that a siRNA for XIAP may be a useful tool for overcoming the resistance to ceramide in human glioma cells.	Ceramides	66-74	X-linked inhibitor of apoptosis	Homo sapiens	163-167
15255262-6	2004	Small interfering RNA (siRNA) on XIAP quenched that resistance in ceramide-resistant human glioma cells (U251SP, T98G, SKAO2, U251MG), indicating that a siRNA for XIAP may be a useful tool for overcoming the resistance to ceramide in human glioma cells.	Ceramides	222-230	X-linked inhibitor of apoptosis	Homo sapiens	33-37
15255262-6	2004	Small interfering RNA (siRNA) on XIAP quenched that resistance in ceramide-resistant human glioma cells (U251SP, T98G, SKAO2, U251MG), indicating that a siRNA for XIAP may be a useful tool for overcoming the resistance to ceramide in human glioma cells.	Ceramides	222-230	X-linked inhibitor of apoptosis	Homo sapiens	163-167
15158440-0	2004	Reduced expression of Bax in ceramide-resistant HL-60 subline.	Ceramides	29-37	BCL2 associated X, apoptosis regulator	Homo sapiens	22-25
15201971-0	2004	Ceramide triggers caspase activation during gamma-radiation-induced apoptosis of human glioma cells lacking functional p53.	Ceramides	0-8	tumor protein p53	Homo sapiens	119-122
15201971-1	2004	We have previously shown that treatment of human glioma U87-MG cells expressing wild-type p53 with a DNA topoisomerase II inhibitor, etoposide resulted in ceramide-dependent apoptotic cell death.	Ceramides	155-163	tumor protein p53	Homo sapiens	90-93
15201971-6	2004	Activation of caspase-3, and formation of ceramide by acid sphingomyelinase, but not by neutral sphingomyelinase, were associated with p53-independent apoptosis.	Ceramides	42-50	tumor protein p53	Homo sapiens	135-138
15201971-10	2004	These results indicate that glioma cells with functional p53 were relatively resistant to gamma-radiation, and that ceramide may play an important role in caspase activation during gamma-radiation-induced apoptosis of glioma cells lacking functional p53.	Ceramides	116-124	tumor protein p53	Homo sapiens	250-253
14979873-4	2004	The sensitizing effect of ceramide accumulation may depend on p38 mitogen-activated protein kinase activation rather than on other ceramide targets.	Ceramides	26-34	mitogen-activated protein kinase 14	Homo sapiens	62-65
15205343-0	2004	Pivotal role of the cell death factor BNIP3 in ceramide-induced autophagic cell death in malignant glioma cells.	Ceramides	47-55	BCL2 interacting protein 3	Homo sapiens	38-43
15205343-5	2004	We additionally demonstrate that ceramide decreases mitochondrial membrane potential and activates the transcription of death-inducing mitochondrial protein, BNIP3, resulting in increased expression levels of its mRNA and protein in malignant glioma cells.	Ceramides	33-41	BCL2 interacting protein 3	Homo sapiens	158-163
15205343-7	2004	These results suggest that ceramide induces autophagic cell death in malignant glioma cells via activation of BNIP3.	Ceramides	27-35	BCL2 interacting protein 3	Homo sapiens	110-115
15051724-8	2004	Cell cycle analysis showed that up-regulation of endogenous nSMase2 correlated with G(0)/G(1) cell cycle arrest and an increase in total ceramide levels (2.4-fold).	Ceramides	137-145	sphingomyelin phosphodiesterase 3	Homo sapiens	60-67
15051724-11	2004	Down-regulation of nSMase2 with specific siRNA increased the cell population of cells in S phase of the cell cycle by 59 +/- 14% and selectively reverted the effects of growth arrest on the increase in levels of very long chain ceramides.	Ceramides	228-237	sphingomyelin phosphodiesterase 3	Homo sapiens	19-26
15032750-0	2004	Acyl-CoA-binding protein, Acb1p, is required for normal vacuole function and ceramide synthesis in Saccharomyces cerevisiae.	Ceramides	77-85	long-chain fatty acid transporter ACB1	Saccharomyces cerevisiae S288C	26-31
15032750-1	2004	In the present study, we show that depletion of acyl-CoA-binding protein, Acb1p, in yeast affects ceramide levels, protein trafficking, vacuole fusion and structure.	Ceramides	98-106	long-chain fatty acid transporter ACB1	Saccharomyces cerevisiae S288C	74-79
15032750-3	2004	Mass spectrometric analysis revealed a dramatic reduction in the content of ceramides in whole-cell lipids and in vacuoles isolated from Acb1p-depleted cells.	Ceramides	76-85	long-chain fatty acid transporter ACB1	Saccharomyces cerevisiae S288C	137-142
15032750-6	2004	We suggest that the reduced ceramide synthesis in Acb1p-depleted cells leads to severely altered vacuole morphology, perturbed vacuole assembly and strong inhibition of homotypic vacuole fusion.	Ceramides	28-36	long-chain fatty acid transporter ACB1	Saccharomyces cerevisiae S288C	50-55
15189345-3	2004	C(2)-ceramide abolishes neurite formation induced by overexpression of PKCepsilon and, in cells overexpressing PKCdelta or PKCtheta, ceramide treatment leads to apoptosis.	Ceramides	5-13	protein kinase C epsilon	Homo sapiens	71-81
15059969-5	2004	In addition, the expression of this NSMase-2 clone in primary hepatocytes led to increased cellular levels of ceramide, indicating that the enzyme is active in situ.	Ceramides	110-118	sphingomyelin phosphodiesterase 3	Rattus norvegicus	36-44
15175033-3	2004	Acid and neutral sphingomyelinase (A- and N-SMase) generate ceramides with structural and signal transduction functions in epidermal proliferation and differentiation.	Ceramides	60-69	sphingomyelin phosphodiesterase 2	Homo sapiens	42-49
15175033-5	2004	We found decreased epidermal A-SMase activity in lesional and non-lesional skin, correlating with reduced stratum corneum ceramide content and disturbed barrier function.	Ceramides	122-130	sphingomyelin phosphodiesterase 1	Homo sapiens	29-36
15181369-1	2004	After 24-hour middle cerebral artery occlusion (MCAO) in spontaneously hypertensive rats, brain ceramide level increased from baseline reached 595% (ischemic core) and 460% (perifocal/penumbral areas); brain glucosylceramide synthase (GCS) activities in these areas simultaneously decreased by 70% and 50%, respectively.	Ceramides	96-104	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	208-233
15181369-1	2004	After 24-hour middle cerebral artery occlusion (MCAO) in spontaneously hypertensive rats, brain ceramide level increased from baseline reached 595% (ischemic core) and 460% (perifocal/penumbral areas); brain glucosylceramide synthase (GCS) activities in these areas simultaneously decreased by 70% and 50%, respectively.	Ceramides	96-104	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	235-238
15181369-4	2004	In ischemic tolerance, GCS appears to modulate otherwise high levels of brain ceramide.	Ceramides	78-86	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	23-26
15189345-8	2004	Taken together, the data indicate that the neurite-inhibiting effect of C(2)-ceramide treatment may be caused by a re-localization of PKCepsilon and thus identify a functional consequence of ceramide effects on PKCepsilon localization.	Ceramides	77-85	protein kinase C epsilon	Homo sapiens	134-144
15189345-8	2004	Taken together, the data indicate that the neurite-inhibiting effect of C(2)-ceramide treatment may be caused by a re-localization of PKCepsilon and thus identify a functional consequence of ceramide effects on PKCepsilon localization.	Ceramides	77-85	protein kinase C epsilon	Homo sapiens	211-221
15155840-0	2004	Ceramide negatively regulates glutathione S-transferase gene transactivation via repression of hepatic nuclear factor-1 that is degraded by the ubiquitin proteasome system.	Ceramides	0-8	hematopoietic prostaglandin D synthase	Rattus norvegicus	30-55
15155840-0	2004	Ceramide negatively regulates glutathione S-transferase gene transactivation via repression of hepatic nuclear factor-1 that is degraded by the ubiquitin proteasome system.	Ceramides	0-8	HNF1 homeobox A	Rattus norvegicus	95-119
15155840-4	2004	This study investigated the role of HNF1 in GSTA2 gene transactivation, the ubiquitin proteasomal degradation of HNF1, and the inhibition of activating HNF1 by ceramide for GSTA2 repression.	Ceramides	160-168	glutathione S-transferase alpha 2	Rattus norvegicus	173-178
15155840-13	2004	In conclusion, the HRE in the GSTA2 promoter region is functionally active for the constitutive and inducible gene expression, and ceramide inhibits GST gene transactivation through decrease in nuclear HNF1, which is degraded by the ubiquitin proteasome system.	Ceramides	131-139	glutathione S-transferase alpha 2	Rattus norvegicus	30-35
15155840-13	2004	In conclusion, the HRE in the GSTA2 promoter region is functionally active for the constitutive and inducible gene expression, and ceramide inhibits GST gene transactivation through decrease in nuclear HNF1, which is degraded by the ubiquitin proteasome system.	Ceramides	131-139	hematopoietic prostaglandin D synthase	Rattus norvegicus	30-33
15155840-13	2004	In conclusion, the HRE in the GSTA2 promoter region is functionally active for the constitutive and inducible gene expression, and ceramide inhibits GST gene transactivation through decrease in nuclear HNF1, which is degraded by the ubiquitin proteasome system.	Ceramides	131-139	HNF1 homeobox A	Rattus norvegicus	202-206
15287503-0	2004	[The molecular machinery CERT for intracellular trafficking of ceramide].	Ceramides	63-71	ceramide transporter 1	Homo sapiens	25-29
15111489-1	2004	In vitro studies revealed that insulin resistance might be associated with the intracellular formation of ceramide, the second messenger in the sphingomyelin signaling pathway.	Ceramides	106-114	insulin	Homo sapiens	31-38
15150117-8	2004	Together, these results demonstrate that cisplatin activates aSMase and induces ceramide production, which triggers the redistribution of CD95 into the plasma membrane rafts.	Ceramides	80-88	Fas cell surface death receptor	Homo sapiens	138-142
14739942-4	2004	We recently identified the endolysosomal aspartate protease cathepsin D (CTSD) as a target for the proapoptotic lipid ceramide.	Ceramides	118-126	cathepsin D	Homo sapiens	60-71
14739942-4	2004	We recently identified the endolysosomal aspartate protease cathepsin D (CTSD) as a target for the proapoptotic lipid ceramide.	Ceramides	118-126	cathepsin D	Homo sapiens	73-77
15130763-3	2004	We and others have shown that the tyrosine kinase p56/Lck is involved in the regulation of apoptosis induced by irradiation or treatment with ceramide but dispensable for death receptor triggered cell death.	Ceramides	142-150	cyclin dependent kinase like 2	Homo sapiens	50-53
15130763-3	2004	We and others have shown that the tyrosine kinase p56/Lck is involved in the regulation of apoptosis induced by irradiation or treatment with ceramide but dispensable for death receptor triggered cell death.	Ceramides	142-150	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	54-57
15111489-7	2004	Insulin sensitivity was related to total ceramide content (r = -0.49, P = 0.01) and to ceramide consisting of palmitic (r = -0.48, P = 0.011), palmitoleic (r = -0.45, P = 0.019), mirystic (r = -0.42, P = 0.028), and nervonic acid (r = -0.39, P = 0.047).	Ceramides	41-49	insulin	Homo sapiens	0-7
15111489-7	2004	Insulin sensitivity was related to total ceramide content (r = -0.49, P = 0.01) and to ceramide consisting of palmitic (r = -0.48, P = 0.011), palmitoleic (r = -0.45, P = 0.019), mirystic (r = -0.42, P = 0.028), and nervonic acid (r = -0.39, P = 0.047).	Ceramides	87-95	insulin	Homo sapiens	0-7
15111489-11	2004	A relationship with the decrease in insulin sensitivity was also observed for ceramides consisting of palmitic (r = -0.68, P = 0.03) and linoleic (r = -0.66, P = 0.038) acid.	Ceramides	78-87	insulin	Homo sapiens	36-43
15294058-4	2004	Fatty acyl-CoA, ceramides and diacylglycerols are known to directly alter various aspects of the insulin signalling cascade.	Ceramides	16-25	insulin	Homo sapiens	97-104
15126630-1	2004	We previously demonstrated that the aspartate protease cathepsin D is activated by ceramide derived from acid sphingomyelinase.	Ceramides	83-91	cathepsin D	Mus musculus	55-66
14970205-0	2004	Ceramide-mediated macroautophagy involves inhibition of protein kinase B and up-regulation of beclin 1.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	56-72
14970205-0	2004	Ceramide-mediated macroautophagy involves inhibition of protein kinase B and up-regulation of beclin 1.	Ceramides	0-8	beclin 1	Homo sapiens	94-102
14970205-4	2004	Ceramide reverted the interleukin 13-dependent inhibition of macroautophagy by interfering with the activation of protein kinase B.	Ceramides	0-8	interleukin 13	Homo sapiens	22-36
14970205-4	2004	Ceramide reverted the interleukin 13-dependent inhibition of macroautophagy by interfering with the activation of protein kinase B.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	114-130
14967819-2	2004	Enforced GCS overexpression has been shown to disrupt ceramide-induced apoptosis and to confer resistance to doxorubicin.	Ceramides	54-62	UDP-glucose ceramide glucosyltransferase	Homo sapiens	9-12
15141021-11	2004	We conclude that selection pressure for resistance to natural product chemotherapy drugs selects for enhanced ceramide metabolism through glucosylceramide synthase in addition to enhanced P-gp expression.	Ceramides	110-118	UDP-glucose ceramide glucosyltransferase	Homo sapiens	138-163
14766899-1	2004	Several studies have shown that ceramide (CER) glucosylation contributes to drug resistance in multidrug-resistant cells and that inhibition of glucosylceramide synthase sensitizes cells to various drug treatments.	Ceramides	32-40	UDP-glucose ceramide glucosyltransferase	Homo sapiens	144-169
14976195-7	2004	WR19L/Fas-SM(-) cells expressing SMS1 cDNA (WR19L/Fas-SMS1) restored the resistance against MbetaCD, the accumulation of SM at the plasma membrane, and SM synthesis by transferring phosphocholine from phosphatidylcholine to ceramide.	Ceramides	224-232	sphingomyelin synthase 1	Mus musculus	33-37
14976195-7	2004	WR19L/Fas-SM(-) cells expressing SMS1 cDNA (WR19L/Fas-SMS1) restored the resistance against MbetaCD, the accumulation of SM at the plasma membrane, and SM synthesis by transferring phosphocholine from phosphatidylcholine to ceramide.	Ceramides	224-232	sphingomyelin synthase 1	Mus musculus	50-58
14769792-1	2004	Ceramide kinase (CERK) catalyzes the conversion of ceramide to ceramide 1-phosphate (C1P) and is known to be activated by calcium.	Ceramides	51-59	ceramide kinase	Rattus norvegicus	0-15
14985352-1	2004	Tumor necrosis factor (TNF) alpha-induced neutral sphingomyelinase-mediated generation of ceramide, a bioactive lipid molecule, is transduced by the adaptor protein FAN, which binds to the intracellular region of the CD120a TNFalpha receptor.	Ceramides	90-98	tumor necrosis factor	Mus musculus	0-33
14985352-1	2004	Tumor necrosis factor (TNF) alpha-induced neutral sphingomyelinase-mediated generation of ceramide, a bioactive lipid molecule, is transduced by the adaptor protein FAN, which binds to the intracellular region of the CD120a TNFalpha receptor.	Ceramides	90-98	neutral sphingomyelinase (N-SMase) activation associated factor	Mus musculus	165-168
14985352-1	2004	Tumor necrosis factor (TNF) alpha-induced neutral sphingomyelinase-mediated generation of ceramide, a bioactive lipid molecule, is transduced by the adaptor protein FAN, which binds to the intracellular region of the CD120a TNFalpha receptor.	Ceramides	90-98	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	217-223
14985352-1	2004	Tumor necrosis factor (TNF) alpha-induced neutral sphingomyelinase-mediated generation of ceramide, a bioactive lipid molecule, is transduced by the adaptor protein FAN, which binds to the intracellular region of the CD120a TNFalpha receptor.	Ceramides	90-98	tumor necrosis factor	Mus musculus	224-232
14769792-1	2004	Ceramide kinase (CERK) catalyzes the conversion of ceramide to ceramide 1-phosphate (C1P) and is known to be activated by calcium.	Ceramides	51-59	ceramide kinase	Rattus norvegicus	17-21
14734550-0	2004	Identification of two RNA cis-elements that function to regulate the 5" splice site selection of Bcl-x pre-mRNA in response to ceramide.	Ceramides	127-135	BCL2 like 1	Homo sapiens	97-102
14734550-14	2004	Therefore, we have identified two ceramide-responsive RNA cis-elements within exon 2 of Bcl-x pre-mRNA, and this is the first report of an RNA cis-element responsive to a bioactive lipid.	Ceramides	34-42	BCL2 like 1	Homo sapiens	88-93
15023539-1	2004	Ceramide has been proposed to be an important signaling intermediate in tumor necrosis factor (TNF)-induced apoptosis in human MCF-7 breast adenocarcinoma cells.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	72-93
15100056-3	2004	Type 2 involves changes in mitochondrial integrity initiated by various effectors like Ca(2+), reactive oxygen species (ROS), Bax, or ceramide, leading to the release of cytochrome c and activation of caspase 9.	Ceramides	134-142	cytochrome c, somatic	Homo sapiens	170-182
15100056-3	2004	Type 2 involves changes in mitochondrial integrity initiated by various effectors like Ca(2+), reactive oxygen species (ROS), Bax, or ceramide, leading to the release of cytochrome c and activation of caspase 9.	Ceramides	134-142	caspase 9	Homo sapiens	201-210
15013522-5	2004	Several anticancer agents, including the cytotoxic retinoid, fenretinide (4-HPR), have been shown to act, at least in part, by increasing tumor cell ceramide via de novo synthesis.	Ceramides	149-157	haptoglobin-related protein	Homo sapiens	76-79
15013522-6	2004	Combinations of 4-HPR and modulators of ceramide action and/or metabolism demonstrated increased anti-tumor activity in pre-clinical models with minimal toxicity for non-malignant cells, and were effective in a p53-independent manner against tumor cell lines resistant to standard cytotoxic agents.	Ceramides	40-48	tumor protein p53	Homo sapiens	211-214
14978734-2	2004	Ceramide treatment causes the round up and the death of A-431 cells that is associated with p38 activation and can be observed in 10 h. Short-time ceramide treatment-induced cell death is not associated with the typical apoptotic phenotypes, such as the translocation of phosphatidylserine (PS) from inner layer to outer layer of the plasma membrane, loss of mitochondrial membrane potential, DNA fragmentation, caspase activation, and PARP or PKC-delta degradation.	Ceramides	0-8	mitogen-activated protein kinase 14	Homo sapiens	92-95
14978734-2	2004	Ceramide treatment causes the round up and the death of A-431 cells that is associated with p38 activation and can be observed in 10 h. Short-time ceramide treatment-induced cell death is not associated with the typical apoptotic phenotypes, such as the translocation of phosphatidylserine (PS) from inner layer to outer layer of the plasma membrane, loss of mitochondrial membrane potential, DNA fragmentation, caspase activation, and PARP or PKC-delta degradation.	Ceramides	0-8	poly(ADP-ribose) polymerase 1	Homo sapiens	436-440
14978734-2	2004	Ceramide treatment causes the round up and the death of A-431 cells that is associated with p38 activation and can be observed in 10 h. Short-time ceramide treatment-induced cell death is not associated with the typical apoptotic phenotypes, such as the translocation of phosphatidylserine (PS) from inner layer to outer layer of the plasma membrane, loss of mitochondrial membrane potential, DNA fragmentation, caspase activation, and PARP or PKC-delta degradation.	Ceramides	147-155	poly(ADP-ribose) polymerase 1	Homo sapiens	436-440
14978734-3	2004	SB202190, a specific inhibitor of p38 mitogen-activated protein (MAP) kinase, but not caspase inhibitor, blocks the cell death induced by short-time ceramide treatment (within 12 h).	Ceramides	149-157	mitogen-activated protein kinase 14	Homo sapiens	34-37
14978734-7	2004	The caspase-independent cell death that occurred in relatively early stage of ceramide treatment is mediated via p38 MAP kinase, which can progress into a stage that is associated with changes of cell cycle events and involves both caspase-dependent and -independent mechanisms.	Ceramides	78-86	mitogen-activated protein kinase 14	Homo sapiens	113-127
15023539-1	2004	Ceramide has been proposed to be an important signaling intermediate in tumor necrosis factor (TNF)-induced apoptosis in human MCF-7 breast adenocarcinoma cells.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	95-98
15023539-2	2004	We compared cell death and signal transduction pathways induced by TNF and ceramide in TNF-sensitive, parental MCF-7 cells to those in TNF-resistant, MCF-7 cells (3E9).	Ceramides	75-83	tumor necrosis factor	Homo sapiens	87-90
15023539-2	2004	We compared cell death and signal transduction pathways induced by TNF and ceramide in TNF-sensitive, parental MCF-7 cells to those in TNF-resistant, MCF-7 cells (3E9).	Ceramides	75-83	tumor necrosis factor	Homo sapiens	87-90
15023539-6	2004	TNF was able to activate JNK/SAPK approximately 30-fold and approximately 5-fold in parental MCF-7 and 3E9 cells, respectively; in contrast, cell-permeable ceramide only weakly stimulated JNK/SAPK activity in either cell type.	Ceramides	156-164	tumor necrosis factor	Homo sapiens	0-3
14722126-1	2004	Sphingosine kinase is a highly conserved enzyme that catalyzes the synthesis of sphingosine 1-phosphate and reduces cellular levels of sphingosine and ceramide.	Ceramides	151-159	Sphingosine kinase 2	Drosophila melanogaster	0-18
14643749-4	2004	The accumulation of ceramide was found to depend on the activation of magnesium-dependent neutral sphingomyelinase (N-SMase), but not on de novo synthesis.	Ceramides	20-28	sphingomyelin phosphodiesterase 2	Rattus norvegicus	90-114
14643749-4	2004	The accumulation of ceramide was found to depend on the activation of magnesium-dependent neutral sphingomyelinase (N-SMase), but not on de novo synthesis.	Ceramides	20-28	sphingomyelin phosphodiesterase 2	Rattus norvegicus	116-123
14643749-8	2004	Thus our data suggest that crocin combats the serum/glucose deprivation-induced ceramide formation in PC-12 cells by increasing GSH levels and prevents the activation of JNK pathway, which is reported to have a role of the signaling cascade downstream ceramide for neuronal cell death.	Ceramides	252-260	mitogen-activated protein kinase 8	Rattus norvegicus	170-173
15469694-2	2004	Here we report the protective role of tTGase in the cell death that is induced by the tumor necrosis factor alpha (TNF-alpha) and ceramide, a product of the TNF-alpha signaling pathway, in human neuroblastoma SH-SY5Y cells.	Ceramides	130-138	transglutaminase 2	Homo sapiens	38-44
15469694-2	2004	Here we report the protective role of tTGase in the cell death that is induced by the tumor necrosis factor alpha (TNF-alpha) and ceramide, a product of the TNF-alpha signaling pathway, in human neuroblastoma SH-SY5Y cells.	Ceramides	130-138	tumor necrosis factor	Homo sapiens	157-166
15469694-9	2004	These results suggest that tTGase expressed by RA treatment plays an important role in the protection of cell death caused by TNF-alpha and ceramide.	Ceramides	140-148	transglutaminase 2	Homo sapiens	27-33
14715667-4	2004	Ceramide-induced apoptosis was inhibited by the PKCdelta-specific inhibitor rottlerin and also was blocked by knockdown of endogenous PKCdelta expression using small interfering RNA.	Ceramides	0-8	protein kinase C delta	Homo sapiens	48-56
14715667-4	2004	Ceramide-induced apoptosis was inhibited by the PKCdelta-specific inhibitor rottlerin and also was blocked by knockdown of endogenous PKCdelta expression using small interfering RNA.	Ceramides	0-8	protein kinase C delta	Homo sapiens	134-142
14715667-5	2004	Ceramide induced the translocation of PKCdelta to the Golgi complex and the concomitant activation of PKCdelta via phosphorylation of Tyr(311) and Tyr(332) in the hinge region of the enzyme.	Ceramides	0-8	protein kinase C delta	Homo sapiens	38-46
14715667-5	2004	Ceramide induced the translocation of PKCdelta to the Golgi complex and the concomitant activation of PKCdelta via phosphorylation of Tyr(311) and Tyr(332) in the hinge region of the enzyme.	Ceramides	0-8	protein kinase C delta	Homo sapiens	102-110
14715667-6	2004	Unphosphorylatable PKCdelta (mutants Y311F and Y332F) could translocate to the Golgi complex in response to ceramide, suggesting that tyrosine phosphorylation is not necessary for translocation.	Ceramides	108-116	protein kinase C delta	Homo sapiens	19-27
14715667-8	2004	These findings suggest that ceramide translocates PKCdelta to the Golgi complex and that PKCdelta is activated by tyrosine phosphorylation in the compartment.	Ceramides	28-36	protein kinase C delta	Homo sapiens	50-58
14715667-9	2004	Furthermore, we utilized species-specific knockdown of PKCdelta by small interfering RNA to study the significance of phosphorylation of Tyr(311) and Tyr(332) in PKCdelta for ceramide-induced apoptosis and found that phosphorylation of Tyr(311) and Tyr(332) is indispensable for ceramide-induced apoptosis.	Ceramides	175-183	protein kinase C delta	Homo sapiens	162-170
14715667-9	2004	Furthermore, we utilized species-specific knockdown of PKCdelta by small interfering RNA to study the significance of phosphorylation of Tyr(311) and Tyr(332) in PKCdelta for ceramide-induced apoptosis and found that phosphorylation of Tyr(311) and Tyr(332) is indispensable for ceramide-induced apoptosis.	Ceramides	279-287	protein kinase C delta	Homo sapiens	55-63
14715667-10	2004	We demonstrate here that the targeting mechanism of PKCdelta, dual regulation of both its activation and translocation to the Golgi complex, is critical for the ceramide-induced apoptotic event.	Ceramides	161-169	protein kinase C delta	Homo sapiens	52-60
14699160-12	2004	The results also suggest a role for Isc1p-generated ceramides in optimal regulation of growth.	Ceramides	52-61	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	36-41
14615385-2	2004	Ceramide inhibition of PLD suppresses PMN function.	Ceramides	0-8	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	23-26
14615385-0	2004	Ceramide inhibition of phospholipase D and its relationship to RhoA and ARF1 translocation in GTP gamma S-stimulated polymorphonuclear leukocytes.	Ceramides	0-8	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	23-38
14615385-4	2004	To investigate the mechanism of ceramide"s inhibitory effect on PLD, we used a cell-free system to examine PLD activity and translocation from cytosol to plasma membrane of ARF, protein kinase C (PKC)alpha and beta, and RhoA, all of which can activate PLD.	Ceramides	32-40	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	64-67
14615385-0	2004	Ceramide inhibition of phospholipase D and its relationship to RhoA and ARF1 translocation in GTP gamma S-stimulated polymorphonuclear leukocytes.	Ceramides	0-8	ras homolog family member A	Homo sapiens	63-67
14615385-0	2004	Ceramide inhibition of phospholipase D and its relationship to RhoA and ARF1 translocation in GTP gamma S-stimulated polymorphonuclear leukocytes.	Ceramides	0-8	ADP ribosylation factor 1	Homo sapiens	72-76
14615385-4	2004	To investigate the mechanism of ceramide"s inhibitory effect on PLD, we used a cell-free system to examine PLD activity and translocation from cytosol to plasma membrane of ARF, protein kinase C (PKC)alpha and beta, and RhoA, all of which can activate PLD.	Ceramides	32-40	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	107-110
14615385-4	2004	To investigate the mechanism of ceramide"s inhibitory effect on PLD, we used a cell-free system to examine PLD activity and translocation from cytosol to plasma membrane of ARF, protein kinase C (PKC)alpha and beta, and RhoA, all of which can activate PLD.	Ceramides	32-40	ras homolog family member A	Homo sapiens	220-224
14615385-4	2004	To investigate the mechanism of ceramide"s inhibitory effect on PLD, we used a cell-free system to examine PLD activity and translocation from cytosol to plasma membrane of ARF, protein kinase C (PKC)alpha and beta, and RhoA, all of which can activate PLD.	Ceramides	32-40	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	107-110
14615385-8	2004	Exogenous RhoA did not restore ceramide-inhibited PLD activity but bound to membranes despite ceramide treatment.	Ceramides	94-102	ras homolog family member A	Homo sapiens	10-14
14615385-9	2004	These observations suggest that, although ceramide may affect RhoA in some systems, ceramide inhibits PLD through another mechanism, perhaps related to the ability of ceramide to inhibit phosphatidylinositol-bisphosphate (PIP2) interaction with PLD.	Ceramides	84-92	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	102-105
14615385-9	2004	These observations suggest that, although ceramide may affect RhoA in some systems, ceramide inhibits PLD through another mechanism, perhaps related to the ability of ceramide to inhibit phosphatidylinositol-bisphosphate (PIP2) interaction with PLD.	Ceramides	84-92	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	102-105
14613483-9	2004	Activation of PP1 by treatment of the cells with ceramide suppressed Ser-23 phosphorylation, as did transfection of the catalytic subunit of PP1.	Ceramides	49-57	inorganic pyrophosphatase 1	Homo sapiens	14-17
14657198-6	2004	Modification of the sphingoid chain also abolished the ability of ceramide to activate PP2Ac.	Ceramides	66-74	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	87-92
14647238-6	2004	Ceramide, which is involved in HPR-induced apoptosis, was also involved in c-Fos induction because its upregulation by HPR was reduced by fumonisin B(1), a ceramide synthase inhibitor.	Ceramides	0-8	haptoglobin-related protein	Homo sapiens	31-34
14647238-6	2004	Ceramide, which is involved in HPR-induced apoptosis, was also involved in c-Fos induction because its upregulation by HPR was reduced by fumonisin B(1), a ceramide synthase inhibitor.	Ceramides	0-8	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	75-80
14647238-6	2004	Ceramide, which is involved in HPR-induced apoptosis, was also involved in c-Fos induction because its upregulation by HPR was reduced by fumonisin B(1), a ceramide synthase inhibitor.	Ceramides	0-8	haptoglobin-related protein	Homo sapiens	119-122
15067322-4	2004	The levels of MAT1A mRNA as well as MAT I/III protein decreased in cultured rat hepatocytes by in situ generation of ceramide from exogenous human placenta ASMase.	Ceramides	117-125	methionine adenosyltransferase 1A	Rattus norvegicus	14-19
15067322-4	2004	The levels of MAT1A mRNA as well as MAT I/III protein decreased in cultured rat hepatocytes by in situ generation of ceramide from exogenous human placenta ASMase.	Ceramides	117-125	sphingomyelin phosphodiesterase 1	Homo sapiens	156-162
14970312-4	2004	Membrane-associated oxidative stress occurs in association with the lipid alterations, and exposure of hippocampal neurons to Abeta induces membrane oxidative stress and the accumulation of ceramide species and cholesterol.	Ceramides	190-198	amyloid beta precursor protein	Homo sapiens	126-131
14617682-5	2004	By contrast, the CB1 cannabinoid receptor antagonist N-(piperidin-1-yl)-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methyl-1H-pyrazole-3-carboximide hydrochloride (SR141716; SR1), capsazepine (vanilloid receptor antagonist), the inhibitors of ceramide generation, or pertussis toxin did not counteract CBD effects.	Ceramides	243-251	cannabinoid receptor 1	Homo sapiens	17-20
14718557-9	2004	Together with the findings that sit4Delta and totDelta cells phenocopy protection against zymocin and the ceramide-induced G1 block, Sit4 is functionally linked to Elongator in cell cycle events targetable by antizymotics.	Ceramides	106-114	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	133-137
14968439-0	2004	The ceramide analog, B13, induces apoptosis in prostate cancer cell lines and inhibits tumor growth in prostate cancer xenografts.	Ceramides	4-12	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	21-24
14630908-0	2004	Rapid shortening of telomere length in response to ceramide involves the inhibition of telomere binding activity of nuclear glyceraldehyde-3-phosphate dehydrogenase.	Ceramides	51-59	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	124-164
14630908-4	2004	During the examination of ceramide-regulated telomere-binding proteins, nuclear glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was identified to associate with both single- and double-stranded telomeric DNA with high specificity in vitro.	Ceramides	26-34	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	80-120
14630908-4	2004	During the examination of ceramide-regulated telomere-binding proteins, nuclear glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was identified to associate with both single- and double-stranded telomeric DNA with high specificity in vitro.	Ceramides	26-34	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	122-127
14630908-6	2004	Further data demonstrated that the nuclear localization of GAPDH is regulated by ceramide in a cell cycle-dependent manner parallel with the inhibition of its telomere binding activity in response to ceramide.	Ceramides	81-89	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	59-64
14630908-6	2004	Further data demonstrated that the nuclear localization of GAPDH is regulated by ceramide in a cell cycle-dependent manner parallel with the inhibition of its telomere binding activity in response to ceramide.	Ceramides	200-208	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	59-64
14630908-9	2004	In contrast, overexpression of nuclear GAPDH resulted in the protection of telomeric DNA in response to exogenous ceramide as well as in response to anticancer drugs, which have been shown to induce endogenous ceramide levels.	Ceramides	114-122	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	39-44
14630908-9	2004	In contrast, overexpression of nuclear GAPDH resulted in the protection of telomeric DNA in response to exogenous ceramide as well as in response to anticancer drugs, which have been shown to induce endogenous ceramide levels.	Ceramides	210-218	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	39-44
14630908-10	2004	Therefore, these results demonstrate a novel function for nuclear GAPDH in the maintenance and/or protection of telomeres and also show that mechanisms of the rapid degradation of telomeres in response to ceramide involve the inhibition of the telomere binding activity of nuclear GAPDH.	Ceramides	205-213	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	66-71
14630908-10	2004	Therefore, these results demonstrate a novel function for nuclear GAPDH in the maintenance and/or protection of telomeres and also show that mechanisms of the rapid degradation of telomeres in response to ceramide involve the inhibition of the telomere binding activity of nuclear GAPDH.	Ceramides	205-213	glyceraldehyde-3-phosphate dehydrogenase	Homo sapiens	281-286
14660582-1	2004	Role of acidic sphingomyelinase-mediated ceramide generation in FAS receptor activation.	Ceramides	41-49	Fas cell surface death receptor	Rattus norvegicus	64-76
14660582-6	2004	In wild-type and FAS-R(-/-) hepatocytes, ceramide elevation was detected as early as 2 min and peaked at 10 min after DCA treatment.	Ceramides	41-49	Fas cell surface death receptor	Rattus norvegicus	17-22
14970312-6	2004	Our findings suggest a sequence of events in the pathogenesis of AD in which Abeta induces membrane-associated oxidative stress, resulting in perturbed ceramide and cholesterol metabolism which, in turn, triggers a neurodegenerative cascade that leads to clinical disease.	Ceramides	152-160	amyloid beta precursor protein	Homo sapiens	77-82
14670935-3	2004	Preincubation of cells with GW4869, an inhibitor of neutral sphingomyelinase (N-SMase), blocked apoC-I-induced apoptosis, an effect that was bypassed by C-2 ceramide.	Ceramides	157-165	sphingomyelin phosphodiesterase 2	Homo sapiens	78-85
14755730-5	2004	Exposure of cultured neurons to the neurotoxic HIV proteins gp120 and Tat resulted in increased cellular levels of sphingomyelin, ceramide, and HNE.	Ceramides	130-138	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	60-65
14755730-6	2004	The ceramide precursor palmitoyl-CoA sensitized neurons to Tat and gp120 toxicity, whereas an inhibitor of ceramide production reduced Tat and gp120-induced increases of ceramide and HNE and protected the neurons from Tat and gp120-induced death.	Ceramides	107-115	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	143-148
14755730-6	2004	The ceramide precursor palmitoyl-CoA sensitized neurons to Tat and gp120 toxicity, whereas an inhibitor of ceramide production reduced Tat and gp120-induced increases of ceramide and HNE and protected the neurons from Tat and gp120-induced death.	Ceramides	107-115	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	143-148
14755730-6	2004	The ceramide precursor palmitoyl-CoA sensitized neurons to Tat and gp120 toxicity, whereas an inhibitor of ceramide production reduced Tat and gp120-induced increases of ceramide and HNE and protected the neurons from Tat and gp120-induced death.	Ceramides	107-115	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	143-148
14755730-6	2004	The ceramide precursor palmitoyl-CoA sensitized neurons to Tat and gp120 toxicity, whereas an inhibitor of ceramide production reduced Tat and gp120-induced increases of ceramide and HNE and protected the neurons from Tat and gp120-induced death.	Ceramides	107-115	inter-alpha-trypsin inhibitor heavy chain 4	Homo sapiens	143-148
14670935-3	2004	Preincubation of cells with GW4869, an inhibitor of neutral sphingomyelinase (N-SMase), blocked apoC-I-induced apoptosis, an effect that was bypassed by C-2 ceramide.	Ceramides	157-165	apolipoprotein C1	Homo sapiens	96-102
14670935-5	2004	ApoC-I and apoC-I-enriched HDL stimulated the generation of ceramide, the release of cytochrome c from mitochondria, and activation of caspase-3 greater than that found in controls, apoC-III, and apoC-I-poor HDL.	Ceramides	60-68	apolipoprotein C1	Homo sapiens	0-6
14670935-5	2004	ApoC-I and apoC-I-enriched HDL stimulated the generation of ceramide, the release of cytochrome c from mitochondria, and activation of caspase-3 greater than that found in controls, apoC-III, and apoC-I-poor HDL.	Ceramides	60-68	apolipoprotein C1	Homo sapiens	11-17
14670935-6	2004	GW4869 inhibited apoC-I-induced production of ceramide and cytochrome c release.	Ceramides	46-54	apolipoprotein C1	Homo sapiens	17-23
14670935-7	2004	CONCLUSIONS: ApoC-I and apoC-I-enriched HDL activate the N-SMase-ceramide signaling pathway, leading to apoptosis in human ASMC, which is an effect that may promote plaque rupture in vivo.	Ceramides	65-73	apolipoprotein C1	Homo sapiens	13-19
14670935-7	2004	CONCLUSIONS: ApoC-I and apoC-I-enriched HDL activate the N-SMase-ceramide signaling pathway, leading to apoptosis in human ASMC, which is an effect that may promote plaque rupture in vivo.	Ceramides	65-73	apolipoprotein C1	Homo sapiens	24-30
14670935-7	2004	CONCLUSIONS: ApoC-I and apoC-I-enriched HDL activate the N-SMase-ceramide signaling pathway, leading to apoptosis in human ASMC, which is an effect that may promote plaque rupture in vivo.	Ceramides	65-73	sphingomyelin phosphodiesterase 2	Homo sapiens	57-64
14748735-8	2004	Sphingomyelinase activity and ceramide levels have been found to increase 7 days after A-beta administration.	Ceramides	30-38	amyloid beta precursor protein	Rattus norvegicus	87-93
14871831-0	2004	Increase of nuclear ceramide through caspase-3-dependent regulation of the "sphingomyelin cycle" in Fas-induced apoptosis.	Ceramides	20-28	caspase 3	Homo sapiens	37-46
14615798-6	2004	The stimulation of annexin binding following osmotic shock is mimicked by addition of ceramide or purified sphingomyelinase and significantly blunted by genetic (aSM-deficient mice) or pharmacologic (50 microM 3,4-dichloroisocoumarin) knockout of sphingomyelinase.	Ceramides	86-94	annexin A11, opposite strand	Mus musculus	19-26
14615798-8	2004	Conversely, osmotic shock-induced annexin binding is potentiated in the presence of sublethal concentrations of ceramide.	Ceramides	112-120	annexin A11, opposite strand	Mus musculus	34-41
14758167-11	2004	However, an abnormal permeability of outer mitochondrial membranes to cytochrome c was observed in all lipopolysaccharide-treated groups and was associated with increased mitochondrial concentrations of Bax and ceramide.	Ceramides	211-219	cytochrome c	Felis catus	70-82
14871831-1	2004	Regardless of the existence of ceramide-related molecules, such as sphingomyelin (SM), neutral sphingomyelinase (nSMase), and SM synthase, in the nucleus, the regulation of ceramide in the nucleus is poorly understood in stress-induced apoptosis.	Ceramides	173-181	sphingomyelin synthase 2	Homo sapiens	126-137
14871831-5	2004	Pretreatment with D-609, a putative SM synthase inhibitor, enhanced Fas-induced increase of ceramide in the nucleus and induction of apoptosis along with increase of Fas-induced inhibition of nuclear SM synthase.	Ceramides	92-100	sphingomyelin synthase 2	Homo sapiens	36-47
14871831-7	2004	A caspase-3 inhibitor, acetyl-Asp-Glu-Val-Asp-chloromethyl ketone, blocked not only Fas-induced increases of apoptosis and ceramide content but also Fas-induced activation of nSMase and inhibition of SM synthase in the nuclear fraction.	Ceramides	123-131	caspase 3	Homo sapiens	2-11
14871831-8	2004	Taken together, it is suggested that the nucleus is a site for ceramide increase and caspase-3 activation in Fas-induced Jurkat T-cell apoptosis and that caspase-3-dependent regulation of the "SM cycle" consisting of nSMase and SM synthase plays a role in Fas-induced ceramide increase in the nucleus.	Ceramides	268-276	caspase 3	Homo sapiens	154-163
14689477-13	2004	The selective expression of SPHK in the zebrin II-immunoreactive PCs may explain their resistance to cell death when ceramide metabolism is disrupted, as in the acid sphingomyelinase knockout model of Niemann-Pick type A/B disease.	Ceramides	117-125	aldolase C, fructose-bisphosphate	Mus musculus	40-49
14720208-0	2004	The role of neutral sphingomyelinase produced ceramide in lipopolysaccharide-mediated expression of inducible nitric oxide synthase.	Ceramides	46-54	sphingomyelin phosphodiesterase 2	Rattus norvegicus	12-36
14720208-0	2004	The role of neutral sphingomyelinase produced ceramide in lipopolysaccharide-mediated expression of inducible nitric oxide synthase.	Ceramides	46-54	nitric oxide synthase 2	Rattus norvegicus	100-131
14720208-2	2004	To delineate the possible role of ceramide in the induction of iNOS, we examined the source of intracellular ceramide and associated signal transduction pathway(s) with the use of inhibitors of intracellular ceramide generation.	Ceramides	34-42	nitric oxide synthase 2	Rattus norvegicus	63-67
14720208-4	2004	MSM-mediated inhibition of iNOS induction was reversed by the supplementation of exogenous C8-ceramide, suggesting that ceramide production by neutral sphingomyelinase (nSMase) is a key mediator in the induction of iNOS.	Ceramides	94-102	nitric oxide synthase 2	Rattus norvegicus	27-31
14720208-4	2004	MSM-mediated inhibition of iNOS induction was reversed by the supplementation of exogenous C8-ceramide, suggesting that ceramide production by neutral sphingomyelinase (nSMase) is a key mediator in the induction of iNOS.	Ceramides	94-102	sphingomyelin phosphodiesterase 2	Rattus norvegicus	143-167
14720208-4	2004	MSM-mediated inhibition of iNOS induction was reversed by the supplementation of exogenous C8-ceramide, suggesting that ceramide production by neutral sphingomyelinase (nSMase) is a key mediator in the induction of iNOS.	Ceramides	94-102	sphingomyelin phosphodiesterase 2	Rattus norvegicus	169-175
14720208-4	2004	MSM-mediated inhibition of iNOS induction was reversed by the supplementation of exogenous C8-ceramide, suggesting that ceramide production by neutral sphingomyelinase (nSMase) is a key mediator in the induction of iNOS.	Ceramides	94-102	nitric oxide synthase 2	Rattus norvegicus	215-219
14720208-9	2004	Our results suggest that ceramide generated by nSMase may be a critical mediator in the regulation of iNOS gene expression via ras-mediated NF-kappaB activation under inflammatory conditions.	Ceramides	25-33	sphingomyelin phosphodiesterase 2	Rattus norvegicus	47-53
14720208-9	2004	Our results suggest that ceramide generated by nSMase may be a critical mediator in the regulation of iNOS gene expression via ras-mediated NF-kappaB activation under inflammatory conditions.	Ceramides	25-33	nitric oxide synthase 2	Rattus norvegicus	102-106
14704790-0	2004	PAF-mediated pulmonary edema: a new role for acid sphingomyelinase and ceramide.	Ceramides	71-79	PCNA clamp associated factor	Homo sapiens	0-3
14704790-2	2004	Here we show that PAF induces pulmonary edema through two mechanisms: acid sphingomyelinase (ASM)-dependent production of ceramide, and activation of the cyclooxygenase pathway.	Ceramides	122-130	PCNA clamp associated factor	Homo sapiens	18-21
14704790-2	2004	Here we show that PAF induces pulmonary edema through two mechanisms: acid sphingomyelinase (ASM)-dependent production of ceramide, and activation of the cyclooxygenase pathway.	Ceramides	122-130	sphingomyelin phosphodiesterase 1	Homo sapiens	70-91
14704790-2	2004	Here we show that PAF induces pulmonary edema through two mechanisms: acid sphingomyelinase (ASM)-dependent production of ceramide, and activation of the cyclooxygenase pathway.	Ceramides	122-130	sphingomyelin phosphodiesterase 1	Homo sapiens	93-96
14704790-3	2004	Agents that interfere with PAF-induced ceramide synthesis, such as steroids or the xanthogenate D609, attenuate pulmonary edema formation induced by PAF, endotoxin or acid instillation.	Ceramides	39-47	PCNA clamp associated factor	Homo sapiens	27-30
14704790-3	2004	Agents that interfere with PAF-induced ceramide synthesis, such as steroids or the xanthogenate D609, attenuate pulmonary edema formation induced by PAF, endotoxin or acid instillation.	Ceramides	39-47	PCNA clamp associated factor	Homo sapiens	149-152
14581477-0	2004	Secreted frizzled-related protein 1 (SFRP1) protects fibroblasts from ceramide-induced apoptosis.	Ceramides	70-78	secreted frizzled related protein 1	Homo sapiens	0-35
14581477-0	2004	Secreted frizzled-related protein 1 (SFRP1) protects fibroblasts from ceramide-induced apoptosis.	Ceramides	70-78	secreted frizzled related protein 1	Homo sapiens	37-42
14581477-5	2004	Our data showed that SFRP1 was significantly up-regulated in cultured human PDLFs during ceramide-induced apoptosis.	Ceramides	89-97	secreted frizzled related protein 1	Homo sapiens	21-26
14732227-5	2004	To further investigate which genes contribute to cell death in C2-ceramide-treated cells, we used the reverse transcription-polymerase chain reaction to assess mRNA levels for five genes in the Bcl-2 family and five genes in the caspases family.	Ceramides	66-74	B cell leukemia/lymphoma 2	Mus musculus	194-199
14697345-7	2004	These results suggest that SMS is a potential target of D609 and inhibition of SMS may contribute to D609-induced tumor cell death via modulation of the cellular levels of ceramide and DAG.	Ceramides	172-180	spermine synthase	Homo sapiens	27-30
14729377-10	2004	These findings suggest that ceramide and D-erythro-analogs of sphingosine have opposite effects on phospholipase A2 activity and thus regulate arachidonic acid release from cells.	Ceramides	28-36	phospholipase A2 group IB	Rattus norvegicus	99-115
14685263-3	2004	This reaction is catalysed by SM synthase, an enzyme whose biological potential can be judged from the roles of diacylglycerol and ceramide as anti- and proapoptotic stimuli, respectively.	Ceramides	131-139	sphingomyelin synthase 2	Homo sapiens	30-41
14697345-7	2004	These results suggest that SMS is a potential target of D609 and inhibition of SMS may contribute to D609-induced tumor cell death via modulation of the cellular levels of ceramide and DAG.	Ceramides	172-180	spermine synthase	Homo sapiens	79-82
14709545-0	2004	Amyloid-beta peptide induces oligodendrocyte death by activating the neutral sphingomyelinase-ceramide pathway.	Ceramides	94-102	sphingomyelin phosphodiesterase 2	Homo sapiens	69-93
14709545-5	2004	In addition, Abeta activated neutral sphingomyelinase (nSMase), but not acidic sphingomyelinase, resulting in increased ceramide generation.	Ceramides	120-128	amyloid beta precursor protein	Homo sapiens	13-18
14709545-5	2004	In addition, Abeta activated neutral sphingomyelinase (nSMase), but not acidic sphingomyelinase, resulting in increased ceramide generation.	Ceramides	120-128	sphingomyelin phosphodiesterase 2	Homo sapiens	29-53
14709545-5	2004	In addition, Abeta activated neutral sphingomyelinase (nSMase), but not acidic sphingomyelinase, resulting in increased ceramide generation.	Ceramides	120-128	sphingomyelin phosphodiesterase 2	Homo sapiens	55-61
14709545-9	2004	These results suggest that Abeta induces OLG death by activating the nSMase-ceramide cascade via an oxidative mechanism.	Ceramides	76-84	amyloid beta precursor protein	Homo sapiens	27-32
14709545-9	2004	These results suggest that Abeta induces OLG death by activating the nSMase-ceramide cascade via an oxidative mechanism.	Ceramides	76-84	sphingomyelin phosphodiesterase 2	Homo sapiens	69-75
14979937-0	2004	Does protein kinase R mediate TNF-alpha- and ceramide-induced increases in expression and activation of matrix metalloproteinases in articular cartilage by a novel mechanism?	Ceramides	45-53	eukaryotic translation initiation factor 2 alpha kinase 2	Bos taurus	5-21
15038664-6	2004	For example, ceramide-induced apoptosis is associated with increased synthesis of a ganglioside, GD3.	Ceramides	13-21	GRDX	Homo sapiens	97-100
14693694-2	2004	Ceramides, either generated via activation of sphingomyelinase or produced by de novo synthesis, induce insulin resistance in cultured cells by inhibitory effects on insulin signaling.	Ceramides	0-9	insulin	Homo sapiens	104-111
14693694-2	2004	Ceramides, either generated via activation of sphingomyelinase or produced by de novo synthesis, induce insulin resistance in cultured cells by inhibitory effects on insulin signaling.	Ceramides	0-9	insulin	Homo sapiens	166-173
14693694-11	2004	This twofold increase in ceramide may be involved in the decrease in Akt phosphorylation observed after insulin infusion and could theoretically play a role in the reduced ability of insulin to stimulate glucose uptake in skeletal muscle from obese subjects.	Ceramides	25-33	AKT serine/threonine kinase 1	Homo sapiens	69-72
14693694-11	2004	This twofold increase in ceramide may be involved in the decrease in Akt phosphorylation observed after insulin infusion and could theoretically play a role in the reduced ability of insulin to stimulate glucose uptake in skeletal muscle from obese subjects.	Ceramides	25-33	insulin	Homo sapiens	104-111
14693694-11	2004	This twofold increase in ceramide may be involved in the decrease in Akt phosphorylation observed after insulin infusion and could theoretically play a role in the reduced ability of insulin to stimulate glucose uptake in skeletal muscle from obese subjects.	Ceramides	25-33	insulin	Homo sapiens	183-190
14761849-13	2004	CONCLUSIONS: A ceramide-PKB-mediated signalling pathway might play a role in radiation-induced apoptosis of oligodendrocytes.	Ceramides	15-23	AKT serine/threonine kinase 1	Rattus norvegicus	24-27
13130125-4	2004	In Chinese hamster ovary (CHO)-K1, HEK-293, and NIH-3T3 cells, D609 caused rapid (1-5 min) and sustained eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation followed by apoptosis after 24 h. Concurrently, D609 stimulated de novo ceramide synthesis and increased ceramide mass 2-fold by 2 h in CHO-K1 cells.	Ceramides	241-249	eukaryotic translation initiation factor 2A	Mus musculus	142-151
13130125-4	2004	In Chinese hamster ovary (CHO)-K1, HEK-293, and NIH-3T3 cells, D609 caused rapid (1-5 min) and sustained eukaryotic initiation factor 2alpha (eIF2alpha) phosphorylation followed by apoptosis after 24 h. Concurrently, D609 stimulated de novo ceramide synthesis and increased ceramide mass 2-fold by 2 h in CHO-K1 cells.	Ceramides	274-282	eukaryotic translation initiation factor 2A	Mus musculus	142-151
13130125-7	2004	Interestingly, short-chain ceramide promoted eIF2alpha phosphorylation and inhibited protein synthesis in CHO-K1 cells, indicating that the effectiveness of endogenous ceramide could be limited by access to signaling pathways.	Ceramides	27-35	eukaryotic translation initiation factor 2A	Cricetulus griseus	45-54
13130125-7	2004	Interestingly, short-chain ceramide promoted eIF2alpha phosphorylation and inhibited protein synthesis in CHO-K1 cells, indicating that the effectiveness of endogenous ceramide could be limited by access to signaling pathways.	Ceramides	168-176	eukaryotic translation initiation factor 2A	Cricetulus griseus	45-54
14523050-13	2004	M-CSF deprivation resulted in activation of acid sphingomyelinase (A-SMase), increased ceramide levels, and a decrease in intracellular Cer-1-P. Exogenously added Cer-1-P inhibited A-SMase in intact BMDMs at concentrations that also prevented apoptosis.	Ceramides	87-95	colony stimulating factor 1	Homo sapiens	0-5
14523050-13	2004	M-CSF deprivation resulted in activation of acid sphingomyelinase (A-SMase), increased ceramide levels, and a decrease in intracellular Cer-1-P. Exogenously added Cer-1-P inhibited A-SMase in intact BMDMs at concentrations that also prevented apoptosis.	Ceramides	87-95	cerberus 1, DAN family BMP antagonist	Homo sapiens	163-168
14523050-15	2004	In conclusion, these data demonstrate that Cer-1-P blocks apoptosis in BMDMs through inhibition of A-SMase, thereby reducing ceramide generation.	Ceramides	125-133	cerberus 1, DAN family BMP antagonist	Homo sapiens	43-48
12967322-0	2003	Ceramide and glutathione define two independently regulated pathways of cell death initiated by p53 in Molt-4 leukaemia cells.	Ceramides	0-8	tumor protein p53	Homo sapiens	96-99
14685229-8	2003	We conclude that CERT mediates the intracellular trafficking of ceramide in a non-vesicular manner.	Ceramides	64-72	ceramide transfer protein	Cricetulus griseus	17-21
12967322-4	2003	In a model of irradiation-induced cell death of Molt-4 leukaemia cells, it was found that ceramide accumulation and glutathione depletion were dependent on p53 up-regulation.	Ceramides	90-98	tumor protein p53	Homo sapiens	156-159
12967322-8	2003	This suggested that a caspase, other than caspase 9, was necessary for ceramide accumulation.	Ceramides	71-79	caspase 9	Homo sapiens	22-29
14505487-12	2003	The stimulation of gene expression by constitutively active PKB-CaaX and inhibition of the insulin effect by ceramide are compatible with a role for PKB in the insulin-dependent induction of GCK and SREBP1.	Ceramides	109-117	insulin	Homo sapiens	91-98
14615069-4	2003	The intracellular ceramide levels were significantly enhanced by the treatment with the anti-Fas antibodies and both CYP3A4 protein and mRNA expression was suppressed by Fas activation in a dose-dependent manner.	Ceramides	18-26	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
14505487-12	2003	The stimulation of gene expression by constitutively active PKB-CaaX and inhibition of the insulin effect by ceramide are compatible with a role for PKB in the insulin-dependent induction of GCK and SREBP1.	Ceramides	109-117	insulin	Homo sapiens	160-167
14505487-12	2003	The stimulation of gene expression by constitutively active PKB-CaaX and inhibition of the insulin effect by ceramide are compatible with a role for PKB in the insulin-dependent induction of GCK and SREBP1.	Ceramides	109-117	glucokinase	Homo sapiens	191-194
14654222-0	2003	Cycloserine and threo-dihydrosphingosine inhibit TNF-alpha-induced cytotoxicity: evidence for the importance of de novo ceramide synthesis in TNF-alpha signaling.	Ceramides	120-128	tumor necrosis factor	Mus musculus	142-151
14663483-4	2003	As a result, Pml(-/-) mice and cells are protected from apoptosis triggered by a number of stimuli such as ionizing radiation, interferon, ceramide, Fas and TNF.	Ceramides	139-147	promyelocytic leukemia	Mus musculus	13-16
14654222-3	2003	In serine-labeled cells, newly (de novo) synthetized labeled ceramide was significantly diminished by threo-DHS alone or together with TNF-alpha, which makes the (dihydro) ceramide synthase the likely target of threo-DHS.	Ceramides	61-69	tumor necrosis factor	Mus musculus	135-144
14609747-5	2003	Oleandrin blocked ceramide-induced NF-kappa B activation.	Ceramides	18-26	nuclear factor kappa B subunit 1	Homo sapiens	35-45
14609747-1	2003	Ceramide (N-acetyl-D-sphingosine), a second messenger for cell signaling induces transcription factors, like nuclear factor-kappa B (NF-kappa B), and activator protein-1 (AP-1) and is involved in inflammation and apoptosis.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	109-131
12960011-6	2003	Increased de novo ceramide formation is probably the most damaging lipid and is a cause of lipoapoptosis, abetted by a decline in tissue Bcl-2.	Ceramides	18-26	BCL2 apoptosis regulator	Homo sapiens	137-142
14609747-1	2003	Ceramide (N-acetyl-D-sphingosine), a second messenger for cell signaling induces transcription factors, like nuclear factor-kappa B (NF-kappa B), and activator protein-1 (AP-1) and is involved in inflammation and apoptosis.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	133-143
14609747-1	2003	Ceramide (N-acetyl-D-sphingosine), a second messenger for cell signaling induces transcription factors, like nuclear factor-kappa B (NF-kappa B), and activator protein-1 (AP-1) and is involved in inflammation and apoptosis.	Ceramides	0-8	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	150-169
14609747-1	2003	Ceramide (N-acetyl-D-sphingosine), a second messenger for cell signaling induces transcription factors, like nuclear factor-kappa B (NF-kappa B), and activator protein-1 (AP-1) and is involved in inflammation and apoptosis.	Ceramides	0-8	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	171-175
14713309-6	2003	Furthermore, we show that ethanol-induced ERK activation triggers the stimulation of cyclo-oxygenase-2 (COX-2) and the release of prostaglandin E2, and that blockade of the mitogen-activated protein kinase kinase (MEK)/ERK pathway by PD98059 abolishes the up-regulation of COX-2 induced by ethanol plus ceramide, and decreases the ethanol-induced apoptosis.	Ceramides	303-311	mitogen-activated protein kinase 1	Homo sapiens	42-45
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	39-47	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	119-146
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	39-47	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	148-151
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	39-47	sphingomyelin phosphodiesterase 2	Homo sapiens	215-239
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	39-47	sphingomyelin phosphodiesterase 2	Homo sapiens	241-247
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	180-188	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	119-146
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	180-188	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	148-151
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	180-188	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	119-146
14563682-4	2003	More specifically we demonstrated that ceramide accumulation induced by resveratrol can be traced to the activation of serine palmitoyltransferase (SPT), the key enzyme of de novo ceramide biosynthetic pathway, and neutral sphingomyelinase (nSMase), a main enzyme involved in the sphingomyelin/ceramide pathway.	Ceramides	180-188	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	148-151
14713309-6	2003	Furthermore, we show that ethanol-induced ERK activation triggers the stimulation of cyclo-oxygenase-2 (COX-2) and the release of prostaglandin E2, and that blockade of the mitogen-activated protein kinase kinase (MEK)/ERK pathway by PD98059 abolishes the up-regulation of COX-2 induced by ethanol plus ceramide, and decreases the ethanol-induced apoptosis.	Ceramides	303-311	mitogen-activated protein kinase kinase 7	Homo sapiens	173-212
14713309-6	2003	Furthermore, we show that ethanol-induced ERK activation triggers the stimulation of cyclo-oxygenase-2 (COX-2) and the release of prostaglandin E2, and that blockade of the mitogen-activated protein kinase kinase (MEK)/ERK pathway by PD98059 abolishes the up-regulation of COX-2 induced by ethanol plus ceramide, and decreases the ethanol-induced apoptosis.	Ceramides	303-311	mitogen-activated protein kinase kinase 7	Homo sapiens	214-217
14713309-6	2003	Furthermore, we show that ethanol-induced ERK activation triggers the stimulation of cyclo-oxygenase-2 (COX-2) and the release of prostaglandin E2, and that blockade of the mitogen-activated protein kinase kinase (MEK)/ERK pathway by PD98059 abolishes the up-regulation of COX-2 induced by ethanol plus ceramide, and decreases the ethanol-induced apoptosis.	Ceramides	303-311	mitogen-activated protein kinase 1	Homo sapiens	219-222
14674699-0	2003	Commitment to apoptosis by ceramides depends on mitochondrial respiratory function, cytochrome c release and caspase-3 activation in Hep-G2 cells.	Ceramides	27-36	cytochrome c, somatic	Homo sapiens	84-96
14674699-0	2003	Commitment to apoptosis by ceramides depends on mitochondrial respiratory function, cytochrome c release and caspase-3 activation in Hep-G2 cells.	Ceramides	27-36	caspase 3	Homo sapiens	109-118
14614956-1	2003	Role of p75NTR in ceramide generation.	Ceramides	18-26	nerve growth factor receptor	Rattus norvegicus	8-14
14614956-13	2003	We found that in sympathetic neurons, selective activation of p75NTR by brain-derived neurotrophin factor or NGF plus K252a induces elevation of ceramide that correlates with SM hydrolysis.	Ceramides	145-153	nerve growth factor receptor	Rattus norvegicus	62-68
12952965-5	2003	This cyt c release was an indispensable prerequisite for effective ceramide signaling, because its inhibition by modulating the mitochondrial megachannel with bonkrekic acid or carboxyatractyloside prevented ceramide-induced AP-2 activation and ICAM-1 expression.	Ceramides	67-75	transcription factor AP-2 alpha	Homo sapiens	225-229
12952965-5	2003	This cyt c release was an indispensable prerequisite for effective ceramide signaling, because its inhibition by modulating the mitochondrial megachannel with bonkrekic acid or carboxyatractyloside prevented ceramide-induced AP-2 activation and ICAM-1 expression.	Ceramides	67-75	intercellular adhesion molecule 1	Homo sapiens	245-251
12952965-0	2003	Mitochondrial cytochrome c release mediates ceramide-induced activator protein 2 activation and gene expression in keratinocytes.	Ceramides	44-52	cytochrome c, somatic	Homo sapiens	14-26
12952965-5	2003	This cyt c release was an indispensable prerequisite for effective ceramide signaling, because its inhibition by modulating the mitochondrial megachannel with bonkrekic acid or carboxyatractyloside prevented ceramide-induced AP-2 activation and ICAM-1 expression.	Ceramides	208-216	cytochrome c, somatic	Homo sapiens	5-10
12952965-0	2003	Mitochondrial cytochrome c release mediates ceramide-induced activator protein 2 activation and gene expression in keratinocytes.	Ceramides	44-52	transcription factor AP-2 alpha	Homo sapiens	61-80
12952965-5	2003	This cyt c release was an indispensable prerequisite for effective ceramide signaling, because its inhibition by modulating the mitochondrial megachannel with bonkrekic acid or carboxyatractyloside prevented ceramide-induced AP-2 activation and ICAM-1 expression.	Ceramides	208-216	transcription factor AP-2 alpha	Homo sapiens	225-229
12952965-2	2003	In the present study, ceramide-induced expression of intercellular adhesion molecule-1 (ICAM-1), which requires activation of transcription factor activator protein 2 (AP-2), was found to be mediated through a mitochondrial pathway.	Ceramides	22-30	intercellular adhesion molecule 1	Homo sapiens	53-86
12952965-2	2003	In the present study, ceramide-induced expression of intercellular adhesion molecule-1 (ICAM-1), which requires activation of transcription factor activator protein 2 (AP-2), was found to be mediated through a mitochondrial pathway.	Ceramides	22-30	intercellular adhesion molecule 1	Homo sapiens	88-94
12952965-5	2003	This cyt c release was an indispensable prerequisite for effective ceramide signaling, because its inhibition by modulating the mitochondrial megachannel with bonkrekic acid or carboxyatractyloside prevented ceramide-induced AP-2 activation and ICAM-1 expression.	Ceramides	208-216	intercellular adhesion molecule 1	Homo sapiens	245-251
12952965-2	2003	In the present study, ceramide-induced expression of intercellular adhesion molecule-1 (ICAM-1), which requires activation of transcription factor activator protein 2 (AP-2), was found to be mediated through a mitochondrial pathway.	Ceramides	22-30	transcription factor AP-2 alpha	Homo sapiens	147-166
12952965-2	2003	In the present study, ceramide-induced expression of intercellular adhesion molecule-1 (ICAM-1), which requires activation of transcription factor activator protein 2 (AP-2), was found to be mediated through a mitochondrial pathway.	Ceramides	22-30	transcription factor AP-2 alpha	Homo sapiens	168-172
14597763-10	2003	These results indicate that proper ceramide compositions through 4-desaturation regulated by ARNT are crucial for maintaining the epidermal barrier function.	Ceramides	35-43	aryl hydrocarbon receptor nuclear translocator	Mus musculus	93-97
12952965-3	2003	Inhibitors of mitochondrial electron transport chain (e.g. rotenone, thenoyltrifluoroacetone, and antimycin A) reduced ceramide-induced ICAM-1 expression.	Ceramides	119-127	intercellular adhesion molecule 1	Homo sapiens	136-142
12952965-4	2003	Stimulation of human keratinocytes with cell-permeant ceramides at concentrations that did not induce apoptosis (no activation of caspases 3, 8, and 9 and no nucleosomal fragmentation) but caused AP-2 activation and ICAM-1 induction released cytochrome c (cyt c) from mitochondria into the cytoplasm of cells.	Ceramides	54-63	transcription factor AP-2 alpha	Homo sapiens	196-200
12952965-4	2003	Stimulation of human keratinocytes with cell-permeant ceramides at concentrations that did not induce apoptosis (no activation of caspases 3, 8, and 9 and no nucleosomal fragmentation) but caused AP-2 activation and ICAM-1 induction released cytochrome c (cyt c) from mitochondria into the cytoplasm of cells.	Ceramides	54-63	intercellular adhesion molecule 1	Homo sapiens	216-222
12952965-4	2003	Stimulation of human keratinocytes with cell-permeant ceramides at concentrations that did not induce apoptosis (no activation of caspases 3, 8, and 9 and no nucleosomal fragmentation) but caused AP-2 activation and ICAM-1 induction released cytochrome c (cyt c) from mitochondria into the cytoplasm of cells.	Ceramides	54-63	cytochrome c, somatic	Homo sapiens	242-254
12952965-4	2003	Stimulation of human keratinocytes with cell-permeant ceramides at concentrations that did not induce apoptosis (no activation of caspases 3, 8, and 9 and no nucleosomal fragmentation) but caused AP-2 activation and ICAM-1 induction released cytochrome c (cyt c) from mitochondria into the cytoplasm of cells.	Ceramides	54-63	cytochrome c, somatic	Homo sapiens	256-261
12952965-5	2003	This cyt c release was an indispensable prerequisite for effective ceramide signaling, because its inhibition by modulating the mitochondrial megachannel with bonkrekic acid or carboxyatractyloside prevented ceramide-induced AP-2 activation and ICAM-1 expression.	Ceramides	67-75	cytochrome c, somatic	Homo sapiens	5-10
14592454-7	2003	Mechanistically, inhibition of telomerase by endogenous ceramide in response to ATRA treatment involves, at least in part, down-regulation of the expression of telomerase reverse transcriptase (hTERT) mRNA, as determined by semi-quantitative RT-PCR, in these cells.	Ceramides	56-64	telomerase reverse transcriptase	Homo sapiens	194-199
14592455-9	2003	ASMase knockout mice retained LPS-induced increases in serum ceramide, thus suggesting that the elevation of VLDL and LDL ceramide content is attributed at least in part to activation of de novo synthesis of ceramide in the liver.	Ceramides	61-69	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
14592455-9	2003	ASMase knockout mice retained LPS-induced increases in serum ceramide, thus suggesting that the elevation of VLDL and LDL ceramide content is attributed at least in part to activation of de novo synthesis of ceramide in the liver.	Ceramides	122-130	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
14592455-9	2003	ASMase knockout mice retained LPS-induced increases in serum ceramide, thus suggesting that the elevation of VLDL and LDL ceramide content is attributed at least in part to activation of de novo synthesis of ceramide in the liver.	Ceramides	122-130	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
12959973-0	2003	Intratesticular delivery of tumor necrosis factor-alpha and ceramide directly abrogates steroidogenic acute regulatory protein expression and Leydig cell steroidogenesis in adult rats.	Ceramides	60-68	steroidogenic acute regulatory protein	Homo sapiens	88-118
12959973-4	2003	Bilateral treatment with cell-permeant short-chain ceramides (C2-cer or C6-cer) reproduced the early (4 h) inhibitory action of TNFalpha on testosterone biosynthesis and testicular StAR expression.	Ceramides	51-60	tumor necrosis factor	Homo sapiens	128-136
12959973-4	2003	Bilateral treatment with cell-permeant short-chain ceramides (C2-cer or C6-cer) reproduced the early (4 h) inhibitory action of TNFalpha on testosterone biosynthesis and testicular StAR expression.	Ceramides	51-60	steroidogenic acute regulatory protein	Homo sapiens	181-185
14563678-4	2003	ACD5 protein shows high specificity for ceramides in vitro.	Ceramides	40-49	Diacylglycerol kinase family protein	Arabidopsis thaliana	0-4
14597763-0	2003	Alteration of the 4-sphingenine scaffolds of ceramides in keratinocyte-specific Arnt-deficient mice affects skin barrier function.	Ceramides	45-54	aryl hydrocarbon receptor nuclear translocator	Mus musculus	80-84
14597763-7	2003	In Arnt-null epidermis, 4-sphingenine was largely replaced by sphinganine and the amounts of ceramides with 4-hydroxysphinganine were greatly decreased, suggesting deficiency of dihydroceramide desaturases that catalyze the formation of both 4-sphingenyl and 4-hydroxysphinganyl moieties.	Ceramides	93-102	aryl hydrocarbon receptor nuclear translocator	Mus musculus	3-7
12975495-8	2003	Liposomal ceramide formulations inhibited phosphorylated Akt levels and stimulated caspase-3/7 activity more effectively than nonliposomal ceramide, events consistent with apoptosis.	Ceramides	10-18	AKT serine/threonine kinase 1	Homo sapiens	57-60
14608042-2	2003	Apoptosis induced by the ceramide analog, C8-ceramine, was inhibited by S1P (ceramine/S1P).	Ceramides	25-33	sphingosine-1-phosphate receptor 1	Mus musculus	72-75
14608042-2	2003	Apoptosis induced by the ceramide analog, C8-ceramine, was inhibited by S1P (ceramine/S1P).	Ceramides	25-33	sphingosine-1-phosphate receptor 1	Mus musculus	86-89
12975495-8	2003	Liposomal ceramide formulations inhibited phosphorylated Akt levels and stimulated caspase-3/7 activity more effectively than nonliposomal ceramide, events consistent with apoptosis.	Ceramides	10-18	caspase 3	Homo sapiens	83-92
14573769-0	2003	Ceramide is involved in r(+)-methanandamide-induced cyclooxygenase-2 expression in human neuroglioma cells.	Ceramides	0-8	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-68
15077187-4	2004	Using diacylglycerol kinase assays to quantify ceramide, we found that the levels of ceramide in mitochondria increased as early as 2 h after UV irradiation and remained elevated at 6 h. The increase in mitochondrial SM and ceramide was inhibited by D609, an inhibitor of sphingomyelinase and SM synthase.	Ceramides	85-93	sphingomyelin synthase 2	Homo sapiens	293-304
15077187-4	2004	Using diacylglycerol kinase assays to quantify ceramide, we found that the levels of ceramide in mitochondria increased as early as 2 h after UV irradiation and remained elevated at 6 h. The increase in mitochondrial SM and ceramide was inhibited by D609, an inhibitor of sphingomyelinase and SM synthase.	Ceramides	85-93	sphingomyelin synthase 2	Homo sapiens	293-304
14560023-0	2003	Ceramide disables 3-phosphoinositide binding to the pleckstrin homology domain of protein kinase B (PKB)/Akt by a PKCzeta-dependent mechanism.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	82-98
14560023-0	2003	Ceramide disables 3-phosphoinositide binding to the pleckstrin homology domain of protein kinase B (PKB)/Akt by a PKCzeta-dependent mechanism.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	100-103
14573769-6	2003	Inhibition of ceramide synthesis with fumonisin B1 was associated with a suppression of R(+)-MA-induced delayed phosphorylations of p38 and p42/44 MAPKs and subsequent COX-2 expression.	Ceramides	14-22	mitogen-activated protein kinase 14	Homo sapiens	132-135
14560023-0	2003	Ceramide disables 3-phosphoinositide binding to the pleckstrin homology domain of protein kinase B (PKB)/Akt by a PKCzeta-dependent mechanism.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	105-108
14560023-0	2003	Ceramide disables 3-phosphoinositide binding to the pleckstrin homology domain of protein kinase B (PKB)/Akt by a PKCzeta-dependent mechanism.	Ceramides	0-8	protein kinase C zeta	Homo sapiens	114-121
14573769-6	2003	Inhibition of ceramide synthesis with fumonisin B1 was associated with a suppression of R(+)-MA-induced delayed phosphorylations of p38 and p42/44 MAPKs and subsequent COX-2 expression.	Ceramides	14-22	erythrocyte membrane protein band 4.2	Homo sapiens	140-143
14560023-1	2003	Ceramide is generated in response to numerous stress-inducing stimuli and has been implicated in the regulation of diverse cellular responses, including cell death, differentiation, and insulin sensitivity.	Ceramides	0-8	insulin	Homo sapiens	186-193
14560023-2	2003	Recent evidence indicates that ceramide may regulate these responses by inhibiting the stimulus-mediated activation of protein kinase B (PKB), a key determinant of cell fate and insulin action.	Ceramides	31-39	protein tyrosine kinase 2 beta	Homo sapiens	119-135
14573769-6	2003	Inhibition of ceramide synthesis with fumonisin B1 was associated with a suppression of R(+)-MA-induced delayed phosphorylations of p38 and p42/44 MAPKs and subsequent COX-2 expression.	Ceramides	14-22	prostaglandin-endoperoxide synthase 2	Homo sapiens	168-173
14560023-2	2003	Recent evidence indicates that ceramide may regulate these responses by inhibiting the stimulus-mediated activation of protein kinase B (PKB), a key determinant of cell fate and insulin action.	Ceramides	31-39	protein tyrosine kinase 2 beta	Homo sapiens	137-140
14560023-2	2003	Recent evidence indicates that ceramide may regulate these responses by inhibiting the stimulus-mediated activation of protein kinase B (PKB), a key determinant of cell fate and insulin action.	Ceramides	31-39	insulin	Homo sapiens	178-185
14560023-5	2003	However, dissociation of the kinase complex and the attendant hormonal activation of PKB were prevented by ceramide.	Ceramides	107-115	protein tyrosine kinase 2 beta	Homo sapiens	85-88
14573769-9	2003	Collectively, our results demonstrate that R(+)-MA induces COX-2 expression in human neuroglioma cells via synthesis of ceramide and subsequent activation of p38 and p42/44 MAPK pathways.	Ceramides	120-128	prostaglandin-endoperoxide synthase 2	Homo sapiens	59-64
14573769-10	2003	Induction of COX-2 expression via ceramide represents a hitherto unknown mechanism by which cannabinoids mediate biological effects within the central nervous system.	Ceramides	34-42	prostaglandin-endoperoxide synthase 2	Homo sapiens	13-18
14563411-1	2003	Ceramide is a lipid second messenger produced by sphingolipid metabolism in cells exposed to a limited number of agonists and in turn triggers important cell responses including protein kinase C (PKC)-alpha activation.	Ceramides	0-8	protein kinase C alpha	Homo sapiens	196-206
14560023-6	2003	Under these circumstances, ceramide activated PKCzeta, leading to phosphorylation of the PKB-PH domain on Thr(34).	Ceramides	27-35	protein kinase C zeta	Homo sapiens	46-53
14560023-6	2003	Under these circumstances, ceramide activated PKCzeta, leading to phosphorylation of the PKB-PH domain on Thr(34).	Ceramides	27-35	protein tyrosine kinase 2 beta	Homo sapiens	89-92
14560023-8	2003	In contrast, a PKB-PH domain with a T34A mutation retained the ability to bind PIP(3) even in the presence of a ceramide-activated PKCzeta and, as such, expression of PKB T34A mutant in L6 cells was resistant to inhibition by ceramide treatment.	Ceramides	112-120	protein tyrosine kinase 2 beta	Homo sapiens	15-18
14560023-8	2003	In contrast, a PKB-PH domain with a T34A mutation retained the ability to bind PIP(3) even in the presence of a ceramide-activated PKCzeta and, as such, expression of PKB T34A mutant in L6 cells was resistant to inhibition by ceramide treatment.	Ceramides	112-120	protein kinase C zeta	Homo sapiens	131-138
14560023-8	2003	In contrast, a PKB-PH domain with a T34A mutation retained the ability to bind PIP(3) even in the presence of a ceramide-activated PKCzeta and, as such, expression of PKB T34A mutant in L6 cells was resistant to inhibition by ceramide treatment.	Ceramides	112-120	protein tyrosine kinase 2 beta	Homo sapiens	167-170
14560023-8	2003	In contrast, a PKB-PH domain with a T34A mutation retained the ability to bind PIP(3) even in the presence of a ceramide-activated PKCzeta and, as such, expression of PKB T34A mutant in L6 cells was resistant to inhibition by ceramide treatment.	Ceramides	226-234	protein tyrosine kinase 2 beta	Homo sapiens	15-18
14560023-8	2003	In contrast, a PKB-PH domain with a T34A mutation retained the ability to bind PIP(3) even in the presence of a ceramide-activated PKCzeta and, as such, expression of PKB T34A mutant in L6 cells was resistant to inhibition by ceramide treatment.	Ceramides	226-234	protein tyrosine kinase 2 beta	Homo sapiens	167-170
14560023-9	2003	Inhibitors of PKCzeta and a kinase-dead PKCzeta both antagonized the inhibitory effect of ceramide on PKB.	Ceramides	90-98	protein kinase C zeta	Homo sapiens	14-21
14560023-9	2003	Inhibitors of PKCzeta and a kinase-dead PKCzeta both antagonized the inhibitory effect of ceramide on PKB.	Ceramides	90-98	protein kinase C zeta	Homo sapiens	40-47
14560023-9	2003	Inhibitors of PKCzeta and a kinase-dead PKCzeta both antagonized the inhibitory effect of ceramide on PKB.	Ceramides	90-98	protein tyrosine kinase 2 beta	Homo sapiens	102-105
14560023-10	2003	Since PKB confers a prosurvival signal and regulates numerous pathways in response to insulin, suppressing its activation by a PKCzeta-dependent process may be one mechanism by which ceramide promotes cell death and induces insulin resistance.	Ceramides	183-191	protein tyrosine kinase 2 beta	Homo sapiens	6-9
14560023-10	2003	Since PKB confers a prosurvival signal and regulates numerous pathways in response to insulin, suppressing its activation by a PKCzeta-dependent process may be one mechanism by which ceramide promotes cell death and induces insulin resistance.	Ceramides	183-191	insulin	Homo sapiens	86-93
14560023-10	2003	Since PKB confers a prosurvival signal and regulates numerous pathways in response to insulin, suppressing its activation by a PKCzeta-dependent process may be one mechanism by which ceramide promotes cell death and induces insulin resistance.	Ceramides	183-191	protein kinase C zeta	Homo sapiens	127-134
14560023-10	2003	Since PKB confers a prosurvival signal and regulates numerous pathways in response to insulin, suppressing its activation by a PKCzeta-dependent process may be one mechanism by which ceramide promotes cell death and induces insulin resistance.	Ceramides	183-191	insulin	Homo sapiens	224-231
14572633-3	2003	Combination with proapoptotic agents such as etoposide, pamidronate, and ceramide resulted in additive proapoptotic effects, whereas Bcl-X(L) protected from apoptosis caused via CD95/Fas stimulation.	Ceramides	73-81	Fas cell surface death receptor	Homo sapiens	178-182
14563411-2	2003	Using a fusion protein comprising bovine PKCalpha and the green fluorescent protein (GFP), we transfected human embryonic kidney (HEK) cells and investigated to which subcellular compartment ceramide triggers PKCalpha redistribution.	Ceramides	191-199	protein kinase C alpha	Homo sapiens	209-217
14563411-3	2003	Stimulation of HEK cells with exogenous C16-ceramide or bacterial sphingomyelinase (bSMase), which leads to increased endogenous ceramide formation, evokes a translocation of PKCalpha to the Golgi compartment.	Ceramides	44-52	protein kinase C alpha	Homo sapiens	175-183
14563411-4	2003	By using deletion mutants of PKCalpha lacking distinct domains in the regulatory region, it is shown that the Ca(2+)-dependent lipid binding C2 domain, but not one of the C1 domains is essentially required for the ceramide-triggered translocation of PKCalpha to the Golgi complex.	Ceramides	214-222	protein kinase C alpha	Homo sapiens	29-37
12902347-0	2003	Nerve growth factor-induced glutamate release is via p75 receptor, ceramide, and Ca(2+) from ryanodine receptor in developing cerebellar neurons.	Ceramides	67-75	nerve growth factor	Homo sapiens	0-19
14563411-4	2003	By using deletion mutants of PKCalpha lacking distinct domains in the regulatory region, it is shown that the Ca(2+)-dependent lipid binding C2 domain, but not one of the C1 domains is essentially required for the ceramide-triggered translocation of PKCalpha to the Golgi complex.	Ceramides	214-222	protein kinase C alpha	Homo sapiens	250-258
14563411-6	2003	In addition, evidence is provided that TPA requires only one of the two C1 subdomains to trigger translocation to the plasma membrane.In summary, our data provide evidence that ceramide either directly or indirectly interacts with the Ca(2+)-dependent lipid binding C2 domain of PKCalpha and thereby induces translocation of the enzyme to the Golgi compartment.	Ceramides	177-185	protein kinase C alpha	Homo sapiens	279-287
14563412-5	2003	TNF-alpha- and Fas-induced apoptosis are associated with both intracellular ceramide generation from sphingomyelin (SM) and release of palmitic-derived FFA, with similar kinetics.	Ceramides	76-84	tumor necrosis factor	Homo sapiens	0-9
14557812-1	2003	Ceramide, generated by the action of acid sphingomyelinase (ASM), has emerged as a biochemical mediator of stimuli as diverse as ionizing radiation, chemotherapy, UVA light, heat, CD95, reperfusion injury, as well as infection with some pathogenic bacteria and viruses.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	37-58
12890677-0	2003	Ceramide enhances cholesterol efflux to apolipoprotein A-I by increasing the cell surface presence of ATP-binding cassette transporter A1.	Ceramides	0-8	apolipoprotein A-I	Cricetulus griseus	40-58
12890677-0	2003	Ceramide enhances cholesterol efflux to apolipoprotein A-I by increasing the cell surface presence of ATP-binding cassette transporter A1.	Ceramides	0-8	phospholipid-transporting ATPase ABCA1	Cricetulus griseus	102-137
12890677-3	2003	Sphingomyelin maintains a preferential interaction with cholesterol in membranes, and its catabolites, especially ceramide, are potent signaling molecules that could play a role in ABCA1 regulation or function.	Ceramides	114-122	phospholipid-transporting ATPase ABCA1	Cricetulus griseus	181-186
12890677-10	2003	Using a cell surface biotinylation method, we found that the total cellular ABCA1 and that at the plasma membrane were increased with ceramide treatment.	Ceramides	134-142	phospholipid-transporting ATPase ABCA1	Cricetulus griseus	76-81
12890677-12	2003	These data suggest that ceramide may increase the plasma membrane content of ABCA1, leading to increased apoA-I binding and cholesterol efflux.	Ceramides	24-32	phospholipid-transporting ATPase ABCA1	Cricetulus griseus	77-82
14557812-1	2003	Ceramide, generated by the action of acid sphingomyelinase (ASM), has emerged as a biochemical mediator of stimuli as diverse as ionizing radiation, chemotherapy, UVA light, heat, CD95, reperfusion injury, as well as infection with some pathogenic bacteria and viruses.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	60-63
14557812-1	2003	Ceramide, generated by the action of acid sphingomyelinase (ASM), has emerged as a biochemical mediator of stimuli as diverse as ionizing radiation, chemotherapy, UVA light, heat, CD95, reperfusion injury, as well as infection with some pathogenic bacteria and viruses.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	180-184
14557812-3	2003	Recently, we proposed a comprehensive model that might explain these diverse functions of ceramide: Upon contacting the relevant stimuli, ASM translocates into and generates ceramide within distinct plasma membrane sphingolipid-enriched microdomains termed rafts.	Ceramides	90-98	sphingomyelin phosphodiesterase 1	Homo sapiens	138-141
14557812-3	2003	Recently, we proposed a comprehensive model that might explain these diverse functions of ceramide: Upon contacting the relevant stimuli, ASM translocates into and generates ceramide within distinct plasma membrane sphingolipid-enriched microdomains termed rafts.	Ceramides	174-182	sphingomyelin phosphodiesterase 1	Homo sapiens	138-141
14760934-4	2003	RESULTS: IL-1 and ceramide, which have been shown to partially mediate IL-1 effects on IEC, activated NF-kappaB levels significantly.	Ceramides	18-26	nuclear factor kappa B subunit 1	Homo sapiens	102-111
12832423-6	2003	When combined with protein kinase C inhibition by staurosporine or rottlerin, breakdown of plasma membrane sphingomyelin or enrichment of the plasma membrane with ceramide also increased IL-6R shedding.	Ceramides	163-171	interleukin 6 receptor	Homo sapiens	187-192
14557071-0	2003	Neutral ceramidase gene: role in regulating ceramide-induced apoptosis.	Ceramides	44-52	N-acylsphingosine amidohydrolase 2	Mus musculus	0-18
14557071-7	2003	We propose that N-CDase is an essential component of an innate detoxifying mechanism to prevent ceramide-induced apoptosis.	Ceramides	96-104	N-acylsphingosine amidohydrolase 2	Mus musculus	16-23
12902347-7	2003	Furthermore, scyphostatin, a sphingomyelinase inhibitor, blocked the NGF-dependent Ca2+ increase and glutamate release, suggesting that a ceramide produced by sphingomyelinase was required for the NGF-stimulated Ca2+ increase and glutamate release.	Ceramides	138-146	nerve growth factor	Homo sapiens	69-72
12902347-7	2003	Furthermore, scyphostatin, a sphingomyelinase inhibitor, blocked the NGF-dependent Ca2+ increase and glutamate release, suggesting that a ceramide produced by sphingomyelinase was required for the NGF-stimulated Ca2+ increase and glutamate release.	Ceramides	138-146	nerve growth factor	Homo sapiens	197-200
12869556-0	2003	Human homologues of LAG1 reconstitute Acyl-CoA-dependent ceramide synthesis in yeast.	Ceramides	57-65	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	20-24
14523222-1	2003	Recent studies have implicated the longevity assurance gene LAG1 in ceramide synthesis.	Ceramides	68-76	ceramide synthase 1	Homo sapiens	60-64
14577330-9	2003	Based on these findings, we propose that oxLDL activates cPLA2 to supply fatty acids required for the cholesterol esterification, through the acceleration of the hydrolytic action of cPLA2 by endogenous ceramide and by oxidized lipids in oxLDL particles in macrophages.	Ceramides	203-211	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	57-62
14577330-9	2003	Based on these findings, we propose that oxLDL activates cPLA2 to supply fatty acids required for the cholesterol esterification, through the acceleration of the hydrolytic action of cPLA2 by endogenous ceramide and by oxidized lipids in oxLDL particles in macrophages.	Ceramides	203-211	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	183-188
12869556-4	2003	Here we show that several human LAG1 homologues can rescue the viability of lag1delta lac1delta yeast cells and restore acyl-CoA-dependent ceramide and sphingolipid biosynthesis.	Ceramides	139-147	ceramide synthase 1	Homo sapiens	32-36
14515991-1	2003	Acid sphingomyelinase (A-SMase, EC 3.1.4.12) catalyzes the lysosomal degradation of sphingomyelin to phosphorylcholine and ceramide.	Ceramides	123-131	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
14515991-1	2003	Acid sphingomyelinase (A-SMase, EC 3.1.4.12) catalyzes the lysosomal degradation of sphingomyelin to phosphorylcholine and ceramide.	Ceramides	123-131	sphingomyelin phosphodiesterase 1	Homo sapiens	23-30
12925201-6	2003	Overexpression of ABCA7 in HeLa cells resulted in increased expression of intracellular and cell surface ceramide and elevated intracellular phosphatidylserine levels.	Ceramides	105-113	ATP binding cassette subfamily A member 7	Homo sapiens	18-23
12944273-1	2003	Ceramides are known to play a major regulatory role in apoptosis by inducing cytochrome c release from mitochondria.	Ceramides	0-9	cytochrome c, somatic	Homo sapiens	77-89
12925201-7	2003	Given the observation that during terminal keratinocyte differentiation intracellular and surface ceramide levels are increased, our results render ABCA7 a candidate regulator of ceramide transport in this process.	Ceramides	98-106	ATP binding cassette subfamily A member 7	Homo sapiens	148-153
12925201-7	2003	Given the observation that during terminal keratinocyte differentiation intracellular and surface ceramide levels are increased, our results render ABCA7 a candidate regulator of ceramide transport in this process.	Ceramides	179-187	ATP binding cassette subfamily A member 7	Homo sapiens	148-153
12934106-0	2003	Ceramide-mediated clustering is required for CD95-DISC formation.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	45-49
12947396-5	2003	In some cells and tissues, BAX is activated downstream of ceramide, regulating commitment to the apoptotic process via release of mitochondrial cytochrome c.	Ceramides	58-66	BCL2 associated X, apoptosis regulator	Homo sapiens	27-30
12947396-5	2003	In some cells and tissues, BAX is activated downstream of ceramide, regulating commitment to the apoptotic process via release of mitochondrial cytochrome c.	Ceramides	58-66	cytochrome c, somatic	Homo sapiens	144-156
12934106-2	2003	Here, we identify the molecular ordering of these events and show that the acid sphingomyelinase (ASM) functions upstream of the DISC to mediate CD95 clustering in ceramide-enriched membrane platforms, an event that is required for DISC formation.	Ceramides	164-172	sphingomyelin phosphodiesterase 1	Homo sapiens	75-96
12934106-2	2003	Here, we identify the molecular ordering of these events and show that the acid sphingomyelinase (ASM) functions upstream of the DISC to mediate CD95 clustering in ceramide-enriched membrane platforms, an event that is required for DISC formation.	Ceramides	164-172	sphingomyelin phosphodiesterase 1	Homo sapiens	98-101
12934106-2	2003	Here, we identify the molecular ordering of these events and show that the acid sphingomyelinase (ASM) functions upstream of the DISC to mediate CD95 clustering in ceramide-enriched membrane platforms, an event that is required for DISC formation.	Ceramides	164-172	Fas cell surface death receptor	Homo sapiens	145-149
12934106-4	2003	This event, however, is both necessary and sufficient to trigger translocation of ASM onto the outer leaflet of the plasma membrane, ASM activation and ceramide release, but insufficient for apoptosis induction.	Ceramides	152-160	sphingomyelin phosphodiesterase 1	Homo sapiens	82-85
12934106-5	2003	Ceramide-mediated CD95 clustering then amplifies the primary CD95 signaling and drives the second step of CD95 signaling, that is, formation of the DISC yielding 100% caspase activity and apoptosis.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	18-22
12934106-5	2003	Ceramide-mediated CD95 clustering then amplifies the primary CD95 signaling and drives the second step of CD95 signaling, that is, formation of the DISC yielding 100% caspase activity and apoptosis.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	61-65
12934106-5	2003	Ceramide-mediated CD95 clustering then amplifies the primary CD95 signaling and drives the second step of CD95 signaling, that is, formation of the DISC yielding 100% caspase activity and apoptosis.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	61-65
12934106-6	2003	These studies suggest that the most parsimonious interpretation of the molecular ordering of the earliest events in CD95 signaling, at least in some cells, is: CD95 ligation-->1% of maximum caspase 8 activation-->ASM translocation-->ceramide generation-->CD95 clustering-->DISC formation-->100% of maximum caspase 8 activation-->apoptosis.	Ceramides	242-250	Fas cell surface death receptor	Homo sapiens	116-120
12934106-6	2003	These studies suggest that the most parsimonious interpretation of the molecular ordering of the earliest events in CD95 signaling, at least in some cells, is: CD95 ligation-->1% of maximum caspase 8 activation-->ASM translocation-->ceramide generation-->CD95 clustering-->DISC formation-->100% of maximum caspase 8 activation-->apoptosis.	Ceramides	242-250	Fas cell surface death receptor	Homo sapiens	160-164
12934106-6	2003	These studies suggest that the most parsimonious interpretation of the molecular ordering of the earliest events in CD95 signaling, at least in some cells, is: CD95 ligation-->1% of maximum caspase 8 activation-->ASM translocation-->ceramide generation-->CD95 clustering-->DISC formation-->100% of maximum caspase 8 activation-->apoptosis.	Ceramides	242-250	Fas cell surface death receptor	Homo sapiens	160-164
12794766-6	2003	Additionally, the cellular ceramide content estimated for PC3 cells was increased after treatment with PD153035, alone or in combination, at a lower dose with OE and Rp-cAMPs.	Ceramides	27-35	chromobox 8	Homo sapiens	58-61
12783875-9	2003	Metabolic labeling studies showed that overexpression of maCER1 caused a decrease in the incorporation of radiolabeled dihydrosphingosine into ceramide and complex sphingolipids but led to a concomitant increase in sphingosine-1-P (S1P) in HeLa cells.	Ceramides	143-151	alkaline ceramidase 1	Mus musculus	57-63
12783875-10	2003	Mass measurement showed that overexpression of maCER1 selectively lowered the cellular levels of D-erythro-C24:1-ceramide, but not other ceramide species and caused an increase in the levels of S1P.	Ceramides	113-121	alkaline ceramidase 1	Mus musculus	47-53
12783875-11	2003	Taken together, these data suggest that maCER1 is a novel alkaline ceramidase with a stringent substrate specificity and that maCER1 is selectively expressed in skin and may have a role in regulating the levels of bioactive lipids ceramide and S1P, as well as complex sphingolipids.	Ceramides	231-239	alkaline ceramidase 1	Mus musculus	40-46
12783875-11	2003	Taken together, these data suggest that maCER1 is a novel alkaline ceramidase with a stringent substrate specificity and that maCER1 is selectively expressed in skin and may have a role in regulating the levels of bioactive lipids ceramide and S1P, as well as complex sphingolipids.	Ceramides	231-239	alkaline ceramidase 1	Mus musculus	126-132
12794766-8	2003	Combined, the results indicated that the simultaneous inhibition of EGFR and PKA signaling cascades might lead to a more massive apoptotic death of metastatic prostatic cancer cells by increasing ceramide accumulation and activating of caspase cascade of a mitochondrial dependent manner.	Ceramides	196-204	epidermal growth factor receptor	Homo sapiens	68-72
12890694-11	2003	Treatment with SK1 RNAi also abolished the effects of exogenous sphingosine and ceramide on PGE2, revealing that the action of sphingosine and ceramide are due to intracellular metabolism into S1P.	Ceramides	80-88	sphingosine kinase 1	Mus musculus	15-18
12885759-6	2003	In mitotic cells, asymmetric distribution of PAR-4 and nestin resulted in one nestin(-)/PAR-4(+) daughter cell, in which ceramide elevation induced apoptosis.	Ceramides	121-129	PRKC, apoptosis, WT1, regulator	Mus musculus	45-50
12885759-6	2003	In mitotic cells, asymmetric distribution of PAR-4 and nestin resulted in one nestin(-)/PAR-4(+) daughter cell, in which ceramide elevation induced apoptosis.	Ceramides	121-129	PRKC, apoptosis, WT1, regulator	Mus musculus	88-93
12890694-11	2003	Treatment with SK1 RNAi also abolished the effects of exogenous sphingosine and ceramide on PGE2, revealing that the action of sphingosine and ceramide are due to intracellular metabolism into S1P.	Ceramides	143-151	sphingosine kinase 1	Mus musculus	15-18
12890694-11	2003	Treatment with SK1 RNAi also abolished the effects of exogenous sphingosine and ceramide on PGE2, revealing that the action of sphingosine and ceramide are due to intracellular metabolism into S1P.	Ceramides	143-151	sphingosine-1-phosphate receptor 1	Mus musculus	193-196
12904547-8	2003	The involvement of Fas antigen was implicated in the apoptotic event since Fas antigen expression was observed after 3 or 4 h stimulation of HL-60 cells with bacterial ceramides.	Ceramides	168-177	Fas cell surface death receptor	Homo sapiens	75-86
12829737-7	2003	We find that the effects of these ceramides on phospholipase D1 activity strongly correlate with their effects on antigen-stimulated Ca2+ mobilization and with their disruption of lipid order.	Ceramides	34-43	phospholipase D1	Rattus norvegicus	47-63
12925779-2	2003	Ceramides and diglycerides are galactosylated within the endoplasmic reticulum by the UDP-galactose:ceramide galactosyltransferase.	Ceramides	0-9	UDP glycosyltransferase 8	Homo sapiens	86-130
12904547-3	2003	Ceramides and SPLs also induced DNA fragmentation and caspase-3 activation, followed by changes in morphology, such as alterations in the size of nuclei and cells, and cell cycle shortening.	Ceramides	0-9	caspase 3	Homo sapiens	54-63
12904547-9	2003	However, a time-course study for caspase-3 activation indicated maximal activity at 1 h after stimulation with bacterial ceramides, suggesting that two (or possibly more) mechanisms of signal transduction, Fas-dependent and Fas-independent, may be involved.	Ceramides	121-130	caspase 3	Homo sapiens	33-42
12904547-8	2003	The involvement of Fas antigen was implicated in the apoptotic event since Fas antigen expression was observed after 3 or 4 h stimulation of HL-60 cells with bacterial ceramides.	Ceramides	168-177	Fas cell surface death receptor	Homo sapiens	19-30
12904547-10	2003	Fas antigen expression and caspase-3 activation by five kinds of SPLs were observed after 3 or 4 h. These results indicate that there is a difference in the response of HL-60 cells to bacterial ceramides and SPLs.	Ceramides	194-203	Fas cell surface death receptor	Homo sapiens	0-11
12904547-10	2003	Fas antigen expression and caspase-3 activation by five kinds of SPLs were observed after 3 or 4 h. These results indicate that there is a difference in the response of HL-60 cells to bacterial ceramides and SPLs.	Ceramides	194-203	caspase 3	Homo sapiens	27-36
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	87-95	mitogen-activated protein kinase kinase kinase 13	Homo sapiens	17-20
12721293-8	2003	The addition of tumor necrosis factor-alpha further enhances the accumulation of LDL-derived ceramide and the rate of apoptosis.	Ceramides	93-101	tumor necrosis factor	Homo sapiens	16-43
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	87-95	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	28-32
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	87-95	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	33-37
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	87-95	tumor necrosis factor	Homo sapiens	129-138
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	87-95	mitogen-activated protein kinase 8	Homo sapiens	190-193
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	173-181	mitogen-activated protein kinase kinase kinase 13	Homo sapiens	17-20
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	173-181	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	28-32
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	173-181	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	33-37
12738796-3	2003	Importantly, the MLK member MLK3/SPRK has been shown recently to be a direct target of ceramide and tumor necrosis factor-alpha (TNF-alpha) and to mediate the TNF-alpha and ceramide-induced JNK activation in Jurkat cells.	Ceramides	173-181	mitogen-activated protein kinase 8	Homo sapiens	190-193
12880980-5	2003	Cytotoxicity of 4-HPR is mediated at least in part by increasing tumor cell ceramide levels and combining 4-HPR with ceramide modulators increased anti-tumor activity in pre-clinical models.	Ceramides	76-84	haptoglobin-related protein	Homo sapiens	18-21
12738796-10	2003	Thus, our findings imply that some of the biological functions of JNK activators, such as TNF-alpha and ceramide, may be attributed to their ability to block cell responses to growth and survival factors acting through the ERK/MAPK pathway.	Ceramides	104-112	mitogen-activated protein kinase 8	Homo sapiens	66-69
12738796-10	2003	Thus, our findings imply that some of the biological functions of JNK activators, such as TNF-alpha and ceramide, may be attributed to their ability to block cell responses to growth and survival factors acting through the ERK/MAPK pathway.	Ceramides	104-112	mitogen-activated protein kinase 1	Homo sapiens	223-226
12738796-10	2003	Thus, our findings imply that some of the biological functions of JNK activators, such as TNF-alpha and ceramide, may be attributed to their ability to block cell responses to growth and survival factors acting through the ERK/MAPK pathway.	Ceramides	104-112	mitogen-activated protein kinase 1	Homo sapiens	227-231
14508111-2	2003	These domains form in response to acid sphingomyelinase (ASM)-induced ceramide generation.	Ceramides	70-78	sphingomyelin phosphodiesterase 1	Homo sapiens	34-55
12832039-9	2003	We demonstrate that caspase-3 was activated after 4 h treatment in the presence of ceramide leading to the cleavage of PARP.	Ceramides	83-91	caspase 3	Homo sapiens	20-29
12832039-9	2003	We demonstrate that caspase-3 was activated after 4 h treatment in the presence of ceramide leading to the cleavage of PARP.	Ceramides	83-91	poly(ADP-ribose) polymerase 1	Homo sapiens	119-123
12750385-11	2003	M-CSF deprivation resulted in activation of acid sphingomyelinase and an increase in ceramide levels.	Ceramides	85-93	colony stimulating factor 1	Homo sapiens	0-5
12750385-13	2003	Ox-LDL completely blocked the increase in acid sphingomyelinase activity as well as the increase in ceramide after M-CSF deprivation.	Ceramides	100-108	colony stimulating factor 1	Homo sapiens	115-120
12750385-16	2003	This in turn prevents ceramide-induced down-regulation of PKB, the activity of which is required to maintain production of Bcl-XL.	Ceramides	22-30	protein tyrosine kinase 2 beta	Homo sapiens	58-61
12750385-16	2003	This in turn prevents ceramide-induced down-regulation of PKB, the activity of which is required to maintain production of Bcl-XL.	Ceramides	22-30	BCL2 like 1	Homo sapiens	123-129
14508111-2	2003	These domains form in response to acid sphingomyelinase (ASM)-induced ceramide generation.	Ceramides	70-78	sphingomyelin phosphodiesterase 1	Homo sapiens	57-60
12767914-0	2003	Ceramide inhibits the potassium channel Kv1.3 by the formation of membrane platforms.	Ceramides	0-8	potassium voltage-gated channel subfamily A member 3	Homo sapiens	40-45
12855648-6	2003	RESULTS: Adenoviral transduction of endothelial cells with pAd-Survivin inhibited growth factor deprivation- or ceramide-induced apoptosis, reduced caspase-3 and -7 generation, and stabilized three-dimensional capillary networks in vitro.	Ceramides	112-120	baculoviral IAP repeat-containing 5	Mus musculus	63-71
12788101-1	2003	Treatment of brain microvessels with endothelin-1 evoked an early decrease in the sphingomyelin levels concomitantly with an increase in those of ceramides.	Ceramides	146-155	endothelin 1	Homo sapiens	37-49
12818738-2	2003	The main lipid classes in SC are cholesterol (CHOL), free fatty acids (FFA) and at least nine classes of ceramides (CER), referred to as CER1 to CER9.	Ceramides	105-114	cerberus 1, DAN family BMP antagonist	Homo sapiens	137-141
12818738-2	2003	The main lipid classes in SC are cholesterol (CHOL), free fatty acids (FFA) and at least nine classes of ceramides (CER), referred to as CER1 to CER9.	Ceramides	116-119	cerberus 1, DAN family BMP antagonist	Homo sapiens	137-141
12767914-4	2003	Transformation of these small rafts to large ceramide-enriched membrane platforms was achieved by stimulation of the endogenous acid sphingomyelinase, addition of exogenous sphingomyelinase or treatment of the cells with C(16)-ceramide and resulted in clustering of Kv1.3 within ceramide-enriched membrane platforms and inhibition of the channel"s activity.	Ceramides	45-53	potassium voltage-gated channel subfamily A member 3	Homo sapiens	266-271
12576296-0	2003	Ceramide accumulation precedes caspase-3 activation during apoptosis of A549 human lung adenocarcinoma cells.	Ceramides	0-8	caspase 3	Homo sapiens	31-40
12749866-9	2003	These results suggest a role for ceramide in apoptosis and differentiation in HL-60 cells, and also suggest that PKC delta might be involved in ceramide- and TPA-induced apoptosis.	Ceramides	144-152	protein kinase C delta	Homo sapiens	113-122
12576296-3	2003	Here we elucidate the link between caspase-3 activation, at the execution phase, and ceramide accumulation, at the commitment phase of apoptosis in A549 human lung adenocarcinoma cells.	Ceramides	85-93	caspase 3	Homo sapiens	35-44
12576296-4	2003	The induction of ceramide accumulation by various triggers of ceramide generation, such as H(2)O(2), C(6)-ceramide, or UDP-glucose-ceramide glucosyltransferase inhibitor dl-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol, triggered the activation of caspase-3.	Ceramides	17-25	caspase 3	Homo sapiens	257-266
12576296-6	2003	Ceramide-mediated apoptosis was blocked by a general caspase inhibitor, Boc-d-fluoromethylketone, and by overexpression of the antiapoptotic protein Bcl-2.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	149-154
12576296-7	2003	Notably, overexpression of Bcl-2 reduced the basal cellular levels of ceramide and prevented the induction of ceramide generation by C(6)-ceramide, which implies ceramide generation as a possible target for the antiapoptotic effects of Bcl-2.	Ceramides	70-78	BCL2 apoptosis regulator	Homo sapiens	27-32
12576296-7	2003	Notably, overexpression of Bcl-2 reduced the basal cellular levels of ceramide and prevented the induction of ceramide generation by C(6)-ceramide, which implies ceramide generation as a possible target for the antiapoptotic effects of Bcl-2.	Ceramides	110-118	BCL2 apoptosis regulator	Homo sapiens	27-32
12576296-7	2003	Notably, overexpression of Bcl-2 reduced the basal cellular levels of ceramide and prevented the induction of ceramide generation by C(6)-ceramide, which implies ceramide generation as a possible target for the antiapoptotic effects of Bcl-2.	Ceramides	110-118	BCL2 apoptosis regulator	Homo sapiens	27-32
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.	Ceramides	14-22	UDP-glucose ceramide glucosyltransferase	Mus musculus	122-147
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.	Ceramides	14-22	UDP-glucose ceramide glucosyltransferase	Mus musculus	149-152
12692077-3	2003	Enzymatic and metabolic analysis demonstrated that GM95/GCS cells expressed a fully functional enzyme, resulting in normal ceramide glycosylation.	Ceramides	123-131	ankyrin repeat domain 29	Mus musculus	51-55
12692077-3	2003	Enzymatic and metabolic analysis demonstrated that GM95/GCS cells expressed a fully functional enzyme, resulting in normal ceramide glycosylation.	Ceramides	123-131	UDP-glucose ceramide glucosyltransferase	Mus musculus	56-59
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.	Ceramides	17-25	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.	Ceramides	17-25	UDP-glucose ceramide glucosyltransferase	Mus musculus	77-80
12729794-0	2003	Transmembrane domain of Bcl-2 is required for inhibition of ceramide synthesis, but not cytochrome c release in the pathway of inostamycin-induced apoptosis.	Ceramides	60-68	BCL2 apoptosis regulator	Homo sapiens	24-29
12649271-0	2003	Ceramide stabilizes beta-site amyloid precursor protein-cleaving enzyme 1 and promotes amyloid beta-peptide biogenesis.	Ceramides	0-8	beta-secretase 1	Homo sapiens	20-73
12649271-9	2003	Pulse-chase and time-course degradation experiments showed that ceramide post-translationally stabilizes the beta-secretase BACE1.	Ceramides	64-72	beta-secretase 1	Homo sapiens	124-129
12649271-10	2003	Taken together, these data indicate that the lipid second messenger ceramide, which is elevated in the brains of Alzheimer"s disease patients, increases the half-life of BACE1 and thereby promotes Abeta biogenesis.	Ceramides	68-76	beta-secretase 1	Homo sapiens	170-175
12729794-3	2003	In the present study, we found that overexpression of Bcl-2 in human small cell lung carcinoma Ms-1 cells inhibited not only the release of cytochrome c from mitochondria into cytosol but also de novo ceramide synthesis induced by inostamycin, a phosphatidylinositol turnover inhibitor.	Ceramides	201-209	BCL2 apoptosis regulator	Homo sapiens	54-59
12729794-6	2003	Thus, the deletion mutant of tarnsmembrane domain of Bcl-2 can suppress inostamycin-induced apoptosis by inhibiting cytochrome c release, a downstream event of ceramide synthesis in the pathway of inostamycin-induced apoptosis.	Ceramides	160-168	BCL2 apoptosis regulator	Homo sapiens	53-58
12729794-6	2003	Thus, the deletion mutant of tarnsmembrane domain of Bcl-2 can suppress inostamycin-induced apoptosis by inhibiting cytochrome c release, a downstream event of ceramide synthesis in the pathway of inostamycin-induced apoptosis.	Ceramides	160-168	cytochrome c, somatic	Homo sapiens	116-128
12578562-7	2003	Cer-Glc-T was found to have a marked preference for ceramide bearing phytosphingosine as sphingoid base.	Ceramides	52-60	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	0-9
12699912-8	2003	Fumonisin B(1) (10 microM), sphinganine, sphingosine and ceramide (1 microM each) significantly repressed PKC-alpha and -delta isoforms at 48 h, whereas all the exogenously added sphingolipids significantly repressed PKC- epsilon and zeta similar to fumonisin B(1).	Ceramides	57-65	protein kinase C alpha	Homo sapiens	106-143
12699912-8	2003	Fumonisin B(1) (10 microM), sphinganine, sphingosine and ceramide (1 microM each) significantly repressed PKC-alpha and -delta isoforms at 48 h, whereas all the exogenously added sphingolipids significantly repressed PKC- epsilon and zeta similar to fumonisin B(1).	Ceramides	57-65	protein kinase C epsilon	Homo sapiens	217-229
12754099-3	2003	C2- and C6-ceramides (cell-permeable ceramide analogs), but not C16-ceramide, induced nuclear factor-kappaB (NF-kappaB) DNA-binding, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and mitochondrial cytochrome c release, indicating that apoptosis occurs through the caspase cascade and the mitochondrial pathway.	Ceramides	11-20	cytochrome c, somatic	Homo sapiens	214-226
12754099-3	2003	C2- and C6-ceramides (cell-permeable ceramide analogs), but not C16-ceramide, induced nuclear factor-kappaB (NF-kappaB) DNA-binding, caspase-3 activation, poly(ADP-ribose) polymerase degradation, and mitochondrial cytochrome c release, indicating that apoptosis occurs through the caspase cascade and the mitochondrial pathway.	Ceramides	11-19	cytochrome c, somatic	Homo sapiens	214-226
12728250-0	2003	TGF-beta1 suppresses apoptosis via differential regulation of MAP kinases and ceramide production.	Ceramides	78-86	transforming growth factor, beta 1	Mus musculus	0-9
12728250-2	2003	Treatment of cells with transforming growth factor-beta1 (TGF-beta1) activated the extracellular signal regulated kinases 1 and 2 (ERK1/ERK2), inhibited the serum deprivation-induced p38 activation and the increase in intracellular ceramide formation, leading to the stimulation of cell proliferation and the suppression of apoptosis.	Ceramides	232-240	transforming growth factor, beta 1	Mus musculus	24-56
12728250-2	2003	Treatment of cells with transforming growth factor-beta1 (TGF-beta1) activated the extracellular signal regulated kinases 1 and 2 (ERK1/ERK2), inhibited the serum deprivation-induced p38 activation and the increase in intracellular ceramide formation, leading to the stimulation of cell proliferation and the suppression of apoptosis.	Ceramides	232-240	transforming growth factor, beta 1	Mus musculus	58-67
12728250-2	2003	Treatment of cells with transforming growth factor-beta1 (TGF-beta1) activated the extracellular signal regulated kinases 1 and 2 (ERK1/ERK2), inhibited the serum deprivation-induced p38 activation and the increase in intracellular ceramide formation, leading to the stimulation of cell proliferation and the suppression of apoptosis.	Ceramides	232-240	mitogen-activated protein kinase 3	Mus musculus	83-129
12728250-2	2003	Treatment of cells with transforming growth factor-beta1 (TGF-beta1) activated the extracellular signal regulated kinases 1 and 2 (ERK1/ERK2), inhibited the serum deprivation-induced p38 activation and the increase in intracellular ceramide formation, leading to the stimulation of cell proliferation and the suppression of apoptosis.	Ceramides	232-240	mitogen-activated protein kinase 3	Mus musculus	131-135
12728250-2	2003	Treatment of cells with transforming growth factor-beta1 (TGF-beta1) activated the extracellular signal regulated kinases 1 and 2 (ERK1/ERK2), inhibited the serum deprivation-induced p38 activation and the increase in intracellular ceramide formation, leading to the stimulation of cell proliferation and the suppression of apoptosis.	Ceramides	232-240	mitogen-activated protein kinase 1	Mus musculus	136-140
12728250-10	2003	TGF-beta1 suppresses the serum-deprivation-induced apoptosis via its distinct effects on complex signaling events involving the activation of ERK1/ERK2 and the inhibition of p38 activation and increased ceramide generation.	Ceramides	203-211	transforming growth factor, beta 1	Mus musculus	0-9
12578840-5	2003	BcR-induced formation of long-chain ceramide species resulted in proteasomal activation and degradation of XIAP and subsequent activation of effector caspases, demonstrating an important cell-biological mechanism through which long-chain ceramides may be involved in the progression of BcR triggering induced apoptosis and subsequent formation of very long-chain ceramide species.	Ceramides	36-44	X-linked inhibitor of apoptosis	Homo sapiens	107-111
12676512-4	2003	Ceramide also is capable of activating protein phosphatases such as protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A).	Ceramides	0-8	inorganic pyrophosphatase 1	Homo sapiens	68-89
12676512-4	2003	Ceramide also is capable of activating protein phosphatases such as protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A).	Ceramides	0-8	inorganic pyrophosphatase 1	Homo sapiens	91-94
12676512-4	2003	Ceramide also is capable of activating protein phosphatases such as protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A).	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	108-122
12676512-4	2003	Ceramide also is capable of activating protein phosphatases such as protein phosphatase 1 (PP1) and protein phosphatase 2A (PP2A).	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	124-128
12676512-5	2003	It is through these protein phosphatases that ceramide can indirectly inhibit kinases that are key components of pro-growth signaling processes such as the classical and novel PKC isoforms and protein kinase B (PKB; also known as Akt).	Ceramides	46-54	protein kinase C zeta	Homo sapiens	176-179
12676512-5	2003	It is through these protein phosphatases that ceramide can indirectly inhibit kinases that are key components of pro-growth signaling processes such as the classical and novel PKC isoforms and protein kinase B (PKB; also known as Akt).	Ceramides	46-54	AKT serine/threonine kinase 1	Homo sapiens	211-214
12676512-5	2003	It is through these protein phosphatases that ceramide can indirectly inhibit kinases that are key components of pro-growth signaling processes such as the classical and novel PKC isoforms and protein kinase B (PKB; also known as Akt).	Ceramides	46-54	AKT serine/threonine kinase 1	Homo sapiens	230-233
12676512-6	2003	However, the mechanisms how ceramide directly activates enzymes such as JNK and PP2A are still not clear.	Ceramides	28-36	mitogen-activated protein kinase 8	Homo sapiens	72-75
12676512-6	2003	However, the mechanisms how ceramide directly activates enzymes such as JNK and PP2A are still not clear.	Ceramides	28-36	protein phosphatase 2 phosphatase activator	Homo sapiens	80-84
12676513-1	2003	Ceramide has been shown to be critically involved in many forms of apoptosis including death triggered by receptors, e.g. CD95 or the tumor necrosis factor receptor, during development, or stress.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	122-126
12676513-3	2003	The release of ceramide by these stimuli is mediated by the acid sphingomyelinase (ASM), an enzyme that is rapidly activated by many apoptotic stimuli.	Ceramides	15-23	sphingomyelin phosphodiesterase 1	Homo sapiens	60-81
12676513-3	2003	The release of ceramide by these stimuli is mediated by the acid sphingomyelinase (ASM), an enzyme that is rapidly activated by many apoptotic stimuli.	Ceramides	15-23	sphingomyelin phosphodiesterase 1	Homo sapiens	83-86
12676513-6	2003	Surface ASM releases ceramide from sphingomyelin that rapidly forms ceramide-enriched platforms in the cell membrane.	Ceramides	21-29	sphingomyelin phosphodiesterase 1	Homo sapiens	8-11
12676513-6	2003	Surface ASM releases ceramide from sphingomyelin that rapidly forms ceramide-enriched platforms in the cell membrane.	Ceramides	68-76	sphingomyelin phosphodiesterase 1	Homo sapiens	8-11
12736045-7	2003	Ceramide levels increased only twofold in PC-3 cells versus 10-fold in LNCaP cells in response to 10 microM 4-HPR.	Ceramides	0-8	haptoglobin-related protein	Homo sapiens	110-113
12736045-8	2003	PC-3 resistance to 4-HPR could be reversed by the addition of tamoxifen or other agents that block the metabolism of ceramide to glucosylceramide, and with tamoxifen this was marked by a ninefold increase in cellular ceramide levels.	Ceramides	117-125	haptoglobin-related protein	Homo sapiens	21-24
12736045-8	2003	PC-3 resistance to 4-HPR could be reversed by the addition of tamoxifen or other agents that block the metabolism of ceramide to glucosylceramide, and with tamoxifen this was marked by a ninefold increase in cellular ceramide levels.	Ceramides	137-145	haptoglobin-related protein	Homo sapiens	21-24
12736045-9	2003	The influence of 4-HPR on ceramide metabolism was shown to be through activation of serine palmitoyltransferase, the rate-limiting enzyme in the ceramide synthesis pathway.	Ceramides	26-34	haptoglobin-related protein	Homo sapiens	19-22
12736045-9	2003	The influence of 4-HPR on ceramide metabolism was shown to be through activation of serine palmitoyltransferase, the rate-limiting enzyme in the ceramide synthesis pathway.	Ceramides	145-153	haptoglobin-related protein	Homo sapiens	19-22
12736045-10	2003	Blocking the ceramide generated by 4-HPR reduced the extent of apoptosis.	Ceramides	13-21	haptoglobin-related protein	Homo sapiens	37-40
12578840-5	2003	BcR-induced formation of long-chain ceramide species resulted in proteasomal activation and degradation of XIAP and subsequent activation of effector caspases, demonstrating an important cell-biological mechanism through which long-chain ceramides may be involved in the progression of BcR triggering induced apoptosis and subsequent formation of very long-chain ceramide species.	Ceramides	238-247	X-linked inhibitor of apoptosis	Homo sapiens	107-111
12578840-5	2003	BcR-induced formation of long-chain ceramide species resulted in proteasomal activation and degradation of XIAP and subsequent activation of effector caspases, demonstrating an important cell-biological mechanism through which long-chain ceramides may be involved in the progression of BcR triggering induced apoptosis and subsequent formation of very long-chain ceramide species.	Ceramides	238-246	X-linked inhibitor of apoptosis	Homo sapiens	107-111
12566438-1	2003	Neutral sphingomyelinase (N-SMase) is one of the key enzymes involved in the generation of ceramide; however, the gene(s) encoding for the mammalian N-SMase is still not well defined.	Ceramides	91-99	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
12706871-0	2003	Ceramide induces cell cycle arrest and upregulates p27kip in nasopharyngeal carcinoma cells.	Ceramides	0-8	dynactin subunit 6	Homo sapiens	51-54
12706871-5	2003	Exposure of CNE2 cells to ceramide resulted in a dose-dependent up-regulation of the cyclin-dependent kinase inhibitor p27 and a decrease of phospho-Akt without reduced expression of total AKT protein.	Ceramides	26-34	dynactin subunit 6	Homo sapiens	119-122
12706871-5	2003	Exposure of CNE2 cells to ceramide resulted in a dose-dependent up-regulation of the cyclin-dependent kinase inhibitor p27 and a decrease of phospho-Akt without reduced expression of total AKT protein.	Ceramides	26-34	AKT serine/threonine kinase 1	Homo sapiens	149-152
12706871-5	2003	Exposure of CNE2 cells to ceramide resulted in a dose-dependent up-regulation of the cyclin-dependent kinase inhibitor p27 and a decrease of phospho-Akt without reduced expression of total AKT protein.	Ceramides	26-34	AKT serine/threonine kinase 1	Homo sapiens	189-192
12706871-7	2003	We concluded that ceramide induced cell cycle arrest in G1 phase in CNE2 cells and p27 up-regulation was involved in this process.	Ceramides	18-26	dynactin subunit 6	Homo sapiens	83-86
12706871-8	2003	In addition, up-regulation of p27 resulting from ceramide treatment may be due to the interruption of Akt, but decrease of phospho-Akt is independent of PI3K function or PTEN protein expression.	Ceramides	49-57	dynactin subunit 6	Homo sapiens	30-33
12706871-8	2003	In addition, up-regulation of p27 resulting from ceramide treatment may be due to the interruption of Akt, but decrease of phospho-Akt is independent of PI3K function or PTEN protein expression.	Ceramides	49-57	AKT serine/threonine kinase 1	Homo sapiens	102-105
12566438-1	2003	Neutral sphingomyelinase (N-SMase) is one of the key enzymes involved in the generation of ceramide; however, the gene(s) encoding for the mammalian N-SMase is still not well defined.	Ceramides	91-99	sphingomyelin phosphodiesterase 2	Homo sapiens	26-33
12566438-1	2003	Neutral sphingomyelinase (N-SMase) is one of the key enzymes involved in the generation of ceramide; however, the gene(s) encoding for the mammalian N-SMase is still not well defined.	Ceramides	91-99	sphingomyelin phosphodiesterase 2	Homo sapiens	149-156
12566438-8	2003	Accordingly, ceramide measurement showed a 60 +/- 15% increase in nSMase2-overexpressing cells compared with the vector-transfected MCF7.	Ceramides	13-21	sphingomyelin phosphodiesterase 3	Homo sapiens	66-73
15041894-6	2003	Key components of TNF signaling include sphingolipids, particularly ceramide generated from acidic sphingomyelinase activation serving as a source for gangliosides.	Ceramides	68-76	tumor necrosis factor	Homo sapiens	18-21
12492401-11	2003	By this pathway, low doses of DHA increase ceramide levels, which leads to inhibition of cdk2 activity and stimulation of PP1 and PP2A.	Ceramides	43-51	cyclin dependent kinase 2	Homo sapiens	89-93
12492401-11	2003	By this pathway, low doses of DHA increase ceramide levels, which leads to inhibition of cdk2 activity and stimulation of PP1 and PP2A.	Ceramides	43-51	inorganic pyrophosphatase 1	Homo sapiens	122-125
12492401-11	2003	By this pathway, low doses of DHA increase ceramide levels, which leads to inhibition of cdk2 activity and stimulation of PP1 and PP2A.	Ceramides	43-51	protein phosphatase 2 phosphatase activator	Homo sapiens	130-134
12644590-2	2003	We have recently reported that eNOS, expressed in an inducible HeLa Tet-off cell line, is activated by tumor necrosis factor-alpha (TNF-alpha) in a previously undescribed pathway that involves the lipid messenger ceramide.	Ceramides	213-221	tumor necrosis factor	Homo sapiens	103-130
12640124-5	2003	Unexpectedly, the caveolin-overexpressing cells also exhibited a significant activation of the phosphatidylinositol 3-kinase (PI3K)/Akt pathway, which additional studies suggested was likely due to decreased neutral sphingomyelinase activity and ceramide synthesis.	Ceramides	246-254	caveolin 1	Homo sapiens	18-26
12785717-8	2003	Ceramides produced in response to heat shock were demonstrated to induce the production of c-jun, leading to apoptosis, and to be upstream of dephosphorylation of serine-rich proteins.	Ceramides	0-9	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	91-96
12684378-0	2003	Ceramide/long-chain base phosphate rheostat in Saccharomyces cerevisiae: regulation of ceramide synthesis by Elo3p and Cka2p.	Ceramides	0-8	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	109-114
12684378-0	2003	Ceramide/long-chain base phosphate rheostat in Saccharomyces cerevisiae: regulation of ceramide synthesis by Elo3p and Cka2p.	Ceramides	0-8	casein kinase 2 catalytic subunit CKA2	Saccharomyces cerevisiae S288C	119-124
12684378-0	2003	Ceramide/long-chain base phosphate rheostat in Saccharomyces cerevisiae: regulation of ceramide synthesis by Elo3p and Cka2p.	Ceramides	87-95	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	109-114
12684378-0	2003	Ceramide/long-chain base phosphate rheostat in Saccharomyces cerevisiae: regulation of ceramide synthesis by Elo3p and Cka2p.	Ceramides	87-95	casein kinase 2 catalytic subunit CKA2	Saccharomyces cerevisiae S288C	119-124
12684378-6	2003	The Elo3 protein is necessary for synthesis of C(26)-CoA, which in wild-type yeast is a source of C(26) fatty acyls found in the ceramide moieties of all sphingolipids.	Ceramides	129-137	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	4-8
12644590-2	2003	We have recently reported that eNOS, expressed in an inducible HeLa Tet-off cell line, is activated by tumor necrosis factor-alpha (TNF-alpha) in a previously undescribed pathway that involves the lipid messenger ceramide.	Ceramides	213-221	tumor necrosis factor	Homo sapiens	132-141
12529332-0	2003	Ceramide-induced and age-associated increase in macrophage COX-2 expression is mediated through up-regulation of NF-kappa B activity.	Ceramides	0-8	cytochrome c oxidase II, mitochondrial	Mus musculus	59-64
12529332-0	2003	Ceramide-induced and age-associated increase in macrophage COX-2 expression is mediated through up-regulation of NF-kappa B activity.	Ceramides	0-8	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	113-123
12529332-1	2003	We have shown that the age-associated increase in lipopolysaccharide (LPS)-stimulated macrophages (M phi) prostaglandin E(2) (PGE(2)) production is because of ceramide-induced up-regulation of cyclooxygenase (COX)-2 transcription that leads to increased COX-2 expression and enzyme activity.	Ceramides	159-167	toll-like receptor 4	Mus musculus	70-73
12529332-1	2003	We have shown that the age-associated increase in lipopolysaccharide (LPS)-stimulated macrophages (M phi) prostaglandin E(2) (PGE(2)) production is because of ceramide-induced up-regulation of cyclooxygenase (COX)-2 transcription that leads to increased COX-2 expression and enzyme activity.	Ceramides	159-167	cytochrome c oxidase II, mitochondrial	Mus musculus	193-215
12529332-1	2003	We have shown that the age-associated increase in lipopolysaccharide (LPS)-stimulated macrophages (M phi) prostaglandin E(2) (PGE(2)) production is because of ceramide-induced up-regulation of cyclooxygenase (COX)-2 transcription that leads to increased COX-2 expression and enzyme activity.	Ceramides	159-167	cytochrome c oxidase II, mitochondrial	Mus musculus	254-259
12529332-2	2003	To determine the mechanism of the age-related and ceramide-dependent increase in COX-2 transcription, we investigated the role of various transcription factors involved in COX-2 gene expression.	Ceramides	50-58	cytochrome c oxidase II, mitochondrial	Mus musculus	81-86
12529332-8	2003	Addition of ceramide to the young M phi, in the presence or absence of LPS, increased NF-kappa B activation in parallel with PGE(2) production.	Ceramides	12-20	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	86-96
12529332-9	2003	Bay 11-7082 or NF-kappa B decoy prevented this ceramide-induced increase in NF-kappa B binding activity and PGE(2) production.	Ceramides	47-55	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	15-25
12529332-9	2003	Bay 11-7082 or NF-kappa B decoy prevented this ceramide-induced increase in NF-kappa B binding activity and PGE(2) production.	Ceramides	47-55	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	76-86
12529332-10	2003	These findings strongly suggest that the age-associated and ceramide-induced increase in COX-2 transcription is mediated through higher NF-kappa B activation, which is, in turn, because of a greater I kappa B degradation in old M phi.	Ceramides	60-68	cytochrome c oxidase II, mitochondrial	Mus musculus	89-94
12529332-10	2003	These findings strongly suggest that the age-associated and ceramide-induced increase in COX-2 transcription is mediated through higher NF-kappa B activation, which is, in turn, because of a greater I kappa B degradation in old M phi.	Ceramides	60-68	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	136-146
12642364-10	2003	Furthermore, N-acetylsphingosine (C2-ceramide), a synthetic cell-permeable ceramide analogue, increased myocyte ROS production, suggesting that TNF-alpha-mediated ROS production and subsequent mtDNA damage were mediated by the sphingomyelin-ceramide signaling pathway.	Ceramides	37-45	tumor necrosis factor	Rattus norvegicus	144-153
12650926-4	2003	A-SMase catalyzes the conversion of sphingomyelin to ceramides, which are pro-apoptotic.	Ceramides	53-62	sphingomyelin phosphodiesterase 1	Homo sapiens	0-7
12650926-5	2003	This action of Sph-1-P prevents the accumulation of ceramides and blocks apoptosis, thereby promoting survival of the macrophages.	Ceramides	52-61	ankyrin 1	Homo sapiens	15-20
12626751-8	2003	Shifting the acc1(ts) cells to 24 degrees C after 2 h of incubation at 37 degrees C resulted in reactivation of the ACC and elevation of the ceramides and very long-chain fatty acid syntheses with normal cell-cycle progression.	Ceramides	141-150	acetyl-CoA carboxylase alpha	Homo sapiens	13-17
12642364-10	2003	Furthermore, N-acetylsphingosine (C2-ceramide), a synthetic cell-permeable ceramide analogue, increased myocyte ROS production, suggesting that TNF-alpha-mediated ROS production and subsequent mtDNA damage were mediated by the sphingomyelin-ceramide signaling pathway.	Ceramides	75-83	tumor necrosis factor	Rattus norvegicus	144-153
12511568-0	2003	Ceramide increases oxidative damage due to inhibition of catalase by caspase-3-dependent proteolysis in HL-60 cell apoptosis.	Ceramides	0-8	catalase	Homo sapiens	57-65
12511568-0	2003	Ceramide increases oxidative damage due to inhibition of catalase by caspase-3-dependent proteolysis in HL-60 cell apoptosis.	Ceramides	0-8	caspase 3	Homo sapiens	69-78
12511568-4	2003	Moreover, acetyl-Asp-Met-Gln-Asp-aldehyde, which dominantly inhibited caspase-3 and blocked the increase of oxidative damage and apoptosis due to C(2)-ceramide-induced catalase depletion at protein and activity levels.	Ceramides	151-159	caspase 3	Homo sapiens	70-79
12515830-4	2003	TGF-beta treatment induced endogenous ceramide levels in a time-dependent manner within 5-15 min of cell stimulation.	Ceramides	38-46	transforming growth factor beta 1	Homo sapiens	0-8
12511568-4	2003	Moreover, acetyl-Asp-Met-Gln-Asp-aldehyde, which dominantly inhibited caspase-3 and blocked the increase of oxidative damage and apoptosis due to C(2)-ceramide-induced catalase depletion at protein and activity levels.	Ceramides	151-159	catalase	Homo sapiens	168-176
12511568-6	2003	Taken together, it is suggested that H(2)O(2) enhances apoptosis in ceramide-pretreated cells, because ceramide increases oxidative damage by inhibition of ROS scavenging ability through caspase-3-dependent proteolysis of catalase.	Ceramides	68-76	caspase 3	Homo sapiens	187-196
12511568-6	2003	Taken together, it is suggested that H(2)O(2) enhances apoptosis in ceramide-pretreated cells, because ceramide increases oxidative damage by inhibition of ROS scavenging ability through caspase-3-dependent proteolysis of catalase.	Ceramides	68-76	catalase	Homo sapiens	222-230
12511568-6	2003	Taken together, it is suggested that H(2)O(2) enhances apoptosis in ceramide-pretreated cells, because ceramide increases oxidative damage by inhibition of ROS scavenging ability through caspase-3-dependent proteolysis of catalase.	Ceramides	103-111	caspase 3	Homo sapiens	187-196
12511568-6	2003	Taken together, it is suggested that H(2)O(2) enhances apoptosis in ceramide-pretreated cells, because ceramide increases oxidative damage by inhibition of ROS scavenging ability through caspase-3-dependent proteolysis of catalase.	Ceramides	103-111	catalase	Homo sapiens	222-230
12668106-2	2003	The suitably protected lactotriose (Lc3) derivatives were successively glycosylated with sialic acid, sialyl-alpha-(2-->3)-D-galactose and/or L-fucose donors in a regio- and stereo-selective manner, to give the protected type I hexa- and hepta-saccharides, respectively, which were then converted to the target gangliosides by the introduction of ceramide and subsequent complete deprotection.	Ceramides	350-358	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	36-39
12637747-6	2003	Suppression of degeneration in arrestin mutant flies expressing ceramidase correlated with a decrease in ceramide levels.	Ceramides	105-113	Arrestin 1	Drosophila melanogaster	31-39
12633609-1	2003	Acid sphingomyelinase (ASM; sphingomyelin phosphodiesterase, EC 3.1.4.12) is the lysosomal enzyme that hydrolyzes sphingomyelin (SPM) to phosphorylcholine and ceramide.	Ceramides	159-167	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
12633609-1	2003	Acid sphingomyelinase (ASM; sphingomyelin phosphodiesterase, EC 3.1.4.12) is the lysosomal enzyme that hydrolyzes sphingomyelin (SPM) to phosphorylcholine and ceramide.	Ceramides	159-167	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
12633609-1	2003	Acid sphingomyelinase (ASM; sphingomyelin phosphodiesterase, EC 3.1.4.12) is the lysosomal enzyme that hydrolyzes sphingomyelin (SPM) to phosphorylcholine and ceramide.	Ceramides	159-167	sphingomyelin phosphodiesterase 1	Homo sapiens	28-59
12525490-0	2003	A role for ceramide, but not diacylglycerol, in the antagonism of insulin signal transduction by saturated fatty acids.	Ceramides	11-19	insulin	Homo sapiens	66-73
12525490-3	2003	These saturated FFAs concomitantly induced the accumulation of ceramide and diacylglycerol, two products of fatty acyl-CoA that have been shown to accumulate in insulin-resistant tissues and to inhibit early steps in insulin signaling.	Ceramides	63-71	insulin	Homo sapiens	161-168
12525490-3	2003	These saturated FFAs concomitantly induced the accumulation of ceramide and diacylglycerol, two products of fatty acyl-CoA that have been shown to accumulate in insulin-resistant tissues and to inhibit early steps in insulin signaling.	Ceramides	63-71	insulin	Homo sapiens	217-224
12525490-4	2003	Preventing de novo ceramide synthesis negated the antagonistic effect of saturated FFAs toward Akt/protein kinase B.	Ceramides	19-27	AKT serine/threonine kinase 1	Homo sapiens	95-98
12525490-4	2003	Preventing de novo ceramide synthesis negated the antagonistic effect of saturated FFAs toward Akt/protein kinase B.	Ceramides	19-27	protein tyrosine kinase 2 beta	Homo sapiens	99-115
12525490-7	2003	Collectively these results identify ceramide as a necessary and sufficient intermediate linking saturated fats to the inhibition of insulin signaling.	Ceramides	36-44	insulin	Homo sapiens	132-139
12431910-8	2003	Both D2 agonists and ceramide specifically induced mitogen-activated protein kinase (ERK1/2), suggesting that ceramide mediates a novel pathway of D2S-induced ERK1/2 activation, leading to cell growth.	Ceramides	21-29	mitogen-activated protein kinase 3	Mus musculus	85-91
12431910-8	2003	Both D2 agonists and ceramide specifically induced mitogen-activated protein kinase (ERK1/2), suggesting that ceramide mediates a novel pathway of D2S-induced ERK1/2 activation, leading to cell growth.	Ceramides	21-29	mitogen-activated protein kinase 3	Mus musculus	159-165
12431910-8	2003	Both D2 agonists and ceramide specifically induced mitogen-activated protein kinase (ERK1/2), suggesting that ceramide mediates a novel pathway of D2S-induced ERK1/2 activation, leading to cell growth.	Ceramides	110-118	mitogen-activated protein kinase 3	Mus musculus	85-91
12431910-8	2003	Both D2 agonists and ceramide specifically induced mitogen-activated protein kinase (ERK1/2), suggesting that ceramide mediates a novel pathway of D2S-induced ERK1/2 activation, leading to cell growth.	Ceramides	110-118	mitogen-activated protein kinase 3	Mus musculus	159-165
12631268-1	2003	Human acid sphingomyelinase (haSMase, EC 3.1.4.12) catalyzes the lysosomal degradation of sphingomyelin to ceramide and phosphorylcholine.	Ceramides	107-115	sphingomyelin phosphodiesterase 1	Homo sapiens	6-27
12588799-5	2003	Interestingly, Parkin acted by delaying mitochondrial swelling and subsequent cytochrome c release and caspase-3 activation observed in ceramide-mediated cell death.	Ceramides	136-144	cytochrome c, somatic	Homo sapiens	78-90
12588799-5	2003	Interestingly, Parkin acted by delaying mitochondrial swelling and subsequent cytochrome c release and caspase-3 activation observed in ceramide-mediated cell death.	Ceramides	136-144	caspase 3	Homo sapiens	103-112
12688321-7	2003	Up-regulation of c-Myc protein evoked by pretreatment with PMA for a short time could disturb the signaling pathway of the ceramide and sphingosine, which are known to function as the endogenous modulators mediating the apoptotic signal of TNF-alpha.	Ceramides	123-131	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	17-22
12594290-2	2003	Within this compartment, the TNF- and IFN-gamma-responsive acid sphingomyelinase (ASMase) generates the signaling molecule ceramide, resulting in the activation of proteases like cathepsin D.	Ceramides	123-131	tumor necrosis factor	Mus musculus	29-32
12594290-2	2003	Within this compartment, the TNF- and IFN-gamma-responsive acid sphingomyelinase (ASMase) generates the signaling molecule ceramide, resulting in the activation of proteases like cathepsin D.	Ceramides	123-131	interferon gamma	Mus musculus	38-47
12594290-2	2003	Within this compartment, the TNF- and IFN-gamma-responsive acid sphingomyelinase (ASMase) generates the signaling molecule ceramide, resulting in the activation of proteases like cathepsin D.	Ceramides	123-131	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	59-80
12594290-2	2003	Within this compartment, the TNF- and IFN-gamma-responsive acid sphingomyelinase (ASMase) generates the signaling molecule ceramide, resulting in the activation of proteases like cathepsin D.	Ceramides	123-131	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	82-88
12594290-2	2003	Within this compartment, the TNF- and IFN-gamma-responsive acid sphingomyelinase (ASMase) generates the signaling molecule ceramide, resulting in the activation of proteases like cathepsin D.	Ceramides	123-131	cathepsin D	Mus musculus	179-190
12688321-7	2003	Up-regulation of c-Myc protein evoked by pretreatment with PMA for a short time could disturb the signaling pathway of the ceramide and sphingosine, which are known to function as the endogenous modulators mediating the apoptotic signal of TNF-alpha.	Ceramides	123-131	tumor necrosis factor	Homo sapiens	240-249
12691738-0	2003	Ceramide-induced neuronal apoptosis is associated with dephosphorylation of Akt, BAD, FKHR, GSK-3beta, and induction of the mitochondrial-dependent intrinsic caspase pathway.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	76-79
12691738-0	2003	Ceramide-induced neuronal apoptosis is associated with dephosphorylation of Akt, BAD, FKHR, GSK-3beta, and induction of the mitochondrial-dependent intrinsic caspase pathway.	Ceramides	0-8	forkhead box O1	Homo sapiens	86-90
12691738-0	2003	Ceramide-induced neuronal apoptosis is associated with dephosphorylation of Akt, BAD, FKHR, GSK-3beta, and induction of the mitochondrial-dependent intrinsic caspase pathway.	Ceramides	0-8	glycogen synthase kinase 3 beta	Homo sapiens	92-101
16120324-0	2003	Cytochrome c dissociation and release from mitochondria by truncated Bid and ceramide.	Ceramides	77-85	cytochrome c, somatic	Homo sapiens	0-12
12691738-4	2003	We show that ceramide treatment initiates a cascade of biochemical alterations associated with cell death: earliest signal transduction changes involve Akt dephosphorylation and inactivation followed by dephosphorylation of proapoptotic regulators such as BAD (proapoptotic Bcl-2 family member), Forkhead family transcription factors, glycogen synthase kinase 3-beta, mitochondrial depolarization and permeabilization, release of cytochrome c into the cytosol, and caspase-3 activation.	Ceramides	13-21	AKT serine/threonine kinase 1	Homo sapiens	152-155
16120324-3	2003	Ceramides did not permeabilize the mitochondrial outer membrane, and stimulated cytochrome c release only in the presence of digitonin.	Ceramides	0-9	cytochrome c, somatic	Homo sapiens	80-92
12691738-4	2003	We show that ceramide treatment initiates a cascade of biochemical alterations associated with cell death: earliest signal transduction changes involve Akt dephosphorylation and inactivation followed by dephosphorylation of proapoptotic regulators such as BAD (proapoptotic Bcl-2 family member), Forkhead family transcription factors, glycogen synthase kinase 3-beta, mitochondrial depolarization and permeabilization, release of cytochrome c into the cytosol, and caspase-3 activation.	Ceramides	13-21	glycogen synthase kinase 3 beta	Homo sapiens	335-366
12563314-4	2003	Failure to generate ceramide-enriched membrane platforms in infected cells results in an unabated inflammatory response, massive release of interleukin (IL)-1 and septic death of mice.	Ceramides	20-28	interleukin 1 complex	Mus musculus	140-158
12691738-4	2003	We show that ceramide treatment initiates a cascade of biochemical alterations associated with cell death: earliest signal transduction changes involve Akt dephosphorylation and inactivation followed by dephosphorylation of proapoptotic regulators such as BAD (proapoptotic Bcl-2 family member), Forkhead family transcription factors, glycogen synthase kinase 3-beta, mitochondrial depolarization and permeabilization, release of cytochrome c into the cytosol, and caspase-3 activation.	Ceramides	13-21	cytochrome c, somatic	Homo sapiens	430-442
12691738-4	2003	We show that ceramide treatment initiates a cascade of biochemical alterations associated with cell death: earliest signal transduction changes involve Akt dephosphorylation and inactivation followed by dephosphorylation of proapoptotic regulators such as BAD (proapoptotic Bcl-2 family member), Forkhead family transcription factors, glycogen synthase kinase 3-beta, mitochondrial depolarization and permeabilization, release of cytochrome c into the cytosol, and caspase-3 activation.	Ceramides	13-21	caspase 3	Homo sapiens	465-474
12576150-6	2003	In addition, we demonstrate that ceramide accumulation correlates with the activation of proximal procaspases-8 and -9 as well as distal caspase-3, prior to the appearance of cell death.	Ceramides	33-41	caspase 3	Mus musculus	137-146
12606757-1	2003	Ceramide, formed by sphingomyelinase, is involved in the expression of cyclooxygenase-2 (COX-2).	Ceramides	0-8	prostaglandin-endoperoxide synthase 2	Mus musculus	71-87
12606757-1	2003	Ceramide, formed by sphingomyelinase, is involved in the expression of cyclooxygenase-2 (COX-2).	Ceramides	0-8	prostaglandin-endoperoxide synthase 2	Mus musculus	89-94
12606757-2	2003	This study examines the effect of C2-ceramide (C2), a cell-permeable ceramide analog, on the lipopolysaccharide (LPS)-inducible COX-2 expression and signaling pathways.	Ceramides	37-45	prostaglandin-endoperoxide synthase 2	Mus musculus	128-133
12493772-0	2003	Lcb4p is a key regulator of ceramide synthesis from exogenous long chain sphingoid base in Saccharomyces cerevisiae.	Ceramides	28-36	sphinganine kinase LCB4	Saccharomyces cerevisiae S288C	0-5
12493772-4	2003	It has been shown that the LCBP phosphatase, Lcb3p, is required for efficient ceramide synthesis from exogenous LCB.	Ceramides	78-86	sphinganine kinase LCB3	Saccharomyces cerevisiae S288C	45-50
12493772-5	2003	Here we present direct evidence that the major LCB kinase, Lcb4p, but not the minor kinase, Lcb5p, regulates synthesis of ceramide from exogenously added LCB.	Ceramides	122-130	sphinganine kinase LCB4	Saccharomyces cerevisiae S288C	59-64
12606947-6	2003	The effect on TNF-induced NF-kappaB activation was selective as adenosine had minimal effect on NF-kappaB activation induced by H(2)O(2), PMA, LPS, okadaic acid, or ceramide, suggesting differences in the pathway leading to NF-kappaB activation by different agents.	Ceramides	165-173	tumor necrosis factor	Homo sapiens	14-17
12646059-8	2003	Treatment with TNFalpha for 5-30 min activated MAPKs (ERK, p38, and JNK), and increased ceramide accumulation.	Ceramides	88-96	tumor necrosis factor	Homo sapiens	15-23
12473648-0	2003	Transient mechanoactivation of neutral sphingomyelinase in caveolae to generate ceramide.	Ceramides	80-88	sphingomyelin phosphodiesterase 2	Homo sapiens	31-55
12473648-3	2003	Hemodynamic stressors from increased vascular flow and pressure in situ rapidly and transiently induce the activity of neutral sphingomyelinase but not that acid sphingomyelinase in a time- and flow rate-dependent manner, followed by the generation of ceramides.	Ceramides	252-261	sphingomyelin phosphodiesterase 2	Homo sapiens	119-143
12565900-4	2003	Protein kinase inhibitor K252a decreased the effect of C2 ceramide in a dose-dependent manner, but the effect of insulin was not changed.	Ceramides	58-66	KIT proto-oncogene receptor tyrosine kinase	Rattus norvegicus	0-14
12565900-10	2003	Moreover, the increased effect of bFGF and dose-dependently decreased effect of C2 ceramide by K252a suggest that different protein kinases are important in bFGF- and ceramide-mediated enhancement of RGC survival rate.	Ceramides	83-91	fibroblast growth factor 2	Rattus norvegicus	157-161
12646059-10	2003	Like TNFalpha, treatment of CLENDO cells with exogenous ceramide significantly induced endothelial apoptosis.	Ceramides	56-64	tumor necrosis factor	Homo sapiens	5-13
12646059-11	2003	Ceramide also activated the JNK pathway, but had no effect on ERK and p38 MAPKs.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	28-31
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.	Ceramides	192-200	glucosylceramidase beta	Homo sapiens	5-28
12562509-0	2003	Ceramide increases mitochondrial free calcium levels via caspase 8 and Bid: role in initiation of cell death.	Ceramides	0-8	caspase 8	Rattus norvegicus	57-66
12424096-5	2003	By Western blot analysis, ceramide-induced NADPH oxidase activation was found to be associated with the translocation of p47(phox) to the membrane.	Ceramides	26-34	pleckstrin	Homo sapiens	121-124
12424096-6	2003	In isolated and pressurized small coronary arteries, N-vanillylnonanamide, apocynin, or uric acid, a peroxynitrite scavenger, largely restored the inhibitory effects of ceramide on bradykinin- and A-23187-induced vasorelaxation.	Ceramides	169-177	kininogen 1	Homo sapiens	181-191
12569071-0	2003	Interleukin-1beta inhibits ATP-induced protein kinase B activation in renal mesangial cells by two different mechanisms: the involvement of nitric oxide and ceramide.	Ceramides	157-165	interleukin 1 beta	Homo sapiens	0-17
12569071-0	2003	Interleukin-1beta inhibits ATP-induced protein kinase B activation in renal mesangial cells by two different mechanisms: the involvement of nitric oxide and ceramide.	Ceramides	157-165	protein tyrosine kinase 2 beta	Homo sapiens	39-55
12569071-11	2003	5 In summary, our data show that IL-1beta exerts both short-term and long-term inhibitory effects on ATP-stimulated PKB activation, the short-term effect probably involves ceramide formation, whereas the long-term effect is due to inducible NO synthase induction and subsequent NO formation.	Ceramides	172-180	interleukin 1 beta	Homo sapiens	33-41
12569071-11	2003	5 In summary, our data show that IL-1beta exerts both short-term and long-term inhibitory effects on ATP-stimulated PKB activation, the short-term effect probably involves ceramide formation, whereas the long-term effect is due to inducible NO synthase induction and subsequent NO formation.	Ceramides	172-180	protein tyrosine kinase 2 beta	Homo sapiens	116-119
12569071-12	2003	These results reveal a further facet in the mechanisms of ceramide- and NO-induced cell death, i.e. by turning off the survival signal elicited by PKB.	Ceramides	58-66	protein tyrosine kinase 2 beta	Homo sapiens	147-150
12700647-2	2003	Although the role of sphingolipids such as ceramides has been suggested to participate in CD95-mediated apoptosis, the exact role of these molecules in this process remains controversial.	Ceramides	43-52	Fas cell surface death receptor	Homo sapiens	90-94
12700652-4	2003	TNF-alpha activated intrinsic and extrinsic apoptosis pathways and increased ceramide and sphingosine levels in irradiated LNCaP cells.	Ceramides	77-85	tumor necrosis factor	Homo sapiens	0-9
12700652-6	2003	Exogenous ceramide and bacterial sphingomyelinase sensitized LNCaP cells to radiation-induced apoptosis and had a synergistic effect on cell death after irradiation with TNF-alpha, but not with CH-11.	Ceramides	10-18	tumor necrosis factor	Homo sapiens	170-179
12700652-7	2003	Cell death effects after exposure to ceramide and irradiation were blocked by the serine protease inhibitor TLCK (Na-p-tosyl-L-lysine-chloromethylketone), but not by the caspase inhibitor z-VAD (2-val-Ala-Asp(oMe)-CH(2)F).	Ceramides	37-45	catenin beta like 1	Homo sapiens	114-118
12700652-8	2003	During LNCaP cell apoptosis induced by exogenous ceramide, we observed activation of caspase-9, but not caspases-8, -3, or -7.	Ceramides	49-57	caspase 9	Homo sapiens	85-94
12700652-9	2003	The effect of ceramide occurred largely via the intrinsic mitochondrial apoptosis pathway and enhanced TNF-alpha, but not CH-11 effects on irradiated cells.	Ceramides	14-22	tumor necrosis factor	Homo sapiens	103-112
12700652-10	2003	The data show that ceramide enhanced activation of the intrinsic apoptotic pathway and enhanced cell death induced by TNF-alpha with or without gamma-irradiation.	Ceramides	19-27	tumor necrosis factor	Homo sapiens	118-127
12700652-11	2003	TNF-alpha and gamma-irradiation elevated levels of endogenous ceramide and activated the intrinsic cell death pathway.	Ceramides	62-70	tumor necrosis factor	Homo sapiens	0-9
12540565-6	2003	Closely following the change in ceramide level was an increase in the expression of globotriaosylceramide (Gb3), the receptor for Stx2.	Ceramides	32-40	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	107-110
12540565-6	2003	Closely following the change in ceramide level was an increase in the expression of globotriaosylceramide (Gb3), the receptor for Stx2.	Ceramides	32-40	syntaxin 2	Homo sapiens	130-134
12562509-0	2003	Ceramide increases mitochondrial free calcium levels via caspase 8 and Bid: role in initiation of cell death.	Ceramides	0-8	BH3 interacting domain death agonist	Rattus norvegicus	71-74
12562509-1	2003	We investigated how the mitochondrial phase of ceramide-mediated cell death is initiated in nerve growth factor (NGF)-differentiated PC12 cells.	Ceramides	47-55	nerve growth factor	Rattus norvegicus	92-111
12562509-1	2003	We investigated how the mitochondrial phase of ceramide-mediated cell death is initiated in nerve growth factor (NGF)-differentiated PC12 cells.	Ceramides	47-55	nerve growth factor	Rattus norvegicus	113-116
12527801-5	2003	We demonstrate that bFGF activates a sphingomyelinase to synthesize ceramide, which, in turn, allows the dissociation of eNOS from caveolin 1 and its translocation to the cytosol in the active form, where it catalyzes the synthesis of NO.	Ceramides	68-76	fibroblast growth factor 2	Homo sapiens	20-24
12527801-5	2003	We demonstrate that bFGF activates a sphingomyelinase to synthesize ceramide, which, in turn, allows the dissociation of eNOS from caveolin 1 and its translocation to the cytosol in the active form, where it catalyzes the synthesis of NO.	Ceramides	68-76	caveolin-1	Cricetulus griseus	131-141
12527801-6	2003	In fact, drugs interfering with sphingomyelinase activity blocked bFGF activation of eNOS, and an increase in ceramide content was detected after bFGF treatment.	Ceramides	110-118	fibroblast growth factor 2	Homo sapiens	146-150
12527801-9	2003	In conclusion, our data show that, in CHO-K1 cells, bFGF regulates the activity of eNOS through a novel intracellular pathway, involving the induction of ceramide synthesis and that the NO released participates in bFGF proliferative activity.	Ceramides	154-162	fibroblast growth factor 2	Homo sapiens	52-56
12545214-6	2003	The second messenger, ceramide, also plays an important role in the regulation of PP2A activity, as well as a plenty of low molecular mass inhibitors of PP2A and other protein phosphatases.	Ceramides	22-30	protein phosphatase 2 phosphatase activator	Homo sapiens	82-86
12545214-6	2003	The second messenger, ceramide, also plays an important role in the regulation of PP2A activity, as well as a plenty of low molecular mass inhibitors of PP2A and other protein phosphatases.	Ceramides	22-30	protein phosphatase 2 phosphatase activator	Homo sapiens	153-157
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	caspase 8	Homo sapiens	12-21
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	caspase 8	Homo sapiens	56-65
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	Fas associated via death domain	Homo sapiens	111-146
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	Fas associated via death domain	Homo sapiens	148-152
12393559-10	2003	DEX-induced caspase-8 activation, like ceramide-induced caspase-8 activation, correlates with the formation of Fas-associated death domain protein (FADD)/caspase-8 complex.	Ceramides	39-47	caspase 8	Homo sapiens	56-65
12408751-6	2003	At the cell surface, receptor clustering in lipid rafts and the formation of endosomes can be facilitated by transient ceramide formation.	Ceramides	119-127	CD177 molecule	Homo sapiens	7-29
12504097-1	2003	We have examined the effects of tumor necrosis factor alpha (TNF alpha) and its second messenger, ceramide, on HMGCoA reductase, the rate-limiting enzyme in the mevalonate pathway.	Ceramides	98-106	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	111-127
12408751-8	2003	Ceramide may affect the permeability of the mitochondrial outer membrane and the release of cytochrome c.	Ceramides	0-8	cytochrome c, somatic	Homo sapiens	92-104
12524240-8	2003	CONCLUSIONS: These findings paint a picture in which the constitutive activation of rac1, via the generation of ceramide, results in mitochondrial oxidative stress and premature endothelial cell senescence.	Ceramides	112-120	Rac family small GTPase 1	Homo sapiens	84-88
14569872-13	2003	CONCLUSION: Ceramide synthesis and sphingomyelin breakdown, caspase activation and reactive oxygen metabolites production are required for the TNF-alpha-induced apoptosis and necrosis which may be regulated dependently on cell cycle.	Ceramides	12-20	tumor necrosis factor	Homo sapiens	143-152
14995068-0	2003	Differential involvement of ceramide in TNFalpha-mediated activation of NF-kappaB in primary human keratinocytes and HaCaT keratinocytes.	Ceramides	28-36	nuclear factor kappa B subunit 1	Homo sapiens	72-81
14995068-0	2003	Differential involvement of ceramide in TNFalpha-mediated activation of NF-kappaB in primary human keratinocytes and HaCaT keratinocytes.	Ceramides	28-36	tumor necrosis factor	Homo sapiens	40-48
14995068-1	2003	The involvement of ceramide signaling in tumor necrosis factor alpha (TNFalpha) mediated nuclear transcription factor kappa B (NF-kappaB) activation was studied.	Ceramides	19-27	tumor necrosis factor	Homo sapiens	41-68
14995068-1	2003	The involvement of ceramide signaling in tumor necrosis factor alpha (TNFalpha) mediated nuclear transcription factor kappa B (NF-kappaB) activation was studied.	Ceramides	19-27	tumor necrosis factor	Homo sapiens	70-78
14995068-1	2003	The involvement of ceramide signaling in tumor necrosis factor alpha (TNFalpha) mediated nuclear transcription factor kappa B (NF-kappaB) activation was studied.	Ceramides	19-27	nuclear factor kappa B subunit 1	Homo sapiens	89-125
14995068-1	2003	The involvement of ceramide signaling in tumor necrosis factor alpha (TNFalpha) mediated nuclear transcription factor kappa B (NF-kappaB) activation was studied.	Ceramides	19-27	nuclear factor kappa B subunit 1	Homo sapiens	127-136
14995068-4	2003	Previously, we could show that TNFalpha induces a ceramide increase in primary human keratinocytes and HaCaT keratinocytes and consequently apoptosis was initiated.	Ceramides	50-58	tumor necrosis factor	Homo sapiens	31-39
14995068-5	2003	It is well known that TNFalpha activates the transcription factor NF-kappaB, but there have been controversial reports on the role of ceramide in TNFalpha-mediated NF-kappaB activation.	Ceramides	134-142	tumor necrosis factor	Homo sapiens	146-154
14995068-5	2003	It is well known that TNFalpha activates the transcription factor NF-kappaB, but there have been controversial reports on the role of ceramide in TNFalpha-mediated NF-kappaB activation.	Ceramides	134-142	nuclear factor kappa B subunit 1	Homo sapiens	164-173
12488331-3	2003	We have previously shown that oocytes lacking acid sphingomyelinase (ASMase; an enzyme that generates the proapoptotic stress sensor ceramide), the aromatic hydrocarbon receptor (Ahr), Bax, or caspase-2 are resistant to apoptosis induced by other chemical toxicants.	Ceramides	133-141	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	46-67
12488331-3	2003	We have previously shown that oocytes lacking acid sphingomyelinase (ASMase; an enzyme that generates the proapoptotic stress sensor ceramide), the aromatic hydrocarbon receptor (Ahr), Bax, or caspase-2 are resistant to apoptosis induced by other chemical toxicants.	Ceramides	133-141	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	69-75
12492473-4	2003	On the basis of measurements of breakdown products, specific inhibitor effects, and previous findings, we suggest that a plasmalogen-selective phospholipase A2 is the ceramide target.	Ceramides	167-175	phospholipase A2 group IB	Homo sapiens	143-159
12492473-7	2003	Quinacrine (phospholipase A2 inhibitor) and 1-O-octadecyl-2-O-methyl-rac-glycerol-3-phosphocholine (CoA-independent transacylase inhibitor) prevented all of these ceramide-elicited effects.	Ceramides	163-171	phospholipase A2 group IB	Homo sapiens	12-28
12492473-12	2003	Furthermore, experiments with Ac-DEVD-CMK (caspase-3 specific inhibitor) have led us to conclude that caspase-3 is downstream of ceramide in activating the brain plasmalogen-selective phospholipase A2.	Ceramides	129-137	cytidine/uridine monophosphate kinase 1	Homo sapiens	38-41
12492473-12	2003	Furthermore, experiments with Ac-DEVD-CMK (caspase-3 specific inhibitor) have led us to conclude that caspase-3 is downstream of ceramide in activating the brain plasmalogen-selective phospholipase A2.	Ceramides	129-137	caspase 3	Homo sapiens	43-52
12492473-12	2003	Furthermore, experiments with Ac-DEVD-CMK (caspase-3 specific inhibitor) have led us to conclude that caspase-3 is downstream of ceramide in activating the brain plasmalogen-selective phospholipase A2.	Ceramides	129-137	caspase 3	Homo sapiens	102-111
12492473-12	2003	Furthermore, experiments with Ac-DEVD-CMK (caspase-3 specific inhibitor) have led us to conclude that caspase-3 is downstream of ceramide in activating the brain plasmalogen-selective phospholipase A2.	Ceramides	129-137	phospholipase A2 group IB	Homo sapiens	184-200
12532151-0	2003	Cell-permeable ceramides increase basal glucose incorporation into triacylglycerols but decrease the stimulation by insulin in 3T3-L1 adipocytes.	Ceramides	15-24	insulin	Homo sapiens	116-123
12532151-1	2003	OBJECTIVE: To investigate mechanisms for the regulation of glucose incorporation into triacylgycerols in adipocytes by ceramides, which mediate some actions of tumour necrosis factor-alpha (TNFalpha).	Ceramides	119-128	tumor necrosis factor	Homo sapiens	190-198
12532151-5	2003	These effects were accompanied by increased GLUT1 synthesis resulting from ceramide-induced activation phosphatidylinositol 3-kinase, ribosomal S6 kinase and mitogen-activated protein kinase.	Ceramides	75-83	solute carrier family 2 member 1	Homo sapiens	44-49
12532151-7	2003	However, C(2)-ceramide decreased the insulin-stimulated component of these signalling pathways and also glucose incorporation into triacylglycerol after 2 h. CONCLUSIONS: Cell-permeable ceramides can mimic some effects of TNFalpha in producing insulin resistance.	Ceramides	186-195	insulin	Homo sapiens	37-44
12532151-7	2003	However, C(2)-ceramide decreased the insulin-stimulated component of these signalling pathways and also glucose incorporation into triacylglycerol after 2 h. CONCLUSIONS: Cell-permeable ceramides can mimic some effects of TNFalpha in producing insulin resistance.	Ceramides	186-195	tumor necrosis factor	Homo sapiens	222-230
12532151-7	2003	However, C(2)-ceramide decreased the insulin-stimulated component of these signalling pathways and also glucose incorporation into triacylglycerol after 2 h. CONCLUSIONS: Cell-permeable ceramides can mimic some effects of TNFalpha in producing insulin resistance.	Ceramides	186-195	insulin	Homo sapiens	244-251
12391098-3	2003	Intratracheal instillation of TNF-alpha in adult rats led to a twofold increase in the amount of surfactant-associated ceramide and tended to decrease levels of sphingomyelin without significantly altering sphingosine or sphinganine content.	Ceramides	119-127	tumor necrosis factor	Rattus norvegicus	30-39
12391098-4	2003	TNF-alpha induction of alveolar ceramide was associated with nearly an 80% increase in acid sphingomyelinase activity recovered in cell-free alveolar lavage.	Ceramides	32-40	tumor necrosis factor	Rattus norvegicus	0-9
12717745-4	2003	Accumulation of TNF-alpha leads to activation of both acid and neutral sphingomyelinases, resulting in high accumulation of ceramides, a second messenger involved in cell apoptosis.	Ceramides	124-133	tumor necrosis factor	Cavia porcellus	16-25
12717745-7	2003	However, NF-kappa B rapidly disappeared after 2 h. It is possible that the initial activation of NF-kappa B was an adaptive response to protect the cells from damage since NF-kappa B is known to inhibit TNF-alpha/ceramide-induced cell apoptosis.	Ceramides	213-221	tumor necrosis factor	Cavia porcellus	203-212
14708343-4	2003	For instance, the early generation of ceramide promoted by TNF is mediated by a neutral sphingomyelinase the activity of which is regulated by the FAN adaptor protein, thereby controlling caspase activation and the cell death programme.	Ceramides	38-46	tumor necrosis factor	Homo sapiens	59-62
12524657-0	2003	Inhibitory effect of ceramide on insulin-induced protein kinase Czeta translocation in rat adipocytes.	Ceramides	21-29	protein kinase C, zeta	Rattus norvegicus	49-69
12524657-1	2003	Ceramide has been confirmed to be a signal mediator of apoptosis that is induced by tumor necrosis factor-alpha (TNF-alpha).	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	84-111
12524657-1	2003	Ceramide has been confirmed to be a signal mediator of apoptosis that is induced by tumor necrosis factor-alpha (TNF-alpha).	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	113-122
12524657-9	2003	These results suggest that ceramide may induce insulin resistance via the suppression of IRS-1-PI3K signaling, and subsequent activation of PKCzeta.	Ceramides	27-35	insulin receptor substrate 1	Rattus norvegicus	89-94
12524657-9	2003	These results suggest that ceramide may induce insulin resistance via the suppression of IRS-1-PI3K signaling, and subsequent activation of PKCzeta.	Ceramides	27-35	protein kinase C, zeta	Rattus norvegicus	140-147
12770554-0	2003	C-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis.	Ceramides	61-69	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
12527887-2	2003	In previous experiments we and others have shown that the tyrosine kinase Lck is required for adequate apoptosis induction in response to ionizing radiation, ceramide incubation and overexpression of the HIV-TAT protein.	Ceramides	158-166	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	74-77
12531545-5	2002	In particular, the present review focuses on the role of neutral sphingomyelinase (N-SMase) in the generation of the proapoptotic ceramide.	Ceramides	130-138	sphingomyelin phosphodiesterase 2	Homo sapiens	57-81
12531545-5	2002	In particular, the present review focuses on the role of neutral sphingomyelinase (N-SMase) in the generation of the proapoptotic ceramide.	Ceramides	130-138	sphingomyelin phosphodiesterase 2	Homo sapiens	83-90
12531547-2	2002	The central role of ASM-released ceramide in the response to those stimuli is confirmed by several genetic studies.	Ceramides	33-41	sphingomyelin phosphodiesterase 1	Homo sapiens	20-23
12531547-3	2002	ASM and ceramide might mediate their biological effects by the activation of several intracellular signaling molecules including cathepsin D, phospholipase A(2) or the kinase suppressor of Ras.	Ceramides	8-16	cathepsin D	Homo sapiens	129-140
12531547-3	2002	ASM and ceramide might mediate their biological effects by the activation of several intracellular signaling molecules including cathepsin D, phospholipase A(2) or the kinase suppressor of Ras.	Ceramides	8-16	phospholipase A2 group IB	Homo sapiens	142-160
12531551-1	2002	Glucosylceramide synthase (GCS) is an enzyme inherent to ceramide metabolism.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
12531551-6	2002	Herein we review the control points of ceramide metabolism with special regard to GCS and the cytotoxic response.	Ceramides	39-47	UDP-glucose ceramide glucosyltransferase	Homo sapiens	82-85
12531555-6	2002	One of these, the de novo ceramide pathway, has been implicated in the lipoapoptosis of beta-cells and myocardiocytes of congenitally obese rats in which leptin action is defective.	Ceramides	26-34	leptin	Rattus norvegicus	154-160
12388538-9	2002	Our results provide the first evidence that increased ceramide biosynthesis is required for 4-HPR-induced endothelial apoptosis and present a molecular mechanism for its antiangiogenic effects.	Ceramides	54-62	haptoglobin-related protein	Homo sapiens	94-97
12482609-1	2002	The neutral ceramidase is a key enzyme in the regulation of cellular ceramide levels.	Ceramides	69-77	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	4-22
12482609-8	2002	In summary, our data clearly show that the ubiquitin/proteasome complex is an important determinant of neutral ceramidase activity and thereby regulates the availability of ceramide.	Ceramides	173-181	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	103-121
12527381-1	2003	Stimulation of CD40 has been previously shown to result in a release of ceramide in small sphingolipid-enriched rafts in the cell membrane [Grassme et al., J. Immunol.	Ceramides	72-80	CD40 antigen	Mus musculus	15-19
12388538-2	2002	Herein we investigate the molecular mechanism of ceramide signaling in endothelial apoptosis induced by fenretinide (N-(4-hydroxyphenyl)retinamide (4-HPR)).	Ceramides	49-57	haptoglobin-related protein	Homo sapiens	150-153
12388538-3	2002	4-HPR, a synthetic derivative of retinoic acid that induces ceramide in tumor cell lines, has been shown to have antiangiogenic effects, but the molecular mechanism of these is largely unknown.	Ceramides	60-68	haptoglobin-related protein	Homo sapiens	2-5
12388538-5	2002	4-HPR (5 microm) increased ceramide levels in endothelial cells 5.3-fold, and the increase in ceramide was required to achieve the apoptotic effect of 4-HPR.	Ceramides	27-35	haptoglobin-related protein	Homo sapiens	2-5
12388538-5	2002	4-HPR (5 microm) increased ceramide levels in endothelial cells 5.3-fold, and the increase in ceramide was required to achieve the apoptotic effect of 4-HPR.	Ceramides	94-102	haptoglobin-related protein	Homo sapiens	153-156
12388538-6	2002	The 4-HPR-induced increase in ceramide was suppressed by inhibitors of ceramide synthesis, fumonisin B(1), myriocin, and l-cycloserine, and 4-HPR transiently activated serine palmitoyltransferase, demonstrating that 4-HPR induced de novo ceramide synthesis.	Ceramides	30-38	haptoglobin-related protein	Homo sapiens	6-9
12388538-6	2002	The 4-HPR-induced increase in ceramide was suppressed by inhibitors of ceramide synthesis, fumonisin B(1), myriocin, and l-cycloserine, and 4-HPR transiently activated serine palmitoyltransferase, demonstrating that 4-HPR induced de novo ceramide synthesis.	Ceramides	30-38	haptoglobin-related protein	Homo sapiens	142-145
12388538-6	2002	The 4-HPR-induced increase in ceramide was suppressed by inhibitors of ceramide synthesis, fumonisin B(1), myriocin, and l-cycloserine, and 4-HPR transiently activated serine palmitoyltransferase, demonstrating that 4-HPR induced de novo ceramide synthesis.	Ceramides	30-38	haptoglobin-related protein	Homo sapiens	142-145
12388538-6	2002	The 4-HPR-induced increase in ceramide was suppressed by inhibitors of ceramide synthesis, fumonisin B(1), myriocin, and l-cycloserine, and 4-HPR transiently activated serine palmitoyltransferase, demonstrating that 4-HPR induced de novo ceramide synthesis.	Ceramides	71-79	haptoglobin-related protein	Homo sapiens	6-9
12388538-6	2002	The 4-HPR-induced increase in ceramide was suppressed by inhibitors of ceramide synthesis, fumonisin B(1), myriocin, and l-cycloserine, and 4-HPR transiently activated serine palmitoyltransferase, demonstrating that 4-HPR induced de novo ceramide synthesis.	Ceramides	71-79	haptoglobin-related protein	Homo sapiens	6-9
12770554-0	2003	C-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis.	Ceramides	61-69	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	25-30
12376552-0	2002	Growth hormone-induced diacylglycerol and ceramide formation via Galpha i3 and Gbeta gamma in GH4 pituitary cells.	Ceramides	42-50	gonadotropin releasing hormone receptor	Rattus norvegicus	0-14
12770554-0	2003	C-Jun N-terminal kinases/c-Jun and p38 pathways cooperate in ceramide-induced neuronal apoptosis.	Ceramides	61-69	mitogen-activated protein kinase 14	Homo sapiens	35-38
12376552-4	2002	GH (EC(50) = 5 nm) stimulated diacylglycerol (DAG) and ceramide formation in parallel by over 10-fold within 15 min and persisting for >3 h. GH-induced DAG/ceramide formation was blocked by pertussis toxin (PTX) implicating G(i)/G(o) proteins and was potentiated 1.5-fold by activation of G(i)/G(o)-coupled dopamine-D2S receptors, which had no effect alone.	Ceramides	55-63	gonadotropin releasing hormone receptor	Rattus norvegicus	0-2
12770554-6	2003	Immunocytochemistry using the same antibodies shows that phospho-JNK are localized in the neurites of control neurons and translocate to the nucleus where phospho-c-Jun concurrently appears upon ceramide-induced apoptosis.	Ceramides	195-203	mitogen-activated protein kinase 8	Homo sapiens	65-68
12376552-4	2002	GH (EC(50) = 5 nm) stimulated diacylglycerol (DAG) and ceramide formation in parallel by over 10-fold within 15 min and persisting for >3 h. GH-induced DAG/ceramide formation was blocked by pertussis toxin (PTX) implicating G(i)/G(o) proteins and was potentiated 1.5-fold by activation of G(i)/G(o)-coupled dopamine-D2S receptors, which had no effect alone.	Ceramides	55-63	gonadotropin releasing hormone receptor	Rattus norvegicus	144-146
12376552-7	2002	In GH(4)ZR(7) cells, GH induced phosphorylation of JAK2 and STAT5, which was blocked by PTX and mimicked by ceramide analogue C2-ceramide or sphingomyelinase treatment to increase endogenous ceramide.	Ceramides	129-137	gonadotropin releasing hormone receptor	Rattus norvegicus	21-23
12376552-4	2002	GH (EC(50) = 5 nm) stimulated diacylglycerol (DAG) and ceramide formation in parallel by over 10-fold within 15 min and persisting for >3 h. GH-induced DAG/ceramide formation was blocked by pertussis toxin (PTX) implicating G(i)/G(o) proteins and was potentiated 1.5-fold by activation of G(i)/G(o)-coupled dopamine-D2S receptors, which had no effect alone.	Ceramides	159-167	gonadotropin releasing hormone receptor	Rattus norvegicus	0-2
12770554-6	2003	Immunocytochemistry using the same antibodies shows that phospho-JNK are localized in the neurites of control neurons and translocate to the nucleus where phospho-c-Jun concurrently appears upon ceramide-induced apoptosis.	Ceramides	195-203	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	163-168
12376552-4	2002	GH (EC(50) = 5 nm) stimulated diacylglycerol (DAG) and ceramide formation in parallel by over 10-fold within 15 min and persisting for >3 h. GH-induced DAG/ceramide formation was blocked by pertussis toxin (PTX) implicating G(i)/G(o) proteins and was potentiated 1.5-fold by activation of G(i)/G(o)-coupled dopamine-D2S receptors, which had no effect alone.	Ceramides	159-167	gonadotropin releasing hormone receptor	Rattus norvegicus	144-146
12376552-7	2002	In GH(4)ZR(7) cells, GH induced phosphorylation of JAK2 and STAT5, which was blocked by PTX and mimicked by ceramide analogue C2-ceramide or sphingomyelinase treatment to increase endogenous ceramide.	Ceramides	129-137	Janus kinase 2	Rattus norvegicus	51-55
12376552-8	2002	We conclude that in GH(4) pituitary cells, GH induces formation of DAG/ceramide via a novel Galpha(i)3/Gbetagamma-dependent pathway.	Ceramides	71-79	gonadotropin releasing hormone receptor	Rattus norvegicus	20-22
12376552-5	2002	Following PTX pretreatment, only PTX-resistant Galpha(i)3, not Galpha(o) or Galpha(i)2, rescued GH-induced DAG/ceramide signaling.	Ceramides	111-119	gonadotropin releasing hormone receptor	Rattus norvegicus	96-98
12770554-7	2003	To determine if ceramide-induced c-Jun activation is responsible for the induction of the apoptotic program, we performed transient transfections of a dominant negative form of c-Jun, truncated in its transactivation region.	Ceramides	16-24	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	33-38
12376552-6	2002	GH-induced DAG/ceramide formation was also blocked in cells expressing Gbetagamma blocker GRK-ct.	Ceramides	15-23	gonadotropin releasing hormone receptor	Rattus norvegicus	0-2
12376552-7	2002	In GH(4)ZR(7) cells, GH induced phosphorylation of JAK2 and STAT5, which was blocked by PTX and mimicked by ceramide analogue C2-ceramide or sphingomyelinase treatment to increase endogenous ceramide.	Ceramides	108-116	gonadotropin releasing hormone receptor	Rattus norvegicus	3-5
12376552-7	2002	In GH(4)ZR(7) cells, GH induced phosphorylation of JAK2 and STAT5, which was blocked by PTX and mimicked by ceramide analogue C2-ceramide or sphingomyelinase treatment to increase endogenous ceramide.	Ceramides	108-116	gonadotropin releasing hormone receptor	Rattus norvegicus	21-23
12376552-7	2002	In GH(4)ZR(7) cells, GH induced phosphorylation of JAK2 and STAT5, which was blocked by PTX and mimicked by ceramide analogue C2-ceramide or sphingomyelinase treatment to increase endogenous ceramide.	Ceramides	108-116	Janus kinase 2	Rattus norvegicus	51-55
12376552-8	2002	We conclude that in GH(4) pituitary cells, GH induces formation of DAG/ceramide via a novel Galpha(i)3/Gbetagamma-dependent pathway.	Ceramides	71-79	gonadotropin releasing hormone receptor	Rattus norvegicus	43-45
12376552-7	2002	In GH(4)ZR(7) cells, GH induced phosphorylation of JAK2 and STAT5, which was blocked by PTX and mimicked by ceramide analogue C2-ceramide or sphingomyelinase treatment to increase endogenous ceramide.	Ceramides	108-116	signal transducer and activator of transcription 5A	Rattus norvegicus	60-65
12770554-7	2003	To determine if ceramide-induced c-Jun activation is responsible for the induction of the apoptotic program, we performed transient transfections of a dominant negative form of c-Jun, truncated in its transactivation region.	Ceramides	16-24	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	177-182
12770554-8	2003	Our results show that DNc-Jun partially protects cortical neurons from ceramide-induced apoptosis.	Ceramides	71-79	solute carrier family 25 member 19	Homo sapiens	22-25
12415011-10	2002	Both forms of caspase-8-dependent cell death were also detected downstream of Fas in Jurkat T-cells, where Fas-dependent PS externalization and delayed ceramide production, which is similar to results shown here in A20 cells, have been reported.	Ceramides	152-160	caspase 8	Homo sapiens	14-23
12482824-7	2002	CONCLUSIONS: SMC proliferation elicited by moderate concentrations of oxLDL involves the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, which leads to extracellular regulated kinase 1/2 activation and DNA synthesis, and the EGFR/PI-3K/Akt pathway, which prevents the apoptotic effect of oxLDL.	Ceramides	103-111	epidermal growth factor receptor	Homo sapiens	233-237
12482824-7	2002	CONCLUSIONS: SMC proliferation elicited by moderate concentrations of oxLDL involves the sphingomyelin/ceramide/sphingosine-1-phosphate pathway, which leads to extracellular regulated kinase 1/2 activation and DNA synthesis, and the EGFR/PI-3K/Akt pathway, which prevents the apoptotic effect of oxLDL.	Ceramides	103-111	AKT serine/threonine kinase 1	Homo sapiens	244-247
12438359-3	2002	We have previously demonstrated that increased ceramide synthesis in host macrophages was involved in the dephosphorylation of extracellular signal-regulated kinase (ERK).	Ceramides	47-55	mitogen-activated protein kinase 1	Mus musculus	166-169
12438359-4	2002	In the present study, we further show that downregulation of ERK by ceramide was found to be associated with the inhibition of activated protein 1 (AP-1) and NF-kappaB transactivation.	Ceramides	68-76	mitogen-activated protein kinase 1	Mus musculus	61-64
12359305-7	2002	Taken together, our results strongly suggest that extracellular sphingomyelinase enhances the BMP-stimulated osteocalcin synthesis via ceramide in osteoblasts and that the effect of ceramide is exerted at a point upstream from p44/p42 MAP kinase.	Ceramides	135-143	bone gamma-carboxyglutamate protein 2	Mus musculus	109-120
12359305-7	2002	Taken together, our results strongly suggest that extracellular sphingomyelinase enhances the BMP-stimulated osteocalcin synthesis via ceramide in osteoblasts and that the effect of ceramide is exerted at a point upstream from p44/p42 MAP kinase.	Ceramides	182-190	mitogen-activated protein kinase 3	Mus musculus	227-230
12359305-7	2002	Taken together, our results strongly suggest that extracellular sphingomyelinase enhances the BMP-stimulated osteocalcin synthesis via ceramide in osteoblasts and that the effect of ceramide is exerted at a point upstream from p44/p42 MAP kinase.	Ceramides	182-190	cyclin-dependent kinase 20	Mus musculus	231-234
12499404-8	2002	Incorporated alpha-GalA was targeted to the lysosome, and hydrolyzed ceramide trihexoside accumulated in the Fabry fibroblasts after 5 days.	Ceramides	69-77	galactosidase alpha	Homo sapiens	13-23
12438359-4	2002	In the present study, we further show that downregulation of ERK by ceramide was found to be associated with the inhibition of activated protein 1 (AP-1) and NF-kappaB transactivation.	Ceramides	68-76	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	158-167
12438359-5	2002	Pharmacological inhibition of ceramide synthesis by Fumonisin B1 restored the induction of AP-1 and NF-kappaB DNA-binding activities in infected BALB/c macrophages.	Ceramides	30-38	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	100-109
12415011-13	2002	Thus, delayed elevation of ceramide is proposed to promote necrosis in those Fas-stimulated cells where caspase-8 activation was insufficient to trigger caspase-3-dependent apoptosis.	Ceramides	27-35	caspase 8	Homo sapiens	104-113
12415011-13	2002	Thus, delayed elevation of ceramide is proposed to promote necrosis in those Fas-stimulated cells where caspase-8 activation was insufficient to trigger caspase-3-dependent apoptosis.	Ceramides	27-35	caspase 3	Homo sapiens	153-162
12444159-8	2002	Piceatannol also inhibited NF-kappaB activated by H(2)O(2), PMA, LPS, okadaic acid, and ceramide.	Ceramides	88-96	nuclear factor kappa B subunit 1	Homo sapiens	27-36
12504027-0	2002	Activation of the Drosophila MLK by ceramide reveals TNF-alpha and ceramide as agonists of mammalian MLK3.	Ceramides	36-44	eiger	Drosophila melanogaster	53-62
12454261-1	2002	Carboxyl ester lipase (CEL), previously named cholesterol esterase or bile salt-stimulated (or dependent) lipase, is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, tri-, di-, and mono-acylglycerols, phospholipids, lysophospholipids, and ceramide.	Ceramides	252-260	carboxyl ester lipase	Homo sapiens	0-21
12454261-1	2002	Carboxyl ester lipase (CEL), previously named cholesterol esterase or bile salt-stimulated (or dependent) lipase, is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, tri-, di-, and mono-acylglycerols, phospholipids, lysophospholipids, and ceramide.	Ceramides	252-260	carboxyl ester lipase	Homo sapiens	23-26
12454261-1	2002	Carboxyl ester lipase (CEL), previously named cholesterol esterase or bile salt-stimulated (or dependent) lipase, is a lipolytic enzyme capable of hydrolyzing cholesteryl esters, tri-, di-, and mono-acylglycerols, phospholipids, lysophospholipids, and ceramide.	Ceramides	252-260	carboxyl ester lipase	Homo sapiens	46-66
12454261-7	2002	Importantly, CEL also participates in chylomicron assembly and secretion, in a mechanism mediated through its ceramide hydrolytic activity.	Ceramides	110-118	carboxyl ester lipase	Homo sapiens	13-16
12435806-4	2002	Here, we show that in U373 MG human astrocytoma cells, CB(1) receptor activation with the cannabinoid agonist delta(8)-tetrahydrocannabinol dimethyl heptyl (HU-210) was coupled to ERK activation and protection from ceramide-induced apoptosis.	Ceramides	215-223	mitogen-activated protein kinase 1	Homo sapiens	180-183
12504027-0	2002	Activation of the Drosophila MLK by ceramide reveals TNF-alpha and ceramide as agonists of mammalian MLK3.	Ceramides	67-75	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	101-105
12504027-3	2002	Here, we demonstrate ceramide as the activator of Drosophila MLK (dMLK) and identify ceramide and TNF-alpha as agonists of mammalian MLK3.	Ceramides	21-29	slipper	Drosophila melanogaster	66-70
12504027-3	2002	Here, we demonstrate ceramide as the activator of Drosophila MLK (dMLK) and identify ceramide and TNF-alpha as agonists of mammalian MLK3.	Ceramides	85-93	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	133-137
12504027-4	2002	dMLK and MLK3 are activated by a ceramide analog and bacterial sphingomyelinase in vivo, whereas a low nanomolar concentration of natural ceramide activates them in vitro.	Ceramides	33-41	slipper	Drosophila melanogaster	0-4
12504027-4	2002	dMLK and MLK3 are activated by a ceramide analog and bacterial sphingomyelinase in vivo, whereas a low nanomolar concentration of natural ceramide activates them in vitro.	Ceramides	33-41	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	9-13
12504027-5	2002	Specific inhibition of dMLK and MLK3 significantly attenuates activation of JNK by ceramide in vivo without affecting ceramide-induced p38 or ERK activation.	Ceramides	83-91	slipper	Drosophila melanogaster	23-27
12504027-5	2002	Specific inhibition of dMLK and MLK3 significantly attenuates activation of JNK by ceramide in vivo without affecting ceramide-induced p38 or ERK activation.	Ceramides	83-91	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	32-36
12504027-5	2002	Specific inhibition of dMLK and MLK3 significantly attenuates activation of JNK by ceramide in vivo without affecting ceramide-induced p38 or ERK activation.	Ceramides	83-91	mitogen-activated protein kinase 8	Homo sapiens	76-79
12504027-7	2002	Thus, the ceramide serves as a common agonist of dMLK and MLK3, and MLK3 contributes to JNK activation induced by TNF-alpha.	Ceramides	10-18	slipper	Drosophila melanogaster	49-53
12504027-7	2002	Thus, the ceramide serves as a common agonist of dMLK and MLK3, and MLK3 contributes to JNK activation induced by TNF-alpha.	Ceramides	10-18	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	58-62
12359735-8	2002	In summary, our data show that NO is able to induce degradation of neutral ceramidase, thereby promoting accumulation of ceramide in the cell.	Ceramides	121-129	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	67-85
12359735-0	2002	Nitric oxide induces degradation of the neutral ceramidase in rat renal mesangial cells and is counterregulated by protein kinase C. Ceramide levels are strongly increased by stimulation of renal mesangial cells with nitric oxide (NO).	Ceramides	133-141	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	40-58
12419308-0	2002	Modulation of CYP3A4 expression by ceramide in human colon carcinoma HT-29 cells.	Ceramides	35-43	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	14-20
12437970-6	2002	Immunoblot analysis of protein extracts from C(2)-ceramide-treated cortical neuronal cultures revealed upregulation of active caspase-9 and caspase-3 protein levels, whereas presence of active caspase-8 immunoreactivity was undetectable in this system.	Ceramides	50-58	caspase 9	Homo sapiens	126-135
12437970-6	2002	Immunoblot analysis of protein extracts from C(2)-ceramide-treated cortical neuronal cultures revealed upregulation of active caspase-9 and caspase-3 protein levels, whereas presence of active caspase-8 immunoreactivity was undetectable in this system.	Ceramides	50-58	caspase 3	Homo sapiens	140-149
12437970-6	2002	Immunoblot analysis of protein extracts from C(2)-ceramide-treated cortical neuronal cultures revealed upregulation of active caspase-9 and caspase-3 protein levels, whereas presence of active caspase-8 immunoreactivity was undetectable in this system.	Ceramides	50-58	caspase 8	Homo sapiens	193-202
12437970-8	2002	Moreover, ceramide-induced cell death was significantly decreased in caspase-9 dominant-negative SH-SY5Y cells, while both caspase-8 dominant-negative cultures and mock-transfected cells showed equally high levels of cell death following C(2)-ceramide treatment.	Ceramides	10-18	caspase 9	Homo sapiens	69-78
12437970-9	2002	Taken together, these data suggest that neuronal death induced by ceramide may be linked to the caspase-9/caspase-3 regulated intrinsic pathway of cellular apoptosis.	Ceramides	66-74	caspase 9	Homo sapiens	96-105
12437970-9	2002	Taken together, these data suggest that neuronal death induced by ceramide may be linked to the caspase-9/caspase-3 regulated intrinsic pathway of cellular apoptosis.	Ceramides	66-74	caspase 3	Homo sapiens	106-115
12437970-0	2002	Ceramide induces neuronal apoptosis through the caspase-9/caspase-3 pathway.	Ceramides	0-8	caspase 9	Homo sapiens	48-57
12437970-0	2002	Ceramide induces neuronal apoptosis through the caspase-9/caspase-3 pathway.	Ceramides	0-8	caspase 3	Homo sapiens	58-67
12437970-2	2002	C(2)-ceramide-induced neuronal loss was accompanied by upregulation of caspase-3 activity, measured by cleavage of its fluorogenic substrate Ac-DEVD-AMC.	Ceramides	5-13	caspase 3	Homo sapiens	71-80
12437970-5	2002	Co-administration of the selective caspase-3 inhibitor z-DEVD-fmk or caspase-9 inhibitor z-LEHD-fmk significantly reduced C(2)-ceramide-induced cell death, while co-application of the caspase-8, inhibitor z-IETD-fmk, was without effect.	Ceramides	127-135	caspase 3	Homo sapiens	35-44
12437970-5	2002	Co-administration of the selective caspase-3 inhibitor z-DEVD-fmk or caspase-9 inhibitor z-LEHD-fmk significantly reduced C(2)-ceramide-induced cell death, while co-application of the caspase-8, inhibitor z-IETD-fmk, was without effect.	Ceramides	127-135	caspase 9	Homo sapiens	69-78
12437970-5	2002	Co-administration of the selective caspase-3 inhibitor z-DEVD-fmk or caspase-9 inhibitor z-LEHD-fmk significantly reduced C(2)-ceramide-induced cell death, while co-application of the caspase-8, inhibitor z-IETD-fmk, was without effect.	Ceramides	127-135	caspase 8	Homo sapiens	184-193
12419308-11	2002	The addition of iNOS antisense oligonucleotide prevented ceramide-mediated induction of iNOS expression and restored CYP3A4 expression.	Ceramides	57-65	nitric oxide synthase 2	Homo sapiens	88-92
12419308-11	2002	The addition of iNOS antisense oligonucleotide prevented ceramide-mediated induction of iNOS expression and restored CYP3A4 expression.	Ceramides	57-65	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	117-123
12419308-12	2002	Wortmannin which is known to inhibit phosphatidylinositol 3-kinase (PI3-K) blocked CYP3A4 suppression by ceramide.	Ceramides	105-113	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	37-66
12419308-12	2002	Wortmannin which is known to inhibit phosphatidylinositol 3-kinase (PI3-K) blocked CYP3A4 suppression by ceramide.	Ceramides	105-113	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	83-89
12419308-13	2002	Taken together, our results demonstrate that ceramide-mediated suppression of CYP3A4 is due to production of NO, which might result from activation of PI3-K.	Ceramides	45-53	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	78-84
12419308-4	2002	In the present study, our studies investigated the effects of ceramide on CYP3A4 expression in human colon carcinoma HT-29 cells.	Ceramides	62-70	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	74-80
12419308-5	2002	Treatment with the cell-permeable ceramide analog C(6)-ceramide to the cells significantly decreased the expression of CYP3A4.	Ceramides	34-42	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	119-125
12419308-7	2002	We found that bacterial sphingomyelinase (SMase) and tumor necrosis factor-alpha (TNF), which are known to increase intracellular ceramide levels, also markedly suppressed the synthesis of CYP3A4.	Ceramides	130-138	tumor necrosis factor	Homo sapiens	53-80
12419308-7	2002	We found that bacterial sphingomyelinase (SMase) and tumor necrosis factor-alpha (TNF), which are known to increase intracellular ceramide levels, also markedly suppressed the synthesis of CYP3A4.	Ceramides	130-138	tumor necrosis factor	Homo sapiens	82-85
12419308-7	2002	We found that bacterial sphingomyelinase (SMase) and tumor necrosis factor-alpha (TNF), which are known to increase intracellular ceramide levels, also markedly suppressed the synthesis of CYP3A4.	Ceramides	130-138	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	189-195
12419308-8	2002	To elucidate whether nitric oxide (NO) participates in suppression of CYP3A4 expression by ceramide, the effects of NO modulators were determined.	Ceramides	91-99	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	70-76
12419308-9	2002	Treatment with N(G)-monomethyl-L-arginine, a competitive inhibitor of inducible nitric oxide synthase (iNOS), was able to protect ceramide-dependent CYP3A4 suppression.	Ceramides	130-138	nitric oxide synthase 2	Homo sapiens	70-101
12419308-9	2002	Treatment with N(G)-monomethyl-L-arginine, a competitive inhibitor of inducible nitric oxide synthase (iNOS), was able to protect ceramide-dependent CYP3A4 suppression.	Ceramides	130-138	nitric oxide synthase 2	Homo sapiens	103-107
12419308-9	2002	Treatment with N(G)-monomethyl-L-arginine, a competitive inhibitor of inducible nitric oxide synthase (iNOS), was able to protect ceramide-dependent CYP3A4 suppression.	Ceramides	130-138	cytochrome P450 family 3 subfamily A member 4	Homo sapiens	149-155
12376561-8	2002	On plastic, neither IGFBP-3 nor -5 alone affected cell viability; although ceramide-induced apoptosis was enhanced by IGFBP-3 but reduced by IGFBP-5.	Ceramides	75-83	insulin like growth factor binding protein 5	Homo sapiens	141-148
12419308-11	2002	The addition of iNOS antisense oligonucleotide prevented ceramide-mediated induction of iNOS expression and restored CYP3A4 expression.	Ceramides	57-65	nitric oxide synthase 2	Homo sapiens	16-20
12213802-2	2002	H2O2 produced early activation of Akt/PKB and also DNA damage that was followed by stabilization of p53 levels, formation of reactive oxygen species (ROS), and generation of ceramide through activation of a glutathione-sensitive neutral sphingomyelinase.	Ceramides	174-182	AKT serine/threonine kinase 1	Homo sapiens	34-41
12213802-0	2002	Ceramide and reactive oxygen species generated by H2O2 induce caspase-3-independent degradation of Akt/protein kinase B.	Ceramides	0-8	caspase 3	Homo sapiens	62-71
12213802-5	2002	Proteolysis of Akt was prevented by exogenous addition of glutathione, indicating a role of ROS and ceramide in Akt degradation.	Ceramides	100-108	AKT serine/threonine kinase 1	Homo sapiens	15-18
12213802-0	2002	Ceramide and reactive oxygen species generated by H2O2 induce caspase-3-independent degradation of Akt/protein kinase B.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	99-102
12213802-10	2002	Our results suggest that strong oxidants generate intracellular ROS and ceramide which in term lead to down-regulation of Akt by dephosphorylation and caspase-3-independent proteolysis.	Ceramides	72-80	AKT serine/threonine kinase 1	Homo sapiens	122-125
12213802-0	2002	Ceramide and reactive oxygen species generated by H2O2 induce caspase-3-independent degradation of Akt/protein kinase B.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	103-119
12213802-10	2002	Our results suggest that strong oxidants generate intracellular ROS and ceramide which in term lead to down-regulation of Akt by dephosphorylation and caspase-3-independent proteolysis.	Ceramides	72-80	caspase 3	Homo sapiens	151-160
12408376-8	2002	Ceramide changes are associated with cell cycle arrest and we observed that all the Cox inhibitors examined increased significantly the number of cells in G0/G1 and reduced the S phase fraction.	Ceramides	0-8	cytochrome c oxidase subunit 4I1	Mus musculus	84-87
12413956-2	2002	Sequencing of the differentially expressed bands identified the serine/threonine protein kinase LIM kinase-1 (LIMK-1), which is involved in the regulation of cytoskeletal organization, as a ceramide-induced gene.	Ceramides	190-198	LIM domain kinase 1	Rattus norvegicus	96-108
12413956-2	2002	Sequencing of the differentially expressed bands identified the serine/threonine protein kinase LIM kinase-1 (LIMK-1), which is involved in the regulation of cytoskeletal organization, as a ceramide-induced gene.	Ceramides	190-198	LIM domain kinase 1	Rattus norvegicus	110-116
12413956-3	2002	The ceramide-triggered upregulation of LIMK-1 was verified by semiquantitative reverse transcriptase-PCR.	Ceramides	4-12	LIM domain kinase 1	Rattus norvegicus	39-45
12413956-4	2002	A detailed time course reveals a first detectable increase in RNA level after 2h of ceramide stimulation which reaches maximal levels after 6h of stimulation and remains elevated up to 24 h. This ceramide-induced gene transcription of LIMK-1 is accompanied by enhanced LIMK-1 protein levels with maximal protein expression seen after 6h of stimulation.	Ceramides	84-92	LIM domain kinase 1	Rattus norvegicus	235-241
12413956-4	2002	A detailed time course reveals a first detectable increase in RNA level after 2h of ceramide stimulation which reaches maximal levels after 6h of stimulation and remains elevated up to 24 h. This ceramide-induced gene transcription of LIMK-1 is accompanied by enhanced LIMK-1 protein levels with maximal protein expression seen after 6h of stimulation.	Ceramides	84-92	LIM domain kinase 1	Rattus norvegicus	269-275
12413956-4	2002	A detailed time course reveals a first detectable increase in RNA level after 2h of ceramide stimulation which reaches maximal levels after 6h of stimulation and remains elevated up to 24 h. This ceramide-induced gene transcription of LIMK-1 is accompanied by enhanced LIMK-1 protein levels with maximal protein expression seen after 6h of stimulation.	Ceramides	196-204	LIM domain kinase 1	Rattus norvegicus	235-241
12413956-4	2002	A detailed time course reveals a first detectable increase in RNA level after 2h of ceramide stimulation which reaches maximal levels after 6h of stimulation and remains elevated up to 24 h. This ceramide-induced gene transcription of LIMK-1 is accompanied by enhanced LIMK-1 protein levels with maximal protein expression seen after 6h of stimulation.	Ceramides	196-204	LIM domain kinase 1	Rattus norvegicus	269-275
12413956-6	2002	Mechanistically, the ceramide-induced LIMK-1 expression is blocked by the Rho kinase inhibitor Y27632, but not by a farnesyl transferase inhibitor, suggesting the involvement of the small G protein Rho, but not Ras and Rac, in the expressional upregulation.	Ceramides	21-29	LIM domain kinase 1	Rattus norvegicus	38-44
12413956-7	2002	Similar to exogenously added ceramide, also interleukin-1beta which is an established activator of the neutral sphingomyelinase that leads to endogenous ceramide formation upregulates LIMK-1 protein expression and activity.	Ceramides	29-37	interleukin 1 beta	Rattus norvegicus	44-61
12413956-7	2002	Similar to exogenously added ceramide, also interleukin-1beta which is an established activator of the neutral sphingomyelinase that leads to endogenous ceramide formation upregulates LIMK-1 protein expression and activity.	Ceramides	29-37	LIM domain kinase 1	Rattus norvegicus	184-190
12413956-7	2002	Similar to exogenously added ceramide, also interleukin-1beta which is an established activator of the neutral sphingomyelinase that leads to endogenous ceramide formation upregulates LIMK-1 protein expression and activity.	Ceramides	153-161	interleukin 1 beta	Rattus norvegicus	44-61
12413956-7	2002	Similar to exogenously added ceramide, also interleukin-1beta which is an established activator of the neutral sphingomyelinase that leads to endogenous ceramide formation upregulates LIMK-1 protein expression and activity.	Ceramides	153-161	LIM domain kinase 1	Rattus norvegicus	184-190
12413956-8	2002	In summary, these data demonstrate for the first time that LIMK-1 is a ceramide-induced gene, thus suggesting that LIMK-1 may act as a link between stress-induced ceramide formation and reorganization of the actin cytoskeleton.	Ceramides	71-79	LIM domain kinase 1	Rattus norvegicus	59-65
12413956-8	2002	In summary, these data demonstrate for the first time that LIMK-1 is a ceramide-induced gene, thus suggesting that LIMK-1 may act as a link between stress-induced ceramide formation and reorganization of the actin cytoskeleton.	Ceramides	71-79	LIM domain kinase 1	Rattus norvegicus	115-121
12413956-8	2002	In summary, these data demonstrate for the first time that LIMK-1 is a ceramide-induced gene, thus suggesting that LIMK-1 may act as a link between stress-induced ceramide formation and reorganization of the actin cytoskeleton.	Ceramides	163-171	LIM domain kinase 1	Rattus norvegicus	59-65
12413956-8	2002	In summary, these data demonstrate for the first time that LIMK-1 is a ceramide-induced gene, thus suggesting that LIMK-1 may act as a link between stress-induced ceramide formation and reorganization of the actin cytoskeleton.	Ceramides	163-171	LIM domain kinase 1	Rattus norvegicus	115-121
12384455-0	2002	Role of ceramide in TNF-alpha-induced impairment of endothelium-dependent vasorelaxation in coronary arteries.	Ceramides	8-16	tumor necrosis factor	Bos taurus	20-29
12384455-1	2002	The present study tested the hypothesis that ceramide, a sphingomylinase metabolite, serves as an second messenger for tumor necrosis factor-alpha (TNF-alpha) to stimulate superoxide production, thereby decreasing endothelium-dependent vasorelaxation in coronary arteries.	Ceramides	45-53	tumor necrosis factor	Bos taurus	119-146
12384455-1	2002	The present study tested the hypothesis that ceramide, a sphingomylinase metabolite, serves as an second messenger for tumor necrosis factor-alpha (TNF-alpha) to stimulate superoxide production, thereby decreasing endothelium-dependent vasorelaxation in coronary arteries.	Ceramides	45-53	tumor necrosis factor	Bos taurus	148-157
12384455-6	2002	In addition, TNF-alpha activated acidic sphingomyelinase and increased ceramide levels in coronary endothelial cells.	Ceramides	71-79	tumor necrosis factor	Bos taurus	13-22
12220618-0	2002	C(2)-ceramide-induced circular smooth muscle cell contraction involves PKC-epsilon and p44/p42 MAPK activation in cat oesophagus.	Ceramides	5-13	protein kinase C epsilon	Homo sapiens	71-82
12220618-0	2002	C(2)-ceramide-induced circular smooth muscle cell contraction involves PKC-epsilon and p44/p42 MAPK activation in cat oesophagus.	Ceramides	5-13	interferon induced protein 44	Homo sapiens	87-90
12220618-0	2002	C(2)-ceramide-induced circular smooth muscle cell contraction involves PKC-epsilon and p44/p42 MAPK activation in cat oesophagus.	Ceramides	5-13	cyclin dependent kinase 20	Homo sapiens	91-94
12220618-0	2002	C(2)-ceramide-induced circular smooth muscle cell contraction involves PKC-epsilon and p44/p42 MAPK activation in cat oesophagus.	Ceramides	5-13	mitogen-activated protein kinase 1	Homo sapiens	95-99
12408376-9	2002	Likewise, addition of a cell-permeable form of ceramide (C6-ceramide) could mimic the effect of Cox inhibitors on both cell cycle and cell growth inhibition.	Ceramides	47-55	cytochrome c oxidase subunit 4I1	Mus musculus	96-99
12200041-4	2002	This function of Lag 1 p results from its participation in ceramide synthesis.	Ceramides	59-67	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	17-24
12404124-1	2002	Activation of acid and neutral sphingomyelinases, and the ensuing generation of ceramide, contributes to the biological effects of tumour necrosis factor-alpha (TNF-alpha), one of which is apoptosis.	Ceramides	80-88	tumor necrosis factor	Homo sapiens	161-170
12399431-4	2002	More specifically, we investigated soluble FasL (sFasL)-activated production of ceramide, a second messenger of the sphingomyelin pathway, and activation of p38(MAPK), a member of the MAPK family.	Ceramides	80-88	Fas ligand	Bos taurus	43-47
12200041-0	2002	LAG1 puts the focus on ceramide signaling.	Ceramides	23-31	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	0-4
12200041-5	2002	Thus, Lag 1 p and its homologues are likely to play a role in ceramide signaling, which affects growth, proliferation, stress resistance, and apoptosis.	Ceramides	62-70	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	6-13
12381813-5	2002	In the presence of glutathione and NGF, exogenous ceramide still enhanced the number of evoked APs, indicating that the sensitizing action of ceramide was downstream of NGF.	Ceramides	50-58	nerve growth factor	Rattus norvegicus	169-172
12390956-10	2002	The partial reversal of this reduction by BH(4) and the diminution of ROS generation by L-NAME suggest that ceramide promotes NADPH oxidase activity of eNOS, leading to ROS formation at the expense of NO synthesis.	Ceramides	108-116	nitric oxide synthase 3	Homo sapiens	152-156
12390956-11	2002	The ceramide-induced upregulation of eNOS gene transcription can be considered an ineffective compensatory mechanism.	Ceramides	4-12	nitric oxide synthase 3	Homo sapiens	37-41
12271467-4	2002	SOD1 overexpression significantly protected against the deleterious effect of reactive oxygen species, ceramide, or N-methyl-D-aspartate (NMDA).	Ceramides	103-111	superoxide dismutase 1, soluble	Mus musculus	0-4
12154098-9	2002	Further, whereas TNF treatment also caused a 75% increase of de novo synthesized ceramide after 20 h of incubation, GW4869, at either 10 or 20 microm, had no effect on this pathway of ceramide generation.	Ceramides	81-89	tumor necrosis factor	Homo sapiens	17-20
12387875-7	2002	Unexpectedly, expression of Bcl-xL prevented tumor necrosis factor-alpha-induced SM hydrolysis and ceramide accumulation but not the decrease in intracellular GSH.	Ceramides	99-107	BCL2 like 1	Homo sapiens	28-34
12387875-7	2002	Unexpectedly, expression of Bcl-xL prevented tumor necrosis factor-alpha-induced SM hydrolysis and ceramide accumulation but not the decrease in intracellular GSH.	Ceramides	99-107	tumor necrosis factor	Homo sapiens	45-72
12387875-8	2002	Furthermore, Bcl-xL inhibited diamide-induced SM hydrolysis and ceramide accumulation but not the decrease in intracellular GSH.	Ceramides	64-72	BCL2 like 1	Homo sapiens	13-19
12387875-9	2002	These results suggest that the site of action of Bcl-xL is downstream of GSH depletion and upstream of ceramide accumulation, and that GSH probably does not exert direct physiologic effects on N-SMase.	Ceramides	103-111	BCL2 like 1	Homo sapiens	49-55
12381813-0	2002	Ceramide, a putative second messenger for nerve growth factor, modulates the TTX-resistant Na(+) current and delayed rectifier K(+) current in rat sensory neurons.	Ceramides	0-8	nerve growth factor	Rattus norvegicus	42-61
12381813-5	2002	In the presence of glutathione and NGF, exogenous ceramide still enhanced the number of evoked APs, indicating that the sensitizing action of ceramide was downstream of NGF.	Ceramides	142-150	nerve growth factor	Rattus norvegicus	35-38
12381813-5	2002	In the presence of glutathione and NGF, exogenous ceramide still enhanced the number of evoked APs, indicating that the sensitizing action of ceramide was downstream of NGF.	Ceramides	142-150	nerve growth factor	Rattus norvegicus	169-172
12381813-13	2002	This NGF-induced sensitization is probably mediated by activation of the sphingomyelin signalling pathway to liberate ceramide(s), wherein ceramide appears to be the second messenger involved in modulating neuronal excitability.	Ceramides	118-126	nerve growth factor	Rattus norvegicus	5-8
12381813-13	2002	This NGF-induced sensitization is probably mediated by activation of the sphingomyelin signalling pathway to liberate ceramide(s), wherein ceramide appears to be the second messenger involved in modulating neuronal excitability.	Ceramides	139-147	nerve growth factor	Rattus norvegicus	5-8
12243760-4	2002	sPLA(2)-induced inhibition of EGF receptor was associated with arachidonic acid release, which was followed by an increase in intracellular ceramide formation.	Ceramides	140-148	phospholipase A2 group X	Homo sapiens	0-7
12385892-5	2002	We show that while both DNR and Ara-C similarly induced early ceramide generation (within 5-20 min) and interphasic apoptosis in all cell models, caspase-8 cleavage was only observed farther downstream (4.5 h) and only in DNR-treated cells.	Ceramides	62-70	ATP binding cassette subfamily C member 6	Homo sapiens	32-35
12385893-5	2002	When various concentrations of adriamycin (ADR) was added to induce apoptosis, the amounts of ceramide detected by NHCER-2 time- and dose-dependently increased in apoptosis-sensitive HL-60 cells as well as by DGK assay, but not in apoptosis-resistant HL-60/ADR cells.	Ceramides	94-102	diacylglycerol kinase beta	Homo sapiens	209-212
12385893-6	2002	After cell fractionation, ceramide levels judged not only by diacylglycerol kinase (DGK) assay but also by NHCER-2 were shown to increase in the microsomal and the nuclear fraction in apoptosis-sensitive cells, but not in apoptosis-resistant cells.	Ceramides	26-34	diacylglycerol kinase beta	Homo sapiens	61-82
12385893-6	2002	After cell fractionation, ceramide levels judged not only by diacylglycerol kinase (DGK) assay but also by NHCER-2 were shown to increase in the microsomal and the nuclear fraction in apoptosis-sensitive cells, but not in apoptosis-resistant cells.	Ceramides	26-34	diacylglycerol kinase beta	Homo sapiens	84-87
12385893-7	2002	Moreover, absolute amounts of ceramide determined by NHCER-2 were well correlated with those by DGK assay.	Ceramides	30-38	diacylglycerol kinase beta	Homo sapiens	96-99
12395108-0	2002	Regulation of nociceptin/orphanin FQ gene expression in astrocytes by ceramide.	Ceramides	70-78	prepronociceptin	Homo sapiens	14-24
12395108-0	2002	Regulation of nociceptin/orphanin FQ gene expression in astrocytes by ceramide.	Ceramides	70-78	prepronociceptin	Homo sapiens	25-36
12395108-2	2002	Since these stimuli dramatically increase nociceptin/orphanin FQ (N/OFQ) gene expression in astrocytes we evaluated the regulation of N/OFQ by ceramide and the signaling mechanisms involved.	Ceramides	143-151	prepronociceptin	Homo sapiens	134-139
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	14-22	prepronociceptin	Homo sapiens	31-36
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	14-22	mitogen-activated protein kinase 14	Homo sapiens	112-115
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	14-22	cAMP responsive element binding protein 1	Homo sapiens	204-208
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	14-22	nuclear factor kappa B subunit 1	Homo sapiens	213-221
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	83-91	prepronociceptin	Homo sapiens	31-36
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	83-91	mitogen-activated protein kinase 14	Homo sapiens	112-115
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	83-91	cAMP responsive element binding protein 1	Homo sapiens	204-208
12395108-3	2002	We found that ceramide induced N/OFQ mRNA levels 22-fold after 24 h. In astrocytes ceramide stimulated the JNK, p38 and ERK MAP kinase pathways and also led to the activation of the transcription factors CREB and NFkappaB.	Ceramides	83-91	nuclear factor kappa B subunit 1	Homo sapiens	213-221
12395108-6	2002	The NFkappaB pathway also appears to be crucial for ceramide-induced N/OFQ gene expression.	Ceramides	52-60	nuclear factor kappa B subunit 1	Homo sapiens	4-12
12395108-6	2002	The NFkappaB pathway also appears to be crucial for ceramide-induced N/OFQ gene expression.	Ceramides	52-60	prepronociceptin	Homo sapiens	69-74
12207171-0	2002	Mitochondrial cytochrome c release precedes transmembrane depolarisation and caspase-3 activation during ceramide-induced apoptosis of Jurkat T cells.	Ceramides	105-113	cytochrome c, somatic	Homo sapiens	14-26
12207171-0	2002	Mitochondrial cytochrome c release precedes transmembrane depolarisation and caspase-3 activation during ceramide-induced apoptosis of Jurkat T cells.	Ceramides	105-113	caspase 3	Homo sapiens	77-86
12207171-4	2002	Subsequent activation of caspase-3 provides the link between these ceramide-induced mitochondrial changes and execution caspases that ultimately result in the physical destruction of the cell.	Ceramides	67-75	caspase 3	Homo sapiens	25-34
12207171-5	2002	Collectively these results demonstrate that ceramide signalling results in caspase-mediated apoptosis via mitochondrial cytochrome c release and are further supportive of the role of ceramide in the amplification of apoptosis.	Ceramides	44-52	cytochrome c, somatic	Homo sapiens	120-132
12207177-4	2002	Bcl-2 located at the ER was shown to interfere with apoptosis induction by Bax, ceramides, ionising radiation, serum withdrawal and c-myc expression.	Ceramides	80-89	BCL2 apoptosis regulator	Homo sapiens	0-5
12243760-4	2002	sPLA(2)-induced inhibition of EGF receptor was associated with arachidonic acid release, which was followed by an increase in intracellular ceramide formation.	Ceramides	140-148	epidermal growth factor	Homo sapiens	30-33
12243760-6	2002	The data presented indicate for the first time that sPLA(2) downregulates the EGF receptor-mediated intracellular signal transduction that may be mediated by arachidonic acid and/or ceramide.	Ceramides	182-190	phospholipase A2 group X	Homo sapiens	52-59
12243760-6	2002	The data presented indicate for the first time that sPLA(2) downregulates the EGF receptor-mediated intracellular signal transduction that may be mediated by arachidonic acid and/or ceramide.	Ceramides	182-190	epidermal growth factor	Homo sapiens	78-81
12204617-1	2002	Ceramidated GLA-60 derivatives 11 and 11" were synthesized from 1 via glycosidation of ceramide derivative 12 as a glycosyl acceptor with GLA-60 derivative 5 as a glycosyl donor, and successive conversion.	Ceramides	87-95	galactosidase alpha	Homo sapiens	12-15
12145310-14	2002	We hypothesize that in eukaryotic cells, Arv1p functions in the sphingolipid metabolic pathway perhaps as a transporter of ceramides between the endoplasmic reticulum and Golgi.	Ceramides	123-132	ARV1 homolog, fatty acid homeostasis modulator	Homo sapiens	41-46
12105227-1	2002	The longevity assurance gene (LAG1) and its homolog (LAC1) are required for acyl-CoA-dependent synthesis of ceramides containing very long acyl chain (e.g. C26) fatty acids in yeast, and a homolog of LAG1, ASC1, confers resistance in plants to fumonisin B(1), an inhibitor of ceramide synthesis.	Ceramides	108-116	ceramide synthase 1	Homo sapiens	30-34
12105227-1	2002	The longevity assurance gene (LAG1) and its homolog (LAC1) are required for acyl-CoA-dependent synthesis of ceramides containing very long acyl chain (e.g. C26) fatty acids in yeast, and a homolog of LAG1, ASC1, confers resistance in plants to fumonisin B(1), an inhibitor of ceramide synthesis.	Ceramides	108-116	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	200-204
12105227-1	2002	The longevity assurance gene (LAG1) and its homolog (LAC1) are required for acyl-CoA-dependent synthesis of ceramides containing very long acyl chain (e.g. C26) fatty acids in yeast, and a homolog of LAG1, ASC1, confers resistance in plants to fumonisin B(1), an inhibitor of ceramide synthesis.	Ceramides	108-116	guanine nucleotide-binding protein subunit beta	Saccharomyces cerevisiae S288C	206-210
12105227-2	2002	To understand further the mechanism of regulation of ceramide synthesis, we now characterize a mammalian homolog of LAG1, upstream of growth and differentiation factor-1 (uog1).	Ceramides	53-61	ceramide synthase 1	Homo sapiens	116-120
12105227-2	2002	To understand further the mechanism of regulation of ceramide synthesis, we now characterize a mammalian homolog of LAG1, upstream of growth and differentiation factor-1 (uog1).	Ceramides	53-61	ceramide synthase 1	Homo sapiens	171-175
12105227-4	2002	Transient transfection of human embryonic kidney 293T cells with uog1 followed by metabolic labeling with [4,5-(3)H]sphinganine or L-3-[(3)H]serine demonstrated that uog1 conferred fumonisin B(1) resistance with respect to the ability of the cells to continue to produce ceramide.	Ceramides	271-279	ceramide synthase 1	Homo sapiens	166-170
12105227-6	2002	Electrospray tandem mass spectrometry confirmed the elevation in sphingolipids and revealed that the ceramides and neutral glycosphingolipids of uog1-transfected cells contain primarily stearic acid (C18), that this enrichment was further increased by FB(1), and that the amount of stearic acid in sphingomyelin was also increased.	Ceramides	101-110	ceramide synthase 1	Homo sapiens	145-149
12105227-9	2002	We propose a role for UOG1 in regulating C18-ceramide (N-stearoyl-sphinganine) synthesis, and we note that not only is this the first case of ceramide formation in mammalian cells with such a high degree of fatty acid specificity, but also that the N-stearoyl-sphinganine produced by UOG1 most significantly impacts neutral glycosphingolipid synthesis.	Ceramides	45-53	ceramide synthase 1	Homo sapiens	22-26
12235122-5	2002	Treatment of SPP-1 transfectants with S1P markedly increased ceramide levels, predominantly in the intracellular membranes, diminished survival, and enhanced apoptosis.	Ceramides	61-69	secreted phosphoprotein 1	Homo sapiens	13-18
12105227-1	2002	The longevity assurance gene (LAG1) and its homolog (LAC1) are required for acyl-CoA-dependent synthesis of ceramides containing very long acyl chain (e.g. C26) fatty acids in yeast, and a homolog of LAG1, ASC1, confers resistance in plants to fumonisin B(1), an inhibitor of ceramide synthesis.	Ceramides	108-117	ceramide synthase 1	Homo sapiens	30-34
12105227-1	2002	The longevity assurance gene (LAG1) and its homolog (LAC1) are required for acyl-CoA-dependent synthesis of ceramides containing very long acyl chain (e.g. C26) fatty acids in yeast, and a homolog of LAG1, ASC1, confers resistance in plants to fumonisin B(1), an inhibitor of ceramide synthesis.	Ceramides	108-117	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	200-204
12105227-1	2002	The longevity assurance gene (LAG1) and its homolog (LAC1) are required for acyl-CoA-dependent synthesis of ceramides containing very long acyl chain (e.g. C26) fatty acids in yeast, and a homolog of LAG1, ASC1, confers resistance in plants to fumonisin B(1), an inhibitor of ceramide synthesis.	Ceramides	108-117	guanine nucleotide-binding protein subunit beta	Saccharomyces cerevisiae S288C	206-210
12473262-0	2002	Gold sodium thiomalate (GSTM) inhibits lipopolysaccharide stimulated tumor necrosis factor-alpha through ceramide pathway.	Ceramides	105-113	tumor necrosis factor	Homo sapiens	69-96
12034359-0	2002	Delayed ERK activation by ceramide reduces melanin synthesis in human melanocytes.	Ceramides	26-34	mitogen-activated protein kinase 1	Homo sapiens	8-11
12473262-3	2002	Ceramide, a structural homolog of LPS and a second messenger in the sphingomyelin signal transduction pathway has been shown to stimulate TNF-alpha production from murine macrophages.	Ceramides	0-8	toll-like receptor 4	Mus musculus	34-37
12473262-3	2002	Ceramide, a structural homolog of LPS and a second messenger in the sphingomyelin signal transduction pathway has been shown to stimulate TNF-alpha production from murine macrophages.	Ceramides	0-8	tumor necrosis factor	Mus musculus	138-147
12473262-7	2002	However, C(2) ceramide stimulated TNF-alpha production in 5 of 10 PBMCs (ceramide responder); it did not do so in the other 5 PBMCs (ceramide non-responder) or the THP-1 cell line.	Ceramides	14-22	tumor necrosis factor	Homo sapiens	34-43
12473262-8	2002	GSTM inhibited LPS stimulated TNF-alpha productions in PBMCs of all 5 ceramide responders both at protein and mRNA expression level.	Ceramides	70-78	interferon regulatory factor 6	Homo sapiens	15-18
12473262-8	2002	GSTM inhibited LPS stimulated TNF-alpha productions in PBMCs of all 5 ceramide responders both at protein and mRNA expression level.	Ceramides	70-78	tumor necrosis factor	Homo sapiens	30-39
12473262-7	2002	However, C(2) ceramide stimulated TNF-alpha production in 5 of 10 PBMCs (ceramide responder); it did not do so in the other 5 PBMCs (ceramide non-responder) or the THP-1 cell line.	Ceramides	73-81	tumor necrosis factor	Homo sapiens	34-43
12473262-9	2002	We also found that GSTM inhibited LPS induced NF-kappaB level only in ceramide responder.	Ceramides	70-78	interferon regulatory factor 6	Homo sapiens	34-37
12473262-7	2002	However, C(2) ceramide stimulated TNF-alpha production in 5 of 10 PBMCs (ceramide responder); it did not do so in the other 5 PBMCs (ceramide non-responder) or the THP-1 cell line.	Ceramides	73-81	tumor necrosis factor	Homo sapiens	34-43
12473262-10	2002	Thus, we for the first time report that GSTM inhibits LPS stimulated TNF-alpha production through ceramide pathway and anti-inflammatory activity of GSTM in treatment of RA may depend on its ability to inhibit NF-kappaB activation and TNF-alpha production.	Ceramides	98-106	interferon regulatory factor 6	Homo sapiens	54-57
12473262-10	2002	Thus, we for the first time report that GSTM inhibits LPS stimulated TNF-alpha production through ceramide pathway and anti-inflammatory activity of GSTM in treatment of RA may depend on its ability to inhibit NF-kappaB activation and TNF-alpha production.	Ceramides	98-106	tumor necrosis factor	Homo sapiens	69-78
12428923-7	2002	Experiments conducted with caspase inhibitors, bongkrekic acid, or DL-PDMP indicated that ceramide triggers mitochondrial collapse, followed by the activation of caspases-9, -8 and -3, and poly(ADP-ribose)polymerase cleavage.	Ceramides	90-98	caspase 8	Homo sapiens	27-34
12428923-7	2002	Experiments conducted with caspase inhibitors, bongkrekic acid, or DL-PDMP indicated that ceramide triggers mitochondrial collapse, followed by the activation of caspases-9, -8 and -3, and poly(ADP-ribose)polymerase cleavage.	Ceramides	90-98	caspase 9	Homo sapiens	162-183
12072440-0	2002	Ceramide mediates age-associated increase in macrophage cyclooxygenase-2 expression.	Ceramides	0-8	prostaglandin-endoperoxide synthase 2	Mus musculus	56-72
12072440-4	2002	Furthermore, the results show that LPS-induced ceramide levels from the old mice are significantly higher than those of young mice, whereas there is no age-related difference in concentration of its down stream metabolite, sphingosine.	Ceramides	47-55	toll-like receptor 4	Mus musculus	35-38
12072440-5	2002	The addition of ceramide in the presence or absence of LPS resulted in a significant increase in PGE(2) production in a dose- and time-dependent manner.	Ceramides	16-24	toll-like receptor 4	Mus musculus	55-58
12072440-7	2002	The ceramide-induced up-regulation in PGE(2) production was mediated through increase in COX activity and transcriptional up-regulation of COX-2 mRNA.	Ceramides	4-12	prostaglandin-endoperoxide synthase 2	Mus musculus	139-144
12011072-4	2002	Clustering of the CD40 ligand is mediated by an association of the ligand with p53, a translocation of acid sphingomyelinase (ASM) to the cell membrane, an activation of the ASM, and a formation of ceramide.	Ceramides	198-206	CD40 molecule	Homo sapiens	18-22
12011072-4	2002	Clustering of the CD40 ligand is mediated by an association of the ligand with p53, a translocation of acid sphingomyelinase (ASM) to the cell membrane, an activation of the ASM, and a formation of ceramide.	Ceramides	198-206	tumor protein p53	Homo sapiens	79-82
12011072-5	2002	Ceramide appears to modify preexisting sphingolipid-rich membrane microdomains to fuse and form ceramide-enriched signaling platforms that serve to cluster CD40 ligand.	Ceramides	0-8	CD40 molecule	Homo sapiens	156-160
12011072-5	2002	Ceramide appears to modify preexisting sphingolipid-rich membrane microdomains to fuse and form ceramide-enriched signaling platforms that serve to cluster CD40 ligand.	Ceramides	96-104	CD40 molecule	Homo sapiens	156-160
12011072-6	2002	Genetic deficiency of p53 or ASM or disruption of ceramide-enriched membrane domains prevents clustering of CD40 ligand.	Ceramides	50-58	CD40 molecule	Homo sapiens	108-112
12147222-0	2002	Modulation of the expression of membrane-bound CD54 (mCD54) and soluble form of CD54 (sCD54) in endothelial cells by glucosyl transferase inhibitor: possible role of ceramide for the shedding of mCD54.	Ceramides	166-174	ATP binding cassette subfamily A member 1	Homo sapiens	32-46
12208520-0	2002	Ceramide generated by acidic sphingomyelinase contributes to tumor necrosis factor-alpha-mediated apoptosis in human colon HT-29 cells through glycosphingolipids formation.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	22-45
12208520-0	2002	Ceramide generated by acidic sphingomyelinase contributes to tumor necrosis factor-alpha-mediated apoptosis in human colon HT-29 cells through glycosphingolipids formation.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	61-88
12208520-2	2002	In the present study we assessed the contribution of acidic sphingomyelinase (ASMase), a ceramide generating enzyme, in tumor necrosis factor (TNF)-mediated apoptosis in human colon HT-29 cells.	Ceramides	89-97	sphingomyelin phosphodiesterase 1	Homo sapiens	53-76
12208520-2	2002	In the present study we assessed the contribution of acidic sphingomyelinase (ASMase), a ceramide generating enzyme, in tumor necrosis factor (TNF)-mediated apoptosis in human colon HT-29 cells.	Ceramides	89-97	sphingomyelin phosphodiesterase 1	Homo sapiens	78-84
12149210-0	2002	Kit signaling inhibits the sphingomyelin-ceramide pathway through PLC gamma 1: implication in stem cell factor radioprotective effect.	Ceramides	41-49	phospholipase C, gamma 1	Mus musculus	66-77
12149210-0	2002	Kit signaling inhibits the sphingomyelin-ceramide pathway through PLC gamma 1: implication in stem cell factor radioprotective effect.	Ceramides	41-49	kit ligand	Mus musculus	94-110
12149210-5	2002	Moreover, SCF stimulation inhibited IR-induced neutral sphingomyelinase (N-SMase) stimulation and ceramide production.	Ceramides	98-106	kit ligand	Mus musculus	10-13
12208496-0	2002	Divergent role of ceramide generated by exogenous sphingomyelinases on NF-kappa B activation and apoptosis in human colon HT-29 cells.	Ceramides	18-26	nuclear factor kappa B subunit 1	Homo sapiens	71-81
12208496-1	2002	This study examined the role of ceramide generated by exogenous sphingomyelinases (SMases) on transcription nuclear factor-kappa B (NF-kappa B) activation and apoptosis in human colon epithelial HT-29 cells.	Ceramides	32-40	nuclear factor kappa B subunit 1	Homo sapiens	108-130
12208496-1	2002	This study examined the role of ceramide generated by exogenous sphingomyelinases (SMases) on transcription nuclear factor-kappa B (NF-kappa B) activation and apoptosis in human colon epithelial HT-29 cells.	Ceramides	32-40	nuclear factor kappa B subunit 1	Homo sapiens	132-142
12147222-0	2002	Modulation of the expression of membrane-bound CD54 (mCD54) and soluble form of CD54 (sCD54) in endothelial cells by glucosyl transferase inhibitor: possible role of ceramide for the shedding of mCD54.	Ceramides	166-174	intercellular adhesion molecule 1	Homo sapiens	47-51
12147222-7	2002	These data provide the possibility that the shedding of mCD54 into sCD54 by metalloproteinase-like enzyme is inhibited by PDMP, in which PDMP-induced accumulation of ceramide may act as a second messenger.	Ceramides	166-174	intercellular adhesion molecule 1	Mus musculus	56-61
12020770-0	2002	Stimulation by de novo-synthesized ceramide of phospholipase A(2)-dependent cholesterol esterification promoted by the uptake of oxidized low-density lipoprotein in macrophages.	Ceramides	35-43	phospholipase A and acyltransferase 1	Homo sapiens	47-62
12130502-0	2002	c-myc proto-oncogene expression in hemophilic synovitis: in vitro studies of the effects of iron and ceramide.	Ceramides	101-109	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-5
12130502-11	2002	Ceramide prevented both the iron-induced increases in HSFC proliferation and c-myc expression.	Ceramides	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	77-82
12020770-6	2002	Furthermore, sphingomyelinase or cell-permeable ceramide induced the release of oleic acid, and this was inhibited by a cPLA(2) inhibitor.	Ceramides	48-56	phospholipase A2 group IVA	Homo sapiens	120-127
12374205-2	2002	We report that differentiated granule cells are capable to form Cer-1-P via ceramide derived from SM degradation at the plasma membrane level.	Ceramides	76-84	cerberus 1, DAN family BMP antagonist	Homo sapiens	64-69
12153720-6	2002	The enzyme hydrolyzed various N-acylsphingosines but not galactosylceramide, GM1a or sphingomyelin, and exhibited a peak of activity at pH 6.5-7.5, and thus was classified as a neutral CDase.	Ceramides	30-48	Ceramidase	Drosophila melanogaster	185-190
12130682-0	2002	Influence of ceramide metabolism on P-glycoprotein function in immature acute myeloid leukemia KG1a cells.	Ceramides	13-21	ATP binding cassette subfamily B member 1	Homo sapiens	36-50
12374208-3	2002	CrmA was also able to block the TNF-alpha-induced increase in ceramide formation in PC12 cells.	Ceramides	62-70	tumor necrosis factor	Rattus norvegicus	32-41
12374208-4	2002	Conversely, if caspase 8 was activated by light-activated Rose Bengal, there was an increase in both ceramide and caspase 3-mediated apoptosis, which was blocked by CrmA overexpression.	Ceramides	101-109	caspase 8	Rattus norvegicus	15-24
12374208-5	2002	This suggested that caspase 8 increases ceramide either by increasing its synthesis or by activating sphingomyelinase.	Ceramides	40-48	caspase 8	Rattus norvegicus	20-29
11953426-9	2002	Since ceramides also support formation of rafts and interact with Raf we propose that Raf may be present at the plasma membrane in two distinct microdomains: in raft regions via association with cholesterol and ceramides and in non-raft regions due to interaction with phosphatidylserine and phosphatidic acid.	Ceramides	6-15	zinc fingers and homeoboxes 2	Homo sapiens	66-69
12006562-1	2002	Ceramides are known to play a major regulatory role in apoptosis by inducing cytochrome c release from mitochondria.	Ceramides	0-9	cytochrome c, somatic	Homo sapiens	77-89
12006562-6	2002	Exogenously added reduced cytochrome c was able to freely permeate the mitochondrial outer membrane with entry to and exit from the intermembrane space facilitated by ceramides in a dose- and time-dependent manner.	Ceramides	167-176	cytochrome c, somatic	Homo sapiens	26-38
12006562-10	2002	These results indicate that the ceramide-induced membrane permeability increases in isolated mitochondria are via ceramide channel formation and not a release mechanism, as the channels that allow cytochrome c to freely permeate are reversible, and are not specific to cytochrome c.	Ceramides	32-40	cytochrome c, somatic	Homo sapiens	197-209
12006562-10	2002	These results indicate that the ceramide-induced membrane permeability increases in isolated mitochondria are via ceramide channel formation and not a release mechanism, as the channels that allow cytochrome c to freely permeate are reversible, and are not specific to cytochrome c.	Ceramides	32-40	cytochrome c, somatic	Homo sapiens	269-281
12139966-2	2002	Inhibition of CGT by D,L-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) caused a marked reduction in a incorporation of [3-14C]serine to CMH in both CHO-K1 and Z65 cells, but resulted in the accumulation of ceramide in Z65 cells in a concentration higher than that in CHO-K1 cells.	Ceramides	222-230	ceramide glucosyltransferase	Cricetulus griseus	14-17
12006573-7	2002	Gene dosage experiments using the sphingolipid long chain sphingoid base (LCB) hydroxylase gene, SUR2, suggest that erg26-1 cells may accumulate LCB, thus placing one point of sterol regulation of sphingolipid synthesis possibly at the level of ceramide metabolism.	Ceramides	245-253	sphingosine hydroxylase	Saccharomyces cerevisiae S288C	97-101
11953426-9	2002	Since ceramides also support formation of rafts and interact with Raf we propose that Raf may be present at the plasma membrane in two distinct microdomains: in raft regions via association with cholesterol and ceramides and in non-raft regions due to interaction with phosphatidylserine and phosphatidic acid.	Ceramides	6-15	zinc fingers and homeoboxes 2	Homo sapiens	86-89
11953426-9	2002	Since ceramides also support formation of rafts and interact with Raf we propose that Raf may be present at the plasma membrane in two distinct microdomains: in raft regions via association with cholesterol and ceramides and in non-raft regions due to interaction with phosphatidylserine and phosphatidic acid.	Ceramides	211-220	zinc fingers and homeoboxes 2	Homo sapiens	86-89
12071851-0	2002	Decreased activity and enhanced nuclear export of CCAAT-enhancer-binding protein beta during inhibition of adipogenesis by ceramide.	Ceramides	123-131	CCAAT enhancer binding protein beta	Homo sapiens	50-85
11950838-0	2002	Ceramide biosynthesis is required for the formation of the oligomeric H+-ATPase Pma1p in the yeast endoplasmic reticulum.	Ceramides	0-8	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	80-85
12074575-1	2002	We have demonstrated previously that IGFBP-5 alone had no effect on cell death but modulated ceramide-induced apoptosis in Hs578T IGF non-responsive cells.	Ceramides	93-101	insulin like growth factor binding protein 5	Homo sapiens	37-44
12074575-6	2002	In summary, all forms of IGFBP-5 modulated ceramide-induced apoptosis in Hs578T cells.	Ceramides	43-51	insulin like growth factor binding protein 5	Homo sapiens	25-32
11956206-7	2002	Membrane but not cytosolic fractions from HEK293 cells transiently transfected with a hCERK expression vector readily phosphorylated ceramide but not sphingosine or other sphingoid bases, diacylglycerol or phosphatidylinositol.	Ceramides	133-141	ceramide kinase	Homo sapiens	86-91
12071851-3	2002	The addition of exogenous N-acetylsphingosine (C2-ceramide) or increasing endogenous ceramide levels inhibited the expression of C/EBPalpha and PPARgamma, and blocked adipocyte development.	Ceramides	50-58	CCAAT enhancer binding protein alpha	Homo sapiens	129-139
12071851-3	2002	The addition of exogenous N-acetylsphingosine (C2-ceramide) or increasing endogenous ceramide levels inhibited the expression of C/EBPalpha and PPARgamma, and blocked adipocyte development.	Ceramides	50-58	peroxisome proliferator activated receptor gamma	Homo sapiens	144-153
12071851-6	2002	Leptomycin B is an inhibitor of CRM1/exportin-1, and reversed the ceramide-induced decrease in nuclear C/EBPbeta at 24 h. Taken together, these data support the hypothesis that ceramide may inhibit adipogenesis, at least in part, by enhancing dephosphorylation and premature nuclear export of C/EBPbeta at a time when its maximal transcriptional activity is required to drive adipogenesis.	Ceramides	66-74	CCAAT enhancer binding protein beta	Homo sapiens	103-112
12071851-6	2002	Leptomycin B is an inhibitor of CRM1/exportin-1, and reversed the ceramide-induced decrease in nuclear C/EBPbeta at 24 h. Taken together, these data support the hypothesis that ceramide may inhibit adipogenesis, at least in part, by enhancing dephosphorylation and premature nuclear export of C/EBPbeta at a time when its maximal transcriptional activity is required to drive adipogenesis.	Ceramides	66-74	CCAAT enhancer binding protein beta	Homo sapiens	293-302
12071851-6	2002	Leptomycin B is an inhibitor of CRM1/exportin-1, and reversed the ceramide-induced decrease in nuclear C/EBPbeta at 24 h. Taken together, these data support the hypothesis that ceramide may inhibit adipogenesis, at least in part, by enhancing dephosphorylation and premature nuclear export of C/EBPbeta at a time when its maximal transcriptional activity is required to drive adipogenesis.	Ceramides	177-185	exportin 1	Homo sapiens	32-36
12071851-6	2002	Leptomycin B is an inhibitor of CRM1/exportin-1, and reversed the ceramide-induced decrease in nuclear C/EBPbeta at 24 h. Taken together, these data support the hypothesis that ceramide may inhibit adipogenesis, at least in part, by enhancing dephosphorylation and premature nuclear export of C/EBPbeta at a time when its maximal transcriptional activity is required to drive adipogenesis.	Ceramides	177-185	exportin 1	Homo sapiens	37-47
12071851-6	2002	Leptomycin B is an inhibitor of CRM1/exportin-1, and reversed the ceramide-induced decrease in nuclear C/EBPbeta at 24 h. Taken together, these data support the hypothesis that ceramide may inhibit adipogenesis, at least in part, by enhancing dephosphorylation and premature nuclear export of C/EBPbeta at a time when its maximal transcriptional activity is required to drive adipogenesis.	Ceramides	177-185	CCAAT enhancer binding protein beta	Homo sapiens	103-112
12071851-6	2002	Leptomycin B is an inhibitor of CRM1/exportin-1, and reversed the ceramide-induced decrease in nuclear C/EBPbeta at 24 h. Taken together, these data support the hypothesis that ceramide may inhibit adipogenesis, at least in part, by enhancing dephosphorylation and premature nuclear export of C/EBPbeta at a time when its maximal transcriptional activity is required to drive adipogenesis.	Ceramides	177-185	CCAAT enhancer binding protein beta	Homo sapiens	293-302
11929874-0	2002	A functional role for the B56 alpha-subunit of protein phosphatase 2A in ceramide-mediated regulation of Bcl2 phosphorylation status and function.	Ceramides	73-81	protein phosphatase 2 regulatory subunit B'alpha	Homo sapiens	26-35
11929874-0	2002	A functional role for the B56 alpha-subunit of protein phosphatase 2A in ceramide-mediated regulation of Bcl2 phosphorylation status and function.	Ceramides	73-81	BCL2 apoptosis regulator	Homo sapiens	105-109
11929874-1	2002	Recently it has been shown that the potent apoptotic agent ceramide activates a mitochondrial protein phosphatase 2A (PP2A) and promotes dephosphorylation of the anti-apoptotic molecule Bcl2 (Ruvolo, P. P., Deng, X., Ito, T., Carr, B. K., and May, W. S. (1999) J. Biol.	Ceramides	59-67	protein phosphatase 2 phosphatase activator	Homo sapiens	118-122
11929874-1	2002	Recently it has been shown that the potent apoptotic agent ceramide activates a mitochondrial protein phosphatase 2A (PP2A) and promotes dephosphorylation of the anti-apoptotic molecule Bcl2 (Ruvolo, P. P., Deng, X., Ito, T., Carr, B. K., and May, W. S. (1999) J. Biol.	Ceramides	59-67	BCL2 apoptosis regulator	Homo sapiens	186-190
11929874-4	2002	In cells expressing Bcl2, dephosphorylation of Bcl2 appears to be required for ceramide-induced cell death because treatment of cells with low doses of the PP2A inhibitor okadaic acid blocks Bcl2 dephosphorylation and promotes cell survival.	Ceramides	79-87	BCL2 apoptosis regulator	Homo sapiens	20-24
11929874-4	2002	In cells expressing Bcl2, dephosphorylation of Bcl2 appears to be required for ceramide-induced cell death because treatment of cells with low doses of the PP2A inhibitor okadaic acid blocks Bcl2 dephosphorylation and promotes cell survival.	Ceramides	79-87	BCL2 apoptosis regulator	Homo sapiens	47-51
11929874-4	2002	In cells expressing Bcl2, dephosphorylation of Bcl2 appears to be required for ceramide-induced cell death because treatment of cells with low doses of the PP2A inhibitor okadaic acid blocks Bcl2 dephosphorylation and promotes cell survival.	Ceramides	79-87	protein phosphatase 2 phosphatase activator	Homo sapiens	156-160
11929874-4	2002	In cells expressing Bcl2, dephosphorylation of Bcl2 appears to be required for ceramide-induced cell death because treatment of cells with low doses of the PP2A inhibitor okadaic acid blocks Bcl2 dephosphorylation and promotes cell survival.	Ceramides	79-87	BCL2 apoptosis regulator	Homo sapiens	47-51
11929874-5	2002	Furthermore, the non-phosphorylatable (i.e. PP2A-resistant) gain-of-function S70E mutant Bcl2 can protect cells from ceramide-induced apoptosis.	Ceramides	117-125	protein phosphatase 2 phosphatase activator	Homo sapiens	44-48
11929874-5	2002	Furthermore, the non-phosphorylatable (i.e. PP2A-resistant) gain-of-function S70E mutant Bcl2 can protect cells from ceramide-induced apoptosis.	Ceramides	117-125	BCL2 apoptosis regulator	Homo sapiens	89-93
11929874-10	2002	It is hypothesized that ceramide regulates PP2A via the B-subunit.	Ceramides	24-32	protein phosphatase 2 phosphatase activator	Homo sapiens	43-47
11929874-11	2002	Thus, understanding the mechanism of how PP2A regulates Bcl2 phosphorylation status and how ceramide might regulate this process requires identification of the regulatory B-subunit of PP2A that comprises the Bcl2 phosphatase.	Ceramides	92-100	protein phosphatase 2 phosphatase activator	Homo sapiens	184-188
11929874-11	2002	Thus, understanding the mechanism of how PP2A regulates Bcl2 phosphorylation status and how ceramide might regulate this process requires identification of the regulatory B-subunit of PP2A that comprises the Bcl2 phosphatase.	Ceramides	92-100	BCL2 apoptosis regulator	Homo sapiens	208-212
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	263-271	protein phosphatase 2 regulatory subunit B'alpha	Homo sapiens	26-35
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	263-271	BCL2 apoptosis regulator	Homo sapiens	97-101
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	263-271	BCL2 apoptosis regulator	Homo sapiens	150-154
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	263-271	BCL2 apoptosis regulator	Homo sapiens	150-154
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	263-271	BCL2 apoptosis regulator	Homo sapiens	150-154
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	470-478	protein phosphatase 2 regulatory subunit B'alpha	Homo sapiens	26-35
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	470-478	BCL2 apoptosis regulator	Homo sapiens	97-101
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	470-478	BCL2 apoptosis regulator	Homo sapiens	150-154
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	470-478	BCL2 apoptosis regulator	Homo sapiens	150-154
11929874-12	2002	Results indicate that the B56 alpha-subunit is a candidate regulatory subunit of the physiologic Bcl2 phosphatase since (a) B56 alpha associates with Bcl2 as evidenced by pull-down experiments, (b) B56 alpha co-localizes with Bcl2 in mitochondrial membranes, (c) ceramide promotes translocation of B56 alpha to mitochondrial membranes, and (d) overexpression of B56 alpha promotes mitochondrial PP2A activity and Bcl2 dephosphorylation and potentiates cell killing with ceramide.	Ceramides	470-478	BCL2 apoptosis regulator	Homo sapiens	150-154
12037683-0	2002	Ceramide induces mitochondrial activation and apoptosis via a Bax-dependent pathway in human carcinoma cells.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	62-65
12037683-3	2002	However, the direct effect of proapoptotic gene products, e.g. Bax, on ceramide-induced death signalling has not yet been studied in detail.	Ceramides	71-79	BCL2 associated X, apoptosis regulator	Homo sapiens	63-66
12037683-4	2002	In the present work, we show by measurement of mitochondrial permeability transition, cytochrome c release, activation of caspase-3 and DNA fragmentation that ceramide-induced apoptosis is marginal in Bax-negative DU 145 cells.	Ceramides	159-167	cytochrome c, somatic	Homo sapiens	86-98
12037683-4	2002	In the present work, we show by measurement of mitochondrial permeability transition, cytochrome c release, activation of caspase-3 and DNA fragmentation that ceramide-induced apoptosis is marginal in Bax-negative DU 145 cells.	Ceramides	159-167	caspase 3	Homo sapiens	122-131
12037683-4	2002	In the present work, we show by measurement of mitochondrial permeability transition, cytochrome c release, activation of caspase-3 and DNA fragmentation that ceramide-induced apoptosis is marginal in Bax-negative DU 145 cells.	Ceramides	159-167	BCL2 associated X, apoptosis regulator	Homo sapiens	201-204
12037683-5	2002	Reconstitution of Bax by generation of DU 145 cells stably expressing this proapoptotic factor, clearly enhanced ceramide-induced apoptosis at all levels of the mitochondrial signalling cascade.	Ceramides	113-121	BCL2 associated X, apoptosis regulator	Homo sapiens	18-21
12037683-6	2002	Using the broad-range caspase inhibitor zVAD-fmk and zDEVD-fmk, an inhibitor of caspase-3-like activities, we demonstrate that the ceramide-induced mitochondrial activation in Bax-transfected DU 145 cells is caspase-independent.	Ceramides	131-139	caspase 3	Homo sapiens	80-89
12037683-6	2002	Using the broad-range caspase inhibitor zVAD-fmk and zDEVD-fmk, an inhibitor of caspase-3-like activities, we demonstrate that the ceramide-induced mitochondrial activation in Bax-transfected DU 145 cells is caspase-independent.	Ceramides	131-139	BCL2 associated X, apoptosis regulator	Homo sapiens	176-179
12037683-8	2002	This influence of Bax on ceramide-induced apoptosis was confirmed in another cellular system: whereas Bax-positive HCT116 wild type cells were very sensitive towards induction of cell death by C(2)-ceramide, sensitivity of Bax knock-out HCT116 cells was significantly reduced.	Ceramides	25-33	BCL2 associated X, apoptosis regulator	Homo sapiens	18-21
12037683-8	2002	This influence of Bax on ceramide-induced apoptosis was confirmed in another cellular system: whereas Bax-positive HCT116 wild type cells were very sensitive towards induction of cell death by C(2)-ceramide, sensitivity of Bax knock-out HCT116 cells was significantly reduced.	Ceramides	25-33	BCL2 associated X, apoptosis regulator	Homo sapiens	102-105
12037683-8	2002	This influence of Bax on ceramide-induced apoptosis was confirmed in another cellular system: whereas Bax-positive HCT116 wild type cells were very sensitive towards induction of cell death by C(2)-ceramide, sensitivity of Bax knock-out HCT116 cells was significantly reduced.	Ceramides	25-33	BCL2 associated X, apoptosis regulator	Homo sapiens	102-105
12037683-9	2002	Thus, we conclude that Bax is a key activator of ceramide-mediated death pathways.	Ceramides	49-57	BCL2 associated X, apoptosis regulator	Homo sapiens	23-26
12222689-0	2002	Increase in ceramide level alters the lysosomal targeting of cathepsin D prior to onset of apoptosis in HT-29 colon cancer cells.	Ceramides	12-20	cathepsin D	Homo sapiens	61-72
12222689-2	2002	In HT-29 colorectal cancer cells increased ceramide levels, induced by exogenous N-acetylsphingosine (NAS, also known as C2-ceramide) or by 1-phenyl-2-(decanoylamino)-3-morpholino-1-propanol (PDMP), inhibited the transport and processing of cathepsin D (CD), a lysosomal protease implicated in apoptosis of tumour cells.	Ceramides	43-51	cathepsin D	Homo sapiens	241-252
12032677-0	2002	Control of ceramide-induced apoptosis by IGF-1: involvement of PI-3 kinase, caspase-3 and catalase.	Ceramides	11-19	insulin like growth factor 1	Homo sapiens	41-46
12032677-0	2002	Control of ceramide-induced apoptosis by IGF-1: involvement of PI-3 kinase, caspase-3 and catalase.	Ceramides	11-19	caspase 3	Homo sapiens	76-98
12032677-3	2002	Either IGF-1 pretreatment or PI-3 kinase overexpression restored ceramide-depleted catalase function, and this restoration was inhibited by wortmannin.	Ceramides	65-73	insulin like growth factor 1	Homo sapiens	7-12
12032677-3	2002	Either IGF-1 pretreatment or PI-3 kinase overexpression restored ceramide-depleted catalase function, and this restoration was inhibited by wortmannin.	Ceramides	65-73	catalase	Homo sapiens	83-91
12032677-4	2002	A catalase inhibitor 3-amino-1h-1, 2, 4-triazole (ATZ) blocked the inhibitory action of IGF-1 on ceramide-induced apoptosis, whereas exogenous purified catalase enhanced it.	Ceramides	97-105	catalase	Homo sapiens	2-10
12032677-4	2002	A catalase inhibitor 3-amino-1h-1, 2, 4-triazole (ATZ) blocked the inhibitory action of IGF-1 on ceramide-induced apoptosis, whereas exogenous purified catalase enhanced it.	Ceramides	97-105	insulin like growth factor 1	Homo sapiens	88-93
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	0-8	caspase 3	Homo sapiens	19-28
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	0-8	insulin like growth factor 1	Homo sapiens	46-51
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	0-8	caspase 3	Homo sapiens	125-134
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	0-8	insulin like growth factor 1	Homo sapiens	196-201
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	0-8	catalase	Homo sapiens	223-231
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	205-213	caspase 3	Homo sapiens	19-28
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	205-213	caspase 3	Homo sapiens	125-134
12032677-5	2002	Ceramide-activated caspase-3 was inhibited by IGF-1/PI-3 kinase and enhanced by wortmannin, while the addition of a specific caspase-3 inhibitor DMQD-CHO significantly enhanced the restoration by IGF-1 of ceramide-depleted catalase function.	Ceramides	205-213	insulin like growth factor 1	Homo sapiens	196-201
12085194-8	2002	Cell death induced by ceramide was significantly reduced by insulin-like growth factor-binding protein-3 in the MCF-10A cells and depleting insulin-like growth factor-binding protein-3 with transforming growth factor-beta in these cells consequently increased their susceptibility to ceramide.	Ceramides	22-30	insulin like growth factor binding protein 3	Homo sapiens	60-104
12085194-8	2002	Cell death induced by ceramide was significantly reduced by insulin-like growth factor-binding protein-3 in the MCF-10A cells and depleting insulin-like growth factor-binding protein-3 with transforming growth factor-beta in these cells consequently increased their susceptibility to ceramide.	Ceramides	284-292	insulin like growth factor binding protein 3	Homo sapiens	140-184
12085194-8	2002	Cell death induced by ceramide was significantly reduced by insulin-like growth factor-binding protein-3 in the MCF-10A cells and depleting insulin-like growth factor-binding protein-3 with transforming growth factor-beta in these cells consequently increased their susceptibility to ceramide.	Ceramides	284-292	transforming growth factor beta 1	Homo sapiens	190-221
12085194-9	2002	In contrast, insulin-like growth factor-binding protein-3 enhanced apoptosis induced by ceramide in the Hs578T cells but transforming growth factor-beta treated Hs578T cells were resistant to apoptosis.	Ceramides	88-96	insulin like growth factor binding protein 3	Homo sapiens	13-57
11950838-7	2002	Furthermore, oligomerization of Pma1p is linked to membrane lipid composition; Pma1p is rendered monomeric in cells depleted of ceramide, suggesting that association with lipid rafts may influence oligomerization.	Ceramides	128-136	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	79-84
11950838-8	2002	Surprisingly, monomeric Pma1p present in ceramide-deficient membranes can be exported from the ER in COPII vesicles in a reaction that is stimulated by Lst1p.	Ceramides	41-49	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	24-29
11950838-8	2002	Surprisingly, monomeric Pma1p present in ceramide-deficient membranes can be exported from the ER in COPII vesicles in a reaction that is stimulated by Lst1p.	Ceramides	41-49	Sfb3p	Saccharomyces cerevisiae S288C	152-157
11939786-8	2002	The incorporation of ceramide, on the other hand, stimulated the sPLA(2) activity significantly.	Ceramides	21-29	phospholipase A2 group IIA	Homo sapiens	65-72
11897496-0	2002	Lithium blocks the PKB and GSK3 dephosphorylation induced by ceramide through protein phosphatase-2A.	Ceramides	61-69	protein tyrosine kinase 2 beta	Homo sapiens	19-22
11897496-0	2002	Lithium blocks the PKB and GSK3 dephosphorylation induced by ceramide through protein phosphatase-2A.	Ceramides	61-69	protein phosphatase 2 phosphatase activator	Homo sapiens	86-100
11897496-4	2002	Since lithium inhibits in vivo the observed protein phosphatase-2A (PP2A) activation induced by ceramide, we hypothesise that the neuroprotective action of lithium may be due to the inhibition of the PP2A activation by apoptotic stimuli.	Ceramides	96-104	protein phosphatase 2 phosphatase activator	Homo sapiens	52-66
11897496-4	2002	Since lithium inhibits in vivo the observed protein phosphatase-2A (PP2A) activation induced by ceramide, we hypothesise that the neuroprotective action of lithium may be due to the inhibition of the PP2A activation by apoptotic stimuli.	Ceramides	96-104	protein phosphatase 2 phosphatase activator	Homo sapiens	68-72
11897496-4	2002	Since lithium inhibits in vivo the observed protein phosphatase-2A (PP2A) activation induced by ceramide, we hypothesise that the neuroprotective action of lithium may be due to the inhibition of the PP2A activation by apoptotic stimuli.	Ceramides	96-104	protein phosphatase 2 phosphatase activator	Homo sapiens	200-204
23345770-8	2002	Our most recent results show that the presence of ceramide 1 and the formation of a liquid phase are crucial elements for the formation of the LPP.	Ceramides	50-58	LIM domain containing preferred translocation partner in lipoma	Homo sapiens	143-146
12069808-8	2002	In the case of PA, S1P and C1P, the products are diacylglycerol (DAG), sphingosine and ceramide, respectively.	Ceramides	87-95	membrane bound transcription factor peptidase, site 1	Homo sapiens	19-30
11986953-1	2002	The retinoid, N-(4-hydroxyphenyl)retinamide (4-HPR), mediates p53-independent cytotoxicity and can increase reactive oxygen species and ceramide in solid tumor cell lines.	Ceramides	136-144	haptoglobin-related protein	Homo sapiens	47-50
11986953-5	2002	Treatment with 4-HPR (9 microM) for 24 h resulted in an 8.9 +/- 1.0-fold (range: 4.9-15.7-fold) increase of ceramide.	Ceramides	108-116	haptoglobin-related protein	Homo sapiens	17-20
11986953-7	2002	Concurrent inhibition of ceramide glycosylation/acylation by d,l-threo-(1-phenyl-2-hexadecanoylamino-3-morpholino-1-propanol) (PPMP) further increased ceramide levels, and synergistically increased 4-HPR cytotoxicity in four of six ALL cell lines.	Ceramides	25-33	haptoglobin-related protein	Homo sapiens	200-203
11986953-8	2002	4-HPR was minimally cytotoxic to peripheral blood mononuclear cells and a lymphoblastoid cell line, and increased ceramide <2-fold.	Ceramides	114-122	haptoglobin-related protein	Homo sapiens	2-5
11986953-9	2002	Thus, 4-HPR was cytotoxic and increased ceramide in ALL cell lines, but not in non-malignant lymphoid cell types.	Ceramides	40-48	haptoglobin-related protein	Homo sapiens	8-11
12643176-4	2002	These impairments appear to be at least indirectly centered on the ability of mitochondria to oxidize fatty acids, possibly through mediation of lipid metabolite levels such as ceramide or diacylglycerol, which are known to directly attenuate insulin signaling.	Ceramides	177-185	insulin	Homo sapiens	243-250
12056568-2	2002	The product-ion spectra of the [M + Li]+ ions of ceramides contain abundant fragment ions that identify the fatty acyl substituent and the long-chain base (LCB) of the molecules, and thus, the structure of ceramides can be easily determined.	Ceramides	49-58	clathrin light chain B	Homo sapiens	156-159
12056568-2	2002	The product-ion spectra of the [M + Li]+ ions of ceramides contain abundant fragment ions that identify the fatty acyl substituent and the long-chain base (LCB) of the molecules, and thus, the structure of ceramides can be easily determined.	Ceramides	206-215	clathrin light chain B	Homo sapiens	156-159
11973615-2	2002	Some reports have indicated that ceramide is either a primary signaling molecule in Fas-induced cell death, or that it functions upstream of Fas by increasing FasL expression.	Ceramides	33-41	Fas ligand	Homo sapiens	159-163
11973615-4	2002	We have approached this problem by studying ceramide-induced apoptosis in unique Jurkat cell clones selected for resistance to membrane-bound FasL-induced death.	Ceramides	44-52	Fas ligand	Homo sapiens	142-146
11973615-11	2002	Because of the parallel resistance of the mutant clones to Fas and to ceramide-induced apoptosis, our data support the notion that ceramide is a second messenger for the Fas/FasL pathway and that serum withdrawal, through production of ceramide, shares a common step with the Fas-mediated apoptotic pathway.	Ceramides	131-139	Fas ligand	Homo sapiens	174-178
11973615-11	2002	Because of the parallel resistance of the mutant clones to Fas and to ceramide-induced apoptosis, our data support the notion that ceramide is a second messenger for the Fas/FasL pathway and that serum withdrawal, through production of ceramide, shares a common step with the Fas-mediated apoptotic pathway.	Ceramides	131-139	Fas ligand	Homo sapiens	174-178
11939786-10	2002	These studies show that group V sPLA(2) is physiologically more important than group IIa enzyme in lipoprotein metabolism, that the sPLA(2) activities are regulated by sphingomyelin and ceramide, and that the pathological effects of sPLA(2) may not be mediated through stimulation of eicosanoid synthesis.	Ceramides	186-194	phospholipase A2 group IIA	Homo sapiens	32-39
11939786-10	2002	These studies show that group V sPLA(2) is physiologically more important than group IIa enzyme in lipoprotein metabolism, that the sPLA(2) activities are regulated by sphingomyelin and ceramide, and that the pathological effects of sPLA(2) may not be mediated through stimulation of eicosanoid synthesis.	Ceramides	186-194	phospholipase A2 group IIA	Homo sapiens	132-139
11939786-10	2002	These studies show that group V sPLA(2) is physiologically more important than group IIa enzyme in lipoprotein metabolism, that the sPLA(2) activities are regulated by sphingomyelin and ceramide, and that the pathological effects of sPLA(2) may not be mediated through stimulation of eicosanoid synthesis.	Ceramides	186-194	phospholipase A2 group IIA	Homo sapiens	132-139
11815603-2	2002	TNF-alpha also stimulates sphingosine kinase, the enzyme that phosphorylates sphingosine to form sphingosine-1-phosphate (SPP), a further metabolite of ceramide.	Ceramides	152-160	tumor necrosis factor	Homo sapiens	0-9
12882362-8	2002	In particular mitogenic stimuli, such as basic fibroblast growth factor (bFGF), rapidly down regulate the cellular levels of ceramide by stimulating sphingomyelin synthase.	Ceramides	125-133	fibroblast growth factor 2	Rattus norvegicus	41-71
11815603-1	2002	In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity.	Ceramides	54-62	nitric oxide synthase 2	Homo sapiens	89-120
11815603-1	2002	In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity.	Ceramides	54-62	nitric oxide synthase 2	Homo sapiens	122-126
11815603-1	2002	In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity.	Ceramides	54-62	tumor necrosis factor	Homo sapiens	139-166
11815603-1	2002	In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity.	Ceramides	54-62	tumor necrosis factor	Homo sapiens	168-177
11815603-1	2002	In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity.	Ceramides	54-62	GTP cyclohydrolase 1	Homo sapiens	219-224
11815603-1	2002	In C6 glioma cells, the sphingolipid second messenger ceramide potentiates expression of inducible nitric-oxide synthase (iNOS) induced by tumor necrosis factor alpha (TNF-alpha) without affecting GTP cyclohydrolase I (GTPCH), the rate-limiting enzyme in the biosynthesis of 6(R)-5,6,7,8-tetrahydrobiopterin (BH(4)), a cofactor required for iNOS activity.	Ceramides	54-62	nitric oxide synthase 2	Homo sapiens	341-345
11880299-6	2002	Ceramide, a CCT inhibitor, was elevated, and linoleic acid, a CCT activator, was decreased in transgenics.	Ceramides	0-8	t-complex protein 1	Mus musculus	12-15
11880299-9	2002	Reduced parenchymal PtdCho synthesis appears to be attributed to CCT enzyme that is physiologically inactivated by ceramide or by diminished availability of activating lipids.	Ceramides	115-123	t-complex protein 1	Mus musculus	65-68
11903061-4	2002	The activity of serine palmitoyltransferase (SPT), which catalyses the rate-limiting step of ceramide synthesis de novo, was remarkably enhanced by THC in C6.9 cells, but not in C6.4 cells.	Ceramides	93-101	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	16-43
11903061-4	2002	The activity of serine palmitoyltransferase (SPT), which catalyses the rate-limiting step of ceramide synthesis de novo, was remarkably enhanced by THC in C6.9 cells, but not in C6.4 cells.	Ceramides	93-101	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	45-48
11903061-6	2002	Changes in SPT activity paralleled changes in ceramide levels.	Ceramides	46-54	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	11-14
12069099-10	2002	Also, in vitro experiments demonstrated that C2-ceramide and ceramide-rich lipid extracts directly activated caspase-3.	Ceramides	48-56	caspase 3	Homo sapiens	109-118
11801602-0	2002	De novo ceramide regulates the alternative splicing of caspase 9 and Bcl-x in A549 lung adenocarcinoma cells.	Ceramides	8-16	caspase 9	Homo sapiens	55-64
11801602-0	2002	De novo ceramide regulates the alternative splicing of caspase 9 and Bcl-x in A549 lung adenocarcinoma cells.	Ceramides	8-16	BCL2 like 1	Homo sapiens	69-74
11801602-4	2002	In this study, the regulation of the alternative processing of pre-mRNA of both caspase 9 and Bcl-x(L) was examined in response to ceramide.	Ceramides	131-139	caspase 9	Homo sapiens	80-89
11801602-4	2002	In this study, the regulation of the alternative processing of pre-mRNA of both caspase 9 and Bcl-x(L) was examined in response to ceramide.	Ceramides	131-139	BCL2 like 1	Homo sapiens	94-102
11801602-5	2002	Treatment of A549 lung adenocarcinoma cells with cell-permeable ceramide, D-e-C(6) ceramide, down-regulated the levels of Bcl-x(L) and caspase 9b mRNA and immunoreactive protein with a concomitant increase in the mRNA and immunoreactive protein levels of Bcl-x(s) and caspase 9 in a dose- and time-dependent manner.	Ceramides	64-72	BCL2 like 1	Homo sapiens	122-130
11801602-5	2002	Treatment of A549 lung adenocarcinoma cells with cell-permeable ceramide, D-e-C(6) ceramide, down-regulated the levels of Bcl-x(L) and caspase 9b mRNA and immunoreactive protein with a concomitant increase in the mRNA and immunoreactive protein levels of Bcl-x(s) and caspase 9 in a dose- and time-dependent manner.	Ceramides	64-72	BCL2 like 1	Homo sapiens	122-127
11801602-5	2002	Treatment of A549 lung adenocarcinoma cells with cell-permeable ceramide, D-e-C(6) ceramide, down-regulated the levels of Bcl-x(L) and caspase 9b mRNA and immunoreactive protein with a concomitant increase in the mRNA and immunoreactive protein levels of Bcl-x(s) and caspase 9 in a dose- and time-dependent manner.	Ceramides	64-72	caspase 9	Homo sapiens	135-144
11801602-5	2002	Treatment of A549 lung adenocarcinoma cells with cell-permeable ceramide, D-e-C(6) ceramide, down-regulated the levels of Bcl-x(L) and caspase 9b mRNA and immunoreactive protein with a concomitant increase in the mRNA and immunoreactive protein levels of Bcl-x(s) and caspase 9 in a dose- and time-dependent manner.	Ceramides	83-91	BCL2 like 1	Homo sapiens	122-130
11801602-5	2002	Treatment of A549 lung adenocarcinoma cells with cell-permeable ceramide, D-e-C(6) ceramide, down-regulated the levels of Bcl-x(L) and caspase 9b mRNA and immunoreactive protein with a concomitant increase in the mRNA and immunoreactive protein levels of Bcl-x(s) and caspase 9 in a dose- and time-dependent manner.	Ceramides	83-91	caspase 9	Homo sapiens	135-144
11801602-6	2002	Pretreatment with calyculin A (5 nm), an inhibitor of protein phosphatase-1 (PP1) and protein phosphatase 2A (PP2A) blocked ceramide-induced alternative splicing in contrast to okadaic acid (10 nm), a specific inhibitor of PP2A at this concentrations in cells, demonstrating a PP1-mediated mechanism.	Ceramides	124-132	inorganic pyrophosphatase 1	Homo sapiens	77-80
11801602-6	2002	Pretreatment with calyculin A (5 nm), an inhibitor of protein phosphatase-1 (PP1) and protein phosphatase 2A (PP2A) blocked ceramide-induced alternative splicing in contrast to okadaic acid (10 nm), a specific inhibitor of PP2A at this concentrations in cells, demonstrating a PP1-mediated mechanism.	Ceramides	124-132	protein phosphatase 2 phosphatase activator	Homo sapiens	94-108
11801602-6	2002	Pretreatment with calyculin A (5 nm), an inhibitor of protein phosphatase-1 (PP1) and protein phosphatase 2A (PP2A) blocked ceramide-induced alternative splicing in contrast to okadaic acid (10 nm), a specific inhibitor of PP2A at this concentrations in cells, demonstrating a PP1-mediated mechanism.	Ceramides	124-132	protein phosphatase 2 phosphatase activator	Homo sapiens	110-114
11801602-6	2002	Pretreatment with calyculin A (5 nm), an inhibitor of protein phosphatase-1 (PP1) and protein phosphatase 2A (PP2A) blocked ceramide-induced alternative splicing in contrast to okadaic acid (10 nm), a specific inhibitor of PP2A at this concentrations in cells, demonstrating a PP1-mediated mechanism.	Ceramides	124-132	protein phosphatase 2 phosphatase activator	Homo sapiens	223-227
11801602-6	2002	Pretreatment with calyculin A (5 nm), an inhibitor of protein phosphatase-1 (PP1) and protein phosphatase 2A (PP2A) blocked ceramide-induced alternative splicing in contrast to okadaic acid (10 nm), a specific inhibitor of PP2A at this concentrations in cells, demonstrating a PP1-mediated mechanism.	Ceramides	124-132	inorganic pyrophosphatase 1	Homo sapiens	277-280
11801602-7	2002	A role for endogenous ceramide in regulating the alternative splicing of caspase 9 and Bcl-x was demonstrated using the chemotherapeutic agent, gemcitabine.	Ceramides	22-30	caspase 9	Homo sapiens	73-82
11801602-7	2002	A role for endogenous ceramide in regulating the alternative splicing of caspase 9 and Bcl-x was demonstrated using the chemotherapeutic agent, gemcitabine.	Ceramides	22-30	BCL2 like 1	Homo sapiens	87-92
11801602-12	2002	Furthermore, doses of D-e-C(6) ceramide that induce the alternative splicing of both caspase 9 and Bcl-x-sensitized A549 cells to daunorubicin.	Ceramides	31-39	caspase 9	Homo sapiens	85-94
11801602-12	2002	Furthermore, doses of D-e-C(6) ceramide that induce the alternative splicing of both caspase 9 and Bcl-x-sensitized A549 cells to daunorubicin.	Ceramides	31-39	BCL2 like 1	Homo sapiens	99-104
12069099-0	2002	Ceramide-dependent caspase 3 activation is prevented by coenzyme Q from plasma membrane in serum-deprived cells.	Ceramides	0-8	caspase 3	Homo sapiens	19-28
11894136-4	2002	We report here substantial evidence that ceramide, resulting from de novo pathway or catabolism modulation, acted as a second messenger of these antitumor drugs in HT29 cells and leads to the activation of caspase-3.	Ceramides	41-49	caspase 3	Homo sapiens	206-215
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.	Ceramides	36-44	choline phosphotransferase 1	Homo sapiens	13-17
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.	Ceramides	36-44	choline phosphotransferase 1	Homo sapiens	14-17
12882362-8	2002	In particular mitogenic stimuli, such as basic fibroblast growth factor (bFGF), rapidly down regulate the cellular levels of ceramide by stimulating sphingomyelin synthase.	Ceramides	125-133	fibroblast growth factor 2	Rattus norvegicus	73-77
12882362-9	2002	Ceramide acts as an intracellular physiological inhibitor of cell growth, being able to counteract the effect of bFGF by inhibiting the MAP kinase pathway.	Ceramides	0-8	fibroblast growth factor 2	Rattus norvegicus	113-117
11792700-0	2002	High density lipoprotein binding to scavenger receptor, Class B, type I activates endothelial nitric-oxide synthase in a ceramide-dependent manner.	Ceramides	121-129	nitric oxide synthase 3	Homo sapiens	82-115
11918706-9	2002	(iii) In cholesterol:human ceramide mixtures in the presence of CER1-lin the long periodicity phase was more prominently present than in the presence of CER1-ol.	Ceramides	27-35	cerberus 1, DAN family BMP antagonist	Homo sapiens	64-68
11792463-8	2002	These results indicate that the serum deprivation induces a rise in the intracellular ceramide level, and that increased ceramide concentration leads to calcium dysregulation and release of cytochrome c followed by caspase-3 activation.	Ceramides	121-129	cytochrome c, somatic	Homo sapiens	190-202
11792463-8	2002	These results indicate that the serum deprivation induces a rise in the intracellular ceramide level, and that increased ceramide concentration leads to calcium dysregulation and release of cytochrome c followed by caspase-3 activation.	Ceramides	121-129	caspase 3	Homo sapiens	215-224
11792700-7	2002	However, HDL binding to SR-BI caused a reversible increase in intracellular ceramide levels from 97 +/- 14 pmol/mg of protein to 501 +/- 21 pmol/mg of protein.	Ceramides	76-84	scavenger receptor class B member 1	Homo sapiens	24-29
11792700-9	2002	We conclude that HDL binding to SR-BI stimulates eNOS by increasing intracellular ceramide levels and is independent of an increase in intracellular calcium or Akt kinase phosphorylation.	Ceramides	82-90	scavenger receptor class B member 1	Homo sapiens	32-37
11777929-0	2002	Nerve growth factor-induced p75-mediated death of cultured hippocampal neurons is age-dependent and transduced through ceramide generated by neutral sphingomyelinase.	Ceramides	119-127	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	28-31
11960374-0	2002	P53 mediates ceramide-induced apoptosis in SKN-SH cells.	Ceramides	13-21	tumor protein p53	Homo sapiens	0-3
11960374-0	2002	P53 mediates ceramide-induced apoptosis in SKN-SH cells.	Ceramides	13-21	hedgehog acyltransferase	Homo sapiens	43-46
11777929-1	2002	Binding of nerve growth factor (NGF) to the p75 neurotrophin receptor (p75) in cultured hippocampal neurons has been reported to cause seemingly contrasting effects, namely ceramide-dependent axonal outgrowth of freshly plated neurons, versus Jun kinase (Jnk)-dependent cell death in older neurons.	Ceramides	173-181	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	44-69
11960374-2	2002	Pretreatment with caspase inhibitors blocks cell death, suggesting that a set of caspase activities including caspase 1, as well as caspase 3, are involved in ceramide-induced apoptosis in SKN-SH cells.	Ceramides	159-167	caspase 1	Homo sapiens	110-119
11960374-2	2002	Pretreatment with caspase inhibitors blocks cell death, suggesting that a set of caspase activities including caspase 1, as well as caspase 3, are involved in ceramide-induced apoptosis in SKN-SH cells.	Ceramides	159-167	caspase 3	Homo sapiens	132-141
11777929-1	2002	Binding of nerve growth factor (NGF) to the p75 neurotrophin receptor (p75) in cultured hippocampal neurons has been reported to cause seemingly contrasting effects, namely ceramide-dependent axonal outgrowth of freshly plated neurons, versus Jun kinase (Jnk)-dependent cell death in older neurons.	Ceramides	173-181	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	44-47
11960374-2	2002	Pretreatment with caspase inhibitors blocks cell death, suggesting that a set of caspase activities including caspase 1, as well as caspase 3, are involved in ceramide-induced apoptosis in SKN-SH cells.	Ceramides	159-167	hedgehog acyltransferase	Homo sapiens	189-192
11960374-4	2002	Ceramide-induced apoptosis is accompanied by accumulation of p53 followed by an increase of Bax and decrease of Bcl-2 levels.	Ceramides	0-8	tumor protein p53	Homo sapiens	61-64
11960374-4	2002	Ceramide-induced apoptosis is accompanied by accumulation of p53 followed by an increase of Bax and decrease of Bcl-2 levels.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	92-95
11960374-4	2002	Ceramide-induced apoptosis is accompanied by accumulation of p53 followed by an increase of Bax and decrease of Bcl-2 levels.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	112-117
11960374-7	2002	These results suggest that p53 regulates the ratio Bcl-2/Bax and the expression/activation of caspases during ceramide-induced apoptosis in SKN-SH cells.	Ceramides	110-118	tumor protein p53	Homo sapiens	27-30
11960374-7	2002	These results suggest that p53 regulates the ratio Bcl-2/Bax and the expression/activation of caspases during ceramide-induced apoptosis in SKN-SH cells.	Ceramides	110-118	BCL2 apoptosis regulator	Homo sapiens	51-56
11960374-7	2002	These results suggest that p53 regulates the ratio Bcl-2/Bax and the expression/activation of caspases during ceramide-induced apoptosis in SKN-SH cells.	Ceramides	110-118	BCL2 associated X, apoptosis regulator	Homo sapiens	57-60
11788605-4	2002	Upon treatment with ATRA, ceramide, the product of an ASMase reaction, accumulated in NB4 cells.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	54-60
11777929-8	2002	These data indicate an initiating role of ceramide generated by neutral sphingomyelinase in the diverse neuronal responses induced by binding of neurotrophins to p75.	Ceramides	42-50	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	162-165
11960374-7	2002	These results suggest that p53 regulates the ratio Bcl-2/Bax and the expression/activation of caspases during ceramide-induced apoptosis in SKN-SH cells.	Ceramides	110-118	caspase 1	Homo sapiens	94-102
11960374-7	2002	These results suggest that p53 regulates the ratio Bcl-2/Bax and the expression/activation of caspases during ceramide-induced apoptosis in SKN-SH cells.	Ceramides	110-118	hedgehog acyltransferase	Homo sapiens	140-143
11882365-0	2002	Ceramide and sphingosine rapidly induce apoptosis of murine mast cells supported by interleukin-3 and stem cell factor.	Ceramides	0-8	interleukin 3	Mus musculus	84-97
11960374-9	2002	Thus ceramide-induced reduction in the Bcl-2/Bax ratio, increase in caspase activity, and apoptosis is dependent upon increases in cellular p53 levels which play a critical role in the regulation of apoptotic cell death.	Ceramides	5-13	BCL2 apoptosis regulator	Homo sapiens	39-44
11960374-9	2002	Thus ceramide-induced reduction in the Bcl-2/Bax ratio, increase in caspase activity, and apoptosis is dependent upon increases in cellular p53 levels which play a critical role in the regulation of apoptotic cell death.	Ceramides	5-13	BCL2 associated X, apoptosis regulator	Homo sapiens	45-48
11960374-9	2002	Thus ceramide-induced reduction in the Bcl-2/Bax ratio, increase in caspase activity, and apoptosis is dependent upon increases in cellular p53 levels which play a critical role in the regulation of apoptotic cell death.	Ceramides	5-13	tumor protein p53	Homo sapiens	140-143
11999738-3	2002	Nine synthetic ceramides were separated by liquid chromatography coupled to tandem mass spectrometry on a C18 bonded silica column.	Ceramides	15-24	Bardet-Biedl syndrome 9	Homo sapiens	106-109
11872660-4	2002	Ceramide is the suggested second messenger of TNF-alpha action, and in this study, we used 3T3-L1 adipocytes to investigate the effects of C(2)-ceramide (a short-chain ceramide analog) on the expression and regulation of PDE3B and lipolysis.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	46-55
11872660-8	2002	In addition to downregulation of PDE3B, the antilipolytic action of insulin was decreased by ceramide treatment.	Ceramides	93-101	insulin	Homo sapiens	68-75
11872660-9	2002	These results, together with data from other studies on PDE3B and lipolysis in diabetic humans and animals, suggest a novel pathway by which ceramide induces insulin resistance.	Ceramides	141-149	phosphodiesterase 3B	Homo sapiens	56-61
11872660-9	2002	These results, together with data from other studies on PDE3B and lipolysis in diabetic humans and animals, suggest a novel pathway by which ceramide induces insulin resistance.	Ceramides	141-149	insulin	Homo sapiens	158-165
11882365-7	2002	CONCLUSION: The present results suggest that ceramide and sphingosine may function as intracellular mediators of apoptotic signals in mast cells, which override survival signals from IL-3 and SCF.	Ceramides	45-53	interleukin 3	Mus musculus	183-187
11882365-7	2002	CONCLUSION: The present results suggest that ceramide and sphingosine may function as intracellular mediators of apoptotic signals in mast cells, which override survival signals from IL-3 and SCF.	Ceramides	45-53	kit ligand	Mus musculus	192-195
11882365-8	2002	In addition, caspases may be partially involved in ceramide- but not sphingosine-mediated apoptosis of mast cells.	Ceramides	51-59	caspase 8	Mus musculus	13-21
11882365-0	2002	Ceramide and sphingosine rapidly induce apoptosis of murine mast cells supported by interleukin-3 and stem cell factor.	Ceramides	0-8	kit ligand	Mus musculus	102-118
11915341-0	2002	[Involvement of p53 in ceramide signaling cascade].	Ceramides	23-31	tumor protein p53	Homo sapiens	16-19
11849427-9	2002	Moreover, SIN-1, a substance that simultaneously releases NO and O(-)(2) and thereby generates peroxynitrite, also stimulated a delayed ceramide formation in endothelial cells but not in mesangial cells.	Ceramides	136-144	MAPK associated protein 1	Homo sapiens	10-15
11854443-0	2002	Vesnarinone causes oxidative damage by inhibiting catalase function through ceramide action in myeloid cell apoptosis.	Ceramides	76-84	catalase	Homo sapiens	50-58
11854443-7	2002	C2-ceramide enhanced vesnarinone-induced inhibition of the ROI-scavenging enzyme catalase at the levels of protein and activity in HL-60 cells; in contrast, however, vesnarinone did not induce ceramide generation, oxidative damage, or catalase depletion in HL-60/ves cells, where vesnarinone could not induce apoptosis.	Ceramides	3-11	catalase	Homo sapiens	81-89
11854443-7	2002	C2-ceramide enhanced vesnarinone-induced inhibition of the ROI-scavenging enzyme catalase at the levels of protein and activity in HL-60 cells; in contrast, however, vesnarinone did not induce ceramide generation, oxidative damage, or catalase depletion in HL-60/ves cells, where vesnarinone could not induce apoptosis.	Ceramides	3-11	catalase	Homo sapiens	235-243
11854443-8	2002	Taken together, the results suggest that vesnarinone induces myeloid cell apoptosis by increasing oxidative damage via ceramide-induced inhibition of catalase function.	Ceramides	119-127	catalase	Homo sapiens	150-158
11829762-0	2002	Ceramide and sphingosine have an antagonistic effect on the plasma-membrane Ca2+-ATPase from human erythrocytes.	Ceramides	0-8	ATPase plasma membrane Ca2+ transporting 2	Homo sapiens	60-87
11724785-0	2002	Dominant-negative suppression of HNF-1 alpha results in mitochondrial dysfunction, INS-1 cell apoptosis, and increased sensitivity to ceramide-, but not to high glucose-induced cell death.	Ceramides	134-142	HNF1 homeobox A	Rattus norvegicus	33-44
11724785-8	2002	In contrast, induction of DN-HNF-1 alpha highly sensitized cells to ceramide toxicity.	Ceramides	68-76	HNF1 homeobox A	Rattus norvegicus	29-40
11822871-5	2002	Moreover, expression of functional p53 protein using a temperature-sensitive human p53val(138) induced ceramide generation by activation of neutral SMase but not acid SMase through ROS formation.	Ceramides	103-111	tumor protein p53	Homo sapiens	35-38
11829762-9	2002	These results, taken together, suggest that ceramide and sphingosine act antagonistically on the plasma-membrane Ca(2+)-ATPase.	Ceramides	44-52	ATPase plasma membrane Ca2+ transporting 2	Homo sapiens	97-126
11822871-5	2002	Moreover, expression of functional p53 protein using a temperature-sensitive human p53val(138) induced ceramide generation by activation of neutral SMase but not acid SMase through ROS formation.	Ceramides	103-111	tumor protein p53	Homo sapiens	83-86
11830497-0	2002	Regulation of polymorphonuclear leukocyte degranulation and oxidant production by ceramide through inhibition of phospholipase D.	Ceramides	82-90	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	113-128
11830497-2	2002	Here it is postulated that increased PLD activity generating phosphatidic acid and diacylglycerol (DAG) is essential for superoxide release and degranulation and that ceramide, previously shown to be generated during PMN activation, inhibits PLD activation, thereby leading to inhibition of PMN function.	Ceramides	167-175	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	242-245
11707431-9	2002	We found that addition of ceramide analogs alone and additively with fatty acids decreased SRE expression and that ceramide analogs reduced levels of the transcriptionally active forms of SREBP-1 and SREBP-2.	Ceramides	115-123	sterol regulatory element binding transcription factor 1	Homo sapiens	188-195
11830497-9	2002	Ceramide may affect protein interactions with PLD in the plasma membrane, thereby attenuating PMN activation.	Ceramides	0-8	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	46-49
11707431-9	2002	We found that addition of ceramide analogs alone and additively with fatty acids decreased SRE expression and that ceramide analogs reduced levels of the transcriptionally active forms of SREBP-1 and SREBP-2.	Ceramides	115-123	sterol regulatory element binding transcription factor 2	Homo sapiens	200-207
11706024-0	2002	Ceramide generation in situ alters leukocyte cytoskeletal organization and beta 2-integrin function and causes complete degranulation.	Ceramides	0-8	potassium calcium-activated channel subfamily M regulatory beta subunit 2	Homo sapiens	75-81
18498489-4	2002	This study shows that this sphinganine-derived ceramide (i.e. C18-dhCer) binds to African-American hair and protects it from weakening caused by chemicals.	Ceramides	47-55	Bardet-Biedl syndrome 9	Homo sapiens	62-65
11830536-3	2002	CLN3 negatively modulates endogenous ceramide levels in NT2 cells and acts upstream of ceramide generation.	Ceramides	37-45	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
11830536-3	2002	CLN3 negatively modulates endogenous ceramide levels in NT2 cells and acts upstream of ceramide generation.	Ceramides	87-95	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
11733511-0	2002	Bile salt-stimulated carboxyl ester lipase influences lipoprotein assembly and secretion in intestine: a process mediated via ceramide hydrolysis.	Ceramides	126-134	carboxyl ester lipase	Mus musculus	21-42
11733511-8	2002	The proximal intestine of CEL(-/-) mice was also found to possess significantly less ceramide hydrolytic activity than that present in CEL(+/+) mice.	Ceramides	85-93	carboxyl ester lipase	Mus musculus	26-29
11733511-12	2002	The mechanism appears to be mediated through CEL hydrolysis of ceramide generated during the lipid absorption process.	Ceramides	63-71	carboxyl ester lipase	Mus musculus	45-48
11829492-9	2002	These histopathological findings in Asah1(+/-) animals correlated with an up to twofold increase in the ceramide content of these tissues and a reduction n AC activity, confirming that the gene insertion event disrupted AC activity and ceramide metabolism.	Ceramides	104-112	N-acylsphingosine amidohydrolase 1	Mus musculus	36-41
11829492-9	2002	These histopathological findings in Asah1(+/-) animals correlated with an up to twofold increase in the ceramide content of these tissues and a reduction n AC activity, confirming that the gene insertion event disrupted AC activity and ceramide metabolism.	Ceramides	236-244	N-acylsphingosine amidohydrolase 1	Mus musculus	36-41
11823712-3	2002	Using cellular models of ischemic tolerance, we have demonstrated that an effector of TNF-alpha-induced preconditioning is ceramide, a sphingolipid messenger in TNF-alpha signaling.	Ceramides	123-131	tumor necrosis factor	Homo sapiens	86-95
11723139-0	2002	Ceramide-induced inhibition of Akt is mediated through protein kinase Czeta: implications for growth arrest.	Ceramides	0-8	AKT serine/threonine kinase 1	Rattus norvegicus	31-34
11723139-0	2002	Ceramide-induced inhibition of Akt is mediated through protein kinase Czeta: implications for growth arrest.	Ceramides	0-8	protein kinase C, zeta	Rattus norvegicus	55-75
11723139-3	2002	Utilizing cultured A7r5 VSMCs, we have now examined the mechanism by which ceramide inhibits Akt phosphorylation/activation.	Ceramides	75-83	AKT serine/threonine kinase 1	Rattus norvegicus	93-96
11723139-4	2002	Our initial studies showed that ceramide-induced inhibition of Akt phosphorylation was not mediated through diminution in phosphoinositide 3-kinase activity.	Ceramides	32-40	AKT serine/threonine kinase 1	Rattus norvegicus	63-66
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	86-94	protein kinase C, zeta	Rattus norvegicus	40-60
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	86-94	protein kinase C, zeta	Rattus norvegicus	62-69
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	86-94	AKT serine/threonine kinase 1	Rattus norvegicus	183-186
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	86-94	protein kinase C, zeta	Rattus norvegicus	209-216
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	152-160	protein kinase C, zeta	Rattus norvegicus	40-60
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	152-160	protein kinase C, zeta	Rattus norvegicus	62-69
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	152-160	AKT serine/threonine kinase 1	Rattus norvegicus	183-186
11723139-5	2002	As we have previously demonstrated that protein kinase Czeta (PKCzeta) is a target of ceramide, we proposed an alternative signaling mechanism by which ceramide induces inhibition of Akt through activation of PKCzeta.	Ceramides	152-160	protein kinase C, zeta	Rattus norvegicus	209-216
11723139-7	2002	In addition, the ability of ceramide to significantly decrease platelet-derived growth factor-induced Akt phosphorylation or cell proliferation was abrogated in A7r5 cells overexpressing a dominant-negative mutant of PKCzeta.	Ceramides	28-36	AKT serine/threonine kinase 1	Rattus norvegicus	102-105
11823712-3	2002	Using cellular models of ischemic tolerance, we have demonstrated that an effector of TNF-alpha-induced preconditioning is ceramide, a sphingolipid messenger in TNF-alpha signaling.	Ceramides	123-131	tumor necrosis factor	Homo sapiens	161-170
11723139-7	2002	In addition, the ability of ceramide to significantly decrease platelet-derived growth factor-induced Akt phosphorylation or cell proliferation was abrogated in A7r5 cells overexpressing a dominant-negative mutant of PKCzeta.	Ceramides	28-36	protein kinase C, zeta	Rattus norvegicus	217-224
11723139-8	2002	Taken together, these data suggest that ceramide-mediated activation of PKCzeta leads to diminished Akt activation and consequent growth arrest in VSMCs.	Ceramides	40-48	protein kinase C, zeta	Rattus norvegicus	72-79
11723139-8	2002	Taken together, these data suggest that ceramide-mediated activation of PKCzeta leads to diminished Akt activation and consequent growth arrest in VSMCs.	Ceramides	40-48	AKT serine/threonine kinase 1	Rattus norvegicus	100-103
11823712-4	2002	TNF-alpha/ceramide-induced preconditioning protected cultured neurons against ischemic death and cultured astrocytes against proinflammatory effects of TNF-alpha.	Ceramides	10-18	tumor necrosis factor	Homo sapiens	0-9
11823712-4	2002	TNF-alpha/ceramide-induced preconditioning protected cultured neurons against ischemic death and cultured astrocytes against proinflammatory effects of TNF-alpha.	Ceramides	10-18	tumor necrosis factor	Homo sapiens	152-161
11841576-0	2002	Ceramide activates microglia to enhance the production/secretion of brain-derived neurotrophic factor (BDNF) without induction of deleterious factors in vitro.	Ceramides	0-8	brain derived neurotrophic factor	Homo sapiens	68-101
11841576-0	2002	Ceramide activates microglia to enhance the production/secretion of brain-derived neurotrophic factor (BDNF) without induction of deleterious factors in vitro.	Ceramides	0-8	brain derived neurotrophic factor	Homo sapiens	103-107
11841576-9	2002	These results indicate that ceramide-induced BDNF release in microglia is mediated by a signaling pathway associated with PKCdelta and/or epsilon, but not with activation of MAPKs, CREB and NFkappaB.	Ceramides	28-36	brain derived neurotrophic factor	Homo sapiens	45-49
11841576-9	2002	These results indicate that ceramide-induced BDNF release in microglia is mediated by a signaling pathway associated with PKCdelta and/or epsilon, but not with activation of MAPKs, CREB and NFkappaB.	Ceramides	28-36	protein kinase C delta	Homo sapiens	122-130
11929536-7	2002	PPH22 overexpression mimics overactive cAMP-PKA (protein kinase A) signalling and PP2A and Sit4 might represent ceramide signalling targets.	Ceramides	112-120	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	91-95
11706021-0	2002	Akt protein kinase inhibits non-apoptotic programmed cell death induced by ceramide.	Ceramides	75-83	AKT serine/threonine kinase 1	Homo sapiens	0-3
11706021-5	2002	Consistent with these characteristics, this ceramide-induced cell death was inhibited neither by the overexpression of Bcl-xL nor by the pan-caspase inhibitor zVAD-fmk.	Ceramides	44-52	BCL2 like 1	Homo sapiens	119-125
11706021-6	2002	However, strikingly, the ceramide-induced non-apoptotic cell death was inhibited by the activation of the Akt/protein kinase B pathway through the expression of a constitutively active version of Akt.	Ceramides	25-33	AKT serine/threonine kinase 1	Homo sapiens	106-109
11706021-6	2002	However, strikingly, the ceramide-induced non-apoptotic cell death was inhibited by the activation of the Akt/protein kinase B pathway through the expression of a constitutively active version of Akt.	Ceramides	25-33	protein tyrosine kinase 2 beta	Homo sapiens	110-126
11706021-6	2002	However, strikingly, the ceramide-induced non-apoptotic cell death was inhibited by the activation of the Akt/protein kinase B pathway through the expression of a constitutively active version of Akt.	Ceramides	25-33	AKT serine/threonine kinase 1	Homo sapiens	196-199
11786023-7	2002	In addition, our analysis of the chimeric proteins supports the model that Raf-1 is a ceramide-activated kinase and that its C1 domain is involved in the ceramide-mediated response.	Ceramides	86-94	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	75-80
11709549-0	2002	Death-associated protein (DAP) kinase plays a central role in ceramide-induced apoptosis in cultured hippocampal neurons.	Ceramides	62-70	death associated protein kinase 1	Mus musculus	0-37
11709549-3	2002	Upon incubation with C(6)-Cer, DAP kinase levels are elevated as early as 1 h after treatment, reaching levels 2-3-fold higher than untreated cells after 4 h. Neurons cultured from DAP kinase-deficient mice were significantly less sensitive to apoptosis induced by C(6)-Cer or by ceramide generated by high concentrations of nerve growth factor.	Ceramides	280-288	death associated protein kinase 1	Mus musculus	31-41
11709549-3	2002	Upon incubation with C(6)-Cer, DAP kinase levels are elevated as early as 1 h after treatment, reaching levels 2-3-fold higher than untreated cells after 4 h. Neurons cultured from DAP kinase-deficient mice were significantly less sensitive to apoptosis induced by C(6)-Cer or by ceramide generated by high concentrations of nerve growth factor.	Ceramides	280-288	death associated protein kinase 1	Mus musculus	181-191
11709549-5	2002	Together, these data demonstrate that DAP kinase plays a central role in ceramide-induced cell death in neurons, but the pathway in which DAP kinase is involved is not the only one via which ceramide can induce apoptosis.	Ceramides	73-81	death associated protein kinase 1	Mus musculus	38-48
11784307-2	2002	Here, we investigate the involvement of death-associated protein (DAP) kinase, initially identified as a positive mediator of the interferon-gamma-induced apoptosis of HeLa cells, in the C(2)-ceramide-induced apoptosis of PC12 cells.	Ceramides	192-200	interferon gamma	Homo sapiens	130-146
11821946-0	2002	Low glucose-enhanced TRAIL cytotoxicity is mediated through the ceramide-Akt-FLIP pathway.	Ceramides	64-72	TNF superfamily member 10	Homo sapiens	21-26
11821946-0	2002	Low glucose-enhanced TRAIL cytotoxicity is mediated through the ceramide-Akt-FLIP pathway.	Ceramides	64-72	AKT serine/threonine kinase 1	Homo sapiens	73-76
11821946-7	2002	The elevation of ceramide may cause dephosphorylation of Akt and maintain dephosphorylation of Akt in the presence of TRAIL and then subsequently down-regulate the expression of FLIP.	Ceramides	17-25	AKT serine/threonine kinase 1	Homo sapiens	57-60
11821946-7	2002	The elevation of ceramide may cause dephosphorylation of Akt and maintain dephosphorylation of Akt in the presence of TRAIL and then subsequently down-regulate the expression of FLIP.	Ceramides	17-25	AKT serine/threonine kinase 1	Homo sapiens	95-98
11821946-7	2002	The elevation of ceramide may cause dephosphorylation of Akt and maintain dephosphorylation of Akt in the presence of TRAIL and then subsequently down-regulate the expression of FLIP.	Ceramides	17-25	TNF superfamily member 10	Homo sapiens	118-123
11821946-8	2002	Taken together, the present studies suggest that glucose deprivation enhances TRAIL-induced cytotoxicity through the ceramide-Akt-FLIP pathway.	Ceramides	117-125	TNF superfamily member 10	Homo sapiens	78-83
11821946-8	2002	Taken together, the present studies suggest that glucose deprivation enhances TRAIL-induced cytotoxicity through the ceramide-Akt-FLIP pathway.	Ceramides	117-125	AKT serine/threonine kinase 1	Homo sapiens	126-129
11751589-0	2002	Ceramide and glucosamine antagonism of alternate signaling pathways regulating insulin- and osmotic shock-induced glucose transporter 4 translocation.	Ceramides	0-8	insulin	Homo sapiens	79-86
11751589-0	2002	Ceramide and glucosamine antagonism of alternate signaling pathways regulating insulin- and osmotic shock-induced glucose transporter 4 translocation.	Ceramides	0-8	solute carrier family 2 member 4	Homo sapiens	114-135
11751589-3	2002	In this study we assessed whether ceramide and/or glucosamine, two known insulin-signaling antagonists, also affected the PI3K/Akt-independent signal.	Ceramides	34-42	insulin	Homo sapiens	73-80
11751589-3	2002	In this study we assessed whether ceramide and/or glucosamine, two known insulin-signaling antagonists, also affected the PI3K/Akt-independent signal.	Ceramides	34-42	AKT serine/threonine kinase 1	Homo sapiens	127-130
11751974-0	2002	Ceramide-rich membrane rafts mediate CD40 clustering.	Ceramides	0-8	CD40 molecule	Homo sapiens	37-41
11835403-1	2002	We have demonstrated previously that IGFBP-5 can confer survival against apoptosis induced by ceramide, C2, or a small synthetic arginine-glycine-aspartic acid (RGD)-containing peptide in a direct manner.	Ceramides	94-102	insulin like growth factor binding protein 5	Homo sapiens	37-44
11835403-12	2002	These data suggest that IGFBP-5 promotes the attachment and survival of Hs578T cells by modulating the balance between ceramide and opposing survival signals.	Ceramides	119-127	insulin like growth factor binding protein 5	Homo sapiens	24-31
11751974-6	2002	Deficiency of ASM, destruction of sphingolipid-rich rafts, or neutralization of surface ceramide prevents CD40 clustering and CD40-initiated cell signaling.	Ceramides	88-96	CD40 molecule	Homo sapiens	106-110
11751974-6	2002	Deficiency of ASM, destruction of sphingolipid-rich rafts, or neutralization of surface ceramide prevents CD40 clustering and CD40-initiated cell signaling.	Ceramides	88-96	CD40 molecule	Homo sapiens	126-130
11751974-4	2002	Surface ASM initiates a release of extracellularly oriented ceramide, which in turn mediates CD40 clustering in sphingolipid-rich membrane domains.	Ceramides	60-68	sphingomyelin phosphodiesterase 1	Homo sapiens	8-11
11751974-7	2002	These findings indicate that the ASM-mediated release of ceramide and/or metabolites of ceramide regulate clustering of CD40, which seems to be a prerequisite for cellular activation via CD40.	Ceramides	57-65	sphingomyelin phosphodiesterase 1	Homo sapiens	33-36
11751974-7	2002	These findings indicate that the ASM-mediated release of ceramide and/or metabolites of ceramide regulate clustering of CD40, which seems to be a prerequisite for cellular activation via CD40.	Ceramides	57-65	CD40 molecule	Homo sapiens	120-124
11751974-4	2002	Surface ASM initiates a release of extracellularly oriented ceramide, which in turn mediates CD40 clustering in sphingolipid-rich membrane domains.	Ceramides	60-68	CD40 molecule	Homo sapiens	93-97
11751974-7	2002	These findings indicate that the ASM-mediated release of ceramide and/or metabolites of ceramide regulate clustering of CD40, which seems to be a prerequisite for cellular activation via CD40.	Ceramides	57-65	CD40 molecule	Homo sapiens	187-191
12037984-0	2002	Acid sphingomyelinase-derived ceramide signaling in apoptosis.	Ceramides	30-38	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
11751974-7	2002	These findings indicate that the ASM-mediated release of ceramide and/or metabolites of ceramide regulate clustering of CD40, which seems to be a prerequisite for cellular activation via CD40.	Ceramides	88-96	sphingomyelin phosphodiesterase 1	Homo sapiens	33-36
11751974-7	2002	These findings indicate that the ASM-mediated release of ceramide and/or metabolites of ceramide regulate clustering of CD40, which seems to be a prerequisite for cellular activation via CD40.	Ceramides	88-96	CD40 molecule	Homo sapiens	120-124
11751974-7	2002	These findings indicate that the ASM-mediated release of ceramide and/or metabolites of ceramide regulate clustering of CD40, which seems to be a prerequisite for cellular activation via CD40.	Ceramides	88-96	CD40 molecule	Homo sapiens	187-191
12241073-2	2002	Direct effects of ceramide on mitochondria (cytochrome c release, respiratory chain inhibition, oxygen radicals production...) have been reported [1, 2] and we previously showed that addition of ceramide to intact cells or isolated mitochondria triggers mitochondrial swelling which appeared to be insensitive to cyclosporin A (CsA) [3, 4].	Ceramides	18-26	cytochrome c, somatic	Homo sapiens	44-56
12241073-2	2002	Direct effects of ceramide on mitochondria (cytochrome c release, respiratory chain inhibition, oxygen radicals production...) have been reported [1, 2] and we previously showed that addition of ceramide to intact cells or isolated mitochondria triggers mitochondrial swelling which appeared to be insensitive to cyclosporin A (CsA) [3, 4].	Ceramides	195-203	cytochrome c, somatic	Homo sapiens	44-56
12453482-9	2002	P75NTR signaling independent of TrkA, such as increased neutral sphingomyelinase (NSMase) activity causing enhanced levels of ceramide, were not detected after exposure of hippocampal neurons to NGF.	Ceramides	126-134	nerve growth factor receptor (TNFR superfamily, member 16)	Mus musculus	0-6
12453482-9	2002	P75NTR signaling independent of TrkA, such as increased neutral sphingomyelinase (NSMase) activity causing enhanced levels of ceramide, were not detected after exposure of hippocampal neurons to NGF.	Ceramides	126-134	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	56-80
12453482-9	2002	P75NTR signaling independent of TrkA, such as increased neutral sphingomyelinase (NSMase) activity causing enhanced levels of ceramide, were not detected after exposure of hippocampal neurons to NGF.	Ceramides	126-134	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	82-88
12219934-9	2002	The actions of TNF-alpha could be only partially mimicked by a cell-permeable analogue of ceramide, thus indicating that actions of this cytokine can not be fully ascribed to an activation of sphingomyelinase.	Ceramides	90-98	tumor necrosis factor	Rattus norvegicus	15-24
12467215-0	2002	P-glycoprotein modulates ceramide-mediated sensitivity of human breast cancer cells to tubulin-binding anticancer drugs.	Ceramides	25-33	ATP binding cassette subfamily B member 1	Homo sapiens	0-14
11675379-10	2001	PD98059, a specific inhibitor of the ERK-activating kinase MEK-1, abolished the TNF-alpha-induced ERK phosphorylation and osteoclast survival, and in these responses the involvement of Grb2 and ceramide was observed.	Ceramides	194-202	mitogen-activated protein kinase 1	Homo sapiens	37-40
11675379-10	2001	PD98059, a specific inhibitor of the ERK-activating kinase MEK-1, abolished the TNF-alpha-induced ERK phosphorylation and osteoclast survival, and in these responses the involvement of Grb2 and ceramide was observed.	Ceramides	194-202	mitogen-activated protein kinase kinase 1	Homo sapiens	59-64
11675379-10	2001	PD98059, a specific inhibitor of the ERK-activating kinase MEK-1, abolished the TNF-alpha-induced ERK phosphorylation and osteoclast survival, and in these responses the involvement of Grb2 and ceramide was observed.	Ceramides	194-202	tumor necrosis factor	Homo sapiens	80-89
11775008-2	2001	Our objective was to evaluate interleukin (IL)-1alpha-induced production of PGE2 and PGF2alpha in endometrial stromal cells (ESC) following treatment with ceramide analogues.	Ceramides	155-163	interleukin 1 alpha	Homo sapiens	30-53
11709400-10	2001	We also consider the recently reported interaction between ANG II and ceramide, a lipid second messenger that mediates cytokine receptor activation.	Ceramides	70-78	angiotensinogen	Homo sapiens	59-65
11775008-13	2001	CONCLUSIONS: These results suggest that IL-1alpha stimulates the production of PGE2 and PGF2alpha by a mechanism that involves the sphingomyelin-ceramide system, and thus that ceramide may be important in increasing the production of PGE2 and PGF2alpha in the human endometrium.	Ceramides	145-153	interleukin 1 alpha	Homo sapiens	40-49
11775008-13	2001	CONCLUSIONS: These results suggest that IL-1alpha stimulates the production of PGE2 and PGF2alpha by a mechanism that involves the sphingomyelin-ceramide system, and thus that ceramide may be important in increasing the production of PGE2 and PGF2alpha in the human endometrium.	Ceramides	176-184	interleukin 1 alpha	Homo sapiens	40-49
11746763-0	2001	Nerve growth factor signaling of p75 induces differentiation and ceramide-mediated apoptosis in Schwann cells cultured from degenerating nerves.	Ceramides	65-73	nerve growth factor	Homo sapiens	0-19
12030784-3	2001	It has also been shown that decreased levels of endogenous ceramide by over-expression of glucosylceramide synthase, which clears ceramide levels by incorporating it into glucosylceramide, results in the development of a multidrug resistant phenotype in cancer cells.	Ceramides	59-67	UDP-glucose ceramide glucosyltransferase	Homo sapiens	90-115
11579085-5	2001	The substitution of Ser(308) to alanine, which mimics the ceramide-induced dephosphorylation at this site, increases Ca(2+)/CaM-independent substrate phosphorylation as well as binding and overall sensitivity of the kinase to CaM.	Ceramides	58-66	calmodulin 1	Homo sapiens	124-127
11579085-5	2001	The substitution of Ser(308) to alanine, which mimics the ceramide-induced dephosphorylation at this site, increases Ca(2+)/CaM-independent substrate phosphorylation as well as binding and overall sensitivity of the kinase to CaM.	Ceramides	58-66	calmodulin 1	Homo sapiens	226-229
11717138-0	2001	Interleukin 1 upregulates ovarian prostaglandin endoperoxide synthase-2 expression: evidence for prostaglandin-dependent/ceramide-independent transcriptional stimulation and for message stabilization.	Ceramides	121-129	interleukin 1 alpha	Homo sapiens	0-13
11717138-0	2001	Interleukin 1 upregulates ovarian prostaglandin endoperoxide synthase-2 expression: evidence for prostaglandin-dependent/ceramide-independent transcriptional stimulation and for message stabilization.	Ceramides	121-129	prostaglandin-endoperoxide synthase 2	Homo sapiens	34-71
11717138-9	2001	Taken together, these findings suggest that the stimulatory effect of IL-1beta on PGS-2 expression is 1) independent of nitric oxide as well as ceramide, 2) dependent on prostaglandin E(2), 3) contingent on de novo protein biosynthesis, and 4) accounted for by both increased transcription and message stabilization.	Ceramides	144-152	interleukin 1 beta	Homo sapiens	70-78
11751455-4	2001	TIAM1 cleavage occurs in multiple cell lines in response to diverse apoptotic stimuli such as ceramide, Fas, and serum deprivation.	Ceramides	94-102	TIAM Rac1 associated GEF 1	Homo sapiens	0-5
11751455-8	2001	Finally, we demonstrate that in cells treated with ceramide, cleavage of TIAM1 coincided with the inactivation of endogenous Rac.	Ceramides	51-59	TIAM Rac1 associated GEF 1	Homo sapiens	73-78
11751455-8	2001	Finally, we demonstrate that in cells treated with ceramide, cleavage of TIAM1 coincided with the inactivation of endogenous Rac.	Ceramides	51-59	AKT serine/threonine kinase 1	Homo sapiens	125-128
11746763-0	2001	Nerve growth factor signaling of p75 induces differentiation and ceramide-mediated apoptosis in Schwann cells cultured from degenerating nerves.	Ceramides	65-73	PC4 and SFRS1 interacting protein 1	Homo sapiens	33-36
11746763-7	2001	In this article, we report that p75(NTR), the low-affinity receptor for all members of neurotrophins, signals both cell differentiation and apoptosis through intracellular ceramide elevation.	Ceramides	172-180	PC4 and SFRS1 interacting protein 1	Homo sapiens	32-35
11746763-7	2001	In this article, we report that p75(NTR), the low-affinity receptor for all members of neurotrophins, signals both cell differentiation and apoptosis through intracellular ceramide elevation.	Ceramides	172-180	neurotensin receptor 1	Homo sapiens	36-39
11746763-8	2001	The final response is dependent on the intracellular ceramide level and Schwann cells modulate their response by changing expression level of p75(NTR).	Ceramides	53-61	PC4 and SFRS1 interacting protein 1	Homo sapiens	142-145
11746763-8	2001	The final response is dependent on the intracellular ceramide level and Schwann cells modulate their response by changing expression level of p75(NTR).	Ceramides	53-61	neurotensin receptor 1	Homo sapiens	146-149
11820739-0	2001	Distinct apoptotic phenotypes induced by radiation and ceramide in both p53-wild-type and p53-mutated lymphoblastoid cells.	Ceramides	55-63	tumor protein p53	Homo sapiens	72-75
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.	Ceramides	26-34	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.	Ceramides	26-34	glucosidase, beta, acid	Mus musculus	151-154
11574545-10	2001	BCG-enhanced calcium influx and the presence of insulin-like growth factor-1 may thus activate a cell survival mechanism that selectively protects developing neurons against ceramide-induced apoptosis by up-regulation of MAPK and reduction of PAR-4 expression.	Ceramides	174-182	insulin-like growth factor 1	Mus musculus	48-76
11746831-7	2001	Moreover, a permeable ceramide was effective in inducing apoptosis in both HL-60 and HL-525 cells, and this induction was caspase-1 and/or -4 dependent because an inhibitor of these caspases abrogated the induced apoptosis.	Ceramides	22-30	caspase 1	Homo sapiens	122-141
11746831-7	2001	Moreover, a permeable ceramide was effective in inducing apoptosis in both HL-60 and HL-525 cells, and this induction was caspase-1 and/or -4 dependent because an inhibitor of these caspases abrogated the induced apoptosis.	Ceramides	22-30	caspase 1	Homo sapiens	182-190
11820739-0	2001	Distinct apoptotic phenotypes induced by radiation and ceramide in both p53-wild-type and p53-mutated lymphoblastoid cells.	Ceramides	55-63	tumor protein p53	Homo sapiens	90-93
11820739-6	2001	Radiation-induced apoptosis is p53-dependent and ceramide-induced apoptosis is p53-independent.	Ceramides	49-57	tumor protein p53	Homo sapiens	79-82
11820739-8	2001	Since p53 is very often dysfunctional in tumour cells, modifying the ceramide pathway is a promising strategy to increase tumour sensitivity to radiation and other anticancer agents.	Ceramides	69-77	tumor protein p53	Homo sapiens	6-9
11698477-0	2001	Ceramide regulates lipopolysaccharide-induced phosphatidylinositol 3-kinase and Akt activity in human alveolar macrophages.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	80-83
12549215-2	2001	Ceramide is generated in response to a number of extracellular inducers(for example: TNF, IL-1 and Fas ligands etc.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	85-88
12549215-5	2001	It has been reported that the C6 ceramide can induce senescence of WI-38 HDF and promote the activity of beta-galactosidase, but, C2 ceramide has no such effect.	Ceramides	33-41	galactosidase beta 1	Homo sapiens	105-123
12549215-7	2001	10 mumol/ml of C6 ceramide treatment for more than 72 hours can induce morphological alterations (such as: enlarged, flattened and irregular cell body), cell cycle arrested at G1 phase and the expression of the senescent histochemical marker-beta-galactosidase in HUVECs.	Ceramides	18-26	galactosidase beta 1	Homo sapiens	242-260
11695990-7	2001	Overexpression of zebrafish caspase-3 induced apoptosis and increased ceramide levels in fish fathead minnow tailbud cells and zebrafish embryos.	Ceramides	70-78	caspase 3, apoptosis-related cysteine peptidase a	Danio rerio	28-37
11695990-10	2001	These findings indicate that the isolated caspase-3 plays an important role in the induction of ceramide generation as well as apoptosis in fish cells and the zebrafish embryo, and suggest that caspase-3 functions as a modulator of the pro-apoptotic signal in development.	Ceramides	96-104	caspase 3, apoptosis-related cysteine peptidase a	Danio rerio	42-51
11695990-10	2001	These findings indicate that the isolated caspase-3 plays an important role in the induction of ceramide generation as well as apoptosis in fish cells and the zebrafish embryo, and suggest that caspase-3 functions as a modulator of the pro-apoptotic signal in development.	Ceramides	96-104	caspase 3, apoptosis-related cysteine peptidase a	Danio rerio	194-203
11697858-0	2001	Ceramide accelerates dephosphorylation of extracellular signal-regulated kinase 1/2 to decrease prostaglandin D(2) production in RBL-2H3 cells.	Ceramides	0-8	mitogen activated protein kinase 3	Rattus norvegicus	42-81
11697858-1	2001	In the present study, the effect of ceramide on antigen-stimulated phosphorylation of extracellular signal-regulated kinase (ERK) in the mechanism responsible for regulating production of prostaglandin (PG) D(2) was investigated in the mast cell line, RBL-2H3 cells.	Ceramides	36-44	Eph receptor B1	Rattus norvegicus	86-123
11697858-1	2001	In the present study, the effect of ceramide on antigen-stimulated phosphorylation of extracellular signal-regulated kinase (ERK) in the mechanism responsible for regulating production of prostaglandin (PG) D(2) was investigated in the mast cell line, RBL-2H3 cells.	Ceramides	36-44	Eph receptor B1	Rattus norvegicus	125-128
11697858-3	2001	Ceramide also inhibited production of PGD(2) and an increase in the activity of cytosolic phospholipase A(2) (cPLA(2)), whereas it did not influence the tyrosine phosphorylation of major cellular proteins in response to antigen.	Ceramides	0-8	phospholipase A2 group IVA	Rattus norvegicus	80-117
11697858-4	2001	The ceramide-induced inhibition of ERK1/2 phosphorylation and of cPLA(2) activation was suppressed by orthovanadate, a tyrosine phosphatase inhibitor, but not by okadaic acid, a serine/threonine phosphatase inhibitor.	Ceramides	4-12	mitogen activated protein kinase 3	Rattus norvegicus	35-41
11697858-4	2001	The ceramide-induced inhibition of ERK1/2 phosphorylation and of cPLA(2) activation was suppressed by orthovanadate, a tyrosine phosphatase inhibitor, but not by okadaic acid, a serine/threonine phosphatase inhibitor.	Ceramides	4-12	phospholipase A2 group IVA	Rattus norvegicus	65-72
11697858-5	2001	Addition of ceramide to the lysate prepared from antigen-stimulated cells reduced the phosphorylated ERK1/2, and orthovanadate effectively prevented the reduction.	Ceramides	12-20	mitogen activated protein kinase 3	Rattus norvegicus	101-107
11697858-6	2001	These results suggest that ceramide accelerates the dephosphorylation of phosphorylated ERK1/2 via activation of a protein tyrosine phosphatase, thus preventing activation of cPLA(2) and production of PGD(2).	Ceramides	27-35	mitogen activated protein kinase 3	Rattus norvegicus	88-94
11697858-6	2001	These results suggest that ceramide accelerates the dephosphorylation of phosphorylated ERK1/2 via activation of a protein tyrosine phosphatase, thus preventing activation of cPLA(2) and production of PGD(2).	Ceramides	27-35	phospholipase A2 group IVA	Rattus norvegicus	175-182
11698477-5	2001	We found that ceramide exposure activated PI 3-kinase and Akt.	Ceramides	14-22	peptidase inhibitor 3	Homo sapiens	42-46
11698477-5	2001	We found that ceramide exposure activated PI 3-kinase and Akt.	Ceramides	14-22	AKT serine/threonine kinase 1	Homo sapiens	58-61
11698477-6	2001	When we blocked LPS-induced ceramide with the inhibitor D609, we blocked LPS-induced PI 3-kinase and Akt activation.	Ceramides	28-36	peptidase inhibitor 3	Homo sapiens	85-89
11698477-6	2001	When we blocked LPS-induced ceramide with the inhibitor D609, we blocked LPS-induced PI 3-kinase and Akt activation.	Ceramides	28-36	AKT serine/threonine kinase 1	Homo sapiens	101-104
11698477-7	2001	Evaluating cell survival after ceramide or LPS exposure, we found that blocking PI 3-kinase induced a significant increase in cell death.	Ceramides	31-39	peptidase inhibitor 3	Homo sapiens	80-84
11698477-9	2001	We found that LPS, to a greater degree than ceramide, induced NF-kappaB translocation to the nucleus.	Ceramides	44-52	nuclear factor kappa B subunit 1	Homo sapiens	62-71
11698477-11	2001	We believe that LPS induction of ceramide results in PI 3-kinase activation and represents a novel effector mechanism that promotes survival of human alveolar macrophages in the setting of pulmonary sepsis.	Ceramides	33-41	peptidase inhibitor 3	Homo sapiens	53-57
11679435-0	2001	Ceramide mediates insulin resistance by tumor necrosis factor-alpha in brown adipocytes by maintaining Akt in an inactive dephosphorylated state.	Ceramides	0-8	insulin	Homo sapiens	18-25
11838965-1	2001	Globotriaosyl ceramide or CD77 functions as a cell surface receptor for toxins of the Shiga toxin/verotoxin family and as a marker for germinal center stage B-cells.	Ceramides	14-22	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	26-30
11668037-1	2001	Transforming growth factor-beta (TGF-beta)-activated kinase 1 (TAK1), a serine/threonine kinase, is reported to function in the signaling pathways of TGF-beta, interleukin 1, and ceramide.	Ceramides	179-187	mitogen activated protein kinase kinase kinase 7	Rattus norvegicus	63-67
11916364-5	2001	Most prominent are: 1) Tyrosine kinase receptors (TRK) induced signaling involving stress or mitogen activated protein kinases (SAPK/MARK) and sphingolipids metabolites (ceramide); 2) G-protein coupled receptor (GPCR) signaling (Galphai, Galphaq) and 3) NF(K) B activation.	Ceramides	170-178	C-X-C motif chemokine receptor 6	Homo sapiens	184-210
11916364-5	2001	Most prominent are: 1) Tyrosine kinase receptors (TRK) induced signaling involving stress or mitogen activated protein kinases (SAPK/MARK) and sphingolipids metabolites (ceramide); 2) G-protein coupled receptor (GPCR) signaling (Galphai, Galphaq) and 3) NF(K) B activation.	Ceramides	170-178	C-X-C motif chemokine receptor 6	Homo sapiens	212-216
11916364-5	2001	Most prominent are: 1) Tyrosine kinase receptors (TRK) induced signaling involving stress or mitogen activated protein kinases (SAPK/MARK) and sphingolipids metabolites (ceramide); 2) G-protein coupled receptor (GPCR) signaling (Galphai, Galphaq) and 3) NF(K) B activation.	Ceramides	170-178	G protein subunit alpha q	Homo sapiens	229-252
11679435-8	2001	Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state.	Ceramides	26-34	tumor necrosis factor	Homo sapiens	47-56
11679435-0	2001	Ceramide mediates insulin resistance by tumor necrosis factor-alpha in brown adipocytes by maintaining Akt in an inactive dephosphorylated state.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	103-106
11679435-8	2001	Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state.	Ceramides	26-34	insulin	Homo sapiens	65-72
11679435-8	2001	Our results indicate that ceramide produced by TNF-alpha induces insulin resistance in brown adipocytes by maintaining Akt in an inactive dephosphorylated state.	Ceramides	26-34	AKT serine/threonine kinase 1	Homo sapiens	119-122
11679435-2	2001	We explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, given that TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	97-105	tumor necrosis factor	Homo sapiens	48-57
11679435-2	2001	We explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, given that TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	97-105	tumor necrosis factor	Homo sapiens	118-127
11679435-2	2001	We explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, given that TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	164-172	tumor necrosis factor	Homo sapiens	48-57
11679435-2	2001	We explored the hypothesis that some effects of TNF-alpha could be mediated by the generation of ceramide, given that TNF-alpha treatment induced the production of ceramide in these primary cells.	Ceramides	164-172	tumor necrosis factor	Homo sapiens	118-127
11679435-3	2001	A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4.	Ceramides	14-22	insulin	Homo sapiens	65-72
11679435-3	2001	A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4.	Ceramides	14-22	insulin	Homo sapiens	103-110
11679435-3	2001	A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4.	Ceramides	14-22	solute carrier family 2 member 4	Homo sapiens	119-124
11679435-3	2001	A short-chain ceramide analog, C2-ceramide, completely precluded insulin-stimulated glucose uptake and insulin-induced GLUT4 translocation to plasma membrane, as determined by Western blot or immunofluorescent localization of GLUT4.	Ceramides	14-22	solute carrier family 2 member 4	Homo sapiens	226-231
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.	Ceramides	25-33	beta-1,3-galactosyltransferase 4	Homo sapiens	164-170
11689465-0	2001	Ceramide inhibition of NF-kappaB activation involves reverse translocation of classical protein kinase C (PKC) isoenzymes: requirement for kinase activity and carboxyl-terminal phosphorylation of PKC for the ceramide response.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	23-32
11689465-0	2001	Ceramide inhibition of NF-kappaB activation involves reverse translocation of classical protein kinase C (PKC) isoenzymes: requirement for kinase activity and carboxyl-terminal phosphorylation of PKC for the ceramide response.	Ceramides	0-8	proline rich transmembrane protein 2	Homo sapiens	88-104
11689465-0	2001	Ceramide inhibition of NF-kappaB activation involves reverse translocation of classical protein kinase C (PKC) isoenzymes: requirement for kinase activity and carboxyl-terminal phosphorylation of PKC for the ceramide response.	Ceramides	0-8	proline rich transmembrane protein 2	Homo sapiens	106-109
11689465-0	2001	Ceramide inhibition of NF-kappaB activation involves reverse translocation of classical protein kinase C (PKC) isoenzymes: requirement for kinase activity and carboxyl-terminal phosphorylation of PKC for the ceramide response.	Ceramides	0-8	proline rich transmembrane protein 2	Homo sapiens	196-199
11689465-0	2001	Ceramide inhibition of NF-kappaB activation involves reverse translocation of classical protein kinase C (PKC) isoenzymes: requirement for kinase activity and carboxyl-terminal phosphorylation of PKC for the ceramide response.	Ceramides	208-216	nuclear factor kappa B subunit 1	Homo sapiens	23-32
11689465-0	2001	Ceramide inhibition of NF-kappaB activation involves reverse translocation of classical protein kinase C (PKC) isoenzymes: requirement for kinase activity and carboxyl-terminal phosphorylation of PKC for the ceramide response.	Ceramides	208-216	proline rich transmembrane protein 2	Homo sapiens	106-109
11689465-0	2001	Ceramide inhibition of NF-kappaB activation involves reverse translocation of classical protein kinase C (PKC) isoenzymes: requirement for kinase activity and carboxyl-terminal phosphorylation of PKC for the ceramide response.	Ceramides	208-216	proline rich transmembrane protein 2	Homo sapiens	196-199
11689465-3	2001	Both exogenous and endogenous ceramide inhibited selectively PKC-mediated activation of NF-kappaB by reverting PKC translocation to the membrane.	Ceramides	30-38	proline rich transmembrane protein 2	Homo sapiens	61-64
11689465-3	2001	Both exogenous and endogenous ceramide inhibited selectively PKC-mediated activation of NF-kappaB by reverting PKC translocation to the membrane.	Ceramides	30-38	nuclear factor kappa B subunit 1	Homo sapiens	88-97
11689465-3	2001	Both exogenous and endogenous ceramide inhibited selectively PKC-mediated activation of NF-kappaB by reverting PKC translocation to the membrane.	Ceramides	30-38	proline rich transmembrane protein 2	Homo sapiens	111-114
11689465-4	2001	Next, confocal and immunofluorescence studies were performed to evaluate the direct effects of ceramide on PKC.	Ceramides	95-103	proline rich transmembrane protein 2	Homo sapiens	107-110
11689465-6	2001	A mutant PKC in which autophosphorylation sites were mutated to alanine (PKC-DA) was resistant to ceramide.	Ceramides	98-106	proline rich transmembrane protein 2	Homo sapiens	9-12
11689465-6	2001	A mutant PKC in which autophosphorylation sites were mutated to alanine (PKC-DA) was resistant to ceramide.	Ceramides	98-106	proline rich transmembrane protein 2	Homo sapiens	73-76
11689465-7	2001	A kinase-inactive mutant (PKC-KR) was also resistant to ceramide action, and the results were supported using kinase inhibitors of the enzyme.	Ceramides	56-64	proline rich transmembrane protein 2	Homo sapiens	26-29
11689465-8	2001	Finally, overexpression of PKC-DA prevented, at least partly, the ability of ceramide to inhibit activation of NF-kappaB.	Ceramides	77-85	proline rich transmembrane protein 2	Homo sapiens	27-30
11689465-8	2001	Finally, overexpression of PKC-DA prevented, at least partly, the ability of ceramide to inhibit activation of NF-kappaB.	Ceramides	77-85	nuclear factor kappa B subunit 1	Homo sapiens	111-120
11689465-9	2001	Taken together, these studies show that ceramide has acute effects on translocation of PKC by inducing reverse translocation, and this reversal requires both the kinase activity of PKC and phosphorylation of the autophosphorylation sites.	Ceramides	40-48	proline rich transmembrane protein 2	Homo sapiens	87-90
11689465-9	2001	Taken together, these studies show that ceramide has acute effects on translocation of PKC by inducing reverse translocation, and this reversal requires both the kinase activity of PKC and phosphorylation of the autophosphorylation sites.	Ceramides	40-48	proline rich transmembrane protein 2	Homo sapiens	181-184
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.	Ceramides	25-33	UDP-glucose ceramide glucosyltransferase	Homo sapiens	44-50
11694593-9	2001	Our results demonstrate that stimulation by TNF-alpha, which increases sphingomyelinase activity and ceramide formation, activates sphingosine kinase, Rho family GTPases, focal adhesion kinase, and paxillin.	Ceramides	101-109	tumor necrosis factor	Homo sapiens	44-53
11694577-5	2001	The sphingolipid synthesis defect in lag1 Delta lac1 Delta cells can be partially corrected by overexpression of YPC1 or YDC1, encoding ceramidases that have been reported to have acyl-CoA-independent ceramide synthesis activity.	Ceramides	201-209	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	37-41
11694577-5	2001	The sphingolipid synthesis defect in lag1 Delta lac1 Delta cells can be partially corrected by overexpression of YPC1 or YDC1, encoding ceramidases that have been reported to have acyl-CoA-independent ceramide synthesis activity.	Ceramides	201-209	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	48-52
11694593-9	2001	Our results demonstrate that stimulation by TNF-alpha, which increases sphingomyelinase activity and ceramide formation, activates sphingosine kinase, Rho family GTPases, focal adhesion kinase, and paxillin.	Ceramides	101-109	paxillin	Homo sapiens	198-206
11694577-5	2001	The sphingolipid synthesis defect in lag1 Delta lac1 Delta cells can be partially corrected by overexpression of YPC1 or YDC1, encoding ceramidases that have been reported to have acyl-CoA-independent ceramide synthesis activity.	Ceramides	201-209	phytoceramidase	Saccharomyces cerevisiae S288C	113-117
11694577-5	2001	The sphingolipid synthesis defect in lag1 Delta lac1 Delta cells can be partially corrected by overexpression of YPC1 or YDC1, encoding ceramidases that have been reported to have acyl-CoA-independent ceramide synthesis activity.	Ceramides	201-209	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	121-125
11694577-7	2001	Moreover, lag1 Delta lac1 Delta cells are resistant to aureobasidin A, an inhibitor of the inositolphosphorylceramide synthase, suggesting that aureobasidin A may be toxic because it leads to increased ceramide levels.	Ceramides	109-117	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	10-14
11694593-10	2001	This novel pathway of ceramide signaling can account for approximately 70% of TNF-alpha-induced stress fiber formation and cytoskeletal reorganization.	Ceramides	22-30	tumor necrosis factor	Homo sapiens	78-87
11597127-0	2001	TNFalpha enhances the DNA single-strand breakage induced by the short-chain lipid hydroperoxide analogue tert-butylhydroperoxide via ceramide-dependent inhibition of complex III followed by enforced superoxide and hydrogen peroxide formation.	Ceramides	133-141	tumor necrosis factor	Homo sapiens	0-8
11694577-7	2001	Moreover, lag1 Delta lac1 Delta cells are resistant to aureobasidin A, an inhibitor of the inositolphosphorylceramide synthase, suggesting that aureobasidin A may be toxic because it leads to increased ceramide levels.	Ceramides	109-117	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	21-25
11694593-0	2001	Tumor necrosis factor-alpha induces stress fiber formation through ceramide production: role of sphingosine kinase.	Ceramides	67-75	tumor necrosis factor	Homo sapiens	0-27
11694593-2	2001	We determined the extent to which ceramide is a second messenger for TNF-alpha-induced signaling leading to cytoskeletal rearrangement in Rat2 fibroblasts.	Ceramides	34-42	tumor necrosis factor	Homo sapiens	69-78
11694603-7	2001	With the addition of S1P with NOE and MAPP as well as with ceramide, treatments reduced the apoptotic response by 30 and 35%, respectively; whereas the addition of S1P with the DMS only and ceramide with DMS treatments reduced the apoptotic response by 60 and 70%, respectively.	Ceramides	190-198	sphingosine-1-phosphate receptor 1	Mus musculus	21-24
11694603-8	2001	Studies using labeled ceramide demonstrated ceramide was metabolized to S1P.	Ceramides	22-30	sphingosine-1-phosphate receptor 1	Mus musculus	72-75
11694603-8	2001	Studies using labeled ceramide demonstrated ceramide was metabolized to S1P.	Ceramides	44-52	sphingosine-1-phosphate receptor 1	Mus musculus	72-75
11597127-3	2001	The TNFalpha-dependent inhibition of complex III appears to be mediated by ceramide.	Ceramides	75-83	tumor necrosis factor	Homo sapiens	4-12
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	79-87	tumor necrosis factor	Homo sapiens	127-135
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	79-87	tumor necrosis factor	Homo sapiens	141-149
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	79-87	tumor necrosis factor	Homo sapiens	141-149
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	176-184	tumor necrosis factor	Homo sapiens	127-135
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	176-184	tumor necrosis factor	Homo sapiens	141-149
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	176-184	tumor necrosis factor	Homo sapiens	141-149
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	176-184	tumor necrosis factor	Homo sapiens	127-135
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	176-184	tumor necrosis factor	Homo sapiens	141-149
11597127-4	2001	Three lines of evidence support this inference: (a) a synthetic cell-permeable ceramide analogue reproduced all the effects of TNFalpha, (b) TNFalpha promoted the formation of ceramide via a mechanism sensitive to inhibition of sphingomyelinases by tricyclodecan-9-yl-xanthogenate and imipramine, and (c) the TNFalpha-mediated enhancement of the tert-butylhydroperoxide-induced DNA-damaging response was prevented under conditions in which ceramide formation was inhibited.	Ceramides	176-184	tumor necrosis factor	Homo sapiens	141-149
11551222-0	2001	Ceramide inhibition of mammalian phospholipase D1 and D2 activities is antagonized by phosphatidylinositol 4,5-bisphosphate.	Ceramides	0-8	phospholipase D1	Homo sapiens	33-49
11641773-9	2001	However, in accordance with a role in lipid-rich microdomains, ceramide by altering membrane composition may function as an amplifier in CD95-mediated apoptosis.	Ceramides	63-71	Fas cell surface death receptor	Homo sapiens	137-141
11574400-2	2001	Ceramide is known to activate both atypical protein kinase C (aPKC) zeta and protein phosphatase (PP) 2A, and each of these effectors has been reported to inhibit PKB.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	163-166
11457826-6	2001	This second phase of activation was first detectable after 2 h of treatment and steadily increased over the next 2 h, reaching maximal values after 4 h. In parallel, a pronounced increase in neutral ceramidase activity was observed, accounting for a constant or even decreased level of ceramide after long-term IL-1beta treatment, despite continuous sphingomyelinase activation.	Ceramides	286-294	N-acylsphingosine amidohydrolase 2	Mus musculus	191-209
11587538-0	2001	Inhibition of ceramide production reverses TNF-induced insulin resistance.	Ceramides	14-22	tumor necrosis factor	Homo sapiens	43-46
11587538-0	2001	Inhibition of ceramide production reverses TNF-induced insulin resistance.	Ceramides	14-22	insulin	Homo sapiens	55-62
11587538-1	2001	Ceramide has been implicated as a mediator of insulin resistance induced by tumor necrosis factor-alpha (TNF) in adipocytes.	Ceramides	0-8	insulin	Homo sapiens	46-53
11587538-1	2001	Ceramide has been implicated as a mediator of insulin resistance induced by tumor necrosis factor-alpha (TNF) in adipocytes.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	76-103
11587538-1	2001	Ceramide has been implicated as a mediator of insulin resistance induced by tumor necrosis factor-alpha (TNF) in adipocytes.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	105-108
11587538-3	2001	Since caveolae may be important sites for crosstalk between tyrosine kinase and sphingolipid signaling pathways, we examined the role of increased caveolar pools of ceramide in regulating tyrosine phosphorylation of the IR and its main substrate, insulin receptor substrate-1 (IRS-1).	Ceramides	165-173	insulin receptor	Homo sapiens	220-222
11587538-5	2001	However, inhibition of TNF-induced caveolar ceramide production reversed the decrease in IR tyrosine phosphorylation in response to TNF.	Ceramides	44-52	tumor necrosis factor	Homo sapiens	23-26
11587538-5	2001	However, inhibition of TNF-induced caveolar ceramide production reversed the decrease in IR tyrosine phosphorylation in response to TNF.	Ceramides	44-52	tumor necrosis factor	Homo sapiens	132-135
11587538-6	2001	These results suggest that TNF-independent increases in caveolar pools of ceramide are not sufficient to inhibit insulin signaling but that in conjunction with other TNF-dependent signals, caveolar pools of ceramide are a critical component for insulin resistance by TNF.	Ceramides	74-82	tumor necrosis factor	Homo sapiens	27-30
11587538-6	2001	These results suggest that TNF-independent increases in caveolar pools of ceramide are not sufficient to inhibit insulin signaling but that in conjunction with other TNF-dependent signals, caveolar pools of ceramide are a critical component for insulin resistance by TNF.	Ceramides	207-215	insulin	Homo sapiens	245-252
11564794-4	2001	N-oleoylethanolamine or D-L-threo 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), which inhibits acid ceramidase or glucosylceramide synthase and then increases endogenous ceramide, enhanced DC apoptosis and ceramide levels in the presence of tumor SN.	Ceramides	133-141	N-acylsphingosine amidohydrolase 1	Mus musculus	106-121
11564794-4	2001	N-oleoylethanolamine or D-L-threo 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), which inhibits acid ceramidase or glucosylceramide synthase and then increases endogenous ceramide, enhanced DC apoptosis and ceramide levels in the presence of tumor SN.	Ceramides	181-189	N-acylsphingosine amidohydrolase 1	Mus musculus	106-121
11564794-4	2001	N-oleoylethanolamine or D-L-threo 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP), which inhibits acid ceramidase or glucosylceramide synthase and then increases endogenous ceramide, enhanced DC apoptosis and ceramide levels in the presence of tumor SN.	Ceramides	181-189	UDP-glucose ceramide glucosyltransferase	Mus musculus	125-150
11564794-9	2001	Tumor SN, N-oleoylethanolamine, or PDMP suppressed Akt, NF-kappaB, and bcl-x(L) in DC, suggesting that the accumulation of ceramide impedes PI3K-mediated survival signals.	Ceramides	123-131	thymoma viral proto-oncogene 1	Mus musculus	51-54
11564794-9	2001	Tumor SN, N-oleoylethanolamine, or PDMP suppressed Akt, NF-kappaB, and bcl-x(L) in DC, suggesting that the accumulation of ceramide impedes PI3K-mediated survival signals.	Ceramides	123-131	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	56-65
11677262-6	2001	The ceramide inhibition of the BK channel was only partly dependent on its inhibition of the L-type Ca(2+) channel.	Ceramides	4-12	potassium calcium-activated channel subfamily M alpha 1	Rattus norvegicus	31-41
11454862-0	2001	Ceramide inhibits axonal growth and nerve growth factor uptake without compromising the viability of sympathetic neurons.	Ceramides	0-8	nerve growth factor	Rattus norvegicus	36-55
11454862-9	2001	Furthermore, we demonstrate that treatment of distal axons with ceramide inhibits the uptake of NGF and low density lipoproteins by distal axons by approximately 70 and 40%, respectively, suggesting that the inhibition of axonal growth by ceramide might be due, at least in part, to impaired endocytosis of NGF.	Ceramides	64-72	nerve growth factor	Rattus norvegicus	96-99
11454862-9	2001	Furthermore, we demonstrate that treatment of distal axons with ceramide inhibits the uptake of NGF and low density lipoproteins by distal axons by approximately 70 and 40%, respectively, suggesting that the inhibition of axonal growth by ceramide might be due, at least in part, to impaired endocytosis of NGF.	Ceramides	64-72	nerve growth factor	Rattus norvegicus	307-310
11454862-9	2001	Furthermore, we demonstrate that treatment of distal axons with ceramide inhibits the uptake of NGF and low density lipoproteins by distal axons by approximately 70 and 40%, respectively, suggesting that the inhibition of axonal growth by ceramide might be due, at least in part, to impaired endocytosis of NGF.	Ceramides	239-247	nerve growth factor	Rattus norvegicus	96-99
11454862-10	2001	However, inhibition of endocytosis of NGF by ceramide could not be ascribed to decreased phosphorylation of TrkA.	Ceramides	45-53	nerve growth factor	Rattus norvegicus	38-41
11551222-7	2001	Ceramides inhibited PLD2 activity, and this inhibition was decreased as PIP2 concentrations increased.	Ceramides	0-9	phospholipase D2	Homo sapiens	20-24
11551222-8	2001	However, C2-ceramide also reversibly inhibited the activity of PLD1 and PLD2 mutants in which binding of PIP2 was decreased, indicating that ceramides are interacting with the catalytic core of the mammalian PLDs.	Ceramides	141-150	phospholipase D1	Homo sapiens	63-67
11551222-8	2001	However, C2-ceramide also reversibly inhibited the activity of PLD1 and PLD2 mutants in which binding of PIP2 was decreased, indicating that ceramides are interacting with the catalytic core of the mammalian PLDs.	Ceramides	141-150	phospholipase D2	Homo sapiens	72-76
11551222-10	2001	Our results provide a novel demonstration that ceramides reversibly inhibit mammalian PLD2 as well as PLD1 activities and that both of these actions are more pronounced when PIP2 concentrations are rate-limiting.	Ceramides	47-56	phospholipase D2	Homo sapiens	86-90
11551222-10	2001	Our results provide a novel demonstration that ceramides reversibly inhibit mammalian PLD2 as well as PLD1 activities and that both of these actions are more pronounced when PIP2 concentrations are rate-limiting.	Ceramides	47-56	phospholipase D1	Homo sapiens	102-106
11551222-1	2001	Ceramides inhibit phospholipase D (PLD) activity in several mammalian cell types.	Ceramides	0-9	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	18-33
11535531-0	2001	Enhanced ceramide generation and induction of apoptosis in human leukemia cells exposed to DT(388)-granulocyte-macrophage colony-stimulating factor (GM-CSF), a truncated diphtheria toxin fused to human GM-CSF.	Ceramides	9-17	colony stimulating factor 2	Homo sapiens	99-147
11535531-0	2001	Enhanced ceramide generation and induction of apoptosis in human leukemia cells exposed to DT(388)-granulocyte-macrophage colony-stimulating factor (GM-CSF), a truncated diphtheria toxin fused to human GM-CSF.	Ceramides	9-17	colony stimulating factor 2	Homo sapiens	149-155
11551222-1	2001	Ceramides inhibit phospholipase D (PLD) activity in several mammalian cell types.	Ceramides	0-9	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	35-38
11535531-2	2001	HL-60/VCR, a multidrug-resistant human myeloid leukemia cell line, and wild-type HL-60 cells were used to study the impact of DT(388)-GM-CSF on metabolism of ceramide, a modulator of apoptosis.	Ceramides	158-166	colony stimulating factor 2	Homo sapiens	134-140
11551222-3	2001	In the present work, we investigated the effects of ceramides in inhibiting both PLD1 and PLD2 and the interaction with another activator, phosphatidylinositol 4,5-bisphosphate (PIP2).	Ceramides	52-61	phospholipase D1	Homo sapiens	81-85
11535531-3	2001	After 48 hours with DT(388)-GM-CSF (10 nM), ceramide levels in HL-60/VCR cells rose 6-fold and viability fell to 10%, whereas GM-CSF alone was without influence.	Ceramides	44-52	colony stimulating factor 2	Homo sapiens	28-34
11535531-10	2001	Diphtheria toxin increased ceramide and decreased sphingomyelin in U-937 cells, a cell line extremely sensitive to diphtheria toxin; exposure to DT(388)-GM-CSF showed sensitivity at less than 1.0 pM.	Ceramides	27-35	colony stimulating factor 2	Homo sapiens	153-159
11551222-3	2001	In the present work, we investigated the effects of ceramides in inhibiting both PLD1 and PLD2 and the interaction with another activator, phosphatidylinositol 4,5-bisphosphate (PIP2).	Ceramides	52-61	phospholipase D2	Homo sapiens	90-94
11566188-0	2001	Bax-dependent apoptosis induced by ceramide in HL-60 cells.	Ceramides	35-43	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
11566188-2	2001	In this study, we show that antisense bax inhibits cytochrome c release, poly(ADP-ribose)polymerase cleavage and cell death induced by ceramide in HL-60 cells.	Ceramides	135-143	BCL2 associated X, apoptosis regulator	Homo sapiens	38-41
11566188-2	2001	In this study, we show that antisense bax inhibits cytochrome c release, poly(ADP-ribose)polymerase cleavage and cell death induced by ceramide in HL-60 cells.	Ceramides	135-143	poly(ADP-ribose) polymerase 1	Homo sapiens	73-99
11566188-3	2001	In addition, ceramide induces translocation of Bax to mitochondria.	Ceramides	13-21	BCL2 associated X, apoptosis regulator	Homo sapiens	47-50
11566188-5	2001	Furthermore, ceramide inhibits the expression of the antiapoptotic protein Bcl-xL with an increase in the ratio of Bax to Bcl-xL.	Ceramides	13-21	BCL2 like 1	Homo sapiens	75-81
11566188-5	2001	Furthermore, ceramide inhibits the expression of the antiapoptotic protein Bcl-xL with an increase in the ratio of Bax to Bcl-xL.	Ceramides	13-21	BCL2 associated X, apoptosis regulator	Homo sapiens	115-118
11566188-5	2001	Furthermore, ceramide inhibits the expression of the antiapoptotic protein Bcl-xL with an increase in the ratio of Bax to Bcl-xL.	Ceramides	13-21	BCL2 like 1	Homo sapiens	122-128
11566188-6	2001	These data provide direct evidence that Bax plays an important role in regulating ceramide-induced apoptosis.	Ceramides	82-90	BCL2 associated X, apoptosis regulator	Homo sapiens	40-43
11502879-0	2001	Glutathione peroxidase-1 overexpression prevents ceramide production and partially inhibits apoptosis in doxorubicin-treated human breast carcinoma cells.	Ceramides	49-57	glutathione peroxidase 1	Homo sapiens	0-24
11502879-7	2001	Interestingly, in addition to a decrease in ROS production, the activation of neutral sphingomyelinase, sphingomyelin hydrolysis, and ceramide generation in response to doxorubicin was impaired in T47D/GPx2 cells compared with control cells.	Ceramides	134-142	glutathione peroxidase 2	Homo sapiens	202-206
11527425-0	2001	Ceramide blocks PDGF-induced DNA synthesis in mesangial cells via inhibition of Akt kinase in the absence of apoptosis.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	80-83
11527425-11	2001	Incubation of mesangial cells with C2 ceramide inhibited PDGF-induced Akt activity.	Ceramides	38-46	AKT serine/threonine kinase 1	Homo sapiens	70-73
11527425-14	2001	These data provide the first evidence that in mesangial cells, ceramide cross-talks with PI 3 kinase-dependent Akt kinase to inhibit PDGF-induced DNA synthesis without inducing apoptosis.	Ceramides	63-71	AKT serine/threonine kinase 1	Homo sapiens	111-114
11502879-3	2001	We selectively investigated the interaction of seleno-glutathione peroxidase-1 (GPx-1), the major enzyme responsible for peroxide detoxification in mammalian cells, with the cytotoxic response of T47D human breast cancer cells to doxorubicin, an anticancer drug known to promote production of ROS and apoptotic mediator ceramide.	Ceramides	320-328	glutathione peroxidase 1	Homo sapiens	47-78
11502879-10	2001	Taken together, these results indicate that GPx-1 can regulate doxorubicin-induced cell death signaling at least in part by interfering with the activation of the sphingomyelin-ceramide pathway.	Ceramides	177-185	glutathione peroxidase 1	Homo sapiens	44-49
11502879-3	2001	We selectively investigated the interaction of seleno-glutathione peroxidase-1 (GPx-1), the major enzyme responsible for peroxide detoxification in mammalian cells, with the cytotoxic response of T47D human breast cancer cells to doxorubicin, an anticancer drug known to promote production of ROS and apoptotic mediator ceramide.	Ceramides	320-328	glutathione peroxidase 1	Homo sapiens	80-85
11441001-8	2001	Taken together, these results show for the first time that both exogenous and endogenous ceramides mediate the modulation of telomerase activity via decreased hTERT promoter activity caused by rapid proteolysis of the ubiquitin-conjugated c-Myc transcription factor.	Ceramides	89-98	telomerase reverse transcriptase	Homo sapiens	159-164
11441001-4	2001	Electrophoretic mobility shift and supershift assays demonstrated that the binding activity of c-Myc transcription factor to the E-box sequence on the hTERT promoter was inhibited in response to C(6)-ceramide at 24 h. These results were also confirmed by transient transfections of A549 cells with pGL3-Basic plasmid constructs containing the functional hTERT promoter and its E-box deleted sequences cloned upstream of a luciferase reporter gene.	Ceramides	200-208	NME/NM23 nucleoside diphosphate kinase 2	Homo sapiens	95-121
11441001-8	2001	Taken together, these results show for the first time that both exogenous and endogenous ceramides mediate the modulation of telomerase activity via decreased hTERT promoter activity caused by rapid proteolysis of the ubiquitin-conjugated c-Myc transcription factor.	Ceramides	89-98	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	239-244
11441001-4	2001	Electrophoretic mobility shift and supershift assays demonstrated that the binding activity of c-Myc transcription factor to the E-box sequence on the hTERT promoter was inhibited in response to C(6)-ceramide at 24 h. These results were also confirmed by transient transfections of A549 cells with pGL3-Basic plasmid constructs containing the functional hTERT promoter and its E-box deleted sequences cloned upstream of a luciferase reporter gene.	Ceramides	200-208	telomerase reverse transcriptase	Homo sapiens	151-156
11523631-5	2001	In other experiments, the ability of C2 ceramide (Cer) to inhibit insulin action and induce IR was assessed as well as the phospholipase C inhibitor D609 to reverse IR induced by these TNF-alpha-like agents.	Ceramides	50-53	insulin	Homo sapiens	66-73
11441001-4	2001	Electrophoretic mobility shift and supershift assays demonstrated that the binding activity of c-Myc transcription factor to the E-box sequence on the hTERT promoter was inhibited in response to C(6)-ceramide at 24 h. These results were also confirmed by transient transfections of A549 cells with pGL3-Basic plasmid constructs containing the functional hTERT promoter and its E-box deleted sequences cloned upstream of a luciferase reporter gene.	Ceramides	200-208	succinate dehydrogenase complex subunit C	Homo sapiens	298-302
11441001-4	2001	Electrophoretic mobility shift and supershift assays demonstrated that the binding activity of c-Myc transcription factor to the E-box sequence on the hTERT promoter was inhibited in response to C(6)-ceramide at 24 h. These results were also confirmed by transient transfections of A549 cells with pGL3-Basic plasmid constructs containing the functional hTERT promoter and its E-box deleted sequences cloned upstream of a luciferase reporter gene.	Ceramides	200-208	telomerase reverse transcriptase	Homo sapiens	354-359
11441001-5	2001	Further analysis using RT-PCR and Western blotting showed that c-Myc protein but not its mRNA levels were decreased in response to C(6)-ceramide at 24 h. The effects of ceramide on the c-Myc protein were shown to be due to a reduction in half-life via increased ubiquitination.	Ceramides	136-144	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	63-68
11441001-6	2001	Similar results were obtained by increased endogenous ceramide levels in response to nontoxic concentrations of daunorubicin, resulting in the inhibition of telomerase and c-Myc activities.	Ceramides	54-62	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	172-177
11441001-7	2001	Furthermore, the elevation of endogenous ceramide by overexpression of bacterial sphingomyelinase after transient transfections also induced the inhibition of telomerase activity with concomitant decreased hTERT and c-Myc protein levels.	Ceramides	41-49	telomerase reverse transcriptase	Homo sapiens	206-211
11441001-7	2001	Furthermore, the elevation of endogenous ceramide by overexpression of bacterial sphingomyelinase after transient transfections also induced the inhibition of telomerase activity with concomitant decreased hTERT and c-Myc protein levels.	Ceramides	41-49	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	216-221
11514235-3	2001	To date, two distinct sphingomyelinases, a lysosomal acid sphingomyelinase (ASM), which is deficient in patients affected with types A and B Niemann-Pick disease (NPD), and a neutral, magnesium-dependent sphingomyelinase (NSM), are candidate enzymes which respond to apoptotic stimulations and cause sphingomyelin hydrolysis and subsequent ceramide generation.	Ceramides	340-348	sphingomyelin phosphodiesterase 1	Homo sapiens	53-74
11514235-3	2001	To date, two distinct sphingomyelinases, a lysosomal acid sphingomyelinase (ASM), which is deficient in patients affected with types A and B Niemann-Pick disease (NPD), and a neutral, magnesium-dependent sphingomyelinase (NSM), are candidate enzymes which respond to apoptotic stimulations and cause sphingomyelin hydrolysis and subsequent ceramide generation.	Ceramides	340-348	sphingomyelin phosphodiesterase 1	Homo sapiens	76-79
11480555-11	2001	Ceramide activates stress-activated protein kinases like c-jun N-terminal kinase (JNK) and thus affects transcription pathways involving c-jun.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	57-80
11466337-2	2001	In a previous study we showed that granulysin induced apoptosis using both caspase- and ceramide-dependent and -independent pathways.	Ceramides	88-96	granulysin	Homo sapiens	35-45
11466337-4	2001	Granulysin-induced death is significantly inhibited by Bcl-2 overexpression and is associated with a rapid (1-5 h) loss of mitochondrial membrane potential, which is not mediated by ceramide generation and is not inhibited by the general caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone.	Ceramides	182-190	granulysin	Homo sapiens	0-10
11466337-5	2001	Ceramide generation induced by granulysin is a slow event, only observable at longer incubation times (12 h).	Ceramides	0-8	granulysin	Homo sapiens	31-41
11466337-7	2001	Ceramide-induced apoptosis is also completely prevented by Bcl-2 overexpression.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	59-64
11454909-0	2001	Rebamipide inhibits ceramide-induced interleukin-8 production in Kato III human gastric cancer cells.	Ceramides	20-28	C-X-C motif chemokine ligand 8	Homo sapiens	37-50
11454909-3	2001	We have recently reported that H. pylori-dependent ceramide production may activate nuclear factor-kappaB and mediate interleukin-8 expression in human gastric cancer cell lines.	Ceramides	51-59	C-X-C motif chemokine ligand 8	Homo sapiens	118-131
11513845-0	2001	Ceramide generation by two distinct pathways in tumor necrosis factor alpha-induced cell death.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	48-75
11513845-2	2001	In this study, we found that blocking de novo ceramide synthesis significantly inhibits ceramide accumulation and subsequent cell death in response to tumor necrosis factor alpha.	Ceramides	46-54	tumor necrosis factor	Homo sapiens	151-178
11513845-2	2001	In this study, we found that blocking de novo ceramide synthesis significantly inhibits ceramide accumulation and subsequent cell death in response to tumor necrosis factor alpha.	Ceramides	88-96	tumor necrosis factor	Homo sapiens	151-178
11513845-3	2001	When cells were pre-treated with glutathione, a proposed cellular regulator of neutral sphingomyelinase, inhibition of ceramide accumulation at early time points was achieved with attenuation of cell death.	Ceramides	119-127	sphingomyelin phosphodiesterase 2	Homo sapiens	79-103
11561905-9	2001	Furthermore, treating Bcl-2 cultures with ceramide (10 microM), a second messenger mediating the RA-initiated death signal in parental cells, no longer caused DNA laddering.	Ceramides	42-50	BCL2 apoptosis regulator	Homo sapiens	22-27
11480555-9	2001	Ceramide levels are elevated in response to diverse stress challenges including chemotherapeutic drug treatment, irradiation, or treatment with pro-death ligands such as tumor necrosis factor alpha, TNF alpha.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	170-197
11480555-9	2001	Ceramide levels are elevated in response to diverse stress challenges including chemotherapeutic drug treatment, irradiation, or treatment with pro-death ligands such as tumor necrosis factor alpha, TNF alpha.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	199-208
11454909-5	2001	Rebamipide inhibited ceramide-induced interleukin-8 expression in a dose-dependent manner.	Ceramides	21-29	C-X-C motif chemokine ligand 8	Homo sapiens	38-51
11454909-6	2001	Rebamipide decreased the ceramide-induced increase of the interleukin-8 mRNA level as assessed by Northern blotting.	Ceramides	25-33	C-X-C motif chemokine ligand 8	Homo sapiens	58-71
11454909-8	2001	Rebamipide inhibited the ceramide-induced degradation of IkappaB-alpha (a major cytoplasmic inhibitor of nuclear factor-kappaB), further supporting that rebamipide inhibits the activation of nuclear factor-kappaB.	Ceramides	25-33	NFKB inhibitor alpha	Homo sapiens	57-70
11480555-11	2001	Ceramide activates stress-activated protein kinases like c-jun N-terminal kinase (JNK) and thus affects transcription pathways involving c-jun.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	82-85
11480555-11	2001	Ceramide activates stress-activated protein kinases like c-jun N-terminal kinase (JNK) and thus affects transcription pathways involving c-jun.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-62
11480555-12	2001	Ceramide activates protein phosphatases such as protein phosphatase 1 (PP1) and protein phosphatase 2 (PP2A).	Ceramides	0-8	inorganic pyrophosphatase 1	Homo sapiens	48-69
11480555-12	2001	Ceramide activates protein phosphatases such as protein phosphatase 1 (PP1) and protein phosphatase 2 (PP2A).	Ceramides	0-8	inorganic pyrophosphatase 1	Homo sapiens	71-74
11480555-12	2001	Ceramide activates protein phosphatases such as protein phosphatase 1 (PP1) and protein phosphatase 2 (PP2A).	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	103-107
11480555-13	2001	Ceramide activation of protein phosphatases has been shown to promote inactivation of a number of pro-growth cellular regulators including the kinases PKC alpha and Akt, Bcl2 and the retinoblastoma protein.	Ceramides	0-8	protein kinase C alpha	Homo sapiens	151-160
11480555-13	2001	Ceramide activation of protein phosphatases has been shown to promote inactivation of a number of pro-growth cellular regulators including the kinases PKC alpha and Akt, Bcl2 and the retinoblastoma protein.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	165-168
11480555-13	2001	Ceramide activation of protein phosphatases has been shown to promote inactivation of a number of pro-growth cellular regulators including the kinases PKC alpha and Akt, Bcl2 and the retinoblastoma protein.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	170-174
11480555-15	2001	Ceramide-induced activation of double-stranded RNA-dependent protein kinase (PKR), a protein kinase important in anti-viral host defense mechanisms and recently implicated in cellular stress pathways, results in the inhibition of protein synthesis as a prelude to cell death.	Ceramides	0-8	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	77-80
11404252-6	2001	Ceramide stimulates sphingomyelinases as effectively as TNF-alpha, thereby amplifying the sphingomyelinase activation, and TNF-alpha, ceramide, and sphingosine all inhibit PC:ceramide phosphocholine transferase (sphingomyelin synthase), the enzyme that restores homeostasis between sphingomyelin and ceramide pools.	Ceramides	175-183	tumor necrosis factor	Homo sapiens	123-132
11369765-1	2001	Sphingolipids such as ceramide are important mediators of apoptosis and growth arrest triggered by ligands such as tumor necrosis factor and Fas-L binding to their receptors.	Ceramides	22-30	Fas ligand (TNF superfamily, member 6)	Mus musculus	141-146
11369765-4	2001	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of approximately 50% over a period of 3 h. Finally, treatment with the de novo inhibitor of ceramide synthesis ISP-1 protected LME6 cells from MNNG-triggered cell death.	Ceramides	28-36	protease, serine 28	Mus musculus	304-309
11369765-4	2001	Treatment with exogenous C2-ceramide and sphingosine led to cell death in both LM and LME6, and treatment of the LME6 cells with MNNG resulted in a transient increase in intracellular ceramide of approximately 50% over a period of 3 h. Finally, treatment with the de novo inhibitor of ceramide synthesis ISP-1 protected LME6 cells from MNNG-triggered cell death.	Ceramides	184-192	protease, serine 28	Mus musculus	304-309
11369765-5	2001	This MNNG-triggered induction of ceramide was not observed in the p53-expressing LM cells, suggesting that it may be down-regulated by p53.	Ceramides	33-41	transformation related protein 53, pseudogene	Mus musculus	135-138
11439243-5	2001	Using these two assays, we show that DJNK activity is stimulated in cultured cells by several treatments that activate mammalian JNKs, including addition of arsenite, vanadate and ceramide derivatives.	Ceramides	180-188	basket	Drosophila melanogaster	37-41
11438587-5	2001	Moreover, p75NTR-dependent survival is blocked by inhibition of ceramide synthesis and rescued by addition of its precursor sphingomyelin.	Ceramides	64-72	nerve growth factor receptor	Homo sapiens	10-16
11438587-7	2001	Thus, ligand-dependent p75NTR regulation of the ceramide pathway mediates survival in certain neurons and may represent an important target for neuroprotective drugs in degenerative diseases involving p75NTR-expressing neurons, such as Alzheimer"s disease.	Ceramides	48-56	nerve growth factor receptor	Homo sapiens	23-29
11438587-7	2001	Thus, ligand-dependent p75NTR regulation of the ceramide pathway mediates survival in certain neurons and may represent an important target for neuroprotective drugs in degenerative diseases involving p75NTR-expressing neurons, such as Alzheimer"s disease.	Ceramides	48-56	nerve growth factor receptor	Homo sapiens	201-207
11337504-2	2001	Glucosylceramide synthase (GCS) transfers glucose from UDP-Glc to ceramide, catalyzing the first glycosylation step in the formation of higher order glycosphingolipids.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	27-30
11335714-8	2001	Finally, stable overexpression of human glucosylceramide synthase, which attenuates ceramide levels by converting ceramide to glucosylceramide, prevented the inhibitory effects of C(6)-ceramide and daunorubicin on telomerase.	Ceramides	84-92	UDP-glucose ceramide glucosyltransferase	Homo sapiens	40-65
11404253-0	2001	CTP:phosphocholine cytidylyltransferase inhibition by ceramide via PKC-alpha, p38 MAPK, cPLA2, and 5-lipoxygenase.	Ceramides	54-62	protein kinase C alpha	Homo sapiens	67-76
11404253-0	2001	CTP:phosphocholine cytidylyltransferase inhibition by ceramide via PKC-alpha, p38 MAPK, cPLA2, and 5-lipoxygenase.	Ceramides	54-62	phospholipase A2 group IVA	Homo sapiens	88-93
11404253-0	2001	CTP:phosphocholine cytidylyltransferase inhibition by ceramide via PKC-alpha, p38 MAPK, cPLA2, and 5-lipoxygenase.	Ceramides	54-62	arachidonate 5-lipoxygenase	Homo sapiens	99-113
11404253-3	2001	In this paper, we explore the signaling pathway employed by TNF-alpha using C2 ceramide as a cell-penetrating sphingolipid representative of the metabolites induced by TNF-alpha.	Ceramides	79-87	tumor necrosis factor	Homo sapiens	60-69
11404253-3	2001	In this paper, we explore the signaling pathway employed by TNF-alpha using C2 ceramide as a cell-penetrating sphingolipid representative of the metabolites induced by TNF-alpha.	Ceramides	79-87	tumor necrosis factor	Homo sapiens	168-177
11391632-2	2001	We blocked ceramide metabolism in a series of variably vincristine-resistant cell lines derived from CCRF-CEM leukemia cells using an inhibitor of glucosylceramide synthase, DL-threo-phenyl-2-hexadecanoylamino-3-pyrrolidino-1-propanol (PPPP).	Ceramides	11-19	UDP-glucose ceramide glucosyltransferase	Homo sapiens	147-172
11431347-1	2001	The retinoid N-(4-hydroxyphenyl)retinamide (4-HPR; fenretinide) is cytotoxic to a variety of cancer cell lines, and we previously showed an association between ceramide generation and 4-HPR cytotoxicity for neuroblastoma cell lines (B. J. Maurer et al., J. Natl.	Ceramides	160-168	haptoglobin-related protein	Homo sapiens	46-49
11431347-1	2001	The retinoid N-(4-hydroxyphenyl)retinamide (4-HPR; fenretinide) is cytotoxic to a variety of cancer cell lines, and we previously showed an association between ceramide generation and 4-HPR cytotoxicity for neuroblastoma cell lines (B. J. Maurer et al., J. Natl.	Ceramides	160-168	haptoglobin-related protein	Homo sapiens	186-189
11431347-4	2001	Here we determine whether the increased ceramide mediated by 4-HPR in the CHLA-90 human neuroblastoma cell line results from de novo ceramide synthesis.	Ceramides	40-48	haptoglobin-related protein	Homo sapiens	63-66
11431347-5	2001	Treatment of CHLA-90 with 4-HPR for 2 h, in the presence of [(3)H]palmitic acid, caused sequential formation of [(3)H]sphinganine (220% over control) and [(3)H]ceramide (160% over control), with sphinganine returning to baseline at 4 h, and ceramide continuing to increase (215% over control).	Ceramides	160-168	haptoglobin-related protein	Homo sapiens	28-31
11431347-5	2001	Treatment of CHLA-90 with 4-HPR for 2 h, in the presence of [(3)H]palmitic acid, caused sequential formation of [(3)H]sphinganine (220% over control) and [(3)H]ceramide (160% over control), with sphinganine returning to baseline at 4 h, and ceramide continuing to increase (215% over control).	Ceramides	241-249	haptoglobin-related protein	Homo sapiens	28-31
11431347-9	2001	Our results show that 4-HPR-mediated ceramide generation is derived from the de novo synthetic pathway by coordinate activation of SPT and ceramide synthase.	Ceramides	37-45	haptoglobin-related protein	Homo sapiens	24-27
11416148-3	2001	We show here that in Rat1 cells expressing an exogenous c-myc allele, distinct apoptotic pathways can be inhibited by Bcl-2 or Bcl-acta yet be distinguished by their sensitivity to Bcl-cb5 as either susceptible (serum withdrawal, taxol, and ceramide) or refractory (etoposide and doxorubicin).	Ceramides	241-249	MYC proto-oncogene, bHLH transcription factor	Rattus norvegicus	56-61
11435466-4	2001	We have now shown that stable expression in human fibroblasts of a dominant negative form of FAN abrogates TNF-induced ceramide generation from sphingomyelin hydrolysis and reduces caspase processing, thus markedly inhibiting TNF-triggered apoptosis.	Ceramides	119-127	neutral sphingomyelinase activation associated factor	Homo sapiens	93-96
11435466-4	2001	We have now shown that stable expression in human fibroblasts of a dominant negative form of FAN abrogates TNF-induced ceramide generation from sphingomyelin hydrolysis and reduces caspase processing, thus markedly inhibiting TNF-triggered apoptosis.	Ceramides	119-127	tumor necrosis factor	Homo sapiens	107-110
11573427-10	2001	C2 ceramide also induced an increase in the expression of the gene MDR1 in both cell lines, while ara C increased the activity of the gene MDR1 only in H9 cells.	Ceramides	3-11	ATP binding cassette subfamily B member 1	Homo sapiens	67-71
11470240-5	2001	Since it has been reported that CPT-I inhibition by etomoxir leads to a further increase in ceramide synthesis, we test the possibility that ceramides were involved in the changes reported.	Ceramides	92-100	carnitine palmitoyltransferase 1B	Homo sapiens	32-37
11470240-5	2001	Since it has been reported that CPT-I inhibition by etomoxir leads to a further increase in ceramide synthesis, we test the possibility that ceramides were involved in the changes reported.	Ceramides	141-150	carnitine palmitoyltransferase 1B	Homo sapiens	32-37
11470240-7	2001	These results indicate that the effects on UCP-3 mRNA levels could be mediated by increased ceramide synthesis.	Ceramides	92-100	uncoupling protein 3	Homo sapiens	43-48
11409897-0	2001	Molecular mechanisms of ceramide-mediated CD95 clustering.	Ceramides	24-32	Fas cell surface death receptor	Homo sapiens	42-46
11409897-2	2001	Here we show that ceramide in sphingolipid-rich membrane rafts mediates clustering of CD95.	Ceramides	18-26	Fas cell surface death receptor	Homo sapiens	86-90
11409897-3	2001	Neutralization of surface ceramide or inhibition of its endogenous generation prevented CD95 clustering.	Ceramides	26-34	Fas cell surface death receptor	Homo sapiens	88-92
11409897-4	2001	Furthermore, application of ceramide at the cell surface triggered clustering of active but not inactive CD95.	Ceramides	28-36	Fas cell surface death receptor	Homo sapiens	105-109
11409897-6	2001	Thus, we conclude that surface ceramide mediates CD95 clustering, which is required for initiation of apoptosis, at least in some cell types.	Ceramides	31-39	Fas cell surface death receptor	Homo sapiens	49-53
11287428-7	2001	Acid sphingomyelinase -/- hepatocytes were defective in Jo2-induced ceramide generation, capping, and apoptosis, and nanomolar concentrations of C(16)-ceramide restored these events.	Ceramides	68-76	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
11459225-2	2001	Ceramide glucosyltransferase (glucosylceramide synthase, GlcT-1, EC 2.4.1.80) catalyzes the initial step in GSL synthesis, the transfer of glucose from UDP-glucose to ceramide.	Ceramides	38-46	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-28
11459225-2	2001	Ceramide glucosyltransferase (glucosylceramide synthase, GlcT-1, EC 2.4.1.80) catalyzes the initial step in GSL synthesis, the transfer of glucose from UDP-glucose to ceramide.	Ceramides	38-46	UDP-glucose ceramide glucosyltransferase	Mus musculus	57-63
11573427-11	2001	The results obtained provide evidence for the contribution of ceramide-mediated signal pathway to the control of MDR1 activity.	Ceramides	62-70	ATP binding cassette subfamily B member 1	Homo sapiens	113-117
11418133-4	2001	Bcl-2 overexpression selectively inhibits apoptosis induced by ceramide and serum factor from AK-5 tumor regressing animals but not actinomycin D and curcumin, whereas the pancaspase inhibitor z-Val-Ala-Asp fluoromethylketone completely blocks apoptosis, irrespective of the inducer used.	Ceramides	63-71	BCL2, apoptosis regulator	Rattus norvegicus	0-5
11279185-0	2001	CD95 signaling via ceramide-rich membrane rafts.	Ceramides	19-27	Fas cell surface death receptor	Homo sapiens	0-4
11279185-2	2001	Here, we show that acid sphingomyelinase (ASM)-released ceramide is essential for clustering of CD95.	Ceramides	56-64	sphingomyelin phosphodiesterase 1	Homo sapiens	19-40
11382404-1	2001	In rat astrocyte-enriched culture, C2 ceramide dose- and time-dependently increased proenkephalin (proENK) mRNA; the significant increase began at 6 h after 30 microM C2 ceramide treatment (about 13-fold) and at 12 h after treatment (about 21-fold).	Ceramides	38-46	proenkephalin	Rattus norvegicus	84-97
11382404-1	2001	In rat astrocyte-enriched culture, C2 ceramide dose- and time-dependently increased proenkephalin (proENK) mRNA; the significant increase began at 6 h after 30 microM C2 ceramide treatment (about 13-fold) and at 12 h after treatment (about 21-fold).	Ceramides	38-46	proenkephalin	Rattus norvegicus	99-105
11279185-2	2001	Here, we show that acid sphingomyelinase (ASM)-released ceramide is essential for clustering of CD95.	Ceramides	56-64	sphingomyelin phosphodiesterase 1	Homo sapiens	42-45
11279185-2	2001	Here, we show that acid sphingomyelinase (ASM)-released ceramide is essential for clustering of CD95.	Ceramides	56-64	Fas cell surface death receptor	Homo sapiens	96-100
11382404-2	2001	In addition, C2 ceramide also increased AP-1 proteins, such as Fra-1, c-Jun, JunB and JunD, and phosphorylation of CREB.	Ceramides	16-24	FOS like 1, AP-1 transcription factor subunit	Rattus norvegicus	63-71
11279185-3	2001	In vitro and in vivo, extracellularly orientated ceramide, released upon CD95-triggered translocation of ASM to the plasma membrane outer surface, enabled clustering of CD95 in sphingolipid-rich membrane rafts and apoptosis induction.	Ceramides	49-57	Fas cell surface death receptor	Homo sapiens	73-77
11382404-2	2001	In addition, C2 ceramide also increased AP-1 proteins, such as Fra-1, c-Jun, JunB and JunD, and phosphorylation of CREB.	Ceramides	16-24	JunB proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	77-81
11382404-2	2001	In addition, C2 ceramide also increased AP-1 proteins, such as Fra-1, c-Jun, JunB and JunD, and phosphorylation of CREB.	Ceramides	16-24	JunD proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	86-90
11382404-2	2001	In addition, C2 ceramide also increased AP-1 proteins, such as Fra-1, c-Jun, JunB and JunD, and phosphorylation of CREB.	Ceramides	16-24	cAMP responsive element binding protein 1	Rattus norvegicus	115-119
11382404-3	2001	The blocking of protein synthesis by cycloheximide (CHX) evokes a further increase of C2 ceramide-induced proENK mRNA and phospho-CREB level, while C2 ceramide-induced increases of AP-1 protein levels were reduced by CHX.	Ceramides	89-97	proenkephalin	Rattus norvegicus	106-112
11279185-3	2001	In vitro and in vivo, extracellularly orientated ceramide, released upon CD95-triggered translocation of ASM to the plasma membrane outer surface, enabled clustering of CD95 in sphingolipid-rich membrane rafts and apoptosis induction.	Ceramides	49-57	sphingomyelin phosphodiesterase 1	Homo sapiens	105-108
11382404-3	2001	The blocking of protein synthesis by cycloheximide (CHX) evokes a further increase of C2 ceramide-induced proENK mRNA and phospho-CREB level, while C2 ceramide-induced increases of AP-1 protein levels were reduced by CHX.	Ceramides	89-97	cAMP responsive element binding protein 1	Rattus norvegicus	130-134
11382404-4	2001	The C2 ceramide-induced proENK mRNA expression was not changed significantly by the pretreatment with H89 (a PKA inhibitor), KN62 (a calcium/calmodulin-dependent protein kinase II inhibitor), and PD98059 (an ERK pathway inhibitor).	Ceramides	7-15	proenkephalin	Rattus norvegicus	24-30
11382404-4	2001	The C2 ceramide-induced proENK mRNA expression was not changed significantly by the pretreatment with H89 (a PKA inhibitor), KN62 (a calcium/calmodulin-dependent protein kinase II inhibitor), and PD98059 (an ERK pathway inhibitor).	Ceramides	7-15	Eph receptor B1	Rattus norvegicus	208-211
11382404-5	2001	However, calphostin C (a PKC inhibitor) and or SB203580 (a p38 inhibitor) partially but significantly reduced C2 ceramide-induced proENK mRNA expression as well as phospho-CREB level.	Ceramides	113-121	mitogen activated protein kinase 14	Rattus norvegicus	59-62
11382404-5	2001	However, calphostin C (a PKC inhibitor) and or SB203580 (a p38 inhibitor) partially but significantly reduced C2 ceramide-induced proENK mRNA expression as well as phospho-CREB level.	Ceramides	113-121	proenkephalin	Rattus norvegicus	130-136
11312266-2	2001	The precise mechanism that p75NTR uses to promote cell death is not certain, but one possibility is that p75NTR-dependent ceramide accumulation inhibits phosphatidylinositol 3-kinase-mediated Akt activation.	Ceramides	122-130	nerve growth factor receptor	Homo sapiens	27-33
11312266-2	2001	The precise mechanism that p75NTR uses to promote cell death is not certain, but one possibility is that p75NTR-dependent ceramide accumulation inhibits phosphatidylinositol 3-kinase-mediated Akt activation.	Ceramides	122-130	nerve growth factor receptor	Homo sapiens	105-111
11382404-6	2001	These results suggest that, in the rat astrocyte-enriched culture, C2 ceramide increases proENK mRNA expression via phosphorylation of CREB rather than the increases of AP-1 protein levels.	Ceramides	70-78	proenkephalin	Rattus norvegicus	89-95
11279185-3	2001	In vitro and in vivo, extracellularly orientated ceramide, released upon CD95-triggered translocation of ASM to the plasma membrane outer surface, enabled clustering of CD95 in sphingolipid-rich membrane rafts and apoptosis induction.	Ceramides	49-57	Fas cell surface death receptor	Homo sapiens	169-173
11382404-6	2001	These results suggest that, in the rat astrocyte-enriched culture, C2 ceramide increases proENK mRNA expression via phosphorylation of CREB rather than the increases of AP-1 protein levels.	Ceramides	70-78	cAMP responsive element binding protein 1	Rattus norvegicus	135-139
11382404-7	2001	Additionally, the activations of PKC and p38, but not PKA, calcium/calmodulin-dependent protein kinase II, and ERK, by C2 ceramide play important regulatory roles in C2 ceramide-induced proENK mRNA expression via activating the CREB.	Ceramides	122-130	mitogen activated protein kinase 14	Rattus norvegicus	41-44
11279185-4	2001	Whereas ASM deficiency, destruction of rafts, or neutralization of surface ceramide prevented CD95 clustering and apoptosis, natural ceramide only rescued ASM-deficient cells.	Ceramides	75-83	Fas cell surface death receptor	Homo sapiens	94-98
11382404-7	2001	Additionally, the activations of PKC and p38, but not PKA, calcium/calmodulin-dependent protein kinase II, and ERK, by C2 ceramide play important regulatory roles in C2 ceramide-induced proENK mRNA expression via activating the CREB.	Ceramides	122-130	proenkephalin	Rattus norvegicus	186-192
11382404-7	2001	Additionally, the activations of PKC and p38, but not PKA, calcium/calmodulin-dependent protein kinase II, and ERK, by C2 ceramide play important regulatory roles in C2 ceramide-induced proENK mRNA expression via activating the CREB.	Ceramides	122-130	cAMP responsive element binding protein 1	Rattus norvegicus	228-232
11312266-2	2001	The precise mechanism that p75NTR uses to promote cell death is not certain, but one possibility is that p75NTR-dependent ceramide accumulation inhibits phosphatidylinositol 3-kinase-mediated Akt activation.	Ceramides	122-130	AKT serine/threonine kinase 1	Homo sapiens	192-195
11279185-5	2001	The data suggest CD95-mediated clustering by ceramide is prerequisite for signaling and death.	Ceramides	45-53	Fas cell surface death receptor	Homo sapiens	17-21
11382404-7	2001	Additionally, the activations of PKC and p38, but not PKA, calcium/calmodulin-dependent protein kinase II, and ERK, by C2 ceramide play important regulatory roles in C2 ceramide-induced proENK mRNA expression via activating the CREB.	Ceramides	169-177	mitogen activated protein kinase 14	Rattus norvegicus	41-44
11382404-7	2001	Additionally, the activations of PKC and p38, but not PKA, calcium/calmodulin-dependent protein kinase II, and ERK, by C2 ceramide play important regulatory roles in C2 ceramide-induced proENK mRNA expression via activating the CREB.	Ceramides	169-177	Eph receptor B1	Rattus norvegicus	111-114
11350735-0	2001	Inhibitory actions of ceramide upon PKC-epsilon/ERK interactions.	Ceramides	22-30	protein kinase C epsilon	Homo sapiens	36-47
11382404-7	2001	Additionally, the activations of PKC and p38, but not PKA, calcium/calmodulin-dependent protein kinase II, and ERK, by C2 ceramide play important regulatory roles in C2 ceramide-induced proENK mRNA expression via activating the CREB.	Ceramides	169-177	proenkephalin	Rattus norvegicus	186-192
11382404-7	2001	Additionally, the activations of PKC and p38, but not PKA, calcium/calmodulin-dependent protein kinase II, and ERK, by C2 ceramide play important regulatory roles in C2 ceramide-induced proENK mRNA expression via activating the CREB.	Ceramides	169-177	cAMP responsive element binding protein 1	Rattus norvegicus	228-232
11350735-0	2001	Inhibitory actions of ceramide upon PKC-epsilon/ERK interactions.	Ceramides	22-30	mitogen-activated protein kinase 1	Homo sapiens	48-51
11350735-1	2001	We have previously shown that interleukin-1 receptor-generated ceramide induces growth arrest in smooth muscle pericytes by inhibiting an upstream kinase in the extracellular signal-regulated kinase (ERK) cascade.	Ceramides	63-71	mitogen-activated protein kinase 1	Homo sapiens	161-198
11350735-1	2001	We have previously shown that interleukin-1 receptor-generated ceramide induces growth arrest in smooth muscle pericytes by inhibiting an upstream kinase in the extracellular signal-regulated kinase (ERK) cascade.	Ceramides	63-71	mitogen-activated protein kinase 1	Homo sapiens	200-203
11350735-2	2001	Here, we now report the mechanism by which ceramide inhibits ERK activity.	Ceramides	43-51	mitogen-activated protein kinase 1	Homo sapiens	61-64
11350735-3	2001	Ceramide renders the human embryonic kidney 293 cells (HEK 293) resistant to the mitogenic actions of growth factors and activators of protein kinase C (PKC).	Ceramides	0-8	protein kinase C epsilon	Homo sapiens	153-156
11350735-4	2001	A role for PKC to mediate ceramide inhibition of growth factor-induced ERK activity and mitogenesis is suggested, as exogenous ceramide directly inhibits both immunoprecipitated and recombinant PKC-epsilon activities.	Ceramides	26-34	protein kinase C epsilon	Homo sapiens	11-14
11350735-4	2001	A role for PKC to mediate ceramide inhibition of growth factor-induced ERK activity and mitogenesis is suggested, as exogenous ceramide directly inhibits both immunoprecipitated and recombinant PKC-epsilon activities.	Ceramides	26-34	mitogen-activated protein kinase 1	Homo sapiens	71-74
11350735-4	2001	A role for PKC to mediate ceramide inhibition of growth factor-induced ERK activity and mitogenesis is suggested, as exogenous ceramide directly inhibits both immunoprecipitated and recombinant PKC-epsilon activities.	Ceramides	127-135	mitogen-activated protein kinase 1	Homo sapiens	71-74
11350735-4	2001	A role for PKC to mediate ceramide inhibition of growth factor-induced ERK activity and mitogenesis is suggested, as exogenous ceramide directly inhibits both immunoprecipitated and recombinant PKC-epsilon activities.	Ceramides	127-135	protein kinase C epsilon	Homo sapiens	194-205
11350735-5	2001	To confirm that PKC-epsilon is necessary for ceramide-inhibited ERK activity, HEK 293 cells were transfected with a dominant-negative mutant of PKC-epsilon (DeltaPKC-epsilon).	Ceramides	45-53	protein kinase C epsilon	Homo sapiens	16-27
11350735-5	2001	To confirm that PKC-epsilon is necessary for ceramide-inhibited ERK activity, HEK 293 cells were transfected with a dominant-negative mutant of PKC-epsilon (DeltaPKC-epsilon).	Ceramides	45-53	mitogen-activated protein kinase 1	Homo sapiens	64-67
11350735-5	2001	To confirm that PKC-epsilon is necessary for ceramide-inhibited ERK activity, HEK 293 cells were transfected with a dominant-negative mutant of PKC-epsilon (DeltaPKC-epsilon).	Ceramides	45-53	protein kinase C epsilon	Homo sapiens	144-155
11415943-0	2001	Rapid reactive oxygen species production by mitochondria in endothelial cells exposed to tumor necrosis factor-alpha is mediated by ceramide.	Ceramides	132-140	tumor necrosis factor	Homo sapiens	89-116
11350735-6	2001	These transfected cells respond to insulin-like growth factor I (IGF-I) with a significantly decreased ERK activity that is not further reduced by ceramide treatment.	Ceramides	147-155	insulin like growth factor 1	Homo sapiens	65-70
11415943-10	2001	Thus, TNF-alpha induces mitochondrial ROS production in HUVEC that primarily occurs at the ubisemiquinone site and is mediated by ceramide-dependent signaling pathways involving CAPK.	Ceramides	130-138	tumor necrosis factor	Homo sapiens	6-15
11350735-8	2001	Ceramide treatment significantly inhibits the IGF-I-induced PKC-epsilon interaction with bioactive phosphorylated ERK.	Ceramides	0-8	insulin like growth factor 1	Homo sapiens	46-51
11350735-8	2001	Ceramide treatment significantly inhibits the IGF-I-induced PKC-epsilon interaction with bioactive phosphorylated ERK.	Ceramides	0-8	protein kinase C epsilon	Homo sapiens	60-71
11350735-8	2001	Ceramide treatment significantly inhibits the IGF-I-induced PKC-epsilon interaction with bioactive phosphorylated ERK.	Ceramides	0-8	mitogen-activated protein kinase 1	Homo sapiens	114-117
11350735-9	2001	Ceramide also inhibits IGF-I-induced PKC-epsilon association with Raf-1, an upstream kinase of ERK.	Ceramides	0-8	insulin like growth factor 1	Homo sapiens	23-28
11350735-9	2001	Ceramide also inhibits IGF-I-induced PKC-epsilon association with Raf-1, an upstream kinase of ERK.	Ceramides	0-8	protein kinase C epsilon	Homo sapiens	37-48
11350735-9	2001	Ceramide also inhibits IGF-I-induced PKC-epsilon association with Raf-1, an upstream kinase of ERK.	Ceramides	0-8	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	66-71
11350735-9	2001	Ceramide also inhibits IGF-I-induced PKC-epsilon association with Raf-1, an upstream kinase of ERK.	Ceramides	0-8	mitogen-activated protein kinase 1	Homo sapiens	95-98
11350735-10	2001	Together, these studies demonstrate that ceramide exerts anti-mitogenic actions by limiting the ability of PKC-epsilon to form a signaling complex with Raf-1 and ERK.	Ceramides	41-49	protein kinase C epsilon	Homo sapiens	107-118
11350735-10	2001	Together, these studies demonstrate that ceramide exerts anti-mitogenic actions by limiting the ability of PKC-epsilon to form a signaling complex with Raf-1 and ERK.	Ceramides	41-49	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	152-165
11422444-0	2001	Ceramide-induced apoptosis in cortical neurons is mediated by an increase in p38 phosphorylation and not by the decrease in ERK phosphorylation.	Ceramides	0-8	mitogen-activated protein kinase 1	Homo sapiens	77-80
11368774-8	2001	Finally, the lipid second messenger ceramide was shown to cause a reduction in Mcl-1 protein translation, probably via its ability to inhibit protein kinase B activation, providing further clues regarding the death-inducing effect of this lipid.	Ceramides	36-44	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	79-84
11387200-0	2001	C26-CoA-dependent ceramide synthesis of Saccharomyces cerevisiae is operated by Lag1p and Lac1p.	Ceramides	18-26	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	80-85
11387200-0	2001	C26-CoA-dependent ceramide synthesis of Saccharomyces cerevisiae is operated by Lag1p and Lac1p.	Ceramides	18-26	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	90-95
11387200-8	2001	The lipid remodelling of GPI-anchored proteins is severely compromised in lag1lac1 double mutants since only few and mostly abnormal ceramides are incorporated into the GPI anchors.	Ceramides	133-142	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	74-82
11387200-9	2001	The participation of Lag1p and Lac1p in ceramide synthesis may explain their role in determining longevity.	Ceramides	40-48	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	21-26
11387200-9	2001	The participation of Lag1p and Lac1p in ceramide synthesis may explain their role in determining longevity.	Ceramides	40-48	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	31-36
11387204-0	2001	The Ca2+ concentration of the endoplasmic reticulum is a key determinant of ceramide-induced apoptosis: significance for the molecular mechanism of Bcl-2 action.	Ceramides	76-84	carbonic anhydrase 2	Homo sapiens	4-7
11387204-0	2001	The Ca2+ concentration of the endoplasmic reticulum is a key determinant of ceramide-induced apoptosis: significance for the molecular mechanism of Bcl-2 action.	Ceramides	76-84	BCL2 apoptosis regulator	Homo sapiens	148-153
11387204-4	2001	All conditions that lowered [Ca2+]er protected HeLa cells from ceramide, a Bcl-2-sensitive apoptotic stimulus, while treatments that increased [Ca2+]er had the opposite effect.	Ceramides	63-71	carbonic anhydrase 2	Homo sapiens	29-32
11387204-4	2001	All conditions that lowered [Ca2+]er protected HeLa cells from ceramide, a Bcl-2-sensitive apoptotic stimulus, while treatments that increased [Ca2+]er had the opposite effect.	Ceramides	63-71	BCL2 apoptosis regulator	Homo sapiens	75-80
11387204-5	2001	Surprisingly, ceramide itself caused the release of Ca2+ from the endoplasmic reticulum and thus [Ca2+] increased both in the cytosol and in the mitochondrial matrix, paralleled by marked alterations in mitochondria morphology.	Ceramides	14-22	carbonic anhydrase 2	Homo sapiens	52-55
11387204-5	2001	Surprisingly, ceramide itself caused the release of Ca2+ from the endoplasmic reticulum and thus [Ca2+] increased both in the cytosol and in the mitochondrial matrix, paralleled by marked alterations in mitochondria morphology.	Ceramides	14-22	carbonic anhydrase 2	Homo sapiens	98-101
11415988-5	2001	Specifically, we report that treatment with angiostatin or ceramide results in the activation of RhoA, an important effector of cytoskeletal structure.	Ceramides	59-67	ras homolog family member A	Homo sapiens	97-101
11446388-8	2001	The treatment with an inhibitor of ceramide-specific glucosyltransferase, N-butyldeoxynojirimysin (NB-DNJ) markedly reduced the intracytoplasmic granular immunofluorescence for GM2 ganglioside in SPMS9 cells, whereas the amount of filipin-positive granules remained unchanged.	Ceramides	35-43	cytochrome b5 domain containing 2	Mus musculus	177-180
11413232-4	2001	We found that tumor necrosis factor-alpha and interferon-gamma exert synergistic inhibitory action on Schwann cell viability via the production of nitric oxide (NO) and ceramide (cer).	Ceramides	169-177	tumor necrosis factor	Homo sapiens	14-41
11413232-4	2001	We found that tumor necrosis factor-alpha and interferon-gamma exert synergistic inhibitory action on Schwann cell viability via the production of nitric oxide (NO) and ceramide (cer).	Ceramides	169-177	interferon gamma	Homo sapiens	46-62
11413232-4	2001	We found that tumor necrosis factor-alpha and interferon-gamma exert synergistic inhibitory action on Schwann cell viability via the production of nitric oxide (NO) and ceramide (cer).	Ceramides	169-172	tumor necrosis factor	Homo sapiens	14-41
11413232-4	2001	We found that tumor necrosis factor-alpha and interferon-gamma exert synergistic inhibitory action on Schwann cell viability via the production of nitric oxide (NO) and ceramide (cer).	Ceramides	169-172	interferon gamma	Homo sapiens	46-62
11355886-1	2001	Ceramide participates in signal transduction of IL-1 and TNF, two cytokines likely involved in cartilage degradation in osteoarthritis.	Ceramides	0-8	tumor necrosis factor	Oryctolagus cuniculus	48-60
11355886-2	2001	We previously showed that ceramide stimulates proteoglycan degradation, mRNA expression of matrix metalloproteinase (MMP)-1, -3, and -13, and pro-MMP-3 production in rabbit cartilage.	Ceramides	26-34	interstitial collagenase	Oryctolagus cuniculus	91-136
11359788-5	2001	In contrast, the anti-apoptotic effect of NGF (studied using the ceramide analogue C2) required p75(NTR) as well as the activation of the transcription factor NF-kB, but neither p140(trkA) nor MAPK was necessary.	Ceramides	65-73	nerve growth factor	Homo sapiens	42-45
11359788-5	2001	In contrast, the anti-apoptotic effect of NGF (studied using the ceramide analogue C2) required p75(NTR) as well as the activation of the transcription factor NF-kB, but neither p140(trkA) nor MAPK was necessary.	Ceramides	65-73	PC4 and SFRS1 interacting protein 1	Homo sapiens	96-99
11359788-5	2001	In contrast, the anti-apoptotic effect of NGF (studied using the ceramide analogue C2) required p75(NTR) as well as the activation of the transcription factor NF-kB, but neither p140(trkA) nor MAPK was necessary.	Ceramides	65-73	neurotensin receptor 1	Homo sapiens	100-103
11313375-0	2001	Ceramide inhibits lipopolysaccharide-mediated nitric oxide synthase and cyclooxygenase-2 induction in macrophages: effects on protein kinases and transcription factors.	Ceramides	0-8	prostaglandin-endoperoxide synthase 2	Mus musculus	72-88
11403420-1	2001	Ceramide has been shown to be a key signaling molecule involved in the apoptotic effect of tumor necrosis factor alpha (TNF-alpha) and other cytokines.	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	91-118
11403420-1	2001	Ceramide has been shown to be a key signaling molecule involved in the apoptotic effect of tumor necrosis factor alpha (TNF-alpha) and other cytokines.	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	120-129
11403420-2	2001	Given the importance of cytokines such as TNF-alpha in myocardial ischemia-reperfusion injury, we hypothesize that ceramide is increased during ischemia or reperfusion, and that the activity of enzymes responsible for its production or breakdown should be increased and/or decreased, respectively.	Ceramides	115-123	tumor necrosis factor	Rattus norvegicus	42-51
11337373-4	2001	When assessed in cell death assays, antisense targeting of survivin abolished the anti-apoptotic function of VEGF against tumor necrosis factor-alpha- or ceramide-induced cell death, enhanced caspase-3 activity, promoted the generation of a approximately 17-kd active caspase-3 subunit, and increased cleavage of the caspase substrate, polyADP ribose polymerase.	Ceramides	154-162	Deterin	Drosophila melanogaster	59-67
11337373-4	2001	When assessed in cell death assays, antisense targeting of survivin abolished the anti-apoptotic function of VEGF against tumor necrosis factor-alpha- or ceramide-induced cell death, enhanced caspase-3 activity, promoted the generation of a approximately 17-kd active caspase-3 subunit, and increased cleavage of the caspase substrate, polyADP ribose polymerase.	Ceramides	154-162	PDGF- and VEGF-related factor 1	Drosophila melanogaster	109-113
11313375-6	2001	The immunocomplex kinase assay indicated that IkappaB kinase activity stimulated by LPS was inhibited by ceramide, which concomitantly reduced the IkappaBalpha degradation caused by LPS within 1-6 h. In concert with the decreased cytosolic p65 protein level, LPS treatment resulted in rapid nuclear accumulation of NF-kappaB subunit p65 and its association with the cAMP-responsive element binding protein.	Ceramides	105-113	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	147-159
11313375-6	2001	The immunocomplex kinase assay indicated that IkappaB kinase activity stimulated by LPS was inhibited by ceramide, which concomitantly reduced the IkappaBalpha degradation caused by LPS within 1-6 h. In concert with the decreased cytosolic p65 protein level, LPS treatment resulted in rapid nuclear accumulation of NF-kappaB subunit p65 and its association with the cAMP-responsive element binding protein.	Ceramides	105-113	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	240-243
11313375-6	2001	The immunocomplex kinase assay indicated that IkappaB kinase activity stimulated by LPS was inhibited by ceramide, which concomitantly reduced the IkappaBalpha degradation caused by LPS within 1-6 h. In concert with the decreased cytosolic p65 protein level, LPS treatment resulted in rapid nuclear accumulation of NF-kappaB subunit p65 and its association with the cAMP-responsive element binding protein.	Ceramides	105-113	v-rel reticuloendotheliosis viral oncogene homolog A (avian)	Mus musculus	333-336
11313375-8	2001	In addition, LPS-induced PKC and p38 mitogen-activated protein kinase activation were overcome by ceramide.	Ceramides	98-106	mitogen-activated protein kinase 14	Mus musculus	33-36
11313375-9	2001	In conclusion, we suggest that ceramide inhibition of LPS-mediated induction of inducible NO synthase and cyclooxygenase-2 is due to reduction of the activation of NF-kappaB and AP-1, which might result from ceramide"s inhibition of LPS-stimulated IkappaB kinase, p38 mitogen-activated protein kinase, and protein kinase C.	Ceramides	31-39	nitric oxide synthase 2, inducible	Mus musculus	80-101
11313375-9	2001	In conclusion, we suggest that ceramide inhibition of LPS-mediated induction of inducible NO synthase and cyclooxygenase-2 is due to reduction of the activation of NF-kappaB and AP-1, which might result from ceramide"s inhibition of LPS-stimulated IkappaB kinase, p38 mitogen-activated protein kinase, and protein kinase C.	Ceramides	31-39	prostaglandin-endoperoxide synthase 2	Mus musculus	106-122
11313375-9	2001	In conclusion, we suggest that ceramide inhibition of LPS-mediated induction of inducible NO synthase and cyclooxygenase-2 is due to reduction of the activation of NF-kappaB and AP-1, which might result from ceramide"s inhibition of LPS-stimulated IkappaB kinase, p38 mitogen-activated protein kinase, and protein kinase C.	Ceramides	31-39	mitogen-activated protein kinase 14	Mus musculus	264-267
11325875-8	2001	It was found that ceramide significantly inhibited bradykinin-induced NO increase within endothelial cells.	Ceramides	18-26	kininogen 1	Bos taurus	51-61
11148216-0	2001	Ceramide regulates protein synthesis by a novel mechanism involving the cellular PKR activator RAX.	Ceramides	0-8	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	81-84
11336794-4	2001	On the other hand, tumor necrosis factor (TNF)-alpha treatment of HUVEC led to an increase in both PAI-1 mRNA expression and protein release, and an enhancement of total ceramide content was also observed.	Ceramides	170-178	tumor necrosis factor	Homo sapiens	19-52
11336794-8	2001	Thus, these data imply the possibility that the subcellular topology of ceramide production determines its lipid mediator function in the regulation of PAI-1 synthesis in HUVEC, because both TNF-alpha and daunorubicin could increase the ceramide levels.	Ceramides	72-80	serpin family E member 1	Homo sapiens	152-157
11336794-8	2001	Thus, these data imply the possibility that the subcellular topology of ceramide production determines its lipid mediator function in the regulation of PAI-1 synthesis in HUVEC, because both TNF-alpha and daunorubicin could increase the ceramide levels.	Ceramides	72-80	tumor necrosis factor	Homo sapiens	191-200
11336794-8	2001	Thus, these data imply the possibility that the subcellular topology of ceramide production determines its lipid mediator function in the regulation of PAI-1 synthesis in HUVEC, because both TNF-alpha and daunorubicin could increase the ceramide levels.	Ceramides	237-245	tumor necrosis factor	Homo sapiens	191-200
11278937-2	2001	We recently reported that the marked decrease in cellular ceramide in primary astrocytes is an early event associated with the mitogenic activity of basic fibroblast growth factor (bFGF) (Riboni, L., Viani, P., Bassi, R., Stabieini, A., and Tettamanti, G. (2000) GLIA 32, 137-145).	Ceramides	58-66	fibroblast growth factor 2	Homo sapiens	149-179
11278937-2	2001	We recently reported that the marked decrease in cellular ceramide in primary astrocytes is an early event associated with the mitogenic activity of basic fibroblast growth factor (bFGF) (Riboni, L., Viani, P., Bassi, R., Stabieini, A., and Tettamanti, G. (2000) GLIA 32, 137-145).	Ceramides	58-66	fibroblast growth factor 2	Homo sapiens	181-185
11278937-3	2001	Here we show that a rapid activation of sphingomyelin biosynthesis appears to be the major mechanism responsible for the fall in ceramide levels induced by bFGF.	Ceramides	129-137	fibroblast growth factor 2	Homo sapiens	156-160
11278937-4	2001	When quiescent astrocytes were treated with bFGF, an increased amount of newly synthesized ceramide (from either l-[(3)H]serine or [(3)H]sphingosine) was directed toward the biosynthesis of sphingomyelin.	Ceramides	91-99	fibroblast growth factor 2	Homo sapiens	44-48
11148216-0	2001	Ceramide regulates protein synthesis by a novel mechanism involving the cellular PKR activator RAX.	Ceramides	0-8	retina and anterior neural fold homeobox	Homo sapiens	95-98
11148216-12	2001	Since RAX is phosphorylated by an as yet undetermined SAPK and ceramide is a potent activator of SAPKs such as JNK, a role for ceramide in the activation of RAX might be possible.	Ceramides	63-71	mitogen-activated protein kinase 9	Homo sapiens	111-114
11360178-3	2001	In Rat-1 cells, a Bcl-2 mutant targeted exclusively to the endoplasmic reticulum (Bcl-cb5) was effective at inhibiting apoptosis induced by serum starvation/myc, or ceramide but not apoptosis induced by etoposide.	Ceramides	165-173	BCL2, apoptosis regulator	Rattus norvegicus	18-23
11148216-12	2001	Since RAX is phosphorylated by an as yet undetermined SAPK and ceramide is a potent activator of SAPKs such as JNK, a role for ceramide in the activation of RAX might be possible.	Ceramides	63-71	retina and anterior neural fold homeobox	Homo sapiens	157-160
11148216-12	2001	Since RAX is phosphorylated by an as yet undetermined SAPK and ceramide is a potent activator of SAPKs such as JNK, a role for ceramide in the activation of RAX might be possible.	Ceramides	127-135	retina and anterior neural fold homeobox	Homo sapiens	6-9
11148216-12	2001	Since RAX is phosphorylated by an as yet undetermined SAPK and ceramide is a potent activator of SAPKs such as JNK, a role for ceramide in the activation of RAX might be possible.	Ceramides	127-135	mitogen-activated protein kinase 9	Homo sapiens	54-58
11148216-12	2001	Since RAX is phosphorylated by an as yet undetermined SAPK and ceramide is a potent activator of SAPKs such as JNK, a role for ceramide in the activation of RAX might be possible.	Ceramides	127-135	mitogen-activated protein kinase 9	Homo sapiens	111-114
11148216-12	2001	Since RAX is phosphorylated by an as yet undetermined SAPK and ceramide is a potent activator of SAPKs such as JNK, a role for ceramide in the activation of RAX might be possible.	Ceramides	127-135	retina and anterior neural fold homeobox	Homo sapiens	157-160
11148216-13	2001	Results indicate that overexpression of exogenous RAX potentiates ceramide-induced killing.	Ceramides	66-74	retina and anterior neural fold homeobox	Homo sapiens	50-53
11148216-15	2001	Since ceramide potently promotes RAX and eukaryotic initiation factor-2alpha phosphorylation, a possible role for ceramide in this process may involve the activation of PKR by RAX.	Ceramides	6-14	retina and anterior neural fold homeobox	Homo sapiens	33-36
11148216-15	2001	Since ceramide potently promotes RAX and eukaryotic initiation factor-2alpha phosphorylation, a possible role for ceramide in this process may involve the activation of PKR by RAX.	Ceramides	114-122	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	169-172
11148216-15	2001	Since ceramide potently promotes RAX and eukaryotic initiation factor-2alpha phosphorylation, a possible role for ceramide in this process may involve the activation of PKR by RAX.	Ceramides	114-122	retina and anterior neural fold homeobox	Homo sapiens	176-179
11148216-16	2001	Since 2-aminopurine, a serine/threonine kinase inhibitor that has previously been shown to inhibit PKR, blocks both the potentiation of ceramide killing by RAX and ceramide-induced inhibition of protein synthesis, ceramide appears to promote PKR activation, at least indirectly.	Ceramides	136-144	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	99-102
11148216-16	2001	Since 2-aminopurine, a serine/threonine kinase inhibitor that has previously been shown to inhibit PKR, blocks both the potentiation of ceramide killing by RAX and ceramide-induced inhibition of protein synthesis, ceramide appears to promote PKR activation, at least indirectly.	Ceramides	136-144	retina and anterior neural fold homeobox	Homo sapiens	156-159
11148216-16	2001	Since 2-aminopurine, a serine/threonine kinase inhibitor that has previously been shown to inhibit PKR, blocks both the potentiation of ceramide killing by RAX and ceramide-induced inhibition of protein synthesis, ceramide appears to promote PKR activation, at least indirectly.	Ceramides	164-172	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	99-102
11148216-16	2001	Since 2-aminopurine, a serine/threonine kinase inhibitor that has previously been shown to inhibit PKR, blocks both the potentiation of ceramide killing by RAX and ceramide-induced inhibition of protein synthesis, ceramide appears to promote PKR activation, at least indirectly.	Ceramides	164-172	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	242-245
11148216-16	2001	Since 2-aminopurine, a serine/threonine kinase inhibitor that has previously been shown to inhibit PKR, blocks both the potentiation of ceramide killing by RAX and ceramide-induced inhibition of protein synthesis, ceramide appears to promote PKR activation, at least indirectly.	Ceramides	164-172	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	99-102
11148216-16	2001	Since 2-aminopurine, a serine/threonine kinase inhibitor that has previously been shown to inhibit PKR, blocks both the potentiation of ceramide killing by RAX and ceramide-induced inhibition of protein synthesis, ceramide appears to promote PKR activation, at least indirectly.	Ceramides	164-172	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	242-245
11400169-3	2001	We have recently shown that nitrosation of the activator protein-1 (AP-1) transcriptional factor is crucial for NO-mediated inhibition of cell death triggered by etoposide or ceramide.	Ceramides	175-183	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	47-66
11400169-3	2001	We have recently shown that nitrosation of the activator protein-1 (AP-1) transcriptional factor is crucial for NO-mediated inhibition of cell death triggered by etoposide or ceramide.	Ceramides	175-183	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	68-72
11259253-5	2001	Similar to apo E, apoptogenic agents such as ceramide and LY 294002, a phosphatidylinositol (PI) 3-kinase inhibitor, induced apoptosis and suppressed androstenedione production.	Ceramides	45-53	apolipoprotein E	Rattus norvegicus	11-16
11282082-0	2001	Loss of cyclin A and G1-cell cycle arrest are a prerequisite of ceramide-induced toxicity in human arterial endothelial cells.	Ceramides	64-72	cyclin A2	Homo sapiens	8-16
11282082-1	2001	BACKGROUND: Ceramide is an important messenger of TNF- and lipid-induced apoptosis.	Ceramides	12-20	tumor necrosis factor	Homo sapiens	50-53
11282082-13	2001	CONCLUSIONS: Ceramide abrogates endothelial cell proliferation independently of apoptosis or necrosis at low concentrations (<or=10 microM) through loss of cyclin A expression with subsequent G1 cell-cycle arrest.	Ceramides	13-21	cyclin A2	Homo sapiens	159-167
11259632-8	2001	Additional studies revealed that apoptosis induced by other JNK-activating stimuli, including ceramide, heat shock, and UV irradiation, was partly suppressed after treatment with JNK1 AS but not JNK2 AS.	Ceramides	94-102	mitogen-activated protein kinase 8	Rattus norvegicus	60-63
11171115-4	2001	Here we show that ceramide analogues specifically prevent the recruitment of the PtdIns(3,4,5)P(3)-binding proteins Akt/protein kinase B (PKB) or the general receptor for phosphoinositides-1 (GRP1).	Ceramides	18-26	AKT serine/threonine kinase 1	Homo sapiens	116-119
11313880-4	2001	Superoxide dismutase (SOD), a selective antioxidant for O2-*, had no effects on p53 expression but inhibited ceramide generation and apoptotic cell death caused by etoposide.	Ceramides	109-117	superoxide dismutase 1	Homo sapiens	0-20
11313880-4	2001	Superoxide dismutase (SOD), a selective antioxidant for O2-*, had no effects on p53 expression but inhibited ceramide generation and apoptotic cell death caused by etoposide.	Ceramides	109-117	superoxide dismutase 1	Homo sapiens	22-25
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Ceramides	141-149	tumor protein p53	Homo sapiens	35-38
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Ceramides	141-149	tumor protein p53	Homo sapiens	81-84
11313880-8	2001	Moreover, expression of functional p53 protein in glioma cells expressing mutant p53 using a temperature-sensitive human p53(Val138) induced ceramide accumulation by the activation of neutral sphingomyelinase which was dependent on the generation of O2-*.	Ceramides	141-149	tumor protein p53	Homo sapiens	81-84
11313880-9	2001	Taken together, these results suggest that p53 may modulate ceramide generation by activation of neutral sphingomyelinase through the formation of O2-*, but not its downstream compounds H2O2 or * OH.	Ceramides	60-68	tumor protein p53	Homo sapiens	43-46
11310790-0	2001	Ceramide inhibits cell proliferation through Akt/PKB inactivation and decreases melanin synthesis in Mel-Ab cells.	Ceramides	0-8	thymoma viral proto-oncogene 1	Mus musculus	45-48
11310790-0	2001	Ceramide inhibits cell proliferation through Akt/PKB inactivation and decreases melanin synthesis in Mel-Ab cells.	Ceramides	0-8	thymoma viral proto-oncogene 1	Mus musculus	49-52
11259760-5	2001	278 C144, 2000) have demonstrated that ceramide, a downstream messenger in TNF-alpha signaling, is a mediator of hypoxia-induced tolerance in neuronal cells.	Ceramides	39-47	tumor necrosis factor	Rattus norvegicus	75-84
11096096-0	2001	Natural ceramide reverses Fas resistance of acid sphingomyelinase(-/-) hepatocytes.	Ceramides	8-16	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	44-65
11096096-8	2001	Overcoming resistance to Fas in asmase(-/-) hepatocytes by natural ceramide is evidence that it is the lack of ceramide and not ASMase which determines the apoptotic phenotype.	Ceramides	67-75	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	32-38
11096096-8	2001	Overcoming resistance to Fas in asmase(-/-) hepatocytes by natural ceramide is evidence that it is the lack of ceramide and not ASMase which determines the apoptotic phenotype.	Ceramides	111-119	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	32-38
11313880-0	2001	p53 regulates ceramide formation by neutral sphingomyelinase through reactive oxygen species in human glioma cells.	Ceramides	14-22	tumor protein p53	Homo sapiens	0-3
11313880-1	2001	The present study was designed to elucidate the relationship between p53 and ceramide, both of which are involved in apoptotic signaling.	Ceramides	77-85	tumor protein p53	Homo sapiens	69-72
11313880-3	2001	p53 activation was followed by the formation of reactive oxygen species (ROS), superoxide anion (O2-*) measured by hydroethidium oxidation into ethidium and hydrogen peroxide (H2O2) measured by oxidation of 2",7"-dichlorofluorescin (DCFH) into 2",7"-dichlorofluorescein (DCF), which was accompanied with ceramide generation through the activation of neutral, but not acid, sphingomyelinase.	Ceramides	304-312	tumor protein p53	Homo sapiens	0-3
11085984-10	2001	TNF-alpha itself stimulated endothelial NO synthase activity to generate NO through a pathway involving its lipid messenger, ceramide.	Ceramides	125-133	tumor necrosis factor	Homo sapiens	0-9
11171115-4	2001	Here we show that ceramide analogues specifically prevent the recruitment of the PtdIns(3,4,5)P(3)-binding proteins Akt/protein kinase B (PKB) or the general receptor for phosphoinositides-1 (GRP1).	Ceramides	18-26	protein tyrosine kinase 2 beta	Homo sapiens	120-136
11171115-4	2001	Here we show that ceramide analogues specifically prevent the recruitment of the PtdIns(3,4,5)P(3)-binding proteins Akt/protein kinase B (PKB) or the general receptor for phosphoinositides-1 (GRP1).	Ceramides	18-26	AKT serine/threonine kinase 1	Homo sapiens	138-141
11171115-4	2001	Here we show that ceramide analogues specifically prevent the recruitment of the PtdIns(3,4,5)P(3)-binding proteins Akt/protein kinase B (PKB) or the general receptor for phosphoinositides-1 (GRP1).	Ceramides	18-26	cytohesin 3	Homo sapiens	150-190
11171115-4	2001	Here we show that ceramide analogues specifically prevent the recruitment of the PtdIns(3,4,5)P(3)-binding proteins Akt/protein kinase B (PKB) or the general receptor for phosphoinositides-1 (GRP1).	Ceramides	18-26	cytohesin 3	Homo sapiens	192-196
11171115-5	2001	Specifically, the short-chain ceramide derivative C2-ceramide inhibited the platelet-derived growth factor (PDGF)-stimulated translocation of full-length Akt/PKB, as well as truncated proteins encoding only the PH domains of Akt/PKB or GRP1.	Ceramides	30-38	AKT serine/threonine kinase 1	Homo sapiens	154-161
11171115-5	2001	Specifically, the short-chain ceramide derivative C2-ceramide inhibited the platelet-derived growth factor (PDGF)-stimulated translocation of full-length Akt/PKB, as well as truncated proteins encoding only the PH domains of Akt/PKB or GRP1.	Ceramides	30-38	AKT serine/threonine kinase 1	Homo sapiens	225-232
11171115-5	2001	Specifically, the short-chain ceramide derivative C2-ceramide inhibited the platelet-derived growth factor (PDGF)-stimulated translocation of full-length Akt/PKB, as well as truncated proteins encoding only the PH domains of Akt/PKB or GRP1.	Ceramides	30-38	cytohesin 3	Homo sapiens	236-240
11179444-0	2001	Tumor necrosis factor-alpha-induced cyclooxygenase-2 expression via sequential activation of ceramide-dependent mitogen-activated protein kinases, and IkappaB kinase 1/2 in human alveolar epithelial cells.	Ceramides	93-101	tumor necrosis factor	Homo sapiens	0-27
11259399-0	2001	Ceramide induces aSMase expression: implications for oxLDL-induced apoptosis.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	17-23
11259399-6	2001	We suggest that in mmLDL-initiated apoptosis 1) enhanced ceramide generation via aSMase appears to be required as well as 2) a positive feedback control of aSMase expression by the increase in intracellular ceramide concentration.	Ceramides	57-65	sphingomyelin phosphodiesterase 1	Homo sapiens	81-87
11259399-6	2001	We suggest that in mmLDL-initiated apoptosis 1) enhanced ceramide generation via aSMase appears to be required as well as 2) a positive feedback control of aSMase expression by the increase in intracellular ceramide concentration.	Ceramides	207-215	sphingomyelin phosphodiesterase 1	Homo sapiens	156-162
11238741-4	2001	Enforced expression of SPHK1 in PC12 cells resulted in significant increases in kinase activity, with corresponding increases in intracellular SPP levels and concomitant decreases in both sphingosine and ceramide, and marked suppression of apoptosis induced by trophic factor withdrawal or by C(2)-ceramide.	Ceramides	204-212	sphingosine kinase 1	Rattus norvegicus	23-28
11238914-9	2001	Tyrosine kinase inhibitor abolished the ceramide-induced activation and tyrosine phosphorylation of delta PKC-GFP.	Ceramides	40-48	TXK tyrosine kinase	Homo sapiens	0-15
11259390-1	2001	Ceramide glycosylation, through glucosylceramide synthase (GCS), allows cellular escape from ceramide-induced programmed cell death.	Ceramides	0-8	UDP-glucose ceramide glucosyltransferase	Homo sapiens	32-57
11259390-1	2001	Ceramide glycosylation, through glucosylceramide synthase (GCS), allows cellular escape from ceramide-induced programmed cell death.	Ceramides	0-8	UDP-glucose ceramide glucosyltransferase	Homo sapiens	59-62
11259390-1	2001	Ceramide glycosylation, through glucosylceramide synthase (GCS), allows cellular escape from ceramide-induced programmed cell death.	Ceramides	40-48	UDP-glucose ceramide glucosyltransferase	Homo sapiens	59-62
11259390-9	2001	Sensitivity to the various drugs by GCS antisense transfection increased 7- to 240-fold and was consistent with the resumption of ceramide-caspase-apoptotic signaling.	Ceramides	130-138	UDP-glucose ceramide glucosyltransferase	Homo sapiens	36-39
11241842-1	2001	Farber disease is a rare, autosomal recessively inherited sphingolipid storage disorder due to the deficient activity of lysosomal acid ceramidase, leading to the accumulation of ceramide in cells and tissues.	Ceramides	179-187	N-acylsphingosine amidohydrolase 1	Homo sapiens	131-146
11179444-0	2001	Tumor necrosis factor-alpha-induced cyclooxygenase-2 expression via sequential activation of ceramide-dependent mitogen-activated protein kinases, and IkappaB kinase 1/2 in human alveolar epithelial cells.	Ceramides	93-101	prostaglandin-endoperoxide synthase 2	Homo sapiens	36-52
11179444-10	2001	All these results suggest that, in NCI-H292 epithelial cells, activation of MAPKs by ceramide contributes to the TNF-alpha signaling that occurs downstream of neutral SMase activation and results in the stimulation of IKK1/2, and NF-kappaB in the COX-2 promoter, followed by initiation of COX-2 expression.	Ceramides	85-93	tumor necrosis factor	Homo sapiens	113-122
11242114-12	2001	Increased de novo ceramide synthesis triggers apoptosis and is associated with massive cell death during neural tube closure, raising the possibility that neural degeneration in HSN1 is due to ceramide-induced apoptotic cell death.	Ceramides	18-26	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	178-182
11179444-10	2001	All these results suggest that, in NCI-H292 epithelial cells, activation of MAPKs by ceramide contributes to the TNF-alpha signaling that occurs downstream of neutral SMase activation and results in the stimulation of IKK1/2, and NF-kappaB in the COX-2 promoter, followed by initiation of COX-2 expression.	Ceramides	85-93	component of inhibitor of nuclear factor kappa B kinase complex	Homo sapiens	218-222
11242114-12	2001	Increased de novo ceramide synthesis triggers apoptosis and is associated with massive cell death during neural tube closure, raising the possibility that neural degeneration in HSN1 is due to ceramide-induced apoptotic cell death.	Ceramides	193-201	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	178-182
11179444-10	2001	All these results suggest that, in NCI-H292 epithelial cells, activation of MAPKs by ceramide contributes to the TNF-alpha signaling that occurs downstream of neutral SMase activation and results in the stimulation of IKK1/2, and NF-kappaB in the COX-2 promoter, followed by initiation of COX-2 expression.	Ceramides	85-93	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	247-252
11179444-10	2001	All these results suggest that, in NCI-H292 epithelial cells, activation of MAPKs by ceramide contributes to the TNF-alpha signaling that occurs downstream of neutral SMase activation and results in the stimulation of IKK1/2, and NF-kappaB in the COX-2 promoter, followed by initiation of COX-2 expression.	Ceramides	85-93	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	289-294
11241551-8	2001	RESULTS: Ceramide caused LNCaP cell death without exhibiting typical signs of apoptosis, such as internucleosomal DNA fragmentation and poly(ADP)-ribose-polymerase (PARP) proteolysis.	Ceramides	9-17	poly(ADP-ribose) polymerase 1	Homo sapiens	136-163
11241551-8	2001	RESULTS: Ceramide caused LNCaP cell death without exhibiting typical signs of apoptosis, such as internucleosomal DNA fragmentation and poly(ADP)-ribose-polymerase (PARP) proteolysis.	Ceramides	9-17	poly(ADP-ribose) polymerase 1	Homo sapiens	165-169
11241551-11	2001	Ceramide induced a strong and prolonged activation of c-Jun N-terminal Kinase (JNK) that correlated very well with the time course of cell death.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	54-77
11241551-11	2001	Ceramide induced a strong and prolonged activation of c-Jun N-terminal Kinase (JNK) that correlated very well with the time course of cell death.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	79-82
11181043-0	2001	UVA radiation stimulates ceramide production: relationship to oxidative stress and potential role in ERK, JNK, and p38 activation.	Ceramides	25-33	mitogen-activated protein kinase 8	Homo sapiens	106-109
11181043-0	2001	UVA radiation stimulates ceramide production: relationship to oxidative stress and potential role in ERK, JNK, and p38 activation.	Ceramides	25-33	mitogen-activated protein kinase 14	Homo sapiens	115-118
11162641-0	2001	Ceramide induces the dephosphorylation and inhibition of constitutively activated Akt in PTEN negative U87mg cells.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	82-85
11241327-4	2001	In many cell types, agents which have been reported to lead to increased intracellular ceramide levels led to an increase in Gadd34 transcript levels.	Ceramides	87-95	protein phosphatase 1 regulatory subunit 15A	Homo sapiens	125-131
11354249-1	2001	Ultraviolet light (UV) activates an acid sphingomyelinase (ASMase) pathway, which hydrolyzes sphingomyeline to ceramide.	Ceramides	111-119	sphingomyelin phosphodiesterase 1	Homo sapiens	36-57
11354249-1	2001	Ultraviolet light (UV) activates an acid sphingomyelinase (ASMase) pathway, which hydrolyzes sphingomyeline to ceramide.	Ceramides	111-119	sphingomyelin phosphodiesterase 1	Homo sapiens	59-65
11354249-2	2001	Ceramide has been found to be a second messenger, which activates the c-jun N-terminal kinase (JNK) that is required for apoptotic cell death.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	70-93
11354249-2	2001	Ceramide has been found to be a second messenger, which activates the c-jun N-terminal kinase (JNK) that is required for apoptotic cell death.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	95-98
11354249-9	2001	Inhibition of ceramide production by desipramine (25-50 microM) reduced UV-induced JNK activation in both 293 and Jurkat cells; and protects 293 cells from UV-induced apoptosis.	Ceramides	14-22	mitogen-activated protein kinase 8	Homo sapiens	83-86
11354249-12	2001	These results suggest that UV-induced JNK activation and apoptosis can be mediated through a ceramide dependent or an independent pathway.	Ceramides	93-101	mitogen-activated protein kinase 8	Homo sapiens	38-41
11161461-0	2001	Interleukin 1 beta (IL-1 beta) action in porcine thyroid cells involves the ceramide signalling pathway.	Ceramides	76-84	interleukin 1 beta	Homo sapiens	0-18
11161461-0	2001	Interleukin 1 beta (IL-1 beta) action in porcine thyroid cells involves the ceramide signalling pathway.	Ceramides	76-84	interleukin 1 beta	Homo sapiens	20-29
11161461-3	2001	In this report we show that IL-1beta induces ceramide formation and sphingomyelin degradation in porcine thyroid cells via the activation of a neutral sphingomyelinase.	Ceramides	45-53	interleukin 1 beta	Homo sapiens	28-36
11161461-3	2001	In this report we show that IL-1beta induces ceramide formation and sphingomyelin degradation in porcine thyroid cells via the activation of a neutral sphingomyelinase.	Ceramides	45-53	sphingomyelin phosphodiesterase 2	Homo sapiens	143-167
11161461-5	2001	We show that both IL-1beta and ceramides lead to an increase of PKCzeta activity.	Ceramides	31-40	protein kinase C zeta	Homo sapiens	64-71
11165240-5	2001	Prevention of ceramide accumulation by AICAR led to a concomitant blockade of the Raf-1/extracellular signal-regulated kinase cascade, which selectively mediates fatty acid-induced apoptosis.	Ceramides	14-22	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	82-87
11162641-0	2001	Ceramide induces the dephosphorylation and inhibition of constitutively activated Akt in PTEN negative U87mg cells.	Ceramides	0-8	phosphatase and tensin homolog	Homo sapiens	89-93
11157748-2	2001	Here we show that yeast lacking the Snc1,2 v-SNAREs, or bearing a temperature-sensitive mutation in the Sso2 t-SNARE, are rescued at restrictive conditions by the addition of ceramide precursors and analogs to the growth medium.	Ceramides	175-183	syntaxin	Saccharomyces cerevisiae S288C	104-108
11308026-1	2001	Acid sphingomyelinase is a water-soluble, lysosomal glycoprotein that catalyzes the degradation of membrane-bound sphingomyelin into phosphorylcholine and ceramide.	Ceramides	155-163	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
11221856-4	2001	Application of ceramide analogues and ceramidase inhibitors induced rapid cell death through activation of various proapoptotic molecules, such as caspases and release of cytochrome c.	Ceramides	15-23	cytochrome c, somatic	Homo sapiens	171-183
11221856-8	2001	Therefore, B13 and related analogues of ceramide and inhibitors of ceramidases offer a promising therapeutic strategy with selective toxicity toward malignant but not normal cells.	Ceramides	40-48	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	11-14
11221891-3	2001	Both TNF-alpha and cell-permeable ceramide have been reported to increase the kinase activity of kinase suppressor of Ras (KSR).	Ceramides	34-42	kinase suppressor of ras 1	Mus musculus	123-126
11221891-5	2001	We report that TNF-alpha, a cell-permeable ceramide, and sphingomyelinase stimulate ERK1/ERK2 activation and increase the phosphoserine content of KSR, which are inhibited by kiKSR expression in intact cells.	Ceramides	43-51	tumor necrosis factor	Mus musculus	15-24
11221891-5	2001	We report that TNF-alpha, a cell-permeable ceramide, and sphingomyelinase stimulate ERK1/ERK2 activation and increase the phosphoserine content of KSR, which are inhibited by kiKSR expression in intact cells.	Ceramides	43-51	mitogen-activated protein kinase 3	Mus musculus	84-88
11221891-5	2001	We report that TNF-alpha, a cell-permeable ceramide, and sphingomyelinase stimulate ERK1/ERK2 activation and increase the phosphoserine content of KSR, which are inhibited by kiKSR expression in intact cells.	Ceramides	43-51	mitogen-activated protein kinase 1	Mus musculus	89-93
11221891-5	2001	We report that TNF-alpha, a cell-permeable ceramide, and sphingomyelinase stimulate ERK1/ERK2 activation and increase the phosphoserine content of KSR, which are inhibited by kiKSR expression in intact cells.	Ceramides	43-51	kinase suppressor of ras 1	Mus musculus	147-150
11281546-5	2001	TNF-alpha stimulates sphingomyelin metabolism and ceramide generation in a variety of cell systems.	Ceramides	50-58	tumor necrosis factor	Rattus norvegicus	0-9
11270673-0	2001	Ceramide impairs the insulin-dependent membrane recruitment of protein kinase B leading to a loss in downstream signalling in L6 skeletal muscle cells.	Ceramides	0-8	insulin	Homo sapiens	21-28
11270673-0	2001	Ceramide impairs the insulin-dependent membrane recruitment of protein kinase B leading to a loss in downstream signalling in L6 skeletal muscle cells.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	63-79
11270673-1	2001	AIMS/HYPOTHESIS: Increased cellular production of ceramide has been implicated in the pathogenesis of insulin resistance and in the impaired utilisation of glucose.	Ceramides	50-58	insulin	Homo sapiens	102-109
11270673-2	2001	In this study we have used L6 muscle cells to investigate the mechanism by which the short-chain ceramide analogue, C2-ceramide, promotes a loss in insulin sensitivity leading to a reduction in insulin stimulated glucose transport and glycogen synthesis.	Ceramides	97-105	insulin	Homo sapiens	148-155
11270673-4	2001	RESULTS: Incubation of L6 muscle cells with ceramide (100 micromol/l) for 2 h led to a complete loss of insulin-stimulated glucose transport and glycogen synthesis.	Ceramides	44-52	insulin	Homo sapiens	104-111
11270673-7	2001	Expression of a membrane-targetted protein kinase B led to its constitutive activation and an increase in glucose transport that was not inhibited by ceramide.	Ceramides	150-158	protein tyrosine kinase 2 beta	Homo sapiens	35-51
11270673-8	2001	CONCLUSIONS/INTERPRETATION: These findings suggest that a defect in protein kinase B recruitment underpins the ceramide-induced loss in insulin sensitivity of key cell responses such as glucose transport and glycogen synthesis in L6 cells.	Ceramides	111-119	protein tyrosine kinase 2 beta	Homo sapiens	68-84
11281546-6	2001	AIMS: The role of exogenous cell-permeable ceramide in modifying MAT I/III mRNA levels and its association with TNF-alpha and IL-6 actions were investigated in rat hepatocytes and H35 hepatoma cells.	Ceramides	43-51	methionine adenosyltransferase 1A	Rattus norvegicus	65-74
11281546-6	2001	AIMS: The role of exogenous cell-permeable ceramide in modifying MAT I/III mRNA levels and its association with TNF-alpha and IL-6 actions were investigated in rat hepatocytes and H35 hepatoma cells.	Ceramides	43-51	interleukin 6	Rattus norvegicus	126-130
11281546-11	2001	TNF-alpha was also a potent antagonist for MAT I/III expression, at 1-20 ng/ml decreased MAT I/III levels and induced endogenous ceramide generation.	Ceramides	129-137	tumor necrosis factor	Rattus norvegicus	0-9
11281546-11	2001	TNF-alpha was also a potent antagonist for MAT I/III expression, at 1-20 ng/ml decreased MAT I/III levels and induced endogenous ceramide generation.	Ceramides	129-137	methionine adenosyltransferase 1A	Rattus norvegicus	43-52
11162568-0	2001	Effect of overexpression of a neutral sphingomyelinase on CD95-induced ceramide production and apoptosis.	Ceramides	71-79	Fas cell surface death receptor	Homo sapiens	58-62
11171373-5	2001	It is possible that overexpression of Bcl2 prevents glucose deprivation-induced ceramide generation, probably by preventing the leakage of hydroperoxide from the mitochondria.	Ceramides	80-88	BCL2 apoptosis regulator	Homo sapiens	38-42
11171373-8	2001	Our results indicate that Bcl2 protects cells from metabolic oxidative stress-induced damage by inhibiting the leakage of hydroperoxide from the mitochondria and subsequently preventing ceramide generation.	Ceramides	186-194	BCL2 apoptosis regulator	Homo sapiens	26-30
11171373-9	2001	Preventing ceramide generation inhibits the signal transduction pathway and results in the suppression of cytochrome c release from the mitochondria.	Ceramides	11-19	cytochrome c, somatic	Homo sapiens	106-118
11169222-0	2001	T-cell receptor downregulation by ceramide-induced caspase activation and cleavage of the zeta chain.	Ceramides	34-42	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	0-15
11169222-6	2001	Thus, a 10--15% downregulation of the TCR was induced following the treatment of the T cells with ceramide for 4 h. A close correlation between TCR downregulation, caspase activation, and cleavage of the zeta chain was found.	Ceramides	98-106	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	38-41
11169222-6	2001	Thus, a 10--15% downregulation of the TCR was induced following the treatment of the T cells with ceramide for 4 h. A close correlation between TCR downregulation, caspase activation, and cleavage of the zeta chain was found.	Ceramides	98-106	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	144-147
11031259-7	2001	Most importantly, the sensitivity to stress could be restored in the asmase(-/-) MEFs by administration of natural ceramide.	Ceramides	115-123	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	69-75
11029458-9	2001	In turn, the induction of differentiation with ceramide in keratinocytes caused an increase in ASK1 expression and activity.	Ceramides	47-55	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	95-99
11167182-11	2001	CONCLUSIONS: Results suggest that IL-1alpha induce the PGHS-2 mRNA and stimulate the production of PGE2 by a mechanism that involves the sphingomyelin-ceramide system.	Ceramides	151-159	interleukin 1 alpha	Homo sapiens	34-43
11167182-11	2001	CONCLUSIONS: Results suggest that IL-1alpha induce the PGHS-2 mRNA and stimulate the production of PGE2 by a mechanism that involves the sphingomyelin-ceramide system.	Ceramides	151-159	prostaglandin-endoperoxide synthase 2	Homo sapiens	55-61
11167182-0	2001	Effect of ceramide analogs on interleukin-1alpha-induced production of prostaglandin E2 by amnion-derived (WISH) cells.	Ceramides	10-18	interleukin 1 alpha	Homo sapiens	30-48
11099485-0	2001	Ceramide binds to the CaLB domain of cytosolic phospholipase A2 and facilitates its membrane docking and arachidonic acid release.	Ceramides	0-8	phospholipase A2 group IVA	Homo sapiens	37-63
11167182-2	2001	Our objective was to measure the level of PGE2 induced by interleukin (IL)-1alpha following treatment with ceramide analogs in amnion-derived cells.	Ceramides	107-115	interleukin 1 alpha	Homo sapiens	58-81
11900368-0	2001	Tumor necrosis factor-alpha, sphingomyelinase and ceramides activate tyrosine kinase, p21Ras and phosphatidylinositol 3-kinase: implications for glucose transport and insulin resistance.	Ceramides	50-59	HRas proto-oncogene, GTPase	Homo sapiens	86-92
11900368-0	2001	Tumor necrosis factor-alpha, sphingomyelinase and ceramides activate tyrosine kinase, p21Ras and phosphatidylinositol 3-kinase: implications for glucose transport and insulin resistance.	Ceramides	50-59	insulin	Homo sapiens	167-174
11361017-10	2001	Induced ceramide levels remained elevated after cotreatment with TNF and zVAD in FADD wt cells.	Ceramides	8-16	tumor necrosis factor	Mus musculus	65-68
11361017-10	2001	Induced ceramide levels remained elevated after cotreatment with TNF and zVAD in FADD wt cells.	Ceramides	8-16	Fas (TNFRSF6)-associated via death domain	Mus musculus	81-85
11361017-12	2001	FB-sensitive ceramide production accompanies, but does not suffice, for apoptosis after Pc 4 photosensitization or TNF.	Ceramides	13-21	tumor necrosis factor	Mus musculus	115-118
11167677-6	2001	The amount of ceramide in NC/Nga Tnd mice under ALC decreased significantly.	Ceramides	14-22	reticulon 4	Mus musculus	29-32
11163340-2	2001	In general, if the modified ceramide had either a hydrogen bond donor or acceptor at C-1 and C-3, including hydrophobic or hydrophilic groups attached to C-1 microstructures formed.	Ceramides	28-36	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	85-96
11163340-5	2001	Ceramides with C-1 and C-3 bridged through a cyclic structure also made microstructures.	Ceramides	0-9	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	15-26
11099485-2	2001	In this study we show that ceramide, which is an early messenger of inflammatory cytokine action, exerts a dual effect on the cytosolic phospholipase A2 (cPLA2), the rate-limiting enzyme in arachidonic acid release and subsequent eicosanoid formation.	Ceramides	27-35	phospholipase A2 group IVA	Homo sapiens	154-159
11099485-5	2001	By use of photoactivatable ceramide analogs, D- and L-[125I]3-trifluoromethyl-3-(m-iodophenyl)diazirine-ceramides (TID-ceramides), we observed a direct interaction of ceramide with cPLA2.	Ceramides	104-112	phospholipase A2 group IVA	Homo sapiens	181-186
11589008-3	2001	Thus transient transfection of LA-N-5 neuroblastoma cells with a reverse-oriented (antisense) PPT1 (AS-PPT1) reduced PPT1 enzyme activity (as measured by an in vitro assay) and increased the susceptibility to apoptosis induced by C2 ceramide.	Ceramides	233-241	palmitoyl-protein thioesterase 1	Homo sapiens	94-98
11589008-3	2001	Thus transient transfection of LA-N-5 neuroblastoma cells with a reverse-oriented (antisense) PPT1 (AS-PPT1) reduced PPT1 enzyme activity (as measured by an in vitro assay) and increased the susceptibility to apoptosis induced by C2 ceramide.	Ceramides	233-241	palmitoyl-protein thioesterase 1	Homo sapiens	100-107
11099485-7	2001	Moreover, recombinant CaLB domain of cPLA2 as well as a mutant deficient in the connecting "hinge" domain of cPLA2, efficiently bound D- and L-TID-ceramides, whereas the catalytic domain did not interact with TID-ceramides.	Ceramides	147-156	phospholipase A2 group IVA	Homo sapiens	37-42
11099485-2	2001	In this study we show that ceramide, which is an early messenger of inflammatory cytokine action, exerts a dual effect on the cytosolic phospholipase A2 (cPLA2), the rate-limiting enzyme in arachidonic acid release and subsequent eicosanoid formation.	Ceramides	27-35	phospholipase A2 group IVA	Homo sapiens	126-152
11099485-7	2001	Moreover, recombinant CaLB domain of cPLA2 as well as a mutant deficient in the connecting "hinge" domain of cPLA2, efficiently bound D- and L-TID-ceramides, whereas the catalytic domain did not interact with TID-ceramides.	Ceramides	147-156	phospholipase A2 group IVA	Homo sapiens	109-114
11099485-8	2001	In vitro binding assays reveal that stearoyl-arachidonyl-phosphatidylcholine (SAPC)-liposomes containing increasing mol% of ceramide lead to an increased association of recombinant cPLA2 to the liposomes.	Ceramides	124-132	phospholipase A2 group IVA	Homo sapiens	181-186
11589008-3	2001	Thus transient transfection of LA-N-5 neuroblastoma cells with a reverse-oriented (antisense) PPT1 (AS-PPT1) reduced PPT1 enzyme activity (as measured by an in vitro assay) and increased the susceptibility to apoptosis induced by C2 ceramide.	Ceramides	233-241	palmitoyl-protein thioesterase 1	Homo sapiens	103-107
11460570-5	2001	A key factor is seen to be accumulation of muscle long chain acyl CoAs, which could alter insulin action via several mechanisms including chronic activation of protein kinase C isoforms or ceramide accumulation.	Ceramides	189-197	insulin	Homo sapiens	90-97
11099485-11	2001	Furthermore, liposomes containing SAPC and sphingomyelin resulted in no better substrate than SAPC liposomes, unless bacterial sphingomyelinase was added to generate ceramide, which then causes a marked increase in cPLA2 activity.	Ceramides	166-174	phospholipase A2 group IVA	Homo sapiens	215-220
11099485-12	2001	These results demonstrate that ceramide can interact directly with cPLA2 via the CaLB domain and thereby serves as a membrane-docking device that facilitates cPLA2 action in inflammatory diseases.	Ceramides	31-39	phospholipase A2 group IVA	Homo sapiens	67-72
11099485-12	2001	These results demonstrate that ceramide can interact directly with cPLA2 via the CaLB domain and thereby serves as a membrane-docking device that facilitates cPLA2 action in inflammatory diseases.	Ceramides	31-39	phospholipase A2 group IVA	Homo sapiens	158-163
11255263-1	2001	Fas receptor and tumor necrosis factor receptor-1 (TNFR1) mediate the activation of acid sphingomyelinase (ASMase), which catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	167-175	TNF receptor superfamily member 1A	Homo sapiens	51-56
11142362-3	2001	The major fragmentation pathways arise from loss of the sugar moiety to yield a lithiated ceramide ion, which undergoes further fragmentation to form multiple fragment ions that confirm the structures of the fatty acid and LCB.	Ceramides	90-98	clathrin light chain B	Homo sapiens	223-226
11204306-2	2001	Ceramide is a recently identified second messenger synthesized in response to cytokines such as tumour necrosis factor alpha (TNF-alpha).	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	126-135
11204306-11	2001	During chronic treatment with TNF-alpha, ceramide levels increased in WKY rat cells but remained unchanged in cells from SHR.	Ceramides	41-49	tumor necrosis factor	Rattus norvegicus	30-39
11204306-13	2001	Short-term incubation with TNF-alpha resulted in a greater increase in ceramide in cells from WKY rats than those from SHR.	Ceramides	71-79	tumor necrosis factor	Rattus norvegicus	27-36
11149666-0	2001	The protective effect of ceramide in immature rat brain hypoxia-ischemia involves up-regulation of bcl-2 and reduction of TUNEL-positive cells.	Ceramides	25-33	BCL2, apoptosis regulator	Rattus norvegicus	99-104
11149666-1	2001	Preconditioning brain with tumor necrosis factor alpha (TNF-alpha) can induce tolerance to experimental hypoxia and stroke and ceramide is a downstream messenger in the TNF-alpha signaling pathway.	Ceramides	127-135	tumor necrosis factor	Rattus norvegicus	27-54
11149666-1	2001	Preconditioning brain with tumor necrosis factor alpha (TNF-alpha) can induce tolerance to experimental hypoxia and stroke and ceramide is a downstream messenger in the TNF-alpha signaling pathway.	Ceramides	127-135	tumor necrosis factor	Rattus norvegicus	56-65
11149666-1	2001	Preconditioning brain with tumor necrosis factor alpha (TNF-alpha) can induce tolerance to experimental hypoxia and stroke and ceramide is a downstream messenger in the TNF-alpha signaling pathway.	Ceramides	127-135	tumor necrosis factor	Rattus norvegicus	169-178
11113186-4	2001	The tsc13 mutant accumulates high levels of long-chain bases as well as ceramides that harbor fatty acids with chain lengths shorter than 26 carbons.	Ceramides	72-81	trans-2-enoyl-CoA reductase (NADPH) TSC13	Saccharomyces cerevisiae S288C	4-9
11255263-1	2001	Fas receptor and tumor necrosis factor receptor-1 (TNFR1) mediate the activation of acid sphingomyelinase (ASMase), which catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	167-175	sphingomyelin phosphodiesterase 1	Homo sapiens	84-105
11255263-1	2001	Fas receptor and tumor necrosis factor receptor-1 (TNFR1) mediate the activation of acid sphingomyelinase (ASMase), which catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	167-175	sphingomyelin phosphodiesterase 1	Homo sapiens	107-113
11282287-15	2000	These results suggest that a ceramide-dependent pathway regulates hCG-stimulated Leydig cell steroidogenesis at the level of cAMP production and at post-cAMP events.	Ceramides	29-37	hypertrichosis 2 (generalised, congenital)	Homo sapiens	66-69
11110682-0	2000	Evidence that ceramide mediates the ability of tumor necrosis factor to modulate primitive human hematopoietic cell fates.	Ceramides	14-22	tumor necrosis factor	Homo sapiens	47-68
11197751-0	2000	Hepatocyte growth factor protects gastric epithelial cells against ceramide-induced apoptosis through induction of cyclooxygenase-2.	Ceramides	67-75	hepatocyte growth factor	Rattus norvegicus	0-24
11197751-0	2000	Hepatocyte growth factor protects gastric epithelial cells against ceramide-induced apoptosis through induction of cyclooxygenase-2.	Ceramides	67-75	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	115-131
11197751-3	2000	In the present study, we examined whether hepatocyte growth factor (HGF)-induced COX-2 affects ceramide-induced apoptosis in RGM-1 gastric epithelial cells.	Ceramides	95-103	hepatocyte growth factor	Rattus norvegicus	42-66
11197751-3	2000	In the present study, we examined whether hepatocyte growth factor (HGF)-induced COX-2 affects ceramide-induced apoptosis in RGM-1 gastric epithelial cells.	Ceramides	95-103	hepatocyte growth factor	Rattus norvegicus	68-71
11107162-0	2000	Release of plasminogen activator inhibitor-1 from human astrocytes is regulated by intracellular ceramide.	Ceramides	97-105	serpin family E member 1	Homo sapiens	11-44
11107162-1	2000	The present study underscores a regulatory role of intracellular ceramide in astrocytes for the release of an extracellular serine protease, tissue-type plasminogen activator (t-PA), and its inhibitor, plasminogen activator inhibitor-1 (PAI-1).	Ceramides	65-73	plasminogen activator, tissue type	Homo sapiens	141-174
11112337-0	2000	Regulation of cyclin-dependent kinase 2 activity by ceramide.	Ceramides	52-60	cyclin dependent kinase 2	Homo sapiens	14-39
11107162-1	2000	The present study underscores a regulatory role of intracellular ceramide in astrocytes for the release of an extracellular serine protease, tissue-type plasminogen activator (t-PA), and its inhibitor, plasminogen activator inhibitor-1 (PAI-1).	Ceramides	65-73	plasminogen activator, tissue type	Homo sapiens	176-180
11112337-5	2000	Employing immunoprecipitation kinase assays, we found that ceramide specifically inhibited cyclin-dependent kinase CDK2, with a mild effect on CDC2 and significantly less effect on CDK4.	Ceramides	59-67	cyclin dependent kinase 2	Homo sapiens	115-119
11110682-2	2000	A similar differential effect on the functional attributes of CD34(+)CD38(-) cells was seen when C2- or C6-ceramide, but not dihydro-C2-ceramide (an inactive analog of ceramide), was substituted for TNF.	Ceramides	107-115	CD34 molecule	Homo sapiens	62-66
11112337-5	2000	Employing immunoprecipitation kinase assays, we found that ceramide specifically inhibited cyclin-dependent kinase CDK2, with a mild effect on CDC2 and significantly less effect on CDK4.	Ceramides	59-67	cyclin dependent kinase 1	Homo sapiens	143-147
11107162-1	2000	The present study underscores a regulatory role of intracellular ceramide in astrocytes for the release of an extracellular serine protease, tissue-type plasminogen activator (t-PA), and its inhibitor, plasminogen activator inhibitor-1 (PAI-1).	Ceramides	65-73	serpin family E member 1	Homo sapiens	202-235
11107162-1	2000	The present study underscores a regulatory role of intracellular ceramide in astrocytes for the release of an extracellular serine protease, tissue-type plasminogen activator (t-PA), and its inhibitor, plasminogen activator inhibitor-1 (PAI-1).	Ceramides	65-73	serpin family E member 1	Homo sapiens	237-242
11112337-5	2000	Employing immunoprecipitation kinase assays, we found that ceramide specifically inhibited cyclin-dependent kinase CDK2, with a mild effect on CDC2 and significantly less effect on CDK4.	Ceramides	59-67	cyclin dependent kinase 4	Homo sapiens	181-185
11107162-3	2000	Interestingly, treatment of the astrocytes with tumor necrosis factor (TNF)-alpha also increased the intracellular ceramide levels but caused the elevation of PAI-1 release without altering the t-PA release.	Ceramides	115-123	tumor necrosis factor	Homo sapiens	48-81
11110682-2	2000	A similar differential effect on the functional attributes of CD34(+)CD38(-) cells was seen when C2- or C6-ceramide, but not dihydro-C2-ceramide (an inactive analog of ceramide), was substituted for TNF.	Ceramides	107-115	CD38 molecule	Homo sapiens	69-73
11107162-4	2000	These data suggest that the generation of ceramide in astrocytes is linked at least with the regulation of PAI-1 release.	Ceramides	42-50	serpin family E member 1	Rattus norvegicus	107-112
11112337-7	2000	Ceramide did not directly inhibit CDK2 in vitro but caused activation of p21, a major class of CDK-inhibitory proteins, and led to a greater association of p21 to CDK2.	Ceramides	0-8	cyclin dependent kinase inhibitor 1A	Homo sapiens	73-76
11112337-7	2000	Ceramide did not directly inhibit CDK2 in vitro but caused activation of p21, a major class of CDK-inhibitory proteins, and led to a greater association of p21 to CDK2.	Ceramides	0-8	cyclin dependent kinase inhibitor 1A	Homo sapiens	156-159
11112337-7	2000	Ceramide did not directly inhibit CDK2 in vitro but caused activation of p21, a major class of CDK-inhibitory proteins, and led to a greater association of p21 to CDK2.	Ceramides	0-8	cyclin dependent kinase 2	Homo sapiens	163-167
11112337-8	2000	Using purified protein phosphatases, we showed that ceramide activated both protein phosphatase 1 and protein phosphatase 2A activities specific for CDK2 in vitro.	Ceramides	52-60	cyclin dependent kinase 2	Homo sapiens	149-153
11110682-3	2000	The addition of D-erythro-MAPP (a specific inhibitor of intracellular ceramide degradation) enhanced the ability of TNF to selectively eliminate long-term culture-initiating cell (LTC-IC) activity.	Ceramides	70-78	tumor necrosis factor	Homo sapiens	116-119
11110682-4	2000	These findings indicate that TNF can directly modulate the ability of CD34(+)CD38(-) cells to maintain their LTC-IC function at doses below those required to initiate apoptosis, cell cycle arrest, or both, and they suggest that this may be mediated by the TNF-induced generation of intracellular ceramide.	Ceramides	296-304	tumor necrosis factor	Homo sapiens	29-32
11110682-4	2000	These findings indicate that TNF can directly modulate the ability of CD34(+)CD38(-) cells to maintain their LTC-IC function at doses below those required to initiate apoptosis, cell cycle arrest, or both, and they suggest that this may be mediated by the TNF-induced generation of intracellular ceramide.	Ceramides	296-304	CD34 molecule	Homo sapiens	70-74
11110682-4	2000	These findings indicate that TNF can directly modulate the ability of CD34(+)CD38(-) cells to maintain their LTC-IC function at doses below those required to initiate apoptosis, cell cycle arrest, or both, and they suggest that this may be mediated by the TNF-induced generation of intracellular ceramide.	Ceramides	296-304	CD38 molecule	Homo sapiens	77-81
11112337-9	2000	Further, calyculin A and okadaic acid, both potent protein phosphatase inhibitors, together almost completely reversed the effects of ceramide on CDK2 inhibition.	Ceramides	134-142	cyclin dependent kinase 2	Homo sapiens	146-150
11112337-11	2000	Ceramide causes an increase in p21 association with CDK2 and through activation of protein phosphatases selectively regulates CDK2.	Ceramides	0-8	cyclin dependent kinase inhibitor 1A	Homo sapiens	31-34
11153078-2	2000	Whereas the HIV-1 nef gene is overexpressed during restricted HIV-1 infection of human astrocytes, our previous results have demonstrated that nef expressed in human U251MG glial cells activates the sphingomyelin pathway triggered by TNF-alpha, increasing ceramide production.	Ceramides	256-264	S100 calcium binding protein B	Homo sapiens	143-146
11112337-11	2000	Ceramide causes an increase in p21 association with CDK2 and through activation of protein phosphatases selectively regulates CDK2.	Ceramides	0-8	cyclin dependent kinase 2	Homo sapiens	52-56
11112337-11	2000	Ceramide causes an increase in p21 association with CDK2 and through activation of protein phosphatases selectively regulates CDK2.	Ceramides	0-8	cyclin dependent kinase 2	Homo sapiens	126-130
11153078-2	2000	Whereas the HIV-1 nef gene is overexpressed during restricted HIV-1 infection of human astrocytes, our previous results have demonstrated that nef expressed in human U251MG glial cells activates the sphingomyelin pathway triggered by TNF-alpha, increasing ceramide production.	Ceramides	256-264	tumor necrosis factor	Homo sapiens	234-243
11080206-6	2000	In the present study, we examined the changes and effect of CDP-choline on ceramide and phospholipids including PtdCho, phosphatidylethanolamine (PtdEtn), phosphatidylinositol (PtdIns), phosphatidylserine (PtdSer), sphingomyelin, and cardiolipin (an exclusive inner mitochondrial membrane lipid essential for electron transport) following ischemia/1-day reperfusion.	Ceramides	75-83	cut like homeobox 1	Homo sapiens	60-63
11106681-6	2000	RESULTS: 4-HPR increased ceramide levels by de novo synthesis.	Ceramides	25-33	haptoglobin-related protein	Homo sapiens	11-14
11106681-10	2000	CONCLUSIONS: Combinations of 4-HPR and modulators of ceramide metabolism may form the basis for a novel chemotherapy that is functional under hypoxic conditions (e.g., such as those within tumors) and is p53 independent and caspase independent.	Ceramides	53-61	tumor protein p53	Homo sapiens	204-207
11303914-0	2000	Early transitory rise in intracellular pH leads to Bax conformation change during ceramide-induced apoptosis.	Ceramides	82-90	BCL2 associated X, apoptosis regulator	Homo sapiens	51-54
11303914-2	2000	Bax has been described as able to kill cells in the absence of caspase activity, therefore we measured Bax in situ during ceramide-induced apoptosis using anti-Bax antibodies and flow cytometry analysis.	Ceramides	122-130	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
11303914-2	2000	Bax has been described as able to kill cells in the absence of caspase activity, therefore we measured Bax in situ during ceramide-induced apoptosis using anti-Bax antibodies and flow cytometry analysis.	Ceramides	122-130	BCL2 associated X, apoptosis regulator	Homo sapiens	103-106
11303914-2	2000	Bax has been described as able to kill cells in the absence of caspase activity, therefore we measured Bax in situ during ceramide-induced apoptosis using anti-Bax antibodies and flow cytometry analysis.	Ceramides	122-130	BCL2 associated X, apoptosis regulator	Homo sapiens	103-106
11303914-3	2000	An early (<30 min) increase in Bax labeling was observed after the addition of several ceramide species to several hemopoietic-related cell types.	Ceramides	90-98	BCL2 associated X, apoptosis regulator	Homo sapiens	34-37
11152958-1	2000	We have investigated the roles of ceramide in Fas signalling leading to phospholipase D (PLD) activation in A20 cells.	Ceramides	34-42	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	89-92
11106681-1	2000	BACKGROUND: We previously reported that N-(4-hydroxyphenyl)retinamide (4-HPR, fenretinide) treatment caused large increases of ceramide levels in neuroblastoma cell lines and induced cell death by a combination of apoptosis and necrosis through p53 (also known as TP53)-independent and caspase-independent pathways.	Ceramides	127-135	haptoglobin-related protein	Homo sapiens	73-76
11106681-2	2000	Our goal was to determine if several molecules that inhibit enzymes involved in ceramide metabolism-L-threo-dihydrosphingosine (safingol), d, l-threo-1-phenyl-2-hexadecanoylamino-3-morpholino-1-propanol (PPMP), and tamoxifen-enhanced 4-HPR-mediated cytotoxicity and/or affected ceramide levels.	Ceramides	80-88	haptoglobin-related protein	Homo sapiens	236-239
11191283-6	2000	However, both ceramide and TNF-alpha potentiated IL-1beta- induced activation of NF-kappaB and iNOS.	Ceramides	14-22	interleukin 1 beta	Rattus norvegicus	49-57
11191283-6	2000	However, both ceramide and TNF-alpha potentiated IL-1beta- induced activation of NF-kappaB and iNOS.	Ceramides	14-22	nitric oxide synthase 2	Rattus norvegicus	95-99
11191283-8	2000	The combination of IL-1beta and IFN-gamma induced apoptosis in RINm5F cells, which was paralleled by a modest increase in acid SMase, whereas ceramide mainly induced necrosis.	Ceramides	142-150	interferon gamma	Rattus norvegicus	32-41
11152959-0	2000	Ceramide-dependent regulation of p42/p44 mitogen-activated protein kinase and c-Jun N-terminal-directed protein kinase in cultured airway smooth muscle cells.	Ceramides	0-8	cyclin dependent kinase 20	Homo sapiens	33-73
11152959-1	2000	Previous studies have demonstrated that a number of biochemical actions of ceramide are mediated through protein kinase signalling pathways, such as p42/p44 mitogen-activated protein kinase (p42/p44 MAPK) and c-Jun N-terminal directed protein kinase (JNK).	Ceramides	75-83	cyclin dependent kinase 20	Homo sapiens	149-189
11152959-1	2000	Previous studies have demonstrated that a number of biochemical actions of ceramide are mediated through protein kinase signalling pathways, such as p42/p44 mitogen-activated protein kinase (p42/p44 MAPK) and c-Jun N-terminal directed protein kinase (JNK).	Ceramides	75-83	cyclin dependent kinase 20	Homo sapiens	149-152
11152959-1	2000	Previous studies have demonstrated that a number of biochemical actions of ceramide are mediated through protein kinase signalling pathways, such as p42/p44 mitogen-activated protein kinase (p42/p44 MAPK) and c-Jun N-terminal directed protein kinase (JNK).	Ceramides	75-83	mitogen-activated protein kinase 3	Homo sapiens	195-203
11152959-1	2000	Previous studies have demonstrated that a number of biochemical actions of ceramide are mediated through protein kinase signalling pathways, such as p42/p44 mitogen-activated protein kinase (p42/p44 MAPK) and c-Jun N-terminal directed protein kinase (JNK).	Ceramides	75-83	mitogen-activated protein kinase 8	Homo sapiens	251-254
11152959-6	2000	The possibility that growth arrest could be mediated by JNK was discounted on the basis that PDGF, as well as ceramide, stimulated JNK in these cells.	Ceramides	110-118	mitogen-activated protein kinase 8	Homo sapiens	131-134
11102964-0	2000	Ceramide-enhanced urokinase-type plasminogen activator (uPA) release is mediated by protein kinase C in cultured microglia.	Ceramides	0-8	plasminogen activator, urokinase	Homo sapiens	18-54
11102964-0	2000	Ceramide-enhanced urokinase-type plasminogen activator (uPA) release is mediated by protein kinase C in cultured microglia.	Ceramides	0-8	plasminogen activator, urokinase	Homo sapiens	56-59
11102964-3	2000	Therefore, in the present study, we examined the effect of ceramide on the release of uPA from cultured microglia.	Ceramides	59-67	plasminogen activator, urokinase	Homo sapiens	86-89
11102964-6	2000	A pharmacological study using a specific PKC activator, phorbol-12-myristate-13-acetate, and a protein kinase C (PKC) inhibitor, bisindolylmaleimide, showed that PKC activation is required in order to release uPA from ceramide-stimulated microglia as well as from nonstimulated microglia.	Ceramides	218-226	protein kinase C delta	Homo sapiens	41-44
11102964-6	2000	A pharmacological study using a specific PKC activator, phorbol-12-myristate-13-acetate, and a protein kinase C (PKC) inhibitor, bisindolylmaleimide, showed that PKC activation is required in order to release uPA from ceramide-stimulated microglia as well as from nonstimulated microglia.	Ceramides	218-226	protein kinase C delta	Homo sapiens	113-116
11102964-6	2000	A pharmacological study using a specific PKC activator, phorbol-12-myristate-13-acetate, and a protein kinase C (PKC) inhibitor, bisindolylmaleimide, showed that PKC activation is required in order to release uPA from ceramide-stimulated microglia as well as from nonstimulated microglia.	Ceramides	218-226	protein kinase C delta	Homo sapiens	113-116
11090283-3	2000	The high affinity of GM2-AP for GM2 is based on specfic recognition of the oligosaccharide moiety as well as the ceramide lipid tail.	Ceramides	113-121	ganglioside GM2 activator	Homo sapiens	21-27
11129654-0	2000	Streptolysin O-permeabilized granulocytes shed L-selectin concomitantly with ceramide generation via neutral sphingomyelinase.	Ceramides	77-85	sphingomyelin phosphodiesterase 2	Homo sapiens	101-125
11129654-4	2000	Cells permeabilized with SLO exhibited a 1.5-fold increase in the activity of neutral sphingomyelinase, which was accompanied by increased ceramide formation.	Ceramides	139-147	sphingomyelin phosphodiesterase 2	Homo sapiens	78-102
11129654-5	2000	L-selectin cleavage was inducible by treatment of cells with bacterial sphingomyelinase, and also through exogenous application of a cell-permeable ceramide analog.	Ceramides	148-156	selectin L	Homo sapiens	0-10
11129654-6	2000	Our data identify a novel path to the shedding process and show that activation of neutral sphingomyelinase with the generation of ceramide is an important event underlying enhanced sheddase function in cells permeabilized by a pore-forming toxin.	Ceramides	131-139	sphingomyelin phosphodiesterase 2	Homo sapiens	83-107
11121143-0	2000	Keloid fibroblasts resist ceramide-induced apoptosis by overexpression of insulin-like growth factor I receptor.	Ceramides	26-34	insulin like growth factor 1	Homo sapiens	74-102
11063615-4	2000	Moreover, we demonstrated that a ceramide analogue with an aromatic ring in the sphingoid moiety is recognized as a substrate by glucosylceramide synthase, which suggests that the observed biological effects are mediated by activation of the ceramide analogue via glucosylation.	Ceramides	33-41	UDP-glucose ceramide glucosyltransferase	Homo sapiens	129-154
11121143-8	2000	Exogenously added insulin-like growth factor I enhanced the resistance of keloid fibroblasts to ceramide-induced apoptosis.	Ceramides	96-104	insulin like growth factor 1	Homo sapiens	18-46
11102528-6	2000	Rac1-induced apoptosis was related to the simultaneous increase in ceramide production and synthesis of FasL.	Ceramides	67-75	Rac family small GTPase 1	Mus musculus	0-4
11102528-11	2000	Thus, Rac1 seems to induce apoptosis by a complex mechanism involving the generation of ceramides and the de novo synthesis of FasL.	Ceramides	88-97	Rac family small GTPase 1	Mus musculus	6-10
10926924-1	2000	Treatment with the lipid second messenger, ceramide, activates extracellular signal-regulated kinase-1/2 (ERK1/2), c-Jun N-terminal kinase, and p38 in human skin fibroblasts and induces their collagenase-1 expression (Reunanen, N., Westermarck, J., Hakkinen, L., Holmstrom, T. H., Elo, I., Eriksson, J. E., and Kahari, V.-M. (1998) J. Biol.	Ceramides	43-51	mitogen-activated protein kinase 1	Homo sapiens	63-104
10926924-1	2000	Treatment with the lipid second messenger, ceramide, activates extracellular signal-regulated kinase-1/2 (ERK1/2), c-Jun N-terminal kinase, and p38 in human skin fibroblasts and induces their collagenase-1 expression (Reunanen, N., Westermarck, J., Hakkinen, L., Holmstrom, T. H., Elo, I., Eriksson, J. E., and Kahari, V.-M. (1998) J. Biol.	Ceramides	43-51	mitogen-activated protein kinase 3	Homo sapiens	106-112
10926924-1	2000	Treatment with the lipid second messenger, ceramide, activates extracellular signal-regulated kinase-1/2 (ERK1/2), c-Jun N-terminal kinase, and p38 in human skin fibroblasts and induces their collagenase-1 expression (Reunanen, N., Westermarck, J., Hakkinen, L., Holmstrom, T. H., Elo, I., Eriksson, J. E., and Kahari, V.-M. (1998) J. Biol.	Ceramides	43-51	mitogen-activated protein kinase 1	Homo sapiens	144-147
11426620-6	2000	Furthermore, cell permeable ceramide, a lipid messenger known to mediate cellular effects of chemotherapeutic drugs and TPA, activated the MDR1 gene and down-regulated PKC.	Ceramides	28-36	ATP binding cassette subfamily B member 1	Homo sapiens	139-143
11082532-4	2000	Like ceramide, daunorubicin also decreased EGF-induced diacylglycerol generation.	Ceramides	5-13	epidermal growth factor	Homo sapiens	43-46
10962008-0	2000	Ceramide directly activates protein kinase C zeta to regulate a stress-activated protein kinase signaling complex.	Ceramides	0-8	mitogen-activated protein kinase 9	Homo sapiens	64-95
10962008-1	2000	We have previously shown that interleukin 1 (IL-1)-receptor-generated ceramide induces growth arrest in smooth muscle pericytes by activating an upstream kinase in the stress-activated protein kinase (SAPK) cascade.	Ceramides	70-78	mitogen-activated protein kinase 9	Homo sapiens	168-199
10962008-1	2000	We have previously shown that interleukin 1 (IL-1)-receptor-generated ceramide induces growth arrest in smooth muscle pericytes by activating an upstream kinase in the stress-activated protein kinase (SAPK) cascade.	Ceramides	70-78	mitogen-activated protein kinase 9	Homo sapiens	201-205
10962008-2	2000	We now report the mechanism by which ceramide activates the SAPK signaling pathway in human embryonic kidney cells (HEK-293).	Ceramides	37-45	mitogen-activated protein kinase 9	Homo sapiens	60-64
10962008-3	2000	We demonstrate that ceramide activation of protein kinase C zeta (PKCzeta) mediates SAPK signal complex formation and subsequent growth suppression.	Ceramides	20-28	protein kinase C zeta	Homo sapiens	66-73
10962008-3	2000	We demonstrate that ceramide activation of protein kinase C zeta (PKCzeta) mediates SAPK signal complex formation and subsequent growth suppression.	Ceramides	20-28	mitogen-activated protein kinase 9	Homo sapiens	84-88
10962008-4	2000	Ceramide directly activates both immunoprecipitated and recombinant human PKCzeta in vitro.	Ceramides	0-8	protein kinase C zeta	Homo sapiens	74-81
10962008-5	2000	Additionally, ceramide activates SAPK activity, which is blocked with a dominant-negative mutant of PKCzeta.	Ceramides	14-22	mitogen-activated protein kinase 9	Homo sapiens	33-37
10962008-5	2000	Additionally, ceramide activates SAPK activity, which is blocked with a dominant-negative mutant of PKCzeta.	Ceramides	14-22	protein kinase C zeta	Homo sapiens	100-107
10962008-6	2000	Co-immunoprecipitation studies reveal that ceramide induces the association of SAPK with PKCzeta, but not with PKCepsilon.	Ceramides	43-51	mitogen-activated protein kinase 9	Homo sapiens	79-83
10962008-6	2000	Co-immunoprecipitation studies reveal that ceramide induces the association of SAPK with PKCzeta, but not with PKCepsilon.	Ceramides	43-51	protein kinase C zeta	Homo sapiens	89-96
10962008-7	2000	In addition, ceramide treatment induces PKCzeta association with phosphorylated SEK and MEKK1, elements of the SAPK signaling complex.	Ceramides	13-21	protein kinase C zeta	Homo sapiens	40-47
10962008-7	2000	In addition, ceramide treatment induces PKCzeta association with phosphorylated SEK and MEKK1, elements of the SAPK signaling complex.	Ceramides	13-21	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	88-93
10962008-7	2000	In addition, ceramide treatment induces PKCzeta association with phosphorylated SEK and MEKK1, elements of the SAPK signaling complex.	Ceramides	13-21	mitogen-activated protein kinase 9	Homo sapiens	111-115
10962008-8	2000	The biological role of ceramide to induce cell cycle arrest is mimicked by overexpression of a constitutively active PKCzeta.	Ceramides	23-31	protein kinase C zeta	Homo sapiens	117-124
10962008-9	2000	Together, these studies demonstrate that ceramide induces cell cycle arrest by enhancing the ability of PKCzeta to form a signaling complex with MEKK1, SEK, and SAPK.	Ceramides	41-49	protein kinase C zeta	Homo sapiens	104-111
10962008-9	2000	Together, these studies demonstrate that ceramide induces cell cycle arrest by enhancing the ability of PKCzeta to form a signaling complex with MEKK1, SEK, and SAPK.	Ceramides	41-49	mitogen-activated protein kinase kinase kinase 1	Homo sapiens	145-150
10962008-9	2000	Together, these studies demonstrate that ceramide induces cell cycle arrest by enhancing the ability of PKCzeta to form a signaling complex with MEKK1, SEK, and SAPK.	Ceramides	41-49	mitogen-activated protein kinase 9	Homo sapiens	161-165
11062012-0	2000	Ceramide induction of COX-2 and PGE(2) in pulmonary A549 cells does not involve activation of NF-kappaB.	Ceramides	0-8	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	22-27
11062012-1	2000	Ceramide is generated by the hydrolysis of membrane sphingomyelin by sphingomyelinase (SMase) and is implicated in multiple signaling pathways, including activation of NF-kappaB.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	168-177
11062012-3	2000	Ceramide and SMase both induced cyclooxygenase (COX)-2 protein expression and stimulated PGE(2) release.	Ceramides	0-8	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	32-54
11062012-5	2000	Both ceramide and SMase were efficient inducers of the extracellular regulated kinase (ERK), but not Jun N-terminal kinase (JNK) or p38 mitogen-activated protein kinase.	Ceramides	5-13	mitogen-activated protein kinase 1	Homo sapiens	55-85
11062012-5	2000	Both ceramide and SMase were efficient inducers of the extracellular regulated kinase (ERK), but not Jun N-terminal kinase (JNK) or p38 mitogen-activated protein kinase.	Ceramides	5-13	mitogen-activated protein kinase 1	Homo sapiens	87-90
11062012-6	2000	Since ERK is implicated in arachidonic acid availability, these data partly explain the ability of ceramide to induce PGE(2) release.	Ceramides	99-107	mitogen-activated protein kinase 1	Homo sapiens	6-9
11058554-10	2000	Exogenous C2 ceramide increased LDH(A4) activity only in cytokine-treated cells, suggesting its involvement as sphingosine precursor in TNFalpha-stimulated LDH(A4) activity via the sphingomyelin hydrolysis pathway.	Ceramides	13-21	tumor necrosis factor	Homo sapiens	136-144
11053253-0	2000	De novo-synthesized ceramide signals apoptosis in astrocytes via extracellular signal-regulated kinase.	Ceramides	20-28	mitogen-activated protein kinase 1	Homo sapiens	65-102
11060030-2	2000	Evidence is provided for a novel mechanism of ceramide formation that mediates solar ultraviolet (UV) A radiation-induced expression of the intercellular adhesion molecule (ICAM)-1.	Ceramides	46-54	intercellular adhesion molecule 1	Homo sapiens	140-180
11060030-3	2000	Similarly to UVA radiation, ceramide stimulation of human keratinocytes induced ICAM-1 mRNA expression and activated the ICAM-1 promoter through transcription factor AP-2.	Ceramides	28-36	intercellular adhesion molecule 1	Homo sapiens	80-86
11060030-3	2000	Similarly to UVA radiation, ceramide stimulation of human keratinocytes induced ICAM-1 mRNA expression and activated the ICAM-1 promoter through transcription factor AP-2.	Ceramides	28-36	intercellular adhesion molecule 1	Homo sapiens	121-127
11060030-3	2000	Similarly to UVA radiation, ceramide stimulation of human keratinocytes induced ICAM-1 mRNA expression and activated the ICAM-1 promoter through transcription factor AP-2.	Ceramides	28-36	transcription factor AP-2 alpha	Homo sapiens	166-170
11060030-4	2000	Ceramide-activated AP-2 and ceramide-induced ICAM-1 reporter gene activation were abrogated through deletion of the AP-2 binding site.	Ceramides	0-8	transcription factor AP-2 alpha	Homo sapiens	19-23
11060030-4	2000	Ceramide-activated AP-2 and ceramide-induced ICAM-1 reporter gene activation were abrogated through deletion of the AP-2 binding site.	Ceramides	0-8	intercellular adhesion molecule 1	Homo sapiens	45-51
11060030-4	2000	Ceramide-activated AP-2 and ceramide-induced ICAM-1 reporter gene activation were abrogated through deletion of the AP-2 binding site.	Ceramides	0-8	transcription factor AP-2 alpha	Homo sapiens	116-120
11060030-4	2000	Ceramide-activated AP-2 and ceramide-induced ICAM-1 reporter gene activation were abrogated through deletion of the AP-2 binding site.	Ceramides	28-36	intercellular adhesion molecule 1	Homo sapiens	45-51
11060030-4	2000	Ceramide-activated AP-2 and ceramide-induced ICAM-1 reporter gene activation were abrogated through deletion of the AP-2 binding site.	Ceramides	28-36	transcription factor AP-2 alpha	Homo sapiens	116-120
11075960-0	2000	Regulation by ceramide of epidermal growth factor signal transduction and mitogenesis in cell lines overexpressing the growth factor receptor.	Ceramides	14-22	receptor-like tyrosine kinase	Mus musculus	119-141
11075960-2	2000	In the present study we evaluated the effect of cell permeant ceramide analogues on ligand-induced tyrosine phosphorylation of the EGF receptor (EGFR), phospholipase Cy (PLCgamma) activity and cell proliferation.	Ceramides	62-70	epidermal growth factor receptor	Mus musculus	131-143
11075960-2	2000	In the present study we evaluated the effect of cell permeant ceramide analogues on ligand-induced tyrosine phosphorylation of the EGF receptor (EGFR), phospholipase Cy (PLCgamma) activity and cell proliferation.	Ceramides	62-70	epidermal growth factor receptor	Mus musculus	145-149
11053253-6	2000	Accordingly, palmitate activated ERK by a process that was dependent on ceramide synthesis de novo and Raf-1, but independent of kinase suppressor of Ras.	Ceramides	72-80	mitogen-activated protein kinase 1	Homo sapiens	33-36
11053253-8	2000	Results show that the Raf-1/ERK cascade is the selective downstream target of de novo-synthesized ceramide in the induction of apoptosis in astrocytes and also highlight the importance of ceramide synthesis de novo in apoptosis of astrocytes, which might have pathophysiological relevance.	Ceramides	98-106	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	22-27
11053253-8	2000	Results show that the Raf-1/ERK cascade is the selective downstream target of de novo-synthesized ceramide in the induction of apoptosis in astrocytes and also highlight the importance of ceramide synthesis de novo in apoptosis of astrocytes, which might have pathophysiological relevance.	Ceramides	98-106	mitogen-activated protein kinase 1	Homo sapiens	28-31
11053253-8	2000	Results show that the Raf-1/ERK cascade is the selective downstream target of de novo-synthesized ceramide in the induction of apoptosis in astrocytes and also highlight the importance of ceramide synthesis de novo in apoptosis of astrocytes, which might have pathophysiological relevance.	Ceramides	188-196	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	22-27
11053253-8	2000	Results show that the Raf-1/ERK cascade is the selective downstream target of de novo-synthesized ceramide in the induction of apoptosis in astrocytes and also highlight the importance of ceramide synthesis de novo in apoptosis of astrocytes, which might have pathophysiological relevance.	Ceramides	188-196	mitogen-activated protein kinase 1	Homo sapiens	28-31
10915783-3	2000	The present study demonstrates selective expression by ceramide of retinoic acid receptor-alpha (RAR-alpha) and retinoic X receptor-alpha (RXR-alpha) in osteoblastic MC3T3-E1 cells and a functional role of SPP-mediated AP-1 in the signaling mechanism of ligand-dependent transcriptional activity of heterodimers of these receptors in the cells.	Ceramides	55-63	retinoic acid receptor, alpha	Mus musculus	67-95
11008213-0	2000	Biomodulatory role of ceramide in basic fibroblast growth factor-induced proliferation of cerebellar astrocytes in primary culture.	Ceramides	22-30	fibroblast growth factor 2	Rattus norvegicus	34-64
11008213-2	2000	Parallel to the bFGF mitogenic effect was a marked, and persistent, decrease in cellular ceramide levels.	Ceramides	89-97	fibroblast growth factor 2	Rattus norvegicus	16-20
11008213-5	2000	In fact, cell growth in bFGF-stimulated astrocytes was inhibited by exogenous ceramide and C2-ceramide, maximal inhibition being obtained at a ceramide concentration of 5-10 microM.	Ceramides	78-86	fibroblast growth factor 2	Rattus norvegicus	24-28
11008213-5	2000	In fact, cell growth in bFGF-stimulated astrocytes was inhibited by exogenous ceramide and C2-ceramide, maximal inhibition being obtained at a ceramide concentration of 5-10 microM.	Ceramides	94-102	fibroblast growth factor 2	Rattus norvegicus	24-28
11008213-8	2000	The administration of antiproliferative doses of ceramide or C2-ceramide, but not of their dihydroderivatives, resulted in a significant inhibition of ERK1/2 activation.	Ceramides	49-57	mitogen activated protein kinase 3	Rattus norvegicus	151-157
11008213-9	2000	In conclusion, our data indicate that the prompt modulation of ceramide levels by bFGF is an early step associated with the signaling pathways responsible for the mitogenic activity of bFGF in astrocytes.	Ceramides	63-71	fibroblast growth factor 2	Rattus norvegicus	82-86
11008213-9	2000	In conclusion, our data indicate that the prompt modulation of ceramide levels by bFGF is an early step associated with the signaling pathways responsible for the mitogenic activity of bFGF in astrocytes.	Ceramides	63-71	fibroblast growth factor 2	Rattus norvegicus	185-189
11025451-7	2000	We also demonstrated that HT-29 cells treated with either 1L-1beta or SNAP induced ceramide production, and addition of C2 or C6 ceramides into cultured HT-29 cells resulted in induction of gamma-GCSh but not MRP1 expression.	Ceramides	129-138	glutamate-cysteine ligase catalytic subunit	Homo sapiens	190-200
11025451-7	2000	We also demonstrated that HT-29 cells treated with either 1L-1beta or SNAP induced ceramide production, and addition of C2 or C6 ceramides into cultured HT-29 cells resulted in induction of gamma-GCSh but not MRP1 expression.	Ceramides	129-138	ATP binding cassette subfamily C member 1	Homo sapiens	209-213
11025451-8	2000	Collectively, our results demonstrate that induction of MRP1 and gamma-GCSh by IL-1beta is regulated, at least in part, by an NO-related signaling, and induction of gamma-GCSh is by NO-related ceramide signaling.	Ceramides	193-201	glutamate-cysteine ligase catalytic subunit	Homo sapiens	165-175
11074596-2	2000	We have demonstrated previously in Hs578T cells that insulin-like growth factor binding protein (IGFBP)-3 can significantly accentuate ceramide (C2)-induced apoptosis, but has no effect on cell death induced by integrin detachment [using an arginine-glycine-aspartic acid (RGD)-containing peptide].	Ceramides	135-143	insulin like growth factor binding protein 3	Homo sapiens	53-105
11068881-1	2000	The effect of ceramide on Ca2+-dependent translocation of cytosolic phospholipase A2 (cPLA2) to membranes was studied.	Ceramides	14-22	phospholipase A2 group IVA	Homo sapiens	86-91
11068881-6	2000	These findings suggest that ceramide in membranes potentiates Ca2+-dependent cPLA2 translocation from cytosol to membranes, probably through modification of membrane phospholipid organization.	Ceramides	28-36	phospholipase A2 group IVA	Homo sapiens	77-82
11228545-2	2000	Here, we evaluate COX-2 mRNA stability in response to treatment with two known endogenous promoters of gastrointestinal cancer, the bile acid (chenodeoxycholate; CD) and ceramide.	Ceramides	170-178	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	18-23
11228545-3	2000	Treatment with CD and ceramide resulted in a 10-fold increase in the level of COX-2 protein and a four-fold lengthening of the half-life of COX-2 mRNA.	Ceramides	22-30	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	78-83
11228545-3	2000	Treatment with CD and ceramide resulted in a 10-fold increase in the level of COX-2 protein and a four-fold lengthening of the half-life of COX-2 mRNA.	Ceramides	22-30	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	140-145
11228545-5	2000	A known inhibitor of mitogen-activated protein (MAP)/extracellular signal-regulated kinase (ERK) kinase (MEK), PD98059, reversed the effects of CD or ceramide to stabilize COX-2 mRNA.	Ceramides	150-158	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	172-177
11228545-7	2000	Treatment with a p38 MAPK inhibitor, PD169316, or transfection with a dominant-negative p38 MAPK construct reversed the effect of CD or ceramide to stabilize COX-2 mRNA.	Ceramides	136-144	mitogen activated protein kinase 14	Rattus norvegicus	17-20
11228545-7	2000	Treatment with a p38 MAPK inhibitor, PD169316, or transfection with a dominant-negative p38 MAPK construct reversed the effect of CD or ceramide to stabilize COX-2 mRNA.	Ceramides	136-144	mitogen activated protein kinase 14	Rattus norvegicus	88-91
11228545-7	2000	Treatment with a p38 MAPK inhibitor, PD169316, or transfection with a dominant-negative p38 MAPK construct reversed the effect of CD or ceramide to stabilize COX-2 mRNA.	Ceramides	136-144	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	158-163
11062251-3	2000	We previously showed that transient expression of constitutively active Akt inhibits ceramide-induced death of hybrid motor neuron 1 cells.	Ceramides	85-93	thymoma viral proto-oncogene 1	Mus musculus	72-75
11007961-5	2000	Other molecular mechanisms that regulate PP2Ac function include phosphorylation, carboxyl methylation, inhibition by intracellular protein inhibitors (I(1)(PP2A) and I(2)(PP2A)), and stimulation by ceramide.	Ceramides	198-206	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	41-46
11007961-5	2000	Other molecular mechanisms that regulate PP2Ac function include phosphorylation, carboxyl methylation, inhibition by intracellular protein inhibitors (I(1)(PP2A) and I(2)(PP2A)), and stimulation by ceramide.	Ceramides	198-206	protein phosphatase 2 phosphatase activator	Homo sapiens	41-45
11068881-0	2000	Acceleration by ceramide of calcium-dependent translocation of phospholipase A2 from cytosol to membranes in platelets.	Ceramides	16-24	phospholipase A2 group IB	Homo sapiens	63-79
11068881-1	2000	The effect of ceramide on Ca2+-dependent translocation of cytosolic phospholipase A2 (cPLA2) to membranes was studied.	Ceramides	14-22	phospholipase A2 group IVA	Homo sapiens	58-84
10915783-3	2000	The present study demonstrates selective expression by ceramide of retinoic acid receptor-alpha (RAR-alpha) and retinoic X receptor-alpha (RXR-alpha) in osteoblastic MC3T3-E1 cells and a functional role of SPP-mediated AP-1 in the signaling mechanism of ligand-dependent transcriptional activity of heterodimers of these receptors in the cells.	Ceramides	55-63	retinoic acid receptor, alpha	Mus musculus	97-106
10915783-3	2000	The present study demonstrates selective expression by ceramide of retinoic acid receptor-alpha (RAR-alpha) and retinoic X receptor-alpha (RXR-alpha) in osteoblastic MC3T3-E1 cells and a functional role of SPP-mediated AP-1 in the signaling mechanism of ligand-dependent transcriptional activity of heterodimers of these receptors in the cells.	Ceramides	55-63	retinoid X receptor alpha	Mus musculus	139-148
10900202-1	2000	In a previous study, we reported that the Saccharomyces cerevisiae gene YPC1 encodes an alkaline ceramidase with a dual activity, catalyzing both hydrolysis and synthesis of yeast ceramide (Mao, C., Xu, R., Bielawska, A., and Obeid, L. M. (2000) J. Biol.	Ceramides	180-188	phytoceramidase	Saccharomyces cerevisiae S288C	72-76
11042022-0	2000	Akt mediates insulin rescue from apoptosis in brown adipocytes: effect of ceramide.	Ceramides	74-82	AKT serine/threonine kinase 1	Homo sapiens	0-3
11023989-2	2000	GD3 ganglioside is rapidly synthesized from accumulated ceramide after the clustering of death-inducing receptors and triggers apoptosis.	Ceramides	56-64	GRDX	Homo sapiens	0-3
11023989-6	2000	We found that endogenous GD3 accumulates within mitochondria of cells undergoing apoptosis after ceramide exposure.	Ceramides	97-105	GRDX	Homo sapiens	25-28
11023989-7	2000	Accordingly, suppression of GD3 synthase (ST8) expression in intact cells substantially prevents ceramide-induced DeltaPsim dissipation, indicating that endogenously synthesized GD3 induces mitochondrial changes in vivo.	Ceramides	97-105	GRDX	Homo sapiens	28-31
11023989-7	2000	Accordingly, suppression of GD3 synthase (ST8) expression in intact cells substantially prevents ceramide-induced DeltaPsim dissipation, indicating that endogenously synthesized GD3 induces mitochondrial changes in vivo.	Ceramides	97-105	Oncogene OVC (ovarian adenocarcinoma oncogene)	Homo sapiens	42-45
11023989-7	2000	Accordingly, suppression of GD3 synthase (ST8) expression in intact cells substantially prevents ceramide-induced DeltaPsim dissipation, indicating that endogenously synthesized GD3 induces mitochondrial changes in vivo.	Ceramides	97-105	GRDX	Homo sapiens	178-181
11001916-7	2000	It is therefore proposed that PKCzeta regulates the PC-PLC/ASMase pathway, and it is hypothesized that the resultant ceramide accumulation mediates the activation of the SEK/JNK module by LPS.	Ceramides	117-125	mitogen-activated protein kinase 8	Homo sapiens	174-177
10959093-2	2000	Acid ceramidase catalyzes the hydrolysis of ceramide, a potent lipid second messenger molecule that promotes apoptosis and inhibits cellular proliferation.	Ceramides	44-52	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
11042022-2	2000	This study investigated the contribution of Akt and p70S6-kinase in insulin rescue from two different apoptotic triggers, serum deprivation and ceramide treatment.	Ceramides	144-152	insulin	Homo sapiens	68-75
11042022-7	2000	Ceramide treatment blunted Akt activity but not PI 3-kinase activity, and insulin and EGF were unable to activate Akt.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	27-30
11042022-8	2000	Ceramide also caused apoptosis in cells transfected with a constitutively active Akt construct, since phosphorylation of Akt was impaired under these experimental conditions.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	81-84
11042022-8	2000	Ceramide also caused apoptosis in cells transfected with a constitutively active Akt construct, since phosphorylation of Akt was impaired under these experimental conditions.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	121-124
10998148-10	2000	Acid sphingomyelinase activity, which is localized in the epidermal lamellar bodies and generates ceramides for extracellular lipid lamellae in the stratum corneum permeability barrier, was reduced in homozygous as well as heterozygous animals.	Ceramides	98-107	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
10998148-12	2000	The reduction in acid sphingomyelinase activity may explain the recently described decreased ratio of ceramides to total lipids in K10 deficient mice.	Ceramides	102-111	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	17-38
11220788-3	2000	One injury-responsive signaling pathway that has recently been characterized in studies of non-neural cells involves cleavage of membrane sphingomyelin by acidic and/or neutral sphingomyelinase (ASMase) resulting in generation of the second messenger ceramide.	Ceramides	251-259	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	195-201
11049693-1	2000	Both ceramide and phospholipase D (PLD) have important roles in a variety of signal transduction pathways.	Ceramides	5-13	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	35-38
11013311-1	2000	Modulation of cytosolic phospholipase A(2) (cPLA(2)) activity by sphingomyelin (SPH), ceramide (Cer), and cholesterol (Chol) was investigated in CHO-2B cells activated by the calcium ionophore A23187 and epinephrine.	Ceramides	86-94	phospholipase A2 group IVA	Homo sapiens	14-51
11013311-1	2000	Modulation of cytosolic phospholipase A(2) (cPLA(2)) activity by sphingomyelin (SPH), ceramide (Cer), and cholesterol (Chol) was investigated in CHO-2B cells activated by the calcium ionophore A23187 and epinephrine.	Ceramides	96-99	phospholipase A2 group IVA	Homo sapiens	14-51
10887171-7	2000	Addition of TNF-alpha led to accumulation of both ceramide and diacylglycerol.	Ceramides	50-58	tumor necrosis factor	Mus musculus	12-21
10998569-5	2000	In fact, considering all the mammalian cell sphingolipids, gangliosides, sulphatides, neutral glycosphingolipids, sphingomyelin and ceramides, it would seem that while the LCB with 18 carbons is the main component of all sphingolipids, only CNS gangliosides contain significant amounts of LCB with 20 carbons.	Ceramides	132-141	clathrin light chain B	Homo sapiens	172-175
11034356-0	2000	Ligation of the WC1 receptor induces gamma delta T cell growth arrest through fumonisin B1-sensitive increases in cellular ceramide.	Ceramides	123-131	ATPase copper transporting beta	Homo sapiens	16-19
11034356-3	2000	We now show that this WC1-mediated growth arrest is associated with an increase in cellular ceramide, in the absence of any measurable changes in acidic/neutral sphingomyelinase activity.	Ceramides	92-100	ATPase copper transporting beta	Homo sapiens	22-25
11034356-4	2000	Moreover, cell-permeable analogues of ceramide also mimicked WC1-induced growth arrest along with an associated decrease in pocket protein expression and phosphorylation status.	Ceramides	38-46	ATPase copper transporting beta	Homo sapiens	61-64
11034356-5	2000	An important role for ceramide in WC1-induced growth arrest was confirmed by demonstrating that the specific ceramide synthase inhibitor fumonisin B1 blocked WC1-induced growth arrest and the associated molecular effects on the pocket proteins.	Ceramides	22-30	ATPase copper transporting beta	Homo sapiens	34-37
11034356-5	2000	An important role for ceramide in WC1-induced growth arrest was confirmed by demonstrating that the specific ceramide synthase inhibitor fumonisin B1 blocked WC1-induced growth arrest and the associated molecular effects on the pocket proteins.	Ceramides	22-30	ATPase copper transporting beta	Homo sapiens	158-161
11034356-7	2000	It is therefore proposed that ligation of WC1 leads to an accumulation in cellular ceramide through activation of ceramide synthase.	Ceramides	83-91	ATPase copper transporting beta	Homo sapiens	42-45
11034356-9	2000	To our knowledge, these results demonstrate for the first time that cell surface receptor-mediated ceramide synthase activation can affect cell fate through increases in cellular ceramide and provide further evidence that the orphan receptor WC1 regulates gammadelta T cell biology through a novel signaling pathway.	Ceramides	99-107	ATPase copper transporting beta	Homo sapiens	242-245
10964506-3	2000	In the present study, we examined the possible involvement of protein kinase C (PKC) and ceramide generation in caspase-3(-like) protease activation induced by inostamycin, a phosphatidylinositol synthesis inhibitor.	Ceramides	89-97	caspase 3	Homo sapiens	112-127
10974027-1	2000	Tumor necrosis factor (TNF) signals cell death and simultaneously induces generation of ceramide.	Ceramides	88-96	tumor necrosis factor	Mus musculus	0-21
10975817-0	2000	Ceramide-induced TCR up-regulation.	Ceramides	0-8	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	17-20
10974027-1	2000	Tumor necrosis factor (TNF) signals cell death and simultaneously induces generation of ceramide.	Ceramides	88-96	tumor necrosis factor	Mus musculus	23-26
10974027-4	2000	In response to TNF, parental L929 cells display a significant increase in intracellular ceramide correlated with an "atypical apoptosis" characterized by membrane blebbing, DNA fragmentation and degradation of poly(ADP-ribose) polymerase despite a lack of caspase activity.	Ceramides	88-96	tumor necrosis factor	Mus musculus	15-18
10974027-6	2000	Pharmacological suppression of AC with N-oleoylethanolamine restored the accumulation of intracellular ceramide as well as the sensitivity of the transfectants to TNF, implying that an enhanced metabolization of intracellular ceramide by AC shifts the balance between intracellular ceramide and SPP levels towards cell survival.	Ceramides	226-234	tumor necrosis factor	Mus musculus	163-166
10974027-6	2000	Pharmacological suppression of AC with N-oleoylethanolamine restored the accumulation of intracellular ceramide as well as the sensitivity of the transfectants to TNF, implying that an enhanced metabolization of intracellular ceramide by AC shifts the balance between intracellular ceramide and SPP levels towards cell survival.	Ceramides	226-234	tumor necrosis factor	Mus musculus	163-166
10974027-7	2000	Correspondingly, inhibition of ceramide production by acid sphingomyelinase also increased survival of TNF-treated L929 cells.	Ceramides	31-39	tumor necrosis factor	Mus musculus	103-106
11000289-10	2000	This indicates the important role of bcl-2 in the regulation of ceramide-mediated signalling pathways in human keratinocytes and supports the involvement of ceramide as a signalling molecule in 1 alpha,25-dihydroxyvitamin D(3)-induced biological responses.	Ceramides	64-72	BCL2 apoptosis regulator	Homo sapiens	37-42
10975817-7	2000	We found that ceramide affected TCR recycling dynamics and induced TCR up-regulation in a concentration- and time-dependent manner.	Ceramides	14-22	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	32-35
10975817-7	2000	We found that ceramide affected TCR recycling dynamics and induced TCR up-regulation in a concentration- and time-dependent manner.	Ceramides	14-22	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	67-70
10975817-8	2000	Experiments applying phosphatase inhibitors indicated that ceramide-induced TCR up-regulation was most probably mediated by serine/threonine protein phosphatase 2A.	Ceramides	59-67	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	76-79
11000289-0	2000	Bcl-2 transfected HaCaT keratinocytes resist apoptotic signals of ceramides, tumor necrosis factor alpha and 1 alpha, 25-dihydroxyvitamin D(3).	Ceramides	66-75	BCL2 apoptosis regulator	Homo sapiens	0-5
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.	Ceramides	294-302	glucosylceramidase beta	Homo sapiens	231-254
11042671-7	2000	In contrast, the increase in ceramide level by an inhibitor of ceramide glucosyltransferase-1, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol caused elevation of the Bax/Bcl-2 ratio and potentiation of caspase-3 activation, thereby resulting in enhancement of etoposide-induced apoptosis.	Ceramides	29-37	BCL2 associated X, apoptosis regulator	Homo sapiens	176-179
11042671-7	2000	In contrast, the increase in ceramide level by an inhibitor of ceramide glucosyltransferase-1, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol caused elevation of the Bax/Bcl-2 ratio and potentiation of caspase-3 activation, thereby resulting in enhancement of etoposide-induced apoptosis.	Ceramides	29-37	BCL2 apoptosis regulator	Homo sapiens	180-185
11042671-7	2000	In contrast, the increase in ceramide level by an inhibitor of ceramide glucosyltransferase-1, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol caused elevation of the Bax/Bcl-2 ratio and potentiation of caspase-3 activation, thereby resulting in enhancement of etoposide-induced apoptosis.	Ceramides	29-37	caspase 3	Homo sapiens	212-221
10996032-0	2000	The effect of a ceramide analog, N-acetylsphingosine on the induction of proliferation and IL-2 synthesis in T cells from young and old F344 rats.	Ceramides	16-24	interleukin 2	Rattus norvegicus	91-95
10996032-2	2000	In the present study, we examined the effects of cell-permeable ceramide analog, N-acetyl-sphingosine (C(2)-ceramide) on the induction of proliferation and interleukin-2 (IL-2) synthesis in T cells from young and old rats.	Ceramides	64-72	interleukin 2	Rattus norvegicus	156-169
10996032-2	2000	In the present study, we examined the effects of cell-permeable ceramide analog, N-acetyl-sphingosine (C(2)-ceramide) on the induction of proliferation and interleukin-2 (IL-2) synthesis in T cells from young and old rats.	Ceramides	64-72	interleukin 2	Rattus norvegicus	171-175
10996032-8	2000	C(2)-ceramide-induced caspase-3 activation and DNA fragmentation was significantly (P<0.5) higher in stimulated T cells from old rats compared to stimulated T cells from young rats.	Ceramides	5-13	caspase 3	Rattus norvegicus	22-31
10997751-0	2000	Involvement of caspase 3- and 8-like proteases in ceramide-induced apoptosis of cardiomyocytes.	Ceramides	50-58	caspase 3	Rattus norvegicus	15-24
10997751-4	2000	In this study, we investigated the role of the cysteinyl aspartate-specific proteases (caspases) in cardiomyocyte apoptosis induced by ceramide.	Ceramides	135-143	caspase 8	Rattus norvegicus	87-95
10997751-6	2000	Caspase 3- and 8-like protease activities are induced in cardiomyocytes by ceramide treatment.	Ceramides	75-83	caspase 3	Rattus norvegicus	0-9
10997751-7	2000	Addition of the tetrapeptide inhibitors for caspases attenuated ceramide-induced apoptosis.	Ceramides	64-72	caspase 8	Rattus norvegicus	44-52
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-47	BCL2 apoptosis regulator	Homo sapiens	96-101
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-47	BCL2 associated X, apoptosis regulator	Homo sapiens	133-136
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-47	BCL2 apoptosis regulator	Homo sapiens	137-142
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-47	caspase 9	Homo sapiens	178-195
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-46	BCL2 apoptosis regulator	Homo sapiens	96-101
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-46	BCL2 associated X, apoptosis regulator	Homo sapiens	133-136
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-46	BCL2 apoptosis regulator	Homo sapiens	137-142
11042671-8	2000	Furthermore, cell-permeable exogenous ceramides (C2- and C6-ceramide) induced downregulation of Bcl-2, leading to an increase in the Bax/Bcl-2 ratio and subsequent activation of caspases-9 and -3.	Ceramides	38-46	caspase 9	Homo sapiens	178-195
11042671-9	2000	Taken together, these results suggest that ceramide may function as a mediator of etoposide-induced apoptosis of C6 glioma cells, which induces increase in the Bax/Bcl-2 ratio followed by release of cytochrome c leading to caspases-9 and -3 activation.	Ceramides	43-51	BCL2 associated X, apoptosis regulator	Homo sapiens	160-163
11042671-9	2000	Taken together, these results suggest that ceramide may function as a mediator of etoposide-induced apoptosis of C6 glioma cells, which induces increase in the Bax/Bcl-2 ratio followed by release of cytochrome c leading to caspases-9 and -3 activation.	Ceramides	43-51	BCL2 apoptosis regulator	Homo sapiens	164-169
11042671-9	2000	Taken together, these results suggest that ceramide may function as a mediator of etoposide-induced apoptosis of C6 glioma cells, which induces increase in the Bax/Bcl-2 ratio followed by release of cytochrome c leading to caspases-9 and -3 activation.	Ceramides	43-51	cytochrome c, somatic	Homo sapiens	199-211
11042671-9	2000	Taken together, these results suggest that ceramide may function as a mediator of etoposide-induced apoptosis of C6 glioma cells, which induces increase in the Bax/Bcl-2 ratio followed by release of cytochrome c leading to caspases-9 and -3 activation.	Ceramides	43-51	caspase 9	Homo sapiens	223-240
10997751-8	2000	The nonselective caspase inhibitor (B-D-FMK) and the caspase 3 (Z-DEVD-FMK) and caspase 8 (Z-IETD-FMK) inhibitors reduced ceramide-induced cardiomyocyte death and significantly inhibited the activation of caspase 3.	Ceramides	122-130	caspase 3	Rattus norvegicus	53-62
10997751-8	2000	The nonselective caspase inhibitor (B-D-FMK) and the caspase 3 (Z-DEVD-FMK) and caspase 8 (Z-IETD-FMK) inhibitors reduced ceramide-induced cardiomyocyte death and significantly inhibited the activation of caspase 3.	Ceramides	122-130	caspase 8	Rattus norvegicus	80-89
10997751-8	2000	The nonselective caspase inhibitor (B-D-FMK) and the caspase 3 (Z-DEVD-FMK) and caspase 8 (Z-IETD-FMK) inhibitors reduced ceramide-induced cardiomyocyte death and significantly inhibited the activation of caspase 3.	Ceramides	122-130	caspase 3	Rattus norvegicus	205-214
10951284-2	2000	In this study, we asked whether sphingomyelin-derived ceramide, resulting from acid-sphingomyelinase activity, is also required for normal barrier function.	Ceramides	54-62	sphingomyelin phosphodiesterase 1	Homo sapiens	79-100
10951284-11	2000	These studies demonstrate an important role for enzymatic processing of sphingomyelin-to-ceramide by acid-sphingomyelinase as a mechanism for generating a portion of the stratum corneum ceramides for permeability barrier homeostasis in mammalian skin.	Ceramides	186-195	sphingomyelin phosphodiesterase 1	Homo sapiens	101-122
10969794-5	2000	Although LNCaP cells are highly resistant to gamma-irradiation-induced apoptosis, they are sensitive to the death-inducing effects of tumor necrosis factor alpha, which also increases ceramide levels in these cells (K. Kimura et al., Cancer Res., 59: 1606-1614, 1999).	Ceramides	184-192	tumor necrosis factor	Homo sapiens	134-161
11045015-6	2000	As an upstream activation of caspase-3, induction of cytochrome c release followed by processing of procaspase-9 was observed by Western blotting, although the formation of intracellular ceramide was not observed.	Ceramides	187-195	caspase 3	Rattus norvegicus	29-38
10910943-4	2000	In addition, in HL60 cells, CD44 ligation with A3D8 mAb fully abrogates the DNR-triggered generation of ceramide, a lipid second messenger involved in the DNR apoptotic signaling pathway.	Ceramides	104-112	CD44 molecule (Indian blood group)	Homo sapiens	28-32
10930579-5	2000	Reconstitution of ceramide, the product of acid sphingomyelinase activity, in imipramine- or SR33557-treated cells restores internalization of the bacteria.	Ceramides	18-26	sphingomyelin phosphodiesterase 1	Homo sapiens	43-64
10919278-2	2000	Recently, it has been reported that tumor necrosis factor-alpha (TNF-alpha) activates the release of ceramide and that ceramide acts as a mediator for the TNF-alpha-induced stimulation of the binding affinity of nuclear factor-KB (NF-KB), a ubiquitous transcription factor of particular importance in immune and inflammatory responses.	Ceramides	101-109	tumor necrosis factor	Homo sapiens	36-63
10919278-2	2000	Recently, it has been reported that tumor necrosis factor-alpha (TNF-alpha) activates the release of ceramide and that ceramide acts as a mediator for the TNF-alpha-induced stimulation of the binding affinity of nuclear factor-KB (NF-KB), a ubiquitous transcription factor of particular importance in immune and inflammatory responses.	Ceramides	101-109	tumor necrosis factor	Homo sapiens	65-74
10981968-7	2000	Binding to CD1b is a highly reversible process and other ceramide-containing glycosphingolipids displace GM1.	Ceramides	57-65	CD1b molecule	Homo sapiens	11-15
10919278-2	2000	Recently, it has been reported that tumor necrosis factor-alpha (TNF-alpha) activates the release of ceramide and that ceramide acts as a mediator for the TNF-alpha-induced stimulation of the binding affinity of nuclear factor-KB (NF-KB), a ubiquitous transcription factor of particular importance in immune and inflammatory responses.	Ceramides	119-127	tumor necrosis factor	Homo sapiens	36-63
10919278-2	2000	Recently, it has been reported that tumor necrosis factor-alpha (TNF-alpha) activates the release of ceramide and that ceramide acts as a mediator for the TNF-alpha-induced stimulation of the binding affinity of nuclear factor-KB (NF-KB), a ubiquitous transcription factor of particular importance in immune and inflammatory responses.	Ceramides	119-127	tumor necrosis factor	Homo sapiens	65-74
10919278-2	2000	Recently, it has been reported that tumor necrosis factor-alpha (TNF-alpha) activates the release of ceramide and that ceramide acts as a mediator for the TNF-alpha-induced stimulation of the binding affinity of nuclear factor-KB (NF-KB), a ubiquitous transcription factor of particular importance in immune and inflammatory responses.	Ceramides	119-127	tumor necrosis factor	Homo sapiens	155-164
10919278-3	2000	In this study we demonstrate that dexamethasone, which reduces the production of ceramide, significantly inhibits TNF-alpha-induced activation of NF-KB, c-Jun N-terminal kinase, also known as stress-activating protein kinase, caspase-3-like cysteine protease, redistribution of cytochrome c, and apoptosis in MC3T3E1 osteoblasts.	Ceramides	81-89	tumor necrosis factor	Homo sapiens	114-123
10919278-3	2000	In this study we demonstrate that dexamethasone, which reduces the production of ceramide, significantly inhibits TNF-alpha-induced activation of NF-KB, c-Jun N-terminal kinase, also known as stress-activating protein kinase, caspase-3-like cysteine protease, redistribution of cytochrome c, and apoptosis in MC3T3E1 osteoblasts.	Ceramides	81-89	cytochrome c, somatic	Homo sapiens	278-290
10919278-4	2000	Compared with TNF-alpha-induced JNK activation, ceramide elicits a more rapid activation of JNK within 30 min.	Ceramides	48-56	mitogen-activated protein kinase 8	Homo sapiens	92-95
10919278-6	2000	This study provides evidence that the release of ceramide may be required as a second messenger in TNF-alpha-induced apoptosis.	Ceramides	49-57	tumor necrosis factor	Homo sapiens	99-108
10919278-7	2000	These results also suggest a regulatory role for dexamethasone in TNF-alpha-induced apoptosis via inhibition of ceramide release.	Ceramides	112-120	tumor necrosis factor	Homo sapiens	66-75
10919278-8	2000	Therefore, our in vitro results suggest that therapies targeted at the inhibition of ceramide release may abrogate inflammatory processes in TNF-alpha-related diseases, including rheumatoid arthritis and periodontitis.	Ceramides	85-93	tumor necrosis factor	Homo sapiens	141-150
10954916-7	2000	NF-kappaB activation induced by serum-activated lipopolysaccharide (SALPS), ceramide, and okadaic acid was also inhibited by overexpression of Bcl-x(L), whereas that by phorbol myristate acetate (PMA) and H2O2 was unaffected.	Ceramides	76-84	nuclear factor kappa B subunit 1	Homo sapiens	0-9
10953034-7	2000	After TNF-alpha challenge, myocardial but not liver production of ceramide was significantly higher in male than in female mice.	Ceramides	66-74	tumor necrosis factor	Mus musculus	6-15
10903735-2	2000	It has been reported that cross-linking Abs to Fas trigger c-Jun N-terminal kinase (JNK) signaling via caspase-mediated activation of MEKK1 (JNK kinase kinase), elevation of ceramide levels or by recruitment of death domain associated protein (DAXX) to Fas.	Ceramides	174-182	mitogen-activated protein kinase 8	Homo sapiens	84-87
10951238-3	2000	An increase in intracellular ceramide level enhanced matrix metalloproteinase 9 production and inhibited cell proliferation in parallel.	Ceramides	29-37	matrix metallopeptidase 9	Homo sapiens	53-79
10954916-7	2000	NF-kappaB activation induced by serum-activated lipopolysaccharide (SALPS), ceramide, and okadaic acid was also inhibited by overexpression of Bcl-x(L), whereas that by phorbol myristate acetate (PMA) and H2O2 was unaffected.	Ceramides	76-84	BCL2 like 1	Homo sapiens	143-151
10899932-6	2000	This study suggests that the inhibition of proinflammatory cytokine-mediated degradation of SM to ceramide by IL-10 and IL-13 is mediated through the activation of PI 3-kinase.	Ceramides	98-106	interleukin 10	Rattus norvegicus	110-115
10899932-0	2000	Interleukin-10 and interleukin-13 inhibit proinflammatory cytokine-induced ceramide production through the activation of phosphatidylinositol 3-kinase.	Ceramides	75-83	interleukin 10	Rattus norvegicus	0-14
10961348-0	2000	Ceramides induce apoptosis in HeLa cells and enhance cytochrome c-induced apoptosis in Xenopus egg extracts.	Ceramides	0-9	cytochrome c, somatic	Homo sapiens	53-65
10899932-0	2000	Interleukin-10 and interleukin-13 inhibit proinflammatory cytokine-induced ceramide production through the activation of phosphatidylinositol 3-kinase.	Ceramides	75-83	interleukin 13	Rattus norvegicus	19-33
10899932-1	2000	Ceramide produced by hydrolysis of plasma membrane sphingomyelin (SM) in different cells including brain cells in response to proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta)] plays an important role in coordinating cellular responses to stress, growth suppression, and apoptosis.	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	153-180
10899932-1	2000	Ceramide produced by hydrolysis of plasma membrane sphingomyelin (SM) in different cells including brain cells in response to proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta)] plays an important role in coordinating cellular responses to stress, growth suppression, and apoptosis.	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	182-191
10899932-1	2000	Ceramide produced by hydrolysis of plasma membrane sphingomyelin (SM) in different cells including brain cells in response to proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta)] plays an important role in coordinating cellular responses to stress, growth suppression, and apoptosis.	Ceramides	0-8	interleukin 1 beta	Rattus norvegicus	194-211
10899932-1	2000	Ceramide produced by hydrolysis of plasma membrane sphingomyelin (SM) in different cells including brain cells in response to proinflammatory cytokines [tumor necrosis factor-alpha (TNF-alpha), interleukin-1beta (IL-1beta)] plays an important role in coordinating cellular responses to stress, growth suppression, and apoptosis.	Ceramides	0-8	interleukin 1 beta	Rattus norvegicus	213-221
10899932-2	2000	The present study underlines the importance of IL-10 and IL-13, cytokines with potent antiinflammatory properties, in inhibiting the proinflammatory cytokine (TNF-alpha and IL-1beta)-mediated degradation of SM to ceramide in rat primary astrocytes.	Ceramides	213-221	interleukin 10	Rattus norvegicus	47-52
10899932-2	2000	The present study underlines the importance of IL-10 and IL-13, cytokines with potent antiinflammatory properties, in inhibiting the proinflammatory cytokine (TNF-alpha and IL-1beta)-mediated degradation of SM to ceramide in rat primary astrocytes.	Ceramides	213-221	interleukin 13	Rattus norvegicus	57-62
10899932-2	2000	The present study underlines the importance of IL-10 and IL-13, cytokines with potent antiinflammatory properties, in inhibiting the proinflammatory cytokine (TNF-alpha and IL-1beta)-mediated degradation of SM to ceramide in rat primary astrocytes.	Ceramides	213-221	tumor necrosis factor	Rattus norvegicus	159-168
10899932-2	2000	The present study underlines the importance of IL-10 and IL-13, cytokines with potent antiinflammatory properties, in inhibiting the proinflammatory cytokine (TNF-alpha and IL-1beta)-mediated degradation of SM to ceramide in rat primary astrocytes.	Ceramides	213-221	interleukin 1 beta	Rattus norvegicus	173-181
10899932-3	2000	Treatment of rat primary astrocytes with TNF-alpha or IL-1beta led to rapid degradation of SM to ceramide, whereas IL-10 and IL-13 by themselves were unable to induce the degradation of SM to ceramide.	Ceramides	97-105	tumor necrosis factor	Rattus norvegicus	41-50
10899932-3	2000	Treatment of rat primary astrocytes with TNF-alpha or IL-1beta led to rapid degradation of SM to ceramide, whereas IL-10 and IL-13 by themselves were unable to induce the degradation of SM to ceramide.	Ceramides	97-105	interleukin 1 beta	Rattus norvegicus	54-62
10899932-4	2000	Interestingly, both IL-10 and IL-13 prevented proinflammatory cytokine-induced degradation of SM to ceramide.	Ceramides	100-108	interleukin 10	Rattus norvegicus	20-25
10899932-4	2000	Interestingly, both IL-10 and IL-13 prevented proinflammatory cytokine-induced degradation of SM to ceramide.	Ceramides	100-108	interleukin 13	Rattus norvegicus	30-35
10899932-5	2000	Both IL-10 and IL-13 caused rapid activation of phosphatidylinositol (PI) 3-kinase, and inhibition of that kinase activity by wortmannin and LY294002 potently blocked the inhibitory effect of IL-10 and IL-13 on proinflammatory cytokine-mediated induction of ceramide production.	Ceramides	258-266	interleukin 10	Rattus norvegicus	5-10
10899932-5	2000	Both IL-10 and IL-13 caused rapid activation of phosphatidylinositol (PI) 3-kinase, and inhibition of that kinase activity by wortmannin and LY294002 potently blocked the inhibitory effect of IL-10 and IL-13 on proinflammatory cytokine-mediated induction of ceramide production.	Ceramides	258-266	interleukin 13	Rattus norvegicus	15-20
10899932-5	2000	Both IL-10 and IL-13 caused rapid activation of phosphatidylinositol (PI) 3-kinase, and inhibition of that kinase activity by wortmannin and LY294002 potently blocked the inhibitory effect of IL-10 and IL-13 on proinflammatory cytokine-mediated induction of ceramide production.	Ceramides	258-266	interleukin 10	Rattus norvegicus	192-197
10964614-0	2000	Ceramide initiates NFkappaB-mediated caspase activation in neuronal apoptosis.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	19-27
10964614-4	2000	In these experimental models, ceramide accumulation mediated activation and nuclear translocation of the transcription factor NFkappaB and cyclin D1 protein expression.	Ceramides	30-38	nuclear factor kappa B subunit 1	Homo sapiens	126-134
10964614-4	2000	In these experimental models, ceramide accumulation mediated activation and nuclear translocation of the transcription factor NFkappaB and cyclin D1 protein expression.	Ceramides	30-38	cyclin D1	Homo sapiens	139-148
10964614-7	2000	Our study suggests that ceramide generation occurs upstream of NFkappaB activation, cell cycle reentry, and caspase activation in the neuronal death pathway.	Ceramides	24-32	nuclear factor kappa B subunit 1	Homo sapiens	63-71
10918609-0	2000	Influence of Bax or Bcl-2 overexpression on the ceramide-dependent apoptotic pathway in glioma cells.	Ceramides	48-56	BCL2 apoptosis regulator	Homo sapiens	20-25
10918609-2	2000	In the present study, the effects of Bcl-2 and Bax on the ceramide-mediated apoptotic pathways were examined in glioma cells overexpressing Bcl-2 or Bax.	Ceramides	58-66	BCL2 apoptosis regulator	Homo sapiens	37-42
10918609-2	2000	In the present study, the effects of Bcl-2 and Bax on the ceramide-mediated apoptotic pathways were examined in glioma cells overexpressing Bcl-2 or Bax.	Ceramides	58-66	BCL2 associated X, apoptosis regulator	Homo sapiens	47-50
10918609-3	2000	Etoposide, cisplatin and tumor necrosis factor-alpha induced apoptosis of C6 rat glioma cells which was associated with ceramide formation due to activation of neutral sphingomyelinase, followed by release of mitochondrial cytochrome c into the cytosol and activation of caspases-9 and -3.	Ceramides	120-128	tumor necrosis factor	Rattus norvegicus	25-52
10918609-8	2000	In contrast, Bcl-2 overexpression resulted in a retardation of the apoptotic process via prevention of cytochrome c release and caspases activation, and ceramide formation was also blocked when Bcl-2 was highly overexpressed in glioma cells.	Ceramides	153-161	BCL2 apoptosis regulator	Homo sapiens	13-18
10918609-8	2000	In contrast, Bcl-2 overexpression resulted in a retardation of the apoptotic process via prevention of cytochrome c release and caspases activation, and ceramide formation was also blocked when Bcl-2 was highly overexpressed in glioma cells.	Ceramides	153-161	BCL2 apoptosis regulator	Homo sapiens	194-199
10918609-9	2000	In addition, transient overexpression of Bcl-xL also exerted inhibitory effects on ceramide formation and apoptotic cell death induced by etoposide.	Ceramides	83-91	BCL2 like 1	Homo sapiens	41-47
10918609-10	2000	These results indicate that Bax promotes apoptosis regardless of ceramide formation and that Bcl-2 or Bcl-xL prevents ceramide formation by repressing neutral sphingomyelinase as well as ceramide-induced cytochrome c release.	Ceramides	118-126	BCL2 apoptosis regulator	Homo sapiens	93-98
10918609-10	2000	These results indicate that Bax promotes apoptosis regardless of ceramide formation and that Bcl-2 or Bcl-xL prevents ceramide formation by repressing neutral sphingomyelinase as well as ceramide-induced cytochrome c release.	Ceramides	118-126	BCL2 like 1	Homo sapiens	102-108
10918609-10	2000	These results indicate that Bax promotes apoptosis regardless of ceramide formation and that Bcl-2 or Bcl-xL prevents ceramide formation by repressing neutral sphingomyelinase as well as ceramide-induced cytochrome c release.	Ceramides	118-126	BCL2 apoptosis regulator	Homo sapiens	93-98
10918609-10	2000	These results indicate that Bax promotes apoptosis regardless of ceramide formation and that Bcl-2 or Bcl-xL prevents ceramide formation by repressing neutral sphingomyelinase as well as ceramide-induced cytochrome c release.	Ceramides	118-126	BCL2 like 1	Homo sapiens	102-108
11229531-7	2000	Activation of caspase-3 by lipid extracts or ceramide was prevented by okadaic acid, indicating the implication of a phosphatase in this process.	Ceramides	45-53	caspase 3	Homo sapiens	14-23
10899932-6	2000	This study suggests that the inhibition of proinflammatory cytokine-mediated degradation of SM to ceramide by IL-10 and IL-13 is mediated through the activation of PI 3-kinase.	Ceramides	98-106	interleukin 13	Rattus norvegicus	120-125
10899932-7	2000	As ceramide induces apoptosis and IL-10 and IL-13 inhibit the induction of ceramide production, we examined the effect of IL-10 and IL-13 on proinflammatory cytokine-mediated apoptosis.	Ceramides	75-83	interleukin 13	Rattus norvegicus	44-49
10899932-8	2000	Inhibition of TNF-alpha-induced apoptosis by IL-10 and IL-13 suggests that the antiapoptotic nature of IL-10 and IL-13 is probably due to the inhibition of ceramide production.	Ceramides	156-164	tumor necrosis factor	Rattus norvegicus	14-23
10899932-8	2000	Inhibition of TNF-alpha-induced apoptosis by IL-10 and IL-13 suggests that the antiapoptotic nature of IL-10 and IL-13 is probably due to the inhibition of ceramide production.	Ceramides	156-164	interleukin 10	Rattus norvegicus	45-50
10899932-8	2000	Inhibition of TNF-alpha-induced apoptosis by IL-10 and IL-13 suggests that the antiapoptotic nature of IL-10 and IL-13 is probably due to the inhibition of ceramide production.	Ceramides	156-164	interleukin 13	Rattus norvegicus	55-60
10899932-8	2000	Inhibition of TNF-alpha-induced apoptosis by IL-10 and IL-13 suggests that the antiapoptotic nature of IL-10 and IL-13 is probably due to the inhibition of ceramide production.	Ceramides	156-164	interleukin 10	Rattus norvegicus	103-108
10899932-8	2000	Inhibition of TNF-alpha-induced apoptosis by IL-10 and IL-13 suggests that the antiapoptotic nature of IL-10 and IL-13 is probably due to the inhibition of ceramide production.	Ceramides	156-164	interleukin 13	Rattus norvegicus	113-118
10859351-7	2000	Enforced expression of mSPP1 in NIH 3T3 fibroblasts not only decreased SPP and enhanced ceramide levels, it also markedly diminished survival and induced the characteristic traits of apoptosis.	Ceramides	88-96	secreted phosphoprotein 1	Mus musculus	23-28
10898586-6	2000	Since ceramide analogues inhibit the mitochondrial respiratory chain, these data imply that ceramide-mediated generation of H(2)O(2) is necessary for the activation of effector caspases-3 and/or -7, and apoptosis.	Ceramides	6-14	caspase 3	Homo sapiens	177-197
10898586-6	2000	Since ceramide analogues inhibit the mitochondrial respiratory chain, these data imply that ceramide-mediated generation of H(2)O(2) is necessary for the activation of effector caspases-3 and/or -7, and apoptosis.	Ceramides	92-100	caspase 3	Homo sapiens	177-197
10997557-1	2000	Binding of tumor necrosis factor-alpha (TNF-alpha) to p60 TNF-alpha receptor induces the activation of sphingomyelinase to generate ceramide, which in turn activates certain protein kinases and phosphatases, resulting in various TNF-alpha-mediated biological effects.	Ceramides	132-140	tumor necrosis factor	Homo sapiens	11-38
10777484-1	2000	Tumor necrosis factor-alpha (TNFalpha)-induced maturation of dendritic cells (DC), with down-regulation of their endocytic ability, has been reported to be mediated by the accumulation of the lipid messenger ceramide.	Ceramides	208-216	tumor necrosis factor	Homo sapiens	0-27
10777484-1	2000	Tumor necrosis factor-alpha (TNFalpha)-induced maturation of dendritic cells (DC), with down-regulation of their endocytic ability, has been reported to be mediated by the accumulation of the lipid messenger ceramide.	Ceramides	208-216	tumor necrosis factor	Homo sapiens	29-37
10777484-4	2000	The intracellular accumulation of ceramide induced by TNFalpha was also inhibited by NO.	Ceramides	34-42	tumor necrosis factor	Homo sapiens	54-62
10777484-5	2000	In addition, NO was found to exert an inhibitory effect downstream of the TNFalpha-triggered ceramide accumulation, because NO donors reversed the inhibition of endocytosis induced by the cell-permeant C(2)-ceramide.	Ceramides	93-101	tumor necrosis factor	Homo sapiens	74-82
10886399-3	2000	A putative effector of CD28-mediated costimulation is the sphingomyelinase enzyme, which generates the potent second messenger ceramide.	Ceramides	127-135	CD28 molecule	Homo sapiens	23-27
10886399-6	2000	Surprisingly, both sphingomyelinase and C2 ceramide strongly inhibited the proliferation of resting T cells stimulated through TCR and CD28 receptors.	Ceramides	43-51	CD28 molecule	Homo sapiens	135-139
10886399-7	2000	Despite these inhibitory effects, neither sphingomyelinase nor C2 ceramide induced apoptosis and we found that upregulation of activation markers CD25 and CD69 could still occur in the presence of sphingomyelinase/C2 ceramide.	Ceramides	217-225	interleukin 2 receptor subunit alpha	Homo sapiens	146-150
10886786-4	2000	In this study we screened a set of murine CD1d-autoreactive T-cell hybridomas with diverse TCR for their reactivity with several glycosylated variants of ceramide, including alphaGalCer.	Ceramides	154-162	CD1d1 antigen	Mus musculus	42-46
10886786-4	2000	In this study we screened a set of murine CD1d-autoreactive T-cell hybridomas with diverse TCR for their reactivity with several glycosylated variants of ceramide, including alphaGalCer.	Ceramides	154-162	T cell receptor alpha variable 6-3	Mus musculus	91-94
10864918-10	2000	Antioxidants and ceramide inhibitors, but not protein kinase C inhibitors, diminished NF-kappaB activation elicited by both Ang II and the AT(2) agonist, while tyrosine kinase inhibitors only decreased Ang II-induced NF-kappaB activity.	Ceramides	17-25	angiogenin	Rattus norvegicus	124-127
10864918-10	2000	Antioxidants and ceramide inhibitors, but not protein kinase C inhibitors, diminished NF-kappaB activation elicited by both Ang II and the AT(2) agonist, while tyrosine kinase inhibitors only decreased Ang II-induced NF-kappaB activity.	Ceramides	17-25	angiotensinogen	Rattus norvegicus	124-130
10869565-1	2000	We report that the expression of mRNA and the activity of UDP-glucose:ceramide (Cer) glucosyltransferase-1 (GlcT-1) of human hepatoma Huh7 and mouse melanoma B16 cells increases after treatment with bacterial sphingomyelinase or upon addition of short-chain Cer.	Ceramides	70-78	UDP-glucose ceramide glucosyltransferase	Homo sapiens	85-106
10869565-1	2000	We report that the expression of mRNA and the activity of UDP-glucose:ceramide (Cer) glucosyltransferase-1 (GlcT-1) of human hepatoma Huh7 and mouse melanoma B16 cells increases after treatment with bacterial sphingomyelinase or upon addition of short-chain Cer.	Ceramides	70-78	UDP-glucose ceramide glucosyltransferase	Homo sapiens	108-114
10869565-1	2000	We report that the expression of mRNA and the activity of UDP-glucose:ceramide (Cer) glucosyltransferase-1 (GlcT-1) of human hepatoma Huh7 and mouse melanoma B16 cells increases after treatment with bacterial sphingomyelinase or upon addition of short-chain Cer.	Ceramides	70-78	MIR7-3 host gene	Homo sapiens	134-138
10910215-7	2000	Moreover, unlike in non-aqueous reversed-phase liquid chromatography (NARP-LC), adding a further unsaturation and two further methylene groups on ceramide results to an increase of retention in pSubFC.	Ceramides	146-154	neuronal pentraxin 2	Homo sapiens	70-74
10834929-4	2000	PLC-gamma1 was fragmented when Molt-4 cells were treated with several apoptotic stimuli such as etoposide, ceramides, and tumor necrosis factor alpha.	Ceramides	107-116	phospholipase C gamma 1	Homo sapiens	0-10
10797307-8	2000	TNF-alpha increased apoptotic cell death, which otherwise remained basal (low serum differentiation medium (LSM), FGF) or low (ceramide).	Ceramides	127-135	tumor necrosis factor	Mus musculus	0-9
10997557-1	2000	Binding of tumor necrosis factor-alpha (TNF-alpha) to p60 TNF-alpha receptor induces the activation of sphingomyelinase to generate ceramide, which in turn activates certain protein kinases and phosphatases, resulting in various TNF-alpha-mediated biological effects.	Ceramides	132-140	tumor necrosis factor	Homo sapiens	40-49
10997557-1	2000	Binding of tumor necrosis factor-alpha (TNF-alpha) to p60 TNF-alpha receptor induces the activation of sphingomyelinase to generate ceramide, which in turn activates certain protein kinases and phosphatases, resulting in various TNF-alpha-mediated biological effects.	Ceramides	132-140	tumor necrosis factor	Homo sapiens	58-67
10997557-1	2000	Binding of tumor necrosis factor-alpha (TNF-alpha) to p60 TNF-alpha receptor induces the activation of sphingomyelinase to generate ceramide, which in turn activates certain protein kinases and phosphatases, resulting in various TNF-alpha-mediated biological effects.	Ceramides	132-140	tumor necrosis factor	Homo sapiens	58-67
10997557-2	2000	We have investigated the role for the sphingomyelin/ceramide pathway in the TNF-alpha-induced upregulation of adhesion molecule expression and tissue factor production of human endothelial cells.	Ceramides	52-60	tumor necrosis factor	Homo sapiens	76-85
10997557-4	2000	C2-ceramide, a highly cell-permeable ceramide analog, was able to stimulate HUVECs to produce tissue factor activity as well as TNF-alpha.	Ceramides	3-11	coagulation factor III, tissue factor	Homo sapiens	94-107
10997557-4	2000	C2-ceramide, a highly cell-permeable ceramide analog, was able to stimulate HUVECs to produce tissue factor activity as well as TNF-alpha.	Ceramides	3-11	tumor necrosis factor	Homo sapiens	128-137
10997557-6	2000	These results suggest that there exist both the ceramide-dependent and -independent pathways in TNF-alpha signal transduction system in human vascular endothelial cells.	Ceramides	48-56	tumor necrosis factor	Homo sapiens	96-105
10844609-13	2000	The oxalate-induced increase in ceramide was also attenuated by pretreatment with AACOCF3, suggesting a role for PLA2.	Ceramides	32-40	phospholipase A2 group IB	Canis lupus familiaris	113-117
10902739-6	2000	RESULTS: The observations establish that A-T cells are equipped with a proficient apoptotic machinery, as demonstrated by their ability to undergo mitochondrial collapse and caspase-3 activation after Fas activation or ceramide treatment.	Ceramides	219-227	caspase 3	Homo sapiens	174-183
10844609-15	2000	CONCLUSIONS: Oxalate exposure produces a marked accumulation of ceramide in renal epithelial cells by a process that is redox sensitive and mediated in part by activation of PLA2.	Ceramides	64-72	phospholipase A2 group IB	Canis lupus familiaris	174-178
10747891-1	2000	Exposure to anti-Fas antibody in Jurkat cells (type II cells), which are characterized by a weak caspase-8 activation at the death-inducing signaling complex (DISC), induced a biphasic increase in ceramide levels.	Ceramides	197-205	caspase 8	Homo sapiens	97-106
10747891-2	2000	The early generation of ceramide preceded transient activation of acidic ceramidase and subsequent production of sphingosine, followed by cytochrome c release, activation of caspases-2, -3, -6, -7, -8, and -9, Bid cleavage, and a later sustained ceramide accumulation.	Ceramides	24-32	cytochrome c, somatic	Homo sapiens	138-150
10747891-2	2000	The early generation of ceramide preceded transient activation of acidic ceramidase and subsequent production of sphingosine, followed by cytochrome c release, activation of caspases-2, -3, -6, -7, -8, and -9, Bid cleavage, and a later sustained ceramide accumulation.	Ceramides	24-32	caspase 2	Homo sapiens	174-208
10747891-2	2000	The early generation of ceramide preceded transient activation of acidic ceramidase and subsequent production of sphingosine, followed by cytochrome c release, activation of caspases-2, -3, -6, -7, -8, and -9, Bid cleavage, and a later sustained ceramide accumulation.	Ceramides	24-32	BH3 interacting domain death agonist	Homo sapiens	210-213
10799564-6	2000	In SV40-WI38, on the other hand, sphingomyelinase washout induced resynthesis of SM due to the action of SMS on ceramide generated at the plasma membrane.	Ceramides	112-120	spermine synthase	Homo sapiens	105-108
10799564-9	2000	The differential activity of SMS may explain the effects of ceramide in NF-kappaB signaling: in the absence of significant SMS activity, ceramide inhibits NF-kappaB, whereas with high SMS, the conversion of the ceramide signal to a diacylglycerol signal by the action of SMS stimulates NF-kappaB.	Ceramides	60-68	spermine synthase	Homo sapiens	29-32
10799564-9	2000	The differential activity of SMS may explain the effects of ceramide in NF-kappaB signaling: in the absence of significant SMS activity, ceramide inhibits NF-kappaB, whereas with high SMS, the conversion of the ceramide signal to a diacylglycerol signal by the action of SMS stimulates NF-kappaB.	Ceramides	137-145	spermine synthase	Homo sapiens	29-32
10799564-9	2000	The differential activity of SMS may explain the effects of ceramide in NF-kappaB signaling: in the absence of significant SMS activity, ceramide inhibits NF-kappaB, whereas with high SMS, the conversion of the ceramide signal to a diacylglycerol signal by the action of SMS stimulates NF-kappaB.	Ceramides	137-145	spermine synthase	Homo sapiens	29-32
10788433-5	2000	Ceramide, a sphingolipid metabolite, may mediate some of the actions of TNF-alpha.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	72-81
10792026-7	2000	The effect of NO, which was cGMP-dependent, was due to inhibition of the TNF-alpha-induced generation of ceramide.	Ceramides	105-113	tumor necrosis factor	Homo sapiens	73-82
10788436-0	2000	Protein tyrosine kinase p56lck is required for ceramide-induced but not tumor necrosis factor-induced activation of NF-kappa B, AP-1, JNK, and apoptosis.	Ceramides	47-55	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	24-30
10792026-0	2000	Nitric oxide inhibits tumor necrosis factor-alpha-induced apoptosis by reducing the generation of ceramide.	Ceramides	98-106	tumor necrosis factor	Homo sapiens	22-49
10792026-3	2000	We have investigated the role of two messengers, ceramide and nitric oxide (NO), on the apoptotic pathway activated in human monocytic U937 cells by tumor necrosis factor-alpha (TNF-alpha) working at its p55 receptor.	Ceramides	49-57	tumor necrosis factor	Homo sapiens	149-176
10792026-3	2000	We have investigated the role of two messengers, ceramide and nitric oxide (NO), on the apoptotic pathway activated in human monocytic U937 cells by tumor necrosis factor-alpha (TNF-alpha) working at its p55 receptor.	Ceramides	49-57	tumor necrosis factor	Homo sapiens	178-187
10792026-6	2000	In combination with TNF-alpha, however, ceramide potentiated, whereas NO inhibited, TNF-alpha-induced TRADD recruitment and caspase 8 activity.	Ceramides	40-48	tumor necrosis factor	Homo sapiens	20-29
10792026-6	2000	In combination with TNF-alpha, however, ceramide potentiated, whereas NO inhibited, TNF-alpha-induced TRADD recruitment and caspase 8 activity.	Ceramides	40-48	TNFRSF1A associated via death domain	Homo sapiens	102-107
10792026-6	2000	In combination with TNF-alpha, however, ceramide potentiated, whereas NO inhibited, TNF-alpha-induced TRADD recruitment and caspase 8 activity.	Ceramides	40-48	caspase 8	Homo sapiens	124-133
10788440-0	2000	Ceramide inhibits protein kinase B/Akt by promoting dephosphorylation of serine 473.	Ceramides	0-8	protein tyrosine kinase 2 beta	Homo sapiens	18-34
10788440-0	2000	Ceramide inhibits protein kinase B/Akt by promoting dephosphorylation of serine 473.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	35-38
10788440-3	2000	We have examined in detail the relationship between ceramide signaling and the activation of an important signaling pathway, phosphatidylinositol (PI) 3-kinase and its downstream target, protein kinase B (PKB).	Ceramides	52-60	protein tyrosine kinase 2 beta	Homo sapiens	187-203
10788436-1	2000	Ceramide has been implicated as an intermediate in the signal transduction of several cytokines including tumor necrosis factor (TNF).	Ceramides	0-8	tumor necrosis factor	Homo sapiens	106-127
10788436-1	2000	Ceramide has been implicated as an intermediate in the signal transduction of several cytokines including tumor necrosis factor (TNF).	Ceramides	0-8	tumor necrosis factor	Homo sapiens	129-132
10788436-2	2000	Both ceramide and TNF activate a wide variety of cellular responses, including NF-kappaB, AP-1, JNK, and apoptosis.	Ceramides	5-13	mitogen-activated protein kinase 8	Homo sapiens	96-99
10788440-3	2000	We have examined in detail the relationship between ceramide signaling and the activation of an important signaling pathway, phosphatidylinositol (PI) 3-kinase and its downstream target, protein kinase B (PKB).	Ceramides	52-60	protein tyrosine kinase 2 beta	Homo sapiens	205-208
10802053-2	2000	Two different CD95 receptor-induced apoptotic pathways are presently known in other cell types: (i) direct activation of caspase-8 and (ii) induction of ceramide-mediated mitochondrial activation, both leading to subsequent caspase-3 activation.	Ceramides	153-161	caspase 3	Homo sapiens	224-233
10788440-5	2000	Addition of cell-permeable ceramide analogs, C(2)- or C(6)-ceramide, caused a partial loss (50-60%) of PKB activation.	Ceramides	27-35	protein tyrosine kinase 2 beta	Homo sapiens	103-106
10802053-0	2000	Resistance to CD95/Fas-induced and ceramide-mediated apoptosis of human melanoma cells is caused by a defective mitochondrial cytochrome c release.	Ceramides	35-43	cytochrome c, somatic	Homo sapiens	126-138
10788436-4	2000	In the present study we investigated the role of the T cell-specific tyrosine kinase p56(lck) in ceramide- and TNF-mediated cellular responses by comparing the responses of Jurkat T cells with JCaM1 cells, isogeneic Lck-deficient T cells.	Ceramides	97-105	cyclin dependent kinase like 2	Homo sapiens	85-88
10788436-4	2000	In the present study we investigated the role of the T cell-specific tyrosine kinase p56(lck) in ceramide- and TNF-mediated cellular responses by comparing the responses of Jurkat T cells with JCaM1 cells, isogeneic Lck-deficient T cells.	Ceramides	97-105	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	89-92
10788436-5	2000	Treatment with ceramide activated NF-kappaB, degraded IkappaBalpha, and induced NF-kappaB-dependent reporter gene expression in a time-dependent manner in Jurkat cells but not in JCaM1 cells, suggesting the critical role of p56(lck) kinase.	Ceramides	15-23	nuclear factor kappa B subunit 1	Homo sapiens	34-66
10788436-5	2000	Treatment with ceramide activated NF-kappaB, degraded IkappaBalpha, and induced NF-kappaB-dependent reporter gene expression in a time-dependent manner in Jurkat cells but not in JCaM1 cells, suggesting the critical role of p56(lck) kinase.	Ceramides	15-23	cyclin dependent kinase like 2	Homo sapiens	224-227
10788436-5	2000	Treatment with ceramide activated NF-kappaB, degraded IkappaBalpha, and induced NF-kappaB-dependent reporter gene expression in a time-dependent manner in Jurkat cells but not in JCaM1 cells, suggesting the critical role of p56(lck) kinase.	Ceramides	15-23	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	228-231
10788436-6	2000	These effects were specific to ceramide, as activation of NF-kappaB by phorbol 12-myristate 13-acetate, lipopolysaccharide, H(2)O(2), and TNF was minimally affected.	Ceramides	31-39	tumor necrosis factor	Homo sapiens	138-141
10788436-7	2000	p56(lck) was also found to be required for ceramide-induced but not TNF-induced AP-1 activation.	Ceramides	43-51	cyclin dependent kinase like 2	Homo sapiens	0-3
10788436-7	2000	p56(lck) was also found to be required for ceramide-induced but not TNF-induced AP-1 activation.	Ceramides	43-51	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	4-7
10788436-8	2000	Similarly, ceramide activated the protein kinases JNK and mitogen-activated protein kinase kinase in Jurkat cells but not in JCaM1 cells.	Ceramides	11-19	mitogen-activated protein kinase 8	Homo sapiens	50-53
10788436-10	2000	Ceramide activated p56(lck) activity in Jurkat cells.	Ceramides	0-8	cyclin dependent kinase like 2	Homo sapiens	19-22
10788436-10	2000	Ceramide activated p56(lck) activity in Jurkat cells.	Ceramides	0-8	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	23-26
10788436-11	2000	Moreover, the reconstitution of JCaM1 cells with p56(lck) tyrosine kinase reversed the ceramide-induced NF-kappaB activation and cytotoxicity.	Ceramides	87-95	cyclin dependent kinase like 2	Homo sapiens	49-73
10788436-12	2000	Overall our results demonstrate that p56(lck) plays a critical role in the activation of NF-kappaB, AP-1, JNK, and apoptosis by ceramide but has minimal or no role in activation of these responses by TNF.	Ceramides	128-136	cyclin dependent kinase like 2	Homo sapiens	37-40
10788436-12	2000	Overall our results demonstrate that p56(lck) plays a critical role in the activation of NF-kappaB, AP-1, JNK, and apoptosis by ceramide but has minimal or no role in activation of these responses by TNF.	Ceramides	128-136	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	41-44
10788437-4	2000	hCG also blocked NF-kappaB activation induced by ceramide.	Ceramides	49-57	chorionic gonadotropin subunit beta 5	Homo sapiens	0-3
10788437-7	2000	AP-1 activation induced by TNF and ceramide was also suppressed by hCG.	Ceramides	35-43	JunB proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-4
10788437-7	2000	AP-1 activation induced by TNF and ceramide was also suppressed by hCG.	Ceramides	35-43	chorionic gonadotropin subunit beta 5	Homo sapiens	67-70
10802053-2	2000	Two different CD95 receptor-induced apoptotic pathways are presently known in other cell types: (i) direct activation of caspase-8 and (ii) induction of ceramide-mediated mitochondrial activation, both leading to subsequent caspase-3 activation.	Ceramides	153-161	Fas cell surface death receptor	Homo sapiens	14-18
10802064-5	2000	hSPHK1 also specifically phosphorylated D-erythro-sphingosine and to a lesser extent sphinganine, but not other lipids, such as D,L-threo-dihydrosphingosine, N, N-dimethylsphingosine, diacylglycerol, ceramide, or phosphatidylinositol.	Ceramides	200-208	sphingosine kinase 1	Homo sapiens	0-6
10857764-0	2000	The role of ceramide in the modulation of intracellular Ca2+ levels by interleukin 1 beta in rat cortical synaptosomes.	Ceramides	12-20	interleukin 1 beta	Rattus norvegicus	71-89
10946159-3	2000	In a number of cell types, TNFalpha regulates cell growth or death, in part, by the hydrolysis of sphingomyelin to ceramide and sphingosine-1-phosphate (SPP).	Ceramides	115-123	tumor necrosis factor	Rattus norvegicus	27-35
10980892-4	2000	The intracellular pathways affected by TNF-alpha include production of ceramide and an alteration in calcium metabolism.	Ceramides	71-79	tumor necrosis factor	Homo sapiens	39-48
10857764-2	2000	We now report that the effects of IL-1beta on [Ca2+]i are mimicked by the sphingolipid metabolite ceramide.	Ceramides	98-106	interleukin 1 beta	Rattus norvegicus	34-42
10857764-3	2000	In cortical synaptosomes ceramide elevates [Ca2+]i in a p42 MAP kinase-dependent manner, and we conclude that the effects of IL-1beta on Ca2+ homeostasis involve ceramide as an upstream component of the p42 MAP kinase pathway.	Ceramides	162-170	interleukin 1 beta	Rattus norvegicus	125-133
10779771-5	2000	However, compared with EGFP-transduced HUVEC, the Bcl-2-transduced cells are resistant to the apoptotic effects of serum and growth factor withdrawal and are also resistant to the induction of apoptosis by staurosporine or by ceramide, with or without TNF.	Ceramides	226-234	BCL2 apoptosis regulator	Homo sapiens	50-55
10754324-6	2000	TNF-alpha and IL-1beta, known to be increased in HIV-encephalitic brains, as well as a cellular product of cytokine stimulation, ceramide, were also shown to induce release of cysteine from hMDM in a dose-dependent manner.	Ceramides	129-137	secreted LY6/PLAUR domain containing 1	Homo sapiens	190-194
10811015-0	2000	Ceramide-mediated stimulation of inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) accumulation in murine macrophages requires tyrosine kinase activity.	Ceramides	0-8	nitric oxide synthase 2, inducible	Mus musculus	33-64
10811015-0	2000	Ceramide-mediated stimulation of inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) accumulation in murine macrophages requires tyrosine kinase activity.	Ceramides	0-8	nitric oxide synthase 2, inducible	Mus musculus	66-70
10811015-0	2000	Ceramide-mediated stimulation of inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) accumulation in murine macrophages requires tyrosine kinase activity.	Ceramides	0-8	tumor necrosis factor	Mus musculus	76-97
10811015-0	2000	Ceramide-mediated stimulation of inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) accumulation in murine macrophages requires tyrosine kinase activity.	Ceramides	0-8	tumor necrosis factor	Mus musculus	99-102
10811015-4	2000	Herein we report that cell-permeable analogs of ceramide up-regulate both inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) production in RAW 264.7 murine macrophages.	Ceramides	48-56	nitric oxide synthase 2, inducible	Mus musculus	74-105
10811015-4	2000	Herein we report that cell-permeable analogs of ceramide up-regulate both inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) production in RAW 264.7 murine macrophages.	Ceramides	48-56	nitric oxide synthase 2, inducible	Mus musculus	107-111
10811015-4	2000	Herein we report that cell-permeable analogs of ceramide up-regulate both inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) production in RAW 264.7 murine macrophages.	Ceramides	48-56	tumor necrosis factor	Mus musculus	117-138
10811015-4	2000	Herein we report that cell-permeable analogs of ceramide up-regulate both inducible nitric oxide synthase (iNOS) and tumor necrosis factor (TNF) production in RAW 264.7 murine macrophages.	Ceramides	48-56	tumor necrosis factor	Mus musculus	140-143
10811015-5	2000	Herbimycin A and genistein, potent natural inhibitors of protein tyrosine (but not serine/threonine) phosphorylation, block ceramide-induced iNOS and TNF production.	Ceramides	124-132	nitric oxide synthase 2, inducible	Mus musculus	141-145
10811015-5	2000	Herbimycin A and genistein, potent natural inhibitors of protein tyrosine (but not serine/threonine) phosphorylation, block ceramide-induced iNOS and TNF production.	Ceramides	124-132	tumor necrosis factor	Mus musculus	150-153
10811015-6	2000	Furthermore, the highly src-family selective pyrazolopyrimidine inhibitor PP1 also blocks ceramide-induced iNOS and TNF production in RAW 264.7 cells.	Ceramides	90-98	Rous sarcoma oncogene	Mus musculus	24-27
10811015-6	2000	Furthermore, the highly src-family selective pyrazolopyrimidine inhibitor PP1 also blocks ceramide-induced iNOS and TNF production in RAW 264.7 cells.	Ceramides	90-98	protein phosphatase 1 catalytic subunit gamma	Mus musculus	74-77
10811015-6	2000	Furthermore, the highly src-family selective pyrazolopyrimidine inhibitor PP1 also blocks ceramide-induced iNOS and TNF production in RAW 264.7 cells.	Ceramides	90-98	nitric oxide synthase 2, inducible	Mus musculus	107-111
10811015-6	2000	Furthermore, the highly src-family selective pyrazolopyrimidine inhibitor PP1 also blocks ceramide-induced iNOS and TNF production in RAW 264.7 cells.	Ceramides	90-98	tumor necrosis factor	Mus musculus	116-119
10811015-7	2000	We found that PP1 also inhibits ceramide-mediated tyrosine phosphorylation of the src-family kinase hck.	Ceramides	32-40	protein phosphatase 1 catalytic subunit gamma	Mus musculus	14-17
10811015-7	2000	We found that PP1 also inhibits ceramide-mediated tyrosine phosphorylation of the src-family kinase hck.	Ceramides	32-40	Rous sarcoma oncogene	Mus musculus	82-85
10811015-7	2000	We found that PP1 also inhibits ceramide-mediated tyrosine phosphorylation of the src-family kinase hck.	Ceramides	32-40	hemopoietic cell kinase	Mus musculus	100-103
10811015-8	2000	These data indicate that src-related tyrosine kinases play a critical role in macrophage activation by ceramide.	Ceramides	103-111	Rous sarcoma oncogene	Mus musculus	25-28
10793354-8	2000	This was accomplished by use of 1alpha,25-dihydroxyvitamin D(3) [1,25(OH)(2)D(3)] and all-trans -retinoic acid to indirectly stimulate PP-2A activity through their capacity to elevated intracellular levels of the second messenger ceramide.	Ceramides	230-238	protein phosphatase 2 phosphatase activator	Homo sapiens	135-140
10830777-0	2000	Ceramide induces cell death in the human prostatic carcinoma cell lines PC3 and DU145 but does not seem to be involved in Fas-mediated apoptosis.	Ceramides	0-8	proprotein convertase subtilisin/kexin type 1	Homo sapiens	72-75
10830777-5	2000	Interestingly, cycloheximide prevented C2-ceramide-induced DNA fragmentation, indicating that ceramide-induced apoptosis in PC3 and DU145 requires new protein synthesis.	Ceramides	42-50	proprotein convertase subtilisin/kexin type 1	Homo sapiens	124-127
10745027-5	2000	On the other hand, activation of protein kinase C (PKC) by 12-O-tetradecanoylphorbol-13-acetate inhibits both H(2)O(2)-induced ceramide production and apoptosis.	Ceramides	127-135	proline rich transmembrane protein 2	Homo sapiens	33-49
10739654-5	2000	In this study, the ceramide analog d-threo-1-phenyl-2-decannoylamino-3-morpholino-1-propanol ([D]-PDMP), which inhibits UDP-glucose-ceramide glucosyltransferase, and addition of GM3 to the culture medium were used to study the effects of GM3 on the EGFR.	Ceramides	19-27	epidermal growth factor receptor	Homo sapiens	249-253
10766421-0	2000	Involvement of p27(kip1) in ceramide-mediated apoptosis in HL-60 cells.	Ceramides	28-36	zinc ribbon domain containing 2	Homo sapiens	15-18
10766421-0	2000	Involvement of p27(kip1) in ceramide-mediated apoptosis in HL-60 cells.	Ceramides	28-36	cyclin dependent kinase inhibitor 1B	Homo sapiens	19-23
10766421-2	2000	In the present study, we examined the expression of p27(kip1) and its relationship to apoptosis induced by ceramide.	Ceramides	107-115	zinc ribbon domain containing 2	Homo sapiens	52-55
10766421-2	2000	In the present study, we examined the expression of p27(kip1) and its relationship to apoptosis induced by ceramide.	Ceramides	107-115	cyclin dependent kinase inhibitor 1B	Homo sapiens	56-60
10766421-4	2000	Ceramide inhibited the kinase activities of cdk2 and cdk4 within 24 h of treatment.	Ceramides	0-8	cyclin dependent kinase 2	Homo sapiens	44-48
10766421-4	2000	Ceramide inhibited the kinase activities of cdk2 and cdk4 within 24 h of treatment.	Ceramides	0-8	cyclin dependent kinase 4	Homo sapiens	53-57
10766421-5	2000	Ceramide-induced inhibition of cdk2 and cdk4 kinase activities was accompanied by increase of p27(kip1) in the cdks complexes.	Ceramides	0-8	cyclin dependent kinase 2	Homo sapiens	31-35
10766421-5	2000	Ceramide-induced inhibition of cdk2 and cdk4 kinase activities was accompanied by increase of p27(kip1) in the cdks complexes.	Ceramides	0-8	cyclin dependent kinase 4	Homo sapiens	40-44
10766421-5	2000	Ceramide-induced inhibition of cdk2 and cdk4 kinase activities was accompanied by increase of p27(kip1) in the cdks complexes.	Ceramides	0-8	zinc ribbon domain containing 2	Homo sapiens	94-97
10766421-5	2000	Ceramide-induced inhibition of cdk2 and cdk4 kinase activities was accompanied by increase of p27(kip1) in the cdks complexes.	Ceramides	0-8	cyclin dependent kinase inhibitor 1B	Homo sapiens	98-102
10766421-6	2000	In addition, we have shown that both the cell death and expression of p27(kip1) protein induced by ceramide were significantly decreased in HL-60 cells overexpressing bcl-2.	Ceramides	99-107	zinc ribbon domain containing 2	Homo sapiens	70-73
10766421-6	2000	In addition, we have shown that both the cell death and expression of p27(kip1) protein induced by ceramide were significantly decreased in HL-60 cells overexpressing bcl-2.	Ceramides	99-107	cyclin dependent kinase inhibitor 1B	Homo sapiens	74-78
10766421-6	2000	In addition, we have shown that both the cell death and expression of p27(kip1) protein induced by ceramide were significantly decreased in HL-60 cells overexpressing bcl-2.	Ceramides	99-107	BCL2 apoptosis regulator	Homo sapiens	167-172
10766421-7	2000	Furthermore, ceramide induced a significant increase in Bax protein expression coincided with increase in p27(kip1) protein level.	Ceramides	13-21	BCL2 associated X, apoptosis regulator	Homo sapiens	56-59
10766421-7	2000	Furthermore, ceramide induced a significant increase in Bax protein expression coincided with increase in p27(kip1) protein level.	Ceramides	13-21	zinc ribbon domain containing 2	Homo sapiens	106-109
10745027-5	2000	On the other hand, activation of protein kinase C (PKC) by 12-O-tetradecanoylphorbol-13-acetate inhibits both H(2)O(2)-induced ceramide production and apoptosis.	Ceramides	127-135	proline rich transmembrane protein 2	Homo sapiens	51-54
10766421-7	2000	Furthermore, ceramide induced a significant increase in Bax protein expression coincided with increase in p27(kip1) protein level.	Ceramides	13-21	cyclin dependent kinase inhibitor 1B	Homo sapiens	110-114
10766421-8	2000	These findings indicate that p27(kip1) may play important roles in mediating ceramide-induced apoptosis and its expression can be regulated by Bax and Bcl-2.	Ceramides	77-85	zinc ribbon domain containing 2	Homo sapiens	29-32
10745027-7	2000	These findings indicate that ceramide, the product of SM hydrolysis, plays an important role in H(2)O(2)-induced apoptosis in HAE cells, and that PKC counteracts ceramide-mediated apoptosis in these cells.	Ceramides	162-170	proline rich transmembrane protein 2	Homo sapiens	146-149
10766421-8	2000	These findings indicate that p27(kip1) may play important roles in mediating ceramide-induced apoptosis and its expression can be regulated by Bax and Bcl-2.	Ceramides	77-85	cyclin dependent kinase inhibitor 1B	Homo sapiens	33-37
10766421-8	2000	These findings indicate that p27(kip1) may play important roles in mediating ceramide-induced apoptosis and its expression can be regulated by Bax and Bcl-2.	Ceramides	77-85	BCL2 associated X, apoptosis regulator	Homo sapiens	143-146
10766421-8	2000	These findings indicate that p27(kip1) may play important roles in mediating ceramide-induced apoptosis and its expression can be regulated by Bax and Bcl-2.	Ceramides	77-85	BCL2 apoptosis regulator	Homo sapiens	151-156
10734114-5	2000	We show that phorbol ester, insulin-like growth factor 1, and a constitutively active PI3K suppress both tumor necrosis factor-induced apoptosis and ceramide generation.	Ceramides	149-157	insulin like growth factor 1	Homo sapiens	28-56
10744629-3	2000	On induction of apoptosis by staurosporin, c-Myc, etoposide, or ceramide, AIF (but not hsp60) translocates to the nucleus.	Ceramides	64-72	apoptosis inducing factor mitochondria associated 1	Homo sapiens	74-77
10739748-4	2000	This disease is thought to be a consequence of inhibition by FB(1) of cellular ceramide synthesis in cells.	Ceramides	79-87	TCF3 fusion partner	Homo sapiens	61-66
10733673-5	2000	A detailed analysis of the lipid species present in the reconstructed epidermis showed that peroxisome proliferator-activated receptor-alpha activation increased the synthesis of ceramides and cholesterol derivatives, thought to be essential structural components of the permeability barrier.	Ceramides	179-188	peroxisome proliferator activated receptor alpha	Homo sapiens	92-140
10733673-7	2000	Furthermore, activation of peroxisome proliferator-activated receptor-alpha led to increased mRNA expression of several key enzymes of ceramide and cholesterol metabolism.	Ceramides	135-143	peroxisome proliferator activated receptor alpha	Homo sapiens	27-75
10733012-10	2000	TF activity in the astrocytoma cells was upregulated 1.5-fold over constitutive levels by a ceramide analogue or the enzyme sphingomyelinase, however the ceramide analogue had no effect on TF activity in the primary astrocytes.	Ceramides	92-100	coagulation factor III, tissue factor	Homo sapiens	0-2
10733012-10	2000	TF activity in the astrocytoma cells was upregulated 1.5-fold over constitutive levels by a ceramide analogue or the enzyme sphingomyelinase, however the ceramide analogue had no effect on TF activity in the primary astrocytes.	Ceramides	154-162	coagulation factor III, tissue factor	Homo sapiens	0-2
10734114-6	2000	Conversely, inhibition of the PI3K pathway with expression of a kinase-dead PI3K both prevented survival signaling and enhanced tumor necrosis factor-induced ceramide generation.	Ceramides	158-166	tumor necrosis factor	Homo sapiens	128-149
10722733-11	2000	In summary, ceramide may efficiently induce HS-induced apoptosis by suppressing anti-apoptotic HSP-70 through a post-transcriptional regulation.	Ceramides	12-20	heat shock protein family A (Hsp70) member 4	Homo sapiens	95-101
10713077-0	2000	Role of c-jun expression increased by heat shock- and ceramide-activated caspase-3 in HL-60 cell apoptosis.	Ceramides	54-62	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	8-13
10722706-1	2000	Engagement of the Fas receptor has been reported to induce ceramide generation via activation of acidic sphingomyelinase (aSMase).	Ceramides	59-67	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	122-128
10722705-0	2000	CD95(Fas/APO-1) signals ceramide generation independent of the effector stage of apoptosis.	Ceramides	24-32	Fas cell surface death receptor	Homo sapiens	0-4
10722705-0	2000	CD95(Fas/APO-1) signals ceramide generation independent of the effector stage of apoptosis.	Ceramides	24-32	Fas cell surface death receptor	Homo sapiens	9-14
10722705-2	2000	Here, we show that CD95-induced ceramide elevation occurs during the initiation phase of apoptosis.	Ceramides	32-40	Fas cell surface death receptor	Homo sapiens	19-23
10722705-6	2000	Ceramide generation induced by FADD was initiator caspase-dependent, being blocked by crmA.	Ceramides	0-8	Fas associated via death domain	Homo sapiens	31-35
10722705-7	2000	Limited pro-caspase 8 overexpression also increased ceramide levels 2.7 +/- 0.2-fold, yet failed, without CHX, to initiate apoptosis.	Ceramides	52-60	caspase 8	Homo sapiens	12-21
10722705-8	2000	Expression of membrane-targeted oligomerized CD-8 caspase 8 induced apoptosis without CHX, yet elevated ceramide only to a level equivalent to limited pro-caspase 8 transfection.	Ceramides	104-112	caspase 8	Homo sapiens	50-59
10722705-10	2000	These investigations provide evidence that ceramide generation is initiator caspase-dependent and occurs prior to commitment to the effector phase of apoptosis, definitively ordering ceramide as proximal in CD95 signaling.	Ceramides	43-51	Fas cell surface death receptor	Homo sapiens	207-211
10722705-10	2000	These investigations provide evidence that ceramide generation is initiator caspase-dependent and occurs prior to commitment to the effector phase of apoptosis, definitively ordering ceramide as proximal in CD95 signaling.	Ceramides	183-191	Fas cell surface death receptor	Homo sapiens	207-211
10722706-1	2000	Engagement of the Fas receptor has been reported to induce ceramide generation via activation of acidic sphingomyelinase (aSMase).	Ceramides	59-67	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	97-120
10713077-11	2000	These results suggested that the ceramide was generated through sphingomyelin hydrolysis by HS-activated neutral, magnesium-dependent sphingomyelinase and that subsequent c-jun expression through activation of caspase-3 played a role in HS-induced HL-60 cell apoptosis.	Ceramides	33-41	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	171-176
10713077-11	2000	These results suggested that the ceramide was generated through sphingomyelin hydrolysis by HS-activated neutral, magnesium-dependent sphingomyelinase and that subsequent c-jun expression through activation of caspase-3 played a role in HS-induced HL-60 cell apoptosis.	Ceramides	33-41	caspase 3	Homo sapiens	210-219
10713077-0	2000	Role of c-jun expression increased by heat shock- and ceramide-activated caspase-3 in HL-60 cell apoptosis.	Ceramides	54-62	caspase 3	Homo sapiens	73-82
10713077-9	2000	When we examined whether the inhibition of c-jun expression by its antisense oligodeoxynucleotides (AS) blocked HS- or C(2)-ceramide-induced apoptosis, AS of c-jun gene inhibited apoptotic morphological changes and DNA fragmentation whereas did not sense oligodeoxynucleotides.	Ceramides	124-132	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	43-48
10713077-10	2000	Moreover, a synthetic tetrapeptide, acetyl-Asp-Met-Gln-Asp-aldehyde (DMQD-CHO), which inhibited the formation of active form of caspase-3 more efficiently than those of caspase-4, -6, -7, and -8, blocked both caspase-3 like activity, c-jun expression and apoptosis induced by HS or C(2)-ceramide, although DMQD-CHO did not affect HS-induced ceramide generation.	Ceramides	287-295	caspase 3	Homo sapiens	128-137
10713077-10	2000	Moreover, a synthetic tetrapeptide, acetyl-Asp-Met-Gln-Asp-aldehyde (DMQD-CHO), which inhibited the formation of active form of caspase-3 more efficiently than those of caspase-4, -6, -7, and -8, blocked both caspase-3 like activity, c-jun expression and apoptosis induced by HS or C(2)-ceramide, although DMQD-CHO did not affect HS-induced ceramide generation.	Ceramides	287-295	caspase 3	Homo sapiens	209-218
10713077-10	2000	Moreover, a synthetic tetrapeptide, acetyl-Asp-Met-Gln-Asp-aldehyde (DMQD-CHO), which inhibited the formation of active form of caspase-3 more efficiently than those of caspase-4, -6, -7, and -8, blocked both caspase-3 like activity, c-jun expression and apoptosis induced by HS or C(2)-ceramide, although DMQD-CHO did not affect HS-induced ceramide generation.	Ceramides	287-295	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	234-239
10702281-0	2000	Uncoupling ceramide glycosylation by transfection of glucosylceramide synthase antisense reverses adriamycin resistance.	Ceramides	11-19	UDP-glucose ceramide glucosyltransferase	Homo sapiens	53-78
10720644-1	2000	The sphingomyelin pathway is now recognized as an important signal transduction system regulating various cellular functions, in which activation of a neutral sphingomyelinase induced by various extracellular stimulants results in selective degradation of sphingomyelin, yielding bioactive lipid intermediates, ceramides and phosphorylcholine.	Ceramides	311-320	sphingomyelin phosphodiesterase 2	Rattus norvegicus	151-175
10702281-5	2000	This was achieved by cellular transfection with glucosylceramide synthase (GCS), the enzyme that converts ceramide to glucosylceramide.	Ceramides	56-64	UDP-glucose ceramide glucosyltransferase	Homo sapiens	75-78
10702281-13	2000	Under adriamycin stress, GCS antisense transfected cells compared with parental cells displayed time- and dose-dependent increases in endogenous ceramide and dramatically higher levels of apoptotic effector, caspase-3.	Ceramides	145-153	UDP-glucose ceramide glucosyltransferase	Homo sapiens	25-28
10731449-5	2000	Increased ceramide formation is associated with an increase in apoptosis in many cell systems and we also observe an increase in caspase-3 like activity and DNA-laddering in these cells.	Ceramides	10-18	caspase 3	Rattus norvegicus	129-138
10694479-9	2000	Our data demonstrated that inhibition of anti-apoptotic kinases, such as Akt and ERK1/2, may play an important role in ceramide-mediated apoptosis of rheumatoid synovial cells.	Ceramides	119-127	AKT serine/threonine kinase 1	Homo sapiens	73-76
10694479-9	2000	Our data demonstrated that inhibition of anti-apoptotic kinases, such as Akt and ERK1/2, may play an important role in ceramide-mediated apoptosis of rheumatoid synovial cells.	Ceramides	119-127	mitogen-activated protein kinase 3	Homo sapiens	81-87
10677376-15	2000	On the basis of these results we propose that, under conditions where ceramide is formed in the plasma membrane, PI-TPbeta plays an important role in restoring the steady-state levels of SM.	Ceramides	70-78	phosphatidylinositol transfer protein, beta	Mus musculus	113-122
10745271-0	2000	Ceramide-induced cell death is independent of the Fas/Fas ligand pathway and is prevented by Nur77 overexpression in A20 B cells.	Ceramides	0-8	Fas ligand	Homo sapiens	54-64
10745271-0	2000	Ceramide-induced cell death is independent of the Fas/Fas ligand pathway and is prevented by Nur77 overexpression in A20 B cells.	Ceramides	0-8	nuclear receptor subfamily 4 group A member 1	Homo sapiens	93-98
10745271-2	2000	While in some experimental systems, ceramide was shown to mediate Fas-induced cell death, in other instances it was claimed to induce the expression of Fas ligand (FasL), killing cells in a caspase-dependent fashion.	Ceramides	36-44	Fas ligand	Homo sapiens	152-162
10745271-2	2000	While in some experimental systems, ceramide was shown to mediate Fas-induced cell death, in other instances it was claimed to induce the expression of Fas ligand (FasL), killing cells in a caspase-dependent fashion.	Ceramides	36-44	Fas ligand	Homo sapiens	164-168
10745271-2	2000	While in some experimental systems, ceramide was shown to mediate Fas-induced cell death, in other instances it was claimed to induce the expression of Fas ligand (FasL), killing cells in a caspase-dependent fashion.	Ceramides	36-44	caspase 6	Homo sapiens	190-197
10745271-6	2000	We also found that overexpression of Nur77, a zinc-finger transcription factor described to upregulate FasL, antagonizes ceramide-induced apoptosis, but not Fas-induced apoptosis.	Ceramides	121-129	nuclear receptor subfamily 4 group A member 1	Homo sapiens	37-42
10745271-6	2000	We also found that overexpression of Nur77, a zinc-finger transcription factor described to upregulate FasL, antagonizes ceramide-induced apoptosis, but not Fas-induced apoptosis.	Ceramides	121-129	Fas ligand	Homo sapiens	103-107
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	58-63
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	tumor protein p53	Homo sapiens	65-68
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	70-73
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	cyclin dependent kinase inhibitor 1B	Homo sapiens	78-85
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	tumor protein p53	Homo sapiens	223-226
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	266-269
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	0-8	cyclin dependent kinase inhibitor 1B	Homo sapiens	274-281
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	161-169	nuclear receptor subfamily 4 group A member 1	Homo sapiens	130-135
10745271-8	2000	Ceramide-induced cell death was associated with increased c-myc, p53, Bax and p27kip1 levels; in contrast, cells transfected with Nur77 (A20Nur77), resistant to ceramide-induced apoptosis, showed a marked downregulation of p53 after ceramide treatment, with neither Bax nor p27kip1 induction.	Ceramides	233-241	nuclear receptor subfamily 4 group A member 1	Homo sapiens	130-135
10726692-0	2000	Ceramide induces apoptosis in neuroblastoma cell cultures resistant to CD95 (Fas/APO-1)-mediated apoptosis.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	71-75
10726692-0	2000	Ceramide induces apoptosis in neuroblastoma cell cultures resistant to CD95 (Fas/APO-1)-mediated apoptosis.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	81-86
11324420-11	2000	The Western blot assay from cell extracts showed that the levels of protein p53 were decreased after ceramide treatment.	Ceramides	101-109	tumor protein p53	Homo sapiens	76-79
11324420-14	2000	CONCLUSION: Ceramide induces apoptosis in Bel7402 cells, related to Bcl-2 down-regulation.	Ceramides	12-20	BCL2 apoptosis regulator	Homo sapiens	68-73
10745271-9	2000	In conclusion, our results suggest that, in the A20 B cell line, Fas and ceramide trigger two distinct pathways and that Nur77 overexpression confers protection against ceramide-mediated apoptosis which correlates with inhibition of p53, Bax and p27kip1 induction.	Ceramides	169-177	nuclear receptor subfamily 4 group A member 1	Homo sapiens	121-126
10752668-3	2000	To determine whether ceramide, a mediator of CD95 and tumour necrosis factor-alpha-induced apoptosis, has similar effects on glucose transport, the human leukaemic cell lines, Jurkat and U937, and human peripheral blood neutrophils were treated with ceramide or sphingomyelinase and the effects on glucose transport determined by measuring [3H]-2-deoxyglucose uptake.	Ceramides	21-29	Fas cell surface death receptor	Homo sapiens	45-49
10669728-0	2000	Caveolin 1-mediated regulation of receptor tyrosine kinase-associated phosphatidylinositol 3-kinase activity by ceramide.	Ceramides	112-120	caveolin 1	Homo sapiens	0-10
10669728-1	2000	Previous studies have indicated that proapoptotic stresses downregulate the phosphatidylinositol 3-kinase [PI(3)K]/Akt survival pathway via the activation of acid-sphingomyelinase (A-SMase) and ceramide production.	Ceramides	194-202	AKT serine/threonine kinase 1	Homo sapiens	115-118
10669728-3	2000	PI(3)K inhibition by ceramide is associated with recruitment of caveolin 1 to PI(3)K-associated receptor complexes within lipid raft microdomains.	Ceramides	21-29	caveolin 1	Homo sapiens	64-74
10669728-4	2000	Overexpression of caveolin 1 alone is sufficient to alter PI(3)K activity and sensitizes fibroblasts to ceramide-induced cell death.	Ceramides	104-112	caveolin 1	Homo sapiens	18-28
10669728-5	2000	Most importantly, antisense expression of caveolin 1 dramatically reduces ceramide-induced PI(3)K deregulation and results in a loss-of-function stress response similar to that in A-SMase-deficient cells.	Ceramides	74-82	caveolin 1	Homo sapiens	42-52
10669728-8	2000	These results led us to propose that stress-induced changes in raft microdomains lead to altered receptor tyrosine kinase signal transduction through the modulation of caveolin 1 by ceramide.	Ceramides	182-190	caveolin 1	Homo sapiens	168-178
10666330-6	2000	C6 ceramide could induce apoptosis in both Fas-resistant cell lines and this was associated with a decrease in BclxL level.	Ceramides	3-11	BCL2 like 1	Homo sapiens	111-116
10778806-7	2000	Ceramide-induced RPE cell death was inhibited by zVAD-fmk, a CPP32-like protease inhibitor.	Ceramides	0-8	caspase 3	Rattus norvegicus	61-66
10778806-8	2000	Our findings indicated that ceramide in RPE cell death functions upstream of CPP32-like proteases.	Ceramides	28-36	caspase 3	Rattus norvegicus	77-82
10737718-11	2000	C6-Ceramide exposure diminished survival of MCF-7 cells; whereas, MCF-7/MDR1 cells were resistant to this short chain ceramide analog.	Ceramides	118-126	ATP binding cassette subfamily B member 1	Homo sapiens	72-76
10714936-0	2000	Ceramide induces expression of the senescence histochemical marker, beta-galactosidase, in human fibroblasts.	Ceramides	0-8	galactosidase beta 1	Homo sapiens	68-86
10714936-3	2000	We investigated the ability of ceramide to induce the expression of beta-Gal and correlated this with cell proliferation.	Ceramides	31-39	galactosidase beta 1	Homo sapiens	68-76
10653652-2	2000	The glycolipid transfer protein (23-24 kDa, pI 9.0) catalyzes the high specificity transfer of lipids that have sugars beta-linked to either a ceramide or a diacylglycerol backbone, such as simple glycolipids and gangliosides, but not the transfer of phospholipids, cholesterol, or cholesterol esters.	Ceramides	143-151	glycolipid transfer protein	Homo sapiens	4-31
10676658-8	2000	This suggests that ceramide may function in detachment-induced endothelial cell apoptosis, originating from inhibition of vitronectin binding to integrins such as alpha(v)beta3 and alpha(v)beta5.	Ceramides	19-27	vitronectin	Bos taurus	122-133
10666416-8	2000	Treatment of cardiac myocytes with extracellular ceramides also activated JNK.	Ceramides	49-58	mitogen-activated protein kinase 8	Homo sapiens	74-77
10666416-12	2000	The results are consistent with a pathway of ceramide-mediated activation of JNK.	Ceramides	45-53	mitogen-activated protein kinase 8	Homo sapiens	77-80
10671221-8	2000	The lck shift is not inducible by co-stimulation through acidic sphingomyelinase or ceramides which even prevent ERK2 activation in PBT.	Ceramides	84-93	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	4-7
10713735-3	2000	We correlate ceramide"s neuroprotective actions with the ability of ceramide to antagonize NGF deprivation-induced oxidative stress and c-jun induction, both of which contribute to apoptosis in this model.	Ceramides	13-21	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	136-141
10713735-3	2000	We correlate ceramide"s neuroprotective actions with the ability of ceramide to antagonize NGF deprivation-induced oxidative stress and c-jun induction, both of which contribute to apoptosis in this model.	Ceramides	68-76	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	136-141
10671221-8	2000	The lck shift is not inducible by co-stimulation through acidic sphingomyelinase or ceramides which even prevent ERK2 activation in PBT.	Ceramides	84-93	mitogen-activated protein kinase 1	Homo sapiens	113-117
10639587-3	2000	Formation of ceramide by acid sphingomyelinase (ASMase) in response to stress has been implicated in apoptotic cell death.	Ceramides	13-21	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	25-46
10639587-3	2000	Formation of ceramide by acid sphingomyelinase (ASMase) in response to stress has been implicated in apoptotic cell death.	Ceramides	13-21	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	48-54
10640300-0	2000	The roles of protein kinase C and tyrosine kinases in mediating endothelin-1-stimulated phospholipase D activity in rat myometrium: differential inhibition by ceramides and cyclic AMP.	Ceramides	159-168	endothelin 1	Rattus norvegicus	64-76
10625668-3	2000	Expression of gp160 in Jurkat T-cells results in increased sensitivity to FAS- and ceramide-mediated apoptosis.	Ceramides	83-91	glutamyl aminopeptidase	Homo sapiens	14-19
10639160-5	2000	An ITF-expressing colonic (HT-ITF1) cell line was resistant to apoptosis induced by serum starvation and ceramide.	Ceramides	105-113	trefoil factor 3	Homo sapiens	3-6
10623638-2	2000	The lipid messenger ceramide is implicated in signal transduction of the catabolic cytokines tumor necrosis factor (TNF) and interleukin-1 (IL-1), as well as in apoptosis.	Ceramides	20-28	tumor necrosis factor	Oryctolagus cuniculus	116-119
10678754-9	2000	Distinct signaling pathways mobilized by NGF and BDNF were also revealed in that NGF but not BDNF stimulated significant production of ceramides, whereas BDNF but not NGF caused persistent activation of mitogen-activated protein kinases.	Ceramides	135-144	nerve growth factor	Rattus norvegicus	41-44
10678754-9	2000	Distinct signaling pathways mobilized by NGF and BDNF were also revealed in that NGF but not BDNF stimulated significant production of ceramides, whereas BDNF but not NGF caused persistent activation of mitogen-activated protein kinases.	Ceramides	135-144	brain-derived neurotrophic factor	Rattus norvegicus	49-53
10678754-9	2000	Distinct signaling pathways mobilized by NGF and BDNF were also revealed in that NGF but not BDNF stimulated significant production of ceramides, whereas BDNF but not NGF caused persistent activation of mitogen-activated protein kinases.	Ceramides	135-144	nerve growth factor	Rattus norvegicus	81-84
10678754-9	2000	Distinct signaling pathways mobilized by NGF and BDNF were also revealed in that NGF but not BDNF stimulated significant production of ceramides, whereas BDNF but not NGF caused persistent activation of mitogen-activated protein kinases.	Ceramides	135-144	nerve growth factor	Rattus norvegicus	81-84
10623638-2	2000	The lipid messenger ceramide is implicated in signal transduction of the catabolic cytokines tumor necrosis factor (TNF) and interleukin-1 (IL-1), as well as in apoptosis.	Ceramides	20-28	tumor necrosis factor	Oryctolagus cuniculus	93-114
10667583-2	2000	Recent studies showed that radiation-induced apoptosis of endothelial cells in vitro and in the lung in vivo is mediated by the lipid second messenger ceramide via activation of acid sphingomyelinase (ASM).	Ceramides	151-159	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	178-199
10667583-2	2000	Recent studies showed that radiation-induced apoptosis of endothelial cells in vitro and in the lung in vivo is mediated by the lipid second messenger ceramide via activation of acid sphingomyelinase (ASM).	Ceramides	151-159	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	201-204
10653009-7	2000	A role for caspase-3-like enzymes in ceramide-induced apoptosis of oligodendroglia may have important implications for approaches to treatment of demyelinating diseases.	Ceramides	37-45	caspase 3	Homo sapiens	11-20
11469335-1	2000	A non natural glycosphingolipid containing the mucin derived, cancer associated disaccharide moiety Galbeta1-->3GalNAc, the T-antigen, alpha linked to a ceramide, has been synthesised via the protected disaccharide glycosyl trichloroacetimidate.	Ceramides	156-164	LOC100508689	Homo sapiens	47-52
10849758-0	2000	Ceramide as an activator lipid of cathepsin D.	Ceramides	0-8	cathepsin D	Homo sapiens	34-45
10849758-1	2000	We have identified the aspartic protease cathepsin D as a novel intracellular target protein for the lipid second messenger ceramide.	Ceramides	124-132	cathepsin D	Homo sapiens	41-52
10849758-2	2000	Ceramide specifically binds to and induces CTSD proteolytic activity.	Ceramides	0-8	cathepsin D	Homo sapiens	43-47
10849758-4	2000	Ceramide accumulation in cells derived from A-ceramidase defective Farber patients correlates with enhanced CTSD activity.	Ceramides	0-8	cathepsin D	Homo sapiens	108-112
10849758-5	2000	These findings suggest that A-SMase-derived ceramide targets endolysosomal CTSD.	Ceramides	44-52	sphingomyelin phosphodiesterase 1	Homo sapiens	28-35
10849758-5	2000	These findings suggest that A-SMase-derived ceramide targets endolysosomal CTSD.	Ceramides	44-52	cathepsin D	Homo sapiens	75-79
10656197-9	2000	In a number of cell types, TNFalpha receptor binding results in the activation of specific signal transduction cascades, including the hydrolysis of sphingomyelin to ceramide.	Ceramides	166-174	tumor necrosis factor	Rattus norvegicus	27-35
10644522-9	2000	HP and TNF-alpha pretreatment cause a two- to threefold increase of intracellular ceramide levels, which coincides with the state of tolerance.	Ceramides	82-90	tumor necrosis factor	Rattus norvegicus	7-16
10644522-13	2000	These results suggest that HP is mediated via ceramide synthesis triggered by TNF-alpha.	Ceramides	46-54	tumor necrosis factor	Rattus norvegicus	78-87
10874474-0	2000	Induction of p53-independent p21 during ceramide-induced G1 arrest in human hepatocarcinoma cells.	Ceramides	40-48	tumor protein p53	Homo sapiens	13-16
10874474-0	2000	Induction of p53-independent p21 during ceramide-induced G1 arrest in human hepatocarcinoma cells.	Ceramides	40-48	H3 histone pseudogene 16	Homo sapiens	29-32
10874474-1	2000	Ceramide is known to induce pRb (retinoblastoma gene product) dephosphorylation through the activation of ceramide-activated protein phosphatase (CAPP) during G1 arrest, but other molecular mechanisms linked to regulation of pRb dephosphorylation during ceramide-induced G1 arrest are poorly understood.	Ceramides	0-8	RB transcriptional corepressor 1	Homo sapiens	28-31
10874474-1	2000	Ceramide is known to induce pRb (retinoblastoma gene product) dephosphorylation through the activation of ceramide-activated protein phosphatase (CAPP) during G1 arrest, but other molecular mechanisms linked to regulation of pRb dephosphorylation during ceramide-induced G1 arrest are poorly understood.	Ceramides	0-8	RB transcriptional corepressor 1	Homo sapiens	225-228
10874474-1	2000	Ceramide is known to induce pRb (retinoblastoma gene product) dephosphorylation through the activation of ceramide-activated protein phosphatase (CAPP) during G1 arrest, but other molecular mechanisms linked to regulation of pRb dephosphorylation during ceramide-induced G1 arrest are poorly understood.	Ceramides	106-114	RB transcriptional corepressor 1	Homo sapiens	28-31
10874474-2	2000	In this paper, we investigated whether p21, a cdk (cyclin-dependent kinase) inhibitor, is involved in the induction of pRb dephosphorylation during ceramide-induced G1 arrest.	Ceramides	148-156	H3 histone pseudogene 16	Homo sapiens	39-42
10874474-2	2000	In this paper, we investigated whether p21, a cdk (cyclin-dependent kinase) inhibitor, is involved in the induction of pRb dephosphorylation during ceramide-induced G1 arrest.	Ceramides	148-156	RB transcriptional corepressor 1	Homo sapiens	119-122
10874474-3	2000	In SK-Hep-1 cells, the addition of ceramide resulted in pRb dephosphorylation and G1 arrest.	Ceramides	35-43	RB transcriptional corepressor 1	Homo sapiens	56-59
10874474-4	2000	The activity of cdk2 was inhibited in response to ceramide during this process.	Ceramides	50-58	cyclin dependent kinase 2	Homo sapiens	16-20
10874474-6	2000	p21 induction was also observed in the Hep3B cells lacking a functional p53 after exposure to ceramide.	Ceramides	94-102	H3 histone pseudogene 16	Homo sapiens	0-3
10874474-6	2000	p21 induction was also observed in the Hep3B cells lacking a functional p53 after exposure to ceramide.	Ceramides	94-102	tumor protein p53	Homo sapiens	72-75
10874474-7	2000	Although p21 is induced in ceramide-treated Hep3B cells, Hep3B cells do not induce G1 arrest, because Hep3B cells are deficient in a functional pRb protein.	Ceramides	27-35	H3 histone pseudogene 16	Homo sapiens	9-12
10874474-7	2000	Although p21 is induced in ceramide-treated Hep3B cells, Hep3B cells do not induce G1 arrest, because Hep3B cells are deficient in a functional pRb protein.	Ceramides	27-35	RB transcriptional corepressor 1	Homo sapiens	144-147
10874474-9	2000	After treatment with ceramide, pRb-expressing cells (pRb+/+), but not pRb-/- cells, were arrested in G1 phase.	Ceramides	21-29	RB transcriptional corepressor 1	Homo sapiens	31-34
10874474-9	2000	After treatment with ceramide, pRb-expressing cells (pRb+/+), but not pRb-/- cells, were arrested in G1 phase.	Ceramides	21-29	RB transcriptional corepressor 1	Homo sapiens	53-56
10874474-9	2000	After treatment with ceramide, pRb-expressing cells (pRb+/+), but not pRb-/- cells, were arrested in G1 phase.	Ceramides	21-29	RB transcriptional corepressor 1	Homo sapiens	53-56
10874474-10	2000	In pRb+/+ cells, ceramide-mediated G1 arrest was accompanied by the accumulation of hypophosphorylated pRb and p21 associated with cdk2.	Ceramides	17-25	RB transcriptional corepressor 1	Homo sapiens	3-6
10874474-10	2000	In pRb+/+ cells, ceramide-mediated G1 arrest was accompanied by the accumulation of hypophosphorylated pRb and p21 associated with cdk2.	Ceramides	17-25	RB transcriptional corepressor 1	Homo sapiens	103-106
10874474-10	2000	In pRb+/+ cells, ceramide-mediated G1 arrest was accompanied by the accumulation of hypophosphorylated pRb and p21 associated with cdk2.	Ceramides	17-25	H3 histone pseudogene 16	Homo sapiens	111-114
10874474-10	2000	In pRb+/+ cells, ceramide-mediated G1 arrest was accompanied by the accumulation of hypophosphorylated pRb and p21 associated with cdk2.	Ceramides	17-25	cyclin dependent kinase 2	Homo sapiens	131-135
10874474-11	2000	Together, these results suggest that p21, induced through p53-independent pathway, participates in the induction of pRb dephosphorylation by inhibiting cdk2 activity during ceramide-mediated G1 arrest in hepatocarcinoma cells.	Ceramides	173-181	H3 histone pseudogene 16	Homo sapiens	37-40
10874474-11	2000	Together, these results suggest that p21, induced through p53-independent pathway, participates in the induction of pRb dephosphorylation by inhibiting cdk2 activity during ceramide-mediated G1 arrest in hepatocarcinoma cells.	Ceramides	173-181	tumor protein p53	Homo sapiens	58-61
10874474-11	2000	Together, these results suggest that p21, induced through p53-independent pathway, participates in the induction of pRb dephosphorylation by inhibiting cdk2 activity during ceramide-mediated G1 arrest in hepatocarcinoma cells.	Ceramides	173-181	RB transcriptional corepressor 1	Homo sapiens	116-119
10874474-11	2000	Together, these results suggest that p21, induced through p53-independent pathway, participates in the induction of pRb dephosphorylation by inhibiting cdk2 activity during ceramide-mediated G1 arrest in hepatocarcinoma cells.	Ceramides	173-181	cyclin dependent kinase 2	Homo sapiens	152-156
10627278-6	2000	3) Stimulation of SV40-transformed fibroblasts by TNF-alpha or CD40 ligand resulted in apoptosis equally well in cells derived from control individuals and from patients affected with Farber disease, having a genetic defect of acid ceramidase activity leading to lysosomal accumulation of ceramide.	Ceramides	289-297	tumor necrosis factor	Homo sapiens	50-59
10772341-0	2000	Specific processing of poly(ADP-ribose) polymerase, accompanied by activation of caspase-3 and elevation/reduction of ceramide/hydrogen peroxide levels, during induction of apoptosis in host HL-60 cells infected by the human granulocytic ehrlichiosis (HGE) agent.	Ceramides	118-126	poly(ADP-ribose) polymerase 1	Homo sapiens	23-50
10627278-6	2000	3) Stimulation of SV40-transformed fibroblasts by TNF-alpha or CD40 ligand resulted in apoptosis equally well in cells derived from control individuals and from patients affected with Farber disease, having a genetic defect of acid ceramidase activity leading to lysosomal accumulation of ceramide.	Ceramides	289-297	CD40 molecule	Homo sapiens	63-67
10666000-5	2000	C2 ceramide produced a concentration-dependent inhibition of fMLP-stimulated superoxide production within the concentration range of 1-30 microM.	Ceramides	3-11	formyl peptide receptor 1	Homo sapiens	61-65
10653586-0	2000	Involvement of caspase-3 and GD3 ganglioside in ceramide-induced apoptosis in Farber disease.	Ceramides	48-56	caspase 3	Homo sapiens	15-24
10653586-0	2000	Involvement of caspase-3 and GD3 ganglioside in ceramide-induced apoptosis in Farber disease.	Ceramides	48-56	GRDX	Homo sapiens	29-32
10653586-3	2000	Because recent studies reported that ceramide accumulation induces GD3 ganglioside formation and apoptosis, we investigated, in tissue obtained via colonoscopy from seriously involved patients, the possible involvement of ceramide in FD colonocyte destruction.	Ceramides	37-45	GRDX	Homo sapiens	67-70
10683565-1	2000	Ceramide, a sphingomyelin-derived second messenger, mediates cellular signals of cytokines such as tumor necrosis factor-alpha that are rapidly produced in the brain in response to vigorous neuronal activity and tissue injury.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	99-126
10563329-2	2000	Identification and characterization of YSR2 and YSR3 have demonstrated that the DHS-1-P phosphatase is an important mediator in the biosynthesis of sphingolipids and in the maintenance of the balance of signaling lipid molecules ceramide, sphingosine, and sphingosine-1-P.	Ceramides	229-237	sphinganine kinase LCB3	Saccharomyces cerevisiae S288C	39-43
10563329-2	2000	Identification and characterization of YSR2 and YSR3 have demonstrated that the DHS-1-P phosphatase is an important mediator in the biosynthesis of sphingolipids and in the maintenance of the balance of signaling lipid molecules ceramide, sphingosine, and sphingosine-1-P.	Ceramides	229-237	sphinganine kinase YSR3	Saccharomyces cerevisiae S288C	48-52
10683565-2	2000	Using whole-cell patch-clamp recordings, the present study examined whether ceramide modulated excitatory postsynaptic currents mediated by ionotropic glutamate receptors in CA1 pyramidal neurons of rat hippocampal slices.	Ceramides	76-84	carbonic anhydrase 1	Rattus norvegicus	174-177
10653520-3	2000	Ceramide has been implicated as a secondary messenger for TNFalpha-induced cell death, but many of the intracellular effects of ceramide are not fully understood.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	58-66
10798219-4	2000	PP 2A has been suggested as a direct in vitro target of ceramide action on cell growth and apoptosis.	Ceramides	56-64	protein phosphatase 2 phosphatase activator	Homo sapiens	0-5
10798219-5	2000	Ceramide also inhibits phorbol myristate acetate-stimulated PLD.	Ceramides	0-8	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	60-63
10653520-6	2000	Treatment with 20 microM ceramide induced apoptosis and this was quickly followed by oncotic necrosis in the TNFalpha-sensitive JB6 (TNFs) cells.	Ceramides	25-33	tumor necrosis factor	Homo sapiens	109-117
10601289-0	1999	CD40 signals apoptosis through FAN-regulated activation of the sphingomyelin-ceramide pathway.	Ceramides	77-85	CD40 molecule	Homo sapiens	0-4
10601289-0	1999	CD40 signals apoptosis through FAN-regulated activation of the sphingomyelin-ceramide pathway.	Ceramides	77-85	neutral sphingomyelinase activation associated factor	Homo sapiens	31-34
10601289-1	1999	The possibility that the sphingomyelin (SM)-ceramide pathway is activated by CD40, a transmembrane glycoprotein belonging to the tumor necrosis factor receptor superfamily and that plays a critical role in the regulation of immune responses has been investigated.	Ceramides	44-52	CD40 molecule	Homo sapiens	77-81
10601289-2	1999	We demonstrate that incubation of Epstein-Barr virus-transformed lymphoid cells with an anti-CD40 antibody acting as an agonist results in the stimulation of a neutral sphingomyelinase, hydrolysis of cellular SM, and concomitant ceramide generation.	Ceramides	229-237	CD40 molecule	Homo sapiens	93-97
11310411-3	2000	ASM catalyses the production of ceramide, a key molecule of apoptosis, from sphingomyelin.	Ceramides	32-40	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
10601289-4	1999	The anti-CD40 antibody, as well as the soluble CD40 ligand induced a decrease in thymidine incorporation and morphological features of apoptosis, which were mimicked by cell-permeant or bacterial sphingomyelinase-produced ceramides.	Ceramides	222-231	CD40 molecule	Homo sapiens	9-13
10601289-4	1999	The anti-CD40 antibody, as well as the soluble CD40 ligand induced a decrease in thymidine incorporation and morphological features of apoptosis, which were mimicked by cell-permeant or bacterial sphingomyelinase-produced ceramides.	Ceramides	222-231	CD40 molecule	Homo sapiens	47-51
10601289-8	1999	Altogether, these results strongly suggest that CD40 ligation can activate via FAN a neutral sphingomyelinase-mediated ceramide pathway that is involved in the cell growth inhibitory effects of CD40.	Ceramides	119-127	CD40 molecule	Homo sapiens	48-52
10601289-8	1999	Altogether, these results strongly suggest that CD40 ligation can activate via FAN a neutral sphingomyelinase-mediated ceramide pathway that is involved in the cell growth inhibitory effects of CD40.	Ceramides	119-127	neutral sphingomyelinase activation associated factor	Homo sapiens	79-82
10601289-8	1999	Altogether, these results strongly suggest that CD40 ligation can activate via FAN a neutral sphingomyelinase-mediated ceramide pathway that is involved in the cell growth inhibitory effects of CD40.	Ceramides	119-127	CD40 molecule	Homo sapiens	194-198
10585263-0	1999	p21 promotes ceramide-induced apoptosis and antagonizes the antideath effect of Bcl-2 in human hepatocarcinoma cells.	Ceramides	13-21	H3 histone pseudogene 16	Homo sapiens	0-3
10593952-4	1999	Although both exogenous ceramide and bacterial SMase stimulate JNK1, GRObeta-induced JNK1 activation is an event probably independent of ceramide generated by A-SMase, since it is maintained in the presence of compounds that block A-SMase activity.	Ceramides	24-32	mitogen-activated protein kinase 8	Rattus norvegicus	63-67
10585289-5	1999	Ceramide, an intermediate of several apoptotic pathways, interferes with growth factor-mediated Akt activation.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	96-99
10585289-6	1999	Ceramide induced endothelial cell death and abolished angiopoietin-1-mediated activation of Akt and the effect on cell survival.	Ceramides	0-8	angiopoietin 1	Homo sapiens	54-68
10585289-6	1999	Ceramide induced endothelial cell death and abolished angiopoietin-1-mediated activation of Akt and the effect on cell survival.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	92-95
10585882-3	1999	The treatment of HL-60 cells with the combination of 1,25(OH)(2)D(3) and IFN-gamma had an additive effect on sphingomyelin hydrolysis, ceramide release and the activity of cytosolic, Mg(2+)-independent, neutral sphingomyelinase.	Ceramides	135-143	interferon gamma	Homo sapiens	73-82
10572248-1	1999	We have demonstrated previously that insulin-like growth factor binding protein (IGFBP)-3 alone has little growth inhibitory effect on Hs578T human breast cancer cells, but that it can dramatically accentuate the apoptotic response to the physiological trigger, ceramide, in an IGF-independent manner.	Ceramides	262-270	insulin like growth factor binding protein 3	Homo sapiens	37-89
10608884-3	1999	Neutral sphingomyelinase (N-SMase) is one of the key enzymes in the generation of ceramide, and recently the cloning of a putative N-SMase was reported.	Ceramides	82-90	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
10608884-3	1999	Neutral sphingomyelinase (N-SMase) is one of the key enzymes in the generation of ceramide, and recently the cloning of a putative N-SMase was reported.	Ceramides	82-90	sphingomyelin phosphodiesterase 2	Homo sapiens	26-33
10608884-3	1999	Neutral sphingomyelinase (N-SMase) is one of the key enzymes in the generation of ceramide, and recently the cloning of a putative N-SMase was reported.	Ceramides	82-90	sphingomyelin phosphodiesterase 2	Homo sapiens	131-138
10585263-3	1999	Previously, we reported that p21 was induced in a p53-independent manner during ceramide-induced apoptosis in human hepatocarcinoma cell lines.	Ceramides	80-88	H3 histone pseudogene 16	Homo sapiens	29-32
10585263-3	1999	Previously, we reported that p21 was induced in a p53-independent manner during ceramide-induced apoptosis in human hepatocarcinoma cell lines.	Ceramides	80-88	tumor protein p53	Homo sapiens	50-53
10590315-0	1999	Possible involvement of cytochrome c release and sequential activation of caspases in ceramide-induced apoptosis in SK-N-MC cells.	Ceramides	86-94	cytochrome c, somatic	Homo sapiens	24-36
10590315-0	1999	Possible involvement of cytochrome c release and sequential activation of caspases in ceramide-induced apoptosis in SK-N-MC cells.	Ceramides	86-94	caspase 2	Homo sapiens	74-82
10590315-1	1999	Ceramide is characterized as a second messenger of apoptosis induced by various agents such as tumor necrosis factor (TNF-alpha), Fas ligand, hydrogen peroxide, heat shock and ionizing radiation.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	118-127
10590315-1	1999	Ceramide is characterized as a second messenger of apoptosis induced by various agents such as tumor necrosis factor (TNF-alpha), Fas ligand, hydrogen peroxide, heat shock and ionizing radiation.	Ceramides	0-8	Fas ligand	Homo sapiens	130-140
10585263-4	1999	In the present study, we investigated the precise role of p21 in ceramide-induced apoptosis in human hepatocarcinoma cells by using a tetracycline-inducible expression system.	Ceramides	65-73	H3 histone pseudogene 16	Homo sapiens	58-61
10585263-6	1999	However, Hep3B/p21 cells were more sensitive to ceramide-induced apoptosis.	Ceramides	48-56	H3 histone pseudogene 16	Homo sapiens	15-18
10585263-8	1999	The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition.	Ceramides	74-82	BCL2 associated X, apoptosis regulator	Homo sapiens	24-27
10585263-8	1999	The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition.	Ceramides	74-82	H3 histone pseudogene 16	Homo sapiens	51-54
10585263-8	1999	The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition.	Ceramides	74-82	H3 histone pseudogene 16	Homo sapiens	133-136
10585263-8	1999	The expression level of Bax was increased in Hep3B/p21 cells treated with ceramide and its expression was more accelerated under the p21-overexpressed condition compared to that of the p21-repressed condition.	Ceramides	74-82	H3 histone pseudogene 16	Homo sapiens	133-136
10585263-10	1999	On the other hand, the levels of p21 and Bax protein were increased by ceramide in another hepatocarcinoma cell line, SK-Hep-1, while the Bcl-2 protein level was not changed.	Ceramides	71-79	H3 histone pseudogene 16	Homo sapiens	33-36
10585263-10	1999	On the other hand, the levels of p21 and Bax protein were increased by ceramide in another hepatocarcinoma cell line, SK-Hep-1, while the Bcl-2 protein level was not changed.	Ceramides	71-79	BCL2 associated X, apoptosis regulator	Homo sapiens	41-44
10585263-10	1999	On the other hand, the levels of p21 and Bax protein were increased by ceramide in another hepatocarcinoma cell line, SK-Hep-1, while the Bcl-2 protein level was not changed.	Ceramides	71-79	DNL-type zinc finger	Homo sapiens	121-126
10585263-11	1999	Overexpression of Bcl-2 not only suppressed apoptosis but also completely prevented induction of p21 and Bax caused by ceramide in SK-Hep-1 cells.	Ceramides	119-127	BCL2 apoptosis regulator	Homo sapiens	18-23
10585263-11	1999	Overexpression of Bcl-2 not only suppressed apoptosis but also completely prevented induction of p21 and Bax caused by ceramide in SK-Hep-1 cells.	Ceramides	119-127	H3 histone pseudogene 16	Homo sapiens	97-100
10585263-11	1999	Overexpression of Bcl-2 not only suppressed apoptosis but also completely prevented induction of p21 and Bax caused by ceramide in SK-Hep-1 cells.	Ceramides	119-127	BCL2 associated X, apoptosis regulator	Homo sapiens	105-108
10585263-11	1999	Overexpression of Bcl-2 not only suppressed apoptosis but also completely prevented induction of p21 and Bax caused by ceramide in SK-Hep-1 cells.	Ceramides	119-127	DNL-type zinc finger	Homo sapiens	134-139
10585263-13	1999	These results suggest that p21 promotes ceramide-induced apoptosis by enhancing the expression of Bax, thereby modulating the molecular ratio of Bcl-2:Bax in human hepatocarcinoma cells.	Ceramides	40-48	H3 histone pseudogene 16	Homo sapiens	27-30
10585263-13	1999	These results suggest that p21 promotes ceramide-induced apoptosis by enhancing the expression of Bax, thereby modulating the molecular ratio of Bcl-2:Bax in human hepatocarcinoma cells.	Ceramides	40-48	BCL2 associated X, apoptosis regulator	Homo sapiens	98-101
10585263-13	1999	These results suggest that p21 promotes ceramide-induced apoptosis by enhancing the expression of Bax, thereby modulating the molecular ratio of Bcl-2:Bax in human hepatocarcinoma cells.	Ceramides	40-48	BCL2 apoptosis regulator	Homo sapiens	145-150
10585263-13	1999	These results suggest that p21 promotes ceramide-induced apoptosis by enhancing the expression of Bax, thereby modulating the molecular ratio of Bcl-2:Bax in human hepatocarcinoma cells.	Ceramides	40-48	BCL2 associated X, apoptosis regulator	Homo sapiens	151-154
10746154-0	1999	Ceramide enhances susceptibility of membrane phospholipids to phospholipase A2 through modification of lipid organization in platelet membranes.	Ceramides	0-8	phospholipase A2 group IB	Homo sapiens	62-78
10746154-1	1999	The effects of ceramide on agonist-stimulated phospholipase A2 (PLA2) activity were studied in platelets.	Ceramides	15-23	phospholipase A2 group IB	Homo sapiens	46-62
10746154-1	1999	The effects of ceramide on agonist-stimulated phospholipase A2 (PLA2) activity were studied in platelets.	Ceramides	15-23	phospholipase A2 group IB	Homo sapiens	64-68
10746154-4	1999	The enhanced arachidonic acid release by exogenous ceramide was completely inhibited by methyl arachidonyl fluorophosphonate, a cytosolic PLA2 inhibitor.	Ceramides	51-59	phospholipase A2 group IB	Homo sapiens	138-142
10746154-6	1999	These results suggest that enrichment of ceramide in membranes causes modification of intermolecular organization, leading to increased susceptibility of substrate phospholipids to PLA2.	Ceramides	41-49	phospholipase A2 group IB	Homo sapiens	181-185
10579332-7	1999	The effect of ceramide was mimicked by interleukin-1beta, a cytokine highly expressed in the pineal that is known to activate the sphingomyelin pathway.	Ceramides	14-22	interleukin 1 beta	Rattus norvegicus	39-56
10610716-1	1999	Acid ceramidase (AC) is the lysosomal enzyme that degrades ceramide into sphingosine and fatty acid.	Ceramides	59-67	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
10579333-0	1999	Ceramide enhances growth hormone (GH)-releasing hormone-stimulated cyclic adenosine 3",5"-monophosphate accumulation but inhibits GH release in rat anterior pituitary cells.	Ceramides	0-8	gonadotropin releasing hormone receptor	Rattus norvegicus	18-32
10579333-0	1999	Ceramide enhances growth hormone (GH)-releasing hormone-stimulated cyclic adenosine 3",5"-monophosphate accumulation but inhibits GH release in rat anterior pituitary cells.	Ceramides	0-8	gonadotropin releasing hormone receptor	Rattus norvegicus	34-36
10579333-0	1999	Ceramide enhances growth hormone (GH)-releasing hormone-stimulated cyclic adenosine 3",5"-monophosphate accumulation but inhibits GH release in rat anterior pituitary cells.	Ceramides	0-8	gonadotropin releasing hormone receptor	Rattus norvegicus	130-132
10579333-1	1999	In this study, the effect of ceramide on GH-releasing hormone (GHRH)-stimulated cAMP accumulation and GH release in rat anterior pituitary cells was investigated.	Ceramides	29-37	growth hormone releasing hormone	Rattus norvegicus	41-61
10579333-1	1999	In this study, the effect of ceramide on GH-releasing hormone (GHRH)-stimulated cAMP accumulation and GH release in rat anterior pituitary cells was investigated.	Ceramides	29-37	growth hormone releasing hormone	Rattus norvegicus	63-67
10579333-1	1999	In this study, the effect of ceramide on GH-releasing hormone (GHRH)-stimulated cAMP accumulation and GH release in rat anterior pituitary cells was investigated.	Ceramides	29-37	gonadotropin releasing hormone receptor	Rattus norvegicus	41-43
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	38-46	gonadotropin releasing hormone receptor	Rattus norvegicus	105-107
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	38-46	growth hormone releasing hormone	Rattus norvegicus	325-329
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	38-46	gonadotropin releasing hormone receptor	Rattus norvegicus	152-154
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	86-94	gonadotropin releasing hormone receptor	Rattus norvegicus	105-107
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	86-94	growth hormone releasing hormone	Rattus norvegicus	325-329
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	86-94	gonadotropin releasing hormone receptor	Rattus norvegicus	152-154
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	86-94	gonadotropin releasing hormone receptor	Rattus norvegicus	105-107
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	86-94	growth hormone releasing hormone	Rattus norvegicus	325-329
10579333-5	1999	To identify the pathway through which ceramide mediated its effect, it was found that ceramide inhibited GH release stimulated by KCl, BayK 8644, and a GH-releasing peptide, but not that stimulated by ionomycin or an activator of protein kinase C. Direct measurement of intracellular Ca2+ revealed that C2-ceramide inhibited GHRH- and KCl-mediated increases in intracellular Ca2+, suggesting that ceramide probably inhibits GH release through inhibition of the L-type Ca2+ channels.	Ceramides	86-94	gonadotropin releasing hormone receptor	Rattus norvegicus	152-154
10579333-6	1999	As for its mechanism on cAMP accumulation, the enhancing effect of ceramide on GHRH-stimulated cAMP accumulation was abolished in the presence of a phosphodiesterase inhibitor, isobutylmethylxanthine, suggesting that ceramide enhances the cAMP response through inhibition of its metabolism.	Ceramides	67-75	growth hormone releasing hormone	Rattus norvegicus	79-83
10579333-6	1999	As for its mechanism on cAMP accumulation, the enhancing effect of ceramide on GHRH-stimulated cAMP accumulation was abolished in the presence of a phosphodiesterase inhibitor, isobutylmethylxanthine, suggesting that ceramide enhances the cAMP response through inhibition of its metabolism.	Ceramides	217-225	growth hormone releasing hormone	Rattus norvegicus	79-83
10579333-7	1999	Taken together, our results suggest that ceramide plays an important role in the regulation of GHRH-stimulated responses in somatotrophs.	Ceramides	41-49	growth hormone releasing hormone	Rattus norvegicus	95-99
10579333-8	1999	By reducing GH secretion while enhancing cAMP accumulation, ceramide may promote the synthesis and storage of GH in rat anterior pituitary cells.	Ceramides	60-68	gonadotropin releasing hormone receptor	Rattus norvegicus	110-112
10610716-1	1999	Acid ceramidase (AC) is the lysosomal enzyme that degrades ceramide into sphingosine and fatty acid.	Ceramides	59-67	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
10570152-3	1999	In this paper we show that CD95-stimulation blocks CRAC and Ca(2+) influx in lymphocytes through the activation of acidic sphingomyelinase (ASM) and ceramide release.	Ceramides	149-157	Fas cell surface death receptor	Homo sapiens	27-31
10606630-2	1999	TNF signaling is mediated by acid and neutral sphingomyelinases (A- and N-SMase), which generate ceramide, an important regulator of proliferation, differentiation, and apoptosis.	Ceramides	97-105	tumor necrosis factor	Mus musculus	0-3
10606630-2	1999	TNF signaling is mediated by acid and neutral sphingomyelinases (A- and N-SMase), which generate ceramide, an important regulator of proliferation, differentiation, and apoptosis.	Ceramides	97-105	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	72-79
10606630-10	1999	Together, these results suggest that TNF-R55 signaling pathways contribute to cutaneous permeability barrier repair through SMase-mediated generation of ceramide.	Ceramides	153-161	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	37-44
10616904-6	1999	In addition, Fas activation of the stress kinases p38 and c-Jun NH2 kinase and the generation of ceramide in response to Fas ligation were blocked in the FADD mutant cell lines.	Ceramides	97-105	Fas associated via death domain	Homo sapiens	154-158
10599977-7	1999	In addition, C2-ceramides and natural ceramides dispersed in a solvent mixture of ethanol and dodecane induced characteristic features of apoptosis in MIN6 cells, mimicking TNF-induced DNA damage.	Ceramides	16-25	tumor necrosis factor	Mus musculus	173-176
10599977-8	1999	We also determined endosomal ceramide production after TNF-alpha (10 nmol/L) treatment in MIN6 cells using the diacylglycerol kinase assay.	Ceramides	29-37	tumor necrosis factor	Mus musculus	55-64
10599977-9	1999	These results suggest that TNF-alpha can cause apoptosis in pancreatic beta cells through TNFR1-linked apoptotic factors, TRADD, FADD, and FLICE, and TNF-induced ceramide production may be involved in the pathways.	Ceramides	162-170	tumor necrosis factor	Mus musculus	27-36
10599977-9	1999	These results suggest that TNF-alpha can cause apoptosis in pancreatic beta cells through TNFR1-linked apoptotic factors, TRADD, FADD, and FLICE, and TNF-induced ceramide production may be involved in the pathways.	Ceramides	162-170	tumor necrosis factor	Mus musculus	27-30
10570178-5	1999	These endosomes containing fluorescent beta(2)m were found close to or within the Golgi apparatus, marked by fluorescent ceramide.	Ceramides	121-129	beta-2-microglobulin	Homo sapiens	39-47
10570152-6	1999	CD95-stimulation or the addition of ceramide prevents store-operated Ca(2+) influx, activation of the transcriptional regulator NFAT, and IL-2 synthesis.	Ceramides	36-44	interleukin 2	Homo sapiens	138-142
10579257-10	1999	The strong correlation we found between cell-associated ceramide and serum TNF-alpha supports the hypothesis that this cytokine plays an important role in activating the sphingomyelin pathway and ceramide generation in patients with sepsis.	Ceramides	56-64	tumor necrosis factor	Homo sapiens	75-84
10582697-4	1999	A Cer analogue with a D-glucuronic acid attached at the primary hydroxyl of N-palmitoyl-D-sphingosine (Cer-beta-glucuronide) was synthesized and evaluated as a substrate for Escherichia coli beta-glucuronidase and colonic digestion, as well as for suppression of early events in colon carcinogenesis in CFI mice treated with 1,2-dimethylhydrazine.	Ceramides	2-5	glucuronidase, beta	Mus musculus	191-209
10842662-7	1999	Interestingly, soluble analogues of ceramide antagonize both insulin"s activation of Akt/PKB as well as its stimulation of glucose transport, consistent with a causal relationship between the two.	Ceramides	36-44	insulin	Homo sapiens	61-68
10842662-7	1999	Interestingly, soluble analogues of ceramide antagonize both insulin"s activation of Akt/PKB as well as its stimulation of glucose transport, consistent with a causal relationship between the two.	Ceramides	36-44	AKT serine/threonine kinase 1	Homo sapiens	89-92
10543999-5	1999	Further investigation revealed that the activity of caspase-3 (CPP32) was elevated after ceramide treatment in Bad-transfected cells compared to that of the cells without Bad transfection, indicating the involvement of caspase cascade.	Ceramides	89-97	caspase 3	Mus musculus	52-61
10543999-5	1999	Further investigation revealed that the activity of caspase-3 (CPP32) was elevated after ceramide treatment in Bad-transfected cells compared to that of the cells without Bad transfection, indicating the involvement of caspase cascade.	Ceramides	89-97	caspase 3	Mus musculus	63-68
10607425-5	1999	Cyclosporin A inhibits induction of JNK function by TCR/CD28, PMA/ionomycin, ceramide, or H(2)O(2), but not induction by UV light or hyperosmolar sorbitol.	Ceramides	77-85	mitogen-activated protein kinase 8	Mus musculus	36-39
11001563-7	1999	A further role of ceramide and N-SMase in atherosclerosis was uncovered by the finding that Ox-LDL and TNF-alpha stimulated N-SMase activity.	Ceramides	18-26	tumor necrosis factor	Homo sapiens	103-112
11001563-7	1999	A further role of ceramide and N-SMase in atherosclerosis was uncovered by the finding that Ox-LDL and TNF-alpha stimulated N-SMase activity.	Ceramides	18-26	sphingomyelin phosphodiesterase 2	Homo sapiens	124-131
10579257-10	1999	The strong correlation we found between cell-associated ceramide and serum TNF-alpha supports the hypothesis that this cytokine plays an important role in activating the sphingomyelin pathway and ceramide generation in patients with sepsis.	Ceramides	196-204	tumor necrosis factor	Homo sapiens	75-84
10552998-3	1999	We investigated the biliary secretion of C6-7-nitro-2,1, 3-benzoxadiazol-4-yl (NBD)-labeled ceramide and its metabolites in Mdr1a/b and Mdr2 knockout mice compared to control mice.	Ceramides	92-100	complement component 6	Mus musculus	41-45
11001565-4	1999	The availability of the cloned aSMase and nSMases discovered so far led to a genetic approach to the verification of the concept that these enzymes in the "sphingomelin cycle" are responsible for the generation of ceramide regarded as a lipophilic second messenger in the intracellular signal cascades activated by e.g. TNF-alpha, Fas ligand or cellular stress.	Ceramides	214-222	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	31-37
11001565-4	1999	The availability of the cloned aSMase and nSMases discovered so far led to a genetic approach to the verification of the concept that these enzymes in the "sphingomelin cycle" are responsible for the generation of ceramide regarded as a lipophilic second messenger in the intracellular signal cascades activated by e.g. TNF-alpha, Fas ligand or cellular stress.	Ceramides	214-222	tumor necrosis factor	Homo sapiens	320-329
11001565-4	1999	The availability of the cloned aSMase and nSMases discovered so far led to a genetic approach to the verification of the concept that these enzymes in the "sphingomelin cycle" are responsible for the generation of ceramide regarded as a lipophilic second messenger in the intracellular signal cascades activated by e.g. TNF-alpha, Fas ligand or cellular stress.	Ceramides	214-222	Fas ligand	Homo sapiens	331-341
11001565-5	1999	All the available evidence derived from the aSMase deficient mouse line and several cell lines overexpressing aSMase and nSMase questions a role of ceramide released by the mammalian sphingomyelinases known so far in intracellular signal transduction.	Ceramides	148-156	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	44-50
11001565-5	1999	All the available evidence derived from the aSMase deficient mouse line and several cell lines overexpressing aSMase and nSMase questions a role of ceramide released by the mammalian sphingomyelinases known so far in intracellular signal transduction.	Ceramides	148-156	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	110-116
11001565-5	1999	All the available evidence derived from the aSMase deficient mouse line and several cell lines overexpressing aSMase and nSMase questions a role of ceramide released by the mammalian sphingomyelinases known so far in intracellular signal transduction.	Ceramides	148-156	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	121-127
11001570-6	1999	Here the molecular mechanisms of TNF-induced activation of sphingomyelinases and the functional consequences of ceramide generation will be discussed.	Ceramides	112-120	tumor necrosis factor	Homo sapiens	33-36
10527636-0	1999	Glycosylation of ceramide potentiates cellular resistance to tumor necrosis factor-alpha-induced apoptosis.	Ceramides	17-25	tumor necrosis factor	Homo sapiens	61-88
10527636-1	1999	Ceramide, as a second messenger, initiates one of the major signal transduction pathways in tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	92-119
10527636-1	1999	Ceramide, as a second messenger, initiates one of the major signal transduction pathways in tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	121-130
10527636-2	1999	Glucosylceramide synthase (GCS) catalyzes glycosylation of ceramide and produces glucosylceramide.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
10527636-7	1999	This work demonstrates that GCS, which catalyzes ceramide glycosylation, potentiates cytotoxic resistance to TNF-alpha.	Ceramides	49-57	UDP-glucose ceramide glucosyltransferase	Homo sapiens	28-31
10527636-7	1999	This work demonstrates that GCS, which catalyzes ceramide glycosylation, potentiates cytotoxic resistance to TNF-alpha.	Ceramides	49-57	tumor necrosis factor	Homo sapiens	109-118
10552998-3	1999	We investigated the biliary secretion of C6-7-nitro-2,1, 3-benzoxadiazol-4-yl (NBD)-labeled ceramide and its metabolites in Mdr1a/b and Mdr2 knockout mice compared to control mice.	Ceramides	92-100	ATP-binding cassette, sub-family B (MDR/TAP), member 1A	Mus musculus	124-129
10531385-12	1999	Importantly, two known mediators of apoptosis, ceramide and GD3 ganglioside, potentiated the induction by Bax of the MPT.	Ceramides	47-55	BCL2 associated X, apoptosis regulator	Homo sapiens	106-109
10531389-4	1999	Treatment of U937 cells with cell-permeant ceramides induced both an increase in ROS generation and JNK activation, and apoptosis, all of which were antioxidant-sensitive.	Ceramides	43-52	mitogen-activated protein kinase 8	Homo sapiens	100-103
10531389-5	1999	In conclusion, DNR-triggered apoptosis implicates a ceramide-mediated, ROS-dependent JNK and activated protein-1 activation.	Ceramides	52-60	mitogen-activated protein kinase 8	Homo sapiens	85-88
10670688-1	1999	Ceramide, ceramide-1-phosphate (C1P) sphingosine (SPH) and sphingosine-1-phosphate (S1P) effects on proliferation and extracellular-signal regulated kinases, ERKs (also known as MAPKs), activation were investigated in human and rat osteoblastic cells.	Ceramides	0-8	mitogen-activated protein kinase 3	Homo sapiens	158-162
10527524-1	1999	Acid ceramidase (N-acylsphingosine amidohydrolase) is the lysosomal enzyme required to hydrolyze the N-acyl linkage between the fatty acid and sphingosine moieties in ceramide.	Ceramides	167-175	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
10523605-0	1999	Binding and antigen presentation of ceramide-containing glycolipids by soluble mouse and human CD1d molecules.	Ceramides	36-44	CD1d molecule	Homo sapiens	95-99
10535965-3	1999	We have explored the role of ceramide analogues in eNOS signaling in cultured bovine aortic endothelial cells (BAEC).	Ceramides	29-37	nitric oxide synthase 3	Bos taurus	51-55
10535965-4	1999	Addition of the ceramide analogue N-acetylsphingosine (C(2)-ceramide; 5 microM) to intact BAEC leads to a significant increase in NO synthase activity (assayed by using the fluorescent indicator 4,5-diaminofluorescein) and translocation of eNOS from the endothelial cell membrane to intracellular sites (measured by using quantitative immunofluorescence techniques); the biologically inactive ceramide N-acetyldihydrosphingosine is entirely without effect.	Ceramides	16-24	nitric oxide synthase 3	Bos taurus	240-244
10535965-4	1999	Addition of the ceramide analogue N-acetylsphingosine (C(2)-ceramide; 5 microM) to intact BAEC leads to a significant increase in NO synthase activity (assayed by using the fluorescent indicator 4,5-diaminofluorescein) and translocation of eNOS from the endothelial cell membrane to intracellular sites (measured by using quantitative immunofluorescence techniques); the biologically inactive ceramide N-acetyldihydrosphingosine is entirely without effect.	Ceramides	60-68	nitric oxide synthase 3	Bos taurus	240-244
10535965-8	1999	Finally, we show that treatment of BAEC with bradykinin causes a significant increase in cellular ceramide content; the response to bradykinin has an EC(50) of 3 nM and is blocked by the bradykinin B(2)-receptor antagonist HOE140.	Ceramides	98-106	kininogen 1	Bos taurus	45-55
10535965-8	1999	Finally, we show that treatment of BAEC with bradykinin causes a significant increase in cellular ceramide content; the response to bradykinin has an EC(50) of 3 nM and is blocked by the bradykinin B(2)-receptor antagonist HOE140.	Ceramides	98-106	kininogen 1	Bos taurus	132-142
10535965-8	1999	Finally, we show that treatment of BAEC with bradykinin causes a significant increase in cellular ceramide content; the response to bradykinin has an EC(50) of 3 nM and is blocked by the bradykinin B(2)-receptor antagonist HOE140.	Ceramides	98-106	kininogen 1	Bos taurus	132-142
10535965-9	1999	Bradykinin-induced ceramide generation could represent a mechanism for longer-term regulation of eNOS activity.	Ceramides	19-27	kininogen 1	Bos taurus	0-10
10535965-9	1999	Bradykinin-induced ceramide generation could represent a mechanism for longer-term regulation of eNOS activity.	Ceramides	19-27	nitric oxide synthase 3	Bos taurus	97-101
10535965-10	1999	Our results suggest that ceramide functions independently of Ca(2+)-regulated pathways to promote activation and translocation of eNOS, and that this lipid mediator may represent a physiological regulator of eNOS in vascular endothelial cells.	Ceramides	25-33	nitric oxide synthase 3	Bos taurus	130-134
10527524-3	1999	This study reports a new assay method to detect acid ceramidase activity in vitro using Bodipy or lissamine rhodamine-conjugated ceramide (C12 ceramide; dodecanoylsphingosine).	Ceramides	129-137	N-acylsphingosine amidohydrolase 1	Homo sapiens	48-63
10482630-9	1999	Moreover, the ceramide level was enhanced by B19 infection and NS-1 expression.	Ceramides	14-22	hormonally up-regulated Neu-associated kinase	Homo sapiens	45-48
10508159-0	1999	Cathepsin D targeted by acid sphingomyelinase-derived ceramide.	Ceramides	54-62	cathepsin D	Homo sapiens	0-11
10508159-0	1999	Cathepsin D targeted by acid sphingomyelinase-derived ceramide.	Ceramides	54-62	sphingomyelin phosphodiesterase 1	Homo sapiens	24-45
10508159-1	1999	Ceramide has been recognized as a common intracellular second messenger for various cytokines, growth factors and other stimuli, such as CD95, chemotherapeutic drugs and stress factors.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	137-141
10508159-6	1999	The results of our study identify cathepsin D as the first endosomal ceramide target that colocalizes with and may mediate downstream signaling effects of A-SMase.	Ceramides	69-77	cathepsin D	Homo sapiens	34-45
10508159-6	1999	The results of our study identify cathepsin D as the first endosomal ceramide target that colocalizes with and may mediate downstream signaling effects of A-SMase.	Ceramides	69-77	sphingomyelin phosphodiesterase 1	Homo sapiens	155-162
10499544-0	1999	Tumor necrosis factor-alpha induces apoptosis in immortalized hypothalamic neurons: involvement of ceramide-generating pathways.	Ceramides	99-107	tumor necrosis factor	Mus musculus	0-27
10499544-5	1999	The involvement of acidic sphingomyelinase in TNF alpha action was demonstrated by the partial prevention of ceramide generation, apoptosis, and reduced cell growth by the inhibitor of the acidic sphingomyelinase-generating pathway, D609, whereas the involvement of ceramide was proved by complete prevention of TNF alpha-induced effects by treatment with okadaic acid at concentrations inhibiting ceramide-dependent protein phosphatase.	Ceramides	109-117	tumor necrosis factor	Mus musculus	46-55
10499544-5	1999	The involvement of acidic sphingomyelinase in TNF alpha action was demonstrated by the partial prevention of ceramide generation, apoptosis, and reduced cell growth by the inhibitor of the acidic sphingomyelinase-generating pathway, D609, whereas the involvement of ceramide was proved by complete prevention of TNF alpha-induced effects by treatment with okadaic acid at concentrations inhibiting ceramide-dependent protein phosphatase.	Ceramides	266-274	tumor necrosis factor	Mus musculus	46-55
10499544-6	1999	The present data indicate that TNF alpha, through activation of ceramide-generating pathways, is able to affect GT1-7 cell viability, suggesting an additional effect that may contribute to the global action of this cytokine on neuroendocrine activities.	Ceramides	64-72	tumor necrosis factor	Mus musculus	31-40
10499544-6	1999	The present data indicate that TNF alpha, through activation of ceramide-generating pathways, is able to affect GT1-7 cell viability, suggesting an additional effect that may contribute to the global action of this cytokine on neuroendocrine activities.	Ceramides	64-72	guanine nucleotide binding protein, alpha transducing 2	Mus musculus	112-117
10493721-0	1999	Ceramide signaling downstream of the p75 neurotrophin receptor mediates the effects of nerve growth factor on outgrowth of cultured hippocampal neurons.	Ceramides	0-8	nerve growth factor receptor	Rattus norvegicus	37-62
10493721-0	1999	Ceramide signaling downstream of the p75 neurotrophin receptor mediates the effects of nerve growth factor on outgrowth of cultured hippocampal neurons.	Ceramides	0-8	nerve growth factor	Rattus norvegicus	87-106
10493721-2	1999	We have analyzed the effects of nerve growth factor (NGF) on the growth of cultured hippocampal pyramidal neurons and examined the possibility that the effects of NGF are mediated via generation of ceramide produced by neutral sphingomyelinase (N-SMase).	Ceramides	198-206	sphingomyelin phosphodiesterase 2	Rattus norvegicus	219-243
10493721-2	1999	We have analyzed the effects of nerve growth factor (NGF) on the growth of cultured hippocampal pyramidal neurons and examined the possibility that the effects of NGF are mediated via generation of ceramide produced by neutral sphingomyelinase (N-SMase).	Ceramides	198-206	sphingomyelin phosphodiesterase 2	Rattus norvegicus	245-252
10493721-4	1999	At this early stage of culture, NGF accelerates neurite formation and outgrowth and induces ceramide formation in a dose-dependent manner.	Ceramides	92-100	nerve growth factor	Rattus norvegicus	32-35
10493721-8	1999	We propose that a neurotrophin-p75NTR-ceramide signaling pathway influences outgrowth of hippocampal neurons.	Ceramides	38-46	nerve growth factor receptor	Rattus norvegicus	31-37
10514462-4	1999	We evaluated for the first time the effect of Bcl-2 expression on the intracellular distribution and production of hydrogen peroxide, under basal conditions and after treatment with apoptosis inducing agents, ceramide analogs and tumor necrosis factor (TNF)-alpha.	Ceramides	209-217	BCL2 apoptosis regulator	Homo sapiens	46-51
10482630-9	1999	Moreover, the ceramide level was enhanced by B19 infection and NS-1 expression.	Ceramides	14-22	influenza virus NS1A binding protein	Homo sapiens	63-67
10440934-5	1999	The activation of MAPKs by heat does not occur in all cell types, because the step(s) downstream of ceramide to activation of Raf-1 protein kinase is missing in myeloid leukemic cells such as HL-60, U937, and K562, while it is present in NIH3T3 fibroblasts.	Ceramides	100-108	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	126-131
10477278-10	1999	Using labelled dihydrosphingosine and dihydrosphingosine-1-P (DHS-1-P), we found that overexpression of YSR2 significantly increased ceramide formation, whereas deletion of YSR2, YSR3, or both, accumulated DHS-1-P, and deletion of YSR2 decreased ceramide formation.	Ceramides	133-141	sphinganine kinase LCB3	Saccharomyces cerevisiae S288C	104-108
10477278-10	1999	Using labelled dihydrosphingosine and dihydrosphingosine-1-P (DHS-1-P), we found that overexpression of YSR2 significantly increased ceramide formation, whereas deletion of YSR2, YSR3, or both, accumulated DHS-1-P, and deletion of YSR2 decreased ceramide formation.	Ceramides	246-254	sphinganine kinase LCB3	Saccharomyces cerevisiae S288C	104-108
10486254-3	1999	We studied the effect of ceramide on the degradation of IkappaB, the cytoplasmic inhibitor of the transcription factor NF-kappaB.	Ceramides	25-33	nuclear factor kappa B subunit 1	Homo sapiens	119-128
10486254-4	1999	We show that ceramide treatment results in reduced levels of phosphorylated IkappaBalpha and degradation of both IkappaBalpha and IkappaBbeta.	Ceramides	13-21	NFKB inhibitor alpha	Homo sapiens	76-88
10486254-4	1999	We show that ceramide treatment results in reduced levels of phosphorylated IkappaBalpha and degradation of both IkappaBalpha and IkappaBbeta.	Ceramides	13-21	NFKB inhibitor alpha	Homo sapiens	113-125
10486254-4	1999	We show that ceramide treatment results in reduced levels of phosphorylated IkappaBalpha and degradation of both IkappaBalpha and IkappaBbeta.	Ceramides	13-21	NFKB inhibitor beta	Homo sapiens	130-141
10486254-5	1999	Ceramide synergised with okadaic acid (OA), a compound which interferes with the protein phosphatase 2A-controlled component of the NF-kappaB activation pathway, enhancing OA-induced IkappaB degradation.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	132-141
10467260-0	1999	Overexpression of Akt (protein kinase B) confers protection against apoptosis and prevents formation of ceramide in response to pro-apoptotic stimuli.	Ceramides	104-112	AKT serine/threonine kinase 1	Homo sapiens	18-21
10467260-7	1999	Ceramide was a more potent activator of CPP32 and an inducer of apoptosis when added as the native form (hydroxy- or nonhydroxy-), rather than the more water-soluble C(2)-ceramide.	Ceramides	0-8	caspase 3	Homo sapiens	40-45
10477698-3	1999	The apoptotic pathway distal to the DISC is intact because ceramide analogs, staurosporine, and granzyme B activate caspase-3 and induce apoptosis.	Ceramides	59-67	caspase 3	Homo sapiens	116-125
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	62-70	endogenous retrovirus group K member 15	Homo sapiens	24-28
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	62-70	AKT serine/threonine kinase 1	Homo sapiens	34-37
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	62-70	AKT serine/threonine kinase 1	Homo sapiens	137-140
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	62-70	AKT serine/threonine kinase 1	Homo sapiens	137-140
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	106-114	endogenous retrovirus group K member 15	Homo sapiens	24-28
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	106-114	AKT serine/threonine kinase 1	Homo sapiens	34-37
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	106-114	AKT serine/threonine kinase 1	Homo sapiens	137-140
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	106-114	AKT serine/threonine kinase 1	Homo sapiens	137-140
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	216-224	endogenous retrovirus group K member 15	Homo sapiens	24-28
10467260-8	1999	Overexpression of PI3K (p110) and Akt protected cells against ceramide-induced apoptosis, suggesting that Ceramide action is upstream of Akt in these cells and suggesting that Akt might be a target for inhibition by ceramide.	Ceramides	216-224	AKT serine/threonine kinase 1	Homo sapiens	34-37
10467260-0	1999	Overexpression of Akt (protein kinase B) confers protection against apoptosis and prevents formation of ceramide in response to pro-apoptotic stimuli.	Ceramides	104-112	protein tyrosine kinase 2 beta	Homo sapiens	23-39
10467260-6	1999	Both neo-transfected and the c-Akt dominant-negative transfected F-11 cells showed increased ceramide formation (twofold) in response to staurosporine, wortmannin, or LY294002; whereas cells with a constitutively active Akt (Myr-Akt) showed no increase in ceramide when treated with staurosporine, wortmannin, or LY294002.	Ceramides	93-101	AKT serine/threonine kinase 1	Homo sapiens	31-34
10467260-6	1999	Both neo-transfected and the c-Akt dominant-negative transfected F-11 cells showed increased ceramide formation (twofold) in response to staurosporine, wortmannin, or LY294002; whereas cells with a constitutively active Akt (Myr-Akt) showed no increase in ceramide when treated with staurosporine, wortmannin, or LY294002.	Ceramides	256-264	AKT serine/threonine kinase 1	Homo sapiens	31-34
10427136-9	1999	We propose that an enhanced capacity to glycosylate ceramide as evidenced in MCF-7-AdrR cells, is a molecular determinant of drug resistance, particularly as regards resistance to ceramide-enhancing agents such as anthracyclines, ionizing radiation, and tumor necrosis factor-alpha.	Ceramides	52-60	tumor necrosis factor	Homo sapiens	254-281
10465274-1	1999	We have recently reported that insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) can significantly increase ceramide-induced apoptosis in an Hs578T breast carcinoma cell line in an IGF-independent manner.	Ceramides	119-127	insulin like growth factor binding protein 3	Homo sapiens	31-81
10465274-1	1999	We have recently reported that insulin-like growth factor (IGF)-binding protein-3 (IGFBP-3) can significantly increase ceramide-induced apoptosis in an Hs578T breast carcinoma cell line in an IGF-independent manner.	Ceramides	119-127	insulin like growth factor binding protein 3	Homo sapiens	83-90
10465274-5	1999	In this study we confirmed that preincubation of Hs578T cells with IGFBP-3 enhances the apoptotic effect of the ceramide analog C2.	Ceramides	112-120	insulin like growth factor binding protein 3	Homo sapiens	67-74
10460829-6	1999	In both organs, the ceramide portion was highly hydroxylated with prevalence of alpha-hydroxylated fatty acids, C18 phytosphingosine in kidney and C18 sphingosine in liver Forssman glycolipid.	Ceramides	20-28	Bardet-Biedl syndrome 9	Homo sapiens	112-115
10460829-6	1999	In both organs, the ceramide portion was highly hydroxylated with prevalence of alpha-hydroxylated fatty acids, C18 phytosphingosine in kidney and C18 sphingosine in liver Forssman glycolipid.	Ceramides	20-28	Bardet-Biedl syndrome 9	Homo sapiens	147-150
10520574-9	1999	Results obtained in dbcAMP (dibutyryladenosine 3":5"-cyclic monophosphate)-stimulated cultures suggest that the observed effects of ceramide on transferrin secretion are secondary to a decrease in cAMP production, whereas the effects of ceramide on lactate and estradiol productions are post-cAMP formation regulatory events.	Ceramides	132-140	transferrin	Homo sapiens	144-155
10510471-0	1999	Potentiation by vitamin D analogs of TNFalpha and ceramide-induced apoptosis in MCF-7 cells is associated with activation of cytosolic phospholipase A2.	Ceramides	50-58	phospholipase A2 group IVA	Homo sapiens	125-151
10510471-7	1999	As assessed by [3H]-arachidonic acid release, cells primed for 48 h with CB1093 (50 nM) showed enhanced cPLA2 activation in response to TNFalpha or ceramide.	Ceramides	148-156	phospholipase A2 group IVA	Homo sapiens	104-109
10510471-9	1999	These results suggest that TNFalpha and vitamin D analogs share a common pathway leading to apoptosis involving cPLA2 activation and/or ceramide generation.	Ceramides	136-144	tumor necrosis factor	Homo sapiens	27-35
10454518-7	1999	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	Ceramides	42-50	mitogen-activated protein kinase 9	Homo sapiens	235-239
10469329-6	1999	Most importantly, the analysis of ceramide subpopulations revealed that the total amount of ceramide 2 was elevated in keratin 10-deficient mice, whereas ceramides 1, 3, 4, and 5 were decreased among total stratum corneum lipids.	Ceramides	92-100	keratin 10	Mus musculus	119-129
10536997-7	1999	Augmentation of DNA synthesis by natural ceramides was more pronounced in tumor necrosis factor alpha (TNFalpha)-sensitive 28-4 cells than in less sensitive 24-2 cells, and TNFalpha-induced proliferation of 28-4 cells was suppressed by the concomitant addition of natural ceramides.	Ceramides	41-50	tumor necrosis factor	Mus musculus	74-101
10536997-7	1999	Augmentation of DNA synthesis by natural ceramides was more pronounced in tumor necrosis factor alpha (TNFalpha)-sensitive 28-4 cells than in less sensitive 24-2 cells, and TNFalpha-induced proliferation of 28-4 cells was suppressed by the concomitant addition of natural ceramides.	Ceramides	41-50	tumor necrosis factor	Mus musculus	103-111
10536997-7	1999	Augmentation of DNA synthesis by natural ceramides was more pronounced in tumor necrosis factor alpha (TNFalpha)-sensitive 28-4 cells than in less sensitive 24-2 cells, and TNFalpha-induced proliferation of 28-4 cells was suppressed by the concomitant addition of natural ceramides.	Ceramides	272-281	tumor necrosis factor	Mus musculus	103-111
10536997-7	1999	Augmentation of DNA synthesis by natural ceramides was more pronounced in tumor necrosis factor alpha (TNFalpha)-sensitive 28-4 cells than in less sensitive 24-2 cells, and TNFalpha-induced proliferation of 28-4 cells was suppressed by the concomitant addition of natural ceramides.	Ceramides	272-281	tumor necrosis factor	Mus musculus	173-181
10536997-9	1999	Our study suggests that ceramide modulation of T cell proliferation depends on the TNFalpha sensitivity and activation level of T cells and that SPC also has a mitogenic potential for T cells.	Ceramides	24-32	tumor necrosis factor	Mus musculus	83-91
10454518-7	1999	In parallel trials, the lethal actions of ceramide (but not of sphingosine) were markedly diminished by pretreatment with diferuloylmethane or expression of TAM-67, confirming the effectiveness of these interventions in suppression of SAPK/AP1-dependent apoptosis.	Ceramides	42-50	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	240-243
10438532-5	1999	The apoptotic effect of TNF-alpha in HL-60 and the transfectants was abrogated by fumonisin, an inhibitor of ceramide generation, and by the peptide Ac-YVAD-BoMK, an inhibitor of caspase-1 and -4.	Ceramides	109-117	tumor necrosis factor	Homo sapiens	24-33
10446195-0	1999	Ceramide generation is sufficient to account for the inhibition of the insulin-stimulated PKB pathway in C2C12 skeletal muscle cells pretreated with palmitate.	Ceramides	0-8	thymoma viral proto-oncogene 1	Mus musculus	90-93
10446195-6	1999	Ceramide, a derivative of palmitate, has recently been associated with similar inhibition of PKB, and here, ceramide levels were found to be elevated 2-fold in palmitate-treated C2C12 cells.	Ceramides	0-8	thymoma viral proto-oncogene 1	Mus musculus	93-96
10446195-7	1999	Incubation of C2C12 cells with ceramide closely reproduced the effects of palmitate, leading to inhibition of glycogen synthesis and PKB and to stimulation of MAP kinase.	Ceramides	31-39	thymoma viral proto-oncogene 1	Mus musculus	133-136
10446195-8	1999	We conclude that palmitate-induced insulin resistance occurs by a mechanism distinct from that of unsaturated FFAs, and involves elevation of ceramide by de novo synthesis, leading to PKB inhibition without affecting IRS-1 function.	Ceramides	142-150	thymoma viral proto-oncogene 1	Mus musculus	184-187
10438532-6	1999	Supplementing HL-525 cells with exogenous ceramides bypassed the PKC-beta deficiency and induced apoptosis, which was also restrained by the caspase-1 and -4 inhibitor.	Ceramides	42-51	caspase 1	Homo sapiens	141-157
10438532-8	1999	We suggest that TNF-alpha-induced apoptosis involves PKC-beta and then ceramide and, in turn, caspase-1 and/or -4, whereas anti-Fas mAb-induced apoptosis utilizes reactive oxygen intermediates and, in turn, caspase-3 and/or -7.	Ceramides	71-79	tumor necrosis factor	Homo sapiens	16-25
10395296-0	1999	Epidermal growth factor inhibits ceramide-induced apoptosis and lowers ceramide levels in primary placental trophoblasts.	Ceramides	33-41	epidermal growth factor	Homo sapiens	0-23
10413587-4	1999	Using IGF-IR-positive fibroblasts we demonstrate here for the first time that ceramide is capable of activating a tyrosine kinase which acts at the level of the IGF-IR to increase cell death.	Ceramides	78-86	insulin-like growth factor I receptor	Mus musculus	6-12
10413587-4	1999	Using IGF-IR-positive fibroblasts we demonstrate here for the first time that ceramide is capable of activating a tyrosine kinase which acts at the level of the IGF-IR to increase cell death.	Ceramides	78-86	insulin-like growth factor I receptor	Mus musculus	161-167
10413587-6	1999	Although the identity of this protein is not known, we speculate that it may link into the Raf kinase signaling pathway; indeed, inhibitors of MEKK reduce ceramide-induced apoptosis, thus substantiating this theory [1, 2].	Ceramides	155-163	mitogen-activated protein kinase kinase kinase 1	Mus musculus	143-147
10413587-8	1999	Finally, the potential hydrolysis of ceramide to sphingosine-1-phosphate was not the cause of increased MAP kinase activation, substantiating the role of an IGF-IR interacting tyrosine kinase, which may be involved in apoptosis.	Ceramides	37-45	insulin-like growth factor I receptor	Mus musculus	157-163
10446931-5	1999	Calcitonin promoted secretion of fluorescence ceramide, a reporter of protein transport from Golgi apparatus to cell surface.	Ceramides	46-54	Calcitonin gene-related peptide	Sus scrofa	0-10
10478474-1	1999	Collision-induced dissociation (CID) spectra of sodium ion complexes ([M+Na]+ ions), produced by FAB-MS of methyl ester derivatives of ganglioside, indicate the length of the fatty acyl chain of the ceramide moieties without chemical degradation.	Ceramides	199-207	FA complementation group B	Homo sapiens	97-100
10395296-0	1999	Epidermal growth factor inhibits ceramide-induced apoptosis and lowers ceramide levels in primary placental trophoblasts.	Ceramides	71-79	epidermal growth factor	Homo sapiens	0-23
10395296-6	1999	Neutral sphingomyelinase also increased ceramide levels but did not induce apoptosis.	Ceramides	40-48	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
10395296-7	1999	Treatment with EGF alone decreased cellular ceramide levels.	Ceramides	44-52	epidermal growth factor	Homo sapiens	15-18
10395296-11	1999	These results implicate sphingolipids as important mediators in trophoblast apoptosis and suggest that the antiapoptotic properties of EGF can in part be explained by its control of ceramide concentrations in trophoblasts.	Ceramides	182-190	epidermal growth factor	Homo sapiens	135-138
10404391-9	1999	Several lines of evidence suggest that TNF alpha activates transcription factor nuclear factor-kappa B (NF kappa B) through activation of protein kinase C (PKC) or the hydrolysis of sphingomyelin to ceramide in a number of cell types.	Ceramides	199-207	tumor necrosis factor	Rattus norvegicus	39-48
10404391-11	1999	Similarly, hydrolysis of sphingomyelin to ceramide, but not activation of PKC, resulted in an increased in IRF-1 mRNA levels in FRTL-5 cells.	Ceramides	42-50	interferon regulatory factor 1	Rattus norvegicus	107-112
10409693-12	1999	These data suggest that PA functions as a specific regulator of PP1 and may reverse or counteract those effects of ceramide that are mediated by PP1, such as apoptosis and retinoblastoma gene product dephosphorylation.	Ceramides	115-123	inorganic pyrophosphatase 1	Homo sapiens	145-148
10428046-0	1999	Induction of the manganese superoxide dismutase gene by sphingomyelinase and ceramide.	Ceramides	77-85	superoxide dismutase 2	Homo sapiens	17-47
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	40-48	superoxide dismutase 2	Homo sapiens	201-231
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	40-48	superoxide dismutase 2	Homo sapiens	233-238
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	161-169	superoxide dismutase 2	Homo sapiens	201-231
10428046-1	1999	The present study reports the effect of ceramide generated by hydrolysis of membrane sphingomyelin with bacterial sphingomyelinase (SMase) and of cell-permeable ceramide analogues on the expression of manganese superoxide dismutase (MnSOD).	Ceramides	161-169	superoxide dismutase 2	Homo sapiens	233-238
10428046-4	1999	A similar effect on the expression of MnSOD was observed with the addition of cell-permeable ceramide analogues (C2 and C6).	Ceramides	93-101	superoxide dismutase 2	Homo sapiens	38-43
10428046-6	1999	Nuclear run-on analysis showed that SMase and ceramide increased the rate of transcription of the MnSOD gene.	Ceramides	46-54	superoxide dismutase 2	Homo sapiens	98-103
10428046-8	1999	Markedly higher expression of mRNA, protein, and activity of MnSOD in skin fibroblasts from patients with Farber disease, a human disorder with pathognomonic accumulation of ceramide due to a deficiency of ceramidase, than in normal skin fibroblasts indicate that ceramide may act as a physiological inducer of MnSOD gene expression.	Ceramides	174-182	superoxide dismutase 2	Homo sapiens	61-66
10428046-8	1999	Markedly higher expression of mRNA, protein, and activity of MnSOD in skin fibroblasts from patients with Farber disease, a human disorder with pathognomonic accumulation of ceramide due to a deficiency of ceramidase, than in normal skin fibroblasts indicate that ceramide may act as a physiological inducer of MnSOD gene expression.	Ceramides	264-272	superoxide dismutase 2	Homo sapiens	61-66
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	24-32	superoxide dismutase 2	Homo sapiens	86-91
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	24-32	superoxide dismutase 2	Homo sapiens	119-124
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	128-136	superoxide dismutase 2	Homo sapiens	86-91
10428046-9	1999	However, stimulation of ceramide-mediated DNA fragmentation by antisense knockdown of MnSOD suggests that induction of MnSOD by ceramide is a protective response of the cell.	Ceramides	128-136	superoxide dismutase 2	Homo sapiens	119-124
10409693-5	1999	Because we recently showed that ceramides activated PP1, we next examined the effects of PA on ceramide stimulation of PP1.	Ceramides	32-41	inorganic pyrophosphatase 1	Homo sapiens	52-55
10409693-5	1999	Because we recently showed that ceramides activated PP1, we next examined the effects of PA on ceramide stimulation of PP1.	Ceramides	32-40	inorganic pyrophosphatase 1	Homo sapiens	52-55
10409693-6	1999	PA inhibited both basal and ceramide-stimulated PP1 activities, and ceramide showed potent and stereoselective activation of PP1 in the presence of PA.	Ceramides	28-36	inorganic pyrophosphatase 1	Homo sapiens	48-51
10409693-6	1999	PA inhibited both basal and ceramide-stimulated PP1 activities, and ceramide showed potent and stereoselective activation of PP1 in the presence of PA.	Ceramides	68-76	inorganic pyrophosphatase 1	Homo sapiens	125-128
10400653-2	1999	The search for potential targets for ceramide action led to the identification of ceramide-activated protein phosphatases, which include protein phosphatase-2A (PP2A) and protein phosphatase-1 (PP1) with roles in regulating apoptosis and cell growth.	Ceramides	37-45	protein phosphatase 2 phosphatase activator	Homo sapiens	145-159
10400650-0	1999	Ceramide induces Bcl2 dephosphorylation via a mechanism involving mitochondrial PP2A.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	17-21
10400650-0	1999	Ceramide induces Bcl2 dephosphorylation via a mechanism involving mitochondrial PP2A.	Ceramides	0-8	protein phosphatase 2 phosphatase activator	Homo sapiens	80-84
10400653-2	1999	The search for potential targets for ceramide action led to the identification of ceramide-activated protein phosphatases, which include protein phosphatase-2A (PP2A) and protein phosphatase-1 (PP1) with roles in regulating apoptosis and cell growth.	Ceramides	37-45	protein phosphatase 2 phosphatase activator	Homo sapiens	161-165
10400650-7	1999	The potent apoptotic agent ceramide can activate a PP2A, suggesting that one potential component of the ceramide-induced death signal may involve the inactivation of Bcl2.	Ceramides	27-35	protein phosphatase 2 phosphatase activator	Homo sapiens	51-55
10400653-2	1999	The search for potential targets for ceramide action led to the identification of ceramide-activated protein phosphatases, which include protein phosphatase-2A (PP2A) and protein phosphatase-1 (PP1) with roles in regulating apoptosis and cell growth.	Ceramides	37-45	inorganic pyrophosphatase 1	Homo sapiens	171-192
10400650-7	1999	The potent apoptotic agent ceramide can activate a PP2A, suggesting that one potential component of the ceramide-induced death signal may involve the inactivation of Bcl2.	Ceramides	27-35	BCL2 apoptosis regulator	Homo sapiens	166-170
10400650-7	1999	The potent apoptotic agent ceramide can activate a PP2A, suggesting that one potential component of the ceramide-induced death signal may involve the inactivation of Bcl2.	Ceramides	104-112	protein phosphatase 2 phosphatase activator	Homo sapiens	51-55
10400653-2	1999	The search for potential targets for ceramide action led to the identification of ceramide-activated protein phosphatases, which include protein phosphatase-2A (PP2A) and protein phosphatase-1 (PP1) with roles in regulating apoptosis and cell growth.	Ceramides	37-45	inorganic pyrophosphatase 1	Homo sapiens	194-197
10400650-7	1999	The potent apoptotic agent ceramide can activate a PP2A, suggesting that one potential component of the ceramide-induced death signal may involve the inactivation of Bcl2.	Ceramides	104-112	BCL2 apoptosis regulator	Homo sapiens	166-170
10400653-8	1999	The addition of 150 mM KCl decreased the basal activity of PP1 and the dose of D-erythro-C18-ceramide necessary to activate PP1c (EC50 = 6.25 microM) and increased the ceramide responsiveness up to 10-17-fold.	Ceramides	93-101	protein phosphatase 1 catalytic subunit gamma	Homo sapiens	124-128
10400650-8	1999	Results indicate that C2-ceramide but not inactive C2-dihydroceramide, was found to specifically activate a mitochondrial PP2A, which rapidly and completely induced Bcl2 dephosphorylation and correlated closely with ceramide-induced cell death.	Ceramides	25-33	protein phosphatase 2 phosphatase activator	Homo sapiens	122-126
10400650-8	1999	Results indicate that C2-ceramide but not inactive C2-dihydroceramide, was found to specifically activate a mitochondrial PP2A, which rapidly and completely induced Bcl2 dephosphorylation and correlated closely with ceramide-induced cell death.	Ceramides	25-33	BCL2 apoptosis regulator	Homo sapiens	165-169
10400650-9	1999	Using a genetic approach, the gain-of-function S70E Bcl2 mutation, which mimics phosphorylation, fails to undergo apoptosis even with the addition of high doses of ceramide (IC50 > 50 microM).	Ceramides	164-172	BCL2 apoptosis regulator	Homo sapiens	52-56
10400653-9	1999	These studies disclose stereospecific activation of PP1 and PP2A by long chain natural ceramides under near physiologic ionic strengths in vitro.	Ceramides	87-96	inorganic pyrophosphatase 1	Homo sapiens	52-55
10400650-10	1999	In contrast, cells overexpressing exogenous wild-type Bcl2 were sensitive to ceramide at dosages where PP2A is fully active and Bcl2 would be expected to be dephosphorylated (IC50 = 14 microM).	Ceramides	77-85	BCL2 apoptosis regulator	Homo sapiens	54-58
10400650-10	1999	In contrast, cells overexpressing exogenous wild-type Bcl2 were sensitive to ceramide at dosages where PP2A is fully active and Bcl2 would be expected to be dephosphorylated (IC50 = 14 microM).	Ceramides	77-85	protein phosphatase 2 phosphatase activator	Homo sapiens	103-107
10400650-11	1999	These findings indicate that in cells expressing functional Bcl2, the mechanism of death action for ceramide may involve, at least in part, a mitochondrial PP2A that dephosphorylates and inactivates Bcl2.	Ceramides	100-108	BCL2 apoptosis regulator	Homo sapiens	60-64
10400650-11	1999	These findings indicate that in cells expressing functional Bcl2, the mechanism of death action for ceramide may involve, at least in part, a mitochondrial PP2A that dephosphorylates and inactivates Bcl2.	Ceramides	100-108	protein phosphatase 2 phosphatase activator	Homo sapiens	156-160
10400650-11	1999	These findings indicate that in cells expressing functional Bcl2, the mechanism of death action for ceramide may involve, at least in part, a mitochondrial PP2A that dephosphorylates and inactivates Bcl2.	Ceramides	100-108	BCL2 apoptosis regulator	Homo sapiens	199-203
10400653-9	1999	These studies disclose stereospecific activation of PP1 and PP2A by long chain natural ceramides under near physiologic ionic strengths in vitro.	Ceramides	87-96	protein phosphatase 2 phosphatase activator	Homo sapiens	60-64
10407065-3	1999	In pig SC at least six subclasses of ceramides (referred to as CER 1, 2-6) are present.	Ceramides	37-46	CER1	Sus scrofa	63-68
10398299-3	1999	NGF also binds to the common neurotrophin receptor (p75(NTR)), a member of the TNFalpha receptor (TNFR-I) superfamily, whose function may be to modulate apoptosis via the release of ceramide and the activation of the transcription factor nuclear factor kappa B (NFkappaB).	Ceramides	182-190	nerve growth factor	Rattus norvegicus	0-3
10398299-3	1999	NGF also binds to the common neurotrophin receptor (p75(NTR)), a member of the TNFalpha receptor (TNFR-I) superfamily, whose function may be to modulate apoptosis via the release of ceramide and the activation of the transcription factor nuclear factor kappa B (NFkappaB).	Ceramides	182-190	nerve growth factor receptor	Rattus norvegicus	52-60
10398299-3	1999	NGF also binds to the common neurotrophin receptor (p75(NTR)), a member of the TNFalpha receptor (TNFR-I) superfamily, whose function may be to modulate apoptosis via the release of ceramide and the activation of the transcription factor nuclear factor kappa B (NFkappaB).	Ceramides	182-190	tumor necrosis factor	Rattus norvegicus	79-87
10398299-3	1999	NGF also binds to the common neurotrophin receptor (p75(NTR)), a member of the TNFalpha receptor (TNFR-I) superfamily, whose function may be to modulate apoptosis via the release of ceramide and the activation of the transcription factor nuclear factor kappa B (NFkappaB).	Ceramides	182-190	TNF receptor superfamily member 1A	Rattus norvegicus	98-104
10403818-0	1999	Involvement of the 92-kDa gelatinase (matrix metalloproteinase-9) in the ceramide-mediated inhibition of human keratinocyte growth.	Ceramides	73-81	matrix metallopeptidase 9	Homo sapiens	38-64
10403818-2	1999	Increasing the ceramide content of keratinocytes with Smase (100 U/ml) or C6-ceramide (1 microM) enhanced matrix metalloproteinase (MMP)-9 production.	Ceramides	15-23	matrix metallopeptidase 9	Homo sapiens	106-138
10403818-4	1999	The inhibition of keratinocyte growth rate induced by ceramide could be annihilated by a peptide hydroxamate MMP inhibitor or an MMP-9 blocking antibody.	Ceramides	54-62	matrix metallopeptidase 9	Homo sapiens	129-134
10393722-10	1999	RESULTS/CONCLUSIONS: In addition to increasing ROS, 4-HPR (2.5-10 microM) statistically significantly increased the level of intracellular ceramide (up to approximately 10-fold; P<.001) in a dose-dependent manner in two neuroblastoma cell lines, one of which is highly resistant to alkylating agents and to etoposide.	Ceramides	139-147	haptoglobin-related protein	Homo sapiens	54-57
10393722-14	1999	IMPLICATIONS: 4-HPR may form the basis for a novel, p53-independent chemotherapy that operates through increased intracellular levels of ceramide and that retains cytotoxicity under reduced oxygen conditions.	Ceramides	137-145	haptoglobin-related protein	Homo sapiens	16-19
10393722-14	1999	IMPLICATIONS: 4-HPR may form the basis for a novel, p53-independent chemotherapy that operates through increased intracellular levels of ceramide and that retains cytotoxicity under reduced oxygen conditions.	Ceramides	137-145	tumor protein p53	Homo sapiens	52-55
10385659-5	1999	Because ceramide may mediate cell death from tumor necrosis factor alpha (TNF-alpha), the ability of RNA synthesis inhibition and NF-kappaB inactivation to sensitize hepatocytes to ceramide toxicity was examined.	Ceramides	8-16	tumor necrosis factor	Rattus norvegicus	74-83
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.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	27-30
10389841-1	1999	Activation of the sphingomyelin/ceramide pathway may mediate interleukin-1-induced beta-cell death (Welsh, N: Interleuken-1beta-induced ceramide and diacylglycerol generation may lead to activation of the c-Jun NH2-terminal kinase and the transcription factor ATF-2 in the insulin-producing cell line RINm5F.	Ceramides	32-40	activating transcription factor 2	Mus musculus	260-265
10389841-1	1999	Activation of the sphingomyelin/ceramide pathway may mediate interleukin-1-induced beta-cell death (Welsh, N: Interleuken-1beta-induced ceramide and diacylglycerol generation may lead to activation of the c-Jun NH2-terminal kinase and the transcription factor ATF-2 in the insulin-producing cell line RINm5F.	Ceramides	136-144	activating transcription factor 2	Mus musculus	260-265
10389841-7	1999	The ceramide effect on cell viability mimicked the effect of the cytokines TNF-alpha, IL-1beta, and IFN-gamma, reported stimulators of sphingomyelin hydrolysis.	Ceramides	4-12	tumor necrosis factor	Mus musculus	75-84
10389841-7	1999	The ceramide effect on cell viability mimicked the effect of the cytokines TNF-alpha, IL-1beta, and IFN-gamma, reported stimulators of sphingomyelin hydrolysis.	Ceramides	4-12	interleukin 1 beta	Mus musculus	86-94
10389841-7	1999	The ceramide effect on cell viability mimicked the effect of the cytokines TNF-alpha, IL-1beta, and IFN-gamma, reported stimulators of sphingomyelin hydrolysis.	Ceramides	4-12	interferon gamma	Mus musculus	100-109
10385659-6	1999	RALA hepatocytes were sensitized to ceramide toxicity by coadministration of actinomycin D (ActD).	Ceramides	36-44	RAS like proto-oncogene A	Rattus norvegicus	0-4
10385659-9	1999	Inhibition of NF-kappaB activation also sensitized RALA hepatocytes to ceramide toxicity, but to a lesser extent than for TNF-alpha.	Ceramides	71-79	RAS like proto-oncogene A	Rattus norvegicus	51-55
10385659-11	1999	The ability of ActD and NF-kappaB inactivation to sensitize RALA hepatocytes to ceramide toxicity suggests that ceramide may act as a downstream mediator of TNF-alpha toxicity.	Ceramides	80-88	RAS like proto-oncogene A	Rattus norvegicus	60-64
10385659-11	1999	The ability of ActD and NF-kappaB inactivation to sensitize RALA hepatocytes to ceramide toxicity suggests that ceramide may act as a downstream mediator of TNF-alpha toxicity.	Ceramides	112-120	RAS like proto-oncogene A	Rattus norvegicus	60-64
10385659-11	1999	The ability of ActD and NF-kappaB inactivation to sensitize RALA hepatocytes to ceramide toxicity suggests that ceramide may act as a downstream mediator of TNF-alpha toxicity.	Ceramides	112-120	tumor necrosis factor	Rattus norvegicus	157-166
10400831-2	1999	Our data indicate that inhibition of methylation reactions by adenosine plus homocysteine, which are known to condense within cells to AdoHcy, markedly potentiated TNF-induced cytotoxicity in MCF7 cells and rendered related TNF-resistant variants, TNF-sensitive by a mechanism independent from the ceramide pathway.	Ceramides	298-306	tumor necrosis factor	Homo sapiens	164-167
10390188-3	1999	Ceramide, a product of sphingomyelin hydrolysis, is a known mediator of apoptotic effects of TNF, IL-1, and gammaIFN.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	93-96
10390188-3	1999	Ceramide, a product of sphingomyelin hydrolysis, is a known mediator of apoptotic effects of TNF, IL-1, and gammaIFN.	Ceramides	0-8	interleukin 1 alpha	Homo sapiens	98-102
10376687-4	1999	In particular, ganglioside GD3 biosynthesis represents an important event for the progression of apoptotic signals generated by CD95 and mediated by ceramide in hematopoietic cells.	Ceramides	149-157	GRDX	Homo sapiens	27-30
10336612-3	1999	However, the SMase-elicited reciprocal alterations in SM and ceramide levels were partially prevented by the PAF treatment.	Ceramides	61-69	PCNA clamp associated factor	Homo sapiens	109-112
10336612-11	1999	In summary, the present data demonstrate that PAF is able to regulate the cellular ceramide levels in brain by accelerating the SM cycle.	Ceramides	83-91	PCNA clamp associated factor	Homo sapiens	46-49
10400831-0	1999	Methyltransferase inhibitor S-adenosyl-L-homocysteine sensitizes human breast carcinoma MCF7 cells and related TNF-resistant derivatives to TNF-mediated cytotoxicity via the ceramide-independent pathway.	Ceramides	174-182	tumor necrosis factor	Homo sapiens	111-114
10400831-0	1999	Methyltransferase inhibitor S-adenosyl-L-homocysteine sensitizes human breast carcinoma MCF7 cells and related TNF-resistant derivatives to TNF-mediated cytotoxicity via the ceramide-independent pathway.	Ceramides	174-182	tumor necrosis factor	Homo sapiens	140-143
10358036-3	1999	AT2 receptor-induced ceramide accumulation preceded the onset of caspase 3 activation and DNA fragmentation.	Ceramides	21-29	angiotensin II receptor, type 2	Rattus norvegicus	0-3
10358036-3	1999	AT2 receptor-induced ceramide accumulation preceded the onset of caspase 3 activation and DNA fragmentation.	Ceramides	21-29	caspase 3	Rattus norvegicus	65-74
10358036-4	1999	AT2 receptor-induced ceramide accumulation did not result from the degradation of complex sphingolipids (SL) such as sphingomyelin or glycosphingolipids, as no changes in neutral or acidic sphingomyelinase activities, sphingomyelin level, nor in cellular glycolipid composition were observed.	Ceramides	21-29	angiotensin II receptor, type 2	Rattus norvegicus	0-3
10358036-6	1999	The AT2 receptor-induced accumulation of ceramide was blocked by inhibitors of the de novo pathway of SL synthesis, beta-chloro-L-alanine and fumonisin B1.	Ceramides	41-49	angiotensin II receptor, type 2	Rattus norvegicus	4-7
10358036-8	1999	Pertussis toxin and orthovanadate blocked AT2 receptor-mediated ceramide production.	Ceramides	64-72	angiotensin II receptor, type 2	Rattus norvegicus	42-45
10358036-9	1999	Taken together our data demonstrate that in PC12W cells the stimulation of AT2 receptor induces the activation of de novo pathway, and a metabolite of this pathway, possibly ceramide, mediates AT2 receptor-induced apoptosis.	Ceramides	174-182	angiotensin II receptor, type 2	Rattus norvegicus	75-78
10358036-9	1999	Taken together our data demonstrate that in PC12W cells the stimulation of AT2 receptor induces the activation of de novo pathway, and a metabolite of this pathway, possibly ceramide, mediates AT2 receptor-induced apoptosis.	Ceramides	174-182	angiotensin II receptor, type 2	Rattus norvegicus	193-196
10400831-5	1999	In conclusion, these results suggest that the methyltransferase inhibitor AdoHcy potentiates TNF-induced cytotoxicity in MCF7 cells and renders TNF-resistant MCF7 clones, TNF-sensitive via the ceramide independent pathway and that FADD and the ICE-like protease are likely necessary components in transducing methylation inhibition/TNF signals for cell death.	Ceramides	193-201	tumor necrosis factor	Homo sapiens	93-96
10400831-5	1999	In conclusion, these results suggest that the methyltransferase inhibitor AdoHcy potentiates TNF-induced cytotoxicity in MCF7 cells and renders TNF-resistant MCF7 clones, TNF-sensitive via the ceramide independent pathway and that FADD and the ICE-like protease are likely necessary components in transducing methylation inhibition/TNF signals for cell death.	Ceramides	193-201	Fas associated via death domain	Homo sapiens	231-235
10348816-7	1999	RESULTS: A cell-permeable ceramide analogue (C2-ceramide) increased IL-8 expression with comparable mRNA induction.	Ceramides	26-34	C-X-C motif chemokine ligand 8	Homo sapiens	68-72
10348816-0	1999	Helicobacter pylori-dependent ceramide production may mediate increased interleukin 8 expression in human gastric cancer cell lines.	Ceramides	30-38	C-X-C motif chemokine ligand 8	Homo sapiens	72-85
10348816-10	1999	CONCLUSIONS: The results suggest a novel role of the sphingomyelin-ceramide pathway, at least in part through NF-kappaB, in IL-8 production induced by H. pylori infection in gastric epithelial cells.	Ceramides	67-75	nuclear factor kappa B subunit 1	Homo sapiens	110-119
10348816-10	1999	CONCLUSIONS: The results suggest a novel role of the sphingomyelin-ceramide pathway, at least in part through NF-kappaB, in IL-8 production induced by H. pylori infection in gastric epithelial cells.	Ceramides	67-75	C-X-C motif chemokine ligand 8	Homo sapiens	124-128
10399097-4	1999	These cells accumulate ceramide as the result of genetic deficiency of acid ceramidase and the ceramidase activator (sap-D), respectively.	Ceramides	23-31	SH2 domain containing 1A	Homo sapiens	117-120
10400316-0	1999	Effect of ceramide on interleukin-6 synthesis in osteoblast-like cells.	Ceramides	10-18	interleukin 6	Mus musculus	22-35
10400316-3	1999	In the present study, among sphingomyelin metabolites, we examined the effect of ceramide on the IL-6 synthesis induced by various agonists in MC3T3-E1 cells.	Ceramides	81-89	interleukin 6	Mus musculus	97-101
10400316-4	1999	C2-ceramide, a cell-permeable ceramide analogue, suppressed the PGE1-induced IL-6 synthesis.	Ceramides	3-11	interleukin 6	Mus musculus	77-81
10400316-12	1999	These results strongly suggest that ceramide modulates the IL-6 synthesis stimulated by various agonists in osteoblasts.	Ceramides	36-44	interleukin 6	Mus musculus	59-63
10399097-5	1999	Amounts of ceramide in fibroblasts from Farber patients and in fibroblasts from sap -/- mouse were increased 2.9-fold and 2.8-fold, respectively, over the level of controls.	Ceramides	11-19	SH2 domain containing 1A	Homo sapiens	80-83
10336437-7	1999	We conclude that the p75(NTR) receptor, while free of NGF, triggers a cascade leading to apoptosis; the cascade includes generation of ceramide and increased caspase activity; and the protective role of NO occurs at step(s) in between the latter events.	Ceramides	135-143	TNF receptor superfamily member 1B	Homo sapiens	21-38
10369458-1	1999	Ceramide, generated by the hydrolysis of sphingomyelin, mediates the actions of several cytokines such as tumour necrosis factor-alpha (TNF-alpha) interferon-gamma and interleukin-1beta (IL-1beta), including their inhibitory effect on tumour proliferation.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	136-145
10336437-0	1999	The p75(NTR)-induced apoptotic program develops through a ceramide-caspase pathway negatively regulated by nitric oxide.	Ceramides	58-66	TNF receptor superfamily member 1B	Homo sapiens	4-7
10336437-0	1999	The p75(NTR)-induced apoptotic program develops through a ceramide-caspase pathway negatively regulated by nitric oxide.	Ceramides	58-66	neurotensin receptor 1	Homo sapiens	8-11
10336437-3	1999	Conversely, exogenous ceramide increased caspase activity and apoptosis in both wild-type and p75(NTR)-expressing cells.	Ceramides	22-30	TNF receptor superfamily member 1B	Homo sapiens	94-97
10336437-3	1999	Conversely, exogenous ceramide increased caspase activity and apoptosis in both wild-type and p75(NTR)-expressing cells.	Ceramides	22-30	neurotensin receptor 1	Homo sapiens	98-101
10336437-4	1999	A new p75(NTR)-expressing clone characterized by low spontaneous apoptosis exhibited high endogenous ceramide and low caspase levels.	Ceramides	101-109	TNF receptor superfamily member 1B	Homo sapiens	6-9
10336437-4	1999	A new p75(NTR)-expressing clone characterized by low spontaneous apoptosis exhibited high endogenous ceramide and low caspase levels.	Ceramides	101-109	neurotensin receptor 1	Homo sapiens	10-13
10344757-3	1999	B-Myb-overexpressing cells showed a diminished cytokine dependence and were resistant to apoptosis induced by doxorubicin, ceramide, and dexamethasone.	Ceramides	123-131	myeloblastosis oncogene-like 2	Mus musculus	0-5
10360645-0	1999	Ceramide triggers p53-dependent apoptosis in genetically defined fibrosarcoma tumour cells.	Ceramides	0-8	tumor protein p53	Homo sapiens	18-21
10360645-8	1999	These results suggest that ceramide-induced apoptosis in tumour cells can be dependent on the status of p53 and imply that p53 is also important for stress-induced apoptotic signal transduction cascades generated at the plasma membrane.	Ceramides	27-35	tumor protein p53	Homo sapiens	104-107
10360645-8	1999	These results suggest that ceramide-induced apoptosis in tumour cells can be dependent on the status of p53 and imply that p53 is also important for stress-induced apoptotic signal transduction cascades generated at the plasma membrane.	Ceramides	27-35	tumor protein p53	Homo sapiens	123-126
10330437-0	1999	A role for neutral sphingomyelinase-mediated ceramide production in T cell receptor-induced apoptosis and mitogen-activated protein kinase-mediated signal transduction.	Ceramides	45-53	sphingomyelin phosphodiesterase 2	Homo sapiens	11-35
10330437-5	1999	These results suggest that ceramide production by activation of neutral sphingomyelinase is an essential component of the TCR signaling machinery.	Ceramides	27-35	sphingomyelin phosphodiesterase 2	Homo sapiens	64-88
10318846-7	1999	Exogenous ceramide bypassed apoptosis resistance in the variant cells, but not in Bcl-2-transfected cells, suggesting that apoptosis signaling induced by CD95, etoposide, and gamma-radiation is subject to common regulation at a level different from that targeted by Bcl-2.	Ceramides	10-18	Fas cell surface death receptor	Homo sapiens	154-158
10318846-7	1999	Exogenous ceramide bypassed apoptosis resistance in the variant cells, but not in Bcl-2-transfected cells, suggesting that apoptosis signaling induced by CD95, etoposide, and gamma-radiation is subject to common regulation at a level different from that targeted by Bcl-2.	Ceramides	10-18	BCL2 apoptosis regulator	Homo sapiens	266-271
10329967-0	1999	TNF-alpha pretreatment prevents subsequent activation of cultured brain cells with TNF-alpha and hypoxia via ceramide.	Ceramides	109-117	tumor necrosis factor	Rattus norvegicus	0-9
10329967-2	1999	Inasmuch as ceramide is known to mediate some of the effects of TNF-alpha, its levels were measured at various times after the TNF-alpha preconditioning.	Ceramides	12-20	tumor necrosis factor	Rattus norvegicus	64-73
10329967-3	1999	We present evidence for the first time that, in normal brain cells, TNF-alpha pretreatment causes a biphasic increase of ceramide levels: an early peak at 15-20 min, when ceramide levels increased 1.9-fold in astrocytes and 2.7-fold in rat brain capillary endothelial cells, and a delayed 2- to 3-fold ceramide increase that occurs 18-24 h after addition of TNF-alpha.	Ceramides	121-129	tumor necrosis factor	Rattus norvegicus	68-77
10329967-3	1999	We present evidence for the first time that, in normal brain cells, TNF-alpha pretreatment causes a biphasic increase of ceramide levels: an early peak at 15-20 min, when ceramide levels increased 1.9-fold in astrocytes and 2.7-fold in rat brain capillary endothelial cells, and a delayed 2- to 3-fold ceramide increase that occurs 18-24 h after addition of TNF-alpha.	Ceramides	171-179	tumor necrosis factor	Rattus norvegicus	68-77
10329967-3	1999	We present evidence for the first time that, in normal brain cells, TNF-alpha pretreatment causes a biphasic increase of ceramide levels: an early peak at 15-20 min, when ceramide levels increased 1.9-fold in astrocytes and 2.7-fold in rat brain capillary endothelial cells, and a delayed 2- to 3-fold ceramide increase that occurs 18-24 h after addition of TNF-alpha.	Ceramides	171-179	tumor necrosis factor	Rattus norvegicus	68-77
10329967-4	1999	The following findings indicate that the delayed ceramide accumulation results in cell unresponsiveness to TNF-alpha: 1) coincident timing of the ceramide peak and the tolerance period, 2) mimicking of preconditioning by addition of exogenous ceramide, and 3) attenuation of preconditioning by fumonisin B1, an inhibitor of ceramide synthesis.	Ceramides	49-57	tumor necrosis factor	Rattus norvegicus	107-116
10224298-3	1999	Enhanced levels of ceramide may be involved in apoptosis signaling following stroke since exogenously added synthetic C2-ceramide increased expression of c-jun and the death-inducing ligands (DILs) CD95-L, TRAIL and TNF-alpha in neuroblastoma cells.	Ceramides	19-27	Fas ligand	Rattus norvegicus	198-204
10224298-3	1999	Enhanced levels of ceramide may be involved in apoptosis signaling following stroke since exogenously added synthetic C2-ceramide increased expression of c-jun and the death-inducing ligands (DILs) CD95-L, TRAIL and TNF-alpha in neuroblastoma cells.	Ceramides	19-27	TNF superfamily member 10	Rattus norvegicus	206-211
10224298-3	1999	Enhanced levels of ceramide may be involved in apoptosis signaling following stroke since exogenously added synthetic C2-ceramide increased expression of c-jun and the death-inducing ligands (DILs) CD95-L, TRAIL and TNF-alpha in neuroblastoma cells.	Ceramides	19-27	tumor necrosis factor	Rattus norvegicus	216-225
10369458-1	1999	Ceramide, generated by the hydrolysis of sphingomyelin, mediates the actions of several cytokines such as tumour necrosis factor-alpha (TNF-alpha) interferon-gamma and interleukin-1beta (IL-1beta), including their inhibitory effect on tumour proliferation.	Ceramides	0-8	interferon gamma	Homo sapiens	147-163
10369458-1	1999	Ceramide, generated by the hydrolysis of sphingomyelin, mediates the actions of several cytokines such as tumour necrosis factor-alpha (TNF-alpha) interferon-gamma and interleukin-1beta (IL-1beta), including their inhibitory effect on tumour proliferation.	Ceramides	0-8	interleukin 1 beta	Homo sapiens	168-185
10369458-1	1999	Ceramide, generated by the hydrolysis of sphingomyelin, mediates the actions of several cytokines such as tumour necrosis factor-alpha (TNF-alpha) interferon-gamma and interleukin-1beta (IL-1beta), including their inhibitory effect on tumour proliferation.	Ceramides	0-8	interleukin 1 beta	Homo sapiens	187-195
10369458-6	1999	IL-1beta produced profound inhibition of LNCaP cell proliferation and caused enhanced ceramide formation.	Ceramides	86-94	interleukin 1 beta	Homo sapiens	0-8
10344598-1	1999	A recent study revealed that ceramide acts as a second messenger in the sphingomyelin pathway and thus plays an important regulatory role in programmed cell death (apoptosis) to cell the lines induced by tumor-necrosis factor (TNF)-alpha and interleukin (IL)-1beta, although its effect remains controversial regarding primary neuronal culture.	Ceramides	29-37	tumor necrosis factor	Homo sapiens	227-237
10344598-1	1999	A recent study revealed that ceramide acts as a second messenger in the sphingomyelin pathway and thus plays an important regulatory role in programmed cell death (apoptosis) to cell the lines induced by tumor-necrosis factor (TNF)-alpha and interleukin (IL)-1beta, although its effect remains controversial regarding primary neuronal culture.	Ceramides	29-37	interleukin 1 beta	Homo sapiens	242-264
10212255-0	1999	A novel pathway for tumor necrosis factor-alpha and ceramide signaling involving sequential activation of tyrosine kinase, p21(ras), and phosphatidylinositol 3-kinase.	Ceramides	52-60	H3 histone pseudogene 16	Homo sapiens	123-126
10212255-7	1999	It is proposed that activation of Ras and PI 3-kinase by ceramide can contribute to signaling effects of TNFalpha that occur downstream of sphingomyelinase activation and result in increased fibroblasts proliferation.	Ceramides	57-65	peptidase inhibitor 3	Homo sapiens	42-46
10212255-7	1999	It is proposed that activation of Ras and PI 3-kinase by ceramide can contribute to signaling effects of TNFalpha that occur downstream of sphingomyelinase activation and result in increased fibroblasts proliferation.	Ceramides	57-65	tumor necrosis factor	Homo sapiens	105-113
10411298-10	1999	We show further that TNF alpha was able to induce [14C]-ceramide accumulation in MA-10 cells and suggest that this sphingolipid may be considered as a transmitter of TNF alpha signals to the StAR protein.	Ceramides	56-64	tumor necrosis factor	Mus musculus	21-30
10222235-3	1999	Short-term incubation of endothelial cells for 20 min reveals that NO and dibutyryl cGMP fail to stimulate an acute ceramide increase, whereas TNF-alpha, a well-known activator of sphingomyelinases, is able to acutely increase ceramide formation.	Ceramides	227-235	tumor necrosis factor	Homo sapiens	143-152
10340476-0	1999	Suppression of ceramide-mediated apoptosis by HSP70.	Ceramides	15-23	heat shock protein family A (Hsp70) member 4	Homo sapiens	46-51
10340476-1	1999	Ceramide has been known as an important second messenger in programmed cell death (apoptosis) which is induced by various stimuli such as the tumor necrosis factor-alpha (TNF-alpha), Fas ligand, and environmental stresses such as UV-irradiation and heat shock.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	142-169
10340476-1	1999	Ceramide has been known as an important second messenger in programmed cell death (apoptosis) which is induced by various stimuli such as the tumor necrosis factor-alpha (TNF-alpha), Fas ligand, and environmental stresses such as UV-irradiation and heat shock.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	171-180
10340476-1	1999	Ceramide has been known as an important second messenger in programmed cell death (apoptosis) which is induced by various stimuli such as the tumor necrosis factor-alpha (TNF-alpha), Fas ligand, and environmental stresses such as UV-irradiation and heat shock.	Ceramides	0-8	Fas ligand	Homo sapiens	183-193
10340476-3	1999	Here, we show that stress-inducible heat shock protein 70 (Hsp70) prevents apoptosis induced by increased level of intracellular ceramide.	Ceramides	129-137	heat shock protein family A (Hsp70) member 4	Homo sapiens	59-64
10340476-4	1999	In T-cell hybridoma DO11.10, we examined the effect of Hsp70 on apoptosis mediated by TNF-alpha, Fas ligation, SMase, and C2-ceramide, all of which elevate intracellular ceramide levels.	Ceramides	125-133	heat shock protein family A (Hsp70) member 4	Homo sapiens	55-60
10340476-6	1999	Similarly, the ceramide-induced c-jun amino-terminal kinase (JNK/SAPK) activation is impaired in cells overexpressing Hsp70.	Ceramides	15-23	mitogen-activated protein kinase 8	Homo sapiens	61-69
10340476-6	1999	Similarly, the ceramide-induced c-jun amino-terminal kinase (JNK/SAPK) activation is impaired in cells overexpressing Hsp70.	Ceramides	15-23	heat shock protein family A (Hsp70) member 4	Homo sapiens	118-123
10340476-7	1999	These data strongly suggest that hsp70 functions as a regulator of apoptosis downstream of ceramide.	Ceramides	91-99	heat shock protein family A (Hsp70) member 4	Homo sapiens	33-38
10411298-10	1999	We show further that TNF alpha was able to induce [14C]-ceramide accumulation in MA-10 cells and suggest that this sphingolipid may be considered as a transmitter of TNF alpha signals to the StAR protein.	Ceramides	56-64	tumor necrosis factor	Mus musculus	166-175
10196212-3	1999	Inhibition of the constitutive levels of Bcl-XL caused 10-25% of the cell population to undergo apoptosis and increased the susceptibility of cells to treatment with low concentrations of staurosporin or ceramide.	Ceramides	204-212	BCL2 like 1	Homo sapiens	41-47
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).	Ceramides	0-9	glucosidase, beta, acid	Mus musculus	151-174
10198223-1	1999	The globotriaosylceramide (Gb3) verotoxin (VT) interaction is one of several examples of glycolipid receptors where the ceramide (or lipid) free oligosaccharides fail to show the expected binding parameters.	Ceramides	17-25	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	27-30
10229201-4	1999	The ability of ceramide to activate the apoptotic protease caspase 3 in HL60 cells but not in B-CLL cells, as well as the lack of correlation of ceramide-mediated killing of different B-CLL isolates with expression of the apoptosis-regulating proteins bcl-2 and bax reinforce the conclusion that ceramide killing of B-CLL cells is by a non-apoptotic mechanism.	Ceramides	15-23	caspase 3	Homo sapiens	59-68
10187863-10	1999	These results suggest that the findings that SNP increased ceramide generation and magnesium-dependent N-SMase activity via caspase-3 are interesting to future study to determine the relation between caspases and sphingolipid metabolites in NO-mediated signaling.	Ceramides	59-67	caspase 3	Homo sapiens	124-133
10101227-8	1999	Kinase activity of each JNK was modestly stimulated in N2A cells by anisomycin but not by ceramide, UV irradiation, or heat shock.	Ceramides	90-98	mitogen-activated protein kinase 8	Mus musculus	24-27
10092612-2	1999	Lipopolysaccharide, cell-permeable ceramide analogs, and bacterial sphingomyelinase led to phosphorylation of the extracellular signal-regulated kinases, c-Jun NH2-terminal kinases, and p38 kinase and induced AP-1 DNA binding in C3H/OuJ (Lpsn) but not in C3H/HeJ (Lpsd) macrophages.	Ceramides	35-43	jun proto-oncogene	Mus musculus	154-159
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.	Ceramides	205-214	prosaposin	Mus musculus	92-96
10092612-11	1999	Thus, ceramide partially mimics lipopolysaccharide in activating the mitogen-activated protein kinases and AP-1 but not in mediating NF-kappaB induction or cytokine production, suggesting a limited role in lipopolysaccharide signaling.	Ceramides	6-14	jun proto-oncogene	Mus musculus	107-111
10092612-2	1999	Lipopolysaccharide, cell-permeable ceramide analogs, and bacterial sphingomyelinase led to phosphorylation of the extracellular signal-regulated kinases, c-Jun NH2-terminal kinases, and p38 kinase and induced AP-1 DNA binding in C3H/OuJ (Lpsn) but not in C3H/HeJ (Lpsd) macrophages.	Ceramides	35-43	jun proto-oncogene	Mus musculus	209-213
10092612-3	1999	Lipopolysaccharide and ceramide mimetics showed distinct kinetics of mitogen-activated protein kinase phosphorylation and AP-1 induction and activated AP-1 complexes with different subunit compositions.	Ceramides	23-31	jun proto-oncogene	Mus musculus	122-126
10092645-11	1999	In accordance with the anti-apoptotic function of BTK, treatment of BTK+ B-lineage leukemic cells with LFM-A13 enhanced their sensitivity to ceramide- or vincristine-induced apoptosis.	Ceramides	141-149	Bruton tyrosine kinase	Homo sapiens	50-53
10092645-11	1999	In accordance with the anti-apoptotic function of BTK, treatment of BTK+ B-lineage leukemic cells with LFM-A13 enhanced their sensitivity to ceramide- or vincristine-induced apoptosis.	Ceramides	141-149	Bruton tyrosine kinase	Homo sapiens	68-71
10092612-3	1999	Lipopolysaccharide and ceramide mimetics showed distinct kinetics of mitogen-activated protein kinase phosphorylation and AP-1 induction and activated AP-1 complexes with different subunit compositions.	Ceramides	23-31	jun proto-oncogene	Mus musculus	151-155
10090938-5	1999	Results indicate that Dex-induced thymocyte apoptosis is attributable to an early ceramide generation caused by the activation of an acidic sphingomyelinase (aSMase).	Ceramides	82-90	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	133-156
10198327-4	1999	Preincubation with herbimycin A, an Src kinase inhibitor (3 microM), inhibited only C2 ceramide-induced PI 3-kinase activation and contraction.	Ceramides	87-95	peptidase inhibitor 3	Homo sapiens	104-108
10198327-6	1999	Western blotting and immunoprecipitation with PI 3-kinase antibodies to the regulatory subunit p85 and the catalytic subunits p110alpha and p110gamma indicated that both endothelin and C2 ceramide interacted with the regulatory subunit p85; endothelin interacted with the catalytic subunits p110alpha and p110gamma, whereas C2 ceramide interacted only with the catalytic subunit p110alpha.	Ceramides	188-196	phosphoinositide-3-kinase regulatory subunit 1	Homo sapiens	95-98
10198327-6	1999	Western blotting and immunoprecipitation with PI 3-kinase antibodies to the regulatory subunit p85 and the catalytic subunits p110alpha and p110gamma indicated that both endothelin and C2 ceramide interacted with the regulatory subunit p85; endothelin interacted with the catalytic subunits p110alpha and p110gamma, whereas C2 ceramide interacted only with the catalytic subunit p110alpha.	Ceramides	188-196	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	126-135
10198327-6	1999	Western blotting and immunoprecipitation with PI 3-kinase antibodies to the regulatory subunit p85 and the catalytic subunits p110alpha and p110gamma indicated that both endothelin and C2 ceramide interacted with the regulatory subunit p85; endothelin interacted with the catalytic subunits p110alpha and p110gamma, whereas C2 ceramide interacted only with the catalytic subunit p110alpha.	Ceramides	188-196	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	140-149
10198327-6	1999	Western blotting and immunoprecipitation with PI 3-kinase antibodies to the regulatory subunit p85 and the catalytic subunits p110alpha and p110gamma indicated that both endothelin and C2 ceramide interacted with the regulatory subunit p85; endothelin interacted with the catalytic subunits p110alpha and p110gamma, whereas C2 ceramide interacted only with the catalytic subunit p110alpha.	Ceramides	188-196	phosphoinositide-3-kinase regulatory subunit 1	Homo sapiens	236-239
10198327-6	1999	Western blotting and immunoprecipitation with PI 3-kinase antibodies to the regulatory subunit p85 and the catalytic subunits p110alpha and p110gamma indicated that both endothelin and C2 ceramide interacted with the regulatory subunit p85; endothelin interacted with the catalytic subunits p110alpha and p110gamma, whereas C2 ceramide interacted only with the catalytic subunit p110alpha.	Ceramides	188-196	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	291-300
10198327-6	1999	Western blotting and immunoprecipitation with PI 3-kinase antibodies to the regulatory subunit p85 and the catalytic subunits p110alpha and p110gamma indicated that both endothelin and C2 ceramide interacted with the regulatory subunit p85; endothelin interacted with the catalytic subunits p110alpha and p110gamma, whereas C2 ceramide interacted only with the catalytic subunit p110alpha.	Ceramides	188-196	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit gamma	Homo sapiens	305-314
10198327-6	1999	Western blotting and immunoprecipitation with PI 3-kinase antibodies to the regulatory subunit p85 and the catalytic subunits p110alpha and p110gamma indicated that both endothelin and C2 ceramide interacted with the regulatory subunit p85; endothelin interacted with the catalytic subunits p110alpha and p110gamma, whereas C2 ceramide interacted only with the catalytic subunit p110alpha.	Ceramides	188-196	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit alpha	Homo sapiens	291-300
10075082-6	1999	Beta-lapachone also suppressed the activation of NF-kappaB by lipopolysaccharide, okadaic acid, and ceramide but had no significant effect on activation by H2O2 or phorbol myristate acetate, indicating that its action is selective.	Ceramides	100-108	nuclear factor kappa B subunit 1	Homo sapiens	49-58
10084970-0	1999	Glucocorticoid receptor-mediated post-ceramide inhibition of the interleukin-1beta-dependent induction of ovarian prostaglandin endoperoxide synthase-2 in rats.	Ceramides	38-46	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	0-23
10084970-0	1999	Glucocorticoid receptor-mediated post-ceramide inhibition of the interleukin-1beta-dependent induction of ovarian prostaglandin endoperoxide synthase-2 in rats.	Ceramides	38-46	interleukin 1 beta	Rattus norvegicus	65-82
10084970-0	1999	Glucocorticoid receptor-mediated post-ceramide inhibition of the interleukin-1beta-dependent induction of ovarian prostaglandin endoperoxide synthase-2 in rats.	Ceramides	38-46	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	114-151
10084970-9	1999	Dexamethasone proved equally effective in suppressing the induction of PGS-2 transcripts by congeners of the sphingomyelin-ceramide cycle (e.g., C-2 ceramide, sphingomyelinase, and sphingosine).	Ceramides	123-131	decorin	Rattus norvegicus	71-76
10084970-12	1999	Taken together, these observations suggest that dexamethasone is capable of glucocorticoid receptor-mediated/post-ceramide suppression of IL-1-supported ovarian PGS-2 transcript, protein, and activity.	Ceramides	114-122	nuclear receptor subfamily 3, group C, member 1	Rattus norvegicus	76-99
10090938-5	1999	Results indicate that Dex-induced thymocyte apoptosis is attributable to an early ceramide generation caused by the activation of an acidic sphingomyelinase (aSMase).	Ceramides	82-90	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	158-164
10090938-6	1999	Caspase activity plays a crucial role in Dex-induced apoptosis and is downstream the aSMase activation in that inhibition of the early ceramide generation inhibits caspase activation and thymocyte death.	Ceramides	135-143	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	85-91
10090938-8	1999	Indeed, PI-PLC inhibition by U73122 totally prevents Dex-induced aSMase activity, ceramide generation, and consequently, caspase activation and apoptosis.	Ceramides	82-90	protein disulfide isomerase associated 3	Mus musculus	8-14
10373346-9	1999	Ceramide also enhanced IGF-induced tyrosine phosphorylation of the IGF-I receptor and activated PI-3 kinase.	Ceramides	0-8	insulin-like growth factor I receptor	Mus musculus	67-81
10197636-11	1999	TNF-alpha increased production of ceramide in LNCaP cells 48 h after exposure.	Ceramides	34-42	tumor necrosis factor	Homo sapiens	0-9
10197636-12	1999	Although irradiation alone had no effect on ceramide production in LNCaP cells, TNF-alpha plus irradiation induced significantly more ceramide than TNF-alpha alone.	Ceramides	134-142	tumor necrosis factor	Homo sapiens	80-89
10197636-13	1999	Ceramide production did not occur immediately after exposure to TNF-alpha, but rather was delayed such that ceramide levels were increased only 24 h after exposure to apoptotic stimuli.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	64-73
10101288-1	1999	A fluorescent analogue of ceramide, C12-NBD-ceramide, was found to be hydrolyzed much faster than 14C-labeled ceramide by alkaline ceramidase from Pseudomonas aeruginosa and neutral ceramidase from mouse liver, while this substrate was relatively resistant to acid ceramidase from plasma of the horseshoe crab.	Ceramides	26-34	N-acylsphingosine amidohydrolase 1	Mus musculus	260-275
10101288-1	1999	A fluorescent analogue of ceramide, C12-NBD-ceramide, was found to be hydrolyzed much faster than 14C-labeled ceramide by alkaline ceramidase from Pseudomonas aeruginosa and neutral ceramidase from mouse liver, while this substrate was relatively resistant to acid ceramidase from plasma of the horseshoe crab.	Ceramides	44-52	N-acylsphingosine amidohydrolase 1	Mus musculus	260-275
10194469-0	1999	Ordering of ceramide formation, caspase activation, and mitochondrial changes during CD95- and DNA damage-induced apoptosis.	Ceramides	12-20	Fas cell surface death receptor	Homo sapiens	85-89
10098845-0	1999	Extended ceramide exposure activates the trkA receptor by increasing receptor homodimer formation.	Ceramides	9-17	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	41-45
10098887-6	1999	THC produced a CB1 receptor-dependent stimulation of sphingomyelin breakdown that was concomitant to an elevation of intracellular ceramide levels.	Ceramides	131-139	cannabinoid receptor 1	Rattus norvegicus	15-18
10098887-8	1999	Furthermore, ceramide activated CPT-I in astrocyte mitochondria.	Ceramides	13-21	carnitine palmitoyltransferase 1B	Rattus norvegicus	32-37
10098887-9	1999	Results thus indicate that cannabinoids stimulate ketogenesis in astrocytes by a mechanism that may rely on CB1 receptor activation, sphingomyelin hydrolysis, and ceramide-mediated activation of CPT-I.	Ceramides	163-171	carnitine palmitoyltransferase 1B	Rattus norvegicus	195-200
10373346-4	1999	Lower ceramide doses were required to induce death in receptor negative compared with receptor positive fibroblasts (P< 0.05 at ceramide doses of 2 microM or greater), not only corroborating evidence that the IGF-I receptor functions as a survival receptor, but also suggesting that ceramide is not inducing apoptosis by suppressing a survival effect of the IGF-IR.	Ceramides	6-14	insulin-like growth factor I receptor	Mus musculus	212-226
10373346-4	1999	Lower ceramide doses were required to induce death in receptor negative compared with receptor positive fibroblasts (P< 0.05 at ceramide doses of 2 microM or greater), not only corroborating evidence that the IGF-I receptor functions as a survival receptor, but also suggesting that ceramide is not inducing apoptosis by suppressing a survival effect of the IGF-IR.	Ceramides	6-14	insulin-like growth factor I receptor	Mus musculus	361-367
10373346-7	1999	Inhibition of MAP kinase, using the MEKK inhibitor, PD98059, significantly reduced ceramide-induced cell death (P< 0.	Ceramides	83-91	mitogen-activated protein kinase kinase kinase 1	Mus musculus	36-40
10373346-11	1999	These results indicate that ceramide is capable of eliciting apparently contradictory events within a single cell type, and suggest that in the presence of an IGF-IR, survival is enhanced because ceramide can activate PI-3 kinase, believed to be an anti-apoptotic enzyme.	Ceramides	28-36	insulin-like growth factor I receptor	Mus musculus	159-165
10527453-5	1999	On the other hand, C-2 ceramide (0.3 microM) as well as other lipid mediators, such as lysophosphatidylcholine and arachidonic acid, were able to elicit a small increase in sPLA2 and potentiate the induction of sPLA2 by TNF-alpha.	Ceramides	23-31	phospholipase A2 group X	Homo sapiens	173-178
10527453-5	1999	On the other hand, C-2 ceramide (0.3 microM) as well as other lipid mediators, such as lysophosphatidylcholine and arachidonic acid, were able to elicit a small increase in sPLA2 and potentiate the induction of sPLA2 by TNF-alpha.	Ceramides	23-31	phospholipase A2 group X	Homo sapiens	211-216
10527453-5	1999	On the other hand, C-2 ceramide (0.3 microM) as well as other lipid mediators, such as lysophosphatidylcholine and arachidonic acid, were able to elicit a small increase in sPLA2 and potentiate the induction of sPLA2 by TNF-alpha.	Ceramides	23-31	tumor necrosis factor	Homo sapiens	220-229
10373346-11	1999	These results indicate that ceramide is capable of eliciting apparently contradictory events within a single cell type, and suggest that in the presence of an IGF-IR, survival is enhanced because ceramide can activate PI-3 kinase, believed to be an anti-apoptotic enzyme.	Ceramides	196-204	insulin-like growth factor I receptor	Mus musculus	159-165
10227679-8	1999	This is not as severe as in G(M2) gangliosidosis as a small amount of G(M2) was metabolized in ML IV cells to ceramide.	Ceramides	110-118	mucolipin TRP cation channel 1	Homo sapiens	95-100
10085144-15	1999	Our study provides the first evidence that GlcT-1 functions to regulate the level of intracellular ceramide by glycosylation of the ceramide when it is present in excess.	Ceramides	99-107	UDP-glucose ceramide glucosyltransferase	Mus musculus	43-49
10085144-15	1999	Our study provides the first evidence that GlcT-1 functions to regulate the level of intracellular ceramide by glycosylation of the ceramide when it is present in excess.	Ceramides	132-140	UDP-glucose ceramide glucosyltransferase	Mus musculus	43-49
10066377-3	1999	Reasoning that VEGF might be modulating apoptotic signal transduction pathways, we examined mechanisms involved in the anti-apoptotic effect of VEGF on starvation- and ceramide-induced apoptosis in HDMEC.	Ceramides	168-176	vascular endothelial growth factor A	Homo sapiens	144-148
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.	Ceramides	0-9	glucosidase, beta, acid	Mus musculus	142-165
10191118-0	1999	CLN3 defines a novel antiapoptotic pathway operative in neurodegeneration and mediated by ceramide.	Ceramides	90-98	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
10191118-6	1999	CLN3 modulates endogenous and vincristine-activated ceramide, and therefore suppresses apoptosis by impacting generation of ceramide.	Ceramides	52-60	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
10191118-6	1999	CLN3 modulates endogenous and vincristine-activated ceramide, and therefore suppresses apoptosis by impacting generation of ceramide.	Ceramides	124-132	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
10037689-3	1999	Ceramide-induced cyto c release is prevented by preincubation of mitochondria with a low concentration (40 nM) of Bcl-2.	Ceramides	0-8	BCL2, apoptosis regulator	Rattus norvegicus	114-119
10066377-8	1999	The presence of VEGF also inhibited the sustained activation of stress-activated protein kinase/c-jun-NH2-kinase (SAPK/JNK) caused by serum starvation and ceramide treatment.	Ceramides	155-163	vascular endothelial growth factor A	Homo sapiens	16-20
10066377-8	1999	The presence of VEGF also inhibited the sustained activation of stress-activated protein kinase/c-jun-NH2-kinase (SAPK/JNK) caused by serum starvation and ceramide treatment.	Ceramides	155-163	mitogen-activated protein kinase 9	Homo sapiens	114-118
10066377-8	1999	The presence of VEGF also inhibited the sustained activation of stress-activated protein kinase/c-jun-NH2-kinase (SAPK/JNK) caused by serum starvation and ceramide treatment.	Ceramides	155-163	mitogen-activated protein kinase 9	Homo sapiens	119-122
10070113-0	1999	TNF-alpha increases ceramide without inducing apoptosis in alveolar type II epithelial cells.	Ceramides	20-28	tumor necrosis factor	Rattus norvegicus	0-9
10070162-1	1999	It has been proposed that ceramide acts as a cellular messenger to mediate tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis.	Ceramides	26-34	tumor necrosis factor	Rattus norvegicus	75-102
10070162-1	1999	It has been proposed that ceramide acts as a cellular messenger to mediate tumor necrosis factor-alpha (TNF-alpha)-induced apoptosis.	Ceramides	26-34	tumor necrosis factor	Rattus norvegicus	104-113
10070162-2	1999	Based on this hypothesis, it was postulated that resistance of some cells to TNF-alpha cytotoxicity was due to an insufficient production of ceramide on stimulation by TNF-alpha.	Ceramides	141-149	tumor necrosis factor	Rattus norvegicus	77-86
10066779-8	1999	In contrast to exogenous NO, tumor necrosis factor (TNF)-alpha stimulates a very rapid and transient increase in ceramide levels within minutes but fails to induce the late-phase ceramide formation.	Ceramides	113-121	tumor necrosis factor	Rattus norvegicus	29-62
10066779-10	1999	Interestingly, NO and TNFalpha cause a chronic activation of acidic and neutral sphingomyelinases, the ceramide-generating enzymes, whereas acidic and neutral ceramidases, the ceramide-metabolizing enzymes, are inhibited by NO, but potently stimulated by TNFalpha.	Ceramides	103-111	tumor necrosis factor	Rattus norvegicus	22-30
10066779-11	1999	Furthermore, in the presence of an acidic ceramidase inhibitor, N-oleoylethanolamine, TNFalpha leads to a sustained accumulation of ceramide and in parallel induces DNA fragmentation.	Ceramides	132-140	tumor necrosis factor	Rattus norvegicus	86-94
10070113-9	1999	The results suggest that ceramide resulting from TNF-alpha activation of sphingomyelin hydrolysis might activate the mitogen-activated protein kinase and nuclear factor-kappaB pathways without increasing programmed cell death in type II cells.	Ceramides	25-33	tumor necrosis factor	Rattus norvegicus	49-58
10070113-2	1999	The purpose of this study was to determine whether endogenous ceramide, generated in response to in vivo administration of tumor necrosis factor-alpha (TNF-alpha), increases apoptosis in primary rat alveolar type II epithelial cells.	Ceramides	62-70	tumor necrosis factor	Rattus norvegicus	123-150
10070113-2	1999	The purpose of this study was to determine whether endogenous ceramide, generated in response to in vivo administration of tumor necrosis factor-alpha (TNF-alpha), increases apoptosis in primary rat alveolar type II epithelial cells.	Ceramides	62-70	tumor necrosis factor	Rattus norvegicus	152-161
10069808-8	1999	mcd4-174 cells synthesize all classes of inositolphosphoceramides, indicating that the GPI protein transport block is not due to deficient ceramide synthesis.	Ceramides	56-64	mannose-ethanolamine phosphotransferase MCD4	Saccharomyces cerevisiae S288C	0-4
10037464-5	1999	Similar time-dependent changes in DNA-PK activity, morphology, and DNA fragmentation occurred when the cells were exposed to either 100 microM ceramide or UV radiation.	Ceramides	143-151	protein kinase, DNA-activated, catalytic subunit	Homo sapiens	34-40
9915989-3	1999	The focus of the current study was to examine the role of ceramide in TNF-alpha-induced Ca2+ regulation.	Ceramides	58-66	tumor necrosis factor	Homo sapiens	70-79
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.	Ceramides	59-67	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	174-177
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.	Ceramides	59-67	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	236-239
10723061-2	1999	In all three cell culture systems, the activation of caspase-3-like activity (CPP32) coincided with the increased formation of ceramide from sphingomyelin and the onset of DNA fragmentation.	Ceramides	127-135	caspase 3	Homo sapiens	53-62
10723061-2	1999	In all three cell culture systems, the activation of caspase-3-like activity (CPP32) coincided with the increased formation of ceramide from sphingomyelin and the onset of DNA fragmentation.	Ceramides	127-135	caspase 3	Homo sapiens	78-83
10082875-0	1999	Protective effects of the TNF-ceramide pathway against glutamate neurotoxicity on cultured mesencephalic neurons.	Ceramides	30-38	tumor necrosis factor	Homo sapiens	26-29
10200557-2	1999	We tested this hypothesis by investigating the role of ceramide in TNF-alpha-initiated apoptotic signaling using the histiocytic lymphoma cell line U937.	Ceramides	55-63	tumor necrosis factor	Homo sapiens	67-76
10070857-0	1999	Activation of integrin and ceramide signalling pathways can inhibit the mitogenic effect of insulin-like growth factor I (IGF-I) in human breast cancer cell lines.	Ceramides	27-35	insulin like growth factor 1	Homo sapiens	92-120
10070857-0	1999	Activation of integrin and ceramide signalling pathways can inhibit the mitogenic effect of insulin-like growth factor I (IGF-I) in human breast cancer cell lines.	Ceramides	27-35	insulin like growth factor 1	Homo sapiens	122-127
10070857-6	1999	Low-dose induction of integrin and ceramide signalling pathways causes cells to be blocked in S-phase, thereby inhibiting the normal cycle of events associated with the IGF-I-induced mitotic signal.	Ceramides	35-43	insulin like growth factor 1	Homo sapiens	169-174
10200557-8	1999	Furthermore, the endogenous ceramide in U937 cells treated with TNF-alpha increases well after the commitment to the apoptotic pathway.	Ceramides	28-36	tumor necrosis factor	Homo sapiens	64-73
10348660-0	1999	Atypical PKC zeta is activated by ceramide, resulting in coactivation of NF-kappaB/JNK kinase and cell survival.	Ceramides	34-42	mitogen-activated protein kinase 8	Rattus norvegicus	83-86
10348660-5	1999	Overexpression of either aPKC isoform, PKC zeta or iota, resulted in enhanced survival of PC12 cells at high doses of ceramide and in ceramide-stimulated Jun N-terminal kinase (JNK), without any apparent effect on mitogen-activated kinase.	Ceramides	134-142	mitogen-activated protein kinase 8	Rattus norvegicus	154-175
10348660-5	1999	Overexpression of either aPKC isoform, PKC zeta or iota, resulted in enhanced survival of PC12 cells at high doses of ceramide and in ceramide-stimulated Jun N-terminal kinase (JNK), without any apparent effect on mitogen-activated kinase.	Ceramides	134-142	mitogen-activated protein kinase 8	Rattus norvegicus	177-180
10348660-6	1999	These findings support a role for ceramide-induced PKC zeta activity in the control of cell survival signaling via a pathway that also activates JNK kinase.	Ceramides	34-42	mitogen-activated protein kinase 8	Rattus norvegicus	145-148
9891021-0	1999	Aryl hydrocarbon receptor regulation of ceramide-induced apoptosis in murine hepatoma 1c1c7 cells.	Ceramides	40-48	aryl-hydrocarbon receptor	Mus musculus	0-25
9915784-2	1999	Several signaling pathways have been implicated for p75 in the absence of Trk receptors, including induction of NF-kappaB and c-Jun kinase activities and increased production of ceramide.	Ceramides	178-186	TNF receptor superfamily member 1B	Homo sapiens	52-55
9891021-9	1999	These results suggest the AHR modulates aspects of ceramide signaling associated with the induction of apoptosis but not cell cycle arrest, and does so by a mechanism that is independent of its interaction with aryl hydrocarbon receptor nuclear translocator and exogenous AHR ligands.	Ceramides	51-59	aryl hydrocarbon receptor	Homo sapiens	26-29
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	0-8	tumor necrosis factor	Mus musculus	146-173
9928956-0	1999	AT2 receptor stimulation induces generation of ceramides in PC12W cells.	Ceramides	47-56	angiotensin II receptor, type 2	Rattus norvegicus	0-3
9928956-2	1999	To further investigate the molecular mechanisms leading to AT2 receptor-induced programmed cell death in PC12W cells we studied the effects of angiotensin II (ANG II) on ceramide levels by HPTLC analysis.	Ceramides	170-178	angiotensinogen	Rattus norvegicus	143-157
9928956-2	1999	To further investigate the molecular mechanisms leading to AT2 receptor-induced programmed cell death in PC12W cells we studied the effects of angiotensin II (ANG II) on ceramide levels by HPTLC analysis.	Ceramides	170-178	angiotensinogen	Rattus norvegicus	159-165
9928956-3	1999	We could demonstrate that ANG II time- (1-10 h) and dose-dependently (10(-8)-5 X 10(-6) M) increased ceramide levels by maximally 175% but did not affect sphingomyelin degradation.	Ceramides	101-109	angiotensinogen	Rattus norvegicus	26-32
9880559-3	1999	Although TNF and IL-1 cause elevation of cellular ceramide, which is thought to act as a second messenger, LPS has been proposed to signal by virtue of structural similarity to ceramide.	Ceramides	50-58	tumor necrosis factor	Mus musculus	9-12
9880559-3	1999	Although TNF and IL-1 cause elevation of cellular ceramide, which is thought to act as a second messenger, LPS has been proposed to signal by virtue of structural similarity to ceramide.	Ceramides	50-58	interleukin 1 complex	Mus musculus	17-21
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	0-8	tumor necrosis factor	Mus musculus	175-178
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	0-8	interleukin 1 beta	Mus musculus	184-201
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	0-8	interleukin 1 complex	Mus musculus	203-207
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	13-21	tumor necrosis factor	Mus musculus	146-173
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	13-21	tumor necrosis factor	Mus musculus	175-178
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	13-21	interleukin 1 beta	Mus musculus	184-201
9880559-2	1999	Ceramide and ceramide-activated enzymes have been implicated in responses to bacterial lipopolysaccharide (LPS) and the proinflammatory cytokines tumor necrosis factor-alpha (TNF) and interleukin-1beta (IL-1).	Ceramides	13-21	interleukin 1 complex	Mus musculus	203-207
10989654-4	1999	Ceramide-induced cyt c release is prevented by a low concentration of Bcl-2.	Ceramides	0-8	BCL2, apoptosis regulator	Rattus norvegicus	70-75
9873062-7	1999	The EC50 values of adriamycin and ceramide were 11-fold (p < 0.0005) and 5-fold (p < 0.005) higher, respectively, in MCF-7/GCS cells compared with MCF-7 cells.	Ceramides	34-42	UDP-glucose ceramide glucosyltransferase	Homo sapiens	129-132
9873062-8	1999	Ceramide resistance displayed by MCF-7/GCS cells closely paralleled the activity of expressed GCS with a correlation coefficient of 0.99.	Ceramides	0-8	UDP-glucose ceramide glucosyltransferase	Homo sapiens	39-42
9873062-8	1999	Ceramide resistance displayed by MCF-7/GCS cells closely paralleled the activity of expressed GCS with a correlation coefficient of 0.99.	Ceramides	0-8	UDP-glucose ceramide glucosyltransferase	Homo sapiens	94-97
9873062-11	1999	This work demonstrates that overexpression of GCS, which catalyzes ceramide glycosylation, induces resistance to adriamycin and ceramide in MCF-7 breast cancer cells.	Ceramides	67-75	UDP-glucose ceramide glucosyltransferase	Homo sapiens	46-49
9873062-11	1999	This work demonstrates that overexpression of GCS, which catalyzes ceramide glycosylation, induces resistance to adriamycin and ceramide in MCF-7 breast cancer cells.	Ceramides	128-136	UDP-glucose ceramide glucosyltransferase	Homo sapiens	46-49
10416029-6	1999	Also, CoQ10 addition decreased ceramide release after serum withdrawal by inhibition of magnesium-dependent plasma membrane neutral-sphingomyelinase.	Ceramides	31-39	sphingomyelin phosphodiesterase 2	Homo sapiens	124-148
9878820-9	1999	The AUR1 gene is necessary for addition of inositol phosphate to ceramide and has been identified as a target of several potent antifungal compounds.	Ceramides	65-73	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	4-8
9864164-0	1999	Ceramide and cyclic adenosine monophosphate (cAMP) induce cAMP response element binding protein phosphorylation via distinct signaling pathways while having opposite effects on myeloid cell survival.	Ceramides	0-8	cAMP responsive element binding protein 1	Homo sapiens	58-95
9864164-6	1999	Ceramide, or sphingomyelinase, like tumor necrosis factor- (TNF-) or the hematopoietic growth factor, interleukin-3 (IL-3), was shown to activate p38 MAPK, which in turn activated MAPKAP kinase-2.	Ceramides	0-8	interleukin 3	Homo sapiens	73-100
9880803-8	1999	These results suggest that ceramide triggers PLC activation through its synergistic action with thrombin, and subsequently potentiates the sequential PKC-MAPK cascade-cPLA2 pathway, thus resulting in enhancement of arachidonic acid release.	Ceramides	27-35	LOC100009319	Oryctolagus cuniculus	45-48
9864164-6	1999	Ceramide, or sphingomyelinase, like tumor necrosis factor- (TNF-) or the hematopoietic growth factor, interleukin-3 (IL-3), was shown to activate p38 MAPK, which in turn activated MAPKAP kinase-2.	Ceramides	0-8	interleukin 3	Homo sapiens	102-115
9864164-6	1999	Ceramide, or sphingomyelinase, like tumor necrosis factor- (TNF-) or the hematopoietic growth factor, interleukin-3 (IL-3), was shown to activate p38 MAPK, which in turn activated MAPKAP kinase-2.	Ceramides	0-8	interleukin 3	Homo sapiens	117-121
9864164-6	1999	Ceramide, or sphingomyelinase, like tumor necrosis factor- (TNF-) or the hematopoietic growth factor, interleukin-3 (IL-3), was shown to activate p38 MAPK, which in turn activated MAPKAP kinase-2.	Ceramides	0-8	MAPK activated protein kinase 2	Homo sapiens	180-195
9864164-8	1999	A selective p38 MAPK inhibitor, SB203580, blocked TNF-- or ceramide-induced CREB phosphorylation, but had no effect on the induction of apoptosis mediated by these agents.	Ceramides	59-67	cAMP responsive element binding protein 1	Homo sapiens	76-80
9880803-0	1999	Stimulation by ceramide of phospholipase A2 activation through a mechanism related to the phospholipase C-initiated signaling pathway in rabbit platelets.	Ceramides	15-23	phospholipase A2	Oryctolagus cuniculus	27-43
9880803-0	1999	Stimulation by ceramide of phospholipase A2 activation through a mechanism related to the phospholipase C-initiated signaling pathway in rabbit platelets.	Ceramides	15-23	LOC100009319	Oryctolagus cuniculus	90-105
9880803-1	1999	To study the involvement of sphingolipids in glycerophospholipid metabolism, the contribution of ceramide to the activation of group IV cytosolic phospholipase A2 (cPLA2) was investigated in platelets using cell-permeable C6-ceramide (N-hexanoylsphingosine).	Ceramides	97-105	phospholipase A2	Oryctolagus cuniculus	146-162
9880803-1	1999	To study the involvement of sphingolipids in glycerophospholipid metabolism, the contribution of ceramide to the activation of group IV cytosolic phospholipase A2 (cPLA2) was investigated in platelets using cell-permeable C6-ceramide (N-hexanoylsphingosine).	Ceramides	97-105	cytosolic phospholipase A2	Oryctolagus cuniculus	164-169
9880803-2	1999	The addition of ceramide led to potentiation of thrombin-induced activation of cPLA2 and mitogen-activated protein kinase (MAPK) as well as arachidonic acid release and lysophosphatidylcholine formation.	Ceramides	16-24	prothrombin	Oryctolagus cuniculus	48-56
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.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	27-30
9880803-8	1999	These results suggest that ceramide triggers PLC activation through its synergistic action with thrombin, and subsequently potentiates the sequential PKC-MAPK cascade-cPLA2 pathway, thus resulting in enhancement of arachidonic acid release.	Ceramides	27-35	prothrombin	Oryctolagus cuniculus	96-104
9880803-2	1999	The addition of ceramide led to potentiation of thrombin-induced activation of cPLA2 and mitogen-activated protein kinase (MAPK) as well as arachidonic acid release and lysophosphatidylcholine formation.	Ceramides	16-24	cytosolic phospholipase A2	Oryctolagus cuniculus	79-84
9880803-5	1999	Ceramide also stimulated thrombin-induced protein kinase C (PKC) activation, but ceramide by itself failed to do so.	Ceramides	0-8	prothrombin	Oryctolagus cuniculus	25-33
9880803-8	1999	These results suggest that ceramide triggers PLC activation through its synergistic action with thrombin, and subsequently potentiates the sequential PKC-MAPK cascade-cPLA2 pathway, thus resulting in enhancement of arachidonic acid release.	Ceramides	27-35	cytosolic phospholipase A2	Oryctolagus cuniculus	167-172
9880803-6	1999	Furthermore, ceramide synergistically enhanced diacylglycerol (DAG) formation and Ca2+ mobilization with thrombin, and also DAG formation with Ca2+-ionophore A23187.	Ceramides	13-21	prothrombin	Oryctolagus cuniculus	105-113
9880803-7	1999	The DAG formation in response to ceramide with thrombin or A23187, as well as arachidonic acid release with thrombin were completely inhibited by U73122, a phospholipase C (PLC) inhibitor.	Ceramides	33-41	prothrombin	Oryctolagus cuniculus	47-55
9880803-7	1999	The DAG formation in response to ceramide with thrombin or A23187, as well as arachidonic acid release with thrombin were completely inhibited by U73122, a phospholipase C (PLC) inhibitor.	Ceramides	33-41	LOC100009319	Oryctolagus cuniculus	156-171
9869656-12	1999	25-Hydroxycholesterol promotes translocation of OSBP to the Golgi apparatus where it appears to stimulate conversion of ceramide to sphingomyelin.	Ceramides	120-128	LOW QUALITY PROTEIN: oxysterol-binding protein 1	Cricetulus griseus	48-52
9880803-7	1999	The DAG formation in response to ceramide with thrombin or A23187, as well as arachidonic acid release with thrombin were completely inhibited by U73122, a phospholipase C (PLC) inhibitor.	Ceramides	33-41	LOC100009319	Oryctolagus cuniculus	173-176
10462066-5	1999	In addition, ceramide generated upon CB1 cannabinoid receptor activation may enhance ketone body production by astrocytes independently of MAPK.	Ceramides	13-21	cannabinoid receptor 1	Homo sapiens	37-40
10419100-0	1999	Tumor necrosis factor-alpha and ceramides in insulin resistance.	Ceramides	32-41	insulin	Homo sapiens	45-52
10419100-1	1999	The present studies tested the hypothesis that some effects of tumor necrosis factor-alpha (TNF-alpha) are mediated by activation of sphingomyelinases and the production of ceramides.	Ceramides	173-182	tumor necrosis factor	Homo sapiens	63-90
10419100-1	1999	The present studies tested the hypothesis that some effects of tumor necrosis factor-alpha (TNF-alpha) are mediated by activation of sphingomyelinases and the production of ceramides.	Ceramides	173-182	tumor necrosis factor	Homo sapiens	92-101
9918791-1	1998	Ceramide glucosyltransferase (glucosylceramide synthase, GlcT-1, EC 2.4.1.80) catalyzes the first step in glycosphingolipid synthesis, the transfer of glucose from UDP-glucose to ceramide.	Ceramides	38-46	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-28
10419100-10	1999	Our work provides further mechanisms whereby TNF-alpha and ceramides produce insulin resistance and decrease the effectiveness of insulin in stimulating glucose disposal from the blood.	Ceramides	59-68	insulin	Homo sapiens	77-84
10419100-10	1999	Our work provides further mechanisms whereby TNF-alpha and ceramides produce insulin resistance and decrease the effectiveness of insulin in stimulating glucose disposal from the blood.	Ceramides	59-68	insulin	Homo sapiens	130-137
9918791-1	1998	Ceramide glucosyltransferase (glucosylceramide synthase, GlcT-1, EC 2.4.1.80) catalyzes the first step in glycosphingolipid synthesis, the transfer of glucose from UDP-glucose to ceramide.	Ceramides	38-46	UDP-glucose ceramide glucosyltransferase	Mus musculus	57-63
9841888-6	1998	These results identify a different mechanism of action for Bcl-xL compared with Bcl-2 and they demonstrate that Bcl-xL targets a point upstream of ceramide generation, whereas Bcl-2 functions downstream of ceramide in the TNFalpha- and camptothecin-activated pathways of apoptosis.	Ceramides	206-214	tumor necrosis factor	Homo sapiens	222-230
9852115-1	1998	Sphingomyelin hydrolysis and ceramide generation catalyzed by sphingomyelinases (SMase) are key components of the signaling pathways in cytokine- and stress-induced cellular responses.	Ceramides	29-37	sphingomyelin phosphodiesterase 2	Rattus norvegicus	81-86
9841888-0	1998	Distinct sites of action of Bcl-2 and Bcl-xL in the ceramide pathway of apoptosis.	Ceramides	52-60	BCL2 apoptosis regulator	Homo sapiens	28-33
9843784-6	1998	Immunoprecipitation and immunoblotting revealed one form of 21-kDa Rho A that translocated from the cytosol to the membrane in response to stimulation by either endothelin (10(-7) M) or ceramide (10(-7) M) ( approximately 30% increase at 30 s that was sustained at 4 min).	Ceramides	186-194	transforming protein RhoA	Oryctolagus cuniculus	67-72
9841888-0	1998	Distinct sites of action of Bcl-2 and Bcl-xL in the ceramide pathway of apoptosis.	Ceramides	52-60	BCL2 like 1	Homo sapiens	38-44
9841888-1	1998	We studied the inhibition of tumour necrosis factor alpha (TNFalpha)- and camptothecin-induced apoptosis by Bcl-2 and Bcl-xL as they relate to the ceramide pathway.	Ceramides	147-155	BCL2 apoptosis regulator	Homo sapiens	108-113
9841888-1	1998	We studied the inhibition of tumour necrosis factor alpha (TNFalpha)- and camptothecin-induced apoptosis by Bcl-2 and Bcl-xL as they relate to the ceramide pathway.	Ceramides	147-155	BCL2 like 1	Homo sapiens	118-124
9841888-4	1998	On the other hand, Bcl-xL prevented the accumulation of endogenous ceramide in response to TNFalpha or camptothecin, whereas Bcl-2 showed little effect on ceramide formation.	Ceramides	67-75	BCL2 like 1	Homo sapiens	19-25
9841888-4	1998	On the other hand, Bcl-xL prevented the accumulation of endogenous ceramide in response to TNFalpha or camptothecin, whereas Bcl-2 showed little effect on ceramide formation.	Ceramides	67-75	tumor necrosis factor	Homo sapiens	91-99
9841888-6	1998	These results identify a different mechanism of action for Bcl-xL compared with Bcl-2 and they demonstrate that Bcl-xL targets a point upstream of ceramide generation, whereas Bcl-2 functions downstream of ceramide in the TNFalpha- and camptothecin-activated pathways of apoptosis.	Ceramides	147-155	BCL2 like 1	Homo sapiens	59-65
9841888-6	1998	These results identify a different mechanism of action for Bcl-xL compared with Bcl-2 and they demonstrate that Bcl-xL targets a point upstream of ceramide generation, whereas Bcl-2 functions downstream of ceramide in the TNFalpha- and camptothecin-activated pathways of apoptosis.	Ceramides	147-155	BCL2 like 1	Homo sapiens	112-118
9841888-6	1998	These results identify a different mechanism of action for Bcl-xL compared with Bcl-2 and they demonstrate that Bcl-xL targets a point upstream of ceramide generation, whereas Bcl-2 functions downstream of ceramide in the TNFalpha- and camptothecin-activated pathways of apoptosis.	Ceramides	206-214	BCL2 like 1	Homo sapiens	59-65
9841888-6	1998	These results identify a different mechanism of action for Bcl-xL compared with Bcl-2 and they demonstrate that Bcl-xL targets a point upstream of ceramide generation, whereas Bcl-2 functions downstream of ceramide in the TNFalpha- and camptothecin-activated pathways of apoptosis.	Ceramides	206-214	BCL2 apoptosis regulator	Homo sapiens	176-181
9829981-4	1998	We therefore semiquantified mRNA of serine palmitoyltransferase (SPT), which catalyzes the first step in ceramide synthesis.	Ceramides	105-113	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	36-63
9829981-4	1998	We therefore semiquantified mRNA of serine palmitoyltransferase (SPT), which catalyzes the first step in ceramide synthesis.	Ceramides	105-113	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	65-68
9829981-8	1998	Triacsin-C, which blocks palmitoyl-CoA synthesis, and L-cycloserine, which blocks SPT activity, completely blocked [3H]ceramide formation from [3H]serine.	Ceramides	119-127	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	82-85
9830045-0	1998	Ceramide regulates the transcription of cyclooxygenase-2.	Ceramides	0-8	prostaglandin-endoperoxide synthase 2	Homo sapiens	40-56
9830045-3	1998	We determined whether ceramide, a lipid second messenger, induced cyclooxygenase-2 (COX-2) in human mammary epithelial cells.	Ceramides	22-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	66-82
9830045-3	1998	We determined whether ceramide, a lipid second messenger, induced cyclooxygenase-2 (COX-2) in human mammary epithelial cells.	Ceramides	22-30	prostaglandin-endoperoxide synthase 2	Homo sapiens	84-89
9830045-4	1998	Treatment of cells with neutral SMase or C2- or C6-ceramide enhanced prostaglandin E2 synthesis and increased levels of COX-2 protein and mRNA.	Ceramides	50-59	prostaglandin-endoperoxide synthase 2	Homo sapiens	120-125
9830045-5	1998	Nuclear runoff assays revealed increased rates of COX-2 transcription after treatment with SMase and C2- and C6-ceramide.	Ceramides	112-120	prostaglandin-endoperoxide synthase 2	Homo sapiens	50-55
9830045-6	1998	Transient transfections utilizing COX-2 promoter deletion constructs and COX-2 promoter constructs in which specific enhancer elements were mutagenized indicated that the effects of ceramide were mediated via a cAMP response element.	Ceramides	182-190	prostaglandin-endoperoxide synthase 2	Homo sapiens	34-39
9830045-6	1998	Transient transfections utilizing COX-2 promoter deletion constructs and COX-2 promoter constructs in which specific enhancer elements were mutagenized indicated that the effects of ceramide were mediated via a cAMP response element.	Ceramides	182-190	prostaglandin-endoperoxide synthase 2	Homo sapiens	73-78
9830045-7	1998	The induction of COX-2 by ceramide was inhibited by calphostin C, an inhibitor of protein kinase C. Induction of COX-2 promoter activity by SMase was blocked by overexpressing kinase-deficient Raf-1.	Ceramides	26-34	prostaglandin-endoperoxide synthase 2	Homo sapiens	17-22
9830045-7	1998	The induction of COX-2 by ceramide was inhibited by calphostin C, an inhibitor of protein kinase C. Induction of COX-2 promoter activity by SMase was blocked by overexpressing kinase-deficient Raf-1.	Ceramides	26-34	prostaglandin-endoperoxide synthase 2	Homo sapiens	113-118
9830045-7	1998	The induction of COX-2 by ceramide was inhibited by calphostin C, an inhibitor of protein kinase C. Induction of COX-2 promoter activity by SMase was blocked by overexpressing kinase-deficient Raf-1.	Ceramides	26-34	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	193-198
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 1	Homo sapiens	60-97
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 1	Homo sapiens	99-102
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 8	Homo sapiens	105-128
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 8	Homo sapiens	130-133
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 14	Homo sapiens	140-176
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 3	Homo sapiens	178-182
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 3	Homo sapiens	226-230
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase kinase 7	Homo sapiens	239-242
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	mitogen-activated protein kinase 1	Homo sapiens	140-143
9830045-8	1998	Triggering of the ceramide pathway also led to increases in extracellular signal-regulated kinase (ERK), c-Jun N-terminal kinase (JNK), and p38 mitogen-activated protein kinase (MAPK) activities; pharmacological inhibitors of MAPK kinase (MEK) and p38 MAPK blocked the induction of COX-2 by SMase.	Ceramides	18-26	prostaglandin-endoperoxide synthase 2	Homo sapiens	282-287
9830045-11	1998	A dominant negative for c-Jun inhibited the activation of COX-2 promoter activity by ceramide.	Ceramides	85-93	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	24-29
9830045-11	1998	A dominant negative for c-Jun inhibited the activation of COX-2 promoter activity by ceramide.	Ceramides	85-93	prostaglandin-endoperoxide synthase 2	Homo sapiens	58-63
9830045-12	1998	Thus, in response to ceramide, increased MAPK signaling activates c-Jun, which, in turn, induces COX-2 gene expression via the cAMP response element in the COX-2 promoter.	Ceramides	21-29	mitogen-activated protein kinase 3	Homo sapiens	41-45
9830045-12	1998	Thus, in response to ceramide, increased MAPK signaling activates c-Jun, which, in turn, induces COX-2 gene expression via the cAMP response element in the COX-2 promoter.	Ceramides	21-29	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	66-71
9830045-12	1998	Thus, in response to ceramide, increased MAPK signaling activates c-Jun, which, in turn, induces COX-2 gene expression via the cAMP response element in the COX-2 promoter.	Ceramides	21-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	97-102
9830045-12	1998	Thus, in response to ceramide, increased MAPK signaling activates c-Jun, which, in turn, induces COX-2 gene expression via the cAMP response element in the COX-2 promoter.	Ceramides	21-29	prostaglandin-endoperoxide synthase 2	Homo sapiens	156-161
9832547-6	1998	Interestingly, VBM1 and VBM2 are allelic to ELO3 and ELO2, two genes that have been shown recently to mediate the elongation of very long chain fatty acids and subsequent ceramide and inositol sphingolipid synthesis.	Ceramides	171-179	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	15-19
10092217-1	1998	The pentameric B subunit of verotoxin (VT) mediates the attachment to cell surface globotriaosyl ceramide (Gb3) to facilitate receptor-mediated endocytosis of the toxin.	Ceramides	97-105	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	107-110
9832547-6	1998	Interestingly, VBM1 and VBM2 are allelic to ELO3 and ELO2, two genes that have been shown recently to mediate the elongation of very long chain fatty acids and subsequent ceramide and inositol sphingolipid synthesis.	Ceramides	171-179	fatty acid elongase ELO2	Saccharomyces cerevisiae S288C	24-28
9832547-6	1998	Interestingly, VBM1 and VBM2 are allelic to ELO3 and ELO2, two genes that have been shown recently to mediate the elongation of very long chain fatty acids and subsequent ceramide and inositol sphingolipid synthesis.	Ceramides	171-179	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	44-48
9832547-6	1998	Interestingly, VBM1 and VBM2 are allelic to ELO3 and ELO2, two genes that have been shown recently to mediate the elongation of very long chain fatty acids and subsequent ceramide and inositol sphingolipid synthesis.	Ceramides	171-179	fatty acid elongase ELO2	Saccharomyces cerevisiae S288C	53-57
9813032-6	1998	Our results show that several lipid enzymes contribute to generation of ceramide in response to TNF and identify glucosylceramide and SM synthase as important regulators of the kinetics and magnitude of intracellular ceramide accumulation.	Ceramides	72-80	tumor necrosis factor	Homo sapiens	96-99
9862448-6	1998	The results indicate that a fall in extracellular ionized Mg2+ concentration produces a rapid and sustained decrease in membrane sphingomyelin and a moderate rise in intracellular ceramide.	Ceramides	180-188	mucin 7, secreted	Homo sapiens	58-61
9862447-2	1998	Interleukin-1beta (IL-1beta) is known to stimulate ceramide formation in rat renal mesangial cells; however, the respective subtype of SMase and its regulation have not been investigated.	Ceramides	51-59	interleukin 1 beta	Rattus norvegicus	0-17
9862447-2	1998	Interleukin-1beta (IL-1beta) is known to stimulate ceramide formation in rat renal mesangial cells; however, the respective subtype of SMase and its regulation have not been investigated.	Ceramides	51-59	interleukin 1 beta	Rattus norvegicus	19-27
9862447-3	1998	We found that IL-1beta induced an increase in endogenous ceramide levels via the action of a neutral SMase but not an acidic SMase in rat mesangial cells.	Ceramides	57-65	interleukin 1 beta	Rattus norvegicus	14-22
9862447-4	1998	Cytokine-induced activation of neutral SMase was inhibited by stimulation of protein kinase C (PKC) by the phorbol ester TPA which caused a reduction of ceramide back to control levels.	Ceramides	153-161	protein kinase C, alpha	Rattus norvegicus	95-98
9862447-6	1998	Long-term incubation (24 h) of mesangial cells with TPA, which downregulates PKC-alpha, -delta, and -epsilon isoenzymes, resulted in a recovery of IL-1beta-stimulated neutral SMase activity as well as ceramide formation.	Ceramides	201-209	interleukin 1 beta	Rattus norvegicus	147-155
9862447-7	1998	These data implicate an important modulatory function of PKC in ceramide production in IL-1beta-activated mesangial cells.	Ceramides	64-72	protein kinase C, alpha	Rattus norvegicus	57-60
9862447-7	1998	These data implicate an important modulatory function of PKC in ceramide production in IL-1beta-activated mesangial cells.	Ceramides	64-72	interleukin 1 beta	Rattus norvegicus	87-95
9813032-0	1998	Tumor necrosis factor induces ceramide oscillations and negatively controls sphingolipid synthases by caspases in apoptotic Kym-1 cells.	Ceramides	30-38	tumor necrosis factor	Homo sapiens	0-21
9813032-2	1998	We show here in Kym-1 rhabdomyosarcoma cells that tumor necrosis factor (TNF)-induced apoptosis is preceded by a multiphasic increase in intracellular ceramide levels.	Ceramides	151-159	tumor necrosis factor	Homo sapiens	50-71
9813032-2	1998	We show here in Kym-1 rhabdomyosarcoma cells that tumor necrosis factor (TNF)-induced apoptosis is preceded by a multiphasic increase in intracellular ceramide levels.	Ceramides	151-159	tumor necrosis factor	Homo sapiens	73-76
9813032-3	1998	Distinct enzymes were found to contribute to three waves of ceramide, neutral sphingomyelinase, ceramide synthase, and acid sphingomyelinase, with peak activities at 1-2, 40, and around 200 min, respectively, the latter coinciding with progression to irreversible damage.	Ceramides	60-68	sphingomyelin phosphodiesterase 2	Homo sapiens	70-94
9815065-2	1998	Cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been shown to increase intracellular ceramide through phospholipase A2 (PLA2)-dependent activation of nSMase.	Ceramides	100-108	tumor necrosis factor	Rattus norvegicus	18-45
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.	Ceramides	17-25	tumor necrosis factor	Homo sapiens	38-41
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.	Ceramides	17-25	sphingomyelin synthase 2	Homo sapiens	86-113
9849882-0	1998	Selective involvement of caspase-3 in ceramide induced apoptosis in AK-5 tumor cells.	Ceramides	38-46	caspase 3	Rattus norvegicus	25-34
9849882-2	1998	The present study demonstrates the activation of caspase-3/CPP-32beta, during apoptosis induced by cell permeable exogenous ceramides, in AK-5 tumor, a spontaneously regressing rat histiocytoma.	Ceramides	124-133	caspase 3	Rattus norvegicus	49-58
9849882-2	1998	The present study demonstrates the activation of caspase-3/CPP-32beta, during apoptosis induced by cell permeable exogenous ceramides, in AK-5 tumor, a spontaneously regressing rat histiocytoma.	Ceramides	124-133	caspase 3	Rattus norvegicus	59-69
9849882-4	1998	In cells overexpressing Bcl-2, a significant decrease in cell death was observed after exogenous addition of ceramides.	Ceramides	109-118	BCL2, apoptosis regulator	Rattus norvegicus	24-29
9849882-5	1998	Furthermore the processing of caspase-3 to its active form upon apoptotic stimulus, and the subsequent cleavage of the substrate PARP, suggested a central role for caspase-3 in the ceramide mediated apoptosis in AK-5 tumor cells.	Ceramides	181-189	caspase 3	Rattus norvegicus	30-39
9849882-5	1998	Furthermore the processing of caspase-3 to its active form upon apoptotic stimulus, and the subsequent cleavage of the substrate PARP, suggested a central role for caspase-3 in the ceramide mediated apoptosis in AK-5 tumor cells.	Ceramides	181-189	caspase 3	Rattus norvegicus	164-173
9824663-0	1998	Tumor necrosis factor-alpha-induced release of plasminogen activator inhibitor-1 from human umbilical vein endothelial cells: involvement of intracellular ceramide signaling event.	Ceramides	155-163	tumor necrosis factor	Homo sapiens	0-27
9824663-0	1998	Tumor necrosis factor-alpha-induced release of plasminogen activator inhibitor-1 from human umbilical vein endothelial cells: involvement of intracellular ceramide signaling event.	Ceramides	155-163	serpin family E member 1	Homo sapiens	47-80
9824663-6	1998	We have previously shown that a cell-permeable ceramide analog, N-acetylsphingosine (C2-ceramide) enhances the PAI-1 release from HUVEC.	Ceramides	47-55	serpin family E member 1	Homo sapiens	111-116
9824663-10	1998	Taken together, these findings suggest that TNF-alpha prominently utilizes the lysosomal acidic SMase-ceramide signaling pathway in the induction of PAI-1 release from HUVEC.	Ceramides	102-110	tumor necrosis factor	Homo sapiens	44-53
9824663-10	1998	Taken together, these findings suggest that TNF-alpha prominently utilizes the lysosomal acidic SMase-ceramide signaling pathway in the induction of PAI-1 release from HUVEC.	Ceramides	102-110	serpin family E member 1	Homo sapiens	149-154
9815065-0	1998	TNF-alpha-induced endothelium-independent vasodilation: a role for phospholipase A2-dependent ceramide signaling.	Ceramides	94-102	tumor necrosis factor	Rattus norvegicus	0-9
9815065-0	1998	TNF-alpha-induced endothelium-independent vasodilation: a role for phospholipase A2-dependent ceramide signaling.	Ceramides	94-102	phospholipase A2 group IB	Rattus norvegicus	67-83
9815065-1	1998	Ceramide is a novel second messenger generated by hydrolysis of membrane sphingomyelin by a neutral sphingomyelinase (nSMase).	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Rattus norvegicus	92-116
9815065-1	1998	Ceramide is a novel second messenger generated by hydrolysis of membrane sphingomyelin by a neutral sphingomyelinase (nSMase).	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Rattus norvegicus	118-124
9815065-2	1998	Cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been shown to increase intracellular ceramide through phospholipase A2 (PLA2)-dependent activation of nSMase.	Ceramides	100-108	tumor necrosis factor	Rattus norvegicus	47-56
9815065-2	1998	Cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been shown to increase intracellular ceramide through phospholipase A2 (PLA2)-dependent activation of nSMase.	Ceramides	100-108	phospholipase A2 group IB	Rattus norvegicus	117-133
9815065-2	1998	Cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been shown to increase intracellular ceramide through phospholipase A2 (PLA2)-dependent activation of nSMase.	Ceramides	100-108	phospholipase A2 group IB	Rattus norvegicus	135-139
9815065-2	1998	Cytokines such as tumor necrosis factor-alpha (TNF-alpha) have been shown to increase intracellular ceramide through phospholipase A2 (PLA2)-dependent activation of nSMase.	Ceramides	100-108	sphingomyelin phosphodiesterase 2	Rattus norvegicus	165-171
9815065-10	1998	In the present study, we tested the hypothesis that ceramide mediates TNF-alpha-induced vasodilation.	Ceramides	52-60	tumor necrosis factor	Rattus norvegicus	70-79
9815065-13	1998	In cultured rat aortic vascular smooth muscle cells, TNF-alpha (10(-7) g/ml) increased intracellular ceramide 1.5-fold over basal level (0.08 nmol/mg protein), which was blocked by the PLA2 antagonist DEDA (50 microM).	Ceramides	101-109	tumor necrosis factor	Rattus norvegicus	53-62
9794783-8	1998	Signalling of the stress response through ceramide appears to play a role in the development of human diseases, including ischaemia/reperfusion injury, insulin resistance and diabetes, atherogenesis, septic shock and ovarian failure.	Ceramides	42-50	insulin	Homo sapiens	152-159
9815065-13	1998	In cultured rat aortic vascular smooth muscle cells, TNF-alpha (10(-7) g/ml) increased intracellular ceramide 1.5-fold over basal level (0.08 nmol/mg protein), which was blocked by the PLA2 antagonist DEDA (50 microM).	Ceramides	101-109	phospholipase A2 group IB	Rattus norvegicus	185-189
9815065-14	1998	We conclude that PLA2 activation and increased ceramide generation play a role in mediating TNF-alpha-induced endothelium-independent vasodilation.	Ceramides	47-55	tumor necrosis factor	Rattus norvegicus	92-101
9806545-3	1998	We also found that Pml is essential for induction of programmed cell death by Fas, tumour necrosis factor alpha (TNF), ceramide and type I and II interferons (IFNs).	Ceramides	119-127	promyelocytic leukemia	Mus musculus	19-22
9810003-8	1998	Ceramide generation occurred in all three variants in response to TNF-alpha treatment, with MCF-7 N cells expressing the greatest increase.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	66-75
9810003-13	1998	Taken together, these results suggest that differences in susceptibility to TNF-alpha-induced apoptosis among MCF-7 breast cancer cell variants may be explained by differences in TNFR expression, ceramide generation, differential expression of the Bcl-2 family of proteins, and protease activation.	Ceramides	196-204	tumor necrosis factor	Homo sapiens	76-85
9884018-6	1998	Recent investigations link ceramide and its analogues to the extracellular signal-regulated kinase (ERK) cascade, stress-activated protein kinase-c-Jun kinase (SAPK/JNK) cascade and apoptotic responses.	Ceramides	27-35	mitogen-activated protein kinase 1	Homo sapiens	61-98
9884018-6	1998	Recent investigations link ceramide and its analogues to the extracellular signal-regulated kinase (ERK) cascade, stress-activated protein kinase-c-Jun kinase (SAPK/JNK) cascade and apoptotic responses.	Ceramides	27-35	mitogen-activated protein kinase 1	Homo sapiens	100-103
9884018-6	1998	Recent investigations link ceramide and its analogues to the extracellular signal-regulated kinase (ERK) cascade, stress-activated protein kinase-c-Jun kinase (SAPK/JNK) cascade and apoptotic responses.	Ceramides	27-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	146-151
9884018-6	1998	Recent investigations link ceramide and its analogues to the extracellular signal-regulated kinase (ERK) cascade, stress-activated protein kinase-c-Jun kinase (SAPK/JNK) cascade and apoptotic responses.	Ceramides	27-35	mitogen-activated protein kinase 8	Homo sapiens	165-168
9884019-2	1998	Diverse kinds of stresses (ultraviolet, irradiation, heat shock and hypoxia) and biological factors (TNF-alpha, IFN-gamma and Fas antibody) require ceramide generation to execute apoptosis.	Ceramides	148-156	tumor necrosis factor	Homo sapiens	101-110
9884019-2	1998	Diverse kinds of stresses (ultraviolet, irradiation, heat shock and hypoxia) and biological factors (TNF-alpha, IFN-gamma and Fas antibody) require ceramide generation to execute apoptosis.	Ceramides	148-156	interferon gamma	Homo sapiens	112-121
9786978-0	1998	Ceramide inhibits inwardly rectifying K+ currents via a Ras- and Raf-1-dependent pathway in cultured oligodendrocytes.	Ceramides	0-8	Raf-1 proto-oncogene, serine/threonine kinase	Rattus norvegicus	65-70
9822324-11	1998	CONCLUSIONS: Human milk bile salt-stimulated milk lipase hydrolyses ceramide and may thus have a role in sphingomyelin digestion, but only after initial hydrolysis to ceramide and phosphorylcholine.	Ceramides	68-76	carboxyl ester lipase	Homo sapiens	45-56
9822324-11	1998	CONCLUSIONS: Human milk bile salt-stimulated milk lipase hydrolyses ceramide and may thus have a role in sphingomyelin digestion, but only after initial hydrolysis to ceramide and phosphorylcholine.	Ceramides	167-175	carboxyl ester lipase	Homo sapiens	45-56
9804618-10	1998	Moreover, the cell-permeable ceramide analog D-erythro-N-octanoylsphingosine, as well as exogenous sphingomyelinase, were able in turn to stimulate MAPK activity, to increase the amount of Raf-1 bound to the particulate cell fraction, and to stimulate glucose metabolism.	Ceramides	29-37	Raf-1 proto-oncogene, serine/threonine kinase	Rattus norvegicus	189-194
9794425-0	1998	Proapoptotic activity of a Trypanosoma cruzi ceramide-containing glycolipid turned on in host macrophages by IFN-gamma.	Ceramides	45-53	interferon gamma	Mus musculus	109-118
9786886-2	1998	A previous study reported that Rpr expression induced generation of the lipid second messenger ceramide and through use of the peptide caspase inhibitor N-benzyloxycarbonyl-VAD-fluoromethylketone(zVAD.fmk ) ordered ceramide generation downstream of caspases in SL2 cells (Pronk, G. J. , Ramer, K., Amiri, P., and Williams, L. T. (1996) Science 271, 808-810).	Ceramides	215-223	reaper	Drosophila melanogaster	31-34
9786886-0	1998	Ceramide generation by the Reaper protein is not blocked by the caspase inhibitor, p35.	Ceramides	0-8	reaper	Drosophila melanogaster	27-33
9786886-2	1998	A previous study reported that Rpr expression induced generation of the lipid second messenger ceramide and through use of the peptide caspase inhibitor N-benzyloxycarbonyl-VAD-fluoromethylketone(zVAD.fmk ) ordered ceramide generation downstream of caspases in SL2 cells (Pronk, G. J. , Ramer, K., Amiri, P., and Williams, L. T. (1996) Science 271, 808-810).	Ceramides	95-103	reaper	Drosophila melanogaster	31-34
9786886-2	1998	A previous study reported that Rpr expression induced generation of the lipid second messenger ceramide and through use of the peptide caspase inhibitor N-benzyloxycarbonyl-VAD-fluoromethylketone(zVAD.fmk ) ordered ceramide generation downstream of caspases in SL2 cells (Pronk, G. J. , Ramer, K., Amiri, P., and Williams, L. T. (1996) Science 271, 808-810).	Ceramides	215-223	Death caspase-1	Drosophila melanogaster	135-142
9786905-7	1998	We also demonstrated that JNK activation does not require ceramide generation since in MCF7 cells transfected with a dominant-negative derivative of FADD (FADD-DN), which are resistant to the cytotoxic action of TNF, TNF induced JNK activation in the absence of ceramide generation.	Ceramides	262-270	mitogen-activated protein kinase 8	Homo sapiens	26-29
9786905-7	1998	We also demonstrated that JNK activation does not require ceramide generation since in MCF7 cells transfected with a dominant-negative derivative of FADD (FADD-DN), which are resistant to the cytotoxic action of TNF, TNF induced JNK activation in the absence of ceramide generation.	Ceramides	262-270	Fas associated via death domain	Homo sapiens	149-153
9786905-7	1998	We also demonstrated that JNK activation does not require ceramide generation since in MCF7 cells transfected with a dominant-negative derivative of FADD (FADD-DN), which are resistant to the cytotoxic action of TNF, TNF induced JNK activation in the absence of ceramide generation.	Ceramides	262-270	Fas associated via death domain	Homo sapiens	155-162
9786886-4	1998	Following copper addition, Rpr protein was detected at 1.5 h and maximal at 2.5 h. Ceramide generation and caspase activation occurred nearly simultaneously, each detectable at 2-2.5 h and maximal at 6 h. Ceramide levels increased from a base line of 5 pmol/nmol lipid phosphorus to a maximum of 10 pmol/nmol lipid phosphorus.	Ceramides	205-213	reaper	Drosophila melanogaster	27-30
9786886-9	1998	These data show that Rpr-induced ceramide generation is upstream or independent of p35-inhibitable caspases and demonstrate differences in the actions of peptide and p35 caspase inhibitors.	Ceramides	33-41	reaper	Drosophila melanogaster	21-24
9756500-0	1998	Src kinase and PI 3-kinase as a transduction pathway in ceramide-induced contraction of colonic smooth muscle.	Ceramides	56-64	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-3
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.	Ceramides	37-45	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	129-154
9756500-2	1998	C2 ceramide induced a rapid increase in Src kinase activity within 15 s, peaked at 1 min, and was sustained up to 8 min.	Ceramides	3-11	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	40-43
9756500-4	1998	Immunoblotting using a phosphospecific anti-Src (416Y) antibody showed a ceramide-induced increase in pp60(src) tyrosine phosphorylation.	Ceramides	73-81	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	44-47
9756500-4	1998	Immunoblotting using a phosphospecific anti-Src (416Y) antibody showed a ceramide-induced increase in pp60(src) tyrosine phosphorylation.	Ceramides	73-81	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	107-110
9756500-5	1998	Immunoprecipitation using an anti-phosphotyrosine antibody followed by Western immunoblotting using a monoclonal IgG anti-phosphoinositide 3-kinase NH2 terminal-SH2 domain antibody showed a ceramide-induced increase in phosphoinositide 3-kinase (PI 3-kinase) tyrosine phosphorylation at a protein mass corresponding to 85 kDa, the regulatory subunit of PI 3-kinase, which contains the Src kinase binding site.	Ceramides	190-198	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	385-388
9756500-8	1998	In summary, we found that 1) the maintenance of sustained contraction is dependent on extracellular Ca2+; 2) ceramide activates a nonreceptor tyrosine kinase pathway through activation of pp60(src) and PI 3-kinase; and 3) the converging signals are probably through activation of MAP kinase.	Ceramides	109-117	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	193-196
9844818-3	1998	We demonstrate that despite this property, Bcr-Abl transformed cells (primitive hematopoietic progenitors or cell lines) remains sensitive to apoptosis induced by Ceramides analogues.	Ceramides	163-172	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	43-50
9763522-18	1998	N-SMase hydrolyzes sphingomyelin into ceramide and phosphocholine.	Ceramides	38-46	sphingomyelin phosphodiesterase 2	Homo sapiens	0-7
10203695-5	1998	Apoptosis induced by exogenous ceramide resembles CD95-mediated apoptosis in that bcl-2 is protective but differs in that NDGA and crm-A have no effect and in that cycloheximide (CHX) inhibits rather than potentiates ceramide-induced cell death.	Ceramides	31-39	Fas cell surface death receptor	Homo sapiens	50-54
10203695-5	1998	Apoptosis induced by exogenous ceramide resembles CD95-mediated apoptosis in that bcl-2 is protective but differs in that NDGA and crm-A have no effect and in that cycloheximide (CHX) inhibits rather than potentiates ceramide-induced cell death.	Ceramides	31-39	BCL2 apoptosis regulator	Homo sapiens	82-87
9788279-4	1998	Treatment with ceramide or its analogues increased survival, both in the presence and absence of NGF.	Ceramides	15-23	nerve growth factor	Mus musculus	97-100
9788279-6	1998	In the presence of the ceramidase inhibitor N-oleoyl ethanolamine, which blocks conversion of ceramide to sphingosine, the addition of natural ceramide-induced cell death, even in the presence of nerve growth factor (NGF).	Ceramides	143-151	nerve growth factor	Mus musculus	217-220
9806330-10	1998	Ceramide, reported to activate on okadaic acid-sensitive phosphatase, mimicked the effects of IGF-1.	Ceramides	0-8	insulin-like growth factor 1	Rattus norvegicus	94-99
9844818-5	1998	In addition to the classical features of apoptosis, we observed that Ceramide-treated CML cells display a rapid and sequential activation of the Bcr-Abl and PI3 kinases.	Ceramides	69-77	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	145-152
9844818-6	1998	We then demonstrated the role of the Bcr-Abl kinase activity in the accelerated response observed in CML cells treated by Ceramide.	Ceramides	122-130	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	37-44
9844818-9	1998	Taken together these results support the hypothesis of at least two independent signaling pathways initiating programmed cell death: one will be involved in apoptosis mediated by signals such as cytokine-starving is blocked by the Bcr-Abl fusion protein while the other one initiated by Ceramide is accelerated by the Bcr-Abl protein.	Ceramides	287-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	231-238
9844818-9	1998	Taken together these results support the hypothesis of at least two independent signaling pathways initiating programmed cell death: one will be involved in apoptosis mediated by signals such as cytokine-starving is blocked by the Bcr-Abl fusion protein while the other one initiated by Ceramide is accelerated by the Bcr-Abl protein.	Ceramides	287-295	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	318-325
9771892-3	1998	Treatment of cells with diverse apoptotic stimuli including TNF, anti-Fas, anticancer drugs, gamma-radiation or ceramide leads to rapid proteolytic cleavage of the 160-kDa form of kinectin to a 120-kDa fragment.	Ceramides	112-120	kinectin 1	Homo sapiens	180-188
9788256-3	1998	Anthroyl derivatives of ceramide and dihydroceramide containing C16, C18, C20, C22, and C24 saturated N-acyl chain could be completely separated to each molecular species by reversed-phase HPLC equipped with fluorescence detector, although some ceramide molecular species containing monoenoic acyl chain were eluted together with saturated dihydroceramide species.	Ceramides	24-32	Bardet-Biedl syndrome 9	Homo sapiens	69-72
9788256-3	1998	Anthroyl derivatives of ceramide and dihydroceramide containing C16, C18, C20, C22, and C24 saturated N-acyl chain could be completely separated to each molecular species by reversed-phase HPLC equipped with fluorescence detector, although some ceramide molecular species containing monoenoic acyl chain were eluted together with saturated dihydroceramide species.	Ceramides	44-52	Bardet-Biedl syndrome 9	Homo sapiens	69-72
9710629-9	1998	These studies demonstrate ceramide"s capacity to inhibit activation of Akt and imply that this is a mechanism of antagonism of insulin-dependent physiological events, such as the peripheral activation of glucose transport and the suppression of apoptosis.	Ceramides	26-34	AKT serine/threonine kinase 1	Homo sapiens	71-74
9743347-5	1998	IL-13 also inhibited NF-kappa B activation by LPS, okadaic acid, H2O2, and ceramide.	Ceramides	75-83	interleukin 13	Homo sapiens	0-5
9743347-5	1998	IL-13 also inhibited NF-kappa B activation by LPS, okadaic acid, H2O2, and ceramide.	Ceramides	75-83	nuclear factor kappa B subunit 1	Homo sapiens	21-31
9743348-5	1998	It also suppressed NF-kappa B activation induced by LPS, okadaic acid, and ceramide.	Ceramides	75-83	nuclear factor kappa B subunit 1	Homo sapiens	19-29
9770326-0	1998	Acid sphingomyelinase-derived ceramide is not required for inflammatory cytokine signalling in murine macrophages.	Ceramides	30-38	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
9727376-10	1998	Exogenous C20:4, as well as PLA2 (in doses simulating Fe-induced deacylation) recapitulated Fe"s ceramide-generating effect.	Ceramides	97-105	phospholipase A2 group IB	Homo sapiens	28-32
9727376-13	1998	CONCLUSIONS: (1) ceramide accumulation during acute cell injury can be an adaptive response to PLA2 activation/C20:4 generation; (2) C20:4-induced ceramidase inhibition, coupled with SMase stimulation, may trigger this result; and (3) these ceramide increments may exert a "biostat" function, helping to offset C20:4/PLA2- and "catalytic" iron-mediated tubular cell death.	Ceramides	17-25	phospholipase A2 group IB	Homo sapiens	95-99
9727376-13	1998	CONCLUSIONS: (1) ceramide accumulation during acute cell injury can be an adaptive response to PLA2 activation/C20:4 generation; (2) C20:4-induced ceramidase inhibition, coupled with SMase stimulation, may trigger this result; and (3) these ceramide increments may exert a "biostat" function, helping to offset C20:4/PLA2- and "catalytic" iron-mediated tubular cell death.	Ceramides	17-25	phospholipase A2 group IB	Homo sapiens	317-321
9725248-3	1998	Both LPS and the cell-permeable ceramide analogue, C2 ceramide, induced significant cell death in IFN-gamma-activated, thioglycollate-elicited peritoneal macrophages after 48 and 24 h, respectively.	Ceramides	32-40	interferon gamma	Mus musculus	98-107
9725248-3	1998	Both LPS and the cell-permeable ceramide analogue, C2 ceramide, induced significant cell death in IFN-gamma-activated, thioglycollate-elicited peritoneal macrophages after 48 and 24 h, respectively.	Ceramides	54-62	interferon gamma	Mus musculus	98-107
9710629-0	1998	Regulation of insulin-stimulated glucose transporter GLUT4 translocation and Akt kinase activity by ceramide.	Ceramides	100-108	insulin	Homo sapiens	14-21
9710629-0	1998	Regulation of insulin-stimulated glucose transporter GLUT4 translocation and Akt kinase activity by ceramide.	Ceramides	100-108	solute carrier family 2 member 4	Homo sapiens	53-58
9710629-0	1998	Regulation of insulin-stimulated glucose transporter GLUT4 translocation and Akt kinase activity by ceramide.	Ceramides	100-108	AKT serine/threonine kinase 1	Homo sapiens	77-80
9710629-2	1998	Recently published reports indicate that ceramide levels are elevated in insulin-responsive tissues of diabetic animals and that agents which trigger ceramide production inhibit insulin signaling.	Ceramides	41-49	insulin	Homo sapiens	73-80
9710629-2	1998	Recently published reports indicate that ceramide levels are elevated in insulin-responsive tissues of diabetic animals and that agents which trigger ceramide production inhibit insulin signaling.	Ceramides	41-49	insulin	Homo sapiens	178-185
9716505-11	1998	These results demonstrate for the first time changes in ceramide during cell cycle progression and suggest that ceramide synthesized de novo might function as an endogenous modulator of Rb protein and cell cycle progression.	Ceramides	56-64	RB transcriptional corepressor 1	Homo sapiens	186-188
9716505-11	1998	These results demonstrate for the first time changes in ceramide during cell cycle progression and suggest that ceramide synthesized de novo might function as an endogenous modulator of Rb protein and cell cycle progression.	Ceramides	112-120	RB transcriptional corepressor 1	Homo sapiens	186-188
9786425-10	1998	We conclude that events downstream of tyrosine phosphorylation and upstream of CPP32 activation, including tyrosine dephosphorylation and possibly ceramide generation, are sensitive to regulation by redox in human NK cells, requiring a reducing environment for optimal protection from apoptosis induced by Fas ligation.	Ceramides	147-155	caspase 3	Homo sapiens	79-84
9736250-0	1998	Identification of ceramide targets in interleukin-1 and tumor necrosis factor-alpha signaling in mesangial cells.	Ceramides	18-26	interleukin 1 alpha	Homo sapiens	38-83
9736250-4	1998	Ceramide was found to bind specifically to and activate protein kinase c-Raf, leading to subsequent activation of the extracellular signal-regulated kinase (ERK) module in mesangial cells.	Ceramides	0-8	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	71-76
9736250-4	1998	Ceramide was found to bind specifically to and activate protein kinase c-Raf, leading to subsequent activation of the extracellular signal-regulated kinase (ERK) module in mesangial cells.	Ceramides	0-8	mitogen-activated protein kinase 1	Homo sapiens	118-155
9736250-4	1998	Ceramide was found to bind specifically to and activate protein kinase c-Raf, leading to subsequent activation of the extracellular signal-regulated kinase (ERK) module in mesangial cells.	Ceramides	0-8	mitogen-activated protein kinase 1	Homo sapiens	157-160
9710629-2	1998	Recently published reports indicate that ceramide levels are elevated in insulin-responsive tissues of diabetic animals and that agents which trigger ceramide production inhibit insulin signaling.	Ceramides	150-158	insulin	Homo sapiens	178-185
9710629-3	1998	In the present series of studies, the short-chain ceramide analog C2-ceramide inhibited insulin-stimulated glucose transport by approximately 50% in 3T3-L1 adipocytes, with similar reductions in hormone-stimulated translocation of the insulin-responsive glucose transporter (GLUT4) and insulin-responsive aminopeptidase.	Ceramides	50-58	insulin	Homo sapiens	88-95
9710629-9	1998	These studies demonstrate ceramide"s capacity to inhibit activation of Akt and imply that this is a mechanism of antagonism of insulin-dependent physiological events, such as the peripheral activation of glucose transport and the suppression of apoptosis.	Ceramides	26-34	insulin	Homo sapiens	127-134
9685387-3	1998	Treatment of rat primary astrocytes with tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta led to marked alteration in cellular redox (decrease in intracellular GSH) and rapid degradation of SM to ceramide.	Ceramides	208-216	tumor necrosis factor	Rattus norvegicus	41-68
9705322-8	1998	SDK1 is a serine kinase with molecular mass 50-60 kDa that is strongly activated by N, N"-dimethylsphingosine and sphingosine, but not by ceramide, sphingosine 1-phosphate, or other sphingo-, phospho-, or glycerolipids tested.	Ceramides	138-146	sidekick cell adhesion molecule 1	Mus musculus	0-4
9712041-7	1998	Granulysin- and ceramide-induced apoptosis are similar in that they both are only minimally inhibited by the more selective cysteine protease p32 (caspase 3)-like caspase inhibitor N-acetyl-Asp-Glu-Val-Asp aldehyde, while they are significantly inhibited by the more general caspase inhibitor benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (Z-VAD-fmk).	Ceramides	16-24	inhibitor of growth family member 2	Homo sapiens	142-145
9712041-10	1998	These data indicate that granulysin induces target cell death by both ceramide- and caspase-dependent and -independent pathways.	Ceramides	70-78	granulysin	Homo sapiens	25-35
9685387-3	1998	Treatment of rat primary astrocytes with tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta led to marked alteration in cellular redox (decrease in intracellular GSH) and rapid degradation of SM to ceramide.	Ceramides	208-216	tumor necrosis factor	Rattus norvegicus	70-79
9685387-3	1998	Treatment of rat primary astrocytes with tumor necrosis factor-alpha (TNF-alpha) or interleukin-1beta led to marked alteration in cellular redox (decrease in intracellular GSH) and rapid degradation of SM to ceramide.	Ceramides	208-216	interleukin 1 beta	Rattus norvegicus	84-101
9699644-3	1998	Exposure to PEdelta53L/TGF-alpha/KDEL decreases the apoptotic threshold through protein synthesis inhibition and simultaneous production of ceramide in tumor cells that lack functional p53 protein.	Ceramides	140-148	transforming growth factor alpha	Homo sapiens	23-32
9716456-0	1998	L-selectin stimulates the neutral sphingomyelinase and induces release of ceramide.	Ceramides	74-82	selectin L	Homo sapiens	0-10
9686602-2	1998	Both PMA and the cell-permeable ceramide, C2-ceramide, caused differentiation of U937 cells, but with distinct cell morphology and CD11b/CD14 surface expression.	Ceramides	32-40	integrin subunit alpha M	Homo sapiens	131-136
9797556-0	1998	Ceramide, a mediator of interleukin 1, tumour necrosis factor alpha, as well as Fas receptor signalling, induces apoptosis of rheumatoid arthritis synovial cells.	Ceramides	0-8	interleukin 1 alpha	Homo sapiens	24-67
9797556-1	1998	OBJECTIVES: To examine the effects of ceramide, which is a lipid second messenger of cell surface receptors, including tumour necrosis factor alpha (TNF alpha), interleukin 1 (IL1), and Fas receptors, on rheumatoid arthritis (RA) synovial cells.	Ceramides	38-46	tumor necrosis factor	Homo sapiens	149-158
9686602-2	1998	Both PMA and the cell-permeable ceramide, C2-ceramide, caused differentiation of U937 cells, but with distinct cell morphology and CD11b/CD14 surface expression.	Ceramides	32-40	CD14 molecule	Homo sapiens	137-141
9681467-4	1998	However, treatment of PC12 cells with C2-ceramide, an analogue of ceramide, the endogenous product produced by the activity of p75NTR-activated sphingomyelinase, mimicked the effects of NGF on cell morphology and stimulation of both APP mRNA levels and APP secretion.	Ceramides	41-49	nerve growth factor receptor	Rattus norvegicus	127-133
9681439-2	1998	Because ceramide is also able to induce NGF secretion and because TNF alpha is a known agonist of the sphingomyelin (SPM)-ceramide pathway, we investigated whether the TNF alpha-induced NGF secretion by primary astrocytes is mediated by ceramide.	Ceramides	8-16	nerve growth factor	Rattus norvegicus	40-43
9681439-4	1998	In marked contrast, inhibition of MAPK counteracted the NGF secretion induced by ceramide.	Ceramides	81-89	nerve growth factor	Rattus norvegicus	56-59
9657974-2	1998	Binding of tumour necrosis factor (TNF) to its 55 kDa receptor (TR55) leads to the generation of ceramide through activation of either acid or neutral sphingomyelinase (A/N-SMase) as well as to potent activation of SAPK/JNK.	Ceramides	97-105	tumor necrosis factor	Mus musculus	11-33
9681439-9	1998	Altogether, our data strongly suggest that TNF alpha-mediated up-regulation of NGF occurs independently of ceramide generation.	Ceramides	107-115	tumor necrosis factor	Rattus norvegicus	43-52
9746206-9	1998	Sphingomyelinase and interleukin-1beta, which are known to activate the sphingomyelin turnover leading to ceramide generation, also induced apoptosis mimicking the effects of ceramide.	Ceramides	106-114	interleukin 1 beta	Homo sapiens	21-38
9746206-9	1998	Sphingomyelinase and interleukin-1beta, which are known to activate the sphingomyelin turnover leading to ceramide generation, also induced apoptosis mimicking the effects of ceramide.	Ceramides	175-183	interleukin 1 beta	Homo sapiens	21-38
9657740-8	1998	Levels of ceramide, a lipid mediator of apoptosis, were measured at 2, 4, 8, 10, and 60 minutes after treatment with ionizing radiation and were substantially reduced in TF-1 cells rescued from apoptosis by GM-CSF compared with apoptotic TF-1 cells.	Ceramides	10-18	colony stimulating factor 2	Homo sapiens	207-213
9657740-9	1998	The largest decrease in ceramide production seen was at 4 minutes postirradiation, with a 46% reduction in ceramide levels in TF-1 cells rescued from apoptosis by GM-CSF compared with those in apoptotic TF-1 cells.	Ceramides	24-32	colony stimulating factor 2	Homo sapiens	163-169
9657740-9	1998	The largest decrease in ceramide production seen was at 4 minutes postirradiation, with a 46% reduction in ceramide levels in TF-1 cells rescued from apoptosis by GM-CSF compared with those in apoptotic TF-1 cells.	Ceramides	107-115	colony stimulating factor 2	Homo sapiens	163-169
9657740-10	1998	Because ceramide has been shown to affect PKCalpha subcellular distribution, these data implicate a role for ceramide in mediating the rapid postirradiation translocation and inhibition of PKCalpha in TF-1 cells not rescued from apoptosis by GM-CSF.	Ceramides	8-16	protein kinase C alpha	Homo sapiens	42-50
9657740-10	1998	Because ceramide has been shown to affect PKCalpha subcellular distribution, these data implicate a role for ceramide in mediating the rapid postirradiation translocation and inhibition of PKCalpha in TF-1 cells not rescued from apoptosis by GM-CSF.	Ceramides	109-117	protein kinase C alpha	Homo sapiens	189-197
9657740-10	1998	Because ceramide has been shown to affect PKCalpha subcellular distribution, these data implicate a role for ceramide in mediating the rapid postirradiation translocation and inhibition of PKCalpha in TF-1 cells not rescued from apoptosis by GM-CSF.	Ceramides	109-117	colony stimulating factor 2	Homo sapiens	242-248
9651362-6	1998	Preceding apoptosis is a TNF-alpha-induced increase in neuronal ceramide levels.	Ceramides	64-72	tumor necrosis factor	Homo sapiens	25-34
9651377-10	1998	Together, these data indicate that involucrin, envoplakin, periplakin, and possibly other structural proteins serve as substrates for the attachment of ceramides by ester linkages to the CE for barrier function in human epidermis.	Ceramides	152-161	involucrin	Homo sapiens	35-45
9651377-10	1998	Together, these data indicate that involucrin, envoplakin, periplakin, and possibly other structural proteins serve as substrates for the attachment of ceramides by ester linkages to the CE for barrier function in human epidermis.	Ceramides	152-161	envoplakin	Homo sapiens	47-57
9642282-4	1998	Cells expressing constitutive HSP72 were shown to have significantly reduced levels of apoptosis after heat, TNFalpha, and ceramide but not after ionizing radiation.	Ceramides	123-131	heat shock protein 1A	Mus musculus	30-35
9649498-4	1998	Ceramide inhibition of PI(3)K is dependent on acid-sphingomyelinase.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	46-67
9649498-5	1998	Down-regulation of PI(3)K by ceramide results in inhibition of the kinase Akt and decreased phosphorylation of the death effector Bad.	Ceramides	29-37	AKT serine/threonine kinase 1	Homo sapiens	74-77
9648862-0	1998	Neurotrophic factors prevent ceramide-induced apoptosis downstream of c-Jun N-terminal kinase activation in PC12 cells.	Ceramides	29-37	mitogen-activated protein kinase 8	Rattus norvegicus	70-93
9648862-3	1998	Ceramide-induced apoptosis was inhibited by nerve growth factor, basic fibroblast growth factor, pituitary adenylyl cyclase-activating peptide, 4-(8-chlorophenylthio)cyclic AMP, and the caspase inhibitor benzyloxycarbonyl-Val-Ala-DL-Asp fluoromethyl ketone (zVAD-FMK).	Ceramides	0-8	nerve growth factor	Rattus norvegicus	44-63
9648862-5	1998	Treatment of PC12 cells with ceramide resulted in a time-dependent increase in JNK activity.	Ceramides	29-37	mitogen-activated protein kinase 8	Rattus norvegicus	79-82
9648862-8	1998	These results indicate that ceramide-induced JNK activation is an early event and may be required for the expression of essential components of the apoptotic machinery.	Ceramides	28-36	mitogen-activated protein kinase 8	Rattus norvegicus	45-48
9648862-9	1998	It is anticipated that neurotrophic factors inhibit ceramide-induced apoptosis by affecting signaling events downstream of JNK activation.	Ceramides	52-60	mitogen-activated protein kinase 8	Rattus norvegicus	123-126
9648886-8	1998	Furthermore, cell-permeable ceramide acted synergistically with the neurotrophin family, which has been previously shown to support Purkinje cell survival.	Ceramides	28-36	brain derived neurotrophic factor	Homo sapiens	68-80
9679455-2	1998	We have shown that photodynamic treatment (PDT), using the phthalocyanine photosensitizer Pc 4 (HOSiPcOSi[CH3]2[CH2]3N[CH3]2), causes increased ceramide generation and subsequent induction of apoptosis in L5178Y-R (LY-R) mouse lymphoma cells.	Ceramides	144-152	proprotein convertase subtilisin/kexin type 4	Mus musculus	90-94
9632721-0	1998	Involvement of de novo ceramide biosynthesis in tumor necrosis factor-alpha/cycloheximide-induced cerebral endothelial cell death.	Ceramides	23-31	tumor necrosis factor	Bos taurus	48-75
9632721-1	1998	Cytokines, including tumor necrosis factor-alpha (TNF-alpha), may elicit cytotoxic response through the sphingomyelin-ceramide signal transduction pathway by activation of sphingomyelinases and the subsequent release of ceramide: the universal lipid second messenger.	Ceramides	118-126	tumor necrosis factor	Bos taurus	21-48
9632721-1	1998	Cytokines, including tumor necrosis factor-alpha (TNF-alpha), may elicit cytotoxic response through the sphingomyelin-ceramide signal transduction pathway by activation of sphingomyelinases and the subsequent release of ceramide: the universal lipid second messenger.	Ceramides	118-126	tumor necrosis factor	Bos taurus	50-59
9632721-1	1998	Cytokines, including tumor necrosis factor-alpha (TNF-alpha), may elicit cytotoxic response through the sphingomyelin-ceramide signal transduction pathway by activation of sphingomyelinases and the subsequent release of ceramide: the universal lipid second messenger.	Ceramides	220-228	tumor necrosis factor	Bos taurus	21-48
9632721-1	1998	Cytokines, including tumor necrosis factor-alpha (TNF-alpha), may elicit cytotoxic response through the sphingomyelin-ceramide signal transduction pathway by activation of sphingomyelinases and the subsequent release of ceramide: the universal lipid second messenger.	Ceramides	220-228	tumor necrosis factor	Bos taurus	50-59
9632721-2	1998	Treatment of bovine cerebral endothelial cells (BCECs) with TNF-alpha for 16 h followed by cycloheximide (CHX) for 6 h resulted in an increase in ceramide accumulation, DNA fragmentation, and cell death.	Ceramides	146-154	tumor necrosis factor	Bos taurus	60-69
9632721-4	1998	TNF-alpha/CHX-mediated ceramide production apparently is not a result of sphingomyelin hydrolysis because sphingomyelin content does not decrease in this death paradigm.	Ceramides	23-31	tumor necrosis factor	Bos taurus	0-9
9632721-6	1998	However, addition of fumonisin B1, a selective ceramide synthase inhibitor, attenuated TNF-alpha/CHX-induced intracellular ceramide elevation and BCEC death.	Ceramides	47-55	tumor necrosis factor	Bos taurus	87-96
9632721-8	1998	Our results show, for the first time, that ceramide derived from de novo synthesis is an alternative mechanism to sphingomyelin hydrolysis in the BCEC death process initiated by TNF-alpha/CHX.	Ceramides	43-51	tumor necrosis factor	Bos taurus	178-187
9632728-0	1998	Inhibition of Akt kinase by cell-permeable ceramide and its implications for ceramide-induced apoptosis.	Ceramides	43-51	thymoma viral proto-oncogene 1	Mus musculus	14-17
9632728-0	1998	Inhibition of Akt kinase by cell-permeable ceramide and its implications for ceramide-induced apoptosis.	Ceramides	77-85	thymoma viral proto-oncogene 1	Mus musculus	14-17
9632728-3	1998	We investigated the possibility that ceramide may decrease antiapoptotic signaling in cells by inhibiting Akt kinase activity.	Ceramides	37-45	thymoma viral proto-oncogene 1	Mus musculus	106-109
9632728-5	1998	These results are consistent with decreased Akt kinase activity being involved in the apoptotic effects of ceramide.	Ceramides	107-115	thymoma viral proto-oncogene 1	Mus musculus	44-47
9632728-6	1998	This possibility is further supported by studies showing that constitutively active Akt kinase decreases C2-ceramide-induced death of HMN1 cells as well as COS-7 cells.	Ceramides	108-116	thymoma viral proto-oncogene 1	Mus musculus	84-87
9632728-9	1998	In sum, our results suggest that inhibition of the key antiapoptotic kinase, Akt, may play an important role in ceramide-induced apoptosis.	Ceramides	112-120	thymoma viral proto-oncogene 1	Mus musculus	77-80
9624136-0	1998	Ceramide activates NFkappaB by inducing the processing of p105.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	19-27
9624136-0	1998	Ceramide activates NFkappaB by inducing the processing of p105.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	58-62
9624136-1	1998	The role of ceramide as a second messenger in tumor necrosis factor (TNF)-mediated signal transduction has been much debated.	Ceramides	12-20	tumor necrosis factor	Homo sapiens	46-67
9624136-1	1998	The role of ceramide as a second messenger in tumor necrosis factor (TNF)-mediated signal transduction has been much debated.	Ceramides	12-20	tumor necrosis factor	Homo sapiens	69-72
9624136-3	1998	In this paper, we directly compare the effects of the cell-permeable ceramide analogue, N-acetylsphingosine (C2-ceramide), with TNF, on NFkappaB function, a transcription factor whose activation is central to many TNF-mediated effects.	Ceramides	69-77	nuclear factor kappa B subunit 1	Homo sapiens	136-144
9624136-3	1998	In this paper, we directly compare the effects of the cell-permeable ceramide analogue, N-acetylsphingosine (C2-ceramide), with TNF, on NFkappaB function, a transcription factor whose activation is central to many TNF-mediated effects.	Ceramides	69-77	tumor necrosis factor	Homo sapiens	214-217
9624136-6	1998	However, electrophoretic mobility shift analysis following cell stimulation with this ceramide analogue revealed a dose-responsive activation of NFkappaB, which was not apparent following cell treatment with the inactive dihydro form.	Ceramides	86-94	nuclear factor kappa B subunit 1	Homo sapiens	145-153
9624136-12	1998	Furthermore, the effect of TNF on NFkappaB activation was rapid, whereas C2-ceramide required an optimal treatment time of 1 h. Interestingly, TNF was found to increase ceramide in cells but only after a 1-h contact time.	Ceramides	76-84	tumor necrosis factor	Homo sapiens	143-146
9624136-13	1998	Our data therefore suggest that ceramide promotes the activation of NFkappaB complexes that lack transactivating activity by enhanced processing of p105.	Ceramides	32-40	nuclear factor kappa B subunit 1	Homo sapiens	68-76
9624136-13	1998	Our data therefore suggest that ceramide promotes the activation of NFkappaB complexes that lack transactivating activity by enhanced processing of p105.	Ceramides	32-40	nuclear factor kappa B subunit 1	Homo sapiens	148-152
9668339-2	1998	While ceramide has been shown to be an important regulatory component of apoptosis induced by tumor necrosis factor alpha and Fas ligand, sphingosine-1-phosphate (SPP), a further metabolite of ceramide, has been implicated as a second messenger in cellular proliferation and survival induced by platelet-derived growth factor, nerve growth factor, and serum.	Ceramides	6-14	tumor necrosis factor	Homo sapiens	94-121
9668339-2	1998	While ceramide has been shown to be an important regulatory component of apoptosis induced by tumor necrosis factor alpha and Fas ligand, sphingosine-1-phosphate (SPP), a further metabolite of ceramide, has been implicated as a second messenger in cellular proliferation and survival induced by platelet-derived growth factor, nerve growth factor, and serum.	Ceramides	6-14	Fas ligand	Homo sapiens	126-136
9668339-5	1998	We propose that the dynamic balance between levels of sphingolipid metabolites, ceramide, and SPP, and consequent regulation of different family members of mitogen-activated protein kinases (JNK versus ERK), is an important factor that determines whether a cell survives or dies.	Ceramides	80-88	mitogen-activated protein kinase 1	Homo sapiens	202-205
9668341-3	1998	In contrast, recent data suggest that neurotrophin-mediated death signals are generated through the interaction of nerve growth factor with the low-affinity neurotrophin receptor, p75NTR, Neurotrophins may signal through p75NTR by stimulating sphingomyelin hydrolysis and generating ceramide in primary cultures of neurons and glial cells as well as in fibroblasts heterologously expressing p75NTR.	Ceramides	283-291	brain derived neurotrophic factor	Homo sapiens	38-50
9668341-3	1998	In contrast, recent data suggest that neurotrophin-mediated death signals are generated through the interaction of nerve growth factor with the low-affinity neurotrophin receptor, p75NTR, Neurotrophins may signal through p75NTR by stimulating sphingomyelin hydrolysis and generating ceramide in primary cultures of neurons and glial cells as well as in fibroblasts heterologously expressing p75NTR.	Ceramides	283-291	nerve growth factor	Homo sapiens	115-134
9668341-3	1998	In contrast, recent data suggest that neurotrophin-mediated death signals are generated through the interaction of nerve growth factor with the low-affinity neurotrophin receptor, p75NTR, Neurotrophins may signal through p75NTR by stimulating sphingomyelin hydrolysis and generating ceramide in primary cultures of neurons and glial cells as well as in fibroblasts heterologously expressing p75NTR.	Ceramides	283-291	brain derived neurotrophic factor	Homo sapiens	157-169
9668341-3	1998	In contrast, recent data suggest that neurotrophin-mediated death signals are generated through the interaction of nerve growth factor with the low-affinity neurotrophin receptor, p75NTR, Neurotrophins may signal through p75NTR by stimulating sphingomyelin hydrolysis and generating ceramide in primary cultures of neurons and glial cells as well as in fibroblasts heterologously expressing p75NTR.	Ceramides	283-291	nerve growth factor receptor	Homo sapiens	180-186
9668341-3	1998	In contrast, recent data suggest that neurotrophin-mediated death signals are generated through the interaction of nerve growth factor with the low-affinity neurotrophin receptor, p75NTR, Neurotrophins may signal through p75NTR by stimulating sphingomyelin hydrolysis and generating ceramide in primary cultures of neurons and glial cells as well as in fibroblasts heterologously expressing p75NTR.	Ceramides	283-291	nerve growth factor receptor	Homo sapiens	221-227
9668341-3	1998	In contrast, recent data suggest that neurotrophin-mediated death signals are generated through the interaction of nerve growth factor with the low-affinity neurotrophin receptor, p75NTR, Neurotrophins may signal through p75NTR by stimulating sphingomyelin hydrolysis and generating ceramide in primary cultures of neurons and glial cells as well as in fibroblasts heterologously expressing p75NTR.	Ceramides	283-291	nerve growth factor receptor	Homo sapiens	221-227
9668341-4	1998	The biochemical characteristics of p75NTR-dependent ceramide generation are discussed relative to the role of ceramide in p75NTR-dependent apoptosis and the activation of NF-kappa B.	Ceramides	52-60	nerve growth factor receptor	Homo sapiens	35-41
9616175-8	1998	Phospholipase D (PLD) activity, which is a target of ceramide action and is required for phagocytosis, was also found primarily in the plasma membrane fractions of FMLP-activated and phagocytosing PMNs.	Ceramides	53-61	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	0-15
9616175-8	1998	Phospholipase D (PLD) activity, which is a target of ceramide action and is required for phagocytosis, was also found primarily in the plasma membrane fractions of FMLP-activated and phagocytosing PMNs.	Ceramides	53-61	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	17-20
9616175-9	1998	Our findings indicate that in human PMNs engaged in phagocytosis, the sphingomyelin cycle is restricted to the plasma membrane where intracellular targets of ceramide action, such as PLD, are localized.	Ceramides	158-166	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	183-186
10200497-4	1998	IL-1 increases beta-cell formation of NO, ceramide, prostaglandins, heat-shock proteins, and activates a protease.	Ceramides	42-50	interleukin 1 alpha	Homo sapiens	0-4
9660181-10	1998	Clusterin mRNA levels were strongly induced in pancreatic acinar AR4-2J cells in response to various apoptotic stimuli (i.e., cycloheximide, staurosporine, ceramide and H2O2) but not with interleukin (IL)-1, IL-4 or IL-6 or heat shock, which do not induce apoptosis in AR4-2J cells.	Ceramides	156-164	clusterin	Rattus norvegicus	0-9
9603985-1	1998	Galactosyltransferases are enzymes which transfer galactose from UDP-Gal to various acceptors with either retention of the anomeric configuration to form alpha1,2-, alpha1,3-, alpha1,4-, and alpha1, 6-linkages, or inversion of the anomeric configuration to form beta1, 3-, beta1,4-, and beta1-ceramide linkages.	Ceramides	293-301	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	262-270
9616231-6	1998	Activation of NF-kappaB and subsequent IL-8 expression in epithelial cells can result from activation of at least two pathways: an exogenous signaling cascade that is activated by ligation of ceramide-associated adhesins such as P. aeruginosa pilin, or endogenous stimulation, suggested to be a consequence of cell stress caused by the accumulation of mutant CFTR in the endoplasmic reticulum.	Ceramides	192-200	nuclear factor kappa B subunit 1	Homo sapiens	14-23
9616231-6	1998	Activation of NF-kappaB and subsequent IL-8 expression in epithelial cells can result from activation of at least two pathways: an exogenous signaling cascade that is activated by ligation of ceramide-associated adhesins such as P. aeruginosa pilin, or endogenous stimulation, suggested to be a consequence of cell stress caused by the accumulation of mutant CFTR in the endoplasmic reticulum.	Ceramides	192-200	CF transmembrane conductance regulator	Homo sapiens	359-363
12671299-12	1998	The exact mechanisms by which MAPK and caspases are activated by these agents are currently unknown, but may involve oxidative modification of glutathione (GSH) and/or protein thiols, and/or generation of secondary messengers, ceramide and calcium, which further activate downstream events.	Ceramides	227-235	mitogen-activated protein kinase 1	Homo sapiens	30-34
9593687-4	1998	Here we show that Nedd4, a ubiquitin-protein ligase containing multiple WW domains and a calcium/lipid-binding domain, is also cleaved during apoptosis induced by a variety of stimuli including Fas-ligation, gamma-radiation, tumor necrosis factor-alpha, C-8 ceramide, and etoposide treatment.	Ceramides	258-266	neural precursor cell expressed, developmentally down-regulated 4	Mus musculus	18-23
9593751-7	1998	HuT-78 cells were also resistant to NF-kappaB activation induced by phorbol ester, H2O2, ceramide, endotoxin, and interleukin-1.	Ceramides	89-97	nuclear factor kappa B subunit 1	Homo sapiens	36-45
9593754-6	1998	In cells overexpressing Cdx1 or Cdx2, tumorigenicity and resistance to apoptosis induced by serum starvation, ceramide, or staurosporine were not changed compared with control cells; yet phorbol ester-stimulated cell migration was decreased by 50%.	Ceramides	110-118	caudal type homeobox 1	Homo sapiens	24-28
9593754-6	1998	In cells overexpressing Cdx1 or Cdx2, tumorigenicity and resistance to apoptosis induced by serum starvation, ceramide, or staurosporine were not changed compared with control cells; yet phorbol ester-stimulated cell migration was decreased by 50%.	Ceramides	110-118	caudal type homeobox 2	Homo sapiens	32-36
9600936-3	1998	Ceramide, a lipid metabolite synthesized upon CD95 receptor triggering, also induces activation of ORCC in cell-attached patch clamp experiments.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	46-50
9582369-5	1998	Besides TNF, phorbol ester-, okadaic acid-, ceramide-, and lipopolysaccharide-induced activation of NF-kappaB was blocked by Mn-SOD, indicating a common pathway of activation.	Ceramides	44-52	nuclear factor kappa B subunit 1	Homo sapiens	100-109
9582369-5	1998	Besides TNF, phorbol ester-, okadaic acid-, ceramide-, and lipopolysaccharide-induced activation of NF-kappaB was blocked by Mn-SOD, indicating a common pathway of activation.	Ceramides	44-52	superoxide dismutase 2	Homo sapiens	125-131
9671089-1	1998	Ceramide, a novel sphingomyelin-derived second messenger mediates cellular signals of cytokines such as tumor necrosis factor-alpha (TNF-alpha).	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	104-131
9671089-1	1998	Ceramide, a novel sphingomyelin-derived second messenger mediates cellular signals of cytokines such as tumor necrosis factor-alpha (TNF-alpha).	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	133-142
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).	Ceramides	176-184	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-28
10200487-0	1998	The growth arrest and downregulation of c-myc transcription induced by ceramide are related events dependent on p21 induction, Rb underphosphorylation and E2F sequestering.	Ceramides	71-79	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	40-45
10200487-0	1998	The growth arrest and downregulation of c-myc transcription induced by ceramide are related events dependent on p21 induction, Rb underphosphorylation and E2F sequestering.	Ceramides	71-79	cyclin dependent kinase inhibitor 1A	Homo sapiens	112-115
10200487-2	1998	Ceramide has been shown to induce growth inhibition, c-myc downmodulation and apoptosis.	Ceramides	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	53-58
10200487-6	1998	Ceramide was also capable of inhibiting the transcriptional activity of a CAT reporter vector driven by E2F binding sites containing c-myc promoter transfected into Hs 27 cells.	Ceramides	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	133-138
10200487-7	1998	The requirement of the pRb protein for ceramide-induced c-myc downregulation was supported by the failure of ceramide to inhibit promoter activity in HeLa cells, in which pRb function is abrogated by the presence of the E7 Papilloma virus oncoprotein, and in pRb-deleted SAOS2 AT cells.	Ceramides	39-47	RB transcriptional corepressor 1	Homo sapiens	23-26
10200487-7	1998	The requirement of the pRb protein for ceramide-induced c-myc downregulation was supported by the failure of ceramide to inhibit promoter activity in HeLa cells, in which pRb function is abrogated by the presence of the E7 Papilloma virus oncoprotein, and in pRb-deleted SAOS2 AT cells.	Ceramides	39-47	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	56-61
10200487-7	1998	The requirement of the pRb protein for ceramide-induced c-myc downregulation was supported by the failure of ceramide to inhibit promoter activity in HeLa cells, in which pRb function is abrogated by the presence of the E7 Papilloma virus oncoprotein, and in pRb-deleted SAOS2 AT cells.	Ceramides	39-47	RB transcriptional corepressor 1	Homo sapiens	171-174
10200487-7	1998	The requirement of the pRb protein for ceramide-induced c-myc downregulation was supported by the failure of ceramide to inhibit promoter activity in HeLa cells, in which pRb function is abrogated by the presence of the E7 Papilloma virus oncoprotein, and in pRb-deleted SAOS2 AT cells.	Ceramides	39-47	RB transcriptional corepressor 1	Homo sapiens	171-174
10200487-8	1998	Ceramide-induced downregulation of the c-myc promoter was restored in SAOS2 #1 cells in which a functional Rb gene was reintroduced.	Ceramides	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	39-44
10200487-9	1998	Our studies demonstrate that pRb dephosphorylation, induced by ceramide, is at least partly necessary for c-myc downregulation, and therefore the CDK-Rb-E2F pathway appears to be a target for the ceramide-induced modulation of cell cycle regulated gene transcription.	Ceramides	63-71	RB transcriptional corepressor 1	Homo sapiens	29-32
10200487-9	1998	Our studies demonstrate that pRb dephosphorylation, induced by ceramide, is at least partly necessary for c-myc downregulation, and therefore the CDK-Rb-E2F pathway appears to be a target for the ceramide-induced modulation of cell cycle regulated gene transcription.	Ceramides	63-71	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	106-111
10200487-9	1998	Our studies demonstrate that pRb dephosphorylation, induced by ceramide, is at least partly necessary for c-myc downregulation, and therefore the CDK-Rb-E2F pathway appears to be a target for the ceramide-induced modulation of cell cycle regulated gene transcription.	Ceramides	196-204	RB transcriptional corepressor 1	Homo sapiens	29-32
9613615-0	1998	A deficiency in Syk enhances ceramide-induced apoptosis in DT40 lymphoma B cells.	Ceramides	29-37	spleen associated tyrosine kinase	Gallus gallus	16-19
9613615-1	1998	Syk deficiency significantly enhanced ceramide-induced apoptosis.	Ceramides	38-46	spleen associated tyrosine kinase	Gallus gallus	0-3
9613615-2	1998	Ectopic expression of wild-type or kinase-inactive Syk rendered Syk-negative cells resistant to ceramide-induced apoptosis.	Ceramides	96-104	spleen associated tyrosine kinase	Gallus gallus	51-54
9613615-2	1998	Ectopic expression of wild-type or kinase-inactive Syk rendered Syk-negative cells resistant to ceramide-induced apoptosis.	Ceramides	96-104	spleen associated tyrosine kinase	Gallus gallus	64-67
9613615-3	1998	Furthermore, ceramide could not activate Syk, indicating that Syk protected DT40 cells from ceramide-induced apoptosis, via a mechanism independent of its activity.	Ceramides	13-21	spleen associated tyrosine kinase	Gallus gallus	62-65
9613615-3	1998	Furthermore, ceramide could not activate Syk, indicating that Syk protected DT40 cells from ceramide-induced apoptosis, via a mechanism independent of its activity.	Ceramides	92-100	spleen associated tyrosine kinase	Gallus gallus	62-65
9613615-4	1998	In addition, a deficiency in Lyn also resulted in the cells becoming susceptible to ceramide-induced apoptosis.	Ceramides	84-92	LYN proto-oncogene, Src family tyrosine kinase	Gallus gallus	29-32
9556624-5	1998	Treatment of MCF7 cells with TNFalpha induced a marked decrease in the level of cellular GSH, which was accompanied by hydrolysis of sphingomyelin and generation of ceramide.	Ceramides	165-173	tumor necrosis factor	Homo sapiens	29-37
9556624-6	1998	Pretreatment of cells with GSH, GSH-methylester, or N-acetylcysteine, a precursor of GSH biosynthesis, inhibited the TNFalpha-induced sphingomyelin hydrolysis and ceramide generation as well as cell death.	Ceramides	163-171	tumor necrosis factor	Homo sapiens	117-125
9605105-2	1998	Among them ceramide, which is formed by cell membrane sphingomyelin, influences the apoptotic signal pathway through Fas antigen.	Ceramides	11-19	Fas cell surface death receptor	Homo sapiens	117-128
9609113-7	1998	cAMP agonists such as SpcAMP (via PKA) and TNF-alpha (recently identified as endogenous inhibitor of insulin action via ceramide) block insulin-stimulated PP-1G phosphorylation with a parallel decrease of PP-1 activity, presumably due to the dissociation of the PP-1 catalytic subunit from the regulatory G-subunit.	Ceramides	120-128	tumor necrosis factor	Rattus norvegicus	43-52
9609113-7	1998	cAMP agonists such as SpcAMP (via PKA) and TNF-alpha (recently identified as endogenous inhibitor of insulin action via ceramide) block insulin-stimulated PP-1G phosphorylation with a parallel decrease of PP-1 activity, presumably due to the dissociation of the PP-1 catalytic subunit from the regulatory G-subunit.	Ceramides	120-128	protein phosphatase 1 catalytic subunit gamma	Rattus norvegicus	155-160
9531568-0	1998	Hypothesis: ceramide conditionally activates atypical protein kinases C, Raf-1 and KSR through binding to their cysteine-rich domains.	Ceramides	12-20	TNF receptor associated factor 3	Homo sapiens	70-78
9531568-0	1998	Hypothesis: ceramide conditionally activates atypical protein kinases C, Raf-1 and KSR through binding to their cysteine-rich domains.	Ceramides	12-20	kinase suppressor of ras 1	Homo sapiens	83-86
9531573-6	1998	Fourth, the SAPK/ERK kinase dominant negative mutant, which attenuated ceramide-induced cell death, did not prevent Fas-induced apoptosis.	Ceramides	71-79	mitogen-activated protein kinase 9	Homo sapiens	12-16
9525894-4	1998	We found that HIV-1 recombinant gp120 (IIIB isolate) could penetrate into a monomolecular film of alpha-hydroxylated galactosylceramide (GalCer-HFA), while ceramides, GluCer, and nonhydroxylated GalCer were totally inactive.	Ceramides	156-165	Envelope surface glycoprotein gp160, precursor	Human immunodeficiency virus 1	32-37
9605434-2	1998	PP2A is activated by ceramide, which is produced by the hydrolysis of membrane sphingomyelin in response to a variety of stress-related stimuli.	Ceramides	21-29	protein phosphatase 2 phosphatase activator	Homo sapiens	0-4
9605434-8	1998	Thus, modulation (both inhibition and activation) of the catatylic activity of ceramide-activated PP2A is demonstrated by certain low molecular weight aromatic compounds.	Ceramides	79-87	protein phosphatase 2 phosphatase activator	Homo sapiens	98-102
9528992-7	1998	The sphingomyelin (N-acylsphingosine-1-phosphocholine, SM) pathway that is initiated by the hydrolysis of SM to ceramide (Cer) has been shown previously to be activated by the Fas ligand/receptor system in a number of different cell types.	Ceramides	112-120	Fas ligand	Rattus norvegicus	176-186
9528992-7	1998	The sphingomyelin (N-acylsphingosine-1-phosphocholine, SM) pathway that is initiated by the hydrolysis of SM to ceramide (Cer) has been shown previously to be activated by the Fas ligand/receptor system in a number of different cell types.	Ceramides	122-125	Fas ligand	Rattus norvegicus	176-186
9528992-16	1998	In conclusion, the sphingomyelin-ceramide cycle that can lead to cell suicide by apoptosis is functional and activated through the Fas ligand/receptor signal transduction pathway, not only in the immune system, but also in thecal/interstitial cells of the ovarian follicle.	Ceramides	33-41	Fas ligand	Rattus norvegicus	131-141
9531315-0	1998	Dual role of ceramide in the control of apoptosis following IL-2 withdrawal.	Ceramides	13-21	interleukin 2	Mus musculus	60-64
9540978-0	1998	Decreased phospholipase D (PLD) activity in ceramide-induced apoptosis of human keratinocyte cell line HaCaT.	Ceramides	44-52	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	10-25
9540978-0	1998	Decreased phospholipase D (PLD) activity in ceramide-induced apoptosis of human keratinocyte cell line HaCaT.	Ceramides	44-52	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	27-30
9562240-0	1998	An accessory role for ceramide in interleukin-1beta induced prostaglandin synthesis.	Ceramides	22-30	interleukin 1 beta	Homo sapiens	34-51
9562240-2	1998	We previously showed that ceramide accumulates in fibroblasts treated with IL-1 and that it enhances IL-1-induced PGE2 production.	Ceramides	26-34	interleukin 1 beta	Homo sapiens	75-79
9562240-2	1998	We previously showed that ceramide accumulates in fibroblasts treated with IL-1 and that it enhances IL-1-induced PGE2 production.	Ceramides	26-34	interleukin 1 beta	Homo sapiens	101-105
9562240-3	1998	The present study was undertaken to determine the mechanism(s) by which ceramide and IL-1 interact to enhance PGE2 production by examining their respective effects on the rate-limiting enzymes in PGE2 synthesis, cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2).	Ceramides	72-80	prostaglandin-endoperoxide synthase 2	Homo sapiens	238-254
9562240-3	1998	The present study was undertaken to determine the mechanism(s) by which ceramide and IL-1 interact to enhance PGE2 production by examining their respective effects on the rate-limiting enzymes in PGE2 synthesis, cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2).	Ceramides	72-80	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	256-261
9562240-3	1998	The present study was undertaken to determine the mechanism(s) by which ceramide and IL-1 interact to enhance PGE2 production by examining their respective effects on the rate-limiting enzymes in PGE2 synthesis, cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2).	Ceramides	72-80	phospholipase A2 group IVA	Homo sapiens	268-294
9562240-3	1998	The present study was undertaken to determine the mechanism(s) by which ceramide and IL-1 interact to enhance PGE2 production by examining their respective effects on the rate-limiting enzymes in PGE2 synthesis, cyclooxygenase-1 (COX-1), cyclooxygenase-2 (COX-2), and cytosolic phospholipase A2 (cPLA2).	Ceramides	72-80	phospholipase A2 group IVA	Homo sapiens	296-301
9562240-5	1998	Conversely, COX-2 mRNA was barely detectable in untreated cells but within 2 h, ceramide or IL-1 alone induced a 5 and 20 fold increase in COX-2 mRNA, respectively.	Ceramides	80-88	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	12-17
9562240-5	1998	Conversely, COX-2 mRNA was barely detectable in untreated cells but within 2 h, ceramide or IL-1 alone induced a 5 and 20 fold increase in COX-2 mRNA, respectively.	Ceramides	80-88	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	139-144
9562240-7	1998	Ceramide however, reduced the length of time required for IL-1 to induce COX-2 protein accumulation and increased COX-2 protein accumulation.	Ceramides	0-8	interleukin 1 beta	Homo sapiens	58-62
9562240-7	1998	Ceramide however, reduced the length of time required for IL-1 to induce COX-2 protein accumulation and increased COX-2 protein accumulation.	Ceramides	0-8	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	73-78
9562240-7	1998	Ceramide however, reduced the length of time required for IL-1 to induce COX-2 protein accumulation and increased COX-2 protein accumulation.	Ceramides	0-8	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	114-119
9562240-10	1998	These observations indicate that, (1) while either ceramide or IL-1 rapidly induced COX-2 mRNA, COX-2 protein only accumulated in IL-1 treated cells after a delay of 6-7 h, (2) IL-1-induced PGE2 synthesis required both COX-2 and cPLA2 protein synthesis and, (3) ceramide enhanced (temporally and quantitatively) IL-1-induced COX-2 protein	Ceramides	51-59	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	84-89
9516458-0	1998	CD95 (Fas/APO-1) induces ceramide formation and apoptosis in the absence of a functional acid sphingomyelinase.	Ceramides	25-33	Fas cell surface death receptor	Homo sapiens	0-4
9516458-0	1998	CD95 (Fas/APO-1) induces ceramide formation and apoptosis in the absence of a functional acid sphingomyelinase.	Ceramides	25-33	Fas cell surface death receptor	Homo sapiens	10-15
9516458-2	1998	It activates the caspase cascade, but also induces ceramide (Cer) production, reportedly involving acid sphingomyelinase (aSMase) activity.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	99-120
9516458-2	1998	It activates the caspase cascade, but also induces ceramide (Cer) production, reportedly involving acid sphingomyelinase (aSMase) activity.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	122-128
9516458-2	1998	It activates the caspase cascade, but also induces ceramide (Cer) production, reportedly involving acid sphingomyelinase (aSMase) activity.	Ceramides	61-64	sphingomyelin phosphodiesterase 1	Homo sapiens	99-120
9516458-2	1998	It activates the caspase cascade, but also induces ceramide (Cer) production, reportedly involving acid sphingomyelinase (aSMase) activity.	Ceramides	61-64	sphingomyelin phosphodiesterase 1	Homo sapiens	122-128
9541007-9	1998	Together, these data indicate that Sph/DMS act independently from ceramide in the apoptosis pathway and further suggest that Sph/DMS act earlier in the pathway than ceramide and are involved upstream of even the early proteases, whereas the point of action for ceramide is downstream of the early proteases but upstream from the late caspases.	Ceramides	165-173	caspase 8	Homo sapiens	334-342
9541007-9	1998	Together, these data indicate that Sph/DMS act independently from ceramide in the apoptosis pathway and further suggest that Sph/DMS act earlier in the pathway than ceramide and are involved upstream of even the early proteases, whereas the point of action for ceramide is downstream of the early proteases but upstream from the late caspases.	Ceramides	165-173	caspase 8	Homo sapiens	334-342
9500792-1	1998	Ceramides deriving from sphingomyelin hydrolysis are important mediators of apoptotic signals originating from Fas (APO-1/CD95).	Ceramides	0-9	Fas cell surface death receptor	Homo sapiens	116-121
9500792-1	1998	Ceramides deriving from sphingomyelin hydrolysis are important mediators of apoptotic signals originating from Fas (APO-1/CD95).	Ceramides	0-9	Fas cell surface death receptor	Homo sapiens	122-126
9500792-5	1998	NPD lymphoblasts also fail to accumulate GD3 ganglioside, a downstream mediator of ceramide-induced cell death (De Maria, R., L. Lenti, F. Malisan, F. D"Agostino, B. Tomassini, A. Zeuner, M.R.	Ceramides	83-91	GRDX	Homo sapiens	41-44
9500792-10	1998	Inefficient apoptosis is due to lack of ASM activity, because proximal signaling from Fas in NPD lymphoblasts is not impaired and apoptosis can be efficiently triggered by passing the ASM defect with exogenous ceramides.	Ceramides	210-219	sphingomyelin phosphodiesterase 1	Homo sapiens	184-187
9506997-0	1998	Ceramide formation leads to caspase-3 activation during hypoxic PC12 cell death.	Ceramides	0-8	caspase 3	Rattus norvegicus	28-37
9506997-1	1998	Inhibitory effects of Bcl-2 on ceramide formation and caspase-3 activation.	Ceramides	31-39	BCL2, apoptosis regulator	Rattus norvegicus	22-27
9506997-10	1998	These results suggest that ceramide generated by activation of neutral magnesium-dependent sphingomyelinase mediates hypoxic cell death and that Bcl-2 has inhibitory effects on ceramide formation and caspase activation.	Ceramides	177-185	BCL2, apoptosis regulator	Rattus norvegicus	145-150
9488730-1	1998	Sphingomyelinase (SMase) activation and ceramide generation have emerged as an important signaling pathway transducing diverse biological effects of cytokine receptors like p55 tumor necrosis factor (TNF) receptor or Fas.	Ceramides	40-48	tumor necrosis factor	Homo sapiens	200-203
9480923-2	1998	To understand the signal transduction pathway of ceramide to the nucleus, in the present study, we examined whether C2-ceramide, a cell permeable ceramide, activates c-fos serum response element (SRE).	Ceramides	119-127	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	166-171
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	152-160	cell division cycle 42	Rattus norvegicus	128-133
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	152-160	ras homolog family member A	Rattus norvegicus	143-147
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	152-160	Rac family small GTPase 1	Rattus norvegicus	276-280
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	152-160	Rac family small GTPase 1	Rattus norvegicus	135-138
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	354-362	cell division cycle 42	Rattus norvegicus	128-133
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	354-362	Rac family small GTPase 1	Rattus norvegicus	135-139
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	354-362	ras homolog family member A	Rattus norvegicus	143-147
9480923-5	1998	By reporter gene analysis following transient transfections with various plasmids expressing a dominant negative mutant form of Cdc42, Rac1 or RhoA, C2-ceramide-induced SRE activation was shown to be selectively repressed by pEXV-RacN17 encoding a dominant negative mutant of Rac1, suggesting that Rac activity is essential for the signalling cascade of ceramide to the nucleus.	Ceramides	354-362	Rac family small GTPase 1	Rattus norvegicus	135-138
9480923-6	1998	In a further study to analyse the downstream mediator of Rac in the ceramide-signalling pathway, we observed that either pretreatment with mepacrine, a potent and specific inhibitor of phospholipase A2, or co-transfection with antisense cytosolic phospholipase A2 (cPLA2) oligonucleotide repressed the C2-ceramide-induced SRE activation selectively, implying a critical role of cPLA2 in C2-ceramide-induced signalling to nucleus.	Ceramides	68-76	Rac family small GTPase 1	Rattus norvegicus	57-60
9480923-8	1998	Together, our findings suggest the critical role of "Rac and subsequent activation of phospholipase A2" in ceramide-signalling to nucleus.	Ceramides	107-115	Rac family small GTPase 1	Rattus norvegicus	53-56
9480923-8	1998	Together, our findings suggest the critical role of "Rac and subsequent activation of phospholipase A2" in ceramide-signalling to nucleus.	Ceramides	107-115	phospholipase A2 group IB	Rattus norvegicus	86-102
10200470-1	1998	Tumor necrosis factor alpha (TNF) or cytotoxic anti-Fas antibodies lead to the activation of apoptotic proteases (caspases) and to sphingomyelinase-mediated ceramide generation.	Ceramides	157-165	tumor necrosis factor	Homo sapiens	0-27
10200470-1	1998	Tumor necrosis factor alpha (TNF) or cytotoxic anti-Fas antibodies lead to the activation of apoptotic proteases (caspases) and to sphingomyelinase-mediated ceramide generation.	Ceramides	157-165	tumor necrosis factor	Homo sapiens	29-32
10200470-3	1998	We report here that rapid apoptosis induced by TNF in U937 cells or anti-Fas in Jurkat cells, in the presence of cycloheximide, induced only a very low increase (<20%) in the cell ceramide content.	Ceramides	183-191	tumor necrosis factor	Homo sapiens	47-50
9541582-0	1998	Ceramide-independent CD28 and TCR signaling but reduced IL-2 secretion in T cells of acid sphingomyelinase-deficient mice.	Ceramides	0-8	CD28 antigen	Mus musculus	21-25
9541582-1	1998	Ceramide generated by lysosomal acid sphingomyelinase (aSMase) has been proposed to contribute to CD28 co-stimulatory signaling pathways.	Ceramides	0-8	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	32-53
9541582-1	1998	Ceramide generated by lysosomal acid sphingomyelinase (aSMase) has been proposed to contribute to CD28 co-stimulatory signaling pathways.	Ceramides	0-8	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	55-61
9541582-1	1998	Ceramide generated by lysosomal acid sphingomyelinase (aSMase) has been proposed to contribute to CD28 co-stimulatory signaling pathways.	Ceramides	0-8	CD28 antigen	Mus musculus	98-102
9541582-6	1998	We conclude that ceramide generated by aSMase is not involved in CD28 signal transduction, but rather a perturbation of the secretory system is responsible for the impaired proliferation of aSMase-deficient splenocytes.	Ceramides	17-25	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	39-45
9541582-6	1998	We conclude that ceramide generated by aSMase is not involved in CD28 signal transduction, but rather a perturbation of the secretory system is responsible for the impaired proliferation of aSMase-deficient splenocytes.	Ceramides	17-25	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	190-196
9609949-2	1998	The present review provides published data and the authors" results suggesting that the content of ceramide and sphingosine in the cell is controlled by the tumor necrosis factor alpha and activators of Fas receptor.	Ceramides	99-107	tumor necrosis factor	Homo sapiens	157-184
9614836-9	1998	When tested by an inhibition ELISA, fraction CLA2-7 inhibited the binding of anticeramide antibodies to a ceramide-coated plate while thin-layer chromatography of fractions CLA2-1 and CLA2-7 showed a spot with an Rf value similar to that of standard ceramide.	Ceramides	81-89	ATPase plasma membrane Ca2+ transporting 3	Homo sapiens	45-51
9614836-9	1998	When tested by an inhibition ELISA, fraction CLA2-7 inhibited the binding of anticeramide antibodies to a ceramide-coated plate while thin-layer chromatography of fractions CLA2-1 and CLA2-7 showed a spot with an Rf value similar to that of standard ceramide.	Ceramides	81-89	ATPase plasma membrane Ca2+ transporting 3	Homo sapiens	45-49
9614836-9	1998	When tested by an inhibition ELISA, fraction CLA2-7 inhibited the binding of anticeramide antibodies to a ceramide-coated plate while thin-layer chromatography of fractions CLA2-1 and CLA2-7 showed a spot with an Rf value similar to that of standard ceramide.	Ceramides	106-114	ATPase plasma membrane Ca2+ transporting 3	Homo sapiens	45-51
9614836-9	1998	When tested by an inhibition ELISA, fraction CLA2-7 inhibited the binding of anticeramide antibodies to a ceramide-coated plate while thin-layer chromatography of fractions CLA2-1 and CLA2-7 showed a spot with an Rf value similar to that of standard ceramide.	Ceramides	106-114	ATPase plasma membrane Ca2+ transporting 3	Homo sapiens	45-49
9454729-5	1998	In the present study, we show that nerve growth factor stimulates sphingomyelin hydrolysis and the concomitant ceramide release in organotypic cultures of otic vesicles.	Ceramides	111-119	nerve growth factor	Homo sapiens	35-54
9454729-7	1998	Ceramide-induced apoptosis was suppressed by insulin-like growth factor-I which is a strong promoter of cell growth and morphogenesis for the developing inner ear.	Ceramides	0-8	insulin like growth factor 1	Homo sapiens	45-73
9499092-3	1998	Ceramides have been described as second messengers induced by TNF-alpha.	Ceramides	0-9	tumor necrosis factor	Homo sapiens	62-71
9499092-6	1998	Moreover, long-chain ceramides induced by treatment with exogenous bacterial sphingomyelinase inhibited HCMV replication in synergy with TNF-alpha.	Ceramides	21-30	tumor necrosis factor	Homo sapiens	137-146
9736335-1	1998	In apoptosis induced by Reaper in Drosophila, as well as in a number of other systems, it has been suggested that the increased synthesis of ceramide might be a consequence of the activation of the caspase/ICE (Interleukin-1beta converting enzyme) protease pathway involved in cell death, implying that ceramide generation might often be the result rather than the cause of apoptosis.	Ceramides	141-149	Death related ICE-like caspase	Drosophila melanogaster	206-209
9736335-1	1998	In apoptosis induced by Reaper in Drosophila, as well as in a number of other systems, it has been suggested that the increased synthesis of ceramide might be a consequence of the activation of the caspase/ICE (Interleukin-1beta converting enzyme) protease pathway involved in cell death, implying that ceramide generation might often be the result rather than the cause of apoptosis.	Ceramides	141-149	Death related ICE-like caspase	Drosophila melanogaster	211-246
9736335-1	1998	In apoptosis induced by Reaper in Drosophila, as well as in a number of other systems, it has been suggested that the increased synthesis of ceramide might be a consequence of the activation of the caspase/ICE (Interleukin-1beta converting enzyme) protease pathway involved in cell death, implying that ceramide generation might often be the result rather than the cause of apoptosis.	Ceramides	303-311	Death related ICE-like caspase	Drosophila melanogaster	206-209
9736335-1	1998	In apoptosis induced by Reaper in Drosophila, as well as in a number of other systems, it has been suggested that the increased synthesis of ceramide might be a consequence of the activation of the caspase/ICE (Interleukin-1beta converting enzyme) protease pathway involved in cell death, implying that ceramide generation might often be the result rather than the cause of apoptosis.	Ceramides	303-311	Death related ICE-like caspase	Drosophila melanogaster	211-246
9769910-10	1998	However, TNF can cause apoptosis of EC when cells are co-treated with either the protein synthesis inhibitor cycloheximide (CHX) or the lipid mediator ceramide (cer).	Ceramides	151-159	tumor necrosis factor	Homo sapiens	9-12
9769910-10	1998	However, TNF can cause apoptosis of EC when cells are co-treated with either the protein synthesis inhibitor cycloheximide (CHX) or the lipid mediator ceramide (cer).	Ceramides	151-154	tumor necrosis factor	Homo sapiens	9-12
9769910-14	1998	These observations suggest that TNF normally acts as an activator of EC but may change from an activator to a killer of EC when combined with agents that release ceramide, such as u.v.	Ceramides	162-170	tumor necrosis factor	Homo sapiens	32-35
9478955-6	1998	Ceramide, a product of sphingomyelin hydrolysis, is also capable of inducing SREBP-1 maturation.	Ceramides	0-8	sterol regulatory element binding transcription factor 1	Homo sapiens	77-84
9478955-7	1998	The mature form of SREBP-1 generated by TNF-alpha, sphingomyelinase or ceramide treatment translocates to the nucleus and binds the sterol regulatory element.	Ceramides	71-79	sterol regulatory element binding transcription factor 1	Homo sapiens	19-26
9478955-9	1998	A unique finding of our studies is that ceramide stimulated SREBP-1 maturation even in the presence of cholesterol and 25-hydroxycholesterol both of which are known suppressors of SREBP-1 maturation.	Ceramides	40-48	sterol regulatory element binding transcription factor 1	Homo sapiens	60-67
9478955-9	1998	A unique finding of our studies is that ceramide stimulated SREBP-1 maturation even in the presence of cholesterol and 25-hydroxycholesterol both of which are known suppressors of SREBP-1 maturation.	Ceramides	40-48	sterol regulatory element binding transcription factor 1	Homo sapiens	180-187
9478955-10	1998	Our findings indicate that ceramide-mediated maturation of SREBP-1 maturation is a novel sterol-independent mechanism by which cholesterol homeostasis may be regulated.	Ceramides	27-35	sterol regulatory element binding transcription factor 1	Homo sapiens	59-66
9478956-7	1998	Altogether these results suggest that signaling through Fas and HLA class I involve caspase(s), targeted by zVAD-fmk, which act upstream of ceramide generation and mitochondrial events, whereas interleukin-1 converting enzyme-like and CPP32-like proteases act downstream of the mitochondria.	Ceramides	140-148	caspase 3	Homo sapiens	235-240
9478967-0	1998	Enhancement of fibroblast collagenase (matrix metalloproteinase-1) gene expression by ceramide is mediated by extracellular signal-regulated and stress-activated protein kinase pathways.	Ceramides	86-94	matrix metallopeptidase 1	Homo sapiens	15-37
9478967-0	1998	Enhancement of fibroblast collagenase (matrix metalloproteinase-1) gene expression by ceramide is mediated by extracellular signal-regulated and stress-activated protein kinase pathways.	Ceramides	86-94	matrix metallopeptidase 1	Homo sapiens	39-65
9478967-1	1998	Inflammatory cytokines tumor necrosis factor-alpha and interleukin-1 trigger the ceramide signaling pathway, initiated by neutral sphingomyelinase-elicited hydrolysis of cell membrane phospholipid sphingomyelin to ceramide, a new lipid second messenger.	Ceramides	81-89	tumor necrosis factor	Homo sapiens	23-50
9478967-1	1998	Inflammatory cytokines tumor necrosis factor-alpha and interleukin-1 trigger the ceramide signaling pathway, initiated by neutral sphingomyelinase-elicited hydrolysis of cell membrane phospholipid sphingomyelin to ceramide, a new lipid second messenger.	Ceramides	214-222	tumor necrosis factor	Homo sapiens	23-50
9478967-2	1998	Here, we show that triggering the ceramide pathway by sphingomyelinase or C2- and C6-ceramide enhances collagenase-1 (matrix metalloproteinase-1; MMP-1) gene expression by fibroblasts.	Ceramides	34-42	matrix metallopeptidase 1	Homo sapiens	118-144
9478967-2	1998	Here, we show that triggering the ceramide pathway by sphingomyelinase or C2- and C6-ceramide enhances collagenase-1 (matrix metalloproteinase-1; MMP-1) gene expression by fibroblasts.	Ceramides	34-42	matrix metallopeptidase 1	Homo sapiens	146-151
9478967-2	1998	Here, we show that triggering the ceramide pathway by sphingomyelinase or C2- and C6-ceramide enhances collagenase-1 (matrix metalloproteinase-1; MMP-1) gene expression by fibroblasts.	Ceramides	85-93	matrix metallopeptidase 1	Homo sapiens	118-144
9478967-2	1998	Here, we show that triggering the ceramide pathway by sphingomyelinase or C2- and C6-ceramide enhances collagenase-1 (matrix metalloproteinase-1; MMP-1) gene expression by fibroblasts.	Ceramides	85-93	matrix metallopeptidase 1	Homo sapiens	146-151
9478967-6	1998	In addition, ceramide-dependent induction of MMP-1 expression is potently prevented by PD 98059, a selective inhibitor of MEK1 activation, and by specific p38 inhibitor SB 203580.	Ceramides	13-21	matrix metallopeptidase 1	Homo sapiens	45-50
9478967-6	1998	In addition, ceramide-dependent induction of MMP-1 expression is potently prevented by PD 98059, a selective inhibitor of MEK1 activation, and by specific p38 inhibitor SB 203580.	Ceramides	13-21	mitogen-activated protein kinase kinase 1	Homo sapiens	122-126
9478967-6	1998	In addition, ceramide-dependent induction of MMP-1 expression is potently prevented by PD 98059, a selective inhibitor of MEK1 activation, and by specific p38 inhibitor SB 203580.	Ceramides	13-21	mitogen-activated protein kinase 1	Homo sapiens	155-158
9478967-7	1998	These results show that triggering the ceramide signaling pathway activates MMP-1 gene expression via three distinct MAPK pathways, i.e. ERK1/2, SAPK/JNK, and p38, and suggest that targeted modulation of the ceramide signaling pathway may offer a novel therapeutic approach for inhibiting collagenolytic activity, e.g. in inflammatory disorders.	Ceramides	39-47	matrix metallopeptidase 1	Homo sapiens	76-81
9478967-7	1998	These results show that triggering the ceramide signaling pathway activates MMP-1 gene expression via three distinct MAPK pathways, i.e. ERK1/2, SAPK/JNK, and p38, and suggest that targeted modulation of the ceramide signaling pathway may offer a novel therapeutic approach for inhibiting collagenolytic activity, e.g. in inflammatory disorders.	Ceramides	39-47	mitogen-activated protein kinase 3	Homo sapiens	137-143
9478967-7	1998	These results show that triggering the ceramide signaling pathway activates MMP-1 gene expression via three distinct MAPK pathways, i.e. ERK1/2, SAPK/JNK, and p38, and suggest that targeted modulation of the ceramide signaling pathway may offer a novel therapeutic approach for inhibiting collagenolytic activity, e.g. in inflammatory disorders.	Ceramides	39-47	mitogen-activated protein kinase 8	Homo sapiens	150-153
9478967-7	1998	These results show that triggering the ceramide signaling pathway activates MMP-1 gene expression via three distinct MAPK pathways, i.e. ERK1/2, SAPK/JNK, and p38, and suggest that targeted modulation of the ceramide signaling pathway may offer a novel therapeutic approach for inhibiting collagenolytic activity, e.g. in inflammatory disorders.	Ceramides	39-47	mitogen-activated protein kinase 1	Homo sapiens	159-162
9478967-7	1998	These results show that triggering the ceramide signaling pathway activates MMP-1 gene expression via three distinct MAPK pathways, i.e. ERK1/2, SAPK/JNK, and p38, and suggest that targeted modulation of the ceramide signaling pathway may offer a novel therapeutic approach for inhibiting collagenolytic activity, e.g. in inflammatory disorders.	Ceramides	208-216	matrix metallopeptidase 1	Homo sapiens	76-81
9450998-0	1998	Regulation of Raf-1 kinase by TNF via its second messenger ceramide and cross-talk with mitogenic signalling.	Ceramides	59-67	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	14-19
9450998-0	1998	Regulation of Raf-1 kinase by TNF via its second messenger ceramide and cross-talk with mitogenic signalling.	Ceramides	59-67	tumor necrosis factor	Homo sapiens	30-33
9450998-2	1998	We have investigated mechanisms of Raf-1 regulation by TNF and its messenger ceramide in cell-free assays, insect and mammalian cell lines.	Ceramides	77-85	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	35-40
9450998-4	1998	Cell-permeable ceramides induced a marked increase of Ras-Raf-1 complexes in cells co-expressing Raf-1 and activated Ras.	Ceramides	15-24	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	58-63
9450998-4	1998	Cell-permeable ceramides induced a marked increase of Ras-Raf-1 complexes in cells co-expressing Raf-1 and activated Ras.	Ceramides	15-24	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	97-102
9450998-5	1998	Likewise, a fast elevation of the endogeneous ceramide level, induced by TNF treatment of human Kym-1 rhabdomyosarcoma cells, was followed by stimulation of Ras-Raf-1 association without significant Raf-1 kinase activation.	Ceramides	46-54	tumor necrosis factor	Homo sapiens	73-76
9450998-5	1998	Likewise, a fast elevation of the endogeneous ceramide level, induced by TNF treatment of human Kym-1 rhabdomyosarcoma cells, was followed by stimulation of Ras-Raf-1 association without significant Raf-1 kinase activation.	Ceramides	46-54	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	161-166
9466577-1	1998	The activation of sphingomyelinase and the generation of ceramide has been proposed to mediate tumor necrosis factor-alpha (TNF-alpha)-induced nuclear factor (NF)-kappaB activation through its second messenger ceramide.	Ceramides	57-65	tumor necrosis factor	Homo sapiens	95-122
9466577-1	1998	The activation of sphingomyelinase and the generation of ceramide has been proposed to mediate tumor necrosis factor-alpha (TNF-alpha)-induced nuclear factor (NF)-kappaB activation through its second messenger ceramide.	Ceramides	57-65	tumor necrosis factor	Homo sapiens	124-133
9466577-1	1998	The activation of sphingomyelinase and the generation of ceramide has been proposed to mediate tumor necrosis factor-alpha (TNF-alpha)-induced nuclear factor (NF)-kappaB activation through its second messenger ceramide.	Ceramides	210-218	tumor necrosis factor	Homo sapiens	95-122
9466577-1	1998	The activation of sphingomyelinase and the generation of ceramide has been proposed to mediate tumor necrosis factor-alpha (TNF-alpha)-induced nuclear factor (NF)-kappaB activation through its second messenger ceramide.	Ceramides	210-218	tumor necrosis factor	Homo sapiens	124-133
9466577-5	1998	The objective of this study was to determine whether TNF-alpha activates the sphingomyelin pathway in human synovial fibroblasts (HSF) and the potential role of ceramide in HSF proliferation and apoptosis.	Ceramides	161-169	interleukin 6	Homo sapiens	173-176
9466577-9	1998	Sphingomyelinase activation was determined by quantitation of sphingomyelin and ceramide radioactivity in [14C]serine-prelabeled HSF cells.	Ceramides	80-88	interleukin 6	Homo sapiens	129-132
9707172-2	1998	Here we show that in U937 and HL60 myeloid leukemia cells and in normal skin fibroblasts, cell-permeant ceramides can trigger neutral sphingomyelinase activation, sphingomyelin hydrolysis, and endogenous ceramide generation regardless of Bcl2 overexpression.	Ceramides	104-113	BCL2 apoptosis regulator	Homo sapiens	238-242
9707172-2	1998	Here we show that in U937 and HL60 myeloid leukemia cells and in normal skin fibroblasts, cell-permeant ceramides can trigger neutral sphingomyelinase activation, sphingomyelin hydrolysis, and endogenous ceramide generation regardless of Bcl2 overexpression.	Ceramides	104-112	BCL2 apoptosis regulator	Homo sapiens	238-242
9719464-0	1998	Induction of p21 during ceramide-mediated apoptosis in human hepatocarcinoma cells.	Ceramides	24-32	H3 histone pseudogene 16	Homo sapiens	13-16
9719464-2	1998	In this study, we investigated the expression of the p21 gene and its relationship to apoptosis induced by ceramide.	Ceramides	107-115	H3 histone pseudogene 16	Homo sapiens	53-56
9719464-6	1998	These findings suggest that ceramide-induced apoptosis is associated with the upregulation of p21 mRNA and protein in a p53-independent pathway.	Ceramides	28-36	H3 histone pseudogene 16	Homo sapiens	94-97
9719464-6	1998	These findings suggest that ceramide-induced apoptosis is associated with the upregulation of p21 mRNA and protein in a p53-independent pathway.	Ceramides	28-36	tumor protein p53	Homo sapiens	120-123
9664074-0	1998	p53-dependent ceramide response to genotoxic stress.	Ceramides	14-22	tumor protein p53	Homo sapiens	0-3
9664074-4	1998	In this study, we investigated the relationship between p53 and ceramide.	Ceramides	64-72	tumor protein p53	Homo sapiens	56-59
9664074-6	1998	In these cells, p53 activation was followed by a dose- and time-dependent increase in endogenous ceramide levels which was not seen in cells lacking functional p53 and treated similarly.	Ceramides	97-105	tumor protein p53	Homo sapiens	16-19
9664074-8	1998	However, in p53-independent systems, such as growth suppression induced by TNF-alpha or serum deprivation, ceramide accumulated irrespective of the upregulation of p53, indicating that p53 regulates ceramide accumulation in only a subset of growth-suppressive pathways.	Ceramides	107-115	tumor protein p53	Homo sapiens	12-15
9664074-10	1998	Also, when cells lacking functional p53, either due to mutation or the expression of the E6 protein of human papilloma virus, were treated with exogenous ceramide, there was equal growth suppression, cell cycle arrest, and apoptosis as compared with cells expressing normal p53.	Ceramides	154-162	tumor protein p53	Homo sapiens	36-39
9664074-10	1998	Also, when cells lacking functional p53, either due to mutation or the expression of the E6 protein of human papilloma virus, were treated with exogenous ceramide, there was equal growth suppression, cell cycle arrest, and apoptosis as compared with cells expressing normal p53.	Ceramides	154-162	tumor protein p53	Homo sapiens	274-277
9664074-12	1998	Instead, they suggest that, in situations where p53 performs a critical regulatory role, such as the response to genotoxic stress, it functions "upstream" of ceramide.	Ceramides	158-166	tumor protein p53	Homo sapiens	48-51
9657974-2	1998	Binding of tumour necrosis factor (TNF) to its 55 kDa receptor (TR55) leads to the generation of ceramide through activation of either acid or neutral sphingomyelinase (A/N-SMase) as well as to potent activation of SAPK/JNK.	Ceramides	97-105	tumor necrosis factor	Mus musculus	35-38
9449644-2	1998	TNF induces receptor-mediated activation of sphingomyelinase, which converts sphingomyelin to ceramide, a mediator of TNF actions.	Ceramides	94-102	tumor necrosis factor-like	Rattus norvegicus	118-121
9449644-12	1998	The addition of TNF increased both the sphingomyelin and ceramide levels 3- to 5-fold in young and old cells.	Ceramides	57-65	tumor necrosis factor-like	Rattus norvegicus	16-19
9449644-0	1998	Tumor necrosis factor, ceramide, transforming growth factor-beta1, and aging reduce Na+/I- symporter messenger ribonucleic acid levels in FRTL-5 cells.	Ceramides	23-31	solute carrier family 5 member 5	Rattus norvegicus	84-100
9449644-2	1998	TNF induces receptor-mediated activation of sphingomyelinase, which converts sphingomyelin to ceramide, a mediator of TNF actions.	Ceramides	94-102	tumor necrosis factor-like	Rattus norvegicus	0-3
9446561-9	1998	Inhibition of ceramide and LPS-mediated induction of iNOS by antioxidant inhibitors of NF-kappaB (N-acetylcysteine and pyrrolidine dithiocarbamate) suggest that the stimulatory effect of ceramide on the induction of iNOS is due to the stimulation of NF-kappaB activation and that cellular redox plays a role in the activation of NF-kappaB and induction of iNOS.	Ceramides	14-22	nitric oxide synthase 2	Rattus norvegicus	216-220
9468284-0	1998	Fas or ceramide induce apoptosis by Ras-regulated phosphoinositide-3-kinase activation.	Ceramides	7-15	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	50-75
9508001-7	1998	However, mRNA levels for serine palmitoyl transferase (SPT), the first committed step for ceramide synthesis, do not increase in parallel.	Ceramides	90-98	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	25-53
9508001-7	1998	However, mRNA levels for serine palmitoyl transferase (SPT), the first committed step for ceramide synthesis, do not increase in parallel.	Ceramides	90-98	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	55-58
9516715-6	1998	In addition, ACTH stimulates the release of ceramide from the glycoinositolphosphoceramide purified from T. cruzi.	Ceramides	44-52	proopiomelanocortin	Homo sapiens	13-17
9446561-9	1998	Inhibition of ceramide and LPS-mediated induction of iNOS by antioxidant inhibitors of NF-kappaB (N-acetylcysteine and pyrrolidine dithiocarbamate) suggest that the stimulatory effect of ceramide on the induction of iNOS is due to the stimulation of NF-kappaB activation and that cellular redox plays a role in the activation of NF-kappaB and induction of iNOS.	Ceramides	14-22	nitric oxide synthase 2	Rattus norvegicus	216-220
9446561-0	1998	Sphingomyelinase and ceramide stimulate the expression of inducible nitric-oxide synthase in rat primary astrocytes.	Ceramides	21-29	nitric oxide synthase 2	Rattus norvegicus	58-89
9446602-0	1998	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	Ceramides	123-131	caspase 6	Homo sapiens	47-55
9446561-9	1998	Inhibition of ceramide and LPS-mediated induction of iNOS by antioxidant inhibitors of NF-kappaB (N-acetylcysteine and pyrrolidine dithiocarbamate) suggest that the stimulatory effect of ceramide on the induction of iNOS is due to the stimulation of NF-kappaB activation and that cellular redox plays a role in the activation of NF-kappaB and induction of iNOS.	Ceramides	187-195	nitric oxide synthase 2	Rattus norvegicus	53-57
9446602-0	1998	Sphingosine 1-phosphate inhibits activation of caspases that cleave poly(ADP-ribose) polymerase and lamins during Fas- and ceramide-mediated apoptosis in Jurkat T lymphocytes.	Ceramides	123-131	poly(ADP-ribose) polymerase 1	Homo sapiens	68-95
9446561-6	1998	Similar to astrocytes, SMase or ceramide analogs also stimulated the LPS- and cytokine-mediated expression of iNOS in the C6 glial cell line.	Ceramides	32-40	nitric oxide synthase 2	Rattus norvegicus	110-114
9446561-11	1998	This study illustrates a novel role of the sphingomyelin-ceramide signaling pathway in stimulating the expression of iNOS via LPS- or cytokine-mediated activation of NF-kappaB in astrocytes.	Ceramides	57-65	nitric oxide synthase 2	Rattus norvegicus	117-121
9464542-5	1998	Nevertheless, both primary CML cells and BCR-ABL+ BAF3 cells show the same dose-dependent sensitivity to TNF-alpha or ceramide-induced apoptosis as their respective normal counterparts.	Ceramides	118-126	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	41-48
9464542-6	1998	In fact, time course studies demonstrated an even faster onset of apoptosis in ceramide-treated BCR-ABL+ BAF3 cells as compared to normal controls.	Ceramides	79-87	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	96-103
9464542-7	1998	BCR-ABL+ cells treated with ceramide also showed a rapid and sequential increase in the tyrosine phosphorylation of p210(BCR-ABL), p46-56SHC and p120Cbl.	Ceramides	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	0-7
9464542-7	1998	BCR-ABL+ cells treated with ceramide also showed a rapid and sequential increase in the tyrosine phosphorylation of p210(BCR-ABL), p46-56SHC and p120Cbl.	Ceramides	28-36	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	121-128
9492297-0	1998	Role of an acidic compartment in tumor-necrosis-factor-alpha-induced production of ceramide, activation of caspase-3 and apoptosis.	Ceramides	83-91	tumor necrosis factor	Homo sapiens	33-60
9419344-4	1998	We now have identified a gene in Saccharomyces cerevisiae, LBP1, that regulates the levels of phosphorylated sphingoid bases and ceramide.	Ceramides	129-137	sphinganine kinase LCB3	Saccharomyces cerevisiae S288C	59-63
9492297-4	1998	In addition, TNF-alpha stimulates the production of ceramide, which also activates the death machinery.	Ceramides	52-60	tumor necrosis factor	Homo sapiens	13-22
9492297-7	1998	This compartment generates at least two signaling pathways that account for the caspase-3 activation and apoptosis induced by TNF-alpha, one involving ceramide and caspase-unrelated adapter molecules and another involving yet unknown lysosomal mediators.	Ceramides	151-159	caspase 3	Homo sapiens	80-89
9492297-7	1998	This compartment generates at least two signaling pathways that account for the caspase-3 activation and apoptosis induced by TNF-alpha, one involving ceramide and caspase-unrelated adapter molecules and another involving yet unknown lysosomal mediators.	Ceramides	151-159	tumor necrosis factor	Homo sapiens	126-135
9492297-8	1998	The apoptosis inhibitor Bcl-2 specifically acts on the ceramide-activated pathway to block caspase-3 activation and apoptosis.	Ceramides	55-63	BCL2 apoptosis regulator	Homo sapiens	24-29
9492297-8	1998	The apoptosis inhibitor Bcl-2 specifically acts on the ceramide-activated pathway to block caspase-3 activation and apoptosis.	Ceramides	55-63	caspase 3	Homo sapiens	91-100
9419344-8	1998	The deletion of LBP1 results in the accumulation of phosphorylated long-chain sphingoid bases and reduced ceramide levels.	Ceramides	106-114	sphinganine kinase LCB3	Saccharomyces cerevisiae S288C	16-20
9762361-1	1998	We have previously demonstrated that exposure of fully differentiated 3T3-L1 adipocytes to TNF results in an activation of at least two separate signal transduction pathways: 1. the sphingomyelinase leading to generation of ceramide and 2. the proliferative and cell growth regulating p44/42 MAP kinase cascade.	Ceramides	224-232	tumor necrosis factor	Homo sapiens	91-94
9439623-2	1998	We demonstrate here that ceramide promotes the down-regulation of protein kinase C (PKC) activity in phorbol ester-stimulated murine polymorphonuclear leukocytes (PMNs).	Ceramides	25-33	protein kinase C, alpha	Mus musculus	84-87
9439623-4	1998	When PMNs were pretreated with cell-permeable ceramide analogue, C2-ceramide, the membrane-associated PKC activity was rapidly down-regulated by phorbol ester stimulation.	Ceramides	46-54	protein kinase C, alpha	Mus musculus	102-105
9439623-7	1998	We found that ceramide strikingly promoted calpain-mediated proteolysis of PKC beta in vitro.	Ceramides	14-22	protein kinase C, beta	Mus musculus	75-83
9439623-8	1998	Ceramide was also shown to inhibit [3H]phorbol 12,13-dibutyrate(PDBu) binding to PKC beta.	Ceramides	0-8	protein kinase C, beta	Mus musculus	81-89
9439623-9	1998	Moreover, we show that ceramide stimulates PKC beta autophosphorylation.	Ceramides	23-31	protein kinase C, beta	Mus musculus	43-51
9439623-10	1998	These results suggest that ceramide directly activates PKC beta and promotes calpain-mediated proteolysis in murine PMNs.	Ceramides	27-35	protein kinase C, beta	Mus musculus	55-63
9821861-5	1998	Withdrawal of these growth factors or inhibition of PI3-kinase with wortmannin or LY294002 activated the pro-apoptotic CPP32 (Yama/Apopain/caspase 3, EC 3.4.22), activated neutral sphingomyelinase and increased ceramide formation in an immortalized dorsal root ganglion cell line F-11.	Ceramides	211-219	caspase 3	Mus musculus	119-124
9821861-5	1998	Withdrawal of these growth factors or inhibition of PI3-kinase with wortmannin or LY294002 activated the pro-apoptotic CPP32 (Yama/Apopain/caspase 3, EC 3.4.22), activated neutral sphingomyelinase and increased ceramide formation in an immortalized dorsal root ganglion cell line F-11.	Ceramides	211-219	caspase 3	Mus musculus	126-130
9821861-5	1998	Withdrawal of these growth factors or inhibition of PI3-kinase with wortmannin or LY294002 activated the pro-apoptotic CPP32 (Yama/Apopain/caspase 3, EC 3.4.22), activated neutral sphingomyelinase and increased ceramide formation in an immortalized dorsal root ganglion cell line F-11.	Ceramides	211-219	caspase 3	Mus musculus	131-138
9821866-1	1998	The verotoxin receptor globotriaosyl ceramide (Gb3) is overexpressed in an ovarian tumour resistant to chemotherapy.	Ceramides	37-45	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	47-50
9860316-0	1998	Radiation-induced apoptosis--the ceramide-SAPK signaling pathway and clinical aspects.	Ceramides	33-41	mitogen-activated protein kinase 9	Homo sapiens	42-46
9860316-5	1998	In this paper we discuss the involvement of a ceramide-mediated stress-activated protein kinase (SAPK) signaling cascade in radiation-induced apoptosis.	Ceramides	46-54	mitogen-activated protein kinase 9	Homo sapiens	64-95
9860316-5	1998	In this paper we discuss the involvement of a ceramide-mediated stress-activated protein kinase (SAPK) signaling cascade in radiation-induced apoptosis.	Ceramides	46-54	mitogen-activated protein kinase 9	Homo sapiens	97-101
9762361-2	1998	In the current study we extend those observations and examine the ability of both TNF and ceramide to activate the stress/cytokine activated p38 MAPK, the JNK and JAK-STAT pathways.	Ceramides	90-98	mitogen-activated protein kinase 8	Homo sapiens	155-158
9438415-0	1998	Restoration of TNF-alpha-induced ceramide generation and apoptosis in resistant human leukemia KG1a cells by the P-glycoprotein blocker PSC833.	Ceramides	33-41	tumor necrosis factor	Homo sapiens	15-24
10200443-2	1998	Here, we demonstrate that Fas receptor-triggered activation of the acidic sphingomyelinase, consumption of sphingomyelin, release of ceramide, and subsequent activation of JNK and p38-K are regulated by caspases.	Ceramides	133-141	mitogen-activated protein kinase 14	Homo sapiens	180-183
9421370-0	1998	Effects of cell-permeable ceramides and tumor necrosis factor-alpha on insulin signaling and glucose uptake in 3T3-L1 adipocytes.	Ceramides	26-35	insulin	Homo sapiens	71-78
9421370-1	1998	Incubation of 3T3-L1 adipocytes with C2- and C6-ceramides (N-acetyl- and N-hexanoylsphingosines) but not dihydro-C2-ceramide increased 2-deoxyglucose uptake in the absence of insulin.	Ceramides	48-57	insulin	Homo sapiens	175-182
9421370-8	1998	Cell-permeable ceramides mimic some effects of TNF-alpha, especially in stimulating basal glucose uptake.	Ceramides	15-24	tumor necrosis factor	Homo sapiens	47-56
9421370-10	1998	Our work provides further mechanisms for the effects of TNF-alpha and ceramides in increasing non-insulin-dependent glucose uptake and decreasing insulin-stimulated uptake in vivo.	Ceramides	70-79	insulin	Homo sapiens	98-105
9421370-10	1998	Our work provides further mechanisms for the effects of TNF-alpha and ceramides in increasing non-insulin-dependent glucose uptake and decreasing insulin-stimulated uptake in vivo.	Ceramides	70-79	insulin	Homo sapiens	146-153
9458713-6	1998	TNF-alpha also increased ceramide levels, and C2-ceramide mimicked the effect of TNF-alpha on SMIT mRNA levels and myo-inositol accumulation in bovine aorta endothelial cells.	Ceramides	25-33	tumor necrosis factor	Bos taurus	0-9
9526097-2	1998	While ceramide has been shown to be an important regulatory component of apoptosis induced by tumor necrosis factor alpha and the Fas ligand, sphingosine-1-phosphate (SPP), a further metabolite of ceramide, has been implicated as a second messenger in cellular proliferation and survival induced by platelet-derived growth factor, neuronal growth factor, and serum.	Ceramides	6-14	tumor necrosis factor	Homo sapiens	94-121
9526097-2	1998	While ceramide has been shown to be an important regulatory component of apoptosis induced by tumor necrosis factor alpha and the Fas ligand, sphingosine-1-phosphate (SPP), a further metabolite of ceramide, has been implicated as a second messenger in cellular proliferation and survival induced by platelet-derived growth factor, neuronal growth factor, and serum.	Ceramides	6-14	Fas ligand	Homo sapiens	130-140
9526097-2	1998	While ceramide has been shown to be an important regulatory component of apoptosis induced by tumor necrosis factor alpha and the Fas ligand, sphingosine-1-phosphate (SPP), a further metabolite of ceramide, has been implicated as a second messenger in cellular proliferation and survival induced by platelet-derived growth factor, neuronal growth factor, and serum.	Ceramides	197-205	Fas ligand	Homo sapiens	130-140
9691465-0	1998	Ceramides perturb the structure of phosphatidylcholine bilayers and modulate the activity of phospholipase A2.	Ceramides	0-9	phospholipase A2 group IB	Homo sapiens	93-109
9691465-4	1998	The long-chain C16-ceramide induced lateral phase separation of the bilayers into gel and liquid crystalline domains and activated PL-A2, as does natural ceramide (Huang et al.	Ceramides	19-27	phospholipase A2 group IB	Homo sapiens	131-136
9691465-6	1998	Taken together, the results strongly suggest a correlation between membrane defects induced by ceramide analogs and their effects on phospholipase A2 activity.	Ceramides	95-103	phospholipase A2 group IB	Homo sapiens	133-149
9691465-7	1998	Furthermore, the effects of short-chain ceramides on PL-A2 are different from those of natural ceramide, indicating that the cell-permeable short-chain ceramide analogs, widely used to study the shpingomyelin-dependent cellular signal transduction pathway, may not completely mimic the natural product.	Ceramides	40-49	phospholipase A2 group IB	Homo sapiens	53-58
9691465-7	1998	Furthermore, the effects of short-chain ceramides on PL-A2 are different from those of natural ceramide, indicating that the cell-permeable short-chain ceramide analogs, widely used to study the shpingomyelin-dependent cellular signal transduction pathway, may not completely mimic the natural product.	Ceramides	40-48	phospholipase A2 group IB	Homo sapiens	53-58
9438415-2	1998	TNF-alpha-induced apoptosis seems to be mediated by a signaling pathway termed "sphingomyelin-ceramide" pathway, which consists of the hydrolysis of sphingomyelin and the production of its breakdown product ceramide.	Ceramides	94-102	tumor necrosis factor	Homo sapiens	0-9
9438415-2	1998	TNF-alpha-induced apoptosis seems to be mediated by a signaling pathway termed "sphingomyelin-ceramide" pathway, which consists of the hydrolysis of sphingomyelin and the production of its breakdown product ceramide.	Ceramides	207-215	tumor necrosis factor	Homo sapiens	0-9
9469581-7	1998	Moreover, the apoptotic capacities of several cytotoxic receptor systems (e.g., CD120a, CD95) and many environmental stresses (e.g., ionizing radiation, heat-shock, oxidative stress) are now known to derive from the activation of multiple signaling cascades by ceramide or, under some circumstances, by sphingosine.	Ceramides	261-269	TNF receptor superfamily member 1A	Homo sapiens	80-86
9769704-3	1998	Breakdown of sphingomyelin to produce ceramide by activation of sphingomyelinase is one of the upstream signalling cascades activated in apoptotic cells in response to stimuli such as TNF.	Ceramides	38-46	tumor necrosis factor	Homo sapiens	184-187
9469597-15	1998	This model is based on the dominant role CER 1 plays in the formation of the long periodicity phase, electron density distribution calculations, and observations, such as i) the bimodal distribution of the fatty acid chain lengths of the ceramides, ii) the phase separation between long-chain ceramides and short-chain ceramides in a monolayer approach, and iii) the absence of swelling of the lamellae upon increasing the water content organization in SC.	Ceramides	238-247	CER1	Sus scrofa	41-46
9469597-15	1998	This model is based on the dominant role CER 1 plays in the formation of the long periodicity phase, electron density distribution calculations, and observations, such as i) the bimodal distribution of the fatty acid chain lengths of the ceramides, ii) the phase separation between long-chain ceramides and short-chain ceramides in a monolayer approach, and iii) the absence of swelling of the lamellae upon increasing the water content organization in SC.	Ceramides	293-302	CER1	Sus scrofa	41-46
9469597-15	1998	This model is based on the dominant role CER 1 plays in the formation of the long periodicity phase, electron density distribution calculations, and observations, such as i) the bimodal distribution of the fatty acid chain lengths of the ceramides, ii) the phase separation between long-chain ceramides and short-chain ceramides in a monolayer approach, and iii) the absence of swelling of the lamellae upon increasing the water content organization in SC.	Ceramides	293-302	CER1	Sus scrofa	41-46
9388194-4	1997	Here we demonstrate that when the human TPx II, a member of this family, is stably overexpressed in Molt-4 leukemia cells, it protects from apoptosis induced by serum deprivation, ceramide, or etoposide.	Ceramides	180-188	thyroid peroxidase	Homo sapiens	40-43
9481450-3	1997	More recently, workers have focused on induction of apoptosis and have shown that daunorubicin stimulates production of the apoptotic mediator, ceramide and that the activity of doxorubicin can be blocked by inhibitors of CD95 (fas).	Ceramides	144-152	Fas cell surface death receptor	Homo sapiens	222-226
9415703-1	1997	We characterized participation of the stress-activated protein kinase (SAPK) cascade in the lethal actions of the cytotoxic lipid messengers ceramide and sphingosine in U937 human monoblastic leukemia cells.	Ceramides	141-149	mitogen-activated protein kinase 9	Homo sapiens	38-69
9450681-0	1997	Induction of nerve growth factor synthesis by sphingomyelinase and ceramide in primary astrocyte cultures.	Ceramides	67-75	nerve growth factor	Rattus norvegicus	13-32
9450681-4	1997	Induction of NGF synthesis by SMase and ceramide was shown to be independent of classical PKC activity.	Ceramides	40-48	nerve growth factor	Rattus norvegicus	13-16
9415703-8	1997	These findings demonstrate that reciprocal alterations in the SAPK and MAPK cascades are associated with the apoptotic influence of either lipid inasmuch as (i) ceramide-mediated lethality is primarily associated with strong stimulation of SAPK and weak inhibition of MAPK, whereas (ii) sphingosine-mediated lethality is primarily associated with weak stimulation of SAPK and strong inhibition of MAPK.	Ceramides	161-169	mitogen-activated protein kinase 9	Homo sapiens	62-66
9415703-8	1997	These findings demonstrate that reciprocal alterations in the SAPK and MAPK cascades are associated with the apoptotic influence of either lipid inasmuch as (i) ceramide-mediated lethality is primarily associated with strong stimulation of SAPK and weak inhibition of MAPK, whereas (ii) sphingosine-mediated lethality is primarily associated with weak stimulation of SAPK and strong inhibition of MAPK.	Ceramides	161-169	mitogen-activated protein kinase 3	Homo sapiens	71-75
9415703-1	1997	We characterized participation of the stress-activated protein kinase (SAPK) cascade in the lethal actions of the cytotoxic lipid messengers ceramide and sphingosine in U937 human monoblastic leukemia cells.	Ceramides	141-149	mitogen-activated protein kinase 9	Homo sapiens	71-75
9415703-8	1997	These findings demonstrate that reciprocal alterations in the SAPK and MAPK cascades are associated with the apoptotic influence of either lipid inasmuch as (i) ceramide-mediated lethality is primarily associated with strong stimulation of SAPK and weak inhibition of MAPK, whereas (ii) sphingosine-mediated lethality is primarily associated with weak stimulation of SAPK and strong inhibition of MAPK.	Ceramides	161-169	mitogen-activated protein kinase 9	Homo sapiens	240-244
9415703-8	1997	These findings demonstrate that reciprocal alterations in the SAPK and MAPK cascades are associated with the apoptotic influence of either lipid inasmuch as (i) ceramide-mediated lethality is primarily associated with strong stimulation of SAPK and weak inhibition of MAPK, whereas (ii) sphingosine-mediated lethality is primarily associated with weak stimulation of SAPK and strong inhibition of MAPK.	Ceramides	161-169	mitogen-activated protein kinase 3	Homo sapiens	268-272
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	mitogen-activated protein kinase 8	Homo sapiens	33-37
9415703-8	1997	These findings demonstrate that reciprocal alterations in the SAPK and MAPK cascades are associated with the apoptotic influence of either lipid inasmuch as (i) ceramide-mediated lethality is primarily associated with strong stimulation of SAPK and weak inhibition of MAPK, whereas (ii) sphingosine-mediated lethality is primarily associated with weak stimulation of SAPK and strong inhibition of MAPK.	Ceramides	161-169	mitogen-activated protein kinase 9	Homo sapiens	240-244
9415703-8	1997	These findings demonstrate that reciprocal alterations in the SAPK and MAPK cascades are associated with the apoptotic influence of either lipid inasmuch as (i) ceramide-mediated lethality is primarily associated with strong stimulation of SAPK and weak inhibition of MAPK, whereas (ii) sphingosine-mediated lethality is primarily associated with weak stimulation of SAPK and strong inhibition of MAPK.	Ceramides	161-169	mitogen-activated protein kinase 3	Homo sapiens	268-272
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	interferon induced protein with tetratricopeptide repeats 2	Homo sapiens	38-41
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	mitogen-activated protein kinase 9	Homo sapiens	42-46
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-89
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	99-104
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	interferon induced protein with tetratricopeptide repeats 2	Homo sapiens	170-173
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	mitogen-activated protein kinase 9	Homo sapiens	174-178
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	200-205
9415703-3	1997	Ceramide robustly stimulated p46-JNK1/p54-JNK2 activity and increased expression of c-jun mRNA and c-Jun protein; in contrast, sphingosine moderately stimulated p46-JNK1/p54-JNK2 and failed to modify c-jun/c-Jun expression.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	206-211
9415703-4	1997	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	Ceramides	151-159	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-42
9415703-4	1997	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	Ceramides	151-159	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-89
9415703-4	1997	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	Ceramides	151-159	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	84-89
9415703-4	1997	Dominant-negative blockade of normal c-Jun activity by transfection with the TAM-67 c-Jun NH2-terminal deletion mutant abolished the lethal actions of ceramide but was without effect on those of sphingosine, indicating that ceramide-related apoptosis is directly dependent on activation of c-Jun, whereas sphingosine-induced cell death proceeds via an unrelated downstream mechanism.	Ceramides	224-232	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	37-42
9415703-5	1997	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/ p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	Ceramides	214-222	mitogen-activated protein kinase 3	Homo sapiens	58-62
9415703-5	1997	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/ p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	Ceramides	214-222	cyclin dependent kinase 20	Homo sapiens	161-164
9415703-5	1997	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/ p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	Ceramides	214-222	mitogen-activated protein kinase 3	Homo sapiens	165-169
9415703-5	1997	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/ p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	Ceramides	214-222	interferon induced protein 44	Homo sapiens	171-174
9415703-5	1997	Characterization of the mitogen-activated protein kinase (MAPK) cascade in these responses revealed a further functional disparity between the two lipids: basal p42-ERK1/ p44-ERK2 activity was gradually reduced by ceramide but immediately and completely suppressed by sphingosine.	Ceramides	214-222	mitogen-activated protein kinase 1	Homo sapiens	175-179
9393854-2	1997	Using different human epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol and ceramide.	Ceramides	252-260	sphingomyelin phosphodiesterase 1	Homo sapiens	156-179
9393854-2	1997	Using different human epithelial cells and primary fibroblasts, we show here an activation of the phosphatidylcholine-specific phospholipase C (PC-PLC) and acidic sphingomyelinase (ASM) by N. gonorrhoeae, resulting in the release of diacylglycerol and ceramide.	Ceramides	252-260	sphingomyelin phosphodiesterase 1	Homo sapiens	181-184
9368039-0	1997	Hydroxylation of Saccharomyces cerevisiae ceramides requires Sur2p and Scs7p.	Ceramides	42-51	sphingosine hydroxylase	Saccharomyces cerevisiae S288C	61-66
9570388-5	1997	Mass spectrometric analysis showed that tumor-derived ganglioside GD3 contained heterogeneous ceramide structures and, interestingly, the ceramide subspecies with shorter fatty acyl chains were selectively shed.	Ceramides	94-102	GRDX	Homo sapiens	66-69
9570388-5	1997	Mass spectrometric analysis showed that tumor-derived ganglioside GD3 contained heterogeneous ceramide structures and, interestingly, the ceramide subspecies with shorter fatty acyl chains were selectively shed.	Ceramides	138-146	GRDX	Homo sapiens	66-69
9368039-0	1997	Hydroxylation of Saccharomyces cerevisiae ceramides requires Sur2p and Scs7p.	Ceramides	42-51	fatty acid alpha-hydroxylase	Saccharomyces cerevisiae S288C	71-76
9368039-5	1997	Characterization of scs7 and sur2 mutants is expected to provide insight into the function of ceramide hydroxylation.	Ceramides	94-102	fatty acid alpha-hydroxylase	Saccharomyces cerevisiae S288C	20-24
9368039-5	1997	Characterization of scs7 and sur2 mutants is expected to provide insight into the function of ceramide hydroxylation.	Ceramides	94-102	sphingosine hydroxylase	Saccharomyces cerevisiae S288C	29-33
9368039-2	1997	Sur2p is required for the hydroxylation of C-4 of the sphingoid moiety of ceramide, and Scs7p is required for the hydroxylation of the very long chain fatty acid.	Ceramides	74-82	sphingosine hydroxylase	Saccharomyces cerevisiae S288C	0-5
9359864-4	1997	The cell-permeable ceramide analogues C2 and C6 each greatly potentiated induction of both CRP and SAA mRNA by IL-6+IL-1beta but did not affect the responses of alpha-fibrinogen to IL-6 or to IL-6+IL-1beta.	Ceramides	19-27	C-reactive protein	Homo sapiens	91-94
9359864-0	1997	The sphingomyelin-ceramide pathway participates in cytokine regulation of C-reactive protein and serum amyloid A, but not alpha-fibrinogen.	Ceramides	18-26	C-reactive protein	Homo sapiens	74-92
9359864-0	1997	The sphingomyelin-ceramide pathway participates in cytokine regulation of C-reactive protein and serum amyloid A, but not alpha-fibrinogen.	Ceramides	18-26	serum amyloid A1 cluster	Homo sapiens	97-112
9359864-4	1997	The cell-permeable ceramide analogues C2 and C6 each greatly potentiated induction of both CRP and SAA mRNA by IL-6+IL-1beta but did not affect the responses of alpha-fibrinogen to IL-6 or to IL-6+IL-1beta.	Ceramides	19-27	serum amyloid A1 cluster	Homo sapiens	99-102
9359864-4	1997	The cell-permeable ceramide analogues C2 and C6 each greatly potentiated induction of both CRP and SAA mRNA by IL-6+IL-1beta but did not affect the responses of alpha-fibrinogen to IL-6 or to IL-6+IL-1beta.	Ceramides	19-27	interleukin 6	Homo sapiens	111-115
9359864-4	1997	The cell-permeable ceramide analogues C2 and C6 each greatly potentiated induction of both CRP and SAA mRNA by IL-6+IL-1beta but did not affect the responses of alpha-fibrinogen to IL-6 or to IL-6+IL-1beta.	Ceramides	19-27	interleukin 1 beta	Homo sapiens	116-124
9359864-4	1997	The cell-permeable ceramide analogues C2 and C6 each greatly potentiated induction of both CRP and SAA mRNA by IL-6+IL-1beta but did not affect the responses of alpha-fibrinogen to IL-6 or to IL-6+IL-1beta.	Ceramides	19-27	interleukin 1 beta	Homo sapiens	197-205
9359864-6	1997	D609, an inhibitor of ceramide production by acidic but not neutral sphingomyelinases, substantially inhibited induction of CRP and SAA by IL-6+IL-1beta.	Ceramides	22-30	C-reactive protein	Homo sapiens	124-127
9359864-7	1997	The ability of C2 and C6 to potentiate the effects of cytokines suggests that the sphingomyelin-ceramide pathway participates in induction of CRP and SAA by IL-6+IL-1beta under these experimental conditions, most likely by transducing the effects of IL-1beta.	Ceramides	96-104	C-reactive protein	Homo sapiens	142-145
9359864-7	1997	The ability of C2 and C6 to potentiate the effects of cytokines suggests that the sphingomyelin-ceramide pathway participates in induction of CRP and SAA by IL-6+IL-1beta under these experimental conditions, most likely by transducing the effects of IL-1beta.	Ceramides	96-104	serum amyloid A1 cluster	Homo sapiens	150-153
9359864-7	1997	The ability of C2 and C6 to potentiate the effects of cytokines suggests that the sphingomyelin-ceramide pathway participates in induction of CRP and SAA by IL-6+IL-1beta under these experimental conditions, most likely by transducing the effects of IL-1beta.	Ceramides	96-104	interleukin 6	Homo sapiens	157-161
9359864-7	1997	The ability of C2 and C6 to potentiate the effects of cytokines suggests that the sphingomyelin-ceramide pathway participates in induction of CRP and SAA by IL-6+IL-1beta under these experimental conditions, most likely by transducing the effects of IL-1beta.	Ceramides	96-104	interleukin 1 beta	Homo sapiens	162-170
9359864-7	1997	The ability of C2 and C6 to potentiate the effects of cytokines suggests that the sphingomyelin-ceramide pathway participates in induction of CRP and SAA by IL-6+IL-1beta under these experimental conditions, most likely by transducing the effects of IL-1beta.	Ceramides	96-104	interleukin 1 beta	Homo sapiens	250-258
9421185-9	1997	The production of ceramide by sphingomyelinase pre-treatment of emulsion particles containing SM leads to a two- to three-fold increase in LPL activity.	Ceramides	18-26	lipoprotein lipase	Homo sapiens	139-142
9388491-6	1997	The expression of c-fos, c-jun and cyclin D1, which are downstream of ERK in the mitogenic pathway were stimulated by thrombin but this stimulation was not affected by ceramide or dihydroceramide.	Ceramides	168-176	G1/S-specific cyclin-D1	Cricetulus griseus	35-44
9581540-0	1997	Transforming growth factor beta1 attenuates ceramide-induced CPP32/Yama activation and apoptosis in human leukaemic HL-60 cells.	Ceramides	44-52	transforming growth factor beta 1	Homo sapiens	0-32
9581540-0	1997	Transforming growth factor beta1 attenuates ceramide-induced CPP32/Yama activation and apoptosis in human leukaemic HL-60 cells.	Ceramides	44-52	caspase 3	Homo sapiens	61-66
9581540-0	1997	Transforming growth factor beta1 attenuates ceramide-induced CPP32/Yama activation and apoptosis in human leukaemic HL-60 cells.	Ceramides	44-52	caspase 3	Homo sapiens	67-71
9426183-12	1997	We also show that a ROS-independent mechanism is activated by IL-1beta in epithelial cells and seems to involve the acidic sphingomyelinase/ceramide transduction pathway.	Ceramides	140-148	interleukin 1 beta	Homo sapiens	62-70
9581540-3	1997	We also found that the addition of a specific tetrapeptide inhibitor of CPP32/Yama, Ac-DEVD-CHO, provided an effective protection against ceramide-induced cell death.	Ceramides	138-146	caspase 3	Homo sapiens	72-77
9581540-3	1997	We also found that the addition of a specific tetrapeptide inhibitor of CPP32/Yama, Ac-DEVD-CHO, provided an effective protection against ceramide-induced cell death.	Ceramides	138-146	caspase 3	Homo sapiens	78-82
9450016-0	1997	Involvement of ceramide and JNK in CD40-mediated growth inhibition.	Ceramides	15-23	CD40 molecule	Homo sapiens	35-39
9581540-4	1997	These results suggested that CPP32/Yama has a central role in ceramide-mediated apoptosis.	Ceramides	62-70	caspase 3	Homo sapiens	29-34
9581540-4	1997	These results suggested that CPP32/Yama has a central role in ceramide-mediated apoptosis.	Ceramides	62-70	caspase 3	Homo sapiens	35-39
9581540-6	1997	Only transforming growth factor beta1 (TGF-beta1) (1 ng/ml) exerted significant prevention of apoptosis induced by C2-ceramide, or by sphingomyelinase (increases intracellular ceramide).	Ceramides	118-126	transforming growth factor beta 1	Homo sapiens	5-37
9581540-6	1997	Only transforming growth factor beta1 (TGF-beta1) (1 ng/ml) exerted significant prevention of apoptosis induced by C2-ceramide, or by sphingomyelinase (increases intracellular ceramide).	Ceramides	118-126	transforming growth factor beta 1	Homo sapiens	39-48
9581540-11	1997	We thus propose that TGF-beta1 rescues ceramide-induced cell death, possibly by maintaining the constant level of Bcl-2, thereby abolishing CPP32/Yama protease activation.	Ceramides	39-47	transforming growth factor beta 1	Homo sapiens	21-30
9581540-11	1997	We thus propose that TGF-beta1 rescues ceramide-induced cell death, possibly by maintaining the constant level of Bcl-2, thereby abolishing CPP32/Yama protease activation.	Ceramides	39-47	BCL2 apoptosis regulator	Homo sapiens	114-119
9581540-11	1997	We thus propose that TGF-beta1 rescues ceramide-induced cell death, possibly by maintaining the constant level of Bcl-2, thereby abolishing CPP32/Yama protease activation.	Ceramides	39-47	caspase 3	Homo sapiens	140-145
9581540-11	1997	We thus propose that TGF-beta1 rescues ceramide-induced cell death, possibly by maintaining the constant level of Bcl-2, thereby abolishing CPP32/Yama protease activation.	Ceramides	39-47	caspase 3	Homo sapiens	146-150
9354428-0	1997	Activated Ki-ras enhances sensitivity of ceramide-induced apoptosis without c-Jun NH2-terminal kinase/stress-activated protein kinase or extracellular signal-regulated kinase activation in human colon cancer cells.	Ceramides	41-49	KRAS proto-oncogene, GTPase	Homo sapiens	10-16
9354428-1	1997	The activation of c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and/or extracellular signal-regulated kinase (ERK) is involved in ceramide-induced apoptosis in certain cells.	Ceramides	155-163	mitogen-activated protein kinase 8	Homo sapiens	45-48
9354428-3	1997	In HKe-3 and HKh-2, the activity of JNK/SAPK increased significantly within 60 min following C2 ceramide stimulation, and some apoptosis followed.	Ceramides	96-104	ribosomal protein S18	Homo sapiens	3-8
9354428-3	1997	In HKe-3 and HKh-2, the activity of JNK/SAPK increased significantly within 60 min following C2 ceramide stimulation, and some apoptosis followed.	Ceramides	96-104	mitogen-activated protein kinase 8	Homo sapiens	36-44
9354428-1	1997	The activation of c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and/or extracellular signal-regulated kinase (ERK) is involved in ceramide-induced apoptosis in certain cells.	Ceramides	155-163	mitogen-activated protein kinase 9	Homo sapiens	83-87
9354428-6	1997	These results suggest that activated Ki-ras contributes to the sensitivity of ceramide-induced apoptosis without JNK/SAPK or ERK activation and that other signaling pathways involved in ceramide-induced apoptosis may be present in human colon cancer cells.	Ceramides	78-86	KRAS proto-oncogene, GTPase	Homo sapiens	37-43
9354428-1	1997	The activation of c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and/or extracellular signal-regulated kinase (ERK) is involved in ceramide-induced apoptosis in certain cells.	Ceramides	155-163	mitogen-activated protein kinase 1	Homo sapiens	96-133
9354428-1	1997	The activation of c-Jun NH2-terminal kinase (JNK)/stress-activated protein kinase (SAPK) and/or extracellular signal-regulated kinase (ERK) is involved in ceramide-induced apoptosis in certain cells.	Ceramides	155-163	mitogen-activated protein kinase 1	Homo sapiens	135-138
9566762-6	1997	The MEF.He clone, but not the MEF.HeJ clone, expressed IL-6 mRNA in response to taxol or ceramide, whereas MEF.HeJ clones as well as the MEF.He clone expressed IL-6 mRNA in response to IL-1alpha.	Ceramides	89-97	interleukin 6	Mus musculus	55-59
9382802-3	1997	JNK/SAPK in BAF3 cells is stimulated by ceramide and also during cell proliferation in response to IL-3 [11], but its role in the apoptotic response is not clear.	Ceramides	40-48	mitogen-activated protein kinase 8	Mus musculus	0-8
9382802-5	1997	Expression of this phosphatase in BAF3 cells prevented ceramide stimulation of JNK/SAPK activity but did not affect apoptosis following IL-3 withdrawal or ceramide treatment.	Ceramides	55-63	mitogen-activated protein kinase 8	Mus musculus	79-87
9382882-6	1997	LPS or TNF-alpha injection was followed within 1 h by tissue generation of the pro-apoptotic lipid ceramide.	Ceramides	99-107	toll-like receptor 4	Mus musculus	0-3
9382882-6	1997	LPS or TNF-alpha injection was followed within 1 h by tissue generation of the pro-apoptotic lipid ceramide.	Ceramides	99-107	tumor necrosis factor	Mus musculus	7-16
9382882-7	1997	TNF-binding protein, which protects against LPS-induced death, blocked LPS-induced ceramide generation and endothelial apoptosis, suggesting systemic TNF is required for both responses.	Ceramides	83-91	tumor necrosis factor	Mus musculus	0-3
9382882-7	1997	TNF-binding protein, which protects against LPS-induced death, blocked LPS-induced ceramide generation and endothelial apoptosis, suggesting systemic TNF is required for both responses.	Ceramides	83-91	toll-like receptor 4	Mus musculus	71-74
9382882-7	1997	TNF-binding protein, which protects against LPS-induced death, blocked LPS-induced ceramide generation and endothelial apoptosis, suggesting systemic TNF is required for both responses.	Ceramides	83-91	tumor necrosis factor	Mus musculus	150-153
9382882-9	1997	Furthermore, intravenous injection of basic fibroblast growth factor, which acts as an intravascular survival factor for endothelial cells, blocked LPS-induced ceramide elevation, endothelial apoptosis and animal death, but did not affect LPS-induced elevation of serum TNF-alpha.	Ceramides	160-168	toll-like receptor 4	Mus musculus	148-151
9382882-10	1997	These investigations demonstrate that LPS induces a disseminated form of endothelial apoptosis, mediated sequentially by TNF and ceramide generation, and suggest that this cascade is mandatory for evolution of the endotoxic syndrome.	Ceramides	129-137	toll-like receptor 4	Mus musculus	38-41
9566762-7	1997	These results indicate that in the responses to LPS, taxol and ceramide, MEF retain the same reactivity as that of the mouse strains from which the MEF were derived, and LPS shares the IL-6 signal transduction pathway with taxol and ceramide, but not with IL-1.	Ceramides	63-71	interleukin 6	Mus musculus	185-189
9566762-7	1997	These results indicate that in the responses to LPS, taxol and ceramide, MEF retain the same reactivity as that of the mouse strains from which the MEF were derived, and LPS shares the IL-6 signal transduction pathway with taxol and ceramide, but not with IL-1.	Ceramides	63-71	interleukin 1 complex	Mus musculus	256-260
9566762-7	1997	These results indicate that in the responses to LPS, taxol and ceramide, MEF retain the same reactivity as that of the mouse strains from which the MEF were derived, and LPS shares the IL-6 signal transduction pathway with taxol and ceramide, but not with IL-1.	Ceramides	233-241	interleukin 6	Mus musculus	185-189
9325280-9	1997	In conclusion, we found that IGFBP-3 had no direct inhibitory effect on Hs578T cells but could accentuate apoptosis induced by the physiological trigger ceramide in an IGF-independent manner.	Ceramides	153-161	insulin like growth factor binding protein 3	Homo sapiens	29-36
9403993-2	1997	Capitalizing on the readily available ganglioside, GM1, we have devised a simple synthesis of labeled GM1 analogues with sulfur in place of oxygen in their linkage to the ceramide residue (SGM1).	Ceramides	171-179	growth differentiation factor 6	Homo sapiens	189-193
9321399-0	1997	Activation of CD95 (APO-1/Fas) signaling by ceramide mediates cancer therapy-induced apoptosis.	Ceramides	44-52	Fas cell surface death receptor	Homo sapiens	14-18
9321399-0	1997	Activation of CD95 (APO-1/Fas) signaling by ceramide mediates cancer therapy-induced apoptosis.	Ceramides	44-52	Fas cell surface death receptor	Homo sapiens	20-25
9321399-2	1997	Ceramide, which accumulates in response to different types of cellular stress such as chemo- and radiotherapy, strongly induced expression of CD95-L, cleavage of caspases and apoptosis.	Ceramides	0-8	Fas ligand	Homo sapiens	142-148
9321399-3	1997	Antisense CD95-L as well as dominant-negative FADD inhibited ceramide- and cellular stress-induced apoptosis.	Ceramides	61-69	Fas ligand	Homo sapiens	10-16
9321399-3	1997	Antisense CD95-L as well as dominant-negative FADD inhibited ceramide- and cellular stress-induced apoptosis.	Ceramides	61-69	Fas associated via death domain	Homo sapiens	46-50
9321399-6	1997	CD95-L expression and apoptosis in NPA fibroblasts were restorable by exogenously added ceramide.	Ceramides	88-96	Fas cell surface death receptor	Homo sapiens	0-4
9321399-8	1997	These data demonstrate that ceramide links cellular stress responses induced by gamma-irradiation or anticancer drugs to the CD95 pathway of apoptosis.	Ceramides	28-36	Fas cell surface death receptor	Homo sapiens	125-129
9346915-2	1997	Ceramide generated by sphingomyelinases (SMases) is known to function as an important second messenger molecule in the signaling pathway of IL-1 and tumor necrosis factor.	Ceramides	0-8	interleukin 1 complex	Mus musculus	140-144
9366247-5	1997	Moreover, in contrast to sphingosine which activates phospholipase D (PLD) leading to an increase in phosphatidic acid levels, sphingomyelinase, but not ceramide analogs, reduced TPA-stimulated PLD activity.	Ceramides	153-161	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	70-73
9282331-0	1997	Induction of intracellular ceramide by interleukin-1 beta in oligodendrocytes.	Ceramides	27-35	interleukin 1 beta	Rattus norvegicus	39-57
9328928-0	1997	Protein kinase C in the developing kidney: isoform expression and effects of ceramide and PKC inhibitors.	Ceramides	77-85	proline rich transmembrane protein 2	Homo sapiens	0-16
9315663-7	1997	Notably, the lack of pRB in these U937-derived clones renders these p53-null cells highly resistant to apoptosis induced by serum withdrawal, calphostin C, and ceramide.	Ceramides	160-168	RB transcriptional corepressor 1	Homo sapiens	21-24
9315663-7	1997	Notably, the lack of pRB in these U937-derived clones renders these p53-null cells highly resistant to apoptosis induced by serum withdrawal, calphostin C, and ceramide.	Ceramides	160-168	tumor protein p53	Homo sapiens	68-71
9305886-1	1997	The current confusion regarding the relevance of endogenous ceramide in mediating CD95/Fas-induced apoptosis is based mainly on (i) discrepancies in kinetics of the ceramide response between different studies using the same apoptotic stimulus and (ii) the observation that late ceramide formation (hours) often parallels apoptosis onset.	Ceramides	60-68	Fas cell surface death receptor	Homo sapiens	82-86
9305886-2	1997	We investigated CD95-induced ceramide formation in Jurkat cells, using two methods (radiolabeling/thin layer chromatography and benzoylation/high performance liquid chromatography), which, unlike the commonly used diglyceride kinase assay, discriminate between ceramide species and de novo formed dihydroceramide.	Ceramides	29-37	Fas cell surface death receptor	Homo sapiens	16-20
9305886-2	1997	We investigated CD95-induced ceramide formation in Jurkat cells, using two methods (radiolabeling/thin layer chromatography and benzoylation/high performance liquid chromatography), which, unlike the commonly used diglyceride kinase assay, discriminate between ceramide species and de novo formed dihydroceramide.	Ceramides	261-269	Fas cell surface death receptor	Homo sapiens	16-20
9305886-5	1997	The majority ( approximately 70%) of the ceramide response remained unaffected when apoptosis was completely inhibited at the level of caspase-3/CPP32 processing by the inhibitor peptide DEVD-CHO.	Ceramides	41-49	caspase 3	Homo sapiens	145-150
9305886-8	1997	The results support the idea that ceramide acts in conjunction with the caspase cascade in CD95-induced apoptosis.	Ceramides	34-42	Fas cell surface death receptor	Homo sapiens	91-95
9295291-3	1997	Short term treatment of PC12 cells with ceramide analogues also resulted in reduced NGF-stimulated TrkA activation, suggesting that p75-mediated increases in sphingomyelinase activity may contribute to this modulatory effect.	Ceramides	40-48	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	99-103
9295291-3	1997	Short term treatment of PC12 cells with ceramide analogues also resulted in reduced NGF-stimulated TrkA activation, suggesting that p75-mediated increases in sphingomyelinase activity may contribute to this modulatory effect.	Ceramides	40-48	nerve growth factor receptor	Rattus norvegicus	132-135
9295291-4	1997	Phosphoamino acid analysis was performed to determine if brain-derived neurotrophic factor- or ceramide-mediated phosphorylation of the TrkA intracellular domain correlated with a reduction in its ligand-induced activation.	Ceramides	95-103	neurotrophic receptor tyrosine kinase 1	Rattus norvegicus	136-140
9287328-4	1997	The effects of nitric oxide thus generated, mediated via cGMP generation, are exerted at at least two sites along the CD95 signaling cascade: one at, or upstream, and the other downstream of ceramide generation.	Ceramides	191-199	Fas cell surface death receptor	Homo sapiens	118-122
9305864-1	1997	Ceramide is a lipid second messenger that mediates the effects of tumor necrosis factor alpha and other agents on cell growth and differentiation.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	66-93
9305864-2	1997	Ceramide is believed to act via activation of protein phosphatase, proline-directed protein kinase, or protein kinase C. Tumor necrosis factor alpha-induced common pathway of apoptosis is associated with an early impairment of mitochondria.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	121-148
9305886-0	1997	CD95/Fas-induced ceramide formation proceeds with slow kinetics and is not blocked by caspase-3/CPP32 inhibition.	Ceramides	17-25	Fas cell surface death receptor	Homo sapiens	0-4
9295281-6	1997	In contrast, exogenous ceramide treatment caused a decrease in cellular Bcl-2 levels.	Ceramides	23-31	BCL2 apoptosis regulator	Homo sapiens	72-77
9278531-5	1997	Levels of ceramide, the precursor of sphingosine, were only slightly decreased by NGF in serum-containing medium.	Ceramides	10-18	nerve growth factor	Rattus norvegicus	82-85
9278531-6	1997	However, NGF decreased the elevation of ceramide induced by serum withdrawal.	Ceramides	40-48	nerve growth factor	Rattus norvegicus	9-12
9282331-8	1997	Surprisingly, long-term exposure (72 h) to increasing concentrations of IL-1 beta, which increases intracellular ceramide, did not induce oligodendroglial cell death.	Ceramides	113-121	interleukin 1 beta	Rattus norvegicus	72-81
9282331-9	1997	These results show that an increase of intracellular ceramide is not sufficient to induce apoptosis in oligodendrocytes and that IL-1 beta signaling through the ceramide pathway in these cells can mediate functions other than programmed cell death.	Ceramides	161-169	interleukin 1 beta	Rattus norvegicus	129-138
9315737-2	1997	Here, we provide evidence that activation of T-lymphocytes via CD40L results in activation of a neutral but not an acidic sphingomyelinase correlating with a consumption of sphingomyelin and a release of ceramide.	Ceramides	204-212	CD40 ligand	Homo sapiens	63-68
9287216-0	1997	Requirement for GD3 ganglioside in CD95- and ceramide-induced apoptosis.	Ceramides	45-53	GRDX	Homo sapiens	16-19
9287216-4	1997	Cell-permeating ceramides, which are potent inducers of apoptosis, also triggered GD3 synthesis.	Ceramides	16-25	GRDX	Homo sapiens	82-85
9335256-4	1997	The neuroprotective actions of TNFalpha and ceramide were abolished in cultures cotreated with kappaB decoy DNA demonstrating a requirement for NF-kappaB activation for prevention of cell death.	Ceramides	44-52	nuclear factor kappa B subunit 1	Homo sapiens	144-153
9335256-5	1997	Levels of manganese superoxide dismutase (Mn-SOD) in neurons were increased following exposure of cultures to TNFalpha and ceramide in control cultures, but not in cultures cotreated with kappaB decoy DNA.	Ceramides	123-131	superoxide dismutase 2	Homo sapiens	10-40
9335256-5	1997	Levels of manganese superoxide dismutase (Mn-SOD) in neurons were increased following exposure of cultures to TNFalpha and ceramide in control cultures, but not in cultures cotreated with kappaB decoy DNA.	Ceramides	123-131	superoxide dismutase 2	Homo sapiens	42-48
9316456-4	1997	In the cells, TNF-alpha induced ceramide production and the addition of exogenous ceramide or sphingomyelinase treatment of the cells simulated TNF-alpha actions.	Ceramides	32-40	tumor necrosis factor	Rattus norvegicus	14-23
9316456-4	1997	In the cells, TNF-alpha induced ceramide production and the addition of exogenous ceramide or sphingomyelinase treatment of the cells simulated TNF-alpha actions.	Ceramides	82-90	tumor necrosis factor	Rattus norvegicus	144-153
9316456-6	1997	We conclude that TNF-alpha, through a sphingomyelinase-ceramide pathway, regulates TSH-induced H2O2 production at steps beyond the Ca2+ mobilization step in the PLC-Ca2+ signaling pathway coupled to TSH.	Ceramides	55-63	tumor necrosis factor	Rattus norvegicus	17-26
9271409-6	1997	Cells that constitutively overexpress hsp70 resist apoptosis induced by ceramide, a lipid signaling molecule that is generated by apoptosis-inducing treatments and is linked to SAPK/JNK activation.	Ceramides	72-80	heat shock protein family A (Hsp70) member 4	Homo sapiens	38-43
9268362-0	1997	Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153.	Ceramides	8-16	Rac family small GTPase 1	Homo sapiens	52-56
9268362-0	1997	Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153.	Ceramides	8-16	mitogen-activated protein kinase 8	Homo sapiens	81-102
9268362-0	1997	Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153.	Ceramides	8-16	mitogen-activated protein kinase 14	Homo sapiens	103-106
9268362-0	1997	Fas- or ceramide-induced apoptosis is mediated by a Rac1-regulated activation of Jun N-terminal kinase/p38 kinases and GADD153.	Ceramides	8-16	DNA damage inducible transcript 3	Homo sapiens	119-126
9268362-2	1997	A signaling cascade from the Fas receptor via ceramide, Ras, Rac1, and JNK/p38-K to GADD153 is demonstrated employing transfection of transdominant inhibitory N17Ras, N17Rac1, c-Jun, or treatment with a specific p38-K inhibitor.	Ceramides	46-54	DNA damage inducible transcript 3	Homo sapiens	84-91
9268362-2	1997	A signaling cascade from the Fas receptor via ceramide, Ras, Rac1, and JNK/p38-K to GADD153 is demonstrated employing transfection of transdominant inhibitory N17Ras, N17Rac1, c-Jun, or treatment with a specific p38-K inhibitor.	Ceramides	46-54	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	176-181
9268362-2	1997	A signaling cascade from the Fas receptor via ceramide, Ras, Rac1, and JNK/p38-K to GADD153 is demonstrated employing transfection of transdominant inhibitory N17Ras, N17Rac1, c-Jun, or treatment with a specific p38-K inhibitor.	Ceramides	46-54	mitogen-activated protein kinase 14	Homo sapiens	212-215
9268362-3	1997	The critical function of this signaling cascade is indicated by prevention of Fas- or C6-ceramide-induced apoptosis after inhibition of Ras, Rac1, or JNK/p38-K.	Ceramides	89-97	Rac family small GTPase 1	Homo sapiens	141-145
9268362-3	1997	The critical function of this signaling cascade is indicated by prevention of Fas- or C6-ceramide-induced apoptosis after inhibition of Ras, Rac1, or JNK/p38-K.	Ceramides	89-97	mitogen-activated protein kinase 8	Homo sapiens	150-153
9268362-3	1997	The critical function of this signaling cascade is indicated by prevention of Fas- or C6-ceramide-induced apoptosis after inhibition of Ras, Rac1, or JNK/p38-K.	Ceramides	89-97	mitogen-activated protein kinase 14	Homo sapiens	154-157
9247485-10	1997	TNF-alpha may inhibit this gene by using sphingomyelin/ceramide as an intracellular signal transduction pathway.	Ceramides	55-63	tumor necrosis factor	Rattus norvegicus	0-9
9281351-1	1997	Apoptosis induced by ligation of either the tumor necrosis factor (TNF) p55 receptor or the Fas/APO-1/CD95 receptor has been suggested to require ceramide as a signaling molecule.	Ceramides	146-154	tumor necrosis factor	Homo sapiens	44-65
9281351-1	1997	Apoptosis induced by ligation of either the tumor necrosis factor (TNF) p55 receptor or the Fas/APO-1/CD95 receptor has been suggested to require ceramide as a signaling molecule.	Ceramides	146-154	tumor necrosis factor	Homo sapiens	67-70
9281351-1	1997	Apoptosis induced by ligation of either the tumor necrosis factor (TNF) p55 receptor or the Fas/APO-1/CD95 receptor has been suggested to require ceramide as a signaling molecule.	Ceramides	146-154	Fas cell surface death receptor	Homo sapiens	96-101
9281351-1	1997	Apoptosis induced by ligation of either the tumor necrosis factor (TNF) p55 receptor or the Fas/APO-1/CD95 receptor has been suggested to require ceramide as a signaling molecule.	Ceramides	146-154	Fas cell surface death receptor	Homo sapiens	102-106
9252342-2	1997	In the present study, inflammatory activation of P388D1 macrophages with bacterial lipopolysaccharide (LPS) and platelet-activating factor (PAF) stimulated a transient accumulation of ceramide.	Ceramides	184-192	patchy fur	Mus musculus	112-138
9252342-2	1997	In the present study, inflammatory activation of P388D1 macrophages with bacterial lipopolysaccharide (LPS) and platelet-activating factor (PAF) stimulated a transient accumulation of ceramide.	Ceramides	184-192	patchy fur	Mus musculus	140-143
9252342-3	1997	Moreover, cell-permeable ceramide mimicked LPS/PAF in triggering arachidonate mobilization in these cells.	Ceramides	25-33	patchy fur	Mus musculus	47-50
9252342-4	1997	LPS/PAF-induced ceramide synthesis did not result from sphingomyelinase activation but from increased de novo synthesis.	Ceramides	16-24	patchy fur	Mus musculus	4-7
9252342-5	1997	Participation of this pathway in arachidonate signaling was detected since fumonisin B1, an inhibitor of de novo ceramide synthesis, was able to inhibit the LPS/PAF-induced response.	Ceramides	113-121	patchy fur	Mus musculus	161-164
9260915-2	1997	Moreover, ectopic expression of bcl-2 can impair apoptosis signaling by most of the cell stresses that activate the ceramide/JNK pathway.	Ceramides	116-124	BCL2 apoptosis regulator	Homo sapiens	32-37
9260915-2	1997	Moreover, ectopic expression of bcl-2 can impair apoptosis signaling by most of the cell stresses that activate the ceramide/JNK pathway.	Ceramides	116-124	mitogen-activated protein kinase 8	Homo sapiens	125-128
9260915-4	1997	Moreover, enforced bcl-2 expression blocked the capacity of C2-ceramide to activate JNK1, indicating bcl-2 functions at the level of JNK1 or upstream of JNK1 in the ceramide/JNK pathway.	Ceramides	63-71	BCL2 apoptosis regulator	Homo sapiens	19-24
9260915-4	1997	Moreover, enforced bcl-2 expression blocked the capacity of C2-ceramide to activate JNK1, indicating bcl-2 functions at the level of JNK1 or upstream of JNK1 in the ceramide/JNK pathway.	Ceramides	63-71	mitogen-activated protein kinase 8	Homo sapiens	84-88
9260915-4	1997	Moreover, enforced bcl-2 expression blocked the capacity of C2-ceramide to activate JNK1, indicating bcl-2 functions at the level of JNK1 or upstream of JNK1 in the ceramide/JNK pathway.	Ceramides	63-71	BCL2 apoptosis regulator	Homo sapiens	101-106
9260915-4	1997	Moreover, enforced bcl-2 expression blocked the capacity of C2-ceramide to activate JNK1, indicating bcl-2 functions at the level of JNK1 or upstream of JNK1 in the ceramide/JNK pathway.	Ceramides	63-71	mitogen-activated protein kinase 8	Homo sapiens	133-137
9260915-4	1997	Moreover, enforced bcl-2 expression blocked the capacity of C2-ceramide to activate JNK1, indicating bcl-2 functions at the level of JNK1 or upstream of JNK1 in the ceramide/JNK pathway.	Ceramides	63-71	mitogen-activated protein kinase 8	Homo sapiens	133-137
9260915-4	1997	Moreover, enforced bcl-2 expression blocked the capacity of C2-ceramide to activate JNK1, indicating bcl-2 functions at the level of JNK1 or upstream of JNK1 in the ceramide/JNK pathway.	Ceramides	63-71	mitogen-activated protein kinase 8	Homo sapiens	84-87
9207149-2	1997	Here, we demonstrate that ceramide, a lipid metabolite synthesized upon Fas receptor ligation, inhibits n-K+ channel activity and induces a tyrosine phosphorylation of the Kv1.3 protein in Jurkat T lymphocytes.	Ceramides	26-34	potassium voltage-gated channel subfamily A member 3	Homo sapiens	172-177
9292957-11	1997	We conclude that proinflammatory cytokines inhibit D1 expression and activity in FRTL-5 cells, in part, by activation of sphingomyelinase and PLA2 that results in (1) competitive inhibition of D1 activity by the enzymatic products ceramide and arachidonic acid and (2) reduction of D1 mRNA stability by protein synthesis-dependent mechanisms.	Ceramides	231-239	phospholipase A2 group IB	Rattus norvegicus	142-146
9206994-10	1997	Although Bcl-2 is a highly efficient inhibitor of mitochondrial alterations (large amplitude swelling + DeltaPsim collapse + release of AIF) induced by prooxidants or cytosols from ceramide-treated cells, it has no effect on the ICE-induced mitochondrial PT and AIF release.	Ceramides	181-189	BCL2 apoptosis regulator	Homo sapiens	9-14
9206994-12	1997	In addition, they provide a plausible explanation of why Bcl-2 fails to interfere with Fas-triggered apoptosis in most cell types, yet prevents ceramide- and prooxidant-induced apoptosis.	Ceramides	144-152	BCL2 apoptosis regulator	Homo sapiens	57-62
9220452-5	1997	The SAPK-mediated apoptosis is also a ceramide-dependent processes.	Ceramides	38-46	mitogen-activated protein kinase 9	Rattus norvegicus	4-8
9220452-10	1997	The IQS provided neuroprotection, suggesting that ceramide-activated SAPK might play a role in IQS-sensitive neuronal death.	Ceramides	50-58	mitogen-activated protein kinase 9	Rattus norvegicus	69-73
9271217-0	1997	Bcl-2 antagonizes apoptotic cell death induced by two new ceramide analogues.	Ceramides	58-66	BCL2 apoptosis regulator	Homo sapiens	0-5
9207149-3	1997	Tyrosine phosphorylation of the n-K+ channel correlated with an activation of the Src-like tyrosine kinase p56lck upon cellular treatment with the ceramide analog C6-ceramide.	Ceramides	147-155	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	107-113
9207084-6	1997	We also determined in the same system that, when utilizing the DAGK assay, increased phosphorylation of substrates that comigrated with ceramide standards was apparent but that this effect was due to an enhancement of DAGK activity rather than increases in levels of cellular ceramides as substrates per se.	Ceramides	136-144	diacylglycerol kinase alpha	Homo sapiens	63-67
9207084-6	1997	We also determined in the same system that, when utilizing the DAGK assay, increased phosphorylation of substrates that comigrated with ceramide standards was apparent but that this effect was due to an enhancement of DAGK activity rather than increases in levels of cellular ceramides as substrates per se.	Ceramides	276-285	diacylglycerol kinase alpha	Homo sapiens	63-67
9207149-4	1997	Because genetic deficiency of p56lck or inhibition of Src-like tyrosine kinases by herbimycin A prevented ceramide-mediated n-K+ channel inhibition and tyrosine phosphorylation, we propose a ceramide-initiated activation of p56lck resulting in tyrosine phosphorylation and inhibition of the n-K+ channel protein.	Ceramides	106-114	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	30-36
9207149-4	1997	Because genetic deficiency of p56lck or inhibition of Src-like tyrosine kinases by herbimycin A prevented ceramide-mediated n-K+ channel inhibition and tyrosine phosphorylation, we propose a ceramide-initiated activation of p56lck resulting in tyrosine phosphorylation and inhibition of the n-K+ channel protein.	Ceramides	106-114	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	224-230
9207149-4	1997	Because genetic deficiency of p56lck or inhibition of Src-like tyrosine kinases by herbimycin A prevented ceramide-mediated n-K+ channel inhibition and tyrosine phosphorylation, we propose a ceramide-initiated activation of p56lck resulting in tyrosine phosphorylation and inhibition of the n-K+ channel protein.	Ceramides	191-199	LCK proto-oncogene, Src family tyrosine kinase	Homo sapiens	30-36
9210401-0	1997	Inhibition of the expression of ornithine decarboxylase and c-Myc by cell-permeant ceramide in difluoromethylornithine-resistant leukaemia cells.	Ceramides	83-91	ornithine decarboxylase, structural 1	Mus musculus	32-55
9240970-0	1997	Serine protease inhibitors block neutral sphingomyelinase activation, ceramide generation, and apoptosis triggered by daunorubicin.	Ceramides	70-78	coagulation factor II, thrombin	Homo sapiens	0-15
9240970-2	1997	Treatment of U937 and HL-60 cells with 0.5-1 microM of the chemotherapeutic drug daunorubicin induced a greater than 30% activation of neutral sphingomyelinase activity within 4-10 min with concomitant sphingomyelin hydrolysis and ceramide generation.	Ceramides	231-239	sphingomyelin phosphodiesterase 2	Homo sapiens	135-159
9240970-3	1997	DNA fragmentation and the classical morphological features of apoptosis were observed within 4-6 h. Pretreatment of cells with the serine protease inhibitors N-tosyl-L-phenylalanyl chloromethyl ketone (20 microM) or dichloroisocoumarin (20 microM) for 30 min inhibited daunorubicin-induced neutral sphingomyelinase activation, sphingomyelin hydrolysis, ceramide generation, and apoptosis.	Ceramides	353-361	coagulation factor II, thrombin	Homo sapiens	131-146
9240970-7	1997	These results suggest that inhibitors of serine proteases can act upstream of ceramide in drug-triggered apoptosis and that neutral sphingomyelinase activation is either directly or indirectly serine protease dependent.	Ceramides	78-86	coagulation factor II, thrombin	Homo sapiens	41-56
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.	Ceramides	101-109	prosaposin	Homo sapiens	183-193
9204210-6	1997	Ceramide storage in prosaposin-deficient cells was also demonstrated by ceramide mass determination.	Ceramides	0-8	prosaposin	Homo sapiens	20-30
9204210-6	1997	Ceramide storage in prosaposin-deficient cells was also demonstrated by ceramide mass determination.	Ceramides	72-80	prosaposin	Homo sapiens	20-30
9204210-7	1997	In contrast to acid ceramidase deficient cells, both the accumulation of ceramide and the reduced in vitro activity of acid ceramidase in cells from prosaposin deficiency could be corrected by addition of purified saposin D. The data confirm that prosaposin is required for lysosomal ceramide degradation, but not for sphingomyelin turnover.	Ceramides	284-292	prosaposin	Homo sapiens	149-159
9182681-0	1997	Mice genetically hyporesponsive to lipopolysaccharide (LPS) exhibit a defect in endocytic uptake of LPS and ceramide.	Ceramides	108-116	toll-like receptor 4	Mus musculus	55-58
9182681-12	1997	As with LPS, we found that binding of fluorescent ceramide by Lpsd and Lpsn macrophages was quantitatively similar, and the label moved rapidly to one to two spots in the perinuclear region in Lpsn mice.	Ceramides	50-58	toll-like receptor 4	Mus musculus	8-11
9182681-14	1997	These results show that cells deficient in responses to LPS exhibit defective vesicular transport of LPS and ceramide and point to a role for vesicular transport in responses to these mediators.	Ceramides	109-117	toll-like receptor 4	Mus musculus	56-59
9202042-0	1997	Phospholipase A2 is necessary for tumor necrosis factor alpha-induced ceramide generation in L929 cells.	Ceramides	70-78	phospholipase A2, group IB, pancreas	Mus musculus	0-16
9202042-0	1997	Phospholipase A2 is necessary for tumor necrosis factor alpha-induced ceramide generation in L929 cells.	Ceramides	70-78	tumor necrosis factor	Mus musculus	34-61
9202042-1	1997	The role of cytosolic phospholipase A2 (cPLA2) in the regulation of ceramide formation was examined in a cell line (L929) responsive to the cytotoxic action of tumor necrosis factor alpha (TNFalpha).	Ceramides	68-76	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	12-38
9202042-1	1997	The role of cytosolic phospholipase A2 (cPLA2) in the regulation of ceramide formation was examined in a cell line (L929) responsive to the cytotoxic action of tumor necrosis factor alpha (TNFalpha).	Ceramides	68-76	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	40-45
9202042-2	1997	In L929 cells, the addition of TNFalpha resulted in the release of arachidonate, which was followed by a prolonged accumulation of ceramide occurring over 5-12 h and reaching 250% over base line.	Ceramides	131-139	tumor necrosis factor	Mus musculus	31-39
9202042-8	1997	The introduction of the cPLA2 gene into C12 cells resulted in partial restoration of TNFalpha-induced arachidonate release, ceramide accumulation, and cytotoxicity.	Ceramides	124-132	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	24-29
9202042-9	1997	This study suggests that cPLA2 is a necessary component in the pathways leading to ceramide accumulation and cell death.	Ceramides	83-91	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	25-30
9252504-9	1997	Ceramide generated during TNF signaling leads to increased production of ROS in mitochondria.	Ceramides	0-8	tumor necrosis factor-like	Rattus norvegicus	26-29
9186373-11	1997	Ceramides (C2 & C6), which were closely related chemically to sphinganine but lacked affinity for the regulatory subunit of PKC, were inactive in this system.	Ceramides	0-9	proline rich transmembrane protein 2	Homo sapiens	128-131
9195956-1	1997	Ceramide inhibits phorbol ester activation of nuclear factor kappaB.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	61-67
9195956-4	1997	We investigated the role of the sphingolipid mediator ceramide in the cytokine-induced signaling mechanisms leading to NF-kappaB activation and cell death.	Ceramides	54-62	nuclear factor kappa B subunit 1	Homo sapiens	119-128
9195956-5	1997	Several lines of evidence presented here suggest that ceramide generated in response to TNFalpha or Fas activation is not involved in NF-kappaB activation.	Ceramides	54-62	tumor necrosis factor	Homo sapiens	88-96
9195956-7	1997	(ii) Ceramide treatment of cells inhibited phorbol ester-induced activation of NF-kappaB.	Ceramides	5-13	nuclear factor kappa B subunit 1	Homo sapiens	79-88
9195956-10	1997	(v) Treatment of Jurkat cells with cross-linking antibodies to APO-1/Fas induced large scale increases in ceramide and apoptosis without affecting NF-kappaB.	Ceramides	106-114	Fas cell surface death receptor	Homo sapiens	63-68
9195956-11	1997	(vi) Ceramide generation in response to Fas activation was inhibited by N-acetyltyrosinylvalinylalanylaspartyl chloromethyl ketone, a peptide inhibitor of interleukin-1beta-converting enzyme-like proteases, whereas TNFalpha-induced NF-kappaB activation was unaffected by the inhibitor.	Ceramides	5-13	tumor necrosis factor	Homo sapiens	215-223
9195956-11	1997	(vi) Ceramide generation in response to Fas activation was inhibited by N-acetyltyrosinylvalinylalanylaspartyl chloromethyl ketone, a peptide inhibitor of interleukin-1beta-converting enzyme-like proteases, whereas TNFalpha-induced NF-kappaB activation was unaffected by the inhibitor.	Ceramides	5-13	nuclear factor kappa B subunit 1	Homo sapiens	232-241
9195956-12	1997	These results show that ceramide accumulation belongs selectively to the apoptotic pathway(s) induced by cytokines, and, if anything, ceramide may participate in negative feedback regulation of NF-kappaB.	Ceramides	134-142	nuclear factor kappa B subunit 1	Homo sapiens	194-203
9210401-12	1997	These results suggest that the inhibition of c-Myc and ODC expression may be early events in the response of leukaemia cells to ceramide.	Ceramides	128-136	myelocytomatosis oncogene	Mus musculus	47-50
9210401-12	1997	These results suggest that the inhibition of c-Myc and ODC expression may be early events in the response of leukaemia cells to ceramide.	Ceramides	128-136	ornithine decarboxylase, structural 1	Mus musculus	55-58
9210401-0	1997	Inhibition of the expression of ornithine decarboxylase and c-Myc by cell-permeant ceramide in difluoromethylornithine-resistant leukaemia cells.	Ceramides	83-91	myelocytomatosis oncogene	Mus musculus	62-65
9210401-2	1997	In difluoromethylornithine-resistant L1210 cells stimulated to growth from quiescence, the cell-permeant analogues of ceramide N-acetylsphingosine (C2-ceramide) and N-hexanoylsphingosine (C6-ceramide) inhibited the induction of ornithine decarboxylase (ODC) activity with IC50 of 8.3 and 1.5 microM respectively.	Ceramides	118-126	ornithine decarboxylase, structural 1	Mus musculus	228-251
9210401-2	1997	In difluoromethylornithine-resistant L1210 cells stimulated to growth from quiescence, the cell-permeant analogues of ceramide N-acetylsphingosine (C2-ceramide) and N-hexanoylsphingosine (C6-ceramide) inhibited the induction of ornithine decarboxylase (ODC) activity with IC50 of 8.3 and 1.5 microM respectively.	Ceramides	118-126	ornithine decarboxylase, structural 1	Mus musculus	253-256
9184074-4	1997	In addition, apoptosis was induced by both native and synthesized ceramide and prevented by YVAD-CHO and DEVD-CHO, suggesting the possible involvement of ceramide in ICE cascade operation.	Ceramides	154-162	caspase 1	Mus musculus	166-169
9196025-6	1997	The mRNA expression in monocytes is sensitive to lipopolysaccharide and ceramide which both strongly increase DIF-2 transcription, while lysophosphatidylcholine results in a weaker upregulation of DIF-2 expression.	Ceramides	72-80	immediate early response 3	Homo sapiens	110-115
9196025-6	1997	The mRNA expression in monocytes is sensitive to lipopolysaccharide and ceramide which both strongly increase DIF-2 transcription, while lysophosphatidylcholine results in a weaker upregulation of DIF-2 expression.	Ceramides	72-80	immediate early response 3	Homo sapiens	197-202
9196025-8	1997	Our results indicate that DIF-2 represents a gene which is regulated in differentiation processes and strongly responsive to lipopolysaccharide, ceramide and lysophosphatidylcholine.	Ceramides	145-153	immediate early response 3	Homo sapiens	26-31
9227535-0	1997	Involvement of ceramide in inhibitory effect of IL-1 beta on L-type Ca2+ current in adult rat ventricular myocytes.	Ceramides	15-23	interleukin 1 beta	Rattus norvegicus	48-57
9227535-3	1997	Exposure of myocytes to 5 ng/ml IL-1 beta elicited a 140% increase in ceramide production within 2 min, as measured with 32P phosphorylation.	Ceramides	70-78	interleukin 1 beta	Rattus norvegicus	32-41
9227535-9	1997	These results suggest that ceramide mediates IL-1 beta-induced suppression of cardiac ICa,L.	Ceramides	27-35	interleukin 1 beta	Rattus norvegicus	45-54
9192094-1	1997	TNF-alpha induced sphingomyelin hydrolysis by sphingomyelinase and both sphingosine and ceramide generation have been reported to be implicated in a number of TNF-alpha responses, including cytotoxicity and apoptosis.	Ceramides	88-96	tumor necrosis factor	Mus musculus	0-9
9192094-1	1997	TNF-alpha induced sphingomyelin hydrolysis by sphingomyelinase and both sphingosine and ceramide generation have been reported to be implicated in a number of TNF-alpha responses, including cytotoxicity and apoptosis.	Ceramides	88-96	tumor necrosis factor	Mus musculus	159-168
9184074-5	1997	To directly demonstrate whether ceramide synthesis operates the ICE cascade, proteolytic activity of ICE- or CPP32-like proteinase was analyzed.	Ceramides	32-40	caspase 1	Mus musculus	64-67
9184074-5	1997	To directly demonstrate whether ceramide synthesis operates the ICE cascade, proteolytic activity of ICE- or CPP32-like proteinase was analyzed.	Ceramides	32-40	caspase 1	Mus musculus	101-105
9184074-5	1997	To directly demonstrate whether ceramide synthesis operates the ICE cascade, proteolytic activity of ICE- or CPP32-like proteinase was analyzed.	Ceramides	32-40	caspase 3	Mus musculus	109-114
9184074-8	1997	These results suggest that ceramide synthesis acts as a dominant regulator in CPT-11-initiated death signaling and sequentially operates the ICE cascade.	Ceramides	27-35	caspase 1	Mus musculus	141-144
9144515-1	1997	In FMLP-activated polymorphonuclear leukocytes (PMNs) challenged with IgG-opsonized erythrocytes (EIgG), the termination of phagocytosis correlates with an accumulation of ceramide, a product of sphingolipid metabolism.	Ceramides	172-180	formyl peptide receptor 1	Homo sapiens	3-7
9148901-3	1997	Since the generation of ceramide has been directly linked with the activation of the transcription factor, NFkappaB, this was investigated as a novel target for the action of daunorubicin.	Ceramides	24-32	nuclear factor kappa B subunit 1	Homo sapiens	107-115
9144515-3	1997	In the present study, we identified p42 and p44 mitogen-actived protein (MAP) kinases, referred to as extracellular signal-regulated kinases ERK2 and ERK1, respectively, as intracellular targets of ceramide action during Fc gammaR-mediated phagocytosis.	Ceramides	198-206	cyclin dependent kinase 20	Homo sapiens	36-39
9144515-3	1997	In the present study, we identified p42 and p44 mitogen-actived protein (MAP) kinases, referred to as extracellular signal-regulated kinases ERK2 and ERK1, respectively, as intracellular targets of ceramide action during Fc gammaR-mediated phagocytosis.	Ceramides	198-206	mitogen-activated protein kinase 1	Homo sapiens	141-145
9144515-3	1997	In the present study, we identified p42 and p44 mitogen-actived protein (MAP) kinases, referred to as extracellular signal-regulated kinases ERK2 and ERK1, respectively, as intracellular targets of ceramide action during Fc gammaR-mediated phagocytosis.	Ceramides	198-206	mitogen-activated protein kinase 3	Homo sapiens	150-154
9094715-6	1997	TNF alpha or ceramide analogs markedly enhance KSR autophosphorylation and its ability to complex with, phosphorylate, and activate Raf-1.	Ceramides	13-21	kinase suppressor of ras 1	Mus musculus	47-50
9141429-8	1997	Ceramide is a second messenger generated by TNF-alpha treatment and is an activator of JNK.	Ceramides	0-8	tumor necrosis factor	Rattus norvegicus	44-53
9141429-8	1997	Ceramide is a second messenger generated by TNF-alpha treatment and is an activator of JNK.	Ceramides	0-8	mitogen-activated protein kinase 8	Rattus norvegicus	87-90
9141429-9	1997	Because JNK activation preceded the elevations in ceramide and TNF-alpha mRNA, these results suggest that increased hepatic TNF-alpha and ceramide may perpetuate JNK induction, but that they are not the initiating signals of JNK activation during reperfusion injury in the transplanted liver.	Ceramides	138-146	mitogen-activated protein kinase 8	Rattus norvegicus	162-165
9141429-9	1997	Because JNK activation preceded the elevations in ceramide and TNF-alpha mRNA, these results suggest that increased hepatic TNF-alpha and ceramide may perpetuate JNK induction, but that they are not the initiating signals of JNK activation during reperfusion injury in the transplanted liver.	Ceramides	138-146	mitogen-activated protein kinase 8	Rattus norvegicus	162-165
9111045-2	1997	Ceramide is a sphingolipid that is generated in the signaling of inflammatory cytokines such as tumor necrosis factor (TNF), which exerts many functional roles depending on the cell type where it is produced.	Ceramides	0-8	tumor necrosis factor-like	Rattus norvegicus	96-117
9111045-2	1997	Ceramide is a sphingolipid that is generated in the signaling of inflammatory cytokines such as tumor necrosis factor (TNF), which exerts many functional roles depending on the cell type where it is produced.	Ceramides	0-8	tumor necrosis factor-like	Rattus norvegicus	119-122
9111045-11	1997	Mitochondria isolated from TNF-treated cells showed an increase (2-3-fold) in the amount of ceramide compared with mitochondria from untreated cells.	Ceramides	92-100	tumor necrosis factor-like	Rattus norvegicus	27-30
9111045-12	1997	These results suggest that mitochondria are a target of ceramide produced in the signaling of TNF whose effect on mitochondrial electron transport chain leads to overproduction of hydrogen peroxide and consequently this phenomena may account for the generation of reactive oxygen species during TNF cytotoxicity.	Ceramides	56-64	tumor necrosis factor-like	Rattus norvegicus	94-97
9111045-12	1997	These results suggest that mitochondria are a target of ceramide produced in the signaling of TNF whose effect on mitochondrial electron transport chain leads to overproduction of hydrogen peroxide and consequently this phenomena may account for the generation of reactive oxygen species during TNF cytotoxicity.	Ceramides	56-64	tumor necrosis factor-like	Rattus norvegicus	295-298
9099747-5	1997	The sphingomyelin pathway is thought to mediate the TNF-alpha-induced activation of NF-kappaB by its second messenger ceramide.	Ceramides	118-126	tumor necrosis factor	Mus musculus	52-61
9099747-5	1997	The sphingomyelin pathway is thought to mediate the TNF-alpha-induced activation of NF-kappaB by its second messenger ceramide.	Ceramides	118-126	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	84-93
9092523-17	1997	However, when challenged with anti-IgM the bcl-xL transfectants produced levels of ceramide similar to wild type cells, suggesting that ceramide formation is upstream of bcl-xL and that it is a major determinant of B-cell death.	Ceramides	83-91	BCL2-like 1	Mus musculus	43-49
9092523-17	1997	However, when challenged with anti-IgM the bcl-xL transfectants produced levels of ceramide similar to wild type cells, suggesting that ceramide formation is upstream of bcl-xL and that it is a major determinant of B-cell death.	Ceramides	136-144	BCL2-like 1	Mus musculus	43-49
9251249-7	1997	Ceramide inhibits PLC delta 1 very weakly.	Ceramides	0-8	phospholipase C delta 1	Homo sapiens	18-29
9251249-8	1997	GM1, which is a ceramide bound glucosidically to the oligosaccharide moiety, was a strong non-competitive inhibitor of PLC delta 1.	Ceramides	16-24	phospholipase C delta 1	Homo sapiens	119-130
9150390-0	1997	Influence of Bcl-2 overexpression on the ceramide pathway in daunorubicin-induced apoptosis of leukemic cells.	Ceramides	41-49	BCL2 apoptosis regulator	Homo sapiens	13-18
9150390-7	1997	In contrast, Bcl-2 overexpression protected the cells against apoptosis induced by ceramide treatment, without preventing the early SM hydrolysis nor the ceramide generation in these cells.	Ceramides	83-91	BCL2 apoptosis regulator	Homo sapiens	13-18
9130145-2	1997	Using primary culture methods, we report that neurons and astrocytes require the activity of the ICE/CED-3 family of proteases to undergo apoptosis induced by staurosporine, ceramide, and serum-free media.	Ceramides	174-182	caspase 1	Homo sapiens	97-100
9130145-2	1997	Using primary culture methods, we report that neurons and astrocytes require the activity of the ICE/CED-3 family of proteases to undergo apoptosis induced by staurosporine, ceramide, and serum-free media.	Ceramides	174-182	intraflagellar transport 43	Homo sapiens	101-106
9094715-6	1997	TNF alpha or ceramide analogs markedly enhance KSR autophosphorylation and its ability to complex with, phosphorylate, and activate Raf-1.	Ceramides	13-21	v-raf-leukemia viral oncogene 1	Mus musculus	132-137
9094715-7	1997	In vitro, low nanomolar concentrations of natural ceramide stimulate KSR to autophosphorylate, and transactivate Raf-1.	Ceramides	50-58	kinase suppressor of ras 1	Mus musculus	69-72
9094715-7	1997	In vitro, low nanomolar concentrations of natural ceramide stimulate KSR to autophosphorylate, and transactivate Raf-1.	Ceramides	50-58	v-raf-leukemia viral oncogene 1	Mus musculus	113-118
9176098-4	1997	C2- or C6-ceramide inhibited O2- release from monocytes primed with LPS (1 ng/ml) or IFN-gamma (100 U/ml), but did not affect unprimed monocytes.	Ceramides	10-18	interferon gamma	Homo sapiens	85-94
9524442-9	1997	P fimbriae that bind the globoseries of glycolipids cause the release of ceramides and activation of the ceramide signaling pathway which contributes to the IL-6 response.	Ceramides	73-82	interleukin 6	Homo sapiens	157-161
9524442-9	1997	P fimbriae that bind the globoseries of glycolipids cause the release of ceramides and activation of the ceramide signaling pathway which contributes to the IL-6 response.	Ceramides	73-81	interleukin 6	Homo sapiens	157-161
9147062-5	1997	The ceramide composition of the parent glycosphingolipids was dominated by the 2-(R)-hydroxy C24:0 fatty acid, cerebronic acid, and C17 sphingoid-bases: 15-methylhexadecasphing-4-enine and 15-methylhexadecaphinganine in approximately equal proportions.	Ceramides	4-12	cytokine like 1	Homo sapiens	132-135
9130266-1	1997	Tumor necrosis factor-alpha induces oligodendrocytes apoptosis, and is known to stimulate the hydrolysis of sphingomyelin to form the lipid mediator, ceramide.	Ceramides	150-158	tumor necrosis factor	Bos taurus	0-27
9079627-0	1997	TAK1 mediates the ceramide signaling to stress-activated protein kinase/c-Jun N-terminal kinase.	Ceramides	18-26	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	0-4
9079627-2	1997	It has recently been reported that ceramide activates stress-activated protein kinase (SAPK, also known as c-Jun NH2-terminal kinase JNK), a subfamily member of mitogen-activated protein kinase superfamily molecules and that the ceramide/SAPK/JNK signaling pathway is required for stress-induced apoptosis.	Ceramides	35-43	mitogen-activated protein kinase 8	Homo sapiens	133-136
9079627-2	1997	It has recently been reported that ceramide activates stress-activated protein kinase (SAPK, also known as c-Jun NH2-terminal kinase JNK), a subfamily member of mitogen-activated protein kinase superfamily molecules and that the ceramide/SAPK/JNK signaling pathway is required for stress-induced apoptosis.	Ceramides	35-43	mitogen-activated protein kinase 8	Homo sapiens	243-246
9079627-2	1997	It has recently been reported that ceramide activates stress-activated protein kinase (SAPK, also known as c-Jun NH2-terminal kinase JNK), a subfamily member of mitogen-activated protein kinase superfamily molecules and that the ceramide/SAPK/JNK signaling pathway is required for stress-induced apoptosis.	Ceramides	229-237	mitogen-activated protein kinase 8	Homo sapiens	133-136
9079627-2	1997	It has recently been reported that ceramide activates stress-activated protein kinase (SAPK, also known as c-Jun NH2-terminal kinase JNK), a subfamily member of mitogen-activated protein kinase superfamily molecules and that the ceramide/SAPK/JNK signaling pathway is required for stress-induced apoptosis.	Ceramides	229-237	mitogen-activated protein kinase 8	Homo sapiens	243-246
9079627-3	1997	However, the molecular mechanism by which ceramide induces SAPK/JNK activation is unknown.	Ceramides	42-50	mitogen-activated protein kinase 8	Homo sapiens	64-67
9079627-4	1997	Here we show that TAK1, a member of the mitogen-activated protein kinase kinase kinase family, is activated by treatment of cells with agents and stresses that induce an increase in ceramide.	Ceramides	182-190	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	18-22
9079627-5	1997	Ceramide itself stimulated the kinase activity of TAK1.	Ceramides	0-8	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	50-54
9079627-7	1997	Furthermore, expression of a kinase-negative form of TAK1 interfered with the activation of SAPK/JNK induced by ceramide.	Ceramides	112-120	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	53-57
9079627-7	1997	Furthermore, expression of a kinase-negative form of TAK1 interfered with the activation of SAPK/JNK induced by ceramide.	Ceramides	112-120	mitogen-activated protein kinase 8	Homo sapiens	97-100
9079627-8	1997	These results indicate that TAK1 may function as a mediator of ceramide signaling to SAPK/JNK activation.	Ceramides	63-71	mitogen-activated protein kinase kinase kinase 7	Homo sapiens	28-32
9079627-8	1997	These results indicate that TAK1 may function as a mediator of ceramide signaling to SAPK/JNK activation.	Ceramides	63-71	mitogen-activated protein kinase 8	Homo sapiens	90-93
9058737-2	1997	In adherent PMNs, the kinetics of ceramide production correspond with the termination of fMLP-stimulated H2O2 release.	Ceramides	34-42	formyl peptide receptor 1	Homo sapiens	89-93
9058737-3	1997	Furthermore, short chain ceramides inhibit fMLP-mediated H2O2 release in adherent PMNs.	Ceramides	25-34	formyl peptide receptor 1	Homo sapiens	43-47
9058737-8	1997	Neutral sphingomyelinase activity paralleled the increase in ceramide, consistent with the generation of ceramide by the hydrolysis of sphingomyelin.	Ceramides	61-69	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
9058737-8	1997	Neutral sphingomyelinase activity paralleled the increase in ceramide, consistent with the generation of ceramide by the hydrolysis of sphingomyelin.	Ceramides	105-113	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
9058737-9	1997	The N-acetyl-conjugated sphingols (C2 ceramides) blocked phosphatidylethanol formation indicating that phospholipase D (PLD) is an intracellular target of ceramide action.	Ceramides	38-47	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	103-118
9058737-9	1997	The N-acetyl-conjugated sphingols (C2 ceramides) blocked phosphatidylethanol formation indicating that phospholipase D (PLD) is an intracellular target of ceramide action.	Ceramides	38-47	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	120-123
9058737-9	1997	The N-acetyl-conjugated sphingols (C2 ceramides) blocked phosphatidylethanol formation indicating that phospholipase D (PLD) is an intracellular target of ceramide action.	Ceramides	38-46	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	103-118
9058737-9	1997	The N-acetyl-conjugated sphingols (C2 ceramides) blocked phosphatidylethanol formation indicating that phospholipase D (PLD) is an intracellular target of ceramide action.	Ceramides	38-46	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	120-123
9069584-3	1997	Interestingly, L-carnitine treatment led to a significant reduction of peripheral blood mononuclear cell-associated ceramide (an intracellular messenger for apoptosis) that correlated with the decrease of apoptotic CD4- and CD8-positive cells.	Ceramides	116-124	CD8a molecule	Homo sapiens	224-227
9054379-0	1997	Alteration of the sphingomyelin/ceramide pathway is associated with resistance of human breast carcinoma MCF7 cells to tumor necrosis factor-alpha-mediated cytotoxicity.	Ceramides	32-40	tumor necrosis factor	Homo sapiens	119-146
9054379-10	1997	Our findings strongly suggest a role of ceramide in the mechanism of cell resistance to TNF-mediated cell death and may be relevant in elucidating the biochemical nature of intracellular messengers leading to such resistance.	Ceramides	40-48	tumor necrosis factor	Homo sapiens	88-91
9069584-9	1997	Our data indicate that L-carnitine is able to inhibit CD95-induced apoptosis of these cells, most likely by preventing sphingomyelin breakdown and consequent ceramide synthesis.	Ceramides	158-166	Fas cell surface death receptor	Homo sapiens	54-58
9069583-4	1997	Interestingly, the L-carnitine treatment, which did not show relevant side effects in four patients, led to a strong and significant reduction of peripheral blood mononuclear cell-associated ceramide, an intracellular messenger of apoptosis, that positively correlated with the decrease of apoptotic CD4- and CD8-positive cells.	Ceramides	191-199	CD4 molecule	Homo sapiens	300-303
9069583-4	1997	Interestingly, the L-carnitine treatment, which did not show relevant side effects in four patients, led to a strong and significant reduction of peripheral blood mononuclear cell-associated ceramide, an intracellular messenger of apoptosis, that positively correlated with the decrease of apoptotic CD4- and CD8-positive cells.	Ceramides	191-199	CD8a molecule	Homo sapiens	309-312
9046335-2	1997	Structure-function relationships of sulfated sialyl Lewis X hexasaccharide ceramides toward E-, P-, and L-selectin binding.	Ceramides	75-84	selectin L	Homo sapiens	104-114
9030540-2	1997	TNF-alpha stimulation of adult feline cardiac myocytes provoked a rapid (<15 min) increase in the hydrolysis of [14C]sphingomyelin in cell-free extracts, as well as an increase in ceramide mass, consistent with cytokine-induced activation of the neutral sphingomyelinase pathway.	Ceramides	183-191	tumor necrosis factor	Homo sapiens	0-9
9070896-2	1997	At physiological temperature the CD2 scissoring mode of the palmitic acid methylenes, and the CH2 rocking mode of the ceramide methylenes, are each split into two components.	Ceramides	118-126	CD2 molecule	Homo sapiens	33-36
9070896-5	1997	The thermotropic behavior of the CD2 stretching vibrations demonstrates that conformational disordering of the palmitic acid commences at 42 degrees C with a transition midpoint of 50 degrees C. The CH2 stretching frequency indicates the ceramide chains remain ordered until 50 degrees C then disorder with a midpoint of 67 degrees C. The results provide a molecular characterization for the complex low temperature (10-40 degrees C) dynamic behavior suggested by recent 2H NMR experiments.	Ceramides	238-246	CD2 molecule	Homo sapiens	33-36
9046335-4	1997	As a result, we found that the 6"-sulfated sLe(x) hexasaccharide ceramides 1-3 have similar binding avidities to L-selectin and their binding to L-selectin appeared somewhat stronger than that of sLe(x).	Ceramides	65-74	selectin L	Homo sapiens	145-155
9046335-3	1997	In order to clarify the real ligand structure of L-selectin proposed by Rosen et al., we first synthesized 6-sulfated sLe(x) hexasaccharide ceramide 1, 6"-sulfated sLe(x) hexasaccharide ceramide 2, and 6,6"-disulfated sLe(x) hexasaccharide ceramide 3 and examined their binding avidities for L-selectin.	Ceramides	140-148	selectin L	Homo sapiens	49-59
9046335-3	1997	In order to clarify the real ligand structure of L-selectin proposed by Rosen et al., we first synthesized 6-sulfated sLe(x) hexasaccharide ceramide 1, 6"-sulfated sLe(x) hexasaccharide ceramide 2, and 6,6"-disulfated sLe(x) hexasaccharide ceramide 3 and examined their binding avidities for L-selectin.	Ceramides	186-194	selectin L	Homo sapiens	49-59
9046335-3	1997	In order to clarify the real ligand structure of L-selectin proposed by Rosen et al., we first synthesized 6-sulfated sLe(x) hexasaccharide ceramide 1, 6"-sulfated sLe(x) hexasaccharide ceramide 2, and 6,6"-disulfated sLe(x) hexasaccharide ceramide 3 and examined their binding avidities for L-selectin.	Ceramides	186-194	selectin L	Homo sapiens	49-59
9013572-7	1997	Inhibition of CPT I by etomoxir enhanced palmitate-induced cell death and led to a further increase in ceramide synthesis.	Ceramides	103-111	carnitine palmitoyltransferase 1b, muscle	Mus musculus	14-19
9046335-4	1997	As a result, we found that the 6"-sulfated sLe(x) hexasaccharide ceramides 1-3 have similar binding avidities to L-selectin and their binding to L-selectin appeared somewhat stronger than that of sLe(x).	Ceramides	65-74	selectin L	Homo sapiens	113-123
9343942-12	1997	HCl), a well-known inhibitor of GlcT-1 (Ceramide: UDP-Glc Glucosyltransferase), an enzyme in the glycolipid synthetic pathway.	Ceramides	40-48	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	32-38
9053448-0	1997	Cytokine response modifier A (CrmA) inhibits ceramide formation in response to tumor necrosis factor (TNF)-alpha: CrmA and Bcl-2 target distinct components in the apoptotic pathway.	Ceramides	45-53	tumor necrosis factor	Homo sapiens	79-112
9053448-0	1997	Cytokine response modifier A (CrmA) inhibits ceramide formation in response to tumor necrosis factor (TNF)-alpha: CrmA and Bcl-2 target distinct components in the apoptotic pathway.	Ceramides	45-53	BCL2 apoptosis regulator	Homo sapiens	123-128
9053448-2	1997	Here, we examine the role of proteases and their relationship to ceramide, a proposed mediator of apoptosis, in the tumor necrosis factor-alpha (TNF-alpha)-induced pathway of cell death.	Ceramides	65-73	tumor necrosis factor	Homo sapiens	116-143
9053448-2	1997	Here, we examine the role of proteases and their relationship to ceramide, a proposed mediator of apoptosis, in the tumor necrosis factor-alpha (TNF-alpha)-induced pathway of cell death.	Ceramides	65-73	tumor necrosis factor	Homo sapiens	145-154
9053448-3	1997	Ceramide induced activation of prICE, the protease that cleaves the death substrate poly(ADP-ribose) polymerase.	Ceramides	0-8	poly(ADP-ribose) polymerase 1	Homo sapiens	84-111
9053448-4	1997	Bcl-2 inhibited ceramide-induced death, but not ceramide generation.	Ceramides	16-24	BCL2 apoptosis regulator	Homo sapiens	0-5
9063586-7	1997	Recent studies have elucidated signal transduction pathways of TGF beta (serine/threonine kinase cascades), TNF alpha (p55 receptor linked to a sphingomyelin-ceramide-NF kappa B pathway), and secreted forms of beta APP (sAPP; receptor guanylate cyclase-cGMP-cGMP-dependent kinase-K+ channel activation).	Ceramides	158-166	transforming growth factor alpha	Mus musculus	63-71
9063586-7	1997	Recent studies have elucidated signal transduction pathways of TGF beta (serine/threonine kinase cascades), TNF alpha (p55 receptor linked to a sphingomyelin-ceramide-NF kappa B pathway), and secreted forms of beta APP (sAPP; receptor guanylate cyclase-cGMP-cGMP-dependent kinase-K+ channel activation).	Ceramides	158-166	tumor necrosis factor	Mus musculus	108-117
9063586-7	1997	Recent studies have elucidated signal transduction pathways of TGF beta (serine/threonine kinase cascades), TNF alpha (p55 receptor linked to a sphingomyelin-ceramide-NF kappa B pathway), and secreted forms of beta APP (sAPP; receptor guanylate cyclase-cGMP-cGMP-dependent kinase-K+ channel activation).	Ceramides	158-166	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	167-177
9013876-6	1997	Furthermore, the peptide inhibitor of interleukin-1beta converting enzyme (ICE)-like proteases, Z-VAD.FMK, completely prevented the nuclear changes induced by ceramide, implicating the involvement of ICE-like protease activation in ceramide-induced apoptosis in PC12 cells.	Ceramides	159-167	caspase 1	Rattus norvegicus	75-78
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.	Ceramides	94-102	fibroblast growth factor 2	Homo sapiens	276-280
8999958-3	1997	Ceramide-induced apoptosis was reported to be blocked by 12-O-tetradecanoylphorbol 13-acetate, a protein kinase C (PKC) activator, but its mechanism remained unclear.	Ceramides	0-8	protein kinase C delta	Homo sapiens	115-118
8999958-5	1997	We here report that N-acetylsphingosine (synthetic membrane-permeable ceramide) induced translocation of PKC-delta and -epsilon isozymes from the membrane to the cytosol within 5 min in human leukemia cell lines.	Ceramides	70-78	protein kinase C delta	Homo sapiens	105-127
8999958-6	1997	Treatment with sphingomyelinase, tumor necrosis factor-alpha, or anti-Fas antibody, all of which can induce apoptosis by generating natural ceramide, similarly induced cytosolic translocation of PKC-delta and -epsilon.	Ceramides	140-148	protein kinase C epsilon	Homo sapiens	195-217
8999958-8	1997	Furthermore, both 12-O-tetradecanoylphorbol 13-acetate and a nonspecific kinase inhibitor, staurosporine, prevented ceramide-induced apoptosis by inhibiting cytosolic translocation of PKC-delta and -epsilon.	Ceramides	116-124	protein kinase C epsilon	Homo sapiens	184-206
9151319-5	1997	This paper provides mechanistic support for the occurrence of apoptosis in this disease: There was marked upregulation of Bcl-2 in brain from the late infantile and juvenile types at the protein and RNA levels both by immunocytochemistry and by Northern blot analysis; there were also a 42% to 197% increase in brain ceramide determinations in brains from three patients with the juvenile type and three patients with the late infantile type.	Ceramides	317-325	BCL2 apoptosis regulator	Homo sapiens	122-127
9151319-7	1997	These results raise the possibility that the intact CLN3 gene is normally antiapoptotic, and that it could be an upstream regulator of ceramide.	Ceramides	135-143	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	52-56
8999958-9	1997	These data suggest that cytosolic translocation of PKC-delta and -epsilon plays an important role in ceramide-mediated apoptosis.	Ceramides	101-109	protein kinase C epsilon	Homo sapiens	51-73
9013876-6	1997	Furthermore, the peptide inhibitor of interleukin-1beta converting enzyme (ICE)-like proteases, Z-VAD.FMK, completely prevented the nuclear changes induced by ceramide, implicating the involvement of ICE-like protease activation in ceramide-induced apoptosis in PC12 cells.	Ceramides	159-167	caspase 1	Rattus norvegicus	200-203
9013876-6	1997	Furthermore, the peptide inhibitor of interleukin-1beta converting enzyme (ICE)-like proteases, Z-VAD.FMK, completely prevented the nuclear changes induced by ceramide, implicating the involvement of ICE-like protease activation in ceramide-induced apoptosis in PC12 cells.	Ceramides	232-240	caspase 1	Rattus norvegicus	75-78
9013876-6	1997	Furthermore, the peptide inhibitor of interleukin-1beta converting enzyme (ICE)-like proteases, Z-VAD.FMK, completely prevented the nuclear changes induced by ceramide, implicating the involvement of ICE-like protease activation in ceramide-induced apoptosis in PC12 cells.	Ceramides	232-240	caspase 1	Rattus norvegicus	200-203
8995404-0	1997	Cell-permeable ceramides prevent the activation of phospholipase D by ADP-ribosylation factor and RhoA.	Ceramides	15-24	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	51-66
8995404-0	1997	Cell-permeable ceramides prevent the activation of phospholipase D by ADP-ribosylation factor and RhoA.	Ceramides	15-24	ras homolog family member A	Homo sapiens	98-102
8995404-7	1997	It is concluded that one mechanism by which ceramides prevent the activation of PLD is inhibition of the translocation to membranes of G-proteins and protein kinase C isoforms that are required for PLD activity.	Ceramides	44-53	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	80-83
8995404-7	1997	It is concluded that one mechanism by which ceramides prevent the activation of PLD is inhibition of the translocation to membranes of G-proteins and protein kinase C isoforms that are required for PLD activity.	Ceramides	44-53	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	198-201
8995404-1	1997	The mechanism of inhibition of phospholipase D (PLD) by ceramides was determined using granulocytes differentiated from human promyelocytic leukemic (HL-60) cells.	Ceramides	56-65	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	31-46
8995404-1	1997	The mechanism of inhibition of phospholipase D (PLD) by ceramides was determined using granulocytes differentiated from human promyelocytic leukemic (HL-60) cells.	Ceramides	56-65	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	48-51
9110068-6	1997	RESULTS: A marked enhancement in the levels of ceramide, a product of the sphingomyelin hydrolysis, was observed in U251MG-Nef upon stimulation with TNF-alpha.	Ceramides	47-55	S100 calcium binding protein B	Homo sapiens	123-126
9000505-0	1997	Ceramides induce a form of apoptosis in human acute lymphoblastic leukemia cells that is inhibited by Bcl-2, but not by CrmA.	Ceramides	0-9	BCL2 apoptosis regulator	Homo sapiens	102-107
9000505-7	1997	In contrast, tetracycline-regulated overexpression of Bcl-2 protected CEM-C7H2 sublines stably transfected with corresponding constructs from ceramide-induced apoptosis.	Ceramides	142-150	BCL2 apoptosis regulator	Homo sapiens	54-59
9000505-8	1997	Thus, in these human leukemia cells, ceramides induce a relatively slow death response that can be prevented by Bcl-2, but is independent of CrmA-inhibitable proteases.	Ceramides	37-46	BCL2 apoptosis regulator	Homo sapiens	112-117
9000505-9	1997	These characteristics distinguish ceramide-induced from other forms of apoptosis, such as Apo-1/Fas-induced cell death where ceramide production has been causally implicated.	Ceramides	34-42	Fas cell surface death receptor	Homo sapiens	90-95
9000505-9	1997	These characteristics distinguish ceramide-induced from other forms of apoptosis, such as Apo-1/Fas-induced cell death where ceramide production has been causally implicated.	Ceramides	125-133	Fas cell surface death receptor	Homo sapiens	90-95
9547591-0	1997	The rise and fall of ceramide and 1,2-diacylglycerol (DAG): modulation by transforming growth factor-beta 1 (TGF beta 1) and by epidermal growth factor (EGF).	Ceramides	21-29	transforming growth factor beta 1	Homo sapiens	74-107
9547591-0	1997	The rise and fall of ceramide and 1,2-diacylglycerol (DAG): modulation by transforming growth factor-beta 1 (TGF beta 1) and by epidermal growth factor (EGF).	Ceramides	21-29	transforming growth factor beta 1	Homo sapiens	109-119
9547591-0	1997	The rise and fall of ceramide and 1,2-diacylglycerol (DAG): modulation by transforming growth factor-beta 1 (TGF beta 1) and by epidermal growth factor (EGF).	Ceramides	21-29	epidermal growth factor	Homo sapiens	128-151
9547591-0	1997	The rise and fall of ceramide and 1,2-diacylglycerol (DAG): modulation by transforming growth factor-beta 1 (TGF beta 1) and by epidermal growth factor (EGF).	Ceramides	21-29	epidermal growth factor	Homo sapiens	153-156
9547591-5	1997	Cell-permeable ceramide analogs stimulate monocytic differentiation of human leukemia (HL60) cells (1), as well as the phosphorylation of the EGF receptor at Thr669 in A431 human epidermoid carcinoma cells (2).	Ceramides	15-23	epidermal growth factor	Homo sapiens	142-145
9547591-7	1997	The present studies aim to investigate the mechanism of TGF beta 1 signaling and to explore whether TGF beta 1"s pathway involves activation of PKC by 1,2-Diacylglycerol (DAG) and/or stimulation of a CAPK by ceramide.	Ceramides	208-216	transforming growth factor beta 1	Homo sapiens	100-110
9547591-8	1997	Ceramide and DAG levels of A431 cells are determined by thin layer chromatography (TLC) after treatment with either TGF beta 1 or with EGF.	Ceramides	0-8	epidermal growth factor	Homo sapiens	135-138
9547591-11	1997	Ceramide levels are reduced 2-fold by TGF beta 1 and almost unaffected by EGF.	Ceramides	0-8	transforming growth factor beta 1	Homo sapiens	38-48
9110068-6	1997	RESULTS: A marked enhancement in the levels of ceramide, a product of the sphingomyelin hydrolysis, was observed in U251MG-Nef upon stimulation with TNF-alpha.	Ceramides	47-55	tumor necrosis factor	Homo sapiens	149-158
9374036-4	1997	In several cell systems ceramide links to the stress-activated protein kinase (SAPK)/c-jun kinase (JNK) cascade to signal apoptosis.	Ceramides	24-32	mitogen-activated protein kinase 8	Homo sapiens	99-102
8978280-4	1997	The activation of the SM cycle by IFN-gamma occurred rapidly, with a decrease of approximately 20% in the SM level observed after 60 minutes with a concomitant increase in ceramide level.	Ceramides	172-180	interferon gamma	Homo sapiens	34-43
9007051-3	1997	In addition to the newly discovered role of ceramide as an intracellular second messenger for tumor necrosis factor-alpha, IL-1beta, and other cytokines, sphingosine, sphingosine-1-phosphate, and other sphingolipid metabolites have recently been demonstrated to modulate cellular calcium homeostasis and cell proliferation.	Ceramides	44-52	tumor necrosis factor	Homo sapiens	94-121
8988042-5	1997	Bcl-2-mediated inhibition of ceramide-induced delta psi m disruption is observed in normal as well as anucleate cells, indicating that bcl-2 acts on an extranuclear pathway of apoptosis.	Ceramides	29-37	BCL2 apoptosis regulator	Homo sapiens	0-5
8988042-5	1997	Bcl-2-mediated inhibition of ceramide-induced delta psi m disruption is observed in normal as well as anucleate cells, indicating that bcl-2 acts on an extranuclear pathway of apoptosis.	Ceramides	29-37	BCL2 apoptosis regulator	Homo sapiens	135-140
8981488-1	1996	In cerebral cortex, endothelin-1 (ET-1) evoked a decrease of 40% in sphingomyelin (SM) levels together with an increase in both ceramide and glycosphingolipid (GSL) levels (100 and 56% respectively).	Ceramides	128-136	endothelin 1	Rattus norvegicus	20-32
8981488-1	1996	In cerebral cortex, endothelin-1 (ET-1) evoked a decrease of 40% in sphingomyelin (SM) levels together with an increase in both ceramide and glycosphingolipid (GSL) levels (100 and 56% respectively).	Ceramides	128-136	endothelin 1	Rattus norvegicus	34-38
8981488-3	1996	By contrast, in cerebellum ET-1 seems to activate the hydrolysis of both SM and GSL, since the peptide evoked a decrease (near 30%) of their levels concomitantly with an increased production of ceramides (200%).	Ceramides	194-203	endothelin 1	Rattus norvegicus	27-31
9160338-6	1997	Phospholipase A2 is inhibited by sphingomyelin, and activated by ceramide and by palmitic acid, one of the products of its own phosphohydrolytic reaction.	Ceramides	65-73	phospholipase A2 group IB	Homo sapiens	0-16
8955085-11	1996	These results suggest that the TNF-alpha and IL-1beta synergize to induce transcriptional down-regulation of the M2 muscarinic receptor, which seems to be mediated through activation of both ceramide and cAMP-dependent protein kinase pathways.	Ceramides	191-199	tumor necrosis factor	Homo sapiens	31-40
8955085-11	1996	These results suggest that the TNF-alpha and IL-1beta synergize to induce transcriptional down-regulation of the M2 muscarinic receptor, which seems to be mediated through activation of both ceramide and cAMP-dependent protein kinase pathways.	Ceramides	191-199	interleukin 1 beta	Homo sapiens	45-53
9007051-3	1997	In addition to the newly discovered role of ceramide as an intracellular second messenger for tumor necrosis factor-alpha, IL-1beta, and other cytokines, sphingosine, sphingosine-1-phosphate, and other sphingolipid metabolites have recently been demonstrated to modulate cellular calcium homeostasis and cell proliferation.	Ceramides	44-52	interleukin 1 beta	Homo sapiens	123-131
9007051-4	1997	Perturbation of sphingolipid metabolism using synthetic and naturally occurring inhibitors of key enzymes of the biosynthetic pathways is aiding the characterization of these processes; for examples, inhibition of cerebroside synthase has indicated a role for ceramide in cellular stress responses including heat shock, and inhibition of ceramide synthase (by fumonisins) has revealed the role of disruption of sphingolipid metabolism in several animal diseases.	Ceramides	260-268	UDP glycosyltransferase 8	Homo sapiens	214-234
8946936-0	1996	Cell-permeable ceramide inhibits the growth of B lymphoma Raji cells lacking TNF-alpha-receptors by inducing G0/G1 arrest but not apoptosis: a new model for dissecting cell-cycle arrest and apoptosis.	Ceramides	15-23	tumor necrosis factor	Homo sapiens	77-86
8940345-6	1996	Tumor necrosis factor-alpha, a stimulator of ceramide production, actively promotes oligonucleosome formation in apoptosis-susceptible, but not in apoptosis-resistant, granulosa cells.	Ceramides	45-53	tumor necrosis factor	Homo sapiens	0-27
8940345-10	1996	More importantly, however, the ability of a physiologically relevant initiator of ceramide biosynthesis, tumor necrosis factor-alpha, to promote cell death is evident only in apoptosis-susceptible granulosa cells collected from atresia-prone prehierarchal follicles.	Ceramides	82-90	tumor necrosis factor	Homo sapiens	105-132
8976196-3	1996	Here, we show that human dendritic cells respond to CD40 ligand, as well as to tumor necrosis factor-alpha and IL-1 beta, with intracellular ceramide accumulation, as they are induced to differentiate.	Ceramides	141-149	CD40 ligand	Homo sapiens	52-63
8976196-3	1996	Here, we show that human dendritic cells respond to CD40 ligand, as well as to tumor necrosis factor-alpha and IL-1 beta, with intracellular ceramide accumulation, as they are induced to differentiate.	Ceramides	141-149	tumor necrosis factor	Homo sapiens	79-106
8976196-3	1996	Here, we show that human dendritic cells respond to CD40 ligand, as well as to tumor necrosis factor-alpha and IL-1 beta, with intracellular ceramide accumulation, as they are induced to differentiate.	Ceramides	141-149	interleukin 1 beta	Homo sapiens	111-120
8946936-1	1996	We examined the effects of a cell-permeable ceramide analog, C2-ceramide, on the growth of TNF-alpha-resistant B lymphoma Raji cells lacking TNF-alpha-receptors (TNF-R).	Ceramides	44-52	tumor necrosis factor	Homo sapiens	91-100
8950029-1	1996	Neutral sphingomyelinase (SMase) can be activated by extracellular signals to produce ceramide, which may affect mitogen-activated protein kinase (MAPK) activities.	Ceramides	86-94	mitogen-activated protein kinase 1	Homo sapiens	147-151
8950992-3	1996	We observed that contrary to the studies in normal B cells, CD40 ligation in carcinoma cell lines and in normal primary epithelial cells resulted in growth inhibition and enhanced susceptibility to apoptosis induced by anti-neoplastic drugs, TNF-alpha, Fas and ceramide.	Ceramides	261-269	CD40 molecule	Homo sapiens	60-64
8920943-0	1996	Ceramide reproduces late appearance of oxidative stress during TNF-mediated cell death in L929 cells.	Ceramides	0-8	tumor necrosis factor	Mus musculus	63-66
8920943-5	1996	Four of the five TNF-resistant clones were also resistant to ceramide and displayed no increase in MTT reduction with either TNF or ceramide.	Ceramides	61-69	tumor necrosis factor	Mus musculus	17-20
8920943-6	1996	The remaining TNF-resistant clone was sensitive to ceramide, displaying an increase in MTT reduction.	Ceramides	51-59	tumor necrosis factor	Mus musculus	14-17
8920943-7	1996	Our results suggest a late increase in superoxide production prior to cellular destruction during TNF and ceramide mediated cell death and support the notion that ceramide can serve as a second messenger for TNF in cell death.	Ceramides	163-171	tumor necrosis factor	Mus musculus	208-211
8895358-0	1996	Tumor necrosis factor-alpha and its second messenger, ceramide, stimulate apoptosis in cultured ovarian follicles.	Ceramides	54-62	tumor necrosis factor	Homo sapiens	0-27
8895373-0	1996	Effects of ceramide and protein kinase C on the regulation of type I 5"-deiodinase in FRTL-5 rat thyroid cells.	Ceramides	11-19	iodothyronine deiodinase 1	Rattus norvegicus	62-82
8895373-3	1996	In a number of cell types, TNF alpha receptor binding results in the activation of specific signal transduction cascades, including protein kinase C (PKC) and the hydrolysis of sphingomyelin to ceramide.	Ceramides	194-202	tumor necrosis factor	Rattus norvegicus	27-36
8910286-10	1996	Our findings indicate that ceramides do not induce A1 but do up-regulate c-jun and induce endothelial death.	Ceramides	27-36	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	73-78
8910286-11	1996	Ceramide-activated endothelial death is also inhibited by A1, suggesting that TNF may initiate divergent survival and death pathways via separate lipid second messengers.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	78-81
8895358-3	1996	Tumor necrosis factor-alpha (TNF alpha) is a cytokine capable of inducing apoptosis in diverse cell types, and the apoptotic effect of TNF alpha is, partially, coupled to the sphingomyelin signaling pathway with ceramide as a second messenger.	Ceramides	212-220	tumor necrosis factor	Homo sapiens	0-27
8895358-3	1996	Tumor necrosis factor-alpha (TNF alpha) is a cytokine capable of inducing apoptosis in diverse cell types, and the apoptotic effect of TNF alpha is, partially, coupled to the sphingomyelin signaling pathway with ceramide as a second messenger.	Ceramides	212-220	tumor necrosis factor	Homo sapiens	29-38
8895358-3	1996	Tumor necrosis factor-alpha (TNF alpha) is a cytokine capable of inducing apoptosis in diverse cell types, and the apoptotic effect of TNF alpha is, partially, coupled to the sphingomyelin signaling pathway with ceramide as a second messenger.	Ceramides	212-220	tumor necrosis factor	Homo sapiens	135-144
8895358-10	1996	A membrane-permeable ceramide analog, C2-ceramide N-acetyl sphingosine, mimicked the effect of TNF alpha and was able to completely abolish the action of FSH at 50 microM.	Ceramides	21-29	tumor necrosis factor	Homo sapiens	95-104
8895358-16	1996	In summary, treatment with TNF alpha or its second messenger, ceramide, stimulates apoptosis of early antral follicles in culture, suggesting a potential role for TNF alpha as an intraovarian regulator of follicle atresia by acting through the ceramide signaling pathway.	Ceramides	62-70	tumor necrosis factor	Homo sapiens	27-36
8895358-16	1996	In summary, treatment with TNF alpha or its second messenger, ceramide, stimulates apoptosis of early antral follicles in culture, suggesting a potential role for TNF alpha as an intraovarian regulator of follicle atresia by acting through the ceramide signaling pathway.	Ceramides	62-70	tumor necrosis factor	Homo sapiens	163-172
8895358-16	1996	In summary, treatment with TNF alpha or its second messenger, ceramide, stimulates apoptosis of early antral follicles in culture, suggesting a potential role for TNF alpha as an intraovarian regulator of follicle atresia by acting through the ceramide signaling pathway.	Ceramides	244-252	tumor necrosis factor	Homo sapiens	27-36
8895358-16	1996	In summary, treatment with TNF alpha or its second messenger, ceramide, stimulates apoptosis of early antral follicles in culture, suggesting a potential role for TNF alpha as an intraovarian regulator of follicle atresia by acting through the ceramide signaling pathway.	Ceramides	244-252	tumor necrosis factor	Homo sapiens	163-172
8898109-0	1996	Ceramide induces apoptosis via CPP32 activation.	Ceramides	0-8	caspase 3	Homo sapiens	31-36
8923461-6	1996	We observed that the action of TNF alpha can be mimicked by ceramide.	Ceramides	60-68	tumor necrosis factor	Homo sapiens	31-40
8923461-8	1996	Levels of c-fos and c-jun proteins also were increased by TNF alpha or ceramide in the presence of DEX.	Ceramides	71-79	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	10-15
8923461-8	1996	Levels of c-fos and c-jun proteins also were increased by TNF alpha or ceramide in the presence of DEX.	Ceramides	71-79	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	20-25
8923461-13	1996	These results suggest that TNF alpha, probably acting through ceramide formation, stimulates the binding of both c-fos and c-jun to the AP-1 element upstream of exon 1.4.	Ceramides	62-70	tumor necrosis factor	Homo sapiens	27-36
8923461-13	1996	These results suggest that TNF alpha, probably acting through ceramide formation, stimulates the binding of both c-fos and c-jun to the AP-1 element upstream of exon 1.4.	Ceramides	62-70	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	113-118
8923461-13	1996	These results suggest that TNF alpha, probably acting through ceramide formation, stimulates the binding of both c-fos and c-jun to the AP-1 element upstream of exon 1.4.	Ceramides	62-70	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	123-128
8878481-6	1996	NGF binding to mature oligodendrocytes expressing the p75 neurotrophin receptor, but not trkA, resulted in a sustained increase of intracellular ceramide and c-Jun amino-terminal kinase (JNK) activity, which are thought to participate in a signal transduction pathway leading to cell death.	Ceramides	145-153	PC4 and SFRS1 interacting protein 1	Homo sapiens	54-57
8898109-4	1996	Furthermore, variant Jurkat cells with defective CPP32 activation were resistant to both anti-Fas- and ceramide-induced apoptosis.	Ceramides	103-111	caspase 3	Homo sapiens	49-54
8898109-5	1996	These results indicate that CPP32 activation is required for ceramide-induced apoptosis, and suggest sphingomyelin-ceramide pathway functions upstream of CPP32.	Ceramides	61-69	caspase 3	Homo sapiens	28-33
8898109-5	1996	These results indicate that CPP32 activation is required for ceramide-induced apoptosis, and suggest sphingomyelin-ceramide pathway functions upstream of CPP32.	Ceramides	115-123	caspase 3	Homo sapiens	154-159
8898109-2	1996	We report here that cell-permeable ceramide induced cleavage and activation of CPP32, a Ced-3/ICE-like protease, but not ICE.	Ceramides	35-43	caspase 3	Homo sapiens	79-84
8898109-2	1996	We report here that cell-permeable ceramide induced cleavage and activation of CPP32, a Ced-3/ICE-like protease, but not ICE.	Ceramides	35-43	caspase 1	Homo sapiens	94-97
8898109-3	1996	Ceramide-induced apoptosis of Jurkat cells was blocked by the CPP32-specific tetrapeptide inhibitor DEVD-CHO, but not by the ICE inhibitor YVAD-CHO.	Ceramides	0-8	caspase 3	Homo sapiens	62-67
8870666-7	1996	In conclusion, the effect of ceramide on GLUT4 gene expression is at the level of transcription, suggesting that another pathway controls mRNA stability.	Ceramides	29-37	solute carrier family 2 member 4	Homo sapiens	41-46
8921873-11	1996	The mammalian LCB2 cDNAs provide valuable reagents for studying the Lcb2 subunit of SPT and for studying how ceramide synthesis is regulated.	Ceramides	109-117	serine palmitoyltransferase long chain base subunit 2	Homo sapiens	14-18
8895515-0	1996	The human retinoblastoma gene product suppresses ceramide-induced apoptosis in human bladder tumor cells.	Ceramides	49-57	RB transcriptional corepressor 1	Homo sapiens	10-24
8895515-1	1996	The retinoblastoma gene product, Rb, has previously been implicated as an obligatory component in the antiproliferative effects mediated by the lipid second messenger, ceramide.	Ceramides	168-176	RB transcriptional corepressor 1	Homo sapiens	4-18
8798752-5	1996	Although ceramide inhibited PMA-induced activation of PLD, it did not inhibit translocation of protein kinase C (PKC) to the membrane in response to PMA.	Ceramides	9-17	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	54-57
8798752-10	1996	Taken together, these data show that ceramide interferes with PKC-mediated activation of PLD.	Ceramides	37-45	protein kinase C alpha	Homo sapiens	62-65
8798752-10	1996	Taken together, these data show that ceramide interferes with PKC-mediated activation of PLD.	Ceramides	37-45	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	89-92
8870666-0	1996	Lipid mediators of insulin resistance: ceramide signalling down-regulates GLUT4 gene transcription in 3T3-L1 adipocytes.	Ceramides	39-47	insulin	Homo sapiens	19-26
8870666-0	1996	Lipid mediators of insulin resistance: ceramide signalling down-regulates GLUT4 gene transcription in 3T3-L1 adipocytes.	Ceramides	39-47	solute carrier family 2 member 4	Homo sapiens	74-79
8798752-0	1996	Ceramide inhibits phospholipase D in a cell-free system.	Ceramides	0-8	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	18-33
8798752-1	1996	Recent evidence in whole cells has implicated ceramide in the regulation of phospholipase D (PLD).	Ceramides	46-54	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	76-91
8798752-1	1996	Recent evidence in whole cells has implicated ceramide in the regulation of phospholipase D (PLD).	Ceramides	46-54	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	93-96
8870666-3	1996	In the same manner as with TNF, treatment of the adipocytes with 1-3 microM C6-ceramide, a membrane-permeable analogue of ceramide, decreased GLUT4 mRNA content by approximately 60%.	Ceramides	79-87	tumor necrosis factor	Homo sapiens	27-30
8870666-8	1996	These data establish that ceramide-initiated signal transduction pathways exist within the adipocyte, and provide a potential mechanism for control of GLUT4 gene expression.	Ceramides	26-34	solute carrier family 2 member 4	Homo sapiens	151-156
8870666-3	1996	In the same manner as with TNF, treatment of the adipocytes with 1-3 microM C6-ceramide, a membrane-permeable analogue of ceramide, decreased GLUT4 mRNA content by approximately 60%.	Ceramides	79-87	solute carrier family 2 member 4	Homo sapiens	142-147
8873967-0	1996	Ceramide-induced nuclear translocation of NF-kappa B is a potential mediator of the apoptotic response to TNF-alpha in murine clonal osteoblasts.	Ceramides	0-8	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	42-52
8903509-3	1996	Tumor necrosis factor-alpha, interleukin 1beta, and nerve growth factor, for example, induce sphingomyelin hydrolysis to ceramide.	Ceramides	121-129	tumor necrosis factor	Mus musculus	0-27
8903509-3	1996	Tumor necrosis factor-alpha, interleukin 1beta, and nerve growth factor, for example, induce sphingomyelin hydrolysis to ceramide.	Ceramides	121-129	interleukin 1 beta	Mus musculus	29-46
8703011-4	1996	To better understand the regulation of the unique pathway for ceramide production in epidermis, we have studied the activity of the enzyme responsible for GlcCer synthesis, ceramide glucosyltransferase (CerGlc transferase), during keratinocyte culture differentiation.	Ceramides	62-70	UDP-glucose ceramide glucosyltransferase	Homo sapiens	173-201
8831497-3	1996	In this study we have examined the role of a recently described TNF signaling pathway involving sphingomyelin activation to generate ceramide, a potential intracellular mediator.	Ceramides	133-141	tumor necrosis factor	Homo sapiens	64-67
8831497-7	1996	Extracellular SMase does not have access to intracellular sphingomyelin, but treatment of ECs with membrane-permeant ceramide analogues still completely fails to activate NF-kappa B and only activates JNK at late times.	Ceramides	117-125	mitogen-activated protein kinase 8	Homo sapiens	201-204
8892112-9	1996	Incubation of cells with bacterial sphingomyelinase and a cell-permeable ceramide stimulated JNK activity, suggesting that the ceramide pathway may play a role in JNK activation, although the time course of activation did not correspond to that of TNF-alpha.	Ceramides	73-81	mitogen-activated protein kinase 8	Homo sapiens	93-96
8892112-9	1996	Incubation of cells with bacterial sphingomyelinase and a cell-permeable ceramide stimulated JNK activity, suggesting that the ceramide pathway may play a role in JNK activation, although the time course of activation did not correspond to that of TNF-alpha.	Ceramides	73-81	mitogen-activated protein kinase 8	Homo sapiens	163-166
8892112-9	1996	Incubation of cells with bacterial sphingomyelinase and a cell-permeable ceramide stimulated JNK activity, suggesting that the ceramide pathway may play a role in JNK activation, although the time course of activation did not correspond to that of TNF-alpha.	Ceramides	73-81	tumor necrosis factor	Homo sapiens	248-257
8892112-9	1996	Incubation of cells with bacterial sphingomyelinase and a cell-permeable ceramide stimulated JNK activity, suggesting that the ceramide pathway may play a role in JNK activation, although the time course of activation did not correspond to that of TNF-alpha.	Ceramides	127-135	mitogen-activated protein kinase 8	Homo sapiens	93-96
8892112-9	1996	Incubation of cells with bacterial sphingomyelinase and a cell-permeable ceramide stimulated JNK activity, suggesting that the ceramide pathway may play a role in JNK activation, although the time course of activation did not correspond to that of TNF-alpha.	Ceramides	127-135	mitogen-activated protein kinase 8	Homo sapiens	163-166
8892112-9	1996	Incubation of cells with bacterial sphingomyelinase and a cell-permeable ceramide stimulated JNK activity, suggesting that the ceramide pathway may play a role in JNK activation, although the time course of activation did not correspond to that of TNF-alpha.	Ceramides	127-135	tumor necrosis factor	Homo sapiens	248-257
8795621-3	1996	We investigated the activation of ICE/CED-3 proteases induced by three apoptotic stimuli (staurosporine, ceramide, and serum withdrawal) in the neuronal cell line GT1-7 and in cells overexpressing Bcl-2.	Ceramides	105-113	caspase 1	Mus musculus	34-37
8873967-0	1996	Ceramide-induced nuclear translocation of NF-kappa B is a potential mediator of the apoptotic response to TNF-alpha in murine clonal osteoblasts.	Ceramides	0-8	tumor necrosis factor	Mus musculus	106-115
8873967-4	1996	Endogenous cellular ceramide concentrations increased within 3 min, and comparable peak levels were observed for 30 min after TNF-alpha treatment.	Ceramides	20-28	tumor necrosis factor	Mus musculus	126-135
8873967-5	1996	Activation of nuclear factor-kappa B (NF-kappa B) was detected after TNF-alpha or synthetic ceramide stimulation.	Ceramides	92-100	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	14-36
8873967-5	1996	Activation of nuclear factor-kappa B (NF-kappa B) was detected after TNF-alpha or synthetic ceramide stimulation.	Ceramides	92-100	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	38-48
8873967-7	1996	Degradation of I kappa B alpha/MAD-3 was observed after 60 min of ceramide treatment.	Ceramides	66-74	nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha	Mus musculus	15-30
8873967-7	1996	Degradation of I kappa B alpha/MAD-3 was observed after 60 min of ceramide treatment.	Ceramides	66-74	Max dimerization protein 3	Mus musculus	31-36
8873967-8	1996	These results indicate that nuclear translocation and activation of NF-kappa B through TNF-alpha generated ceramide may be one important apoptotic signaling pathway in MC3T3-E1 cells.	Ceramides	107-115	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	68-78
8873967-8	1996	These results indicate that nuclear translocation and activation of NF-kappa B through TNF-alpha generated ceramide may be one important apoptotic signaling pathway in MC3T3-E1 cells.	Ceramides	107-115	tumor necrosis factor	Mus musculus	87-96
8873967-9	1996	The osteoblastic apoptosis triggered by TNF-alpha-generated ceramide may explain the inhibition of bone formation during severe bone inflammation.	Ceramides	60-68	tumor necrosis factor	Mus musculus	40-49
8702918-1	1996	Stimulation of [3H]serine-labeled A431 cells with tumor necrosis factor-alpha (TNFalpha) or bacterial sphingomyelinase (SMase) resulted in a rapid decrease (approximately 50% by 15 min) in cellular [3H]sphingomyelin content and generation of the lipid moiety [3H]ceramide, which remained elevated 60 min later.	Ceramides	263-271	tumor necrosis factor	Homo sapiens	50-77
8891691-9	1996	Utilization of this branch of the ceramide signaling pathway may be cell type specific or may be specific for the LIF mRNA response.	Ceramides	34-42	LIF interleukin 6 family cytokine	Homo sapiens	114-117
8751967-8	1996	Furthermore, the degradation rate of fluorescent sphingomyelin into ceramide in keratinocytes was increased by IFN-gamma, suggesting that IFN-gamma activates sphingomyelin hydrolysis in keratinocytes.	Ceramides	68-76	interferon gamma	Homo sapiens	111-120
8751967-8	1996	Furthermore, the degradation rate of fluorescent sphingomyelin into ceramide in keratinocytes was increased by IFN-gamma, suggesting that IFN-gamma activates sphingomyelin hydrolysis in keratinocytes.	Ceramides	68-76	interferon gamma	Homo sapiens	138-147
8751967-9	1996	These observations suggest the possible role of ceramide in IFN-gamma-induced ICAM-1 and HLA-DR expression on keratinocytes.	Ceramides	48-56	interferon gamma	Homo sapiens	60-69
8751967-9	1996	These observations suggest the possible role of ceramide in IFN-gamma-induced ICAM-1 and HLA-DR expression on keratinocytes.	Ceramides	48-56	intercellular adhesion molecule 1	Homo sapiens	78-84
8958448-3	1996	Murine interleukin-2 (IL-2) dependent T-lymphocyte CTLL cells, murine fibroblasts Swiss 3R3 cells, and murine fibroblast BALB/C A31 cells metabolize exogenously added sphingosine to ceramide.	Ceramides	182-190	interleukin 2	Mus musculus	7-20
8958448-3	1996	Murine interleukin-2 (IL-2) dependent T-lymphocyte CTLL cells, murine fibroblasts Swiss 3R3 cells, and murine fibroblast BALB/C A31 cells metabolize exogenously added sphingosine to ceramide.	Ceramides	182-190	interleukin 2	Mus musculus	22-26
8702918-1	1996	Stimulation of [3H]serine-labeled A431 cells with tumor necrosis factor-alpha (TNFalpha) or bacterial sphingomyelinase (SMase) resulted in a rapid decrease (approximately 50% by 15 min) in cellular [3H]sphingomyelin content and generation of the lipid moiety [3H]ceramide, which remained elevated 60 min later.	Ceramides	263-271	tumor necrosis factor	Homo sapiens	79-87
8702918-2	1996	Sphingomyelin hydrolysis in response to TNFalpha or bacterial SMase resulted in a time-dependent decrease in the phosphorylation state of c-Jun protein, an effect that was also observed in cells treated with the membrane-permeable ceramide analogue N-hexanoylsphingosine (C6-ceramide).	Ceramides	231-239	tumor necrosis factor	Homo sapiens	40-48
8702918-2	1996	Sphingomyelin hydrolysis in response to TNFalpha or bacterial SMase resulted in a time-dependent decrease in the phosphorylation state of c-Jun protein, an effect that was also observed in cells treated with the membrane-permeable ceramide analogue N-hexanoylsphingosine (C6-ceramide).	Ceramides	231-239	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	138-143
8683130-9	1996	From these results, we concluded that ceramide is needed for certain TNF-mediated cellular responses, but it alone may not be sufficient.	Ceramides	38-46	tumor necrosis factor	Homo sapiens	69-72
8695867-2	1996	Although sphingomyelin (SPM) hydrolysis and ceramide generation may function as an important mediator in TNF alpha signaling, the molecular mechanisms of the signaling pathway(s) are still not well understood.	Ceramides	44-52	tumor necrosis factor	Homo sapiens	105-114
8695867-5	1996	TNF alpha triggered in KG1a cells neither SPM hydrolysis nor ceramide generation, but induced SPM synthesis and ceramide breakdown as well as dose-dependent cell proliferation.	Ceramides	61-69	tumor necrosis factor	Homo sapiens	0-9
8695867-5	1996	TNF alpha triggered in KG1a cells neither SPM hydrolysis nor ceramide generation, but induced SPM synthesis and ceramide breakdown as well as dose-dependent cell proliferation.	Ceramides	112-120	tumor necrosis factor	Homo sapiens	0-9
8695867-6	1996	In contrast, TNF alpha induced in U937 SPM hydrolysis and ceramide generation as well as dose-dependent cell death.	Ceramides	58-66	tumor necrosis factor	Homo sapiens	13-22
8753774-0	1996	Activation of phospholipase D in human fibroblasts by ceramide and sphingosine: evaluation of their modulatory role in bradykinin stimulation of phospholipase D.	Ceramides	54-62	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	14-29
8753774-1	1996	In the present study the modulatory action of exogenous short-chain ceramide and sphingosine on phospholipase D (PLD) activity in young and old human fibroblasts was examined.	Ceramides	68-76	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	96-111
8753774-1	1996	In the present study the modulatory action of exogenous short-chain ceramide and sphingosine on phospholipase D (PLD) activity in young and old human fibroblasts was examined.	Ceramides	68-76	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	113-116
8753774-2	1996	Sphingosine and also ceramide, thus far described as a negative modulator of PLD, were able to activate PLD.	Ceramides	21-29	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	77-80
8753774-2	1996	Sphingosine and also ceramide, thus far described as a negative modulator of PLD, were able to activate PLD.	Ceramides	21-29	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	104-107
8751717-3	1996	Phospholipases (PLA2, PLC, PLD, sphingomyelinase) are pivotal in the generation of these LM including eicosanoids, platelet activating factor (PAF), diacylglycerides, ceramide, and other newly discovered bioactive autacoids.	Ceramides	167-175	phospholipase A2 group IB	Homo sapiens	16-20
8751717-3	1996	Phospholipases (PLA2, PLC, PLD, sphingomyelinase) are pivotal in the generation of these LM including eicosanoids, platelet activating factor (PAF), diacylglycerides, ceramide, and other newly discovered bioactive autacoids.	Ceramides	167-175	heparan sulfate proteoglycan 2	Homo sapiens	22-25
8751717-3	1996	Phospholipases (PLA2, PLC, PLD, sphingomyelinase) are pivotal in the generation of these LM including eicosanoids, platelet activating factor (PAF), diacylglycerides, ceramide, and other newly discovered bioactive autacoids.	Ceramides	167-175	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	27-30
8757882-4	1996	Cell-permeable analogs of ceramide induced the expression of many LPS-inducible genes; however, the expression of interferon-inducible protein 10 (IP-10) and interferon consensus sequence-binding protein (ICSBP) mRNAs was significantly lower than that induced by LPS.	Ceramides	26-34	interferon regulatory factor 8	Mus musculus	205-210
8706124-6	1996	Acid sphingomyelinase knockout mice also expressed defects in radiation-induced ceramide generation and apoptosis in vivo.	Ceramides	80-88	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
8706867-0	1996	CPP32 inhibition prevents Fas-induced ceramide generation and apoptosis in human cells.	Ceramides	38-46	caspase 3	Homo sapiens	0-5
8692926-0	1996	Ceramide-binding and activation defines protein kinase c-Raf as a ceramide-activated protein kinase.	Ceramides	0-8	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	55-60
8692926-1	1996	Interleukin 1 is the prototype of an inflammatory cytokine, and evidence suggests that it uses the sphingomyelin pathway and ceramide production to trigger mitogen-activated protein kinase (MAPK) activation and subsequent gene expression required for acute inflammatory processes.	Ceramides	125-133	interleukin 1 alpha	Homo sapiens	0-13
8692926-3	1996	It is observed that ceramide specifically binds to and activates protein kinase c-Raf, leading to a subsequent activation of the MAPK cascade.	Ceramides	20-28	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	80-85
8692926-5	1996	These data identify protein kinase c-Raf as a specific molecular target for interleukin 1 beta-stimulated ceramide formation and demonstrate that ceramide is a lipid cofactor participating in regulation of c-Raf activity.	Ceramides	106-114	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	35-40
8692926-5	1996	These data identify protein kinase c-Raf as a specific molecular target for interleukin 1 beta-stimulated ceramide formation and demonstrate that ceramide is a lipid cofactor participating in regulation of c-Raf activity.	Ceramides	106-114	interleukin 1 beta	Homo sapiens	76-94
8692926-5	1996	These data identify protein kinase c-Raf as a specific molecular target for interleukin 1 beta-stimulated ceramide formation and demonstrate that ceramide is a lipid cofactor participating in regulation of c-Raf activity.	Ceramides	146-154	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	35-40
8692926-5	1996	These data identify protein kinase c-Raf as a specific molecular target for interleukin 1 beta-stimulated ceramide formation and demonstrate that ceramide is a lipid cofactor participating in regulation of c-Raf activity.	Ceramides	146-154	interleukin 1 beta	Homo sapiens	76-94
8692926-5	1996	These data identify protein kinase c-Raf as a specific molecular target for interleukin 1 beta-stimulated ceramide formation and demonstrate that ceramide is a lipid cofactor participating in regulation of c-Raf activity.	Ceramides	146-154	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	206-211
8757935-4	1996	Upstream inputs are diverse, and include small GTPases (primarily Rac and Cdc42; secondarily Ras) acting through mammalian homologs of the yeast Ste20 kinase, other kinase subfamilies (e.g. GC kinase) and ceramide, a putative second messenger for certain TNF-alpha actions.	Ceramides	205-213	AKT serine/threonine kinase 1	Homo sapiens	66-69
8757935-4	1996	Upstream inputs are diverse, and include small GTPases (primarily Rac and Cdc42; secondarily Ras) acting through mammalian homologs of the yeast Ste20 kinase, other kinase subfamilies (e.g. GC kinase) and ceramide, a putative second messenger for certain TNF-alpha actions.	Ceramides	205-213	cell division cycle 42	Homo sapiens	74-79
8757935-4	1996	Upstream inputs are diverse, and include small GTPases (primarily Rac and Cdc42; secondarily Ras) acting through mammalian homologs of the yeast Ste20 kinase, other kinase subfamilies (e.g. GC kinase) and ceramide, a putative second messenger for certain TNF-alpha actions.	Ceramides	205-213	mitogen-activated protein kinase kinase kinase kinase 2	Homo sapiens	190-199
8683130-2	1996	In the present report we used this system to investigate the role of ceramide in TNF action.	Ceramides	69-77	tumor necrosis factor	Homo sapiens	81-84
8683130-4	1996	To investigate the roles of ceramide in TNF action, we used ((2-isopropyl-1-(4-[3-N-methyl-N-(3,4-dimethoxy-phenethyl)amino] propyloxy)benzenesulfonyl))indolizine (SR33557), a potent inhibitor of acidic but not neutral sphingomyelinase (SMase).	Ceramides	28-36	tumor necrosis factor	Homo sapiens	40-43
8683130-7	1996	Since ceramide has been shown to play a role in TNF-mediated activation of nuclear factor-kappa B (NF-kappa B), we examined the effect of SR33557 on this early cellular response of TNF.	Ceramides	6-14	tumor necrosis factor	Homo sapiens	48-51
8683130-7	1996	Since ceramide has been shown to play a role in TNF-mediated activation of nuclear factor-kappa B (NF-kappa B), we examined the effect of SR33557 on this early cellular response of TNF.	Ceramides	6-14	nuclear factor kappa B subunit 1	Homo sapiens	75-97
8683130-7	1996	Since ceramide has been shown to play a role in TNF-mediated activation of nuclear factor-kappa B (NF-kappa B), we examined the effect of SR33557 on this early cellular response of TNF.	Ceramides	6-14	nuclear factor kappa B subunit 1	Homo sapiens	99-109
8657285-1	1996	Ceramide is an important regulatory participant of programmed cell death (apoptosis) induced by tumour-necrosis factor (TNF)-alpha and Fas ligand, members of the TNF superfamily.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	96-130
8657285-5	1996	Finally sphingosine-1-phosphate not only stimulates the extracellular signal-regulated kinase (ERK) pathway, it counteracts the ceramide-induced activation of stress-activated protein kinase (SAPK/JNK).	Ceramides	128-136	mitogen-activated protein kinase 8	Homo sapiens	197-200
8657285-1	1996	Ceramide is an important regulatory participant of programmed cell death (apoptosis) induced by tumour-necrosis factor (TNF)-alpha and Fas ligand, members of the TNF superfamily.	Ceramides	0-8	Fas ligand	Homo sapiens	135-145
8662871-14	1996	A similar inhibition was observed upon pretreatment of cells with fumonisin B1 or ISP-1, both of which block the synthesis of ceramide, a common precursor of both GSLs and SM.	Ceramides	126-134	protease, serine 28	Mus musculus	82-87
8664339-5	1996	Ceramide derived from neutral SMase activation is thought to be involved in modulating CAPK and MAP kinases, PLA2 (arachidonic acid mobilization), and CAPP while ceramide generated through acid SMase activation appears to be primarily involved in NF-kappa B activation.	Ceramides	0-8	phospholipase A2 group IB	Homo sapiens	109-113
8741670-2	1996	Tumor necrosis factor-alpha, anti-Fas antibody, anticancer drugs, radiation or heat shock induce apoptosis through generation of ceramide by activation of sphingomyelinase or ceramide synthase.	Ceramides	129-137	tumor necrosis factor	Homo sapiens	0-27
8741670-4	1996	We have found that ceramide induces the transcription of c-jun gene and increases the DNA binding activity of transcription factor AP-1 in human myelogenous leukemia HL-60 cells, and that activation of c-jun/AP-1 by ceramide(presumably through activation of Jun N-terminal kinase/stress-activated protein kinase) may be involved in the signaling pathway leading to apoptosis.	Ceramides	19-27	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-62
8741670-4	1996	We have found that ceramide induces the transcription of c-jun gene and increases the DNA binding activity of transcription factor AP-1 in human myelogenous leukemia HL-60 cells, and that activation of c-jun/AP-1 by ceramide(presumably through activation of Jun N-terminal kinase/stress-activated protein kinase) may be involved in the signaling pathway leading to apoptosis.	Ceramides	19-27	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	131-135
8741670-4	1996	We have found that ceramide induces the transcription of c-jun gene and increases the DNA binding activity of transcription factor AP-1 in human myelogenous leukemia HL-60 cells, and that activation of c-jun/AP-1 by ceramide(presumably through activation of Jun N-terminal kinase/stress-activated protein kinase) may be involved in the signaling pathway leading to apoptosis.	Ceramides	19-27	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	202-207
8741670-4	1996	We have found that ceramide induces the transcription of c-jun gene and increases the DNA binding activity of transcription factor AP-1 in human myelogenous leukemia HL-60 cells, and that activation of c-jun/AP-1 by ceramide(presumably through activation of Jun N-terminal kinase/stress-activated protein kinase) may be involved in the signaling pathway leading to apoptosis.	Ceramides	19-27	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	208-212
8741670-4	1996	We have found that ceramide induces the transcription of c-jun gene and increases the DNA binding activity of transcription factor AP-1 in human myelogenous leukemia HL-60 cells, and that activation of c-jun/AP-1 by ceramide(presumably through activation of Jun N-terminal kinase/stress-activated protein kinase) may be involved in the signaling pathway leading to apoptosis.	Ceramides	216-224	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	131-135
8741670-4	1996	We have found that ceramide induces the transcription of c-jun gene and increases the DNA binding activity of transcription factor AP-1 in human myelogenous leukemia HL-60 cells, and that activation of c-jun/AP-1 by ceramide(presumably through activation of Jun N-terminal kinase/stress-activated protein kinase) may be involved in the signaling pathway leading to apoptosis.	Ceramides	216-224	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	202-207
8741670-4	1996	We have found that ceramide induces the transcription of c-jun gene and increases the DNA binding activity of transcription factor AP-1 in human myelogenous leukemia HL-60 cells, and that activation of c-jun/AP-1 by ceramide(presumably through activation of Jun N-terminal kinase/stress-activated protein kinase) may be involved in the signaling pathway leading to apoptosis.	Ceramides	216-224	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	208-212
8664339-6	1996	While there is no apparent cross-talk between these two ceramide-mediated signalling pathways, there is likely to be significant cross-talk between ceramide signalling and other signal transduction pathways (e.g., the PKC and MAP kinase pathways).	Ceramides	148-156	protein kinase C zeta	Homo sapiens	218-221
8664339-7	1996	Other downstream targets for ceramide action include Cox, IL-6 and IL-2 gene expression, PKC zeta, Vav, Rb, c-Myc, c-Fos, c-Jun and other transcriptional regulators.	Ceramides	29-37	cytochrome c oxidase subunit 8A	Homo sapiens	53-56
8664339-7	1996	Other downstream targets for ceramide action include Cox, IL-6 and IL-2 gene expression, PKC zeta, Vav, Rb, c-Myc, c-Fos, c-Jun and other transcriptional regulators.	Ceramides	29-37	interleukin 6	Homo sapiens	58-62
8664339-7	1996	Other downstream targets for ceramide action include Cox, IL-6 and IL-2 gene expression, PKC zeta, Vav, Rb, c-Myc, c-Fos, c-Jun and other transcriptional regulators.	Ceramides	29-37	interleukin 2	Homo sapiens	67-71
8664339-7	1996	Other downstream targets for ceramide action include Cox, IL-6 and IL-2 gene expression, PKC zeta, Vav, Rb, c-Myc, c-Fos, c-Jun and other transcriptional regulators.	Ceramides	29-37	protein kinase C zeta	Homo sapiens	89-97
8664339-7	1996	Other downstream targets for ceramide action include Cox, IL-6 and IL-2 gene expression, PKC zeta, Vav, Rb, c-Myc, c-Fos, c-Jun and other transcriptional regulators.	Ceramides	29-37	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	122-127
8641202-1	1996	In granulosa cells labeled to isotopic steady-state with [3H]serine, addition of interleukin-1 beta (IL1 beta) or bacterial sphingomyelinase (SMase) induced a rapid decrease (approximately 60% by 10 min) in cellular [3H]Sphingomyelin content and a prolonged generation (up to 60 min) of [3H]ceramide, the immediate lipid-moiety generated in response to sphingomyelin hydrolysis.	Ceramides	291-299	interleukin 1 beta	Homo sapiens	81-99
8641202-1	1996	In granulosa cells labeled to isotopic steady-state with [3H]serine, addition of interleukin-1 beta (IL1 beta) or bacterial sphingomyelinase (SMase) induced a rapid decrease (approximately 60% by 10 min) in cellular [3H]Sphingomyelin content and a prolonged generation (up to 60 min) of [3H]ceramide, the immediate lipid-moiety generated in response to sphingomyelin hydrolysis.	Ceramides	291-299	interleukin 1 beta	Homo sapiens	101-109
8641197-9	1996	Cell permeable ceramide analogs, C2, C6, and Sphingomyelinase mimicked the effects of TNF-alpha on PP-1 inhibition.	Ceramides	15-23	tumor necrosis factor	Rattus norvegicus	86-95
8641202-2	1996	In FSH-treated cells, IL1 beta (0.3-30 ng/ml) inhibited progesterone biosynthesis in a dose-dependent manner, an effect that was also observed in cells exposed to increasing concentrations of bacterial SMase (0.003-0.3 U/ml) or the membrane-permeable ceramide analogue N-hexanoylsphingosine (C6-cer:0.1-10 microM).	Ceramides	251-259	interleukin 1 beta	Homo sapiens	22-30
8641197-10	1996	Furthermore, TNF-alpha treatment was accompanied by an increase in cellular ceramide levels, with concomitant reductions in sphingomyelin.	Ceramides	76-84	tumor necrosis factor	Rattus norvegicus	13-22
8641197-11	1996	We conclude that TNF-alpha blocks insulin-stimulated glycogen synthesis by inhibiting PP-1 activation via ceramide release.	Ceramides	106-114	tumor necrosis factor	Rattus norvegicus	17-26
8641202-0	1996	Interleukin-1 beta stimulates sphingomyelin hydrolysis in cultured granulosa cells: evidence for a regulatory role of ceramide on progesterone and prostaglandin biosynthesis.	Ceramides	118-126	interleukin 1 beta	Homo sapiens	0-18
8641202-7	1996	Although the effect on PGHS-2 messenger RNA may account for the facilitatory role of ceramide on IL1 beta-induced PGE2 biosynthesis, neither SMase nor the membrane-permeant ceramide analogue were able to augment prostaglandin accumulation in the presence of exogenously added arachidonate precursor.	Ceramides	85-93	prostaglandin-endoperoxide synthase 2	Homo sapiens	23-29
8641202-7	1996	Although the effect on PGHS-2 messenger RNA may account for the facilitatory role of ceramide on IL1 beta-induced PGE2 biosynthesis, neither SMase nor the membrane-permeant ceramide analogue were able to augment prostaglandin accumulation in the presence of exogenously added arachidonate precursor.	Ceramides	85-93	interleukin 1 beta	Homo sapiens	97-105
8641202-8	1996	Collectively, whereas these results show that ceramide triggers a negative-effector pathway that is both necessary and sufficient to reproduce the inhibitory effect of IL1 beta on FSH-stimulated granulosa cell steroidogenesis, they also support the notion that sphingomyelin hydrolysis may be important for cytokine-induced PGHS-2 expression but not sufficient to reproduce IL1 beta-stimulated PGE2 biosynthesis.	Ceramides	46-54	interleukin 1 beta	Homo sapiens	168-176
8641202-8	1996	Collectively, whereas these results show that ceramide triggers a negative-effector pathway that is both necessary and sufficient to reproduce the inhibitory effect of IL1 beta on FSH-stimulated granulosa cell steroidogenesis, they also support the notion that sphingomyelin hydrolysis may be important for cytokine-induced PGHS-2 expression but not sufficient to reproduce IL1 beta-stimulated PGE2 biosynthesis.	Ceramides	46-54	prostaglandin-endoperoxide synthase 2	Homo sapiens	324-330
8641202-8	1996	Collectively, whereas these results show that ceramide triggers a negative-effector pathway that is both necessary and sufficient to reproduce the inhibitory effect of IL1 beta on FSH-stimulated granulosa cell steroidogenesis, they also support the notion that sphingomyelin hydrolysis may be important for cytokine-induced PGHS-2 expression but not sufficient to reproduce IL1 beta-stimulated PGE2 biosynthesis.	Ceramides	46-54	interleukin 1 beta	Homo sapiens	374-382
8662702-2	1996	Ceramide generation by stimulated sphingomyelinase activity has been implicated in tumor necrosis factor alpha (TNF) signaling of apoptosis and differentiation.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	83-110
8662702-2	1996	Ceramide generation by stimulated sphingomyelinase activity has been implicated in tumor necrosis factor alpha (TNF) signaling of apoptosis and differentiation.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	112-115
8662702-3	1996	We examined the role of ceramide in a major action of TNF: the initiation of inflammatory events.	Ceramides	24-32	tumor necrosis factor	Homo sapiens	54-57
8662702-5	1996	TNF induced only a small increase in ceramide: using lower doses of sphingomyelinase to mimic this we found that small amounts of ceramide did not induce protein expression, but still rapidly activated Raf-1, mitogen-activated protein/extracellular regulated kinase (ERK) kinase (MEK) and ERKs.	Ceramides	37-45	tumor necrosis factor	Homo sapiens	0-3
8662702-5	1996	TNF induced only a small increase in ceramide: using lower doses of sphingomyelinase to mimic this we found that small amounts of ceramide did not induce protein expression, but still rapidly activated Raf-1, mitogen-activated protein/extracellular regulated kinase (ERK) kinase (MEK) and ERKs.	Ceramides	130-138	tumor necrosis factor	Homo sapiens	0-3
8662702-5	1996	TNF induced only a small increase in ceramide: using lower doses of sphingomyelinase to mimic this we found that small amounts of ceramide did not induce protein expression, but still rapidly activated Raf-1, mitogen-activated protein/extracellular regulated kinase (ERK) kinase (MEK) and ERKs.	Ceramides	130-138	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	202-207
8662702-5	1996	TNF induced only a small increase in ceramide: using lower doses of sphingomyelinase to mimic this we found that small amounts of ceramide did not induce protein expression, but still rapidly activated Raf-1, mitogen-activated protein/extracellular regulated kinase (ERK) kinase (MEK) and ERKs.	Ceramides	130-138	mitogen-activated protein kinase 1	Homo sapiens	267-270
8662702-5	1996	TNF induced only a small increase in ceramide: using lower doses of sphingomyelinase to mimic this we found that small amounts of ceramide did not induce protein expression, but still rapidly activated Raf-1, mitogen-activated protein/extracellular regulated kinase (ERK) kinase (MEK) and ERKs.	Ceramides	130-138	mitogen-activated protein kinase kinase 7	Homo sapiens	280-283
8662702-5	1996	TNF induced only a small increase in ceramide: using lower doses of sphingomyelinase to mimic this we found that small amounts of ceramide did not induce protein expression, but still rapidly activated Raf-1, mitogen-activated protein/extracellular regulated kinase (ERK) kinase (MEK) and ERKs.	Ceramides	130-138	mitogen-activated protein kinase 1	Homo sapiens	289-293
8662702-6	1996	TNF additionally caused rapid p38 and JNK-1 mitogen-activated protein kinase activation and efficient NF-kappaB translocation, which could not be achieved even by high levels of ceramide.	Ceramides	178-186	tumor necrosis factor	Homo sapiens	0-3
8662702-7	1996	Thus activation of the ERK cascade alone is an incomplete endothelial cell stimulus, and the TNF receptor generates at least two signals: Raf-1 activation, which could be ceramide-dependent; and ceramide-independent efficient NF-kappaB translocation and activation of p38 and JNK-1 mitogen-activated kinases.	Ceramides	171-179	tumor necrosis factor	Homo sapiens	93-96
8662702-7	1996	Thus activation of the ERK cascade alone is an incomplete endothelial cell stimulus, and the TNF receptor generates at least two signals: Raf-1 activation, which could be ceramide-dependent; and ceramide-independent efficient NF-kappaB translocation and activation of p38 and JNK-1 mitogen-activated kinases.	Ceramides	171-179	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	138-143
8662702-7	1996	Thus activation of the ERK cascade alone is an incomplete endothelial cell stimulus, and the TNF receptor generates at least two signals: Raf-1 activation, which could be ceramide-dependent; and ceramide-independent efficient NF-kappaB translocation and activation of p38 and JNK-1 mitogen-activated kinases.	Ceramides	195-203	tumor necrosis factor	Homo sapiens	93-96
8662781-7	1996	Initial inhibition was observed as early as 4.5 h after treatment of cells with C6-ceramide, and the activity was completely lost by 13 h. Inhibition of PKCalpha activity was seen at concentrations of ceramide as low as 5 microM with maximal effects occurring at a concentration of 15 microM.	Ceramides	83-91	protein kinase C alpha	Homo sapiens	153-161
8662781-3	1996	In Molt-4 cells, phorbol 12-myristate 13-acetate (PMA) induced retinoblastoma gene product (Rb) phosphorylation, and ceramide inhibited this effect, suggesting an inhibitory effect of ceramide on the protein kinase C (PKC) pathway, the primary target of PMA.	Ceramides	117-125	protein kinase C alpha	Homo sapiens	218-221
8662781-5	1996	To determine the effects of ceramide on PKC, we developed an immunoprecipitation assay for PKCalpha activity.	Ceramides	28-36	protein kinase C alpha	Homo sapiens	91-99
8684259-2	1996	This study corroborates the above result and also gives evidence for the presence of antibodies to the nonpolar ceramide (Cer) moiety of GalC.	Ceramides	112-120	galactosylceramidase	Homo sapiens	137-141
8684259-2	1996	This study corroborates the above result and also gives evidence for the presence of antibodies to the nonpolar ceramide (Cer) moiety of GalC.	Ceramides	122-125	galactosylceramidase	Homo sapiens	137-141
8662983-6	1996	Exogenous sphingomyelinase and ceramides, known to be formed by activation of p55 TNFR, inhibit IR and IRS-1 tyrosine phosphorylation and convert IRS-1 into an inhibitor of IR tyrosine kinase in vitro.	Ceramides	31-40	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	78-81
8662983-6	1996	Exogenous sphingomyelinase and ceramides, known to be formed by activation of p55 TNFR, inhibit IR and IRS-1 tyrosine phosphorylation and convert IRS-1 into an inhibitor of IR tyrosine kinase in vitro.	Ceramides	31-40	tumor necrosis factor receptor superfamily, member 1a	Mus musculus	82-86
8662983-6	1996	Exogenous sphingomyelinase and ceramides, known to be formed by activation of p55 TNFR, inhibit IR and IRS-1 tyrosine phosphorylation and convert IRS-1 into an inhibitor of IR tyrosine kinase in vitro.	Ceramides	31-40	insulin receptor substrate 1	Mus musculus	103-108
8662983-6	1996	Exogenous sphingomyelinase and ceramides, known to be formed by activation of p55 TNFR, inhibit IR and IRS-1 tyrosine phosphorylation and convert IRS-1 into an inhibitor of IR tyrosine kinase in vitro.	Ceramides	31-40	insulin receptor substrate 1	Mus musculus	146-151
8643573-0	1996	Bcl-2 interrupts the ceramide-mediated pathway of cell death.	Ceramides	21-29	BCL2 apoptosis regulator	Homo sapiens	0-5
8643573-2	1996	In this study, we examine the relationship between the ceramide-mediated pathway of growth suppression and the bcl-2 protooncogene.	Ceramides	55-63	BCL2 apoptosis regulator	Homo sapiens	111-116
8643573-7	1996	Overexpression of bcl-2 prevented apoptosis in response to ceramide, suggesting that bcl-2 acts at a point downstream of ceramide.	Ceramides	59-67	BCL2 apoptosis regulator	Homo sapiens	18-23
8643573-7	1996	Overexpression of bcl-2 prevented apoptosis in response to ceramide, suggesting that bcl-2 acts at a point downstream of ceramide.	Ceramides	59-67	BCL2 apoptosis regulator	Homo sapiens	85-90
8643573-7	1996	Overexpression of bcl-2 prevented apoptosis in response to ceramide, suggesting that bcl-2 acts at a point downstream of ceramide.	Ceramides	121-129	BCL2 apoptosis regulator	Homo sapiens	18-23
8643573-7	1996	Overexpression of bcl-2 prevented apoptosis in response to ceramide, suggesting that bcl-2 acts at a point downstream of ceramide.	Ceramides	121-129	BCL2 apoptosis regulator	Homo sapiens	85-90
8662781-11	1996	Taken together, these results suggested that ceramide caused inactivation of PKCalpha.	Ceramides	45-53	protein kinase C alpha	Homo sapiens	77-85
8662781-12	1996	Since PKC requires phosphorylation for activity, we determined the effects of ceramide on phosphorylation of PKCalpha.	Ceramides	78-86	protein kinase C alpha	Homo sapiens	6-9
8662781-12	1996	Since PKC requires phosphorylation for activity, we determined the effects of ceramide on phosphorylation of PKCalpha.	Ceramides	78-86	protein kinase C alpha	Homo sapiens	109-117
8662781-14	1996	In addition, okadaic acid, a potent phosphatase inhibitor, slightly stimulated PKC activity and blocked the effects of ceramide on PKCalpha inhibition.	Ceramides	119-127	protein kinase C alpha	Homo sapiens	131-139
8662781-15	1996	These results demonstrate that ceramide causes inhibition/inactivation of PKCalpha and suggest these effects of ceramide may be mediated by a protein phosphatase.	Ceramides	31-39	protein kinase C alpha	Homo sapiens	74-82
8645194-6	1996	Moreover, ceramide can suppress growth factor- or sphingosine-induced ERK activation as well as proliferation.	Ceramides	10-18	Eph receptor B1	Rattus norvegicus	70-73
8681429-3	1996	The action of PAP-2 could terminate signalling by these bioactive lipids and at the same time generates compounds such as diacylglycerol, sphingosine and ceramide which are also potent signalling molecules.	Ceramides	154-162	phospholipid phosphatase 1	Homo sapiens	14-19
8665940-14	1996	Cell-permeable ceramide analogs mimicked the TNF-alpha effect on MAPK inhibition and PP-2A activation.	Ceramides	15-23	tumor necrosis factor	Rattus norvegicus	45-54
8645194-4	1996	In contrast, inflammatory cytokines or cell-permeable ceramide analogues activate SAPK but not ERK.	Ceramides	54-62	mitogen-activated protein kinase 9	Rattus norvegicus	82-86
8645194-5	1996	Ceramide, but not sphingosine, induces interleukin-6 secretion, a marker of an inflamed phenotype.	Ceramides	0-8	interleukin 6	Rattus norvegicus	39-52
8645213-1	1996	The novel lipid second messenger, ceramide, specifically induced poly(ADP-ribose) polymerase cleavage through activation of the protease prICE.	Ceramides	34-42	poly(ADP-ribose) polymerase 1	Homo sapiens	65-92
8645213-2	1996	Over-expression of Bcl-2 inhibited ceramide-induced poly(ADP-ribose) polymerase proteolysis and protected cells from ceramide-induced death.	Ceramides	35-43	BCL2 apoptosis regulator	Homo sapiens	19-24
8645213-2	1996	Over-expression of Bcl-2 inhibited ceramide-induced poly(ADP-ribose) polymerase proteolysis and protected cells from ceramide-induced death.	Ceramides	35-43	poly(ADP-ribose) polymerase 1	Homo sapiens	52-79
8645213-2	1996	Over-expression of Bcl-2 inhibited ceramide-induced poly(ADP-ribose) polymerase proteolysis and protected cells from ceramide-induced death.	Ceramides	117-125	BCL2 apoptosis regulator	Homo sapiens	19-24
8726216-3	1996	Recent studies using cultured human fibroblasts have shown that TNF alpha stimulates the activity of neutral sphingomyelinase (SMase) which hydrolyses sphingomyelin (SM) generating ceramide and changing membrane components including cholesterol.	Ceramides	181-189	tumor necrosis factor	Homo sapiens	64-73
8626598-1	1996	Previously we showed that interleukin 1 beta stimulates the conversion of sphingomyelin to ceramide in the caveolae fraction of normal human fibroblasts.	Ceramides	91-99	interleukin 1 beta	Homo sapiens	26-44
8645177-7	1996	In this context, short-chain ceramides are poor stimulators of ERKs in ASM cells, and sphingosine is inactive, whereas both sphingolipids are powerful activators of the JNK module.	Ceramides	29-38	mitogen-activated protein kinase 1	Homo sapiens	63-67
8645177-9	1996	Therefore, in blocking ceramide-stimulated ERK-2 activity, cyclic AMP may allow the ceramide-dependent activation of JNK to programme cells to opt out of the cell cycle.	Ceramides	23-31	mitogen-activated protein kinase 1	Homo sapiens	43-48
8645177-9	1996	Therefore, in blocking ceramide-stimulated ERK-2 activity, cyclic AMP may allow the ceramide-dependent activation of JNK to programme cells to opt out of the cell cycle.	Ceramides	23-31	mitogen-activated protein kinase 8	Homo sapiens	117-120
8645177-9	1996	Therefore, in blocking ceramide-stimulated ERK-2 activity, cyclic AMP may allow the ceramide-dependent activation of JNK to programme cells to opt out of the cell cycle.	Ceramides	84-92	mitogen-activated protein kinase 1	Homo sapiens	43-48
8645177-9	1996	Therefore, in blocking ceramide-stimulated ERK-2 activity, cyclic AMP may allow the ceramide-dependent activation of JNK to programme cells to opt out of the cell cycle.	Ceramides	84-92	mitogen-activated protein kinase 8	Homo sapiens	117-120
8647130-6	1996	In contrast, sphingosine and cell-permeable ceramides elicit the prominent tyrosyl phosphorylation and activation of JNK, are poor stimulators of ERK-2, and do not induce the phosphorylation of p70(56K).	Ceramides	44-53	mitogen-activated protein kinase 8	Homo sapiens	117-120
8647130-6	1996	In contrast, sphingosine and cell-permeable ceramides elicit the prominent tyrosyl phosphorylation and activation of JNK, are poor stimulators of ERK-2, and do not induce the phosphorylation of p70(56K).	Ceramides	44-53	mitogen-activated protein kinase 1	Homo sapiens	146-151
8647130-6	1996	In contrast, sphingosine and cell-permeable ceramides elicit the prominent tyrosyl phosphorylation and activation of JNK, are poor stimulators of ERK-2, and do not induce the phosphorylation of p70(56K).	Ceramides	44-53	ubiquitin associated and SH3 domain containing B	Homo sapiens	194-197
8647130-9	1996	For instance, both ceramide and sphingosine will elicit growth arrest via activation of JNK, whereas sphingosine phosphate will potentiate growth-factor-stimulated DNA synthesis, a consequence of the activation of ERK-2, Furthermore, under certain conditions, sphingosine and ceramide stimulate cAMP formation, a negative modulator of cell growth, whereas sphingosine phosphate depresses cAMP, thereby enhancing its own growth-promoting properties.	Ceramides	19-27	mitogen-activated protein kinase 8	Homo sapiens	88-91
8647130-9	1996	For instance, both ceramide and sphingosine will elicit growth arrest via activation of JNK, whereas sphingosine phosphate will potentiate growth-factor-stimulated DNA synthesis, a consequence of the activation of ERK-2, Furthermore, under certain conditions, sphingosine and ceramide stimulate cAMP formation, a negative modulator of cell growth, whereas sphingosine phosphate depresses cAMP, thereby enhancing its own growth-promoting properties.	Ceramides	276-284	mitogen-activated protein kinase 1	Homo sapiens	214-219
8626623-0	1996	Sphingomyelinase and ceramide suppress insulin-induced tyrosine phosphorylation of the insulin receptor substrate-1.	Ceramides	21-29	insulin receptor substrate 1	Rattus norvegicus	87-115
8626623-8	1996	A similar impact on IRS-1 tyrosine phosphorylation was observed after addition of cell-permeable ceramide analogs (C2 and C6).	Ceramides	97-105	insulin receptor substrate 1	Rattus norvegicus	20-25
8626623-9	1996	Comparable changes in IRS-1 tyrosine phosphorylation and electrophoretic mobility were found after exposure of cells to either TNF, SMase, or ceramide.	Ceramides	142-150	insulin receptor substrate 1	Rattus norvegicus	22-27
8626526-0	1996	Interleukin-1 beta-induced ceramide and diacylglycerol generation may lead to activation of the c-Jun NH2-terminal kinase and the transcription factor ATF2 in the insulin-producing cell line RINm5F.	Ceramides	27-35	interleukin 1 beta	Rattus norvegicus	0-18
8621602-0	1996	Regulatory role of ceramide in interleukin (IL)-1 beta-induced E-selectin expression in human umbilical vein endothelial cells.	Ceramides	19-27	interleukin 1 beta	Homo sapiens	31-54
8621602-0	1996	Regulatory role of ceramide in interleukin (IL)-1 beta-induced E-selectin expression in human umbilical vein endothelial cells.	Ceramides	19-27	selectin E	Homo sapiens	63-73
8621602-1	1996	Ceramide enhances IL-1 beta action, but is not sufficient for E-selectin expression.	Ceramides	0-8	interleukin 1 beta	Homo sapiens	18-27
8621602-11	1996	IL-1 beta induced sphingomyelin hydrolysis to ceramide; intracellular ceramide level increased to 182% of control value at 30 min.	Ceramides	46-54	interleukin 1 beta	Homo sapiens	0-9
8621602-11	1996	IL-1 beta induced sphingomyelin hydrolysis to ceramide; intracellular ceramide level increased to 182% of control value at 30 min.	Ceramides	70-78	interleukin 1 beta	Homo sapiens	0-9
8626526-0	1996	Interleukin-1 beta-induced ceramide and diacylglycerol generation may lead to activation of the c-Jun NH2-terminal kinase and the transcription factor ATF2 in the insulin-producing cell line RINm5F.	Ceramides	27-35	activating transcription factor 2	Rattus norvegicus	151-155
8626526-3	1996	It was found that IL-1beta induced a transient increase (2-5 min) in ceramide and diacylglycerol, which was not paralleled by an increase in ceramide 1-phosphate and phosphatidic acid.	Ceramides	69-77	interleukin 1 beta	Rattus norvegicus	18-26
8626526-5	1996	The cell-permeable ceramide analogue N-acetylsphingosine and the phorbol ester phorbol 12-myristate 13-acetate (PMA) both induced the phosphorylation and increased the activities of the protein kinase JNK1 and the transcription factor ATF2.	Ceramides	19-27	activating transcription factor 2	Rattus norvegicus	235-239
17180092-0	1996	Educational Corner: Ceramide-mediated pathways in FAS/APO-1 signalling.	Ceramides	20-28	Fas cell surface death receptor	Homo sapiens	54-59
8660316-0	1996	Bradykinin increases ceramide and sphingosine content in human fibroblasts: possible involvement of glycosphingolipids.	Ceramides	21-29	kininogen 1	Homo sapiens	0-10
8660316-5	1996	The observation that the labeled glycosphingolipid pool is decreased upon BK stimulation would rather suggest that the peptide increases ceramide cellular content by rapidly mobilizing neutral glycolipids.	Ceramides	137-145	kininogen 1	Homo sapiens	74-76
8660316-6	1996	Even though the physiological relevance of ceramide and sphingosine increase induced by BK is not known, it is noteworthy that glycosphingolipids may participate in this lipid signalling pathway.	Ceramides	43-51	kininogen 1	Homo sapiens	88-90
8617770-3	1996	Here we report that an N-terminal truncation of one of these candidate signal transducers, FADD/MORT1, abrogates CD95-induced apoptosis, ceramide generation, and activation of the cell death protease Yama/CPP32.	Ceramides	137-145	Fas associated via death domain	Homo sapiens	91-95
8626526-11	1996	It is concluded that IL-1beta-stimulated formation of ceramide and diacylglycerol may contribute to JNK1 and ATF2 transcription factor activation, which may be a necessary (but not sufficient) step in beta-cell nitric-oxide synthase induction.	Ceramides	54-62	interleukin 1 beta	Rattus norvegicus	21-29
8626526-11	1996	It is concluded that IL-1beta-stimulated formation of ceramide and diacylglycerol may contribute to JNK1 and ATF2 transcription factor activation, which may be a necessary (but not sufficient) step in beta-cell nitric-oxide synthase induction.	Ceramides	54-62	activating transcription factor 2	Rattus norvegicus	109-113
8607825-0	1996	Role of ceramide in stimulation of the transcription of cytosolic phospholipase A2 and cyclooxygenase 2.	Ceramides	8-16	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	56-82
8607825-0	1996	Role of ceramide in stimulation of the transcription of cytosolic phospholipase A2 and cyclooxygenase 2.	Ceramides	8-16	prostaglandin-endoperoxide synthase 2	Mus musculus	87-103
8607825-5	1996	In this study, we evaluated the role of ceramide in TNF-signaling in L929 cells.	Ceramides	40-48	tumor necrosis factor	Mus musculus	52-55
8607825-6	1996	L929 cells generated ceramide in response to TNF, whereas the TNF-resistant sublines did not.	Ceramides	21-29	tumor necrosis factor	Mus musculus	45-48
8607825-7	1996	The addition of an exogenous cell-permeable ceramide analogue resulted in the elevated expression of cPLA2 and cyclooxygenase 2 mRNAs in the cells.	Ceramides	44-52	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	101-106
8607825-7	1996	The addition of an exogenous cell-permeable ceramide analogue resulted in the elevated expression of cPLA2 and cyclooxygenase 2 mRNAs in the cells.	Ceramides	44-52	prostaglandin-endoperoxide synthase 2	Mus musculus	111-127
8607825-8	1996	These results suggest the role of ceramide to amplify the magnitude of signals generated through the PLA2 pathway.	Ceramides	34-42	phospholipase A2, group V	Mus musculus	101-105
8607851-0	1996	Ceramide induces structural defects into phosphatidylcholine bilayers and activates phospholipase A2.	Ceramides	0-8	LOC104974671	Bos taurus	84-100
8607851-4	1996	The observed structural effects of ceramide correlated with ceramide-induced activation of cobra venom phospholipase A2 (PL-A2).	Ceramides	35-43	LOC104974671	Bos taurus	103-119
8607851-4	1996	The observed structural effects of ceramide correlated with ceramide-induced activation of cobra venom phospholipase A2 (PL-A2).	Ceramides	35-43	LOC104974671	Bos taurus	121-126
8607851-4	1996	The observed structural effects of ceramide correlated with ceramide-induced activation of cobra venom phospholipase A2 (PL-A2).	Ceramides	60-68	LOC104974671	Bos taurus	103-119
8607851-4	1996	The observed structural effects of ceramide correlated with ceramide-induced activation of cobra venom phospholipase A2 (PL-A2).	Ceramides	60-68	LOC104974671	Bos taurus	121-126
8607851-5	1996	Ceramide activated PL-A2 in a concentration-dependent manner, with a significant effect observed at 5 mol% ceramide, which caused an approximately 3-fold increase in PL-A2 activity.	Ceramides	0-8	LOC104974671	Bos taurus	19-24
8607851-5	1996	Ceramide activated PL-A2 in a concentration-dependent manner, with a significant effect observed at 5 mol% ceramide, which caused an approximately 3-fold increase in PL-A2 activity.	Ceramides	0-8	LOC104974671	Bos taurus	166-171
8607851-5	1996	Ceramide activated PL-A2 in a concentration-dependent manner, with a significant effect observed at 5 mol% ceramide, which caused an approximately 3-fold increase in PL-A2 activity.	Ceramides	107-115	LOC104974671	Bos taurus	19-24
8607851-5	1996	Ceramide activated PL-A2 in a concentration-dependent manner, with a significant effect observed at 5 mol% ceramide, which caused an approximately 3-fold increase in PL-A2 activity.	Ceramides	107-115	LOC104974671	Bos taurus	166-171
8607851-6	1996	The results showing activation of PL-A2 by ceramide illustrate an additional feature of the biological effects of this second messenger and suggest the possibility of cross-talk between the sphingomyelinase and PL-A2 signal transduction pathways.	Ceramides	43-51	LOC104974671	Bos taurus	34-39
8617770-3	1996	Here we report that an N-terminal truncation of one of these candidate signal transducers, FADD/MORT1, abrogates CD95-induced apoptosis, ceramide generation, and activation of the cell death protease Yama/CPP32.	Ceramides	137-145	Fas associated via death domain	Homo sapiens	96-101
8617770-3	1996	Here we report that an N-terminal truncation of one of these candidate signal transducers, FADD/MORT1, abrogates CD95-induced apoptosis, ceramide generation, and activation of the cell death protease Yama/CPP32.	Ceramides	137-145	Fas cell surface death receptor	Homo sapiens	113-117
8628997-0	1996	Requirement of an ICE-like protease for induction of apoptosis and ceramide generation by REAPER.	Ceramides	67-75	Death related ICE-like caspase	Drosophila melanogaster	18-21
8604026-4	1996	Tumor necrosis factor alpha (TNF-alpha) mediates some of its actions by triggering sphingomyelinase to generate ceramide.	Ceramides	112-120	tumor necrosis factor	Homo sapiens	0-27
8604026-4	1996	Tumor necrosis factor alpha (TNF-alpha) mediates some of its actions by triggering sphingomyelinase to generate ceramide.	Ceramides	112-120	tumor necrosis factor	Homo sapiens	29-38
8604026-7	1996	Ceramide did so by extending the lag period in the cells" response to TNF-alpha.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	70-79
8604026-9	1996	Remarkably, however, ceramide inhibited cell spreading or the respiratory burst only if added together with TNF-alpha or within the next few minutes.	Ceramides	21-29	tumor necrosis factor	Homo sapiens	108-117
8604026-10	1996	Neutrophils ignored ceramide if it was added later, even if the TNF-alpha-triggered respiratory burst had not yet commenced.	Ceramides	20-28	tumor necrosis factor	Homo sapiens	64-73
8604026-11	1996	These features suggest that an early, brief elevation of ceramide in response to TNF-alpha could mediate the lag period.	Ceramides	57-65	tumor necrosis factor	Homo sapiens	81-90
8628997-4	1996	RPR-induced apoptosis was associated with increased ceramide production that was also blocked by Z-VAD-fmk, which suggests that ceramide generation requires an ICE-like protease as well.	Ceramides	52-60	reaper	Drosophila melanogaster	0-3
8628997-4	1996	RPR-induced apoptosis was associated with increased ceramide production that was also blocked by Z-VAD-fmk, which suggests that ceramide generation requires an ICE-like protease as well.	Ceramides	128-136	reaper	Drosophila melanogaster	0-3
8600023-1	1996	Certain mammalian growth modulators, such as tumor necrosis factor alpha, interleukin-1beta, and gamma-interferon, induce an antiproliferative response-terminal differentiation, apoptosis, or cell cycle arrest-through a novel signal transduction pathway mediated by the lipid ceramide as a second messenger.	Ceramides	276-284	tumor necrosis factor	Homo sapiens	45-72
8600023-1	1996	Certain mammalian growth modulators, such as tumor necrosis factor alpha, interleukin-1beta, and gamma-interferon, induce an antiproliferative response-terminal differentiation, apoptosis, or cell cycle arrest-through a novel signal transduction pathway mediated by the lipid ceramide as a second messenger.	Ceramides	276-284	interleukin 1 beta	Homo sapiens	74-91
8646815-1	1996	Farber disease is an inborn lysosomal storage disorder characterized by accumulation of ceramide in the patient"s tissues due to the deficient activity of acid ceramidase.	Ceramides	88-96	N-acylsphingosine amidohydrolase 1	Homo sapiens	155-170
8628997-4	1996	RPR-induced apoptosis was associated with increased ceramide production that was also blocked by Z-VAD-fmk, which suggests that ceramide generation requires an ICE-like protease as well.	Ceramides	128-136	Death related ICE-like caspase	Drosophila melanogaster	160-163
8628997-0	1996	Requirement of an ICE-like protease for induction of apoptosis and ceramide generation by REAPER.	Ceramides	67-75	reaper	Drosophila melanogaster	90-96
8674577-0	1996	Activation of NF kappa B and potentiation of TNF-induced NF kappa B activation by ceramide analogues in leukemic cell lines despite the absence of an observed sphingomyelinase signalling event.	Ceramides	82-90	nuclear factor kappa B subunit 1	Homo sapiens	14-24
8562342-7	1996	In TNF-resistant variant cells, activation of PK35 in response to TNF-alpha or ceramide was practically nil.	Ceramides	79-87	tumor necrosis factor	Homo sapiens	3-6
8674577-0	1996	Activation of NF kappa B and potentiation of TNF-induced NF kappa B activation by ceramide analogues in leukemic cell lines despite the absence of an observed sphingomyelinase signalling event.	Ceramides	82-90	tumor necrosis factor	Homo sapiens	45-48
8562342-8	1996	These findings suggest that activation of PK35 through the ceramide pathway may play an important role in signal transduction of TNF-alpha in the Kasumi-1 cell line, while the decreased activation of PK35 may explain the insensitivity of the variant cells towards TNF-alpha.	Ceramides	59-67	tumor necrosis factor	Homo sapiens	129-138
8562955-7	1996	We show that stimulation with a synthetic ceramide analog results in JNK activation as well as apoptosis, suggesting ceramide release occurs proximal to JNK activation in Fas signaling.	Ceramides	42-50	mitogen-activated protein kinase 9	Homo sapiens	69-72
8562955-7	1996	We show that stimulation with a synthetic ceramide analog results in JNK activation as well as apoptosis, suggesting ceramide release occurs proximal to JNK activation in Fas signaling.	Ceramides	42-50	mitogen-activated protein kinase 9	Homo sapiens	153-156
8674577-0	1996	Activation of NF kappa B and potentiation of TNF-induced NF kappa B activation by ceramide analogues in leukemic cell lines despite the absence of an observed sphingomyelinase signalling event.	Ceramides	82-90	nuclear factor kappa B subunit 1	Homo sapiens	57-67
8592146-1	1996	The death of dopaminergic and other neurons in primary cultures of the mesencephalon could be induced by treatment with ceramide, as in lymphocytes where it mediates activation by the cytokines tumor necrosis factor-alpha and interleukin-1 beta of a novel sphingomyelin-dependent signaling pathway leading to apoptosis.	Ceramides	120-128	tumor necrosis factor	Homo sapiens	194-221
8641566-10	1996	Taken altogether, these findings demonstrate that TNF or UV light activate sphingomyelinase that leads to the generation of ceramide resulting in activation of AP24 and DNA fragmentation in sensitive cells.	Ceramides	124-132	tumor necrosis factor	Homo sapiens	50-53
8592146-1	1996	The death of dopaminergic and other neurons in primary cultures of the mesencephalon could be induced by treatment with ceramide, as in lymphocytes where it mediates activation by the cytokines tumor necrosis factor-alpha and interleukin-1 beta of a novel sphingomyelin-dependent signaling pathway leading to apoptosis.	Ceramides	120-128	interleukin 1 beta	Homo sapiens	226-244
8567691-3	1996	GCS activity was monitored throughout purification using UDP-Glc and a fluorescent ceramide analog as substrates.	Ceramides	83-91	UDP-glucose ceramide glucosyltransferase	Rattus norvegicus	0-3
8843466-7	1996	Because FB1 has a close molecular resemblance to sphinganine, it interferes with ceramide biosynthesis and, hence, the processes that it regulates, which is thought to explain its carcinogenic properties.	Ceramides	81-89	TCF3 fusion partner	Homo sapiens	8-11
8567950-8	1996	However C2-ceramide, a cell permeant synthetic analog of ceramide, could efficiently induce apoptosis in T-LPL and T-PBL when added exogenously.	Ceramides	11-19	lipoprotein lipase	Homo sapiens	107-110
9371227-0	1996	Vitamin D3 and ceramide reduce the invasion of tumor cells through extracellular matrix components by elevating protein phosphatase-2A.	Ceramides	15-23	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	120-134
9371227-4	1996	The cellular PP-2A activity could be stimulated by addition of C2-ceramide to LLC-LN7 lysates, or by incubating cells with either C2-ceramide or with a noncalcemic analog of vitamin D3, which has previously been shown to stimulate the release of ceramide.	Ceramides	66-74	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	13-18
9160353-1	1996	Ceramide has emerged as a novel lipid mediator of tumor necrosis factor (TNF)-induced apoptosis.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	50-71
9160353-1	1996	Ceramide has emerged as a novel lipid mediator of tumor necrosis factor (TNF)-induced apoptosis.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	73-76
9160353-3	1996	The present study demonstrates that ceramide-induced internucleosomal DNA cleavage is temporally associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta.	Ceramides	36-44	poly(ADP-ribose) polymerase 1	Homo sapiens	137-164
9160353-3	1996	The present study demonstrates that ceramide-induced internucleosomal DNA cleavage is temporally associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta.	Ceramides	36-44	poly(ADP-ribose) polymerase 1	Homo sapiens	166-170
9160353-3	1996	The present study demonstrates that ceramide-induced internucleosomal DNA cleavage is temporally associated with proteolytic cleavage of poly(ADP-ribose) polymerase (PARP) and protein kinase C (PKC) delta.	Ceramides	36-44	protein kinase C delta	Homo sapiens	176-204
9160353-4	1996	Overexpression of baculovirus protein p35 blocked ceramide-induced DNA fragmentation and proteolytic activity, whereas overexpression of cowpox virus protein CrmA had no effect on these events.	Ceramides	50-58	interleukin 12A	Homo sapiens	38-41
8960353-4	1996	Conversely, activation of sphingomyelinase by agonists (e.g., tumor necrosis factor-alpha) causes ceramide production that inhibits cell division and produces apoptosis.	Ceramides	98-106	tumor necrosis factor	Homo sapiens	62-89
8960353-8	1996	Tumor necrosis factor-alpha causes insulin resistance, which may be partly explained by ceramide production.	Ceramides	88-96	tumor necrosis factor	Homo sapiens	0-27
8960353-8	1996	Tumor necrosis factor-alpha causes insulin resistance, which may be partly explained by ceramide production.	Ceramides	88-96	insulin	Homo sapiens	35-42
8960353-9	1996	Cell-permeable ceramides decrease insulin-stimulated glucose uptake in 3T3-L1 adipocytes after 2-24 h, whereas they stimulate basal glucose uptake.	Ceramides	15-24	insulin	Homo sapiens	34-41
8960353-11	1996	They appear to rely on the differential effects of ceramides on the translocation of GLUT1-and GLUT4-containing vesicles.	Ceramides	51-60	solute carrier family 2 member 1	Homo sapiens	85-90
8960353-11	1996	They appear to rely on the differential effects of ceramides on the translocation of GLUT1-and GLUT4-containing vesicles.	Ceramides	51-60	solute carrier family 2 member 4	Homo sapiens	95-100
17180067-0	1996	BCL-2 suppresses ceramide-induced cell killing.	Ceramides	17-25	BCL2 apoptosis regulator	Homo sapiens	0-5
8618884-4	1995	The levels of alpha B-crystallin, as measured by Northern blot and immunoblot analyses, were increased by the addition of an exogenous short-chain ceramide, N-acetylsphingosine, or by increasing endogenous intracellular ceramide by inhibition of glucosylceramide synthase.	Ceramides	220-228	crystallin, alpha B	Mus musculus	14-32
8550818-3	1995	We have studied the effects of synthetic ceramides and sphingomyelinase as possible regulators of IL-6 gene expression in a human astrocytoma cell line.	Ceramides	41-50	interleukin 6	Homo sapiens	98-102
8550818-4	1995	The synthetic ceramides C2- and C6-ceramide as well as the enzyme sphingomyelinase were able to induce IL-6 gene transcription and protein synthesis in a dose-dependent manner with maximal IL-6 mRNA levels being reached after 4 h of ceramide treatment.	Ceramides	14-23	interleukin 6	Homo sapiens	103-107
8618884-0	1995	Ceramide formation during heat shock: a potential mediator of alpha B-crystallin transcription.	Ceramides	0-8	crystallin, alpha B	Mus musculus	62-80
8550818-4	1995	The synthetic ceramides C2- and C6-ceramide as well as the enzyme sphingomyelinase were able to induce IL-6 gene transcription and protein synthesis in a dose-dependent manner with maximal IL-6 mRNA levels being reached after 4 h of ceramide treatment.	Ceramides	14-23	interleukin 6	Homo sapiens	189-193
8550818-4	1995	The synthetic ceramides C2- and C6-ceramide as well as the enzyme sphingomyelinase were able to induce IL-6 gene transcription and protein synthesis in a dose-dependent manner with maximal IL-6 mRNA levels being reached after 4 h of ceramide treatment.	Ceramides	14-22	interleukin 6	Homo sapiens	103-107
8550818-4	1995	The synthetic ceramides C2- and C6-ceramide as well as the enzyme sphingomyelinase were able to induce IL-6 gene transcription and protein synthesis in a dose-dependent manner with maximal IL-6 mRNA levels being reached after 4 h of ceramide treatment.	Ceramides	14-22	interleukin 6	Homo sapiens	189-193
8618884-1	1995	Ceramide has been identified as a potential second messenger that may mediate cell differentiation and apoptosis after exposure to hormonal agonists such as 1 alpha, 25-dihydroxyvitamin D3, tumor necrosis factor alpha, or gamma-interferon.	Ceramides	0-8	tumor necrosis factor	Mus musculus	190-217
8618884-1	1995	Ceramide has been identified as a potential second messenger that may mediate cell differentiation and apoptosis after exposure to hormonal agonists such as 1 alpha, 25-dihydroxyvitamin D3, tumor necrosis factor alpha, or gamma-interferon.	Ceramides	0-8	interferon gamma	Mus musculus	222-238
7487982-0	1995	Tumor necrosis factor alpha increases tyrosine phosphorylation of a 23-kDa nuclear protein in U937 cells through ceramide signaling pathway.	Ceramides	113-121	tumor necrosis factor	Homo sapiens	0-27
8618884-3	1995	We report that in NIH WT-3T3 cells, ceramide induces an enhancement of gene transcription of alpha B-crystallin, a small heat shock protein.	Ceramides	36-44	crystallin, alpha B	Mus musculus	93-111
8618884-4	1995	The levels of alpha B-crystallin, as measured by Northern blot and immunoblot analyses, were increased by the addition of an exogenous short-chain ceramide, N-acetylsphingosine, or by increasing endogenous intracellular ceramide by inhibition of glucosylceramide synthase.	Ceramides	147-155	crystallin, alpha B	Mus musculus	14-32
8610279-0	1995	Sphingomyelinase and cell-permeable ceramide analogs increase the release of plasminogen activator inhibitor-1 from cultured endothelial cells.	Ceramides	36-44	serpin family E member 1	Homo sapiens	77-110
8610279-5	1995	Cell-permeable ceramide analogs also enhanced the release of PAI-1 from cultured HUVEC in concentration- and time-dependent manners.	Ceramides	15-23	serpin family E member 1	Homo sapiens	61-66
8610279-10	1995	These results suggest that ceramide, generated via "SM cycle", acts as a lipid mediator of PAI-1 release from vascular endothelial cells, and may contribute to a better understanding of the pathogenesis of the PAI-1-associated thrombotic disorders.	Ceramides	27-35	serpin family E member 1	Homo sapiens	91-96
8610279-10	1995	These results suggest that ceramide, generated via "SM cycle", acts as a lipid mediator of PAI-1 release from vascular endothelial cells, and may contribute to a better understanding of the pathogenesis of the PAI-1-associated thrombotic disorders.	Ceramides	27-35	serpin family E member 1	Homo sapiens	210-215
8846779-2	1995	Fas/APO-1 cross-linking by mAbs resulted in membrane sphingomyelin hydrolysis and ceramide generation by the action of both neutral and acidic sphingomyelinases.	Ceramides	82-90	Fas cell surface death receptor	Homo sapiens	4-9
19245473-0	1995	Inhibition of human neutrophil elastase by wheat ceramides.	Ceramides	49-58	elastase, neutrophil expressed	Homo sapiens	20-39
19245473-3	1995	Human neutrophil elastase (HNE) can be inhibited by long-chain fatty acids and their derivatives; it was therefore postulated that plant ceramides could be inhibitors of HNE.	Ceramides	137-146	elastase, neutrophil expressed	Homo sapiens	6-25
7592995-0	1995	Requirement of AP-1 for ceramide-induced apoptosis in human leukemia HL-60 cells.	Ceramides	24-32	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	15-19
7592995-2	1995	In this work, we demonstrate that the levels of c-jun mRNA, c-Jun protein, and DNA binding activity of a nuclear transcription factor AP-1 to 12-o-tetradecanoylphorbol 13-acetate responsive elements all increased following treatment with the cell-permeable ceramide, N-acetylsphingosine in human leukemia HL-60 cells.	Ceramides	257-265	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	48-53
7592995-2	1995	In this work, we demonstrate that the levels of c-jun mRNA, c-Jun protein, and DNA binding activity of a nuclear transcription factor AP-1 to 12-o-tetradecanoylphorbol 13-acetate responsive elements all increased following treatment with the cell-permeable ceramide, N-acetylsphingosine in human leukemia HL-60 cells.	Ceramides	257-265	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	134-138
7592995-5	1995	Ceramide-induced growth inhibition and DNA fragmentation were both prevented by treatment with curcumin, 1,7-bis[4-hydroxy-3-methoxy-phenyl]-1,6-heptadiene-3,5-dione (an inhibitor of AP-1 activation), or antisense oligonucleotides for c-jun.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	183-187
7592995-5	1995	Ceramide-induced growth inhibition and DNA fragmentation were both prevented by treatment with curcumin, 1,7-bis[4-hydroxy-3-methoxy-phenyl]-1,6-heptadiene-3,5-dione (an inhibitor of AP-1 activation), or antisense oligonucleotides for c-jun.	Ceramides	0-8	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	235-240
7592995-6	1995	These results suggest that the transcription factor AP-1 is critical for apoptosis in HL-60 cells and that an intracellular sphingolipid mediator, ceramide, modulates a signal transduction inducing apoptosis through AP-1 activation.	Ceramides	147-155	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	216-220
7595516-2	1995	The enzyme UDP-galactose:ceramide galactosyltransferase (CGalT) catalyzes the final step of the synthesis of GalC: the transfer of galactose to ceramide.	Ceramides	25-33	UDP glycosyltransferase 8	Homo sapiens	57-62
7595516-2	1995	The enzyme UDP-galactose:ceramide galactosyltransferase (CGalT) catalyzes the final step of the synthesis of GalC: the transfer of galactose to ceramide.	Ceramides	25-33	galactosylceramidase	Homo sapiens	109-113
7559661-0	1995	Regulation of cytochrome P450 2C11 (CYP2C11) gene expression by interleukin-1, sphingomyelin hydrolysis, and ceramides in rat hepatocytes.	Ceramides	109-118	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	14-34
7559661-0	1995	Regulation of cytochrome P450 2C11 (CYP2C11) gene expression by interleukin-1, sphingomyelin hydrolysis, and ceramides in rat hepatocytes.	Ceramides	109-118	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	36-43
7559661-2	1995	We have examined the role of sphingomyelin hydrolysis to ceramide in the suppression of CYP2C11, a major constitutive form of cytochrome P450, by interleukin-1.	Ceramides	57-65	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	88-95
7559661-3	1995	Treatment of rat hepatocytes cultured on matrigel with interleukin-1 beta caused a rapid turnover of sphingomyelin and an increase in cellular ceramide, with no change in cellular phosphatidylcholine.	Ceramides	143-151	interleukin 1 beta	Rattus norvegicus	55-73
7559661-8	1995	These results are consistent with a role for ceramide or a related sphingolipid in mediating the down-regulation of CYP2C11, the induction of alpha 1-acid glycoprotein, and perhaps other cellular effects of interleukin-1 in hepatocytes.	Ceramides	45-53	cytochrome P450, subfamily 2, polypeptide 11	Rattus norvegicus	116-123
7477354-8	1995	Moreover, in intact HL-60 cells, CAP kinase complexes with Raf1 and, in response to TNF and ceramide analogues, phosphorylates and activates Raf1, implicating CAP kinase as a link between the TNF receptor and Raf1.	Ceramides	92-100	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	141-145
7477354-8	1995	Moreover, in intact HL-60 cells, CAP kinase complexes with Raf1 and, in response to TNF and ceramide analogues, phosphorylates and activates Raf1, implicating CAP kinase as a link between the TNF receptor and Raf1.	Ceramides	92-100	tumor necrosis factor	Homo sapiens	192-195
7477354-8	1995	Moreover, in intact HL-60 cells, CAP kinase complexes with Raf1 and, in response to TNF and ceramide analogues, phosphorylates and activates Raf1, implicating CAP kinase as a link between the TNF receptor and Raf1.	Ceramides	92-100	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	141-145
7592974-5	1995	The ceramide produced in response to IL-1 beta blocked platelet-derived growth factor-stimulated DNA synthesis.	Ceramides	4-12	interleukin 1 beta	Homo sapiens	37-46
7591052-6	1995	Cellular levels of diacylglycerol and ceramide, products of PLC activity, accumulated beginning 3 to 4 h after infection of cells with wild-type bacteria.	Ceramides	38-46	perlecan (heparan sulfate proteoglycan 2)	Mus musculus	60-63
7559485-7	1995	Inflammatory cytokines, including interleukin-1, and tumor necrosis factor-alpha, stimulated sphingomyelinase but not ceramidase activity, a result consistent with the cellular accumulation of the ceramide, apoptidic, differentiating second messenger.	Ceramides	197-205	tumor necrosis factor	Rattus norvegicus	34-80
17180030-0	1995	Inhibition of ceramide-induced apoptosis by Bcl-2.	Ceramides	14-22	BCL2 apoptosis regulator	Homo sapiens	44-49
17180030-1	1995	Ceramide, a long chain sphingolipid that is generated intracellularly upon hydrolysis of membrane-associated sphingomyelin, has recently been implicated as a second messenger-like molecule that is produced distal to ligation of the tumour necrosis factor receptor type 1 (TNFR1), as well as the related Fas (CD95/Apo-1) molecule.	Ceramides	0-8	TNF receptor superfamily member 1A	Homo sapiens	232-270
17180030-1	1995	Ceramide, a long chain sphingolipid that is generated intracellularly upon hydrolysis of membrane-associated sphingomyelin, has recently been implicated as a second messenger-like molecule that is produced distal to ligation of the tumour necrosis factor receptor type 1 (TNFR1), as well as the related Fas (CD95/Apo-1) molecule.	Ceramides	0-8	TNF receptor superfamily member 1A	Homo sapiens	272-277
17180030-1	1995	Ceramide, a long chain sphingolipid that is generated intracellularly upon hydrolysis of membrane-associated sphingomyelin, has recently been implicated as a second messenger-like molecule that is produced distal to ligation of the tumour necrosis factor receptor type 1 (TNFR1), as well as the related Fas (CD95/Apo-1) molecule.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	308-312
17180030-1	1995	Ceramide, a long chain sphingolipid that is generated intracellularly upon hydrolysis of membrane-associated sphingomyelin, has recently been implicated as a second messenger-like molecule that is produced distal to ligation of the tumour necrosis factor receptor type 1 (TNFR1), as well as the related Fas (CD95/Apo-1) molecule.	Ceramides	0-8	Fas cell surface death receptor	Homo sapiens	313-318
17180030-5	1995	Here we show that exposure to synthetic ceramides triggers apoptosis in the human T lymphoblastoid cell lines, CEM and Jurkat, and that overexpression of the apoptosis-repressor protein, Bcl-2, renders these cells resistant to the apoptosis-inducing effects of ceramide, as well as to several other stimuli.	Ceramides	40-49	BCL2 apoptosis regulator	Homo sapiens	187-192
17180030-5	1995	Here we show that exposure to synthetic ceramides triggers apoptosis in the human T lymphoblastoid cell lines, CEM and Jurkat, and that overexpression of the apoptosis-repressor protein, Bcl-2, renders these cells resistant to the apoptosis-inducing effects of ceramide, as well as to several other stimuli.	Ceramides	40-48	BCL2 apoptosis regulator	Homo sapiens	187-192
8580709-7	1995	Recent studies indicate that p75 dramatically influences Trk activity and ligand interactions, and may mediate signals through the ceramide second-messenger pathway.	Ceramides	131-139	PC4 and SFRS1 interacting protein 1	Homo sapiens	29-32
17180030-6	1995	Since exposure to ceramides can result in either cell proliferation, differentiation, cycle arrest, or death, the level of Bcl-2 expression in a cell may be an important factor in determining the outcome of signals that result in intracellular generation of this sphingolipid.	Ceramides	18-27	BCL2 apoptosis regulator	Homo sapiens	123-128
7657695-8	1995	Addition of exogenous ceramide, to circumvent the FB1 block, restored GP-2 and Na/K-ATPase sorting to the apical and basal-lateral membranes, respectively.	Ceramides	22-30	glycoprotein 2	Canis lupus familiaris	70-81
7559390-8	1995	These data suggest that ceramide may act as a second messenger for a subset of TNF alpha"s biochemical and biological effects.	Ceramides	24-32	tumor necrosis factor	Homo sapiens	79-88
7545682-11	1995	Since Abl was also found to block apoptosis mediated by ceramide, a recently proposed downstream effector of the apoptotic pathway initiated by Fas, we propose that Abl exerts its protective effects downstream of the early Fas-initiated signaling events.	Ceramides	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	6-9
7545682-11	1995	Since Abl was also found to block apoptosis mediated by ceramide, a recently proposed downstream effector of the apoptotic pathway initiated by Fas, we propose that Abl exerts its protective effects downstream of the early Fas-initiated signaling events.	Ceramides	56-64	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	165-168
7561863-3	1995	The results also show that, in the Trembler mouse sciatic nerves: (a) The severely deficient sphingolipid biosynthesis results from the constitution of a qualitatively and quantitatively abnormal fatty acid substrate pool destined for metabolism via the ceramide pathway, which ensures the totality of the galactocerebroside labeling and two-thirds of that of sphingomyelin.	Ceramides	254-262	peripheral myelin protein 22	Mus musculus	35-43
8941755-3	1995	Apoptosis induced by ceramide in HL-60 cells requires the presence of c-jun protooncogene.	Ceramides	21-29	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	70-75
8941755-6	1995	These results indicate that ceramide controls cell differentiation and proliferation through apoptosis by activating the nuclear transcriptional factor AP-1.	Ceramides	28-36	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	152-156
7559390-2	1995	A potential second messenger for these signaling pathways is ceramide, which is generated when TNF alpha activates sphingomyelinases.	Ceramides	61-69	tumor necrosis factor	Homo sapiens	95-104
7545303-4	1995	Because resistant cell lines expressed the Fas antigen, these results indicate that these cells have a defect in the proximal signaling events leading to ceramide generation.	Ceramides	154-162	Fas cell surface death receptor	Homo sapiens	43-54
7629499-10	1995	Transfection with the antiapoptotic protooncogene Bcl-2 simultaneously inhibits mitochondrial alterations and apoptotic cell death triggered by steroids or ceramide.	Ceramides	156-164	BCL2 apoptosis regulator	Homo sapiens	50-55
7634330-1	1995	The sphingomyelin pathway, which is initiated by sphingomyelin hydrolysis to generate the second messenger ceramide, signals apoptosis for tumor necrosis factor alpha, Fas, and ionizing radiation.	Ceramides	107-115	tumor necrosis factor	Homo sapiens	139-166
7629516-0	1995	Ceramide induces interleukin 6 gene expression in human fibroblasts.	Ceramides	0-8	interleukin 6	Homo sapiens	17-30
7629516-1	1995	We previously reported that ceramide, the immediate product of sphingomyelin hydrolysis, increases in response to interleukin (IL)-1 beta and plays a role in modulating IL-1 beta-mediated prostaglandin E2 production and cyclooxygenase gene expression in human fibroblasts (Ballou, L. R., C. P. Chao, M. A. Holness, S. C. Barker, and R. Raghow.	Ceramides	28-36	interleukin 1 beta	Homo sapiens	114-137
7650365-2	1995	One such lipid, ceramide, generated from membrane sphingomyelin following stimulation with TNF-alpha, IL-1 beta, or IFN-gamma, activates ceramide-activated kinase (CAK).	Ceramides	16-24	tumor necrosis factor	Mus musculus	91-100
7650365-2	1995	One such lipid, ceramide, generated from membrane sphingomyelin following stimulation with TNF-alpha, IL-1 beta, or IFN-gamma, activates ceramide-activated kinase (CAK).	Ceramides	16-24	interleukin 1 beta	Mus musculus	102-111
7650365-2	1995	One such lipid, ceramide, generated from membrane sphingomyelin following stimulation with TNF-alpha, IL-1 beta, or IFN-gamma, activates ceramide-activated kinase (CAK).	Ceramides	16-24	interferon gamma	Mus musculus	116-125
7650365-3	1995	A recent study demonstrated that LPS activated CAK without generating ceramide, suggesting that the LPS stimulation of cells mimics the second messenger function of ceramide.	Ceramides	165-173	toll-like receptor 4	Mus musculus	33-36
7650365-3	1995	A recent study demonstrated that LPS activated CAK without generating ceramide, suggesting that the LPS stimulation of cells mimics the second messenger function of ceramide.	Ceramides	165-173	toll-like receptor 4	Mus musculus	100-103
7650365-4	1995	To compare ceramide to LPS signaling, we assessed the ability of LPS-responsive (Lpsn) and LPS-hyporesponsive (Lpsd) macrophages to respond directly to ceramide for enhanced expression of LPS-inducible genes.	Ceramides	152-160	toll-like receptor 4	Mus musculus	65-68
7650365-6	1995	These results suggest that a common critical molecule, encoded by the Lps gene, regulates both ceramide and LPS signaling pathways.	Ceramides	95-103	toll-like receptor 4	Mus musculus	70-73
7629516-1	1995	We previously reported that ceramide, the immediate product of sphingomyelin hydrolysis, increases in response to interleukin (IL)-1 beta and plays a role in modulating IL-1 beta-mediated prostaglandin E2 production and cyclooxygenase gene expression in human fibroblasts (Ballou, L. R., C. P. Chao, M. A. Holness, S. C. Barker, and R. Raghow.	Ceramides	28-36	interleukin 1 beta	Homo sapiens	169-178
7629516-6	1995	Here we describe the effects of ceramide in another IL-1 beta-mediated process in these cells, the induction of IL-6 production.	Ceramides	32-40	interleukin 1 beta	Homo sapiens	52-61
7629516-6	1995	Here we describe the effects of ceramide in another IL-1 beta-mediated process in these cells, the induction of IL-6 production.	Ceramides	32-40	interleukin 6	Homo sapiens	112-116
7629516-8	1995	Both D-erythro-C2-ceramide (a cell-permeable analogue of natural ceramide) and D-threo-C2-ceramide were potent inducers of IL-6 production, while neither L isomer of ceramide was effective.	Ceramides	18-26	interleukin 6	Homo sapiens	123-127
7629516-8	1995	Both D-erythro-C2-ceramide (a cell-permeable analogue of natural ceramide) and D-threo-C2-ceramide were potent inducers of IL-6 production, while neither L isomer of ceramide was effective.	Ceramides	65-73	interleukin 6	Homo sapiens	123-127
7629516-9	1995	Compared with IL-1 beta-induced IL-6 production, cells treated with ceramide or exogenous sphingomyelinase induced 82 and 50% of maximal IL-1 beta-induced IL-6 levels by 6 h, respectively; by 24 h all three treatments induced similar levels of IL-6 production.	Ceramides	68-76	interleukin 6	Homo sapiens	32-36
7629516-9	1995	Compared with IL-1 beta-induced IL-6 production, cells treated with ceramide or exogenous sphingomyelinase induced 82 and 50% of maximal IL-1 beta-induced IL-6 levels by 6 h, respectively; by 24 h all three treatments induced similar levels of IL-6 production.	Ceramides	68-76	interleukin 1 beta	Homo sapiens	137-146
7629516-9	1995	Compared with IL-1 beta-induced IL-6 production, cells treated with ceramide or exogenous sphingomyelinase induced 82 and 50% of maximal IL-1 beta-induced IL-6 levels by 6 h, respectively; by 24 h all three treatments induced similar levels of IL-6 production.	Ceramides	68-76	interleukin 6	Homo sapiens	155-159
7629516-9	1995	Compared with IL-1 beta-induced IL-6 production, cells treated with ceramide or exogenous sphingomyelinase induced 82 and 50% of maximal IL-1 beta-induced IL-6 levels by 6 h, respectively; by 24 h all three treatments induced similar levels of IL-6 production.	Ceramides	68-76	interleukin 6	Homo sapiens	155-159
7790893-0	1995	Ceramide prevents neuronal programmed cell death induced by nerve growth factor deprivation.	Ceramides	0-8	nerve growth factor	Homo sapiens	60-79
7629516-10	1995	Ceramide-induced IL-6 messenger RNA could be detected within 1 h of treatment and reached maximal levels by 24 h. These findings suggest that ceramide may play a role in the regulation of IL-6 gene expression.	Ceramides	0-8	interleukin 6	Homo sapiens	17-21
7629516-10	1995	Ceramide-induced IL-6 messenger RNA could be detected within 1 h of treatment and reached maximal levels by 24 h. These findings suggest that ceramide may play a role in the regulation of IL-6 gene expression.	Ceramides	0-8	interleukin 6	Homo sapiens	188-192
7629516-10	1995	Ceramide-induced IL-6 messenger RNA could be detected within 1 h of treatment and reached maximal levels by 24 h. These findings suggest that ceramide may play a role in the regulation of IL-6 gene expression.	Ceramides	142-150	interleukin 6	Homo sapiens	17-21
7629516-10	1995	Ceramide-induced IL-6 messenger RNA could be detected within 1 h of treatment and reached maximal levels by 24 h. These findings suggest that ceramide may play a role in the regulation of IL-6 gene expression.	Ceramides	142-150	interleukin 6	Homo sapiens	188-192
7542883-7	1995	Sphingomyelinase and ceramide (Cer) induced internucleosomal DNA fragmentation was also inhibited by herbimycin A, supporting the hypothesis that Cer may be a novel second messenger mediating the cytotoxic effect of TNF alpha.	Ceramides	21-29	tumor necrosis factor	Homo sapiens	216-225
7621875-0	1995	Sphingomyelin-ceramide turnover in CD28 costimulatory signaling.	Ceramides	14-22	CD28 molecule	Homo sapiens	35-39
7621875-2	1995	Ligation of CD28 initiated sphingomyelin hydrolysis and generated ceramide.	Ceramides	66-74	CD28 molecule	Homo sapiens	12-16
7621875-5	1995	Stabilization of interleukin-2 mRNA was also observed in C6-ceramide-treated cells.	Ceramides	60-68	interleukin 2	Homo sapiens	17-30
7607324-0	1995	Ceramide inhibits pancreatic beta-cell insulin production and mitogenesis and mimics the actions of interleukin-1 beta.	Ceramides	0-8	insulin	Homo sapiens	39-46
7607324-0	1995	Ceramide inhibits pancreatic beta-cell insulin production and mitogenesis and mimics the actions of interleukin-1 beta.	Ceramides	0-8	interleukin 1 beta	Homo sapiens	100-118
7607324-2	1995	The effects of endogenously generated and exogenously delivered ceramide on long-term insulin secretion and replication by pancreatic beta-cells were investigated, and compared to the effects of interleukin 1 beta (IL-1 beta).	Ceramides	64-72	insulin	Homo sapiens	86-93
7607324-3	1995	Generation of beta-cell ceramide by exogenous sphingomyelinase, or addition of cell-permeant ceramide analogs C2-ceramide and C6-ceramide, caused inhibitor effects on beta-cell insulin production and mitogenesis mimicing those evoked by IL-1 beta.	Ceramides	24-32	insulin	Homo sapiens	177-184
7607324-3	1995	Generation of beta-cell ceramide by exogenous sphingomyelinase, or addition of cell-permeant ceramide analogs C2-ceramide and C6-ceramide, caused inhibitor effects on beta-cell insulin production and mitogenesis mimicing those evoked by IL-1 beta.	Ceramides	24-32	interleukin 1 beta	Homo sapiens	237-246
7607324-4	1995	Hence, ceramide may be involved in transducing the cytostatic and cytotoxic actions of IL-1 beta in the beta-cell.	Ceramides	7-15	interleukin 1 beta	Homo sapiens	87-96
8530143-5	1995	SMase and its product ceramide induce degradation of the NF-kappa B inhibitor I kappa B as well as NF-kappa B activation.	Ceramides	22-30	nuclear factor kappa B subunit 1	Homo sapiens	57-67
8530143-5	1995	SMase and its product ceramide induce degradation of the NF-kappa B inhibitor I kappa B as well as NF-kappa B activation.	Ceramides	22-30	nuclear factor kappa B subunit 1	Homo sapiens	99-109
8530143-8	1995	Ceramide generated by nSMase directs the activation of proline-directed serin/threonine protein kinases and phospholipase A2 and ceramide produced by aSMase triggers the activation of NF-kappa B.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	22-28
8530143-8	1995	Ceramide generated by nSMase directs the activation of proline-directed serin/threonine protein kinases and phospholipase A2 and ceramide produced by aSMase triggers the activation of NF-kappa B.	Ceramides	0-8	phospholipase A2 group IB	Homo sapiens	108-124
8530143-8	1995	Ceramide generated by nSMase directs the activation of proline-directed serin/threonine protein kinases and phospholipase A2 and ceramide produced by aSMase triggers the activation of NF-kappa B.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	150-156
8530143-8	1995	Ceramide generated by nSMase directs the activation of proline-directed serin/threonine protein kinases and phospholipase A2 and ceramide produced by aSMase triggers the activation of NF-kappa B.	Ceramides	0-8	nuclear factor kappa B subunit 1	Homo sapiens	184-194
8530143-8	1995	Ceramide generated by nSMase directs the activation of proline-directed serin/threonine protein kinases and phospholipase A2 and ceramide produced by aSMase triggers the activation of NF-kappa B.	Ceramides	129-137	sphingomyelin phosphodiesterase 1	Homo sapiens	150-156
8530143-8	1995	Ceramide generated by nSMase directs the activation of proline-directed serin/threonine protein kinases and phospholipase A2 and ceramide produced by aSMase triggers the activation of NF-kappa B.	Ceramides	129-137	nuclear factor kappa B subunit 1	Homo sapiens	184-194
7790893-2	1995	We found that a cell-permeable ceramide analogue prevented neuronal PCD when applied to established sympathetic neuron primary cultures at the time of nerve growth factor (NGF) deprivation.	Ceramides	31-39	nerve growth factor	Homo sapiens	151-170
7790893-2	1995	We found that a cell-permeable ceramide analogue prevented neuronal PCD when applied to established sympathetic neuron primary cultures at the time of nerve growth factor (NGF) deprivation.	Ceramides	31-39	nerve growth factor	Homo sapiens	172-175
7790893-7	1995	Given the recent findings that the SM cycle is activated to increase the intracellular ceramide level on NGF binding to the low-affinity NGF receptor (LNGFR) and that NGF binding to LNGFR suppresses apoptosis in neuronal cell lines, our results suggest the possibility of the SM cycle as a signaling mechanism transducing the PCD-preventing activity of NGF.	Ceramides	87-95	nerve growth factor	Homo sapiens	105-108
7600574-5	1995	The Niemann-Pick mouse might facilitate studies on the function of aSMase in the generation of ceramide as proposed second messenger in the intracellular signaling pathways and across the plasma membrane.	Ceramides	95-103	protein interacting with PRKCA 1	Homo sapiens	12-16
7600574-5	1995	The Niemann-Pick mouse might facilitate studies on the function of aSMase in the generation of ceramide as proposed second messenger in the intracellular signaling pathways and across the plasma membrane.	Ceramides	95-103	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	67-73
7790893-7	1995	Given the recent findings that the SM cycle is activated to increase the intracellular ceramide level on NGF binding to the low-affinity NGF receptor (LNGFR) and that NGF binding to LNGFR suppresses apoptosis in neuronal cell lines, our results suggest the possibility of the SM cycle as a signaling mechanism transducing the PCD-preventing activity of NGF.	Ceramides	87-95	nerve growth factor	Homo sapiens	137-140
7790893-7	1995	Given the recent findings that the SM cycle is activated to increase the intracellular ceramide level on NGF binding to the low-affinity NGF receptor (LNGFR) and that NGF binding to LNGFR suppresses apoptosis in neuronal cell lines, our results suggest the possibility of the SM cycle as a signaling mechanism transducing the PCD-preventing activity of NGF.	Ceramides	87-95	nerve growth factor	Homo sapiens	137-140
7790893-7	1995	Given the recent findings that the SM cycle is activated to increase the intracellular ceramide level on NGF binding to the low-affinity NGF receptor (LNGFR) and that NGF binding to LNGFR suppresses apoptosis in neuronal cell lines, our results suggest the possibility of the SM cycle as a signaling mechanism transducing the PCD-preventing activity of NGF.	Ceramides	87-95	nerve growth factor	Homo sapiens	137-140
7572287-3	1995	Ceramides, which have been shown to be effectors of TNF-alpha, are ineffective in inhibiting phosphorylation, whereas sphingomyelinase mimics TNF-alpha in this action.	Ceramides	0-9	tumor necrosis factor	Homo sapiens	52-61
7769132-1	1995	Hydrolysis of glucosylceramides (GlcCer) by beta-glucocerebrosidase generates ceramides, critical components of the epidermal permeability barrier.	Ceramides	22-31	glucosidase, beta, acid	Mus musculus	44-67
7759998-3	1995	CD28 engagement triggers the activation of an acidic sphingomyelinase (A-SMase), which results in the generation of ceramide, an important lipid messenger intermediate.	Ceramides	116-124	CD28 molecule	Homo sapiens	0-4
7759998-3	1995	CD28 engagement triggers the activation of an acidic sphingomyelinase (A-SMase), which results in the generation of ceramide, an important lipid messenger intermediate.	Ceramides	116-124	sphingomyelin phosphodiesterase 1	Homo sapiens	46-69
7759998-3	1995	CD28 engagement triggers the activation of an acidic sphingomyelinase (A-SMase), which results in the generation of ceramide, an important lipid messenger intermediate.	Ceramides	116-124	sphingomyelin phosphodiesterase 1	Homo sapiens	71-78
7544978-1	1995	Recent studies indicate that tumor necrosis factor (TNF) and interleukin 1 (IL-1) stimulate cells via the intracellular messenger ceramide.	Ceramides	130-138	tumor necrosis factor	Homo sapiens	29-50
7544978-1	1995	Recent studies indicate that tumor necrosis factor (TNF) and interleukin 1 (IL-1) stimulate cells via the intracellular messenger ceramide.	Ceramides	130-138	tumor necrosis factor	Homo sapiens	52-55
7544978-1	1995	Recent studies indicate that tumor necrosis factor (TNF) and interleukin 1 (IL-1) stimulate cells via the intracellular messenger ceramide.	Ceramides	130-138	interleukin 1 alpha	Homo sapiens	61-80
7720683-3	1995	In FSH-primed cells, TNF alpha inhibited P450-AROM activity in a dose-dependent manner, an effect that was also observed in cells treated with bacterial sphingomyelinase (SMase 0.003-0.3 U/ml) or increasing concentrations (0.1-10 microM) of N-acetylsphingosine (C2-cer) a membrane-permeable analogue of ceramide.	Ceramides	303-311	tumor necrosis factor	Homo sapiens	21-30
7744740-1	1995	Acid ceramidase (N-acylsphingosine deacylase, EC 3.5.1.23) is the lysosomal enzyme catalyzing the hydrolysis of ceramide to sphingosine and free fatty acid.	Ceramides	112-120	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
7744003-0	1995	PKC zeta is a molecular switch in signal transduction of TNF-alpha, bifunctionally regulated by ceramide and arachidonic acid.	Ceramides	96-104	protein kinase C zeta	Homo sapiens	0-8
7744003-0	1995	PKC zeta is a molecular switch in signal transduction of TNF-alpha, bifunctionally regulated by ceramide and arachidonic acid.	Ceramides	96-104	tumor necrosis factor	Homo sapiens	57-66
7744003-3	1995	In this study we investigated the relationship of ceramide and AA in regulating an atypical PKC isozyme, PKC zeta.	Ceramides	50-58	protein kinase C zeta	Homo sapiens	92-95
7744003-3	1995	In this study we investigated the relationship of ceramide and AA in regulating an atypical PKC isozyme, PKC zeta.	Ceramides	50-58	protein kinase C zeta	Homo sapiens	105-113
7744003-5	1995	[14C]ceramide specifically binds to and regulates kinase activity of PKC zeta in a biphasic manner.	Ceramides	5-13	protein kinase C zeta	Homo sapiens	69-77
7744003-8	1995	Interestingly, AA competes for ceramide binding and inhibits basal and ceramide-stimulated PKC zeta kinase activity at < 100 nM.	Ceramides	71-79	protein kinase C zeta	Homo sapiens	91-99
7744003-10	1995	Based on the bifunctional modulation of PKC zeta by the lipid messengers ceramide and AA, a model of TNF signal pathways is suggested in which PKC zeta takes a central position, acting as a molecular switch between mitogenic and growth inhibitory signals of TNF-alpha.	Ceramides	73-81	protein kinase C zeta	Homo sapiens	40-48
7744003-10	1995	Based on the bifunctional modulation of PKC zeta by the lipid messengers ceramide and AA, a model of TNF signal pathways is suggested in which PKC zeta takes a central position, acting as a molecular switch between mitogenic and growth inhibitory signals of TNF-alpha.	Ceramides	73-81	protein kinase C zeta	Homo sapiens	143-151
7738000-10	1995	PTPase inhibitors also blocked NF-kappa B activation induced by phorbol ester, ceramide, and interleukin-1 but not that activated by okadaic acid.	Ceramides	79-87	protein tyrosine phosphatase non-receptor type 22	Homo sapiens	0-6
7738000-10	1995	PTPase inhibitors also blocked NF-kappa B activation induced by phorbol ester, ceramide, and interleukin-1 but not that activated by okadaic acid.	Ceramides	79-87	nuclear factor kappa B subunit 1	Homo sapiens	31-41
7720683-1	1995	In [3H]serine-labelled granulosa cells treatment with TNF alpha (10 ng/ml) resulted in a transient decrease in cellular [3H]sphingomyelin and generation of [3H]ceramide that remained elevated 60 min later.	Ceramides	160-168	tumor necrosis factor	Homo sapiens	54-63
7720683-3	1995	In FSH-primed cells, TNF alpha inhibited P450-AROM activity in a dose-dependent manner, an effect that was also observed in cells treated with bacterial sphingomyelinase (SMase 0.003-0.3 U/ml) or increasing concentrations (0.1-10 microM) of N-acetylsphingosine (C2-cer) a membrane-permeable analogue of ceramide.	Ceramides	303-311	cytochrome P450 family 19 subfamily A member 1	Homo sapiens	41-50
7720683-4	1995	These results support the notion that sphingomyelin degradation to a bioeffector molecule ceramide, may be an early event involved in TNF alpha-induced signal transduction in granulosa cells.	Ceramides	90-98	tumor necrosis factor	Homo sapiens	134-143
7742354-0	1995	Inhibition of acyl-CoA:cholesterol acyltransferase in Chinese hamster ovary (CHO) cells by short-chain ceramide and dihydroceramide.	Ceramides	103-111	sterol O-acyltransferase 1	Cricetulus griseus	14-50
7727545-1	1995	Acid sphingomyelinase (ASM) is the lysosomal enzyme required to hydrolyze sphingomyelin into ceramide and phosphocholine.	Ceramides	93-101	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
7727545-1	1995	Acid sphingomyelinase (ASM) is the lysosomal enzyme required to hydrolyze sphingomyelin into ceramide and phosphocholine.	Ceramides	93-101	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
7742354-11	1995	Thus, N-acyl chain length could influence inhibition, either by altering the effective concentration of ceramide in membranes or affinity for the ACAT enzyme.	Ceramides	104-112	sterol O-acyltransferase 1	Cricetulus griseus	146-150
7742354-12	1995	Short-chain ceramides and dihydroceramides are the first ACAT inhibitors described with structural similarity to a naturally occurring compound.	Ceramides	12-21	sterol O-acyltransferase 1	Cricetulus griseus	57-61
7701566-2	1995	A sphingomyelin cycle has been identified whereby the action of certain extracellular agents (such as tumor necrosis factor alpha) results in activation of a sphingomyelinase, which cleaves membrane sphingomyelin, to generate cellular ceramide.	Ceramides	235-243	tumor necrosis factor	Homo sapiens	102-129
7552072-8	1995	There is some evidence that IL-1 and TNF activate sphingomyelinase in the cell membrane to generate ceramide, which may have a signalling function.	Ceramides	100-108	tumor necrosis factor	Homo sapiens	37-40
7794804-5	1995	The U-A20 and U-V20 clones were also resistant to endonucleolytic DNA cleavage associated with exposure to tumor necrosis factor or ceramide.	Ceramides	132-140	ERCC excision repair 1, endonuclease non-catalytic subunit	Homo sapiens	14-19
7592537-11	1995	D-Threo-PDMP but not the L-threo isomer inhibited both LacCer and GM3 synthases as well as GlcCer synthase, suggesting that the ceramide-like structure of the D-PDMP molecule interacted stereospecifically with these GSL-synthesizing enzymes.	Ceramides	128-136	granulocyte macrophage antigen 3	Mus musculus	66-69
7867010-0	1995	Suppression of Bcl-2 messenger RNA production may mediate apoptosis after ionizing radiation, tumor necrosis factor alpha, and ceramide.	Ceramides	127-135	BCL2 apoptosis regulator	Homo sapiens	15-20
7867010-1	1995	Recent studies have proposed that tumor necrosis factor alpha (TNF-alpha) and ionizing radiation induce apoptosis by activating hydrolysis of sphingomyelin to ceramide.	Ceramides	159-167	tumor necrosis factor	Homo sapiens	34-61
7867010-1	1995	Recent studies have proposed that tumor necrosis factor alpha (TNF-alpha) and ionizing radiation induce apoptosis by activating hydrolysis of sphingomyelin to ceramide.	Ceramides	159-167	tumor necrosis factor	Homo sapiens	63-72
7867010-5	1995	These results suggest that modulation of Bcl-2 gene expression may be a target for ceramide-mediated apoptosis following exposure to ionizing radiation and TNF-alpha.	Ceramides	83-91	BCL2 apoptosis regulator	Homo sapiens	41-46
7867010-5	1995	These results suggest that modulation of Bcl-2 gene expression may be a target for ceramide-mediated apoptosis following exposure to ionizing radiation and TNF-alpha.	Ceramides	83-91	tumor necrosis factor	Homo sapiens	156-165
7852361-12	1995	Therefore, it appears that ceramide mediates in part the inhibitory effect of GlcCer synthase inhibition on IGF-1-induced cell proliferation in 3T3 cells.	Ceramides	27-35	insulin-like growth factor 1	Mus musculus	108-113
7702579-8	1995	Both XN-1 and XN-2 had an identical pentaoligosaccharide structure, but differed in their ceramide moiety.	Ceramides	90-98	nuclear receptor corepressor 1 L homeolog	Xenopus laevis	5-18
7890607-6	1995	The data provide strong evidence that ceramide can negatively regulate the translocation of PKC-alpha but not PKC-epsilon and further suggest that PKC-alpha may be involved in regulating phospholipase D activity.	Ceramides	38-46	protein kinase C, alpha	Mus musculus	92-101
7578992-11	1995	As a third signaling pathway, TNF/LT employ the sphingomyelinase (SMase)-mediated hydrolysis of membrane sphingomyelin (SM) to ceramide.	Ceramides	127-135	tumor necrosis factor	Homo sapiens	30-33
7806975-5	1994	However, a correspondingly significant decrease in sulfoglycolipid and ceramide concentration was observed in the cpk/cpk kidneys.	Ceramides	71-79	cystin 1	Mus musculus	114-117
7525558-5	1994	Cell permeable ceramides also stimulated tyrosine phosphorylation of the M(r) 110,000-130,000 band as well as p125FAK, but the effect was less pronounced than that of sphingosine.	Ceramides	15-24	PTK2 protein tyrosine kinase 2	Mus musculus	110-117
7929315-12	1994	A soluble analog of ceramide, C6-ceramide, was found to inhibit serum-stimulated DAG accumulation and PLD activation in young cells.	Ceramides	20-28	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	102-105
7929315-13	1994	These data demonstrate for the first time a defect in PLD activation in cellular senescence and suggest that ceramide may be responsible for the inhibition of this pathway.	Ceramides	109-117	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	54-57
7930586-7	1994	Moreover, when Daudi cells were treated with a ceramide analogue, 1-phenyl-2-(decanoylamino)-3-morpholino-1-propanol, Gb2 and Gb3 synthesis was inhibited and a concomitant reduction in IFN-induced ISGF3 activation was noted.	Ceramides	47-55	gamma-aminobutyric acid type B receptor subunit 2	Homo sapiens	118-121
7930586-7	1994	Moreover, when Daudi cells were treated with a ceramide analogue, 1-phenyl-2-(decanoylamino)-3-morpholino-1-propanol, Gb2 and Gb3 synthesis was inhibited and a concomitant reduction in IFN-induced ISGF3 activation was noted.	Ceramides	47-55	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	126-129
7930586-7	1994	Moreover, when Daudi cells were treated with a ceramide analogue, 1-phenyl-2-(decanoylamino)-3-morpholino-1-propanol, Gb2 and Gb3 synthesis was inhibited and a concomitant reduction in IFN-induced ISGF3 activation was noted.	Ceramides	47-55	interferon regulatory factor 9	Homo sapiens	197-202
7523573-4	1994	Crosslinking of CD95 with DX2 resulted in the activation of a sphingomyelinase (SMase) in promyelocytic U937 cells, as well as in other human tumor cell lines and in CD95-transfected murine cells, as demonstrated by induction of in vivo sphingomyelin (SM) hydrolysis and generation of ceramide.	Ceramides	285-293	Fas cell surface death receptor	Homo sapiens	16-20
7817665-1	1994	To elucidate the mechanisms that are involved in the decrease of ceramide levels in atopic dry skin and in aged skin, we examined both the activities of beta-glucocerebrosidase, which is a major enzyme in ceramide production, and of ceramidase, which is an essential enzyme in ceramide degradation, in the stratum corneum of atopic dry skin and aged skin.	Ceramides	65-73	glucosylceramidase beta	Homo sapiens	153-176
7817665-1	1994	To elucidate the mechanisms that are involved in the decrease of ceramide levels in atopic dry skin and in aged skin, we examined both the activities of beta-glucocerebrosidase, which is a major enzyme in ceramide production, and of ceramidase, which is an essential enzyme in ceramide degradation, in the stratum corneum of atopic dry skin and aged skin.	Ceramides	205-213	glucosylceramidase beta	Homo sapiens	153-176
7817665-1	1994	To elucidate the mechanisms that are involved in the decrease of ceramide levels in atopic dry skin and in aged skin, we examined both the activities of beta-glucocerebrosidase, which is a major enzyme in ceramide production, and of ceramidase, which is an essential enzyme in ceramide degradation, in the stratum corneum of atopic dry skin and aged skin.	Ceramides	205-213	glucosylceramidase beta	Homo sapiens	153-176
7798945-2	1995	The main and earliest formed 3H-metabolites of [Sph-3H]GM1 were GM2, asialo-GM1 asialo-GM2, and lactose-ceramide, and those of [Sph-3H]GM2 were asialo-GM2 and lactose-ceramide.	Ceramides	104-112	coenzyme Q10A	Mus musculus	55-58
7798945-2	1995	The main and earliest formed 3H-metabolites of [Sph-3H]GM1 were GM2, asialo-GM1 asialo-GM2, and lactose-ceramide, and those of [Sph-3H]GM2 were asialo-GM2 and lactose-ceramide.	Ceramides	167-175	coenzyme Q10A	Mus musculus	55-58
7527398-4	1994	Ceramide has been proposed as an intracellular mediator of IL-1 action, but C2-ceramide or sphingosine stimulated predominantly MBP-specific kinase activity in fibroblasts and had no effect in HepG2 cells.	Ceramides	0-8	interleukin 1 alpha	Homo sapiens	59-63
7988686-1	1994	Treatment of human neutrophils with tumor necrosis factor-alpha (TNF-alpha) resulted in an increase in concentration of ceramide and its catabolite, sphingosine.	Ceramides	120-128	tumor necrosis factor	Homo sapiens	36-63
7988686-1	1994	Treatment of human neutrophils with tumor necrosis factor-alpha (TNF-alpha) resulted in an increase in concentration of ceramide and its catabolite, sphingosine.	Ceramides	120-128	tumor necrosis factor	Homo sapiens	65-74
7988686-5	1994	These results indicate that sphingosine deacylated from ceramide may be an endogenous modulator mediating apoptotic signals by TNF-alpha in neutrophils.	Ceramides	56-64	tumor necrosis factor	Homo sapiens	127-136
7964160-0	1994	The role of diacylglycerol and ceramide in tumor necrosis factor and interleukin-1 signal transduction.	Ceramides	31-39	tumor necrosis factor	Homo sapiens	43-64
7964160-0	1994	The role of diacylglycerol and ceramide in tumor necrosis factor and interleukin-1 signal transduction.	Ceramides	31-39	interleukin 1 alpha	Homo sapiens	69-82
7964160-3	1994	Two lipid second messengers have been found to transmit TNF and IL-1 intracellular signals: 1,2-diacylglycerol (DAG), generated by a phosphatidylcholine-specific phospholipase C, and ceramide, generated by sphingomyelinase (SMase).	Ceramides	183-191	tumor necrosis factor	Homo sapiens	56-59
7964160-3	1994	Two lipid second messengers have been found to transmit TNF and IL-1 intracellular signals: 1,2-diacylglycerol (DAG), generated by a phosphatidylcholine-specific phospholipase C, and ceramide, generated by sphingomyelinase (SMase).	Ceramides	183-191	interleukin 1 alpha	Homo sapiens	64-68
7964161-6	1994	In the past three years, several groups reported that IL-1 and tumor necrosis factor (TNF) rapidly induce sphingomyelin turnover in various types of cells, producing ceramide, which may act as a second messenger molecule in an intracellular signaling cascade.	Ceramides	166-174	interleukin 1 alpha	Homo sapiens	54-58
7964161-6	1994	In the past three years, several groups reported that IL-1 and tumor necrosis factor (TNF) rapidly induce sphingomyelin turnover in various types of cells, producing ceramide, which may act as a second messenger molecule in an intracellular signaling cascade.	Ceramides	166-174	tumor necrosis factor	Homo sapiens	63-84
7964161-6	1994	In the past three years, several groups reported that IL-1 and tumor necrosis factor (TNF) rapidly induce sphingomyelin turnover in various types of cells, producing ceramide, which may act as a second messenger molecule in an intracellular signaling cascade.	Ceramides	166-174	tumor necrosis factor	Homo sapiens	86-89
7929233-9	1994	In this reconstitution system, we can also demonstrate the activation of NF-kappa B by ceramide, but this activation is not tyrosine kinase-dependent.	Ceramides	87-95	nuclear factor kappa B subunit 1	Homo sapiens	73-83
7929233-10	1994	Overall, our results indicate that intermediates required for NF-kappa B activation by TNF or ceramide are membrane-bound, but the mechanism of activation by TNF is most likely different from that of ceramide.	Ceramides	94-102	nuclear factor kappa B subunit 1	Homo sapiens	62-72
7929233-10	1994	Overall, our results indicate that intermediates required for NF-kappa B activation by TNF or ceramide are membrane-bound, but the mechanism of activation by TNF is most likely different from that of ceramide.	Ceramides	200-208	nuclear factor kappa B subunit 1	Homo sapiens	62-72
7523573-7	1994	These data indicate that CD95 cross-linking induces SM breakdown and ceramide production through an acidic SMase, thus providing the first information regarding early signal generation from CD95, and may be relevant in defining the biochemical nature of intracellular messengers leading to apoptotic cell death.	Ceramides	69-77	Fas cell surface death receptor	Homo sapiens	25-29
7923351-5	1994	Ceramide generated by N-SMase directs the activation of proline-directed serine/threonine protein kinase(s) and phospholipase A2.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	22-29
7923351-5	1994	Ceramide generated by N-SMase directs the activation of proline-directed serine/threonine protein kinase(s) and phospholipase A2.	Ceramides	0-8	phospholipase A2 group IB	Homo sapiens	112-128
8079174-2	1994	Nerve growth factor can activate the sphingomyelin cycle, generating the putative-lipid second messenger ceramide.	Ceramides	105-113	nerve growth factor	Mus musculus	0-19
8079174-3	1994	In T9 glioma cells, addition of a cell-permeable ceramide analog mimicked the effects of nerve growth factor on cell growth inhibition and process formation.	Ceramides	49-57	nerve growth factor	Mus musculus	89-108
7806975-5	1994	However, a correspondingly significant decrease in sulfoglycolipid and ceramide concentration was observed in the cpk/cpk kidneys.	Ceramides	71-79	cystin 1	Mus musculus	118-121
8046331-2	1994	In this pathway, TNF-receptor interaction initiates sphingomyelin hydrolysis to ceramide by a sphingomyelinase.	Ceramides	80-88	tumor necrosis factor	Bos taurus	17-20
7954976-2	1994	The product (SR-12GM1) was quantitatively converted to SR-12GM2 by treatment with bovine testes beta-galactosidase and in intact cultured human skin fibroblasts was catabolized to sulforhodamine GM2, GM3 and ceramide; the latter product was further converted to sphingomyelin.	Ceramides	208-216	galactosidase beta 1	Bos taurus	96-114
8053910-1	1994	Human acid sphingomyelinase (ASM) hydrolyses sphingomyelin to ceramide and phosphocholine.	Ceramides	62-70	sphingomyelin phosphodiesterase 1	Homo sapiens	6-27
8053910-1	1994	Human acid sphingomyelinase (ASM) hydrolyses sphingomyelin to ceramide and phosphocholine.	Ceramides	62-70	sphingomyelin phosphodiesterase 1	Homo sapiens	29-32
7533016-1	1994	The L2/HNK-1 carbohydrate epitope has been shown to carry an unusual 3"-sulfoglucuronic acid linked O-glycosidically through a neolactosyl-type backbone to a ceramide residue.	Ceramides	158-166	beta-1,3-glucuronyltransferase 1	Homo sapiens	7-12
8046331-4	1994	The present studies show that ionizing radiation, like TNF, induces rapid sphingomyelin hydrolysis to ceramide and apoptosis in bovine aortic endothelial cells.	Ceramides	102-110	tumor necrosis factor	Bos taurus	55-58
8034585-2	1994	Stimulation of adherent neutrophils with formyl-Met-Leu-Phe (fMLP) resulted in the accumulation of ceramide at a time when H2O2 release is terminated.	Ceramides	99-107	formyl peptide receptor 1	Homo sapiens	41-59
8034680-3	1994	Tumor necrosis factor alpha (TNF alpha) and interleukin-1, besides activating the phospholipase C-mediated breakdown of phosphatidylcholine, also generate ceramide, which is produced by stimulation of sphingomyelin hydrolysis.	Ceramides	155-163	tumor necrosis factor	Homo sapiens	0-27
8034680-3	1994	Tumor necrosis factor alpha (TNF alpha) and interleukin-1, besides activating the phospholipase C-mediated breakdown of phosphatidylcholine, also generate ceramide, which is produced by stimulation of sphingomyelin hydrolysis.	Ceramides	155-163	tumor necrosis factor	Homo sapiens	29-38
8034680-3	1994	Tumor necrosis factor alpha (TNF alpha) and interleukin-1, besides activating the phospholipase C-mediated breakdown of phosphatidylcholine, also generate ceramide, which is produced by stimulation of sphingomyelin hydrolysis.	Ceramides	155-163	interleukin 1 alpha	Homo sapiens	44-57
8034729-1	1994	Extracellular agonists such as tumor necrosis factor-alpha (TNF-alpha) activate the sphingomyelin cycle leading to the generation of ceramide.	Ceramides	133-141	tumor necrosis factor	Homo sapiens	31-58
8034729-1	1994	Extracellular agonists such as tumor necrosis factor-alpha (TNF-alpha) activate the sphingomyelin cycle leading to the generation of ceramide.	Ceramides	133-141	tumor necrosis factor	Homo sapiens	60-69
8034729-2	1994	Ceramide has been suggested as an important mediator of the effect of TNF-alpha on growth inhibition, c-myc down-regulation, apoptosis, and the activation of the nuclear factor kappa B.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	70-79
8034729-2	1994	Ceramide has been suggested as an important mediator of the effect of TNF-alpha on growth inhibition, c-myc down-regulation, apoptosis, and the activation of the nuclear factor kappa B.	Ceramides	0-8	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	102-107
8034729-5	1994	In intact HL-60 cells ceramide induced down-regulation of c-myc RNA levels.	Ceramides	22-30	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	58-63
8034729-8	1994	Therefore, ceramide appeared to inhibit c-myc expression via a mechanism identical with that of TNF-alpha.	Ceramides	11-19	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	40-45
8034729-12	1994	Moreover, okadaic acid inhibited the effects of ceramide and TNF-alpha on c-myc down-regulation.	Ceramides	48-56	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	74-79
8034729-14	1994	These results demonstrate that CAPP is important for ceramide-induced down-regulation of c-myc in myeloid leukemia cells.	Ceramides	53-61	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	89-94
8034585-2	1994	Stimulation of adherent neutrophils with formyl-Met-Leu-Phe (fMLP) resulted in the accumulation of ceramide at a time when H2O2 release is terminated.	Ceramides	99-107	formyl peptide receptor 1	Homo sapiens	61-65
8034585-3	1994	H2O2 release in fMLP-stimulated neutrophils was suppressed in a concentration-dependent manner by the exogenous addition of several free sphingoid amines and short chain ceramides.	Ceramides	170-179	formyl peptide receptor 1	Homo sapiens	16-20
8034585-11	1994	These findings demonstrate that C2 ceramides inhibit H2O2 generation in fMLP-stimulated neutrophils via protein kinase C- or sphingoid base-independent mechanisms.	Ceramides	35-44	formyl peptide receptor 1	Homo sapiens	72-76
7986582-1	1994	Ceramide, an intracellular lipid mediator of tumor necrosis factor alpha (TNF-alpha) action, was studied for its effects on the expression of the proviral human immunodeficiency virus type 1 genome in latently infected myelomonocytic cell lines U-1IIIB and OM-10.1.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	74-77
8027186-7	1994	Since Shiga toxin receptors (Gb3) in butyric acid-treated A431 cells seem to have a ceramide moiety with longer fatty acids than in untreated cells, the possibility exists that fatty acid composition of the receptor is important for sorting to the ER.	Ceramides	84-92	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	29-32
8207213-3	1994	The following experiments both confirm that the addition of ceramide to cells can activate NF-kappa B and demonstrate that a 48-h pretreatment with phorbol 12-myristate (PMA) results in the loss of the ceramide-induced NF-kappa B response.	Ceramides	202-210	nuclear factor kappa B subunit 1	Homo sapiens	91-101
8207213-3	1994	The following experiments both confirm that the addition of ceramide to cells can activate NF-kappa B and demonstrate that a 48-h pretreatment with phorbol 12-myristate (PMA) results in the loss of the ceramide-induced NF-kappa B response.	Ceramides	202-210	nuclear factor kappa B subunit 1	Homo sapiens	219-229
8207213-6	1994	Supplementary data demonstrates that TNF-alpha, ceramide, and PMA activate a human cytomegalovirus-(HCMV) beta gal construct (promoter is responsive to NF-kappa B) that was stably transfected into the TNF receptor-bearing tumor cell line, SW480.	Ceramides	48-56	nuclear factor kappa B subunit 1	Homo sapiens	152-162
8207213-9	1994	This data suggests that although ceramide and 1,2-diacylglycerol (DAG) pathways may contribute to TNF-alpha activation of NF-kappa B, impedance of these pathways does not block TNF-alpha from activating NF-kappa B nor induction of the functional activation of the NF-kappa B responsive reporter construct, HCMV.	Ceramides	33-41	tumor necrosis factor	Homo sapiens	98-107
8207213-9	1994	This data suggests that although ceramide and 1,2-diacylglycerol (DAG) pathways may contribute to TNF-alpha activation of NF-kappa B, impedance of these pathways does not block TNF-alpha from activating NF-kappa B nor induction of the functional activation of the NF-kappa B responsive reporter construct, HCMV.	Ceramides	33-41	nuclear factor kappa B subunit 1	Homo sapiens	122-132
8188652-5	1994	I kappa B-alpha degradation could be directly induced by addition of sphingomyelinase or synthetic ceramide to a cell-free system, indicating a stringent coupling of SMase to the NF-kappa B activation pathway.	Ceramides	99-107	NFKB inhibitor alpha	Homo sapiens	0-15
8188652-5	1994	I kappa B-alpha degradation could be directly induced by addition of sphingomyelinase or synthetic ceramide to a cell-free system, indicating a stringent coupling of SMase to the NF-kappa B activation pathway.	Ceramides	99-107	nuclear factor kappa B subunit 1	Homo sapiens	179-189
8161785-2	1994	Recent investigations have shown that TNF can use a signal transduction pathway in HL-60 cells involving sphingomyelin hydrolysis to ceramide with subsequent stimulation of a ceramide-linked kinase.	Ceramides	133-141	tumor necrosis factor	Homo sapiens	38-41
8161785-5	1994	In addition, anti-TNF antibodies blocked much of the effect of both sphingomyelinase and the synthetic ceramide analog on virus expression, suggesting that, although signaling is initiated through the sphingomyelin pathway, it is sustained by autocrine TNF synthesis.	Ceramides	103-111	tumor necrosis factor	Homo sapiens	18-21
8161785-5	1994	In addition, anti-TNF antibodies blocked much of the effect of both sphingomyelinase and the synthetic ceramide analog on virus expression, suggesting that, although signaling is initiated through the sphingomyelin pathway, it is sustained by autocrine TNF synthesis.	Ceramides	103-111	tumor necrosis factor	Homo sapiens	253-256
8021269-2	1994	TNF-alpha and IL-1 beta are known to initiate signaling through a pathway involving hydrolysis of sphingomyelin to ceramide (Kolesnick, R. N., and Golde, D. W. (1994) Cell 77, 325-328).	Ceramides	115-123	tumor necrosis factor	Homo sapiens	0-9
8021269-2	1994	TNF-alpha and IL-1 beta are known to initiate signaling through a pathway involving hydrolysis of sphingomyelin to ceramide (Kolesnick, R. N., and Golde, D. W. (1994) Cell 77, 325-328).	Ceramides	115-123	interleukin 1 beta	Homo sapiens	14-23
8207213-2	1994	Recent studies demonstrate that the sphingomyelinase-ceramide pathway plays a potential role in the activation of nuclear factor-kappa B (NF-kappa B) by TNF-alpha.	Ceramides	53-61	nuclear factor kappa B subunit 1	Homo sapiens	114-136
8207213-2	1994	Recent studies demonstrate that the sphingomyelinase-ceramide pathway plays a potential role in the activation of nuclear factor-kappa B (NF-kappa B) by TNF-alpha.	Ceramides	53-61	nuclear factor kappa B subunit 1	Homo sapiens	138-148
8207213-2	1994	Recent studies demonstrate that the sphingomyelinase-ceramide pathway plays a potential role in the activation of nuclear factor-kappa B (NF-kappa B) by TNF-alpha.	Ceramides	53-61	tumor necrosis factor	Homo sapiens	153-162
8207213-3	1994	The following experiments both confirm that the addition of ceramide to cells can activate NF-kappa B and demonstrate that a 48-h pretreatment with phorbol 12-myristate (PMA) results in the loss of the ceramide-induced NF-kappa B response.	Ceramides	60-68	nuclear factor kappa B subunit 1	Homo sapiens	91-101
8207213-3	1994	The following experiments both confirm that the addition of ceramide to cells can activate NF-kappa B and demonstrate that a 48-h pretreatment with phorbol 12-myristate (PMA) results in the loss of the ceramide-induced NF-kappa B response.	Ceramides	60-68	nuclear factor kappa B subunit 1	Homo sapiens	219-229
8199203-2	1994	An inverse relationship between the cellular concentrations of ceramide and the proliferative capacity of human T-lymphocytes was observed for cells treated with either interleukin-2 or phorbol ester plus ionomycin.	Ceramides	63-71	interleukin 2	Homo sapiens	169-182
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.	Ceramides	22-30	glucosidase, beta, acid	Mus musculus	34-57
7986582-4	1994	These observations suggest that the TNF-ceramide signaling system may be involved in the regulation of HIV expression in certain myeloid cell types.	Ceramides	40-48	tumor necrosis factor	Homo sapiens	36-39
8141790-6	1994	As it has been reported that ceramide might act as a second messenger to mediate many of the effects of TNF alpha, the effects of exogenous sphingomyelinase and the cell-permeable ceramide analogue, C2- ceramide, on production of superoxide anions, induction of priming in response to formylmethionyl-leucyl-phenylalanine, and cell-shape change were examined.	Ceramides	29-37	tumor necrosis factor	Homo sapiens	104-113
8132572-1	1994	The participation of cell ceramide in tumor necrosis factor (TNF)-alpha-stimulated NF-kappa B activation in Jurkat T cells and HL-60 cells was studied.	Ceramides	26-34	tumor necrosis factor	Homo sapiens	38-71
8132572-1	1994	The participation of cell ceramide in tumor necrosis factor (TNF)-alpha-stimulated NF-kappa B activation in Jurkat T cells and HL-60 cells was studied.	Ceramides	26-34	nuclear factor kappa B subunit 1	Homo sapiens	83-93
8081245-1	1994	We have investigated the effects of an inhibitor of ceramide biosynthesis on the glycosylphosphatidylinositol (GPI)-anchoring and intracellular transport of the yeast Gas1 protein.	Ceramides	52-60	1,3-beta-glucanosyltransferase GAS1	Saccharomyces cerevisiae S288C	167-171
8254018-0	1993	Release of ceramide after membrane sphingomyelin hydrolysis decreases the basolateral secretion of triacylglycerol and apolipoprotein B in cultured human intestinal cells.	Ceramides	11-19	apolipoprotein B	Homo sapiens	119-135
8307965-1	1994	Treatment of HL-60 cells with a 1 alpha,25-dihydroxyvitamin D3 induces activation of a neutral sphingomyelinase (SMase), resulting in a decrease in sphingomyelin (SM) levels and an increase in ceramide levels in a proposed "sphingomyelin cycle" of cell regulation (Okazaki, T., Bell, R., and Hannun, Y.	Ceramides	193-201	sphingomyelin phosphodiesterase 2	Homo sapiens	87-111
8169783-1	1994	Transferrin was incorporated into the external surface of liposomes that were previously derivatized with ceramides.	Ceramides	106-115	transferrin	Homo sapiens	0-11
8086039-4	1994	Three lines of evidence, rapid kinetics of activation of the sphingomyelin pathway by tumor necrosis factor (TNF) alpha, the ability of cell-permeable ceramide analogs to bypass receptor activation and mimic the effect of TNF alpha, and reconstitution of this cascade in a cell-free system, support the concept that the sphingomyelin pathway serves to signal TNF alpha-induced monocytic differentiation.	Ceramides	151-159	tumor necrosis factor	Homo sapiens	222-231
8086040-5	1994	GD3, a dominant ganglioside on malignant melanoma, was modified by ozone cleavage of the double bond in the ceramide backbone, an aldehyde group introduced and used for coupling via reductive amination to epsilon-amino-lysyl groups of proteins.	Ceramides	108-116	GRDX	Homo sapiens	0-3
8261439-6	1994	The optimal procedure involved ozone cleavage of the double bond of GD3 in the ceramide backbone, introducing an aldehyde group, and coupling to aminolysyl groups of proteins by reductive amination.	Ceramides	79-87	GRDX	Homo sapiens	68-71
8278410-1	1994	The potential involvement of ceramide-related signaling processes in the induction of apoptosis by tumor necrosis factor alpha was assessed by multiple biochemical strategies in the human leukemic cell lines HL-60 and U937 and the murine fibrosarcoma cell lines L929/LM and WEHI 164/13.	Ceramides	29-37	tumor necrosis factor	Homo sapiens	99-126
8278410-2	1994	Exposure of these cells to tumor necrosis factor alpha resulted in internucleosomal cleavage of genomic DNA, yielding laddered patterns of oligonucleosomal fragments characteristic of apoptosis when resolved by agarose gel electrophoresis; similar responses were observed after exposure to exogenous sphingomyelinase or synthetic ceramides.	Ceramides	330-339	tumor necrosis factor	Homo sapiens	27-54
8278410-6	1994	Phospholipase A2 and arachidonic acid failed to promote DNA fragmentation, as did phospholipase D. Characterization of DNA strand breaks by alkaline and neutral elution analyses confirmed that ceramide action was restricted to breakage of mature, double-stranded DNA but not of nascent DNA.	Ceramides	193-201	phospholipase A2 group IB	Homo sapiens	0-16
8408075-7	1993	We now demonstrate that the addition of both Cer-1-phosphate (Cer-1-P) and a short-acyl chain analog of Cer-1-P,N-hexanoylsphingosine-1-phosphate (C6-Cer-1-P) to cultured cells and a variety of subcellular fractions results in rapid degradation to Cer and C6-Cer, respectively.	Ceramides	45-48	cerberus 1, DAN family BMP antagonist	Rattus norvegicus	62-67
8349660-0	1993	Tumor necrosis factor-alpha (TNF-alpha) signal transduction through ceramide.	Ceramides	68-76	tumor necrosis factor	Homo sapiens	0-27
8376408-4	1993	As shown previously, TNF (1 nM) induced a marked increase in nuclear NF-kappa B binding in human leukemia (HL-60) cells within 5 min, and elevated binding was detected for as long as 1 h. Addition of a maximally effective concentration of sphingomyelinase, 0.1 units.ml-1, induced a 50% reduction in sphingomyelin content by 5 min from a basal level of 560 pmol.10(6) cells-1 and a quantitative increase in ceramide levels from 89 pmol.10(6) cells-1.	Ceramides	407-415	tumor necrosis factor	Homo sapiens	21-24
8376408-6	1993	A cell-permeable ceramide analog, C8-ceramide, which mimics biologic effects of TNF-alpha, also enhanced nuclear NF-kappa B activation within minutes.	Ceramides	17-25	tumor necrosis factor	Homo sapiens	80-89
8376408-6	1993	A cell-permeable ceramide analog, C8-ceramide, which mimics biologic effects of TNF-alpha, also enhanced nuclear NF-kappa B activation within minutes.	Ceramides	17-25	nuclear factor kappa B subunit 1	Homo sapiens	113-123
8376408-8	1993	Further, TNF-alpha induced elevation in ceramide content by 2 min to 185% of control but did not affect DG levels.	Ceramides	40-48	tumor necrosis factor	Homo sapiens	9-18
8376361-2	1993	Signal transduction for tumor necrosis factor-alpha and interleukin-1 involves sphingomyelin hydrolysis to ceramide and stimulation of a ceramide-activated serine/threonine protein kinase (Mathias, S., Younes, A., Kan, C., Orlow, I., Joseph, C., and Kolesnick, R. (1993) Science 259, 519-522).	Ceramides	107-115	interleukin 1 alpha	Homo sapiens	56-69
8349660-0	1993	Tumor necrosis factor-alpha (TNF-alpha) signal transduction through ceramide.	Ceramides	68-76	tumor necrosis factor	Homo sapiens	29-38
8349660-4	1993	In this study, we investigated the role of ceramide as an intracellular mediator of TNF-alpha action.	Ceramides	43-51	tumor necrosis factor	Homo sapiens	84-93
8349660-9	1993	Thus, ceramide functions as a selective mediator of the cytostatic/cytotoxic effects of TNF-alpha and plays a positive feedback role in activation of NF-kappa B.	Ceramides	6-14	tumor necrosis factor	Homo sapiens	88-97
8349660-9	1993	Thus, ceramide functions as a selective mediator of the cytostatic/cytotoxic effects of TNF-alpha and plays a positive feedback role in activation of NF-kappa B.	Ceramides	6-14	nuclear factor kappa B subunit 1	Homo sapiens	150-160
8405660-4	1993	Synaptic plasma membrane vesicles (SPMV) from rat brain synthesized ceramide-phosphoethanolamine (SpE), an analogue of sphingomyelin (SpC) from phosphatidylethanolamine (PE) and ceramide.	Ceramides	68-76	surfactant protein C	Rattus norvegicus	134-137
8456305-1	1993	Sphingomyelin hydrolysis and ceramide generation have been implicated in a signal transduction pathway that mediates the effects of tumor necrosis factor-alpha (TNF-alpha) and other agents on cell growth and differentiation.	Ceramides	29-37	tumor necrosis factor	Homo sapiens	132-159
7686898-2	1993	In some circumstances, TNF may use a signal transduction pathway involving hydrolysis of sphingomyelin to ceramide and stimulation of a ceramide-activated protein kinase.	Ceramides	106-114	tumor necrosis factor	Homo sapiens	23-26
7686898-9	1993	The cell-permeable ceramide analogs, C2- and C6-ceramide, which mimic effects of TNF, also induced p42mapk phosphorylation within seconds.	Ceramides	19-27	tumor necrosis factor	Homo sapiens	81-84
7686898-9	1993	The cell-permeable ceramide analogs, C2- and C6-ceramide, which mimic effects of TNF, also induced p42mapk phosphorylation within seconds.	Ceramides	19-27	cyclin dependent kinase 20	Homo sapiens	99-102
7686898-9	1993	The cell-permeable ceramide analogs, C2- and C6-ceramide, which mimic effects of TNF, also induced p42mapk phosphorylation within seconds.	Ceramides	48-56	tumor necrosis factor	Homo sapiens	81-84
7686898-9	1993	The cell-permeable ceramide analogs, C2- and C6-ceramide, which mimic effects of TNF, also induced p42mapk phosphorylation within seconds.	Ceramides	48-56	cyclin dependent kinase 20	Homo sapiens	99-102
8456305-1	1993	Sphingomyelin hydrolysis and ceramide generation have been implicated in a signal transduction pathway that mediates the effects of tumor necrosis factor-alpha (TNF-alpha) and other agents on cell growth and differentiation.	Ceramides	29-37	tumor necrosis factor	Homo sapiens	161-170
8424175-2	1993	Tumor necrosis factor-alpha uses a signal transduction pathway that involves sphingomyelin hydrolysis to ceramide and stimulation of a ceramide-activated protein kinase.	Ceramides	105-113	tumor necrosis factor	Mus musculus	0-27
8424175-3	1993	In intact EL4 thymoma cells, IL-1 beta similarly stimulated a rapid decrease of sphingomyelin and an elevation of ceramide, and enhanced ceramide-activated protein kinase activity.	Ceramides	114-122	interleukin 1 beta	Mus musculus	29-38
1325455-4	1992	It is demonstrated that the TNF signaling cascade, i.e. stimulation of protein kinase C, sphingomyelinase, and phospholipase A2, production of the second messengers diacylglycerol and ceramide, can occur completely through exclusive binding of TNF to TR55.	Ceramides	184-192	tumor necrosis factor	Homo sapiens	28-31
1444464-11	1992	From these data, we conclude that SP-A binds to galactosylceramide and asialo-GM2, and that both saccharide and ceramide moieties in the glycolipid molecule are important for the binding of SP-A to glycolipids.	Ceramides	58-66	surfactant protein A1	Rattus norvegicus	34-38
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.	Ceramides	186-194	surfactant protein D	Rattus norvegicus	52-56
8379453-9	1993	Ceramide released as a consequence of N-SMase reaction would then carry out various biological phenomena, such as cell proliferation and differentiation.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	38-45
8379453-15	1993	We can safely conclude that N-SMase action may be required to carry out a myriad of important cellular functions either directly or by cholesterol mobilization, or generation of ceramide, ceramide-1-phosphate, and sphingoid bases.	Ceramides	178-186	sphingomyelin phosphodiesterase 2	Homo sapiens	28-35
1330325-2	1992	Central to this TNF signaling route is the second messenger-like molecule ceramide, which is generated by sphingomyelin (SM) breakdown catalyzed by a sphingomyelinase (SMase).	Ceramides	74-82	tumor necrosis factor	Homo sapiens	16-19
1330325-6	1992	A model is proposed in which a TNF-responsive PC-PLC via DAG couples to an acidic SMase, resulting in the generation of ceramide, which eventually triggers rapid induction of nuclear NF-kappa B activity.	Ceramides	120-128	tumor necrosis factor	Homo sapiens	31-34
1330325-6	1992	A model is proposed in which a TNF-responsive PC-PLC via DAG couples to an acidic SMase, resulting in the generation of ceramide, which eventually triggers rapid induction of nuclear NF-kappa B activity.	Ceramides	120-128	heparan sulfate proteoglycan 2	Homo sapiens	49-52
1330325-6	1992	A model is proposed in which a TNF-responsive PC-PLC via DAG couples to an acidic SMase, resulting in the generation of ceramide, which eventually triggers rapid induction of nuclear NF-kappa B activity.	Ceramides	120-128	nuclear factor kappa B subunit 1	Homo sapiens	183-193
1400321-4	1992	Because sphingosine and ceramide are interconvertable, we extended previous studies by treating cells with C2-ceramide (C2-cer), a membrane-soluble analogue of ceramide, and found that C2-cer stimulates IL-1-mediated PGE2 production to the same degree as sphingosine.	Ceramides	110-118	interleukin 1 beta	Homo sapiens	203-207
1400321-9	1992	IL-1 treatment induced the hydrolysis of a significant fraction of prelabeled sphingomyelin which was accompanied by increased levels of intracellular ceramide.	Ceramides	151-159	interleukin 1 beta	Homo sapiens	0-4
1325455-4	1992	It is demonstrated that the TNF signaling cascade, i.e. stimulation of protein kinase C, sphingomyelinase, and phospholipase A2, production of the second messengers diacylglycerol and ceramide, can occur completely through exclusive binding of TNF to TR55.	Ceramides	184-192	phospholipase A2 group IB	Homo sapiens	111-127
1325455-4	1992	It is demonstrated that the TNF signaling cascade, i.e. stimulation of protein kinase C, sphingomyelinase, and phospholipase A2, production of the second messengers diacylglycerol and ceramide, can occur completely through exclusive binding of TNF to TR55.	Ceramides	184-192	tumor necrosis factor	Homo sapiens	244-247
1740330-1	1992	Acid sphingomyelinase (ASM; HGMW-approved symbol, SMPD1) is the lysosomal phosphodiesterase that hydrolyzes sphingomyelin to ceramide and phosphocholine.	Ceramides	125-133	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
1637497-1	1992	A comparison of the two major ceramide molecular species (d18:1-C18:0 and d20:1-C18:0) of synaptosomal gangliosides GM1, GD1a+GT1a, GD1b, GT1b, revealed a difference between the ceramide composition of ethanol-sensitive LS and ethanol-insensitive SS whole brain synaptosomal gangliosides.	Ceramides	30-38	coenzyme Q10A	Mus musculus	116-119
1313189-2	1992	TNF-alpha signaling may involve sphingomyelin hydrolysis to ceramide by a sphingomyelinase and stimulation of a ceramide-activated protein kinase.	Ceramides	60-68	tumor necrosis factor	Homo sapiens	0-9
1313189-3	1992	In a cell-free system, TNF-alpha induced a rapid reduction in membrane sphingomyelin content and a quantitative elevation in ceramide concentrations.	Ceramides	125-133	tumor necrosis factor	Homo sapiens	23-32
1565290-1	1992	1-Alpha, 25-dihydroxyvitamin D3, tumor necrosis factor alpha, and gamma-interferon induce sphingomyelin turnover to ceramide in HL-60 cells.	Ceramides	116-124	tumor necrosis factor	Homo sapiens	33-60
1431599-10	1992	In summary, mammalian epidermis contains an usually high percentage (approximately 75%) of beta-glucocerebrosidase activity, and the concentration of activity in the more differentiated cell layers may account for the replacement of glucosylceramide by ceramides in the outer epidermis.	Ceramides	253-262	glucosylceramidase beta	Homo sapiens	91-114
1577827-9	1992	Selected components among the neutral glycolipids are bound by radiolabeled human SP-A; these are identified by TLC-LSIMS as predominantly ceramide mono- and disaccharides (human surfactant) and ceramide tri- and tetrasaccharides (rat surfactant and type II cells).	Ceramides	139-147	surfactant protein A1	Homo sapiens	82-86
1577827-9	1992	Selected components among the neutral glycolipids are bound by radiolabeled human SP-A; these are identified by TLC-LSIMS as predominantly ceramide mono- and disaccharides (human surfactant) and ceramide tri- and tetrasaccharides (rat surfactant and type II cells).	Ceramides	195-203	surfactant protein A1	Homo sapiens	82-86
1312955-0	1992	Influence of phospholipid environment on the phosphatidylethanolamine: ceramide-phosphorylethanolamine transferase activity in rat liver plasma membranes.	Ceramides	71-79	phosphate cytidylyltransferase 2, ethanolamine	Rattus norvegicus	80-114
1378088-0	1992	Reactivity of two anti-galactosyl ceramide antibodies towards myelin basic protein.	Ceramides	34-42	myelin basic protein	Mus musculus	62-82
1740330-1	1992	Acid sphingomyelinase (ASM; HGMW-approved symbol, SMPD1) is the lysosomal phosphodiesterase that hydrolyzes sphingomyelin to ceramide and phosphocholine.	Ceramides	125-133	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
1740330-1	1992	Acid sphingomyelinase (ASM; HGMW-approved symbol, SMPD1) is the lysosomal phosphodiesterase that hydrolyzes sphingomyelin to ceramide and phosphocholine.	Ceramides	125-133	sphingomyelin phosphodiesterase 1	Homo sapiens	50-55
1946418-3	1991	Ceramide may have second-messenger function because it induces epidermal growth factor receptor phosphorylation, presumably on Thr-669 in A-431 cells.	Ceramides	0-8	epidermal growth factor receptor	Homo sapiens	63-95
1946418-12	1991	Because tumor necrosis factor (TNF) alpha rapidly induces sphingomyelin hydrolysis to ceramide during monocytic differentiation of HL-60 cells, its effects on kinase activity were assessed.	Ceramides	86-94	tumor necrosis factor	Homo sapiens	8-41
1824846-8	1991	Together with studies on the enzymic degradation of GM2 derivatives with modifications in the ceramide portion, these results indicate that mainly steric hindrance by adjacent lipid molecules impedes the access of Hex A to membrane-bound GM2 (whose degradation therefore depends on solubilization by the GM2 activator) and in addition that the interaction between the GM2.	Ceramides	94-102	hexosaminidase subunit alpha	Homo sapiens	214-219
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.	Ceramides	22-30	beta-1,3-galactosyltransferase 4	Homo sapiens	123-129
1874747-0	1991	Ceramide stimulates epidermal growth factor receptor phosphorylation in A431 human epidermoid carcinoma cells.	Ceramides	0-8	epidermal growth factor receptor	Homo sapiens	20-52
2004772-1	1991	Human acid sphingomyelinase (SMPD1) is the lysosomal phosphodiesterase that cleaves sphingomyelin to ceramide and phosphocholine.	Ceramides	101-109	sphingomyelin phosphodiesterase 1	Homo sapiens	6-27
2004772-1	1991	Human acid sphingomyelinase (SMPD1) is the lysosomal phosphodiesterase that cleaves sphingomyelin to ceramide and phosphocholine.	Ceramides	101-109	sphingomyelin phosphodiesterase 1	Homo sapiens	29-34
1845977-10	1991	Cell-permeable ceramide also caused prompt down-regulation of mRNA for the c-myc protooncogene.	Ceramides	15-23	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	75-80
1845977-11	1991	The time course of c-myc down-regulation was consistent with the action of ceramide as the mediator of TNF alpha action.	Ceramides	75-83	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	19-24
1845977-11	1991	The time course of c-myc down-regulation was consistent with the action of ceramide as the mediator of TNF alpha action.	Ceramides	75-83	tumor necrosis factor	Homo sapiens	103-112
2177172-1	1990	Synaptic plasma membrane vesicles (SPMV) from brains of normal and Trembler mice synthesized ceramide-phosphoethanolamine, and analogue of sphingomyelin from phosphatidylethanolamine (PE) and ceramide.	Ceramides	93-101	peripheral myelin protein 22	Mus musculus	67-75
33806766-3	2021	One of the ways melanoma alters sphingolipid rheostat is via over-expression of lysosomal acid ceramidase (AC), which catalyses the hydrolysis of pro-apoptotic long-chain ceramides into sphingosine and fatty acid.	Ceramides	171-180	N-acylsphingosine amidohydrolase 1	Homo sapiens	90-105
33766731-12	2021	We found that ASAH1 inhibition increased peroxisome biogenesis through ceramide-mediated PPARgamma activation.	Ceramides	71-79	N-acylsphingosine amidohydrolase 1	Mus musculus	14-19
33766731-12	2021	We found that ASAH1 inhibition increased peroxisome biogenesis through ceramide-mediated PPARgamma activation.	Ceramides	71-79	peroxisome proliferator activated receptor gamma	Mus musculus	89-98
33766731-13	2021	ASAH1 loss increased ceramide and peroxisome-derived ROS, which in turn inhibited melanoma growth.	Ceramides	21-29	N-acylsphingosine amidohydrolase 1	Mus musculus	0-5
33821992-6	2021	We demonstrated that restoration of ELOVL6 levels in BTZ-resistant MM cells resensitized them to BTZ largely via upregulation of ELOVL6-dependent ceramide species, which was a prerequisite for BTZ-induced ER stress and cell death in these cells.	Ceramides	146-154	ELOVL family member 6, elongation of long chain fatty acids (yeast)	Mus musculus	36-42
33821992-6	2021	We demonstrated that restoration of ELOVL6 levels in BTZ-resistant MM cells resensitized them to BTZ largely via upregulation of ELOVL6-dependent ceramide species, which was a prerequisite for BTZ-induced ER stress and cell death in these cells.	Ceramides	146-154	ELOVL family member 6, elongation of long chain fatty acids (yeast)	Mus musculus	129-135
33821992-7	2021	Our data characterize ELOVL6 as a major clinically relevant regulator of MM cell resistance to BTZ, which can emerge from the impaired ability of these cells to alter ceramide composition in response to BTZ.	Ceramides	167-175	ELOVL family member 6, elongation of long chain fatty acids (yeast)	Mus musculus	22-28
2391709-3	1990	We have developed a rapid method to detect Shiga toxin and SLT-I (Verotoxin 1) based on their binding to globotriosyl ceramide (Gb3).	Ceramides	118-126	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	128-131
33939982-6	2021	While ORMDL3-KO modestly increased dihydroceramide and ceramide levels, ORMDL-TKO cells had dramatic increases in the accumulation of these sphingolipid precursors.	Ceramides	42-50	ORMDL sphingolipid biosynthesis regulator 3	Homo sapiens	6-12
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.	Ceramides	115-123	ORMDL sphingolipid biosynthesis regulator 1	Homo sapiens	21-31
33806766-3	2021	One of the ways melanoma alters sphingolipid rheostat is via over-expression of lysosomal acid ceramidase (AC), which catalyses the hydrolysis of pro-apoptotic long-chain ceramides into sphingosine and fatty acid.	Ceramides	171-180	N-acylsphingosine amidohydrolase 1	Homo sapiens	107-109
32466342-5	2020	CTL1-mediated choline uptake is associated with cell viability, and the functional inhibition of CTL1 by Amb4269951 may promote apoptotic cell death via ceramide-induced suppression of the expression of survivin, an apoptotic inhibitory factor.	Ceramides	153-161	solute carrier family 44 member 1	Homo sapiens	0-4
33815291-4	2021	A significant number of studies have described the involvement of ceramides and other sphingolipids in the inhibition of insulin-signaling pathway in both skeletal muscles and the liver.	Ceramides	66-75	insulin	Homo sapiens	121-128
33800208-3	2021	The role of CerS2, which mainly synthesizes C22-C24 ceramides, was investigated in immune responses elicited by airway inflammation using CerS2 null mice.	Ceramides	52-61	ceramide synthase 2	Mus musculus	12-17
33814423-0	2021	Cerebrospinal Fluid C18 Ceramide Associates with Markers of Alzheimer"s Disease and Inflammation at the Pre- and Early Stages of Dementia.	Ceramides	24-32	Bardet-Biedl syndrome 9	Homo sapiens	20-23
33814423-10	2021	CONCLUSION: Higher levels of C18 ceramide associated with increased AD pathology and inflammation, suggesting its potential value as a therapeutic target.	Ceramides	33-41	Bardet-Biedl syndrome 9	Homo sapiens	29-32
33233706-5	2020	The activities of SM deacylase and acid ceramidase (aCDase) were measured using SM and ceramide as substrates by tandem mass spectrometry by monitoring the production of SPC and sphingosine, respectively.	Ceramides	87-95	N-acylsphingosine amidohydrolase 1	Homo sapiens	35-50
33233706-5	2020	The activities of SM deacylase and acid ceramidase (aCDase) were measured using SM and ceramide as substrates by tandem mass spectrometry by monitoring the production of SPC and sphingosine, respectively.	Ceramides	87-95	N-acylsphingosine amidohydrolase 1	Rattus norvegicus	52-58
33233706-11	2020	These results provide new insights into the essential role of SM deacylase expressed as an aCDase-degrading beta-subunit that evokes the ceramide deficiency in AD skin.	Ceramides	137-145	N-acylsphingosine amidohydrolase 1	Homo sapiens	91-97
32466342-5	2020	CTL1-mediated choline uptake is associated with cell viability, and the functional inhibition of CTL1 by Amb4269951 may promote apoptotic cell death via ceramide-induced suppression of the expression of survivin, an apoptotic inhibitory factor.	Ceramides	153-161	solute carrier family 44 member 1	Homo sapiens	97-101
12538495-0	2003	Possible role of ceramide as an indicator of chemoresistance: decrease of the ceramide content via activation of glucosylceramide synthase and sphingomyelin synthase in chemoresistant leukemia.	Ceramides	17-25	UDP-glucose ceramide glucosyltransferase	Homo sapiens	113-138
33033923-11	2020	Five glycosylated ceramides were increased in insulin autoantibody (IAA) positive adolescent subjects compared to adolescent subjects without this autoantibody.	Ceramides	18-27	insulin	Homo sapiens	46-53
19074599-2	2009	In most GPI anchors this modified diacylglycerol-based anchor is subsequently transformed into a ceramide-containing anchor, a reaction which requires Cwh43.	Ceramides	97-105	Cwh43p	Saccharomyces cerevisiae S288C	151-156
12538495-9	2003	Therefore, it is suggested that a decrease of the ceramide level via activation of GCS and SMS is associated with the chemoresistant condition in leukemia, probably in relation to Bcl-2 but not to MDR-1 expression.	Ceramides	50-58	UDP-glucose ceramide glucosyltransferase	Homo sapiens	83-86
12538495-9	2003	Therefore, it is suggested that a decrease of the ceramide level via activation of GCS and SMS is associated with the chemoresistant condition in leukemia, probably in relation to Bcl-2 but not to MDR-1 expression.	Ceramides	50-58	BCL2 apoptosis regulator	Homo sapiens	180-185
24777581-8	2014	On the other hand, the loss of HL, EL, or both raised the plasma concentrations for select molecular species of phosphatidylcholine, cholesteryl ester, diacylglycerol, sphingomyelin, ceramide, plasmanylcholine, and plasmenylcholine.	Ceramides	183-191	lipase, hepatic	Mus musculus	31-33
12538495-4	2003	A lower level of ceramide with higher activities of glucosylceramide synthase (GCS) and sphingomyelin synthase (SMS) was detected in HL-60/ADR cells than in HL-60 cells.	Ceramides	17-25	UDP-glucose ceramide glucosyltransferase	Homo sapiens	52-77
12538495-4	2003	A lower level of ceramide with higher activities of glucosylceramide synthase (GCS) and sphingomyelin synthase (SMS) was detected in HL-60/ADR cells than in HL-60 cells.	Ceramides	17-25	UDP-glucose ceramide glucosyltransferase	Homo sapiens	79-82
12538495-5	2003	In contrast, HL-60/GCS cells, overexpressing GCS, significantly inhibited DOX-induced ceramide increase and apoptosis.	Ceramides	86-94	UDP-glucose ceramide glucosyltransferase	Homo sapiens	19-22
12538495-5	2003	In contrast, HL-60/GCS cells, overexpressing GCS, significantly inhibited DOX-induced ceramide increase and apoptosis.	Ceramides	86-94	UDP-glucose ceramide glucosyltransferase	Homo sapiens	45-48
12538495-7	2003	In vivo, the level of ceramide was lower in chemoresistant leukemia patients (6.4 +/- 1.8 pmol/nmol phosphate; n = 14) than in chemosensitive patients (9.5 +/- 2.7 pmol/nmol phosphate; n = 9), and the activities of GCS and SMS were more than 2-fold higher in chemoresistant leukemia cells than in chemosensitive cells.	Ceramides	22-30	UDP-glucose ceramide glucosyltransferase	Homo sapiens	215-218
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	18-24
34962430-8	2022	Ceramides prevented insulin-induced phosphorylation of PKB and NDRG1, but not of Nedd4-2.	Ceramides	0-9	insulin	Homo sapiens	20-27
34962430-8	2022	Ceramides prevented insulin-induced phosphorylation of PKB and NDRG1, but not of Nedd4-2.	Ceramides	0-9	protein tyrosine kinase 2 beta	Homo sapiens	55-58
34962430-8	2022	Ceramides prevented insulin-induced phosphorylation of PKB and NDRG1, but not of Nedd4-2.	Ceramides	0-9	N-myc downstream regulated 1	Homo sapiens	63-68
34962430-9	2022	The ceramide metabolite sphingosine 1-phosphate induced phosphorylation of Nedd4-2.	Ceramides	4-12	NEDD4 like E3 ubiquitin protein ligase	Homo sapiens	75-82
34962430-11	2022	Sphingosine 1-phosphate might protect Nedd4-2 against ceramide-induced insulin resistance.	Ceramides	54-62	NEDD4 like E3 ubiquitin protein ligase	Homo sapiens	38-45
34962430-11	2022	Sphingosine 1-phosphate might protect Nedd4-2 against ceramide-induced insulin resistance.	Ceramides	54-62	insulin	Homo sapiens	71-78
34492164-4	2022	Using this strain, we investigated the effect of a decrease in ceramide synthesis on TOR complex 2 (TORC2)-Ypk1 signaling, which senses the complex sphingolipid level at the plasma membrane and promotes sphingolipid biosynthesis.	Ceramides	63-71	serine/threonine protein kinase YPK1	Saccharomyces cerevisiae S288C	107-111
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	26-34	NLR family pyrin domain containing 3	Homo sapiens	121-126
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	26-34	NLR family pyrin domain containing 3	Homo sapiens	148-153
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	36-39	sphingomyelin phosphodiesterase 1	Homo sapiens	18-24
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	36-39	NLR family pyrin domain containing 3	Homo sapiens	92-119
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	36-39	NLR family pyrin domain containing 3	Homo sapiens	121-126
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	36-39	NLR family pyrin domain containing 3	Homo sapiens	148-153
9520418-2	1998	Ceramide, its primary catabolic intermediate, is released by either acid sphingomyelinase or neutral sphingomyelinase (nSMase) and has emerged as a potential lipid signaling molecule.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	119-125
9520418-6	1998	Their stimulation by tumor necrosis factor alpha leads only to a moderately elevated ceramide concentration.	Ceramides	85-93	tumor necrosis factor	Homo sapiens	21-48
9520418-9	1998	The cloned nSMase will facilitate further controlled experiments aiming at the definition of a possible role of ceramide as signal transduction molecule.	Ceramides	112-120	sphingomyelin phosphodiesterase 2	Homo sapiens	11-17
34813948-5	2022	In Acsl1-/- mice, epidermal ceramide (EOS) (Cer(EOS)) containing omega-O-esterified linoleic acid, a lipid essential for the skin barrier, was significantly reduced.	Ceramides	28-36	acyl-CoA synthetase long-chain family member 1	Mus musculus	3-8
34974112-1	2022	beta-galactosylceramidase (GALC) is a lysosomal enzyme that removes beta-galactose from beta-galactosylceramide, leading to the formation of the oncosuppressor metabolite ceramide.	Ceramides	171-179	galactosylceramidase	Homo sapiens	27-31
34969174-3	2022	The metabolite of ASMase, ceramide (Cer), activates the inflammatory response by activating Nod-like receptor protein 3 (NLRP3) in macrophages, and NLRP3 is also involved in the EMT process.	Ceramides	26-34	NLR family pyrin domain containing 3	Homo sapiens	92-119
34951654-0	2021	Activation of neutral sphingomyelinase 2 through hyperglycemia contributes to endothelial apoptosis via vesicle-bound intercellular transfer of ceramides.	Ceramides	144-153	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	14-40
34951654-6	2021	The increased packaging of ceramide into lEVs after hyperglycemic injury was shown to be dependent on neutral sphingomyelinase 2 (nSMase2), which was upregulated in glucose-treated HCAECs.	Ceramides	27-35	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	102-128
34951654-6	2021	The increased packaging of ceramide into lEVs after hyperglycemic injury was shown to be dependent on neutral sphingomyelinase 2 (nSMase2), which was upregulated in glucose-treated HCAECs.	Ceramides	27-35	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	130-137
34954721-4	2022	Ceramides, such as sphingolipids are also produced intracellularly and have signalling actions in regulating cell metabolism including effects on inflammation, and potentially have a mechanistic role in the development of insulin resistance.	Ceramides	0-9	insulin	Homo sapiens	222-229
34951654-9	2021	To generate lEVs with high levels of C16 ceramide, ceramide was applied exogenously and shown to be effectively packaged into the lEVs, which then induced apoptosis in lEV-recipient HCAECs via activation of caspase 3.	Ceramides	51-59	caspase 3	Mus musculus	207-216
34954108-0	2022	Ablation of ORMDL3 impairs adipose tissue thermogenesis and insulin sensitivity by increasing ceramide generation.	Ceramides	94-102	ORM1-like 3 (S. cerevisiae)	Mus musculus	12-18
34958030-7	2022	The cellular and medium contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 and increased in the cells overexpressing apoE4.	Ceramides	36-45	apolipoprotein E	Homo sapiens	97-102
34958030-7	2022	The cellular and medium contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 and increased in the cells overexpressing apoE4.	Ceramides	36-45	apolipoprotein E	Homo sapiens	105-110
34958030-7	2022	The cellular and medium contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 and increased in the cells overexpressing apoE4.	Ceramides	36-45	apolipoprotein E	Homo sapiens	153-158
34958030-9	2022	The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4.	Ceramides	25-34	apolipoprotein E	Homo sapiens	86-91
34958030-9	2022	The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4.	Ceramides	25-34	apolipoprotein E	Homo sapiens	94-99
34958030-9	2022	The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4.	Ceramides	25-34	apolipoprotein E	Homo sapiens	102-107
34958030-9	2022	The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4.	Ceramides	25-34	apolipoprotein E	Homo sapiens	179-184
34958030-9	2022	The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4.	Ceramides	25-34	apolipoprotein E	Homo sapiens	187-192
34958030-9	2022	The cellular contents of ceramides decreased in the order of the cells overexpressing apoE3 > apoE2 = apoE4 and those in medium decreased in the order of the cells overexpressing apoE3 > apoE2, while increased in the cells overexpressing apoE4.	Ceramides	25-34	apolipoprotein E	Homo sapiens	238-243
34958030-10	2022	CONCLUSION: The modulation of apoM and S1P might partly explain the protective effects of apoE2 against Alzheimer"s disease, and the modulation of ceramides might be one of the mechanisms explaining the association of apoE4 with the development of Alzheimer"s disease.	Ceramides	147-156	apolipoprotein E	Homo sapiens	218-223
34954108-11	2022	Importantly, ceramide levels were elevated in the adipose tissue of Ormdl3-/- mice.	Ceramides	13-21	ORM1-like 3 (S. cerevisiae)	Mus musculus	68-74
34954108-12	2022	In addition, the reduction in thermogenesis and increase in bodyweight caused by Ormdl3 deficiency could be rescued by inhibiting the production of ceramides.	Ceramides	148-157	ORM1-like 3 (S. cerevisiae)	Mus musculus	81-87
34931016-10	2021	In conclusion, sortilin knockdown in the prefrontal cortex and hippocampus plays an important role in ameliorating depressive-like behavior induced by CUMS, which is mainly evidenced by decreasing the trafficking of ASM from the trans-Golgi network to the lysosome and reducing the ceramide levels.	Ceramides	282-290	sortilin 1	Mus musculus	15-23
34931016-0	2021	Sortilin deletion in the prefrontal cortex and hippocampus ameliorates depressive-like behaviors in mice via regulating ASM/ceramide signaling.	Ceramides	124-132	sortilin 1	Mus musculus	0-8
34931016-8	2021	We revealed that sortilin facilitated acid sphingomyelinase (ASM)/ceramide signaling, which activated RhoA/ROCK2 signaling, ultimately causing the transformation of dendritic spine dynamics.	Ceramides	66-74	sortilin 1	Mus musculus	17-25
34931016-8	2021	We revealed that sortilin facilitated acid sphingomyelinase (ASM)/ceramide signaling, which activated RhoA/ROCK2 signaling, ultimately causing the transformation of dendritic spine dynamics.	Ceramides	66-74	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	38-59
34914638-4	2022	It was first found by us that miR-148a deficiency dramatically increased mouse gut dysbiosis through upregulating Cers5 expression, which promoted ceramide synthesis afterward.	Ceramides	147-155	microRNA 148a	Mus musculus	30-38
34931016-8	2021	We revealed that sortilin facilitated acid sphingomyelinase (ASM)/ceramide signaling, which activated RhoA/ROCK2 signaling, ultimately causing the transformation of dendritic spine dynamics.	Ceramides	66-74	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	61-64
34931016-8	2021	We revealed that sortilin facilitated acid sphingomyelinase (ASM)/ceramide signaling, which activated RhoA/ROCK2 signaling, ultimately causing the transformation of dendritic spine dynamics.	Ceramides	66-74	ras homolog family member A	Mus musculus	102-106
34931016-8	2021	We revealed that sortilin facilitated acid sphingomyelinase (ASM)/ceramide signaling, which activated RhoA/ROCK2 signaling, ultimately causing the transformation of dendritic spine dynamics.	Ceramides	66-74	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	107-112
34987511-3	2021	As demonstrated in experimental and observational clinical studies, the transient and stress-triggered release of a sphingomyelinase, SMPD1, into circulation and subsequent ceramide generation provides a promising target for FDA-approved drugs.	Ceramides	173-181	sphingomyelin phosphodiesterase 1	Homo sapiens	134-139
34987511-6	2021	Consistent with increased ceramide levels derived from the inert membrane constituent sphingomyelin, increased activity of acid sphingomyelinase (ASM) accurately distinguished the patient cohort undergoing intensive care from healthy controls.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	123-144
34987511-6	2021	Consistent with increased ceramide levels derived from the inert membrane constituent sphingomyelin, increased activity of acid sphingomyelinase (ASM) accurately distinguished the patient cohort undergoing intensive care from healthy controls.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	146-149
34647453-6	2021	Further, we found that this ceramide accumulation on LPs was orchestrated by ceramide synthase 2, inhibition of which hampers phagosomal maturation.	Ceramides	28-36	ceramide synthase 2	Homo sapiens	77-96
34944757-4	2021	METHODS AND RESULTS: In 25 FH subjects, heterozygotes or compound heterozygotes for different LDL receptor mutations, untargeted lipidomic revealed significant reductions in 26 lipid classes belonging to phosphatidylcholine (PC), sphingomyelin (SM), ceramide (CER), cholesteryl ester (CE), triacylglycerol (TG) and phosphatidylinositol (PI).	Ceramides	250-258	low density lipoprotein receptor	Homo sapiens	27-29
34944757-4	2021	METHODS AND RESULTS: In 25 FH subjects, heterozygotes or compound heterozygotes for different LDL receptor mutations, untargeted lipidomic revealed significant reductions in 26 lipid classes belonging to phosphatidylcholine (PC), sphingomyelin (SM), ceramide (CER), cholesteryl ester (CE), triacylglycerol (TG) and phosphatidylinositol (PI).	Ceramides	250-258	low density lipoprotein receptor	Homo sapiens	94-106
34944757-4	2021	METHODS AND RESULTS: In 25 FH subjects, heterozygotes or compound heterozygotes for different LDL receptor mutations, untargeted lipidomic revealed significant reductions in 26 lipid classes belonging to phosphatidylcholine (PC), sphingomyelin (SM), ceramide (CER), cholesteryl ester (CE), triacylglycerol (TG) and phosphatidylinositol (PI).	Ceramides	260-263	low density lipoprotein receptor	Homo sapiens	27-29
34944757-4	2021	METHODS AND RESULTS: In 25 FH subjects, heterozygotes or compound heterozygotes for different LDL receptor mutations, untargeted lipidomic revealed significant reductions in 26 lipid classes belonging to phosphatidylcholine (PC), sphingomyelin (SM), ceramide (CER), cholesteryl ester (CE), triacylglycerol (TG) and phosphatidylinositol (PI).	Ceramides	260-263	low density lipoprotein receptor	Homo sapiens	94-106
34944757-9	2021	The mechanism underlying these changes likely involves the de novo synthesis of SM and CER through the activation of the key enzyme sphingomyelin synthase by oxidized LDL and argues for a multifaceted system leading to vascular improvement in users of PCSK-9 inhibitors.	Ceramides	87-90	proprotein convertase subtilisin/kexin type 9	Homo sapiens	252-258
34914638-10	2022	Our study clarified that ceramide promoted CRC development through increasing gut dysbiosis, further resulting in the increase of cholesterol esterification in a special way of SOAT1-dependent.	Ceramides	25-33	sterol O-acyltransferase 1	Homo sapiens	177-182
34914638-4	2022	It was first found by us that miR-148a deficiency dramatically increased mouse gut dysbiosis through upregulating Cers5 expression, which promoted ceramide synthesis afterward.	Ceramides	147-155	ceramide synthase 5	Mus musculus	114-119
34846852-5	2021	Based on structure-activity relationship studies, we proposed the ability of the compounds to act as light chain 3 (LC3) interactors, similar to cardiolipin or ceramide, triggering mitophagy via Pink1/Parkin.	Ceramides	160-168	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	101-114
34914638-6	2022	Meanwhile, increased level of ceramide correlated with the significant enhancements on both beta-catenin activity and colorectal tumorigenesis in a fashion of TLR4-dependent.	Ceramides	30-38	catenin (cadherin associated protein), beta 1	Mus musculus	92-104
34846852-5	2021	Based on structure-activity relationship studies, we proposed the ability of the compounds to act as light chain 3 (LC3) interactors, similar to cardiolipin or ceramide, triggering mitophagy via Pink1/Parkin.	Ceramides	160-168	PTEN induced kinase 1	Homo sapiens	195-200
34914638-6	2022	Meanwhile, increased level of ceramide correlated with the significant enhancements on both beta-catenin activity and colorectal tumorigenesis in a fashion of TLR4-dependent.	Ceramides	30-38	toll-like receptor 4	Mus musculus	159-163
34915026-3	2022	As ceramides are the sole source for sphingomyelins, we hypothesized that ceramide synthase (CerS)-derived ceramides regulate ABCB1 activity.	Ceramides	3-12	ATP binding cassette subfamily B member 1	Homo sapiens	126-131
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.	Ceramides	172-180	Diacylglycerol kinase family protein	Arabidopsis thaliana	77-81
34919775-6	2022	Comparison of the level of reactive oxygen species (ROS), salicylic acid (SA), and ceramides in the wild-type and acer acd5 plants at different developmental stages indicated that the acer acd5 mutant exhibited constitutive activation of SA and ROS signaling, which occurred simultaneously with the alteration of ceramides.	Ceramides	83-92	Diacylglycerol kinase family protein	Arabidopsis thaliana	119-123
34919775-6	2022	Comparison of the level of reactive oxygen species (ROS), salicylic acid (SA), and ceramides in the wild-type and acer acd5 plants at different developmental stages indicated that the acer acd5 mutant exhibited constitutive activation of SA and ROS signaling, which occurred simultaneously with the alteration of ceramides.	Ceramides	83-92	Diacylglycerol kinase family protein	Arabidopsis thaliana	189-193
34919775-6	2022	Comparison of the level of reactive oxygen species (ROS), salicylic acid (SA), and ceramides in the wild-type and acer acd5 plants at different developmental stages indicated that the acer acd5 mutant exhibited constitutive activation of SA and ROS signaling, which occurred simultaneously with the alteration of ceramides.	Ceramides	313-322	Diacylglycerol kinase family protein	Arabidopsis thaliana	119-123
34919775-7	2022	Overexpressing NahG in the acer acd5 mutant could completely suppress its cell death and ceramide accumulation, while BTH treatment restored its phenotype again.	Ceramides	89-97	Diacylglycerol kinase family protein	Arabidopsis thaliana	32-36
34919775-9	2022	Ceramides accumulated in the plasma membrane of acer acd5, directly binding and activating the NADPH oxidase RbohD and promoting H2 O2 generation and SA- or defense-related gene activation.	Ceramides	0-9	Diacylglycerol kinase family protein	Arabidopsis thaliana	53-57
34919775-9	2022	Ceramides accumulated in the plasma membrane of acer acd5, directly binding and activating the NADPH oxidase RbohD and promoting H2 O2 generation and SA- or defense-related gene activation.	Ceramides	0-9	respiratory burst oxidase homologue D	Arabidopsis thaliana	109-114
34919775-0	2022	Ceramides regulate defense response by binding to RbohD in Arabidopsis.	Ceramides	0-9	respiratory burst oxidase homologue D	Arabidopsis thaliana	50-55
34910213-2	2022	The fatty acid hydroxylase mutant fah1 fah2 exhibits high ceramide levels and moderately elevated LCB levels.	Ceramides	58-66	ferulic acid 5-hydroxylase 1	Arabidopsis thaliana	34-38
34910213-2	2022	The fatty acid hydroxylase mutant fah1 fah2 exhibits high ceramide levels and moderately elevated LCB levels.	Ceramides	58-66	fatty acid hydroxylase 2	Arabidopsis thaliana	39-43
34915026-3	2022	As ceramides are the sole source for sphingomyelins, we hypothesized that ceramide synthase (CerS)-derived ceramides regulate ABCB1 activity.	Ceramides	107-116	ATP binding cassette subfamily B member 1	Homo sapiens	126-131
34915026-8	2022	We demonstrated that chemoresistance to doxorubicin in ABCB1high cells was partially reversed by inhibitors of de novo ceramide synthesis (L-cycloserine) and CerS (fumonisin B1) in cell viability assays.	Ceramides	119-127	ATP binding cassette subfamily B member 1	Homo sapiens	55-60
34915026-11	2022	Furthermore, CerS6-targeting siRNA shifted ceramide and sphingomyelin composition to ultra long-chain species (C22-C26).	Ceramides	43-51	ceramide synthase 6	Homo sapiens	13-18
34915026-13	2022	We conclude that a critical balance in ceramide/sphingomyelin species is prerequisite to ABCB1 expression and functionalization, which could be targeted to reverse MDR in renal cancers.	Ceramides	39-47	ATP binding cassette subfamily B member 1	Homo sapiens	89-94
34893994-9	2022	It indicated that ceramide metabolic balance might be a mainly disordered, performing higher synthesis and lower hydrolysis, with the ratio of SMPD1/SGMS2 up-regulated significantly (p<0.05) in ox-LDL induced group.	Ceramides	18-26	sphingomyelin phosphodiesterase 1	Homo sapiens	143-148
34893994-9	2022	It indicated that ceramide metabolic balance might be a mainly disordered, performing higher synthesis and lower hydrolysis, with the ratio of SMPD1/SGMS2 up-regulated significantly (p<0.05) in ox-LDL induced group.	Ceramides	18-26	sphingomyelin synthase 2	Homo sapiens	149-154
34096319-5	2021	Sphingomyelin/ ceramide biosynthesis is dysregulated in GCTB due to alterations in the expression of SMS1, SMS2, and nSMase2.	Ceramides	15-23	sphingomyelin synthase 1	Homo sapiens	101-105
34947980-5	2021	Ceramide transfer protein (CERT) dictates the ratio of ceramide to sphingomyelin within the cell.	Ceramides	55-63	ceramide transporter 1	Homo sapiens	0-25
34947980-5	2021	Ceramide transfer protein (CERT) dictates the ratio of ceramide to sphingomyelin within the cell.	Ceramides	55-63	ceramide transporter 1	Homo sapiens	27-31
34514546-0	2021	Altered ceramide metabolism is a feature in the extracellular vesicle-mediated spread of alpha-synuclein in Lewy body disorders.	Ceramides	8-16	synuclein alpha	Homo sapiens	89-104
34514546-7	2021	Our in vitro studies demonstrate that LBD EV constitute a "pathological package" capable of inducing aggregation of wild-type alpha-synuclein, mediated through a combination of alpha-synuclein-ceramide interaction and the presence of pathological forms of alpha-synuclein.	Ceramides	193-201	synuclein alpha	Homo sapiens	126-141
34514546-7	2021	Our in vitro studies demonstrate that LBD EV constitute a "pathological package" capable of inducing aggregation of wild-type alpha-synuclein, mediated through a combination of alpha-synuclein-ceramide interaction and the presence of pathological forms of alpha-synuclein.	Ceramides	193-201	synuclein alpha	Homo sapiens	177-192
34096319-5	2021	Sphingomyelin/ ceramide biosynthesis is dysregulated in GCTB due to alterations in the expression of SMS1, SMS2, and nSMase2.	Ceramides	15-23	sphingomyelin synthase 2	Homo sapiens	107-111
34096319-5	2021	Sphingomyelin/ ceramide biosynthesis is dysregulated in GCTB due to alterations in the expression of SMS1, SMS2, and nSMase2.	Ceramides	15-23	sphingomyelin phosphodiesterase 3	Homo sapiens	117-124
34424821-1	2021	CPT1C, which is expressed in hippocampus, influences ceramide level, endogenous cannabinoid and oxidation process, as well as plays an important role in various brain functions such as learning.	Ceramides	53-61	carnitine palmitoyltransferase 1c	Mus musculus	0-5
34399014-9	2021	Levels of cytotoxic sphingosine and ceramide were higher in the corpus callosum of SphK2-/- mice, and in contrast to WT mice, did not decline following cuprizone withdrawal in SphK2-/- mice.	Ceramides	36-44	sphingosine kinase 2	Mus musculus	83-88
34363204-7	2021	We then focus on the temporal dynamics of sphingolipid biosynthesis and emphasise the modulatory role of some sphingolipid species (i.e. sphingomyelins, ceramides and glycosphingolipids) on the pro-inflammatory and pro-resolution phases of LPS/TLR4 activation in macrophages.	Ceramides	153-162	toll like receptor 4	Homo sapiens	244-248
34851150-9	2021	Interestingly, DCHP exposure also led to higher circulating ceramides in a PXR-dependent manner.	Ceramides	60-69	nuclear receptor subfamily 1, group I, member 2	Mus musculus	75-78
34851150-10	2021	DCHP-mediated PXR activation stimulated the expression of intestinal genes mediating lipogenesis and ceramide synthesis.	Ceramides	101-109	nuclear receptor subfamily 1, group I, member 2	Mus musculus	14-17
34851150-13	2021	Our studies demonstrate that DCHP activated PXR to induce hypercholesterolemia and ceramide production in mice.	Ceramides	83-91	nuclear receptor subfamily 1, group I, member 2	Mus musculus	44-47
34399014-12	2021	We propose that persistently high levels of sphingosine and ceramide, a direct consequence of SphK2 deficiency, may block remyelination.	Ceramides	60-68	sphingosine kinase 2	Mus musculus	94-99
34793833-7	2021	We showed that binding of ceramide and its analogs to TRAM2 correlated with their ability to induce RAT of TM4SF20.	Ceramides	26-34	translocation associated membrane protein 2	Rattus norvegicus	54-59
34793833-7	2021	We showed that binding of ceramide and its analogs to TRAM2 correlated with their ability to induce RAT of TM4SF20.	Ceramides	26-34	transmembrane 4 L six family member 20	Rattus norvegicus	107-114
34940574-6	2021	The isolated ceramides, including Cer-1, Cer-2, Cer-3, Cer-4, Cer-5 and Cer-6 showed promising antiviral activity against SARS-CoV-2 when investigated using in silico approaches by preventing its attachment to human cells and/or inhibiting its viral replication.	Ceramides	13-22	cerberus 1, DAN family BMP antagonist	Homo sapiens	34-39
34600152-3	2021	This study assessed the therapeutic potential of dihydroceramide desaturase 1 (Des1) inhibition, the last enzyme involved in de novo ceramide synthesis, to mitigate the vascular effects of the PBUT indoxyl sulfate (IS).	Ceramides	133-141	delta 4-desaturase, sphingolipid 1	Homo sapiens	79-83
34454928-4	2021	This study aimed to investigate whether ACC2 inhibition-induced compositional changes in bioactive lipids, especially diacylglycerol and ceramide, within skeletal muscle contribute to the improved insulin resistance.	Ceramides	137-145	acetyl-CoA carboxylase beta	Rattus norvegicus	40-44
34707072-5	2021	The expression of ceramide synthase 3 (CerS3), which binds ultra-long-chain fatty acids to sphingosine to produce ceramides found in the skin, was also increased.	Ceramides	114-123	ceramide synthase 3	Homo sapiens	18-37
34707072-5	2021	The expression of ceramide synthase 3 (CerS3), which binds ultra-long-chain fatty acids to sphingosine to produce ceramides found in the skin, was also increased.	Ceramides	114-123	ceramide synthase 3	Homo sapiens	39-44
34785538-5	2022	Loss of SPTLC2 prevents the synthesis of mitochondrial sphingolipids and protects from palmitate-induced mitochondrial toxicity, a process dependent on mitochondrial ceramides.	Ceramides	166-175	serine palmitoyltransferase long chain base subunit 2	Homo sapiens	8-14
34877496-2	2021	Deficiencies in the human dihydroceramide desaturase gene, DEGS1, increase the dihydroceramide-to-ceramide ratio and cause hypomyelinating leukodystrophy.	Ceramides	98-106	delta 4-desaturase, sphingolipid 1	Homo sapiens	59-64
34877496-8	2021	Together, DEGS1/Ifc controls the dihydroceramide-to-ceramide ratio and enhances exosome secretion by promoting ILV formation and preventing the autophagic degradation of MVEs.	Ceramides	52-60	delta 4-desaturase, sphingolipid 1	Homo sapiens	10-15
34877496-8	2021	Together, DEGS1/Ifc controls the dihydroceramide-to-ceramide ratio and enhances exosome secretion by promoting ILV formation and preventing the autophagic degradation of MVEs.	Ceramides	52-60	infertile crescent	Drosophila melanogaster	16-19
34869633-10	2021	Consistently, real-time PCR showed that periplocymarin significantly abolished the induction of the genes involved in the de novo synthesis of ceramide, i.e., CerS2, CerS4, CerS5, and CerS6, and the induction was attributed to the treatment of DOX.	Ceramides	143-151	ceramide synthase 2	Rattus norvegicus	159-164
34869633-10	2021	Consistently, real-time PCR showed that periplocymarin significantly abolished the induction of the genes involved in the de novo synthesis of ceramide, i.e., CerS2, CerS4, CerS5, and CerS6, and the induction was attributed to the treatment of DOX.	Ceramides	143-151	ceramide synthase 4	Rattus norvegicus	166-171
34869633-10	2021	Consistently, real-time PCR showed that periplocymarin significantly abolished the induction of the genes involved in the de novo synthesis of ceramide, i.e., CerS2, CerS4, CerS5, and CerS6, and the induction was attributed to the treatment of DOX.	Ceramides	143-151	ceramide synthase 5	Rattus norvegicus	173-178
34869633-10	2021	Consistently, real-time PCR showed that periplocymarin significantly abolished the induction of the genes involved in the de novo synthesis of ceramide, i.e., CerS2, CerS4, CerS5, and CerS6, and the induction was attributed to the treatment of DOX.	Ceramides	143-151	ceramide synthase 6	Rattus norvegicus	184-189
34454928-5	2021	In skeletal muscle of normal rats, treatment of the ACC2 inhibitor compound 2e significantly decreased both diacylglycerol and ceramide levels while having no significant impact on other lipid metabolite levels.	Ceramides	127-135	acetyl-CoA carboxylase beta	Rattus norvegicus	52-56
34454928-10	2021	These findings suggest that ACC2 inhibition decreases diacylglycerol and ceramide accumulation within skeletal muscle by enhancing acyl-CoA breakdown, leading to attenuation of lipid-induced insulin resistance and subsequent diabetes progression.	Ceramides	73-81	acetyl-CoA carboxylase beta	Rattus norvegicus	28-32
34618068-2	2021	Ceramides, key intermediates in sphingolipid metabolism, are phosphorylated by the ceramide kinase ACCELERATED CELL DEATH5 (ACD5).	Ceramides	0-9	Diacylglycerol kinase family protein	Arabidopsis thaliana	99-122
34739556-2	2022	Sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b), a lipid modifying enzyme that converts sphingomyelin to ceramide in the cell membrane, is expressed in macrophages and regulates Toll-like receptor (TLR) 4 signaling by altering cell membrane fluidity.	Ceramides	112-120	sphingomyelin phosphodiesterase acid like 3B	Homo sapiens	0-44
34739556-2	2022	Sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b), a lipid modifying enzyme that converts sphingomyelin to ceramide in the cell membrane, is expressed in macrophages and regulates Toll-like receptor (TLR) 4 signaling by altering cell membrane fluidity.	Ceramides	112-120	sphingomyelin phosphodiesterase acid like 3B	Homo sapiens	46-53
34739556-2	2022	Sphingomyelin phosphodiesterase acid-like 3b (SMPDL3b), a lipid modifying enzyme that converts sphingomyelin to ceramide in the cell membrane, is expressed in macrophages and regulates Toll-like receptor (TLR) 4 signaling by altering cell membrane fluidity.	Ceramides	112-120	toll like receptor 4	Homo sapiens	185-211
34805145-3	2021	We have previously demonstrated that the release of palmitate-stimulated EVs is dependent on the de novo synthesis of ceramide, which is trafficked by the ceramide transport protein, STARD11.	Ceramides	118-126	ceramide transporter 1	Homo sapiens	183-190
34805145-3	2021	We have previously demonstrated that the release of palmitate-stimulated EVs is dependent on the de novo synthesis of ceramide, which is trafficked by the ceramide transport protein, STARD11.	Ceramides	155-163	ceramide transporter 1	Homo sapiens	183-190
34805145-4	2021	The trafficking of ceramide is a critical step in the release of lipotoxic EVs, as cells deficient in STARD11 do not release palmitate-stimulated EVs.	Ceramides	19-27	ceramide transporter 1	Homo sapiens	102-109
34805145-11	2021	Haptoglobin, vascular non-inflammatory molecule-1, and insulin-like growth factor-binding protein complex acid labile subunit were commonly detected in NASH and hepatocyte-derived ceramide-dependent EVs.	Ceramides	180-188	haptoglobin	Homo sapiens	0-11
34805145-11	2021	Haptoglobin, vascular non-inflammatory molecule-1, and insulin-like growth factor-binding protein complex acid labile subunit were commonly detected in NASH and hepatocyte-derived ceramide-dependent EVs.	Ceramides	180-188	vanin 1	Homo sapiens	13-49
34618068-2	2021	Ceramides, key intermediates in sphingolipid metabolism, are phosphorylated by the ceramide kinase ACCELERATED CELL DEATH5 (ACD5).	Ceramides	0-9	Diacylglycerol kinase family protein	Arabidopsis thaliana	124-128
34618068-3	2021	The loss of ACD5 function leads to ceramide accumulation and spontaneous cell death.	Ceramides	35-43	Diacylglycerol kinase family protein	Arabidopsis thaliana	12-16
34618068-8	2021	Together, our findings show that JAs accelerate cell death in acd5 mutants, possibly by modulating sphingolipid metabolism and increasing ceramide levels.	Ceramides	138-146	Diacylglycerol kinase family protein	Arabidopsis thaliana	62-66
34418535-1	2021	Sphingomyelin synthase (SMS), which comprises of two isozymes, SMS1 and SMS2, is the only enzyme that generates sphingomyelin (SM) by transferring phosphocholine of phosphatidylcholine to ceramide in mammals.	Ceramides	188-196	sphingomyelin synthase 1	Homo sapiens	63-67
34731610-2	2021	Here, we identify sphingomyelin phosphodiesterase 1 (SMPD1), an enzyme that regulates the conversion of sphingomyelin to ceramide, as an actionable drug target in GBM.	Ceramides	121-129	sphingomyelin phosphodiesterase 1	Homo sapiens	18-51
34731610-2	2021	Here, we identify sphingomyelin phosphodiesterase 1 (SMPD1), an enzyme that regulates the conversion of sphingomyelin to ceramide, as an actionable drug target in GBM.	Ceramides	121-129	sphingomyelin phosphodiesterase 1	Homo sapiens	53-58
34418535-1	2021	Sphingomyelin synthase (SMS), which comprises of two isozymes, SMS1 and SMS2, is the only enzyme that generates sphingomyelin (SM) by transferring phosphocholine of phosphatidylcholine to ceramide in mammals.	Ceramides	188-196	sphingomyelin synthase 2	Homo sapiens	72-76
34482548-9	2021	This study suggests that the intracellular metabolism of palmitate and elevation of metabolites, including ceramide and phospholipids, are responsible for the palmitate-mediated induction of the potent orexigen Npy.	Ceramides	107-115	neuropeptide Y	Homo sapiens	211-214
34688657-1	2021	The lipid molecule ceramide is transported from the endoplasmic reticulum to the Golgi apparatus for sphingomyelin production via the ceramide transport protein (CERT), encoded by CERT1.	Ceramides	19-27	ceramide transporter 1	Homo sapiens	162-166
34688657-1	2021	The lipid molecule ceramide is transported from the endoplasmic reticulum to the Golgi apparatus for sphingomyelin production via the ceramide transport protein (CERT), encoded by CERT1.	Ceramides	134-142	ceramide transporter 1	Homo sapiens	162-166
34398463-3	2021	As glycosphingolipid biosynthesis starts from ceramide glycosylation by glucosylceramide synthase (GCS), inhibiting GCS in the brain is a promising strategy for neurological GD.	Ceramides	46-54	UDP-glucose ceramide glucosyltransferase	Mus musculus	72-97
34398463-3	2021	As glycosphingolipid biosynthesis starts from ceramide glycosylation by glucosylceramide synthase (GCS), inhibiting GCS in the brain is a promising strategy for neurological GD.	Ceramides	46-54	UDP-glucose ceramide glucosyltransferase	Mus musculus	99-102
34365584-6	2021	Lipid and gene expression analyses confirmed an elevated level of the n-3 PUFA eicosapentaenoic acid (EPA) in the plasma and brain, blocking of TBI-mediated increase of Cer in the brain, and decrease in TBI-mediated induction of Cer biosynthetic and inflammatory gene expression in the brain of the Fat1+ mice.	Ceramides	229-232	FAT atypical cadherin 1	Mus musculus	299-303
34273578-4	2021	Indeed, excessive hypothalamic de novo ceramide synthesis have been shown to result in the establishment of central insulin resistance, endoplasmic reticulum stress and inflammation.	Ceramides	39-47	insulin	Homo sapiens	116-123
34365584-7	2021	Our results demonstrate that suppression of ceramide biosynthesis and inflammatory factors in Fat1+-transgenic mice is associated with significant protection against the visual, motor, and emotional deficits caused by mild TBI.	Ceramides	44-52	FAT atypical cadherin 1	Mus musculus	94-98
34456156-1	2021	Lysosomal beta-galactosylceramidase (GALC) removes beta-galactose from beta-galactosylceramide, thus generating the oncosuppressor metabolite ceramide.	Ceramides	142-150	galactosylceramidase	Homo sapiens	37-41
34257427-7	2021	Moreover, saturated fat raises IHTG more than polyunsaturated or monounsaturated fats, with adverse effects on insulin sensitivity, which are probably mediated in part by increased ceramide synthesis.	Ceramides	181-189	insulin	Homo sapiens	111-118
34285405-5	2021	These extracellular factors perturb the intracellular concentration of a range of intermediates, including ceramide and other lipids, leading to defects in responsiveness of cells to insulin.	Ceramides	107-115	insulin	Homo sapiens	183-190
34405428-0	2021	Protein-bound ceramide levels in the epidermis of transglutaminase 1-deficient mice.	Ceramides	14-22	transglutaminase 1, K polypeptide	Mus musculus	50-68
34727637-6	2021	Methods: The ceramide C6 (an extracellular signaling-regulated kinases 1 and 2 (ERK1/2) activator) and MHY1485 (a mTOR activator) were used to treat rabbit adipose-derived stem cells (ADSCs) with or without acetate, respectively.	Ceramides	13-21	mitogen-activated protein kinase 3	Homo sapiens	80-86
34727637-10	2021	Activation of ERK1/2 and mTOR by respective addition in media with ceramide C6 and MHY1485 significantly attenuated decreased lipid deposition and increased HSL expression caused by acetate.	Ceramides	67-75	mitogen-activated protein kinase 3	Homo sapiens	14-20
34727637-10	2021	Activation of ERK1/2 and mTOR by respective addition in media with ceramide C6 and MHY1485 significantly attenuated decreased lipid deposition and increased HSL expression caused by acetate.	Ceramides	67-75	mechanistic target of rapamycin kinase	Homo sapiens	25-29
34727637-10	2021	Activation of ERK1/2 and mTOR by respective addition in media with ceramide C6 and MHY1485 significantly attenuated decreased lipid deposition and increased HSL expression caused by acetate.	Ceramides	67-75	lipase E, hormone sensitive type	Homo sapiens	157-160
34686591-0	2021	Ceramide accumulation induces mitophagy and impairs beta-oxidation in PINK1 deficiency.	Ceramides	0-8	PTEN induced kinase 1	Homo sapiens	70-75
34776936-0	2021	Effects of Sex, Age, and Apolipoprotein E Genotype on Brain Ceramides and Sphingosine-1-Phosphate in Alzheimer"s Disease and Control Mice.	Ceramides	60-69	apolipoprotein E	Mus musculus	25-41
34612290-5	2021	The simulations show that the spike tries to maximize the contacts with stratum corneum lipids, particularly ceramides, with substantial hydrogen bonding.	Ceramides	109-118	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	30-35
34686882-0	2022	Formation of keto-type ceramides in palmoplantar keratoderma based on biallelic KDSR mutations in patients.	Ceramides	23-32	3-ketodihydrosphingosine reductase	Homo sapiens	80-84
34686591-6	2021	Here, we identified ceramide to play a crucial role in PINK1-related PD that was previously linked almost exclusively to mitochondrial dysfunction.	Ceramides	20-28	PTEN induced kinase 1	Homo sapiens	55-60
34686591-10	2021	As a result of the ceramide accumulation, beta-oxidation in PINK1 mutants was decreased, which was rescued by lowering ceramide levels.	Ceramides	19-27	PTEN induced kinase 1	Homo sapiens	60-65
34686591-10	2021	As a result of the ceramide accumulation, beta-oxidation in PINK1 mutants was decreased, which was rescued by lowering ceramide levels.	Ceramides	119-127	PTEN induced kinase 1	Homo sapiens	60-65
34686882-8	2022	Formation of keto-type ceramides is probably due to a bottle neck in metabolic flux through KDSR and a bypass by ceramide synthases, which highlights the importance of tight intermediate regulation during sphingolipid anabolism and reveals substrate deprivation as potential therapy.	Ceramides	23-32	3-ketodihydrosphingosine reductase	Homo sapiens	92-96
34608263-0	2022	The acid sphingomyelinase/ceramide system in COVID-19.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
34615856-0	2021	ECHS1, an interacting protein of LASP1, induces sphingolipid-metabolism imbalance to promote colorectal cancer progression by regulating ceramide glycosylation.	Ceramides	137-145	enoyl-CoA hydratase, short chain 1	Homo sapiens	0-5
34615856-0	2021	ECHS1, an interacting protein of LASP1, induces sphingolipid-metabolism imbalance to promote colorectal cancer progression by regulating ceramide glycosylation.	Ceramides	137-145	LIM and SH3 protein 1	Homo sapiens	33-38
34615856-4	2021	Mechanistic studies of the underlying tumor-supportive oncometabolism indicate that ECHS1 enables altering ceramide (Cer) metabolism that increases glycosphingolipid synthesis (HexCer) by promoting UDP-glucose ceramide glycosyltransferase (UGCG).	Ceramides	107-115	enoyl-CoA hydratase, short chain 1	Homo sapiens	84-89
34615856-4	2021	Mechanistic studies of the underlying tumor-supportive oncometabolism indicate that ECHS1 enables altering ceramide (Cer) metabolism that increases glycosphingolipid synthesis (HexCer) by promoting UDP-glucose ceramide glycosyltransferase (UGCG).	Ceramides	107-115	UDP-glucose ceramide glucosyltransferase	Homo sapiens	198-238
34615856-4	2021	Mechanistic studies of the underlying tumor-supportive oncometabolism indicate that ECHS1 enables altering ceramide (Cer) metabolism that increases glycosphingolipid synthesis (HexCer) by promoting UDP-glucose ceramide glycosyltransferase (UGCG).	Ceramides	107-115	UDP-glucose ceramide glucosyltransferase	Homo sapiens	240-244
34615856-4	2021	Mechanistic studies of the underlying tumor-supportive oncometabolism indicate that ECHS1 enables altering ceramide (Cer) metabolism that increases glycosphingolipid synthesis (HexCer) by promoting UDP-glucose ceramide glycosyltransferase (UGCG).	Ceramides	117-120	enoyl-CoA hydratase, short chain 1	Homo sapiens	84-89
34615856-4	2021	Mechanistic studies of the underlying tumor-supportive oncometabolism indicate that ECHS1 enables altering ceramide (Cer) metabolism that increases glycosphingolipid synthesis (HexCer) by promoting UDP-glucose ceramide glycosyltransferase (UGCG).	Ceramides	117-120	UDP-glucose ceramide glucosyltransferase	Homo sapiens	198-238
34615856-4	2021	Mechanistic studies of the underlying tumor-supportive oncometabolism indicate that ECHS1 enables altering ceramide (Cer) metabolism that increases glycosphingolipid synthesis (HexCer) by promoting UDP-glucose ceramide glycosyltransferase (UGCG).	Ceramides	117-120	UDP-glucose ceramide glucosyltransferase	Homo sapiens	240-244
34770770-3	2021	ER stress induces iPLA2beta-mediated generation of pro-apoptotic ceramides via neutral sphingomyelinase (NSMase).	Ceramides	65-74	phospholipase A2 group VI	Homo sapiens	18-27
34770770-3	2021	ER stress induces iPLA2beta-mediated generation of pro-apoptotic ceramides via neutral sphingomyelinase (NSMase).	Ceramides	65-74	sphingomyelin phosphodiesterase 2	Homo sapiens	79-103
34770770-3	2021	ER stress induces iPLA2beta-mediated generation of pro-apoptotic ceramides via neutral sphingomyelinase (NSMase).	Ceramides	65-74	sphingomyelin phosphodiesterase 2	Homo sapiens	105-111
34418572-2	2021	Inhibition of sphingosine kinase isoform 1 (SK1) within this pathway, leads to a buildup of sphingosine and ceramide, two molecules directly linked to cell apoptosis, while decreasing the intracellular concentration of sphingosine-1-phosphate (S1P), a molecule linked to cellular proliferation.	Ceramides	108-116	sphingosine kinase 1	Homo sapiens	14-42
34418572-2	2021	Inhibition of sphingosine kinase isoform 1 (SK1) within this pathway, leads to a buildup of sphingosine and ceramide, two molecules directly linked to cell apoptosis, while decreasing the intracellular concentration of sphingosine-1-phosphate (S1P), a molecule linked to cellular proliferation.	Ceramides	108-116	sphingosine kinase 1	Homo sapiens	44-47
34608263-1	2022	Acid sphingomyelinase (ASM) cleaves sphingomyelin into the highly lipophilic ceramide, which forms large gel-like rafts/platforms in the plasma membrane.	Ceramides	77-85	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
34608263-1	2022	Acid sphingomyelinase (ASM) cleaves sphingomyelin into the highly lipophilic ceramide, which forms large gel-like rafts/platforms in the plasma membrane.	Ceramides	77-85	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
34608263-3	2022	Lowering the amount of ceramide or ceramide blockade due to inhibitors of ASM, genetic downregulation of ASM, anti-ceramide antibodies or degradation by neutral ceramidase protected against infection with SARS-CoV-2.	Ceramides	23-31	sphingomyelin phosphodiesterase 1	Homo sapiens	74-77
34608263-3	2022	Lowering the amount of ceramide or ceramide blockade due to inhibitors of ASM, genetic downregulation of ASM, anti-ceramide antibodies or degradation by neutral ceramidase protected against infection with SARS-CoV-2.	Ceramides	35-43	sphingomyelin phosphodiesterase 1	Homo sapiens	74-77
34608263-8	2022	The ASM/ceramide system provides a framework for a better understanding of the infection of cells by SARS-CoV-2 and the clinical, antiviral, and anti-inflammatory effects of functional inhibitors of ASM.	Ceramides	8-16	sphingomyelin phosphodiesterase 1	Homo sapiens	4-7
34608263-8	2022	The ASM/ceramide system provides a framework for a better understanding of the infection of cells by SARS-CoV-2 and the clinical, antiviral, and anti-inflammatory effects of functional inhibitors of ASM.	Ceramides	8-16	sphingomyelin phosphodiesterase 1	Homo sapiens	199-202
34174696-5	2021	CD300a or CD300f binding to externalized phosphatidylserine or extracellular ceramides, respectively, inhibits FcepsilonRI-mediated mast cell activation.	Ceramides	77-86	CD300a molecule	Homo sapiens	0-6
34638448-5	2021	Increasing levels of IL6, IL8, CXCL16, MPIF1, and YKL40 correlated with increasing levels of ceramide in both cohorts.	Ceramides	93-101	interleukin 6	Homo sapiens	21-24
34638448-5	2021	Increasing levels of IL6, IL8, CXCL16, MPIF1, and YKL40 correlated with increasing levels of ceramide in both cohorts.	Ceramides	93-101	C-X-C motif chemokine ligand 8	Homo sapiens	26-29
34638448-5	2021	Increasing levels of IL6, IL8, CXCL16, MPIF1, and YKL40 correlated with increasing levels of ceramide in both cohorts.	Ceramides	93-101	C-X-C motif chemokine ligand 16	Homo sapiens	31-37
34638448-5	2021	Increasing levels of IL6, IL8, CXCL16, MPIF1, and YKL40 correlated with increasing levels of ceramide in both cohorts.	Ceramides	93-101	C-C motif chemokine ligand 23	Homo sapiens	39-44
34638448-5	2021	Increasing levels of IL6, IL8, CXCL16, MPIF1, and YKL40 correlated with increasing levels of ceramide in both cohorts.	Ceramides	93-101	chitinase 3 like 1	Homo sapiens	50-55
34174696-5	2021	CD300a or CD300f binding to externalized phosphatidylserine or extracellular ceramides, respectively, inhibits FcepsilonRI-mediated mast cell activation.	Ceramides	77-86	CD300 molecule like family member f	Homo sapiens	10-16
34791626-10	2021	These findings indicated the protective effects of VEGF in confronting the ceramide-induced cardiomyocyte apoptosis, and would devote therapeutic targets for cardiovascular safeguard in dealing with fatty acid stress.	Ceramides	75-83	vascular endothelial growth factor A	Rattus norvegicus	51-55
34499916-3	2021	Acid sphingomyelinase (ASMase) is one of the major enzymes responsible for the stress-induced generation of ceramides.	Ceramides	108-117	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
34499916-3	2021	Acid sphingomyelinase (ASMase) is one of the major enzymes responsible for the stress-induced generation of ceramides.	Ceramides	108-117	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-29
34656931-12	2021	INTERPRETATION: Ceramide-S1P signalling promotes ARSI resistance, which can be reversed with SPHK inhibitors.	Ceramides	16-24	sphingosine kinase 1	Homo sapiens	93-97
34499916-13	2021	These results provide evidence that ceramides can induce RGC cell death by acting directly, as well as indirectly via the secretion of TNF-alpha from optic nerve head astrocytes.	Ceramides	36-45	tumor necrosis factor	Mus musculus	135-144
34499916-14	2021	In vivo studies in mice provide evidence that ceramides derived through the activity of ASMase contribute to ocular hypertensive injury.	Ceramides	46-55	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	88-94
34371064-11	2021	Stimulation of oestrogen receptor alpha (ERalpha) by oestradiol down-regulates ceramide synthesis in hypothalamic neuronal GT1-7 cells but no in microglial SIM-A9 cells.	Ceramides	79-87	estrogen receptor 1 (alpha)	Mus musculus	41-48
34371064-12	2021	In contrast, genetic inactivation of ERalpha in VMH upregulates ceramide synthesis.	Ceramides	64-72	estrogen receptor 1 (alpha)	Mus musculus	37-44
34142167-0	2021	Geniposide ameliorates chronic unpredictable mild stress induced depression-like behavior through inhibition of ceramide-PP2A signaling via the PI3K/Akt/GSK3beta axis.	Ceramides	112-120	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	121-125
34474170-0	2021	Inhibition of ceramide de novo synthesis ameliorates meibomian gland dysfunction induced by SCD1 deficiency.	Ceramides	14-22	stearoyl-Coenzyme A desaturase 1	Mus musculus	92-96
34474170-4	2021	However, inhibition of serine palmitoyltransferase, the initial enzyme in ceramide biosynthesis, improved meibomian gland metabolism and morphology in SCD1-deficient mice, resulting in normal cell differentiation and reduced inflammation infiltration, cell apoptosis, and keratinization.	Ceramides	74-82	stearoyl-Coenzyme A desaturase 1	Mus musculus	151-155
34363020-0	2021	M6A methylation of DEGS2, a key ceramide-synthesizing enzyme, is involved in colorectal cancer progression through ceramide synthesis.	Ceramides	32-40	delta 4-desaturase, sphingolipid 2	Homo sapiens	19-24
34363020-0	2021	M6A methylation of DEGS2, a key ceramide-synthesizing enzyme, is involved in colorectal cancer progression through ceramide synthesis.	Ceramides	115-123	delta 4-desaturase, sphingolipid 2	Homo sapiens	19-24
34363020-8	2021	Moreover, ceramide synthesis was suppressed due to DEGS2 upregulation mediated by m6A modification in CRC tissues.	Ceramides	10-18	delta 4-desaturase, sphingolipid 2	Homo sapiens	51-56
34142167-0	2021	Geniposide ameliorates chronic unpredictable mild stress induced depression-like behavior through inhibition of ceramide-PP2A signaling via the PI3K/Akt/GSK3beta axis.	Ceramides	112-120	thymoma viral proto-oncogene 1	Mus musculus	149-152
34142167-0	2021	Geniposide ameliorates chronic unpredictable mild stress induced depression-like behavior through inhibition of ceramide-PP2A signaling via the PI3K/Akt/GSK3beta axis.	Ceramides	112-120	glycogen synthase kinase 3 alpha	Mus musculus	153-161
34142167-7	2021	Geniposide is able to reduce the levels of ceramide and lower the activity of acid sphingomyelinase (ASM) in hippocampus; besides, ASM inhibitor (amitriptyline) can decrease the concentration of ceramide and ameliorate depressive-like behaviors of mice.	Ceramides	43-51	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	131-134
34142167-7	2021	Geniposide is able to reduce the levels of ceramide and lower the activity of acid sphingomyelinase (ASM) in hippocampus; besides, ASM inhibitor (amitriptyline) can decrease the concentration of ceramide and ameliorate depressive-like behaviors of mice.	Ceramides	195-203	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	78-99
34142167-7	2021	Geniposide is able to reduce the levels of ceramide and lower the activity of acid sphingomyelinase (ASM) in hippocampus; besides, ASM inhibitor (amitriptyline) can decrease the concentration of ceramide and ameliorate depressive-like behaviors of mice.	Ceramides	195-203	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	131-134
34616654-3	2021	ORMDL3 not only regulates major human rhinovirus receptor intercellular adhesion molecule 1 expression, but also plays pivotal roles in viral infection through metabolisms of ceramide and sphingosine-1-phosphate, endoplasmic reticulum (ER) stress, ER-Golgi interface and glycolysis.	Ceramides	175-183	ORMDL sphingolipid biosynthesis regulator 3	Homo sapiens	0-6
34638539-10	2021	AUCs calculated from ROC curves indicated ceramides C16:0, C18:0, C24:1, sphingosine and SPTLC1 as putative biomarkers of disease evolution.	Ceramides	42-51	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	89-95
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.	Ceramides	168-176	glucosylceramidase beta	Homo sapiens	71-92
34374401-5	2021	SFF administration reduced ceramide levels in both serum and colonic tissue of HFD-fed mice, as well as reduced expression of SPT and CerS genes, which encode enzymes crucial to the biosynthesis of ceramides regulated by FXR signaling.	Ceramides	27-35	nuclear receptor subfamily 1, group H, member 4	Mus musculus	221-224
34374401-5	2021	SFF administration reduced ceramide levels in both serum and colonic tissue of HFD-fed mice, as well as reduced expression of SPT and CerS genes, which encode enzymes crucial to the biosynthesis of ceramides regulated by FXR signaling.	Ceramides	198-207	nuclear receptor subfamily 1, group H, member 4	Mus musculus	221-224
34374401-7	2021	Taken together, the results suggested that SFF increased TUDCA levels by remodeling gut microbiota, and TUDCA, a natural FXR antagonist, inhibited the FXR/SHP signaling pathway to reduce colon-derived biosynthesis of ceramide, thereby improving insulin resistance in the diet-induced obese (DIO) mice.	Ceramides	217-225	nuclear receptor subfamily 1, group H, member 4	Mus musculus	121-124
34374401-7	2021	Taken together, the results suggested that SFF increased TUDCA levels by remodeling gut microbiota, and TUDCA, a natural FXR antagonist, inhibited the FXR/SHP signaling pathway to reduce colon-derived biosynthesis of ceramide, thereby improving insulin resistance in the diet-induced obese (DIO) mice.	Ceramides	217-225	nuclear receptor subfamily 1, group H, member 4	Mus musculus	151-154
34374401-7	2021	Taken together, the results suggested that SFF increased TUDCA levels by remodeling gut microbiota, and TUDCA, a natural FXR antagonist, inhibited the FXR/SHP signaling pathway to reduce colon-derived biosynthesis of ceramide, thereby improving insulin resistance in the diet-induced obese (DIO) mice.	Ceramides	217-225	nuclear receptor subfamily 0, group B, member 2	Mus musculus	155-158
34604081-13	2021	Overexpression of ceramide synthase 5 that specifically produces C16 ceramide enables erianin to induce apoptosis in castration-resistant prostate cancer cells.	Ceramides	69-77	ceramide synthase 5	Homo sapiens	18-37
34616654-3	2021	ORMDL3 not only regulates major human rhinovirus receptor intercellular adhesion molecule 1 expression, but also plays pivotal roles in viral infection through metabolisms of ceramide and sphingosine-1-phosphate, endoplasmic reticulum (ER) stress, ER-Golgi interface and glycolysis.	Ceramides	175-183	intercellular adhesion molecule 1	Homo sapiens	58-91
34062255-5	2021	Genes which encode key enzymes for the synthesis of long chain bases (LCBs) and ceramides were periodically transcribed during the mitotic cell cycle, having a peak at G1/S, and required SWI4 for full transcription at this stage.	Ceramides	80-89	SBF complex DNA-binding subunit SWI4	Saccharomyces cerevisiae S288C	187-191
34621698-2	2021	SLs are generated intracellularly in a stepwise manner, starting with the generation of the sphingoid long chain base (LCB), followed by N-acylation of the LCB to form ceramide, which can be subsequently metabolized to sphingomyelin and glycosphingolipids.	Ceramides	168-176	clathrin light chain B	Homo sapiens	156-159
34417267-0	2021	Surplus Ceramides: An Added Twist in the Tale of TREM2 and Insulin Resistance.	Ceramides	8-17	twist family bHLH transcription factor 1	Homo sapiens	28-33
34417267-0	2021	Surplus Ceramides: An Added Twist in the Tale of TREM2 and Insulin Resistance.	Ceramides	8-17	triggering receptor expressed on myeloid cells 2	Homo sapiens	49-54
34417267-0	2021	Surplus Ceramides: An Added Twist in the Tale of TREM2 and Insulin Resistance.	Ceramides	8-17	insulin	Homo sapiens	59-66
34431499-7	2021	Omics analysis showed toxic species such as diacylglycerides and ceramides in Tgfbeta3+/- mice, and dysregulated mitochondrial metabolism.	Ceramides	65-74	transforming growth factor, beta 3	Mus musculus	78-86
34180563-9	2021	Consistent with this, B. cinerea-induced ceramide accumulation requires PAD4 or EDS1.	Ceramides	41-49	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	72-76
34180563-0	2021	The immune components EDS1 and PAD4 are required for cell death caused by overaccumulation of ceramides in Arabidopsis.	Ceramides	94-103	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	22-26
34180563-9	2021	Consistent with this, B. cinerea-induced ceramide accumulation requires PAD4 or EDS1.	Ceramides	41-49	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	80-84
34180563-0	2021	The immune components EDS1 and PAD4 are required for cell death caused by overaccumulation of ceramides in Arabidopsis.	Ceramides	94-103	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	31-35
34180563-5	2021	The accelerated cell death 5 (acd5) mutants accumulate ceramides due to a defect in ceramide kinase and show spontaneous cell death.	Ceramides	55-64	Diacylglycerol kinase family protein	Arabidopsis thaliana	30-34
34180563-6	2021	Loss of function of EDS1, PAD4, or SALICYLIC ACID INDUCTION DEFICIENT 2 (SID2) in the acd5 background suppressed the acd5 cell-death phenotype and prevented ceramide accumulation.	Ceramides	157-165	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	20-24
34180563-6	2021	Loss of function of EDS1, PAD4, or SALICYLIC ACID INDUCTION DEFICIENT 2 (SID2) in the acd5 background suppressed the acd5 cell-death phenotype and prevented ceramide accumulation.	Ceramides	157-165	ADC synthase superfamily protein	Arabidopsis thaliana	35-71
34180563-6	2021	Loss of function of EDS1, PAD4, or SALICYLIC ACID INDUCTION DEFICIENT 2 (SID2) in the acd5 background suppressed the acd5 cell-death phenotype and prevented ceramide accumulation.	Ceramides	157-165	ADC synthase superfamily protein	Arabidopsis thaliana	73-77
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	50-58	TRAM, LAG1 and CLN8 (TLC) lipid-sensing domain containing protein	Arabidopsis thaliana	73-77
34180563-6	2021	Loss of function of EDS1, PAD4, or SALICYLIC ACID INDUCTION DEFICIENT 2 (SID2) in the acd5 background suppressed the acd5 cell-death phenotype and prevented ceramide accumulation.	Ceramides	157-165	Diacylglycerol kinase family protein	Arabidopsis thaliana	86-90
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	50-58	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	104-108
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	50-58	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	110-114
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	150-158	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	104-108
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	150-158	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	110-114
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	174-182	TRAM, LAG1 and CLN8 (TLC) lipid-sensing domain containing protein	Arabidopsis thaliana	73-77
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	174-182	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	104-108
34180563-10	2021	Finally, examination of plants overexpressing the ceramide synthase gene LAG1 HOMOLOGUE2 suggested that EDS1, PAD4, and SA are involved in long-chain ceramide metabolism and ceramide-associated cell death.	Ceramides	174-182	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	110-114
34180563-11	2021	Collectively, our observations reveal that EDS1 and PAD4 mediate ceramide (especially long-chain ceramide) metabolism and associated cell death, by SA-dependent and SA-independent pathways.	Ceramides	65-73	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	43-47
34180563-11	2021	Collectively, our observations reveal that EDS1 and PAD4 mediate ceramide (especially long-chain ceramide) metabolism and associated cell death, by SA-dependent and SA-independent pathways.	Ceramides	65-73	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	52-56
34180563-11	2021	Collectively, our observations reveal that EDS1 and PAD4 mediate ceramide (especially long-chain ceramide) metabolism and associated cell death, by SA-dependent and SA-independent pathways.	Ceramides	97-105	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	43-47
34180563-11	2021	Collectively, our observations reveal that EDS1 and PAD4 mediate ceramide (especially long-chain ceramide) metabolism and associated cell death, by SA-dependent and SA-independent pathways.	Ceramides	97-105	alpha/beta-Hydrolases superfamily protein	Arabidopsis thaliana	52-56
34503116-4	2021	Ceramide kinase (CERK) catalyzes the phosphorylation of ceramide to ceramide 1-phosphate, which regulates various cellular functions including cell growth and migration.	Ceramides	56-64	ceramide kinase	Mus musculus	0-15
34514718-9	2021	Correction of DeltaF508-CFTR trafficking with VX445 + VX661 decreased some sphingomyelins and all ceramides, but exacerbated increases in dihydroceramides.	Ceramides	98-107	CF transmembrane conductance regulator	Homo sapiens	24-28
34503116-4	2021	Ceramide kinase (CERK) catalyzes the phosphorylation of ceramide to ceramide 1-phosphate, which regulates various cellular functions including cell growth and migration.	Ceramides	56-64	ceramide kinase	Homo sapiens	17-21
34401974-13	2021	In summary, protecting mitochondria via inhibiting VDAC1 oligomerization attenuated hepatocyte ferroptosis by restoring ceramide and cardiolipin content in AILI.	Ceramides	120-128	voltage dependent anion channel 1	Homo sapiens	51-56
34458595-1	2021	The acid beta-glucocerebrosidase (GCase) enzyme cleaves glucosylceramide into glucose and ceramide.	Ceramides	90-98	glucosidase, beta, acid	Mus musculus	9-32
34458595-1	2021	The acid beta-glucocerebrosidase (GCase) enzyme cleaves glucosylceramide into glucose and ceramide.	Ceramides	90-98	glucosidase, beta, acid	Mus musculus	34-39
34401974-11	2021	Knockdown of Smpd1 and Taz expression responsible for ceramide and cardiolipin synthesis, respectively, aggravated APAP-induced mitochondrial dysfunction and ferroptosis in hepatocytes, whereas Taz overexpression protected against these processes.	Ceramides	54-62	sphingomyelin phosphodiesterase 1	Homo sapiens	13-18
34502095-0	2021	A Dansyl-Modified Sphingosine Kinase Inhibitor DPF-543 Enhanced De Novo Ceramide Generation.	Ceramides	72-80	sphingosine kinase 1	Homo sapiens	18-36
34502095-3	2021	In this regard, SPHK/S1P axis regulation has been a specific issue in the anticancer strategy to turn accumulated sphingosine (SPN) into cytotoxic ceramides (Cers).	Ceramides	147-156	sphingosine kinase 1	Homo sapiens	16-20
34502095-3	2021	In this regard, SPHK/S1P axis regulation has been a specific issue in the anticancer strategy to turn accumulated sphingosine (SPN) into cytotoxic ceramides (Cers).	Ceramides	158-162	sphingosine kinase 1	Homo sapiens	16-20
34445706-3	2021	The majority of the literature implies that ASM hydrolyses solely sphingomyelin to generate ceramide and ignores its ability to degrade further substrates.	Ceramides	92-100	sphingomyelin phosphodiesterase 1	Homo sapiens	44-47
34401974-11	2021	Knockdown of Smpd1 and Taz expression responsible for ceramide and cardiolipin synthesis, respectively, aggravated APAP-induced mitochondrial dysfunction and ferroptosis in hepatocytes, whereas Taz overexpression protected against these processes.	Ceramides	54-62	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	23-26
34436382-7	2021	IGF-1 treatment of myotubes had a significant impact on the levels of diacylglycerol (DG) and ceramide (Cer) in secreted EVs.	Ceramides	94-102	insulin-like growth factor 1	Mus musculus	0-5
34400330-0	2022	Silencing of ceramide synthase 2 in hepatocytes modulates plasma ceramide biomarkers predictive of cardiovascular death.	Ceramides	65-73	ceramide synthase 2	Homo sapiens	13-32
34436382-7	2021	IGF-1 treatment of myotubes had a significant impact on the levels of diacylglycerol (DG) and ceramide (Cer) in secreted EVs.	Ceramides	104-107	insulin-like growth factor 1	Mus musculus	0-5
34422083-11	2021	Conclusion: GQD can inhibit the FXR/ceramide signaling pathway, regulate endoplasmic reticulum stress, enhance the CS activity of liver mitochondria, reduce the acetyl CoA level and PC activity of liver mitochondria, inhibit hepatic gluconeogenesis, protect islet beta-cells, and control blood glucose.	Ceramides	36-44	nuclear receptor subfamily 1, group H, member 4	Rattus norvegicus	32-35
34382511-3	2022	SK1 is highly expressed in colorectal cancer, its inhibitors suppress the formation of S1P and increase ceramide levels having a pro-apoptotic function.	Ceramides	104-112	sphingosine kinase 1	Homo sapiens	0-3
34422083-0	2021	Effect of Gegen Qinlian Decoction on Hepatic Gluconeogenesis in ZDF Rats with Type 2 Diabetes Mellitus Based on the Farnesol X Receptor/Ceramide Signaling Pathway Regulating Mitochondrial Metabolism and Endoplasmic Reticulum Stress.	Ceramides	136-144	nuclear receptor subfamily 1, group H, member 4	Rattus norvegicus	116-135
34361066-0	2021	N-Palmitoyl Serinol Stimulates Ceramide Production through a CB1-Dependent Mechanism in In Vitro Model of Skin Inflammation.	Ceramides	31-39	cannabinoid receptor 1	Homo sapiens	61-64
34422083-2	2021	Farnesol X receptor (FXR)/ceramide signaling pathway plays an important role in regulating cholesterol metabolism, lipid homeostasis, and the absorption of fat and vitamins in diet.	Ceramides	26-34	nuclear receptor subfamily 1, group H, member 4	Rattus norvegicus	0-19
34422083-2	2021	Farnesol X receptor (FXR)/ceramide signaling pathway plays an important role in regulating cholesterol metabolism, lipid homeostasis, and the absorption of fat and vitamins in diet.	Ceramides	26-34	nuclear receptor subfamily 1, group H, member 4	Rattus norvegicus	21-24
34422083-4	2021	Objective: To investigate the effect of Gegen Qinlian Decoction (GQD) on hepatic gluconeogenesis in obese T2DM rats based on the FXR/ceramide signaling pathway regulating mitochondrial metabolism and endoplasmic reticulum stress (ERS).	Ceramides	133-141	nuclear receptor subfamily 1, group H, member 4	Rattus norvegicus	129-132
34288516-4	2021	Counteracting the deleterious effects of high-fat diets (HFDs) rich in saturated fat either by inhibiting synthesis or by promoting degradation of ceramides mitigates insulin resistance and ectopic lipid accumulation (Meikle and Summers 2017).	Ceramides	147-156	insulin	Homo sapiens	167-174
34361066-5	2021	Accordingly, an IL-4-mediated decrease in cellular ceramide levels was significantly stimulated in human epidermal keratinocytes (KC) following PS treatment through both de novo ceramide synthesis- and sphingomyelin hydrolysis-pathways.	Ceramides	178-186	interleukin 4	Homo sapiens	16-20
34361066-8	2021	These studies demonstrate that an analog of endocannabinoid, PS, stimulates the generation of specific ceramide species as well as the total amount of ceramides via the endocannabinoid receptor CB1-dependent mechanism, thereby resulting in the enhancement of epidermal permeability barrier function.	Ceramides	151-160	cannabinoid receptor 1	Homo sapiens	194-197
34361066-3	2021	It is widely accepted that the endocannabinoid system (ECS) can modulate a number of biological responses in the central nerve system, prior studies revealed that activation of endocannabinoid receptor CB1, a key component of ECS, triggers the generation of ceramides that mediate neuronal cell fate.	Ceramides	258-267	cannabinoid receptor 1	Homo sapiens	202-205
34361066-5	2021	Accordingly, an IL-4-mediated decrease in cellular ceramide levels was significantly stimulated in human epidermal keratinocytes (KC) following PS treatment through both de novo ceramide synthesis- and sphingomyelin hydrolysis-pathways.	Ceramides	51-59	interleukin 4	Homo sapiens	16-20
34359242-3	2021	Ceramide stimulation downregulated the overall abundance of phosphorylated (p) protein kinase B (AKT), p-mechanistic target of rapamycin (mTOR), and p-eukaryotic elongation factor 2 (eEF2).	Ceramides	0-8	AKT serine/threonine kinase 1	Bos taurus	97-100
34359242-3	2021	Ceramide stimulation downregulated the overall abundance of phosphorylated (p) protein kinase B (AKT), p-mechanistic target of rapamycin (mTOR), and p-eukaryotic elongation factor 2 (eEF2).	Ceramides	0-8	mechanistic target of rapamycin kinase	Bos taurus	103-136
34270128-1	2022	Reportedly, decreases in fatty acid (FA) chain length of ceramide (CER) are associated with interferon-gamma (IFN-gamma), which shows increased expression in psoriasis.	Ceramides	57-65	interferon gamma	Mus musculus	92-108
34359242-3	2021	Ceramide stimulation downregulated the overall abundance of phosphorylated (p) protein kinase B (AKT), p-mechanistic target of rapamycin (mTOR), and p-eukaryotic elongation factor 2 (eEF2).	Ceramides	0-8	mechanistic target of rapamycin kinase	Bos taurus	138-142
34270128-1	2022	Reportedly, decreases in fatty acid (FA) chain length of ceramide (CER) are associated with interferon-gamma (IFN-gamma), which shows increased expression in psoriasis.	Ceramides	57-65	interferon gamma	Mus musculus	110-119
34270128-1	2022	Reportedly, decreases in fatty acid (FA) chain length of ceramide (CER) are associated with interferon-gamma (IFN-gamma), which shows increased expression in psoriasis.	Ceramides	67-70	interferon gamma	Mus musculus	92-108
34359242-3	2021	Ceramide stimulation downregulated the overall abundance of phosphorylated (p) protein kinase B (AKT), p-mechanistic target of rapamycin (mTOR), and p-eukaryotic elongation factor 2 (eEF2).	Ceramides	0-8	eukaryotic translation elongation factor 2	Bos taurus	149-181
34270128-1	2022	Reportedly, decreases in fatty acid (FA) chain length of ceramide (CER) are associated with interferon-gamma (IFN-gamma), which shows increased expression in psoriasis.	Ceramides	67-70	interferon gamma	Mus musculus	110-119
34359242-3	2021	Ceramide stimulation downregulated the overall abundance of phosphorylated (p) protein kinase B (AKT), p-mechanistic target of rapamycin (mTOR), and p-eukaryotic elongation factor 2 (eEF2).	Ceramides	0-8	eukaryotic translation elongation factor 2	Bos taurus	183-187
34359242-7	2021	Ceramide stimulation decreased the overall protein abundance of the Na-coupled neutral amino acid transporter SLC38A1 and branched-chain alpha-ketoacid dehydrogenase kinase (BCKDK).	Ceramides	0-8	solute carrier family 38 member 1	Bos taurus	110-117
34359242-7	2021	Ceramide stimulation decreased the overall protein abundance of the Na-coupled neutral amino acid transporter SLC38A1 and branched-chain alpha-ketoacid dehydrogenase kinase (BCKDK).	Ceramides	0-8	branched chain keto acid dehydrogenase kinase	Bos taurus	122-172
34359242-7	2021	Ceramide stimulation decreased the overall protein abundance of the Na-coupled neutral amino acid transporter SLC38A1 and branched-chain alpha-ketoacid dehydrogenase kinase (BCKDK).	Ceramides	0-8	branched chain keto acid dehydrogenase kinase	Bos taurus	174-179
34359242-9	2021	Circulating ceramides might affect amino acid, insulin signaling, and glutathione metabolism in dairy cow adipose tissue.	Ceramides	12-21	insulin	Bos taurus	47-54
34232291-9	2021	CONCLUSIONS: A ceramide-based CERT-HBP was established to evaluate risk of MACE in hypertensive patients at high cardiovascular risk.	Ceramides	15-23	ceramide transporter 1	Homo sapiens	30-34
34118203-6	2021	MYC-overexpressing cells require ceramide, whereas AURKB requires ESCRT to release high levels of EVs.	Ceramides	33-41	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	0-3
34298889-9	2021	Moreover, decreased sphingomyelins together with normal ceramides and sphingomyelin synthase activity reveal the importance of ACBD3 in ceramide transport from ER to Golgi.	Ceramides	136-144	acyl-CoA binding domain containing 3	Homo sapiens	127-132
34232291-9	2021	CONCLUSIONS: A ceramide-based CERT-HBP was established to evaluate risk of MACE in hypertensive patients at high cardiovascular risk.	Ceramides	15-23	heme binding protein 1	Homo sapiens	35-38
34209043-4	2021	Here, we report the impairment of ceramide kinase (CerK), the enzyme responsible for the phosphorylation of ceramide to C1P, associated with the accomplishment of atrophic phenotype in various experimental models of SkM atrophy: in vivo animal model bearing the C26 adenocarcinoma or Lewis lung carcinoma tumors, in human and murine SkM cells treated with the conditioned medium obtained from cancer cells or with the glucocorticoid dexamethasone.	Ceramides	108-116	ceramide kinase	Homo sapiens	34-49
34105193-2	2021	Increased synthesis of ceramides is linked to decreased insulin sensitivity of tissues.	Ceramides	23-32	INS	Equus caballus	56-63
34105193-3	2021	Conversely, activation of the insulin signaling pathway can downregulate ceramide synthesis.	Ceramides	73-81	INS	Equus caballus	30-37
34105193-5	2021	HYPOTHESES: Horses with insulin dysregulation will have a plasma sphingolipid profile characterized by increased ceramide concentrations.	Ceramides	113-121	INS	Equus caballus	24-31
34105193-6	2021	The plasma sphingolipid profile will have decreased ceramide concentrations after acute activation of the insulin signaling pathway by oral glucose testing.	Ceramides	52-60	INS	Equus caballus	106-113
34105193-14	2021	A high plasma ceramide concentration can indicate insulin dysregulation in horses.	Ceramides	14-22	INS	Equus caballus	50-57
34211180-6	2021	Moreover, we identify Cers4, encoding ceramide synthase 4, catalysing de novo ceramide synthesis, as a MYC target gene.	Ceramides	78-86	ceramide synthase 4	Mus musculus	22-27
34211180-6	2021	Moreover, we identify Cers4, encoding ceramide synthase 4, catalysing de novo ceramide synthesis, as a MYC target gene.	Ceramides	78-86	ceramide synthase 4	Mus musculus	38-57
34211180-6	2021	Moreover, we identify Cers4, encoding ceramide synthase 4, catalysing de novo ceramide synthesis, as a MYC target gene.	Ceramides	78-86	myelocytomatosis oncogene	Mus musculus	103-106
34211180-7	2021	Finally, we show that administration of the MYC inhibitor 10058-F4 has beneficial effects on high-fat-diet-induced metabolic disorders, and is accompanied by increased GLP-1 and reduced ceramide levels in serum.	Ceramides	186-194	myelocytomatosis oncogene	Mus musculus	44-47
34211181-0	2021	Gutting out Myc to decrease ceramides.	Ceramides	28-37	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	12-15
34089907-2	2021	Ceramides have been linked to oxidative stress-mediated apoptotic intracellular signalling and the enzyme neutral sphingomyelinase (nSMase) is, in part, responsible for generating these ceramides through the hydrolysis of sphingomyelin.	Ceramides	0-9	sphingomyelin phosphodiesterase 2	Homo sapiens	106-130
34089907-2	2021	Ceramides have been linked to oxidative stress-mediated apoptotic intracellular signalling and the enzyme neutral sphingomyelinase (nSMase) is, in part, responsible for generating these ceramides through the hydrolysis of sphingomyelin.	Ceramides	0-9	sphingomyelin phosphodiesterase 2	Homo sapiens	132-138
34089907-2	2021	Ceramides have been linked to oxidative stress-mediated apoptotic intracellular signalling and the enzyme neutral sphingomyelinase (nSMase) is, in part, responsible for generating these ceramides through the hydrolysis of sphingomyelin.	Ceramides	186-195	sphingomyelin phosphodiesterase 2	Homo sapiens	106-130
34089907-2	2021	Ceramides have been linked to oxidative stress-mediated apoptotic intracellular signalling and the enzyme neutral sphingomyelinase (nSMase) is, in part, responsible for generating these ceramides through the hydrolysis of sphingomyelin.	Ceramides	186-195	sphingomyelin phosphodiesterase 2	Homo sapiens	132-138
34089907-8	2021	These findings suggest that nSMase associated with SS mitochondria may play a role in intracellular signalling processes involving ceramides in skeletal muscle and nSMase2 may be the key isoform, specifically in slow twitch muscle like soleus.	Ceramides	131-140	sphingomyelin phosphodiesterase 2	Homo sapiens	28-34
34197026-3	2021	Two approaches for rendering the SWCNT sensors for insulin are compared, using surface functionalization with either a natural insulin aptamer with known affinity to insulin, or a synthetic lipid-poly(ethylene glycol) (PEG) (C16 -PEG(2000Da)-Ceramide), both of which show a modulation of the emitted fluorescence in response to insulin.	Ceramides	242-250	insulin	Homo sapiens	51-58
34197026-3	2021	Two approaches for rendering the SWCNT sensors for insulin are compared, using surface functionalization with either a natural insulin aptamer with known affinity to insulin, or a synthetic lipid-poly(ethylene glycol) (PEG) (C16 -PEG(2000Da)-Ceramide), both of which show a modulation of the emitted fluorescence in response to insulin.	Ceramides	242-250	insulin	Homo sapiens	328-335
34197026-4	2021	Although the PEGylated-lipid has no prior affinity to insulin, the response of C16 -PEG(2000Da)-Ceramide-SWCNTs to insulin is more stable and reproducible compared to the insulin aptamer-SWCNTs.	Ceramides	96-104	insulin	Homo sapiens	54-61
34197026-4	2021	Although the PEGylated-lipid has no prior affinity to insulin, the response of C16 -PEG(2000Da)-Ceramide-SWCNTs to insulin is more stable and reproducible compared to the insulin aptamer-SWCNTs.	Ceramides	96-104	insulin	Homo sapiens	115-122
34209043-4	2021	Here, we report the impairment of ceramide kinase (CerK), the enzyme responsible for the phosphorylation of ceramide to C1P, associated with the accomplishment of atrophic phenotype in various experimental models of SkM atrophy: in vivo animal model bearing the C26 adenocarcinoma or Lewis lung carcinoma tumors, in human and murine SkM cells treated with the conditioned medium obtained from cancer cells or with the glucocorticoid dexamethasone.	Ceramides	108-116	ceramide kinase	Homo sapiens	51-55
34209043-6	2021	Gene silencing of CerK promotes the up-regulation of atrogin-1/MAFbx expression, which was also observed after cell treatment with C8-ceramide, a biologically active ceramide analogue.	Ceramides	166-174	F-box protein 32	Homo sapiens	53-62
34157971-13	2021	The high levels of interferon (IFN)gamma not only in skin, but also in brain likely account for a significant decline in esterified very-long-chain N-acyl fatty acids in brain ceramides, again mimicking known IFNgamma-induced changes in AD.	Ceramides	176-185	interferon gamma	Mus musculus	209-217
34097992-0	2021	The Aryl Hydrocarbon Receptor Activates Ceramide Biosynthesis in Mice Contributing to Hepatic Lipogenesis.	Ceramides	40-48	aryl-hydrocarbon receptor	Mus musculus	4-29
34097992-2	2021	Here we report that AHR activation by TCDF (24 microg/kg body weight given orally for five days) induced significant elevation of hepatic lipids including ceramides in mice, was associated with increased expression of key ceramide biosynthetic genes, and increased activity of their respective enzymes.	Ceramides	155-164	aryl-hydrocarbon receptor	Mus musculus	20-23
34097992-2	2021	Here we report that AHR activation by TCDF (24 microg/kg body weight given orally for five days) induced significant elevation of hepatic lipids including ceramides in mice, was associated with increased expression of key ceramide biosynthetic genes, and increased activity of their respective enzymes.	Ceramides	222-230	aryl-hydrocarbon receptor	Mus musculus	20-23
34097992-5	2021	Taken together, our results revealed that AHR activation results in the up-regulation of Sptlc2, leading to ceramide accumulation, thus promoting lipogenesis, which can induce hepatic lipid accumulation.	Ceramides	108-116	aryl-hydrocarbon receptor	Mus musculus	42-45
34097992-5	2021	Taken together, our results revealed that AHR activation results in the up-regulation of Sptlc2, leading to ceramide accumulation, thus promoting lipogenesis, which can induce hepatic lipid accumulation.	Ceramides	108-116	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	89-95
34222257-8	2021	Acid sphingomyelinase (ASM) is vital for the generation of ceramide and functional inhibition of ASM by drugs like amitriptyline reduced SARS-CoV-2 entry into the epithelial cells.	Ceramides	59-67	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
34222257-8	2021	Acid sphingomyelinase (ASM) is vital for the generation of ceramide and functional inhibition of ASM by drugs like amitriptyline reduced SARS-CoV-2 entry into the epithelial cells.	Ceramides	59-67	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
34429698-0	2021	Effects of Glycogen on Ceramide Production in Cultured Human Keratinocytes via Acid Sphingomyelinase Activation.	Ceramides	23-31	sphingomyelin phosphodiesterase 1	Homo sapiens	79-100
34208778-0	2021	Inhibition of Ceramide Synthesis Reduces alpha-Synuclein Proteinopathy in a Cellular Model of Parkinson"s Disease.	Ceramides	14-22	synuclein alpha	Homo sapiens	41-56
34909730-4	2021	The amounts of C24 and C26 free fatty acids and C24 and C26 ceramides-oxidized exclusively in peroxisomes-were reduced in the epidermis of ft/ft mice despite increased lipid synthesis, similar to that seen in human ADL edpidermis.	Ceramides	60-69	sarcoglycan alpha	Homo sapiens	215-218
34135326-5	2021	The structure of the ceramide acyl chain still affects these domains, as co-clustering with the glycosylphosphatidylinositol (GPI)-anchored protein CD59 occurs only when GM1 contains the fully saturated C16:0 acyl chain, and not C16:1.	Ceramides	21-29	CD59 molecule (CD59 blood group)	Homo sapiens	148-152
34179008-3	2021	Ceramide can be phosphorylated by ceramide kinase (CERK) to generate ceramide-1-phosphate, a cytoprotective signaling molecule that has been widely studied in multiple tissues and organs, including the developing otocyst.	Ceramides	0-8	ceramide kinase	Gallus gallus	34-49
34102611-4	2021	We identified acid ceramidase (ASAH1), a lysosomal enzyme that cleaves ceramide into sphingosine and fatty acid, as being highly elevated in senescent cells.	Ceramides	71-79	N-acylsphingosine amidohydrolase 1	Homo sapiens	14-29
34102611-4	2021	We identified acid ceramidase (ASAH1), a lysosomal enzyme that cleaves ceramide into sphingosine and fatty acid, as being highly elevated in senescent cells.	Ceramides	71-79	N-acylsphingosine amidohydrolase 1	Homo sapiens	31-36
34179008-3	2021	Ceramide can be phosphorylated by ceramide kinase (CERK) to generate ceramide-1-phosphate, a cytoprotective signaling molecule that has been widely studied in multiple tissues and organs, including the developing otocyst.	Ceramides	0-8	ceramide kinase	Gallus gallus	51-55
34179008-5	2021	Using chicken otocysts, we show that genes for CERK and other enzymes of ceramide metabolism are expressed during the early stages of inner ear development and that CERK is developmentally regulated at the otic vesicle stage.	Ceramides	73-81	ceramide kinase	Gallus gallus	47-51
34179008-5	2021	Using chicken otocysts, we show that genes for CERK and other enzymes of ceramide metabolism are expressed during the early stages of inner ear development and that CERK is developmentally regulated at the otic vesicle stage.	Ceramides	73-81	ceramide kinase	Gallus gallus	165-169
34069652-7	2021	This review confirms that ceramides are associated with hypothalamic dysfunction in response to metaflammation, endoplasmic reticulum (ER) stress, and lipotoxicity, leading to insulin/leptin resistance.	Ceramides	26-35	insulin	Homo sapiens	176-183
34071826-2	2021	Recently, the acid sphingomyelinase (ASM)/ceramide system has been implicated in the pathogenesis of MDD.	Ceramides	42-50	sphingomyelin phosphodiesterase 1	Homo sapiens	14-35
34071826-2	2021	Recently, the acid sphingomyelinase (ASM)/ceramide system has been implicated in the pathogenesis of MDD.	Ceramides	42-50	sphingomyelin phosphodiesterase 1	Homo sapiens	37-40
34071826-3	2021	ASM is a lysosomal glycoprotein that catalyzes the hydrolysis of sphingomyelin, an abundant component of membranes, into the bioactive sphingolipid ceramide, which impacts signaling pathways.	Ceramides	148-156	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
34069652-7	2021	This review confirms that ceramides are associated with hypothalamic dysfunction in response to metaflammation, endoplasmic reticulum (ER) stress, and lipotoxicity, leading to insulin/leptin resistance.	Ceramides	26-35	leptin	Homo sapiens	184-190
34088014-2	2021	Mutations in the N-acylsphingosine amidohydrolase (ASAH1) gene, which encodes for the enzyme acid ceramidase (ACDase), cause ceramides to accumulate in the body.	Ceramides	125-134	N-acylsphingosine amidohydrolase 1	Homo sapiens	51-56
34062962-5	2021	Instead, our results suggest that ASAH1 activity is important for preventing the accumulation of long chain ceramides such as C16-ceramide.	Ceramides	108-117	N-acylsphingosine amidohydrolase 1	Homo sapiens	34-39
34505020-13	2021	Different sexes had opposite correlations with ceramide and IL-5, respectively, suggesting that therapeutic strategies targeting ceramide should be different between sexes.	Ceramides	129-137	interleukin 5	Homo sapiens	60-64
34088014-2	2021	Mutations in the N-acylsphingosine amidohydrolase (ASAH1) gene, which encodes for the enzyme acid ceramidase (ACDase), cause ceramides to accumulate in the body.	Ceramides	125-134	N-acylsphingosine amidohydrolase 1	Homo sapiens	93-108
34088014-2	2021	Mutations in the N-acylsphingosine amidohydrolase (ASAH1) gene, which encodes for the enzyme acid ceramidase (ACDase), cause ceramides to accumulate in the body.	Ceramides	125-134	N-acylsphingosine amidohydrolase 1	Homo sapiens	110-116
34602551-4	2021	Up-regulation of ceramide levels via de novo and salvage synthesis pathways is reported in Abeta-treated cells and brains with AD; however, the effects of Abeta on ceramide decomposition pathways have not been elucidated.	Ceramides	17-25	amyloid beta precursor protein	Homo sapiens	91-96
34602551-4	2021	Up-regulation of ceramide levels via de novo and salvage synthesis pathways is reported in Abeta-treated cells and brains with AD; however, the effects of Abeta on ceramide decomposition pathways have not been elucidated.	Ceramides	17-25	amyloid beta precursor protein	Homo sapiens	155-160
34602551-4	2021	Up-regulation of ceramide levels via de novo and salvage synthesis pathways is reported in Abeta-treated cells and brains with AD; however, the effects of Abeta on ceramide decomposition pathways have not been elucidated.	Ceramides	164-172	amyloid beta precursor protein	Homo sapiens	155-160
35379526-3	2022	ELOVL1 catalyzes fatty acid elongation to produce very long-chain fatty acids (VLCFAs; >=C21), most of which are components of sphingolipids such as ceramides and sphingomyelins.	Ceramides	149-158	ELOVL fatty acid elongase 1	Homo sapiens	0-6
34171322-11	2021	In summary, long-chain oxygenated ceramide metabolism is dysregulated at the lipidomic level in psoriasis, likely driven by the transcriptional differences also observed, and we identified ZIC1 as a potential regulatory target for future therapeutic interventions.	Ceramides	34-42	Zic family member 1	Homo sapiens	189-193
35462006-2	2022	The enzyme neutral sphingomyelinase 2 (nSMase2) is involved in the biogenesis of ceramide and extracellular vesicles (EVs), both of which are dysregulated in PLH, CI, and MDD.	Ceramides	81-89	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	11-37
35462006-2	2022	The enzyme neutral sphingomyelinase 2 (nSMase2) is involved in the biogenesis of ceramide and extracellular vesicles (EVs), both of which are dysregulated in PLH, CI, and MDD.	Ceramides	81-89	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	39-46
35429745-5	2022	In the preliminary phase of the study, gradually aggravated hepatic hypoxia and varying levels of ceramides were observed with the development of type 2 diabetes mellitus (T2DM) due to increasing HIF-2alpha accumulation.	Ceramides	98-107	endothelial PAS domain protein 1	Mus musculus	196-206
35483419-6	2022	Using large unilamellar vesicles, we found that upon replacing 10 mol% DPPC with either C16:0 or C18:0 ceramide, or 16:0 diacylglycerol (dag), lipid domains persisted to higher temperatures.	Ceramides	103-111	Bardet-Biedl syndrome 9	Homo sapiens	97-100
34993951-2	2022	In the stratum corneum (SC), beta- glucocerebrosidase (GBA) mediates transformation of glucosylceramide (GlcCER) into ceramide (CER) and cholesterol into glucosylcholesterol (GlcChol).	Ceramides	118-126	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).	Ceramides	128-131	glucosylceramidase beta	Homo sapiens	55-58
35635926-0	2022	Withdrawal: Ceramide stabilizes beta-site amyloid precursor protein-cleaving enzyme 1 and promotes amyloid beta-peptide biogenesis.	Ceramides	12-20	beta-secretase 1	Homo sapiens	32-85
35331697-2	2022	Recent data indicate a unique role for neutral sphingomyelinase (nSMase) in the control of ceramide-dependent exosome release and inflammatory pathways.	Ceramides	91-99	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	39-63
35331697-2	2022	Recent data indicate a unique role for neutral sphingomyelinase (nSMase) in the control of ceramide-dependent exosome release and inflammatory pathways.	Ceramides	91-99	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	65-71
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.	Ceramides	112-120	glucosylceramidase beta	Homo sapiens	62-66
35624221-8	2022	Treatment with LCL521 or simvastatin to inhibit ASAH1 or HMGCR, respectively, resulted in accumulation of ceramide at the cell surface of PGCC and prevented PGCC progeny formation.	Ceramides	106-114	N-acylsphingosine amidohydrolase 1	Homo sapiens	48-53
35624221-8	2022	Treatment with LCL521 or simvastatin to inhibit ASAH1 or HMGCR, respectively, resulted in accumulation of ceramide at the cell surface of PGCC and prevented PGCC progeny formation.	Ceramides	106-114	3-hydroxy-3-methylglutaryl-CoA reductase	Homo sapiens	57-62
35608326-5	2022	Sphingolipid quantifications showed that ceramides with C16:0 side-chains accumulated in both plant species, and this response was largely unchanged in the SA-induction deficient2 (sid2-1) mutant.	Ceramides	41-50	ADC synthase superfamily protein	Arabidopsis thaliana	181-185
35615758-4	2022	The protein encoded by PNPLA1 acts as a unique transacylase that specifically transfers linoleic acid from triglyceride to omega-hydroxy fatty acid in ceramide, thus giving rise to omega-O-acylceramide, a particular class of sphingolipids that is essential for skin barrier function.	Ceramides	151-159	patatin like phospholipase domain containing 1	Homo sapiens	23-29
35625985-7	2022	CERK inhibition induces ceramide-mediated cell death in tamoxifen-resistant cells.	Ceramides	24-32	ceramide kinase	Homo sapiens	0-4
35584813-4	2022	Sphingolipids such as ceramides are among the most deleterious and bioactive metabolites that accrue, as they participate in selective insulin resistance, dyslipidemia, oxidative stress and apoptosis.	Ceramides	22-31	insulin	Homo sapiens	135-142
35626132-8	2022	However, cotreatment with diTFPP and ceramide downregulated the protein level of CERS2 and increased oxidative and endoplasmic reticulum (ER) stress.	Ceramides	37-45	ceramide synthase 2	Homo sapiens	81-86
35626132-9	2022	Furthermore, insufficient LAMP2 glycosylation induced by diTFPP/ceramide cotreatment may cause the failure of autophagosome-lysosome fusion, eventually lowering the threshold for triggering cell death in response to C2-ceramide.	Ceramides	64-72	lysosomal associated membrane protein 2	Homo sapiens	26-31
35551349-10	2022	The main serum lipids that distinguished both Parkinson"s disease patients and LRRK2 mutation carriers from controls included species of ceramide, triacylglycerol, sphingomyelin, acylcarnitine, phosphatidylcholine and lysophosphatidylethanolamine.	Ceramides	137-145	leucine rich repeat kinase 2	Homo sapiens	79-84
35625985-10	2022	Consequently, ET-resistant breast cancer models have a unique dependence on CERK as its activity can inhibit de novo ceramide production.	Ceramides	117-125	ceramide kinase	Homo sapiens	76-80
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	203-211	patatin-like phospholipase domain containing 2	Mus musculus	31-37
35439015-2	2022	Binding of STx to Gb3 is a prerequisite for its internalization into the host cells, and the ceramide"s fatty acid of Gb3 has been shown to influence STx binding.	Ceramides	93-101	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	18-21
35439015-2	2022	Binding of STx to Gb3 is a prerequisite for its internalization into the host cells, and the ceramide"s fatty acid of Gb3 has been shown to influence STx binding.	Ceramides	93-101	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	118-121
35513703-4	2022	Ceramide, which serves a central role in sphingolipid metabolism, is generated by ceramide synthases (CerS1-6).	Ceramides	0-8	ceramide synthase 1	Homo sapiens	102-109
35601829-5	2022	Furthermore, combined exposure to HFD and unpredictable stress caused a synergistic increase in C16:0, C16:1, and C18:0 ceramides in both sexes and C18:1 and C24:1 in males.	Ceramides	120-129	Bardet-Biedl syndrome 9	Homo sapiens	114-117
35508142-4	2022	Moreover, we also show that a GPI-AP with a C26 ceramide moiety is monitored by the GPI-glycan remodelase Ted1, which, in turn, is required for receptor-mediated export of GPI-APs.	Ceramides	48-56	Ted1p	Saccharomyces cerevisiae S288C	106-110
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	213-216	lipase, hormone sensitive	Mus musculus	39-43
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	213-216	acyl-CoA synthetase long-chain family member 1	Mus musculus	45-50
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.	Ceramides	44-47	CCHC-type zinc finger nucleic acid binding protein	Homo sapiens	110-151
35508667-1	2022	Ectopic ceramide accumulation in insulin-responsive tissues contributes to the development of obesity and impairs insulin sensitivity.	Ceramides	8-16	insulin	Homo sapiens	33-40
35508667-2	2022	Moreover, pharmacological inhibition of serine palmitoyl transferase (SPT), the first enzyme essential for ceramide biosynthesis using myriocin in rodents reduces body weight and improves insulin sensitivity and associated metabolic indices.	Ceramides	107-115	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	40-68
35508667-2	2022	Moreover, pharmacological inhibition of serine palmitoyl transferase (SPT), the first enzyme essential for ceramide biosynthesis using myriocin in rodents reduces body weight and improves insulin sensitivity and associated metabolic indices.	Ceramides	107-115	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	70-73
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	213-216	lipoprotein lipase	Mus musculus	55-58
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	203-211	lipase, hormone sensitive	Mus musculus	39-43
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	203-211	acyl-CoA synthetase long-chain family member 1	Mus musculus	45-50
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	203-211	lipoprotein lipase	Mus musculus	55-58
35529487-5	2022	Increased expression levels of Pnpla2, Lipe, Acsl1 and Lpl likely increase intracellular free fatty acids, which can then be used for subsequent synthesis of other lipids, such as sphingomyelin (SM) and ceramide (Cer).	Ceramides	213-216	patatin-like phospholipase domain containing 2	Mus musculus	31-37
35560527-8	2022	Integration with transcriptome data identified candidate enzymes for IHC validation: Delta4-Desaturase, Sphingolipid 1 (DEGS1) which desaturates dihydroceramide to ceramide, and Delta5 and Delta6-Desaturases (fatty acid desaturases, FADS1 and FADS2), responsible for polyunsaturation.	Ceramides	164-172	delta 4-desaturase, sphingolipid 1	Homo sapiens	120-125
35513574-5	2022	We found that the expression levels of Sptlc1 and Sptlc2, the major SPT subunits, were upregulated and that the cellular concentrations of ceramide and dihydroceramide were elevated by acute ER stress inducers in primary hepatocytes and HepG2 cells.	Ceramides	139-147	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	39-45
35294847-1	2022	Sphingomyelin phosphodiesterase 1 (SMPD1) converts sphingomyelin into ceramide and phosphocholine; hence, loss of SMPD1 function causes abnormal accumulation of sphingomyelin in lysosomes, which results in the lipid-storage disorder Niemann-Pick disease (types A and B).	Ceramides	70-78	sphingomyelin phosphodiesterase 1	Homo sapiens	0-33
35294847-1	2022	Sphingomyelin phosphodiesterase 1 (SMPD1) converts sphingomyelin into ceramide and phosphocholine; hence, loss of SMPD1 function causes abnormal accumulation of sphingomyelin in lysosomes, which results in the lipid-storage disorder Niemann-Pick disease (types A and B).	Ceramides	70-78	sphingomyelin phosphodiesterase 1	Homo sapiens	35-40
35294847-1	2022	Sphingomyelin phosphodiesterase 1 (SMPD1) converts sphingomyelin into ceramide and phosphocholine; hence, loss of SMPD1 function causes abnormal accumulation of sphingomyelin in lysosomes, which results in the lipid-storage disorder Niemann-Pick disease (types A and B).	Ceramides	70-78	sphingomyelin phosphodiesterase 1	Homo sapiens	114-119
35294847-5	2022	Both ZNT complexes contribute to cellular sphingolipid metabolism by activating SMPD1 because cells lacking the functions of the two complexes exhibited a reduced ceramide to sphingomyelin content ratio in terms of their dominant molecular species and an increase in the sphingomyelin content in terms of three minor species.	Ceramides	163-171	sphingomyelin phosphodiesterase 1	Homo sapiens	80-85
35429112-1	2022	Emerging studies indicate that intracellular eukaryotic ceramide species directly activate cathepsin B (CatB), a lysosomal-cysteine-protease, in the cytoplasm of osteoclast precursors (OCPs) leading to elevated RANKL-mediated osteoclastogenesis and inflammatory osteolysis.	Ceramides	56-64	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	211-216
35513574-5	2022	We found that the expression levels of Sptlc1 and Sptlc2, the major SPT subunits, were upregulated and that the cellular concentrations of ceramide and dihydroceramide were elevated by acute ER stress inducers in primary hepatocytes and HepG2 cells.	Ceramides	139-147	serine palmitoyltransferase long chain base subunit 2	Homo sapiens	50-56
35245521-2	2022	Ceramide, a central molecule of sphingolipid metabolism, is phosphorylated to ceramide-1-phosphate (C1P) by ceramide kinase (CerK).	Ceramides	0-8	ceramide kinase	Mus musculus	108-123
35245521-2	2022	Ceramide, a central molecule of sphingolipid metabolism, is phosphorylated to ceramide-1-phosphate (C1P) by ceramide kinase (CerK).	Ceramides	0-8	ceramide kinase	Mus musculus	125-129
35513574-8	2022	Liver-specific Sptlc2 transgenic mice exhibited increased ceramide levels in the liver and elevated fasting glucose levels.	Ceramides	58-66	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	15-21
35513574-10	2022	Collectively, these results demonstrate that ER stress induces activation of the de novo biosynthesis of ceramide and contributes to the progression of hepatic insulin resistance via the reduced phosphorylation of IRbeta in hepatocytes.	Ceramides	105-113	insulin receptor	Mus musculus	214-220
35462437-8	2022	RESULTS: The expressions of genes related to keratinisation (LCE, PSORS1C2, IVL, and KRT17), triglyceride synthesis and storage (PLIN2, DGAT2, and CIDEA), wax synthesis (FAR2), ceramide synthesis (GBA2, SMPD3, and SPTLC3), antimicrobial peptides (DEFB1), and intercellular adhesion (CDSN), all of which are related to the skin barrier, are lower in children with AD than in healthy children.	Ceramides	177-185	perilipin 2	Homo sapiens	129-134
35421371-5	2022	Lipid analysis of VAP-A-knockdown EVs revealed reductions in the EV biogenesis lipid ceramide.	Ceramides	85-93	VAMP associated protein A	Homo sapiens	18-23
35421371-6	2022	Knockdown of the VAP-A-binding ceramide transfer protein CERT led to similar defects in EV RNA content.	Ceramides	31-39	VAMP associated protein A	Homo sapiens	17-22
35421371-6	2022	Knockdown of the VAP-A-binding ceramide transfer protein CERT led to similar defects in EV RNA content.	Ceramides	31-39	ceramide transporter 1	Homo sapiens	57-61
35421371-7	2022	Imaging experiments revealed that VAP-A promotes luminal filling of multivesicular bodies (MVBs), CERT localizes to MVBs, and the ceramide-generating enzyme neutral sphingomyelinase 2 colocalizes with VAP-A-positive ER.	Ceramides	130-138	sphingomyelin phosphodiesterase 3	Homo sapiens	157-183
35421371-7	2022	Imaging experiments revealed that VAP-A promotes luminal filling of multivesicular bodies (MVBs), CERT localizes to MVBs, and the ceramide-generating enzyme neutral sphingomyelinase 2 colocalizes with VAP-A-positive ER.	Ceramides	130-138	VAMP associated protein A	Homo sapiens	201-206
35421371-8	2022	We propose that ceramide transfer via VAP-A-CERT linkages drives the biogenesis of a select RNA-containing EV population.	Ceramides	16-24	VAMP associated protein A	Homo sapiens	38-43
35421371-8	2022	We propose that ceramide transfer via VAP-A-CERT linkages drives the biogenesis of a select RNA-containing EV population.	Ceramides	16-24	ceramide transporter 1	Homo sapiens	44-48
35260314-0	2022	Association between KLF6 rs3750861 polymorphism and plasma ceramide concentrations in post-menopausal women with type 2 diabetes.	Ceramides	59-67	Kruppel like factor 6	Homo sapiens	20-24
35260314-7	2022	CONCLUSIONS: The C/T or T/T genotypes of rs3750861 in the KLF6 gene were closely associated with higher levels of specific plasma ceramides in post-menopausal women with T2DM.	Ceramides	130-139	Kruppel like factor 6	Homo sapiens	58-62
35462437-8	2022	RESULTS: The expressions of genes related to keratinisation (LCE, PSORS1C2, IVL, and KRT17), triglyceride synthesis and storage (PLIN2, DGAT2, and CIDEA), wax synthesis (FAR2), ceramide synthesis (GBA2, SMPD3, and SPTLC3), antimicrobial peptides (DEFB1), and intercellular adhesion (CDSN), all of which are related to the skin barrier, are lower in children with AD than in healthy children.	Ceramides	177-185	diacylglycerol O-acyltransferase 2	Homo sapiens	136-141
35462437-8	2022	RESULTS: The expressions of genes related to keratinisation (LCE, PSORS1C2, IVL, and KRT17), triglyceride synthesis and storage (PLIN2, DGAT2, and CIDEA), wax synthesis (FAR2), ceramide synthesis (GBA2, SMPD3, and SPTLC3), antimicrobial peptides (DEFB1), and intercellular adhesion (CDSN), all of which are related to the skin barrier, are lower in children with AD than in healthy children.	Ceramides	177-185	cell death inducing DFFA like effector a	Homo sapiens	147-152
35443029-0	2022	Ceramide-induced integrated stress response overcomes Bcl-2 inhibitor resistance in acute myeloid leukemia.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	54-59
35134389-1	2022	Neutral ceramidase is a hydrolase of ceramide that has been implicated in multiple biologic processes, including inflammation and oncogenesis.	Ceramides	37-45	N-acylsphingosine amidohydrolase 2	Homo sapiens	0-18
35134389-6	2022	To better understand the function of ceramide, biochemical and cellular assays for enzymatic activity were developed and validated to identify inhibitors of human neutral ceramidase (nCDase).	Ceramides	37-45	N-acylsphingosine amidohydrolase 2	Homo sapiens	163-181
35439525-10	2022	The Degs2 and Fa2h genes, which are responsible for ceramide hydroxylation, were expressed in the purified intercalated cells.	Ceramides	52-60	delta(4)-desaturase, sphingolipid 2	Mus musculus	4-9
35134389-6	2022	To better understand the function of ceramide, biochemical and cellular assays for enzymatic activity were developed and validated to identify inhibitors of human neutral ceramidase (nCDase).	Ceramides	37-45	N-acylsphingosine amidohydrolase 2	Homo sapiens	183-189
35439525-10	2022	The Degs2 and Fa2h genes, which are responsible for ceramide hydroxylation, were expressed in the purified intercalated cells.	Ceramides	52-60	fatty acid 2-hydroxylase	Mus musculus	14-18
35061523-3	2022	Rather, insulin resistance is caused, at least in part, by the presence of high concentrations of harmful lipid metabolites, such as diacylglycerols and ceramides in muscle.	Ceramides	153-162	insulin	Homo sapiens	8-15
35422650-0	2022	alpha-Lipoic Acid Reduces Ceramide Synthesis and Neuroinflammation in the Hypothalamus of Insulin-Resistant Rats, While in the Cerebral Cortex Diminishes the beta-Amyloid Accumulation.	Ceramides	26-34	insulin	Homo sapiens	90-97
35409383-1	2022	The ceramide transport protein (CERT) delivers ceramide from the endoplasmic reticulum (ER) to the Golgi apparatus, where ceramide is converted to sphingomyelin (SM).	Ceramides	47-55	ceramide transporter 1	Homo sapiens	4-30
35409383-1	2022	The ceramide transport protein (CERT) delivers ceramide from the endoplasmic reticulum (ER) to the Golgi apparatus, where ceramide is converted to sphingomyelin (SM).	Ceramides	47-55	ceramide transporter 1	Homo sapiens	32-36
35409383-1	2022	The ceramide transport protein (CERT) delivers ceramide from the endoplasmic reticulum (ER) to the Golgi apparatus, where ceramide is converted to sphingomyelin (SM).	Ceramides	122-130	ceramide transporter 1	Homo sapiens	4-30
35409383-1	2022	The ceramide transport protein (CERT) delivers ceramide from the endoplasmic reticulum (ER) to the Golgi apparatus, where ceramide is converted to sphingomyelin (SM).	Ceramides	122-130	ceramide transporter 1	Homo sapiens	32-36
35409383-7	2022	Moreover, we found that de novo synthesis of SM with very-long acyl chains preferentially increases via a CERT-independent mechanism under hyperosmotic-stressed cells, providing an insight into a CERT-independent ceramide transport pathway for de novo synthesis of SM.	Ceramides	213-221	ceramide transporter 1	Homo sapiens	196-200
35409370-3	2022	A ceramide-S1P rheostat regulates ROS-induced mitochondrial dysfunction, apoptotic/anti-apoptotic Bcl-2 family proteins and signaling pathways, leading to apoptosis, survival, cell proliferation, inflammation and fibrosis in the kidney.	Ceramides	2-10	BCL2 apoptosis regulator	Homo sapiens	98-103
35409370-4	2022	Ceramide inhibits the mitochondrial respiration chain and induces ceramide channel formation and the closure of voltage-dependent anion channels, leading to mitochondrial dysfunction, altered Bcl-2 family protein expression, ROS generation and disturbed calcium homeostasis.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	192-197
35409370-9	2022	Thus, a ceramide-SphKs/S1P rheostat modulates oxidant-induced kidney injury by affecting mitochondrial function, ROS production, Bcl-2 family proteins, calcium homeostasis and their downstream signaling pathways.	Ceramides	8-16	BCL2 apoptosis regulator	Homo sapiens	129-134
35373347-0	2022	Ectopic accumulation of ceramide in cardiomyocytes modulates alcoholic cardiomyopathy via the TLR4-dependent pathway.	Ceramides	24-32	toll-like receptor 4	Mus musculus	94-98
35373347-10	2022	As a ceramide precursor, PA induces intracellular ceramide generation through TLR4 signaling, which could be abolished by an inhibitor of ceramide synthesis.	Ceramides	5-13	toll-like receptor 4	Rattus norvegicus	78-82
35373347-10	2022	As a ceramide precursor, PA induces intracellular ceramide generation through TLR4 signaling, which could be abolished by an inhibitor of ceramide synthesis.	Ceramides	50-58	toll-like receptor 4	Rattus norvegicus	78-82
35373347-10	2022	As a ceramide precursor, PA induces intracellular ceramide generation through TLR4 signaling, which could be abolished by an inhibitor of ceramide synthesis.	Ceramides	138-146	toll-like receptor 4	Rattus norvegicus	78-82
35373347-11	2022	Furthermore, mechanistic investigations demonstrated that pharmacological or genetic inhibition of TLR4 attenuated PA-induced cell death and the corresponding ceramide production.	Ceramides	159-167	toll-like receptor 4	Rattus norvegicus	99-103
35373347-13	2022	CONCLUSIONS: Overall, our findings demonstrate that ceramide accumulation plays a crucial role in alcoholic cardiomyopathy, which was partially mediated through the TLR4-dependent pathway.	Ceramides	52-60	toll-like receptor 4	Mus musculus	165-169
35464162-3	2022	Here, its cytotoxic, cytostatic and apoptotic effects are investigated in combination with serine palmitoyltransferase (SPT), the first enzyme of de novo pathway of ceramide production, inhibitor myriocin on MOLM-13 and MV4-11 cells.	Ceramides	165-173	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	91-118
35065241-3	2022	In addition, LPS was shown to activate RhoA by inducing transient receptor potential channel 6 (TRPC6) overexpression and calcium influx through the ASMase/ceramide pathway, and activation of RhoA further induced the cytoskeletal rearrangement of PMVECs and destruction of intercellular junctions, ultimately leading to early acute PMVEC barrier dysfunction.	Ceramides	156-164	ras homolog family member A	Rattus norvegicus	39-43
35065241-3	2022	In addition, LPS was shown to activate RhoA by inducing transient receptor potential channel 6 (TRPC6) overexpression and calcium influx through the ASMase/ceramide pathway, and activation of RhoA further induced the cytoskeletal rearrangement of PMVECs and destruction of intercellular junctions, ultimately leading to early acute PMVEC barrier dysfunction.	Ceramides	156-164	transient receptor potential cation channel, subfamily C, member 6	Rattus norvegicus	56-94
35065241-3	2022	In addition, LPS was shown to activate RhoA by inducing transient receptor potential channel 6 (TRPC6) overexpression and calcium influx through the ASMase/ceramide pathway, and activation of RhoA further induced the cytoskeletal rearrangement of PMVECs and destruction of intercellular junctions, ultimately leading to early acute PMVEC barrier dysfunction.	Ceramides	156-164	transient receptor potential cation channel, subfamily C, member 6	Rattus norvegicus	96-101
35508055-4	2022	Recent studies revealed that patients with unstable coronary artery disease (CAD) presented increased plasma ceramide levels (especially C16, C18, and C24:1).	Ceramides	109-117	Bardet-Biedl syndrome 9	Homo sapiens	142-145
35464162-3	2022	Here, its cytotoxic, cytostatic and apoptotic effects are investigated in combination with serine palmitoyltransferase (SPT), the first enzyme of de novo pathway of ceramide production, inhibitor myriocin on MOLM-13 and MV4-11 cells.	Ceramides	165-173	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	120-123
35181339-0	2022	Fatty acid transport protein 2 interacts with ceramide synthase 2 to promote ceramide synthesis.	Ceramides	77-85	solute carrier family 27 (fatty acid transporter), member 2	Mus musculus	0-30
35065241-4	2022	However, regarding apoptosis-dependent delayed barrier dysfunction, the ceramide-induced de novo synthesis pathway in paracellular cells induced the apoptosis of PMVECs, in which Txnip overexpression inhibited Trx activity and subsequently activated ASK1 in the context of LPS-induced PMVEC apoptosis, acting upstream of the ceramide-induced activation of p38 MAPK and JNK.	Ceramides	72-80	thioredoxin interacting protein	Rattus norvegicus	179-184
35065241-4	2022	However, regarding apoptosis-dependent delayed barrier dysfunction, the ceramide-induced de novo synthesis pathway in paracellular cells induced the apoptosis of PMVECs, in which Txnip overexpression inhibited Trx activity and subsequently activated ASK1 in the context of LPS-induced PMVEC apoptosis, acting upstream of the ceramide-induced activation of p38 MAPK and JNK.	Ceramides	72-80	thioredoxin 1	Rattus norvegicus	210-213
35065241-4	2022	However, regarding apoptosis-dependent delayed barrier dysfunction, the ceramide-induced de novo synthesis pathway in paracellular cells induced the apoptosis of PMVECs, in which Txnip overexpression inhibited Trx activity and subsequently activated ASK1 in the context of LPS-induced PMVEC apoptosis, acting upstream of the ceramide-induced activation of p38 MAPK and JNK.	Ceramides	72-80	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	250-254
35065241-4	2022	However, regarding apoptosis-dependent delayed barrier dysfunction, the ceramide-induced de novo synthesis pathway in paracellular cells induced the apoptosis of PMVECs, in which Txnip overexpression inhibited Trx activity and subsequently activated ASK1 in the context of LPS-induced PMVEC apoptosis, acting upstream of the ceramide-induced activation of p38 MAPK and JNK.	Ceramides	72-80	mitogen-activated protein kinase 8	Rattus norvegicus	369-372
35065241-4	2022	However, regarding apoptosis-dependent delayed barrier dysfunction, the ceramide-induced de novo synthesis pathway in paracellular cells induced the apoptosis of PMVECs, in which Txnip overexpression inhibited Trx activity and subsequently activated ASK1 in the context of LPS-induced PMVEC apoptosis, acting upstream of the ceramide-induced activation of p38 MAPK and JNK.	Ceramides	325-333	thioredoxin interacting protein	Rattus norvegicus	179-184
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	52-60	thioredoxin interacting protein	Rattus norvegicus	157-162
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	52-60	thioredoxin 1	Rattus norvegicus	163-166
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	52-60	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	167-171
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	52-60	mitogen activated protein kinase 14	Rattus norvegicus	172-175
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	74-82	thioredoxin interacting protein	Rattus norvegicus	157-162
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	74-82	thioredoxin 1	Rattus norvegicus	163-166
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	74-82	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	167-171
35181339-0	2022	Fatty acid transport protein 2 interacts with ceramide synthase 2 to promote ceramide synthesis.	Ceramides	77-85	ceramide synthase 2	Mus musculus	46-65
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	74-82	mitogen activated protein kinase 14	Rattus norvegicus	172-175
35065241-5	2022	At the same time, in rats with LPS- or exogenous C8 ceramide-induced ALI, ceramide was demonstrated to play an important role in lung injury by inducing the Txnip/TRX/ASK1/P38 and JNK pathways.	Ceramides	74-82	mitogen-activated protein kinase 8	Rattus norvegicus	180-183
35065241-6	2022	Thus, the Txnip/TRX/ASK1/p38 and JNK pathways might be involved in ceramide-mediated PMVEC apoptosis in LPS-induced ALI.	Ceramides	67-75	thioredoxin interacting protein	Rattus norvegicus	10-15
35181339-6	2022	In addition, transfection of cells with FATP1, FATP2 or FATP4 increased ceramide levels although only FATP2 and 4 increased dihydroceramide levels, consistent with their known intracellular locations.	Ceramides	72-80	solute carrier family 27 (fatty acid transporter), member 1	Mus musculus	40-45
35065241-6	2022	Thus, the Txnip/TRX/ASK1/p38 and JNK pathways might be involved in ceramide-mediated PMVEC apoptosis in LPS-induced ALI.	Ceramides	67-75	thioredoxin 1	Rattus norvegicus	16-19
35181339-6	2022	In addition, transfection of cells with FATP1, FATP2 or FATP4 increased ceramide levels although only FATP2 and 4 increased dihydroceramide levels, consistent with their known intracellular locations.	Ceramides	72-80	solute carrier family 27 (fatty acid transporter), member 2	Mus musculus	47-52
35065241-6	2022	Thus, the Txnip/TRX/ASK1/p38 and JNK pathways might be involved in ceramide-mediated PMVEC apoptosis in LPS-induced ALI.	Ceramides	67-75	mitogen-activated protein kinase kinase kinase 5	Rattus norvegicus	20-24
35065241-6	2022	Thus, the Txnip/TRX/ASK1/p38 and JNK pathways might be involved in ceramide-mediated PMVEC apoptosis in LPS-induced ALI.	Ceramides	67-75	mitogen activated protein kinase 14	Rattus norvegicus	25-28
35181339-6	2022	In addition, transfection of cells with FATP1, FATP2 or FATP4 increased ceramide levels although only FATP2 and 4 increased dihydroceramide levels, consistent with their known intracellular locations.	Ceramides	72-80	solute carrier family 27 (fatty acid transporter), member 4	Mus musculus	56-61
35065241-6	2022	Thus, the Txnip/TRX/ASK1/p38 and JNK pathways might be involved in ceramide-mediated PMVEC apoptosis in LPS-induced ALI.	Ceramides	67-75	mitogen-activated protein kinase 8	Rattus norvegicus	33-36
35470585-5	2022	Within-tissue analysis showed higher mean levels of ceramide species linked to insulin resistance, such as Cer(d18:1/18:0) and Cer(d18:1/16:0), in visceral tissue of prediabetic/diabetic patients compared with nondiabetic subjects and higher content of Cer(d18:1/14:0) in subcutaneous tissue of insulin-resistant female patients compared with prediabetic/diabetic males.	Ceramides	52-60	insulin	Homo sapiens	79-86
35470585-5	2022	Within-tissue analysis showed higher mean levels of ceramide species linked to insulin resistance, such as Cer(d18:1/18:0) and Cer(d18:1/16:0), in visceral tissue of prediabetic/diabetic patients compared with nondiabetic subjects and higher content of Cer(d18:1/14:0) in subcutaneous tissue of insulin-resistant female patients compared with prediabetic/diabetic males.	Ceramides	52-60	insulin	Homo sapiens	295-302
35470585-6	2022	Statistically significant differences in mean levels of ceramide species between insulin-resistant African American and insulin-resistant Caucasian patients were not evident in visceral or subcutaneous tissue.	Ceramides	56-64	insulin	Homo sapiens	81-88
35470585-6	2022	Statistically significant differences in mean levels of ceramide species between insulin-resistant African American and insulin-resistant Caucasian patients were not evident in visceral or subcutaneous tissue.	Ceramides	56-64	insulin	Homo sapiens	120-127
35470585-8	2022	Knowledge of the accumulated ceramides/dihydroceramides may reflect on the prelipolytic state that leads the lipotoxic phase of insulin resistance and may shed light on the predisposition to insulin resistance by gender.	Ceramides	29-38	insulin	Homo sapiens	128-135
35470585-8	2022	Knowledge of the accumulated ceramides/dihydroceramides may reflect on the prelipolytic state that leads the lipotoxic phase of insulin resistance and may shed light on the predisposition to insulin resistance by gender.	Ceramides	29-38	insulin	Homo sapiens	191-198
35066761-2	2022	Recent studies provide data that ceramide metabolism impairment may play a role in the pathogenesis of synucleinopathies due to its influence on alpha-synuclein accumulation.	Ceramides	33-41	synuclein alpha	Homo sapiens	145-160
35360085-1	2022	Alkaline sphingomyelinase (alk-SMase) is phospholipase that creates ceramides and inactivates platelet activating factors during metabolism, and is linked to digestion and cancer prevention.	Ceramides	68-77	ectonucleotide pyrophosphatase/phosphodiesterase 7	Mus musculus	27-36
35365625-8	2022	Ceramide synthesis through the ceramide synthase 2 de novo pathway is regulated by UPR kinase Perk.	Ceramides	0-8	ceramide synthase 2	Mus musculus	31-50
35365625-8	2022	Ceramide synthesis through the ceramide synthase 2 de novo pathway is regulated by UPR kinase Perk.	Ceramides	0-8	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	94-98
35365625-9	2022	Inactivation of CerS2 in mice reduces systemic and muscle ceramide signals and muscle UPR activation.	Ceramides	58-66	ceramide synthase 2	Mus musculus	16-21
35409270-8	2022	Epidermal lipid analysis revealed that the ceramide level was significantly higher upon application of the NHE1 activator cream on 3D-cultured skin, compared to application of a vehicle cream.	Ceramides	43-51	solute carrier family 9 member A1	Homo sapiens	107-111
35351872-7	2022	AdipoRon ameliorated insulin resistance, fibrosis, M1-dominant inflammation, and apoptosis in association with reduced accumulations of free fatty acid, triglycerides, and TLR4-related ceramide in the heart.	Ceramides	185-193	toll-like receptor 4	Mus musculus	172-176
35351872-10	2022	It also increased acid ceramidase activity which reduced ceramide and increased sphingosine-1 phosphate levels in the heart of db/db mice and cultured human cardiomyocytes.	Ceramides	57-65	N-acylsphingosine amidohydrolase 1	Mus musculus	18-33
35406045-0	2022	Effects of Isocaloric Fructose Restriction on Ceramide Levels in Children with Obesity and Cardiometabolic Risk: Relation to Hepatic De Novo Lipogenesis and Insulin Sensitivity.	Ceramides	46-54	insulin	Homo sapiens	157-164
35406045-3	2022	Ceramides are bioactive sphingolipids whose dysregulated metabolism contribute to lipotoxicity, insulin resistance, and CMR.	Ceramides	0-9	insulin	Homo sapiens	96-103
35406045-8	2022	Change in each primary ceramide species correlated negatively with composite insulin sensitivity index (CISI).	Ceramides	23-31	insulin	Homo sapiens	77-84
35406045-10	2022	These results suggest that ceramides decrease in response to dietary fructose restriction, negatively correlate with insulin sensitivity, and may represent an intermediary link between hepatic DNL, insulin resistance, and CMR.	Ceramides	27-36	insulin	Homo sapiens	117-124
35406045-10	2022	These results suggest that ceramides decrease in response to dietary fructose restriction, negatively correlate with insulin sensitivity, and may represent an intermediary link between hepatic DNL, insulin resistance, and CMR.	Ceramides	27-36	insulin	Homo sapiens	198-205
35254894-4	2022	Loss of beta cell FIT2 and LDs reduces insulin secretion, increases intracellular ceramides, stimulates ER stress, and exacerbates diet-induced diabetes in mice.	Ceramides	82-91	fat storage-inducing transmembrane protein 2	Mus musculus	18-22
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.	Ceramides	169-177	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.	Ceramides	169-177	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.	Ceramides	169-177	glucosylceramidase beta	Homo sapiens	83-101
35328730-5	2022	miRNAs play a part in modifying the expression of cardiac transcription factors (miR-335-5p), increasing cell cycle trigger factors (miR-126-3p), interfering with ceramide synthesis (miR-320a), inducing apoptosis (miR-634 and miR-122), suppressing production of interleukins (miR-217), and reducing cell proliferation (miR-218).	Ceramides	163-171	microRNA 320a	Homo sapiens	183-191
35294243-3	2022	Here, we demonstrate that following membrane perforation by bacterial cholesterol-dependent cytolysins, calcium influx activates mixed lineage kinase 3 independently of protein kinase C or ceramide generation.	Ceramides	189-197	mitogen-activated protein kinase kinase kinase 11	Homo sapiens	129-151
35241663-1	2022	The acid sphingomyelinase (ASM)/ceramide system may provide a useful framework for better understanding SARS-CoV-2 infection and the repurposing of psychotropic medications functionally inhibiting the acid sphingomyelinase/ceramide system (named FIASMA psychotropic medications) against COVID-19.	Ceramides	32-40	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
35370720-16	2022	Impressively, NGR1 inhibited the synthesis of diacylglycerol (DAG) and ceramide and promoted fatty acid oxidation (FAO) in vivo.	Ceramides	71-79	reticulon 4 receptor	Mus musculus	14-18
35370720-17	2022	Moreover, NGR1 significantly promoted expression of CPT-1A, the key enzyme in FAO pathway, and down-regulated the expression of GPAT and SPT, which were the key enzymes catalyzing production of DAG and ceramide.	Ceramides	202-210	reticulon 4 receptor	Mus musculus	10-14
35370720-17	2022	Moreover, NGR1 significantly promoted expression of CPT-1A, the key enzyme in FAO pathway, and down-regulated the expression of GPAT and SPT, which were the key enzymes catalyzing production of DAG and ceramide.	Ceramides	202-210	glycerol-3-phosphate acyltransferase, mitochondrial	Rattus norvegicus	128-132
35241663-1	2022	The acid sphingomyelinase (ASM)/ceramide system may provide a useful framework for better understanding SARS-CoV-2 infection and the repurposing of psychotropic medications functionally inhibiting the acid sphingomyelinase/ceramide system (named FIASMA psychotropic medications) against COVID-19.	Ceramides	32-40	sphingomyelin phosphodiesterase 1	Homo sapiens	27-30
35241663-1	2022	The acid sphingomyelinase (ASM)/ceramide system may provide a useful framework for better understanding SARS-CoV-2 infection and the repurposing of psychotropic medications functionally inhibiting the acid sphingomyelinase/ceramide system (named FIASMA psychotropic medications) against COVID-19.	Ceramides	32-40	sphingomyelin phosphodiesterase 1	Homo sapiens	201-222
35241663-1	2022	The acid sphingomyelinase (ASM)/ceramide system may provide a useful framework for better understanding SARS-CoV-2 infection and the repurposing of psychotropic medications functionally inhibiting the acid sphingomyelinase/ceramide system (named FIASMA psychotropic medications) against COVID-19.	Ceramides	223-231	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
35241663-1	2022	The acid sphingomyelinase (ASM)/ceramide system may provide a useful framework for better understanding SARS-CoV-2 infection and the repurposing of psychotropic medications functionally inhibiting the acid sphingomyelinase/ceramide system (named FIASMA psychotropic medications) against COVID-19.	Ceramides	223-231	sphingomyelin phosphodiesterase 1	Homo sapiens	27-30
35241663-1	2022	The acid sphingomyelinase (ASM)/ceramide system may provide a useful framework for better understanding SARS-CoV-2 infection and the repurposing of psychotropic medications functionally inhibiting the acid sphingomyelinase/ceramide system (named FIASMA psychotropic medications) against COVID-19.	Ceramides	223-231	sphingomyelin phosphodiesterase 1	Homo sapiens	201-222
35066602-10	2022	Positive associations of ceramide C22:0/C24:0 and their precursors with homeostasis model assessment of insulin resistance suggested that the synthesis of the ceramides might be involved in insulin resistance.	Ceramides	25-33	insulin	Homo sapiens	104-111
35066602-10	2022	Positive associations of ceramide C22:0/C24:0 and their precursors with homeostasis model assessment of insulin resistance suggested that the synthesis of the ceramides might be involved in insulin resistance.	Ceramides	25-33	insulin	Homo sapiens	190-197
35066602-10	2022	Positive associations of ceramide C22:0/C24:0 and their precursors with homeostasis model assessment of insulin resistance suggested that the synthesis of the ceramides might be involved in insulin resistance.	Ceramides	159-168	insulin	Homo sapiens	104-111
35066602-10	2022	Positive associations of ceramide C22:0/C24:0 and their precursors with homeostasis model assessment of insulin resistance suggested that the synthesis of the ceramides might be involved in insulin resistance.	Ceramides	159-168	insulin	Homo sapiens	190-197
35060604-5	2022	Clustering and integration of CFTR into ceramide-rich platforms are abolished by the disease mutations F508del and S13F and rescued by the CFTR modulators elexacaftor+tezacaftor.	Ceramides	40-48	CF transmembrane conductance regulator	Homo sapiens	30-34
35060604-5	2022	Clustering and integration of CFTR into ceramide-rich platforms are abolished by the disease mutations F508del and S13F and rescued by the CFTR modulators elexacaftor+tezacaftor.	Ceramides	40-48	CF transmembrane conductance regulator	Homo sapiens	139-143
35269833-9	2022	Nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX) is activated by DPE and results in increased ceramide production by sphingomyelinase activation in HDF.	Ceramides	111-119	dual oxidase 2	Homo sapiens	0-59
35151662-4	2022	For example, neutral ceramidase (nCDase) is an enzyme responsible for converting ceramide into sphingosine, which is then phosphorylated to become sphingosine-1-phosphate, and our lab previously demonstrated that nCDase knockout (nCDase-/-) in mouse embryonic fibroblasts led to resistance to nutrient and energy deprivation-induced cell death via upregulation of autophagic flux.	Ceramides	81-89	N-acylsphingosine amidohydrolase 2	Mus musculus	13-31
35151662-4	2022	For example, neutral ceramidase (nCDase) is an enzyme responsible for converting ceramide into sphingosine, which is then phosphorylated to become sphingosine-1-phosphate, and our lab previously demonstrated that nCDase knockout (nCDase-/-) in mouse embryonic fibroblasts led to resistance to nutrient and energy deprivation-induced cell death via upregulation of autophagic flux.	Ceramides	81-89	N-acylsphingosine amidohydrolase 2	Mus musculus	33-39
35151662-4	2022	For example, neutral ceramidase (nCDase) is an enzyme responsible for converting ceramide into sphingosine, which is then phosphorylated to become sphingosine-1-phosphate, and our lab previously demonstrated that nCDase knockout (nCDase-/-) in mouse embryonic fibroblasts led to resistance to nutrient and energy deprivation-induced cell death via upregulation of autophagic flux.	Ceramides	81-89	N-acylsphingosine amidohydrolase 2	Mus musculus	213-219
35151662-4	2022	For example, neutral ceramidase (nCDase) is an enzyme responsible for converting ceramide into sphingosine, which is then phosphorylated to become sphingosine-1-phosphate, and our lab previously demonstrated that nCDase knockout (nCDase-/-) in mouse embryonic fibroblasts led to resistance to nutrient and energy deprivation-induced cell death via upregulation of autophagic flux.	Ceramides	81-89	N-acylsphingosine amidohydrolase 2	Mus musculus	230-236
35269833-10	2022	We identified that ceramide-1-phosphate (C1P) (produced from ceramide by ceramide kinase activation) activates MMP-1 and MMP-3 through activation of arachidonate cascade, followed by STAT 1- and STAT 3-dependent transcriptional activation.	Ceramides	61-69	matrix metallopeptidase 1	Homo sapiens	111-116
35330102-0	2022	Inhibition of Ceramide Glycosylation Enhances Cisplatin Sensitivity in Cholangiocarcinoma by Limiting the Activation of the ERK Signaling Pathway.	Ceramides	14-22	mitogen-activated protein kinase 1	Homo sapiens	124-127
35269833-10	2022	We identified that ceramide-1-phosphate (C1P) (produced from ceramide by ceramide kinase activation) activates MMP-1 and MMP-3 through activation of arachidonate cascade, followed by STAT 1- and STAT 3-dependent transcriptional activation.	Ceramides	61-69	matrix metallopeptidase 3	Homo sapiens	121-126
35015730-0	2022	Inhibition of ceramide accumulation in AdipoR1-/- mice increases photoreceptor survival and improves vision.	Ceramides	14-22	adiponectin receptor 1	Mus musculus	39-46
35015730-5	2022	We discovered an accumulation of ceramides in the AdipoR1-/- retina, likely due to insufficient ceramidase activity for healthy retina function, resulting in photoreceptor death.	Ceramides	33-42	adiponectin receptor 1	Homo sapiens	50-57
35015730-9	2022	These results highlight the importance of ADIPOR1 ceramidase in the retina, and show that pharmacological inhibition of ceramide generation can provide a therapeutic strategy for ADIPOR1-related retinopathy.	Ceramides	120-128	adiponectin receptor 1	Mus musculus	42-49
35015730-9	2022	These results highlight the importance of ADIPOR1 ceramidase in the retina, and show that pharmacological inhibition of ceramide generation can provide a therapeutic strategy for ADIPOR1-related retinopathy.	Ceramides	120-128	adiponectin receptor 1	Mus musculus	179-186
35181782-0	2022	Lysosomal ceramides regulate Cathepsin B-mediated processing of saposin C and glucocerebrosidase activity.	Ceramides	10-19	cathepsin B	Homo sapiens	29-40
35184720-4	2022	In the past decade, ceramides have gained attention due to their accumulation in certain tissues and their suggested role in initiating insulin resistance.	Ceramides	20-29	insulin	Homo sapiens	136-143
35184720-5	2022	This study aims to determine the association of specific ceramides and their major metabolizing enzymes with obesity-associated insulin resistance.	Ceramides	57-66	insulin	Homo sapiens	128-135
35181782-5	2022	Here, we found that ceramide activates cathepsin B, and identified a novel role for cathepsin B in mediating prosaposin cleavage to form saposin C, the lysosomal coactivator of GCase.	Ceramides	20-28	cathepsin B	Homo sapiens	39-50
35181782-5	2022	Here, we found that ceramide activates cathepsin B, and identified a novel role for cathepsin B in mediating prosaposin cleavage to form saposin C, the lysosomal coactivator of GCase.	Ceramides	20-28	cathepsin B	Homo sapiens	84-95
35181782-7	2022	Conversely, increasing ceramide production by inhibiting acid ceramidase activity, was sufficient to upregulate cathepsin B and saposin C-mediated activation of GCase.	Ceramides	23-31	cathepsin B	Homo sapiens	112-123
35216212-0	2022	Natural Ligand-Mimetic and Nonmimetic Inhibitors of the Ceramide Transport Protein CERT.	Ceramides	56-64	ceramide transporter 1	Homo sapiens	83-87
35203316-3	2022	Acid sphingomyelinase (ASMase) hydrolyzes sphingomyelin into ceramide and phosphorylcholine.	Ceramides	61-69	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
35203316-3	2022	Acid sphingomyelinase (ASMase) hydrolyzes sphingomyelin into ceramide and phosphorylcholine.	Ceramides	61-69	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
35203316-8	2022	We hypothesized that imipramine could decrease hippocampal neuronal death by reducing ceramide via the inhibition of ASMase after hypoglycemia.	Ceramides	86-94	sphingomyelin phosphodiesterase 1	Homo sapiens	117-123
35216212-3	2022	The ceramide transport protein CERT, a typical LTP, mediates the ER-to-Golgi transport of ceramide at an ER-distal Golgi membrane contact zone.	Ceramides	4-12	ceramide transporter 1	Homo sapiens	31-35
35216212-3	2022	The ceramide transport protein CERT, a typical LTP, mediates the ER-to-Golgi transport of ceramide at an ER-distal Golgi membrane contact zone.	Ceramides	90-98	ceramide transporter 1	Homo sapiens	31-35
35216212-5	2022	Since then, various ceramide-resembling compounds have been found to act as CERT inhibitors.	Ceramides	20-28	ceramide transporter 1	Homo sapiens	76-80
35159039-5	2022	The high S1P:Ceramide intracellular ratio in MM cells protected c-Myc protein stability in a PP2A-dependent manner.	Ceramides	13-21	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	64-69
35222477-4	2022	Next, the remodeling enzyme Per1p (Post-Glycosylphosphatidylinositol Attachment to Proteins phospholipase 3 -PGAP3- in mammals) removes a short, unsaturated fatty acid of phosphatidylinositol (PI) that is replaced with a very long-chain saturated fatty acid or ceramide to complete lipid remodeling.	Ceramides	261-269	1-cysteine peroxiredoxin 1	Arabidopsis thaliana	28-33
35211530-10	2022	Conclusions: Our findings demonstrated that ceramide metabolism disturbance might play a vital role in TAD development by aggravating aortic inflammation through the NLRP3 pathway, possibly providing a new target for pharmacological therapy and a potential biomarker of TAD.	Ceramides	44-52	NLR family pyrin domain containing 3	Homo sapiens	166-171
35159039-5	2022	The high S1P:Ceramide intracellular ratio in MM cells protected c-Myc protein stability in a PP2A-dependent manner.	Ceramides	13-21	protein phosphatase 2 phosphatase activator	Homo sapiens	93-97
35111371-1	2022	Ceramide is a core molecule of sphingolipid metabolism that causes selective insulin resistance and dyslipidemia.	Ceramides	0-8	insulin	Homo sapiens	77-84
35059910-2	2022	However, how resveratrol exerts its anti-leukemic actions by modulating anti-apoptotic ceramide catabolism enzymes, mainly sphingosine kinase (SK-1) and glucosylceramide synthase (GCS), in FLT3-ITD AML remains unclear.	Ceramides	87-95	sphingosine kinase 1	Homo sapiens	143-147
35104807-0	2022	Sortilin drives hypertension by modulating sphingolipid/ceramide homeostasis and by triggering oxidative stress.	Ceramides	56-64	sortilin 1	Homo sapiens	0-8
35104807-6	2022	Mechanistically, they demonstrate that sortilin altered sphingolipid/ceramide homeostasis, initiating a signaling cascade that, from sphingosine-1-phosphate (S1P), leads to the augmented production of reactive oxygen species.	Ceramides	69-77	sortilin 1	Homo sapiens	39-47
35059910-2	2022	However, how resveratrol exerts its anti-leukemic actions by modulating anti-apoptotic ceramide catabolism enzymes, mainly sphingosine kinase (SK-1) and glucosylceramide synthase (GCS), in FLT3-ITD AML remains unclear.	Ceramides	87-95	UDP-glucose ceramide glucosyltransferase	Homo sapiens	153-178
35054078-8	2022	Sphingolipids are known to be a modulator of insulin resistance, and our results indicate that ceramide measurements in early pregnancy may help with GDM screening.	Ceramides	95-103	insulin	Homo sapiens	45-52
35053491-8	2022	Amb544925 and ceramide increased SMPD4 expression and suppressed surivivin expression.	Ceramides	14-22	sphingomyelin phosphodiesterase 4	Mus musculus	33-38
35053491-11	2022	CONCLUSIONS: The plant-derived CTL1 inhibitor Amb544925 is a lead compound of a new anticancer agent exhibiting antitumor effects and inhibition of cell migration through the ceramide/survivin pathway.	Ceramides	175-183	solute carrier family 44, member 1	Mus musculus	31-35
35053491-11	2022	CONCLUSIONS: The plant-derived CTL1 inhibitor Amb544925 is a lead compound of a new anticancer agent exhibiting antitumor effects and inhibition of cell migration through the ceramide/survivin pathway.	Ceramides	175-183	baculoviral IAP repeat-containing 5	Mus musculus	184-192
2730890-9	1989	In analogy to the findings in vivo, in the Hep-G2 cells more 16:0, 18:0 and 24:0 ceramides were converted to sphingomyelin than 18:1 or 18:2 ceramides.	Ceramides	81-90	DNL-type zinc finger	Homo sapiens	43-46
35005872-4	2022	Lipidomic analysis of UV-exposed skin showed shifts to the composition of ceramide subclasses essential in repairing and strengthening the SC barrier (including CER1(EOS), CER3(NP), and CER6(AP)) and reduced very long-chain acyl moieties.	Ceramides	74-82	cerberus 1, DAN family BMP antagonist	Homo sapiens	161-165
35005872-5	2022	Gene expression analysis and immunohistochemical staining of key enzymes (aSMase, DES1, CerS5, CerS3) suggested that lipid alterations can be attributed to changes within the ceramide biosynthesis process.	Ceramides	175-183	ceramide synthase 3	Homo sapiens	95-100
2730890-9	1989	In analogy to the findings in vivo, in the Hep-G2 cells more 16:0, 18:0 and 24:0 ceramides were converted to sphingomyelin than 18:1 or 18:2 ceramides.	Ceramides	141-150	DNL-type zinc finger	Homo sapiens	43-46
2666433-0	1989	Rapid method to detect shiga toxin and shiga-like toxin I based on binding to globotriosyl ceramide (Gb3), their natural receptor.	Ceramides	91-99	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	101-104
2666433-2	1989	These toxins have the same biologic activities and according to recent studies also share the same binding receptor, globotriosyl ceramide (Gb3).	Ceramides	130-138	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	140-143
2644572-2	1989	We have previously shown that this toxin specifically binds to a glycolipid receptor-globotriosyl ceramide (Gb3).	Ceramides	98-106	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	108-111
2426269-13	1986	Since the axis of ceramide, which is inserted in the lipid bilayer, is perpendicular to the plane of type 2 chain, the epitope recognized by the antibody KH1 is located at the external nonpolar surface of the carbohydrate chain that is overlaid on the lipid bilayer.	Ceramides	18-26	potassium voltage-gated channel modifier subfamily F member 1	Homo sapiens	154-157
3571286-6	1987	In addition, small amounts of lactotetraosylceramide, a blood group H-active triglycosylceramide with the structure of Fuc alpha 1-2Gal-Hex-Cer (where Fuc is fucose, Hex is hexose, and Cer is ceramide), and dihexosylceramides were identified in some cases.	Ceramides	44-52	hematopoietically expressed homeobox	Homo sapiens	136-139
3571286-6	1987	In addition, small amounts of lactotetraosylceramide, a blood group H-active triglycosylceramide with the structure of Fuc alpha 1-2Gal-Hex-Cer (where Fuc is fucose, Hex is hexose, and Cer is ceramide), and dihexosylceramides were identified in some cases.	Ceramides	44-52	hematopoietically expressed homeobox	Homo sapiens	166-169
3928791-11	1985	2-Hydroxy-C16 fatty acid was a major component of one of the ceramide monohexosides.	Ceramides	61-69	galectin 1B	Gallus gallus	10-13
4086474-7	1985	The epithelial mono- and diglycosylceramide compounds had an unusual ceramide composition with mainly C18 and C20 trihydroxy long chain bases in combination with C22-C24 hydroxy fatty acids in contrast to the non-epithelial glycolipids which contained mainly C18 dihydroxy long chain bases in combination with C16-C24 non-hydroxy fatty acids.	Ceramides	35-43	Bardet-Biedl syndrome 9	Homo sapiens	102-105
4086474-7	1985	The epithelial mono- and diglycosylceramide compounds had an unusual ceramide composition with mainly C18 and C20 trihydroxy long chain bases in combination with C22-C24 hydroxy fatty acids in contrast to the non-epithelial glycolipids which contained mainly C18 dihydroxy long chain bases in combination with C16-C24 non-hydroxy fatty acids.	Ceramides	35-43	Bardet-Biedl syndrome 9	Homo sapiens	259-262
2409238-6	1985	Increased molar proportions of ceramide tri- and tetra-saccharides occurred in the two glioma lines which had the greatest increases in NK resistance following IFN exposure.	Ceramides	31-39	interferon alpha 1	Homo sapiens	160-163
4009062-6	1985	Free ceramide content of CDA-II erythrocytes was two times greater than the control value and the fatty acid composition was also altered.	Ceramides	5-13	SEC23 homolog B, COPII coat complex component	Homo sapiens	25-31
3967657-5	1985	In addition, we have observed that threo-sphingosine C-5 and C-4 of ceramide and D-glucosyl-ceramide resonate near 129.5 ppm and 133.5 ppm, respectively, with a signal separation of about 4 ppm.	Ceramides	68-76	complement C5	Homo sapiens	53-56
3967657-5	1985	In addition, we have observed that threo-sphingosine C-5 and C-4 of ceramide and D-glucosyl-ceramide resonate near 129.5 ppm and 133.5 ppm, respectively, with a signal separation of about 4 ppm.	Ceramides	68-76	complement C4A (Rodgers blood group)	Homo sapiens	61-64
6853556-4	1983	Sugar analysis reveals that all 11 gangliosides contain the same base structure, Gal(beta 1-3)GalNAc(beta 1-4)Gal(beta 1-4)Glc(beta 1-1) ceramide, which is gangliotetraosylceramide.	Ceramides	137-145	hemoglobin, beta adult major chain	Mus musculus	85-91
6853556-4	1983	Sugar analysis reveals that all 11 gangliosides contain the same base structure, Gal(beta 1-3)GalNAc(beta 1-4)Gal(beta 1-4)Glc(beta 1-1) ceramide, which is gangliotetraosylceramide.	Ceramides	137-145	hemoglobin, beta adult major chain	Mus musculus	101-107
6853556-4	1983	Sugar analysis reveals that all 11 gangliosides contain the same base structure, Gal(beta 1-3)GalNAc(beta 1-4)Gal(beta 1-4)Glc(beta 1-1) ceramide, which is gangliotetraosylceramide.	Ceramides	137-145	hemoglobin, beta adult major chain	Mus musculus	101-107
6853556-4	1983	Sugar analysis reveals that all 11 gangliosides contain the same base structure, Gal(beta 1-3)GalNAc(beta 1-4)Gal(beta 1-4)Glc(beta 1-1) ceramide, which is gangliotetraosylceramide.	Ceramides	137-145	hemoglobin, beta adult major chain	Mus musculus	127-135
7076419-6	1982	The hydrolysis of ceramide by this enzyme was stimulated approximately 75% in the presence of fatty acid-free bovine serum albumin at the concentration of 3.33 X 10(-5) M.	Ceramides	18-26	albumin	Sus scrofa	117-130
6214615-2	1982	Although the activity of galactosyltransferase with ceramides containing hydroxy fatty acids quadrupled in normal male littermates between 14 and 20 days, hardly any increase was observed in the mutant and the activity was less than 10% of control above 20 days of age.	Ceramides	52-61	glycoprotein alpha-galactosyltransferase 1	Rattus norvegicus	25-46
6814427-7	1982	Deficiency of acid ceramidase activity in fibroblasts from patients with Farber disease and intermediate activities in obligate heterozygotes were demonstrated with all ceramides examined except for N-hexanoylsphingosine (C(6:0)/C(18:1)), whereas alkaline ceramidase activity was unaffected.	Ceramides	169-178	N-acylsphingosine amidohydrolase 1	Homo sapiens	14-29
6814495-1	1982	An accumulation of ceramide associated with the deficiency of acid ceramidase has been demonstrated in cultured diploid skin fibroblasts from a patient with Farber"s disease.	Ceramides	19-27	N-acylsphingosine amidohydrolase 1	Homo sapiens	62-77
60462-8	1976	The reaction to bela Glc NAc1 leads to 3 beta Gall leads to 4 Glc leads to ceramide (structure 4), which is the precursor of all blood group glycolipids, was consistently high in many cases of tumor glycolipid than that of normal glycolipid.	Ceramides	75-83	nucleus accumbens associated 1	Homo sapiens	25-29
6954491-4	1982	Because these glycolipids with Lex and NeuAc alpha 2 leads to 6Gal structures are developmentally regulated and are highly expressed in certain tumors, ceramide composition may affect development, differentiation, and oncogenesis.	Ceramides	152-160	fucosyltransferase 4	Homo sapiens	31-34
7095839-4	1982	These two gangliosides have the same carbohydrate chain, NeuAc(alpha 2-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)Glc(SNH), but they differ in their ceramide moiety.	Ceramides	179-187	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	93-99
7095839-4	1982	These two gangliosides have the same carbohydrate chain, NeuAc(alpha 2-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)Glc(SNH), but they differ in their ceramide moiety.	Ceramides	179-187	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	93-99
6253377-4	1980	During the biosynthesis of sphingomyelins, phosphocholine is being transferred from the donor CDP-choline to the primary alcohol group of ceramides.	Ceramides	138-147	cut like homeobox 1	Homo sapiens	94-97
208366-0	1978	Effect of detergents on ceramide-3 hydrolysis by alpha-galactosidase A.	Ceramides	24-32	galactosidase alpha	Homo sapiens	49-70
7095839-4	1982	These two gangliosides have the same carbohydrate chain, NeuAc(alpha 2-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)Glc(SNH), but they differ in their ceramide moiety.	Ceramides	179-187	UDP-GlcNAc:betaGal beta-1,3-N-acetylglucosaminyltransferase 2	Homo sapiens	77-83
7095839-4	1982	These two gangliosides have the same carbohydrate chain, NeuAc(alpha 2-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)GlcNAc(beta 1-3)Gal(beta 1-4)Glc(SNH), but they differ in their ceramide moiety.	Ceramides	179-187	eukaryotic translation elongation factor 1 beta 2 pseudogene 2	Homo sapiens	93-101
1148270-3	1975	One was identified as a hexaglycoslyceramide with the following composition and sequence: fucose-hexose(fucose)-hexosamine-hexose-hexose-ceramide, with a terminal saccharide structure similar to blood group Leb determinants.	Ceramides	36-44	mucin 5AC, oligomeric mucus/gel-forming	Homo sapiens	207-210
5769961-0	1969	[On the C18-and C20-sphingosine content of ceramides and sphingomyelins from the grey and white matter of the human brain].	Ceramides	43-52	Bardet-Biedl syndrome 9	Homo sapiens	8-11
5441240-5	1970	Some ions, formed by cleavage between C-3 and C-4 in the long-chain base, indicate the phytosphingosine nature of the ceramide.	Ceramides	118-126	complement C3	Homo sapiens	38-41
5441240-5	1970	Some ions, formed by cleavage between C-3 and C-4 in the long-chain base, indicate the phytosphingosine nature of the ceramide.	Ceramides	118-126	complement C4A (Rodgers blood group)	Homo sapiens	46-49
33900381-3	2021	We here determined whether the levels of macrophage glycerophospholipids, sphingolipids including ceramides, triacylglycerides, and cytokine release could be altered by FATP4 inactivation.	Ceramides	98-107	solute carrier family 27 (fatty acid transporter), member 4	Mus musculus	169-174
16742444-3	1966	Ceramide lactoside could be degraded to ceramide, galactose and glucose by mixtures of rat-brain beta-galactosidase and ox-brain beta-glucosidase.	Ceramides	40-48	galactosidase, beta 1	Rattus norvegicus	97-115
33912962-5	2022	Furthermore, we discover that the SMP domain of PDZD8 binds glycerophospholipids and ceramides both in vivo and in vitro, and that the SMP domain can transport lipids between membranes in vitro.	Ceramides	85-94	PDZ domain containing 8	Homo sapiens	48-53
33647448-3	2021	Specifically, we looked at activation of the acid sphingomyelinase (ASMase)/ceramide pathway, which leads to generation of reactive oxygen species (ROS) and induction of oxidative stress that may result in vascular injury.	Ceramides	76-84	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	45-66
33647448-3	2021	Specifically, we looked at activation of the acid sphingomyelinase (ASMase)/ceramide pathway, which leads to generation of reactive oxygen species (ROS) and induction of oxidative stress that may result in vascular injury.	Ceramides	76-84	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	68-74
34050932-2	2021	Preclinical and clinical evidence suggest that the (ASM)/ceramide system may be central to SARS-CoV-2 infection.	Ceramides	57-65	sphingomyelin phosphodiesterase 1	Homo sapiens	52-55
33900381-7	2021	Under basal conditions, FATP4/Fatp4 deficiency decreased the levels of ceramides and induced an upregulation of mannose receptor CD206 expression.	Ceramides	71-80	solute carrier family 27 (fatty acid transporter), member 4	Mus musculus	24-29
33900381-7	2021	Under basal conditions, FATP4/Fatp4 deficiency decreased the levels of ceramides and induced an upregulation of mannose receptor CD206 expression.	Ceramides	71-80	solute carrier family 27 (fatty acid transporter), member 4	Mus musculus	30-35
34045496-1	2021	Acid ceramidase (AC) is a lysosomal hydrolase encoded by the ASAH1 gene, which cleaves ceramides into sphingosine and fatty acid.	Ceramides	87-96	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
33864951-4	2021	Ceramides may be key players in promoting an obesity-induced inflammatory environment due to their ability to activate key pathways such as Toll-like receptor 4 (TLR4) and NLR pyrin domain containing receptor 3 (Nlrp3), while studies have shown that inhibition of ceramide synthesis gives rise to an anti-inflammatory environment.	Ceramides	0-9	toll like receptor 4	Homo sapiens	140-160
33864951-4	2021	Ceramides may be key players in promoting an obesity-induced inflammatory environment due to their ability to activate key pathways such as Toll-like receptor 4 (TLR4) and NLR pyrin domain containing receptor 3 (Nlrp3), while studies have shown that inhibition of ceramide synthesis gives rise to an anti-inflammatory environment.	Ceramides	0-9	toll like receptor 4	Homo sapiens	162-166
33864951-4	2021	Ceramides may be key players in promoting an obesity-induced inflammatory environment due to their ability to activate key pathways such as Toll-like receptor 4 (TLR4) and NLR pyrin domain containing receptor 3 (Nlrp3), while studies have shown that inhibition of ceramide synthesis gives rise to an anti-inflammatory environment.	Ceramides	0-9	NLR family pyrin domain containing 3	Homo sapiens	212-217
34045496-1	2021	Acid ceramidase (AC) is a lysosomal hydrolase encoded by the ASAH1 gene, which cleaves ceramides into sphingosine and fatty acid.	Ceramides	87-96	N-acylsphingosine amidohydrolase 1	Homo sapiens	61-66
34033896-3	2021	Acid ceramidase (AC) is a lysosomal enzyme that hydrolyzes ceramide (N-acylsphingosine), which resembles NAAA in structure and function.	Ceramides	59-67	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
34033896-3	2021	Acid ceramidase (AC) is a lysosomal enzyme that hydrolyzes ceramide (N-acylsphingosine), which resembles NAAA in structure and function.	Ceramides	59-67	N-acylethanolamine acid amidase	Homo sapiens	105-109
34033896-3	2021	Acid ceramidase (AC) is a lysosomal enzyme that hydrolyzes ceramide (N-acylsphingosine), which resembles NAAA in structure and function.	Ceramides	69-86	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
34033896-3	2021	Acid ceramidase (AC) is a lysosomal enzyme that hydrolyzes ceramide (N-acylsphingosine), which resembles NAAA in structure and function.	Ceramides	69-86	N-acylethanolamine acid amidase	Homo sapiens	105-109
34004484-3	2021	Recent studies have highlighted circulating ceramides as novel biomarkers of coronary artery disease, type-2 diabetes and insulin resistance.	Ceramides	44-53	insulin	Homo sapiens	122-129
33991313-1	2021	Dihydroceramide desaturase (Degs1) catalyses the introduction of a 4,5-trans double bond into dihydroceramide to form ceramide.	Ceramides	7-15	delta 4-desaturase, sphingolipid 1	Homo sapiens	28-33
33991313-4	2021	Therefore, 4-HPR or celecoxib appear to stimulate the de novo ceramide pathway (with the exception of C24:0 ceramide), using native Degs1, and thereby promote PARP cleavage and LC3B-I/II processing (autophagy/apoptosis).	Ceramides	62-70	haptoglobin-related protein	Homo sapiens	13-16
33991313-4	2021	Therefore, 4-HPR or celecoxib appear to stimulate the de novo ceramide pathway (with the exception of C24:0 ceramide), using native Degs1, and thereby promote PARP cleavage and LC3B-I/II processing (autophagy/apoptosis).	Ceramides	62-70	delta 4-desaturase, sphingolipid 1	Homo sapiens	132-137
33991313-5	2021	The ubiquitin-proteasomal degradation of Degs1 is positively linked to cell survival via XBP-1s and results in a concomitant increase in dihydroceramides and a decrease in C24:0 ceramide levels.	Ceramides	144-152	delta 4-desaturase, sphingolipid 1	Homo sapiens	41-46
33991313-9	2021	The de novo synthesis of ceramide or the ubiquitin-proteasomal degradation of Degs1 in response to anti-oxidants, retinol derivatives and phenolic compounds appear to involve sensors, and for rectifier function, this might be Degs1 itself.	Ceramides	25-33	delta 4-desaturase, sphingolipid 1	Homo sapiens	78-83
33991313-9	2021	The de novo synthesis of ceramide or the ubiquitin-proteasomal degradation of Degs1 in response to anti-oxidants, retinol derivatives and phenolic compounds appear to involve sensors, and for rectifier function, this might be Degs1 itself.	Ceramides	25-33	delta 4-desaturase, sphingolipid 1	Homo sapiens	226-231
34026750-3	2021	Acid ceramidase is a lipid hydrolase that modulates the levels of ceramide, and as such has a potential therapeutic role in many human diseases where ceramide has been implicated.	Ceramides	66-74	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
34026750-3	2021	Acid ceramidase is a lipid hydrolase that modulates the levels of ceramide, and as such has a potential therapeutic role in many human diseases where ceramide has been implicated.	Ceramides	150-158	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
33957567-1	2021	Sphingomyelin (SM) can be converted into ceramide (Cer) by neutral sphingomyelinase (NSM) and acid sphingomyelinase (ASM).	Ceramides	41-49	sphingomyelin phosphodiesterase 2	Homo sapiens	59-83
34026750-8	2021	In addition, elevated ceramide and sphingosine levels were observed in the IR group compared to sham, and were markedly reduced when pretreated with acid ceramidase.	Ceramides	22-30	N-acylsphingosine amidohydrolase 1	Mus musculus	149-164
33951438-3	2021	Here, we show that activated T cells isolated from aging mice have elevated C14/C16 ceramide accumulation in mitochondria, generated by ceramide synthase 6, leading to mitophagy/mitochondrial dysfunction.	Ceramides	84-92	ceramide synthase 6	Mus musculus	136-155
34017832-0	2021	Ceramide-Induced Lysosomal Biogenesis and Exocytosis in Early-Onset Preeclampsia Promotes Exosomal Release of SMPD1 Causing Endothelial Dysfunction.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	110-115
34017832-5	2021	In vitro and in vivo experiments demonstrate that ceramide increases TFEB expression and nuclear translocation and induces lysosomal formation and exocytosis.	Ceramides	50-58	transcription factor EB	Homo sapiens	69-73
34017832-6	2021	Further, we show that TFEB directly regulates the expression of lysosomal sphingomyelin phosphodiesterase (L-SMPD1) that degrades sphingomyelin to ceramide.	Ceramides	147-155	transcription factor EB	Homo sapiens	22-26
34017832-6	2021	Further, we show that TFEB directly regulates the expression of lysosomal sphingomyelin phosphodiesterase (L-SMPD1) that degrades sphingomyelin to ceramide.	Ceramides	147-155	sphingomyelin phosphodiesterase 1	Homo sapiens	74-105
34017832-7	2021	In early-onset preeclampsia, ceramide-induced lysosomal exocytosis carries L-SMPD1 to the apical membrane of the syncytial epithelium, resulting in ceramide accumulation in lipid rafts and release of active L-SMPD1 via ceramide-enriched exosomes into the maternal circulation.	Ceramides	29-37	sphingomyelin phosphodiesterase 1	Homo sapiens	77-82
34017832-7	2021	In early-onset preeclampsia, ceramide-induced lysosomal exocytosis carries L-SMPD1 to the apical membrane of the syncytial epithelium, resulting in ceramide accumulation in lipid rafts and release of active L-SMPD1 via ceramide-enriched exosomes into the maternal circulation.	Ceramides	29-37	sphingomyelin phosphodiesterase 1	Homo sapiens	209-214
34017832-7	2021	In early-onset preeclampsia, ceramide-induced lysosomal exocytosis carries L-SMPD1 to the apical membrane of the syncytial epithelium, resulting in ceramide accumulation in lipid rafts and release of active L-SMPD1 via ceramide-enriched exosomes into the maternal circulation.	Ceramides	148-156	sphingomyelin phosphodiesterase 1	Homo sapiens	77-82
34017832-7	2021	In early-onset preeclampsia, ceramide-induced lysosomal exocytosis carries L-SMPD1 to the apical membrane of the syncytial epithelium, resulting in ceramide accumulation in lipid rafts and release of active L-SMPD1 via ceramide-enriched exosomes into the maternal circulation.	Ceramides	148-156	sphingomyelin phosphodiesterase 1	Homo sapiens	77-82
33957567-1	2021	Sphingomyelin (SM) can be converted into ceramide (Cer) by neutral sphingomyelinase (NSM) and acid sphingomyelinase (ASM).	Ceramides	41-49	sphingomyelin phosphodiesterase 1	Homo sapiens	94-115
33957567-1	2021	Sphingomyelin (SM) can be converted into ceramide (Cer) by neutral sphingomyelinase (NSM) and acid sphingomyelinase (ASM).	Ceramides	41-49	sphingomyelin phosphodiesterase 1	Homo sapiens	117-120
33938457-5	2021	Sphingomyelin phosphodiesterase 3 (SMPD3), which is involved in ceramide synthesis in the intestine, was identified as an FXR target gene.	Ceramides	64-72	nuclear receptor subfamily 1, group H, member 4	Mus musculus	122-125
33957567-1	2021	Sphingomyelin (SM) can be converted into ceramide (Cer) by neutral sphingomyelinase (NSM) and acid sphingomyelinase (ASM).	Ceramides	51-54	sphingomyelin phosphodiesterase 2	Homo sapiens	59-83
33938457-6	2021	SMPD3 overexpression or C16:0 ceramide supplementation eliminated the improvements in atherosclerosis in FxrDeltaIE ApoE-/- mice.	Ceramides	30-38	apolipoprotein E	Mus musculus	116-120
33957567-1	2021	Sphingomyelin (SM) can be converted into ceramide (Cer) by neutral sphingomyelinase (NSM) and acid sphingomyelinase (ASM).	Ceramides	51-54	sphingomyelin phosphodiesterase 1	Homo sapiens	94-115
33938457-7	2021	Administration of GUDCA or GW4869, an SMPD3 inhibitor, elicited therapeutic effects on established atherosclerosis in ApoE-/- mice by decreasing circulating ceramide levels.	Ceramides	157-165	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	38-43
33957567-1	2021	Sphingomyelin (SM) can be converted into ceramide (Cer) by neutral sphingomyelinase (NSM) and acid sphingomyelinase (ASM).	Ceramides	51-54	sphingomyelin phosphodiesterase 1	Homo sapiens	117-120
33938457-7	2021	Administration of GUDCA or GW4869, an SMPD3 inhibitor, elicited therapeutic effects on established atherosclerosis in ApoE-/- mice by decreasing circulating ceramide levels.	Ceramides	157-165	apolipoprotein E	Mus musculus	118-122
33705961-3	2021	Mature CMs derived from hiPSC exposed to the diabetic-like environment or transfected with plasmids overexpressing serine-palmitoyltransferase long chain base subunit 1 (SPTLC1), a subunit of the serine-palmitoyltransferase (SPT) complex, resulted in increased intracellular ceramide levels.	Ceramides	275-283	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	170-176
33934437-5	2021	Following knockdown, CEBPgamma and YBX1 were found to be independently associated with reductions in ceramide-dependent lamellipodia formation as well as migration activity, while only CEBPgamma may have induced CERS6 expression through specific binding to Y-box.	Ceramides	101-109	CCAAT enhancer binding protein gamma	Homo sapiens	21-30
33934437-5	2021	Following knockdown, CEBPgamma and YBX1 were found to be independently associated with reductions in ceramide-dependent lamellipodia formation as well as migration activity, while only CEBPgamma may have induced CERS6 expression through specific binding to Y-box.	Ceramides	101-109	Y-box binding protein 1	Homo sapiens	35-39
33630410-4	2021	Accumulation of these ceramides is associated with insulin resistance, de novo lipogenesis, and inflammation1 , thus increasing the risk of cardiometabolic diseases such as type 2 diabetes (T2D) and atherosclerosis.	Ceramides	22-31	insulin	Homo sapiens	51-58
33727246-2	2021	Neutral sphingomyelinase 2 (nSMase2), encoded by SMPD3, catalyzes the breakdown of sphingomyelin to produce the anti-oncometabolite ceramide.	Ceramides	132-140	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	0-26
33727246-2	2021	Neutral sphingomyelinase 2 (nSMase2), encoded by SMPD3, catalyzes the breakdown of sphingomyelin to produce the anti-oncometabolite ceramide.	Ceramides	132-140	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	28-35
33727246-2	2021	Neutral sphingomyelinase 2 (nSMase2), encoded by SMPD3, catalyzes the breakdown of sphingomyelin to produce the anti-oncometabolite ceramide.	Ceramides	132-140	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	49-54
33727246-5	2021	In wild-type mice, nSMase2 overexpressing tumors showed accumulation of both ceramide and CD8+ tumor-infiltrating lymphocytes, and this was associated with increased level of transcripts encoding IFNgamma and CXCL9.	Ceramides	77-85	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	19-26
33855746-8	2021	The emollients MPS and ceramide partially restored the epidermal function and alleviated the skin inflammation in Flg-/- mice with CPT-induced AD-like dermatitis.	Ceramides	23-31	filaggrin	Mus musculus	114-117
33938457-3	2021	The serum levels of fibroblast growth factor 19 (FGF19), which is encoded by an FXR target gene, were much higher in patients with hypercholesterolemia than in control subjects and were positively related to circulating ceramide levels, indicating a link between intestinal FXR, ceramide metabolism, and atherosclerosis.	Ceramides	220-228	fibroblast growth factor 19	Homo sapiens	20-47
33938457-3	2021	The serum levels of fibroblast growth factor 19 (FGF19), which is encoded by an FXR target gene, were much higher in patients with hypercholesterolemia than in control subjects and were positively related to circulating ceramide levels, indicating a link between intestinal FXR, ceramide metabolism, and atherosclerosis.	Ceramides	220-228	fibroblast growth factor 19	Homo sapiens	49-54
33938457-3	2021	The serum levels of fibroblast growth factor 19 (FGF19), which is encoded by an FXR target gene, were much higher in patients with hypercholesterolemia than in control subjects and were positively related to circulating ceramide levels, indicating a link between intestinal FXR, ceramide metabolism, and atherosclerosis.	Ceramides	220-228	nuclear receptor subfamily 1 group H member 4	Homo sapiens	80-83
33938457-3	2021	The serum levels of fibroblast growth factor 19 (FGF19), which is encoded by an FXR target gene, were much higher in patients with hypercholesterolemia than in control subjects and were positively related to circulating ceramide levels, indicating a link between intestinal FXR, ceramide metabolism, and atherosclerosis.	Ceramides	279-287	fibroblast growth factor 19	Homo sapiens	20-47
33938457-3	2021	The serum levels of fibroblast growth factor 19 (FGF19), which is encoded by an FXR target gene, were much higher in patients with hypercholesterolemia than in control subjects and were positively related to circulating ceramide levels, indicating a link between intestinal FXR, ceramide metabolism, and atherosclerosis.	Ceramides	279-287	fibroblast growth factor 19	Homo sapiens	49-54
33938457-3	2021	The serum levels of fibroblast growth factor 19 (FGF19), which is encoded by an FXR target gene, were much higher in patients with hypercholesterolemia than in control subjects and were positively related to circulating ceramide levels, indicating a link between intestinal FXR, ceramide metabolism, and atherosclerosis.	Ceramides	279-287	nuclear receptor subfamily 1 group H member 4	Homo sapiens	80-83
33938457-5	2021	Sphingomyelin phosphodiesterase 3 (SMPD3), which is involved in ceramide synthesis in the intestine, was identified as an FXR target gene.	Ceramides	64-72	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	0-33
33938457-5	2021	Sphingomyelin phosphodiesterase 3 (SMPD3), which is involved in ceramide synthesis in the intestine, was identified as an FXR target gene.	Ceramides	64-72	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	35-40
33545384-3	2021	SM is synthesized by sphingomyelin synthase 1 and 2 (SMS1 and SMS2) which utilizes ceramide and phosphatidylcholine, as two substrates, to produce SM and diacylglyceride.	Ceramides	83-91	sphingomyelin synthase 1	Mus musculus	21-51
33545384-3	2021	SM is synthesized by sphingomyelin synthase 1 and 2 (SMS1 and SMS2) which utilizes ceramide and phosphatidylcholine, as two substrates, to produce SM and diacylglyceride.	Ceramides	83-91	sphingomyelin synthase 1	Mus musculus	53-57
33705961-6	2021	Further, ceramide accumulation increased mitochondrial fission regulators such as dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF) as well as auto/mitophagic proteins LC3B and PINK-1 compared to control.	Ceramides	9-17	dynamin 1 like	Homo sapiens	82-107
33705961-6	2021	Further, ceramide accumulation increased mitochondrial fission regulators such as dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF) as well as auto/mitophagic proteins LC3B and PINK-1 compared to control.	Ceramides	9-17	dynamin 1 like	Homo sapiens	109-113
33705961-6	2021	Further, ceramide accumulation increased mitochondrial fission regulators such as dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF) as well as auto/mitophagic proteins LC3B and PINK-1 compared to control.	Ceramides	9-17	microtubule associated protein 1 light chain 3 beta	Homo sapiens	190-194
33705961-6	2021	Further, ceramide accumulation increased mitochondrial fission regulators such as dynamin-related protein 1 (DRP1) and mitochondrial fission factor (MFF) as well as auto/mitophagic proteins LC3B and PINK-1 compared to control.	Ceramides	9-17	PTEN induced kinase 1	Homo sapiens	199-205
33568795-5	2021	Mouse models of metabolic disease have demonstrated that inhibition of intestinal FXR signalling reduces obesity, insulin resistance and fatty liver disease by modulation of hepatic and gut bacteria-mediated BA metabolism, and intestinal ceramide synthesis.	Ceramides	238-246	nuclear receptor subfamily 1, group H, member 4	Mus musculus	82-85
33760130-0	2021	Ceramide induces the apoptosis of non-small cell lung cancer cells through the Txnip/Trx1 complex.	Ceramides	0-8	thioredoxin interacting protein	Homo sapiens	79-84
33760130-0	2021	Ceramide induces the apoptosis of non-small cell lung cancer cells through the Txnip/Trx1 complex.	Ceramides	0-8	thioredoxin	Homo sapiens	85-89
33760130-4	2021	Thus, it was hypothesized that ceramide induces apoptosis in lung adenocarcinoma cells (A549 and PC9) by modulating the Txnip/Trx1 complex.	Ceramides	31-39	thioredoxin interacting protein	Homo sapiens	120-125
33760130-4	2021	Thus, it was hypothesized that ceramide induces apoptosis in lung adenocarcinoma cells (A549 and PC9) by modulating the Txnip/Trx1 complex.	Ceramides	31-39	thioredoxin	Homo sapiens	126-130
33760130-6	2021	Hoechst 33258 staining and flow cytometry were used to detect cell apoptosis, and the positional association between Txnip and Trx1 upregulated by ceramide was observed by immunofluorescence confocal microscopy.	Ceramides	147-155	thioredoxin interacting protein	Homo sapiens	117-122
33760130-6	2021	Hoechst 33258 staining and flow cytometry were used to detect cell apoptosis, and the positional association between Txnip and Trx1 upregulated by ceramide was observed by immunofluorescence confocal microscopy.	Ceramides	147-155	thioredoxin	Homo sapiens	127-131
33760130-8	2021	The results revealed that ceramide treatment resulted in the upregulation of Txnip and in the reduction of Trx1 activities.	Ceramides	26-34	thioredoxin interacting protein	Homo sapiens	77-82
33760130-8	2021	The results revealed that ceramide treatment resulted in the upregulation of Txnip and in the reduction of Trx1 activities.	Ceramides	26-34	thioredoxin	Homo sapiens	107-111
33760130-11	2021	On the whole, the present study demonstrates that ceramide induces the apoptosis of lung cancer cells by regulating the Txnip/Trx1 complex.	Ceramides	50-58	thioredoxin interacting protein	Homo sapiens	120-125
33760130-11	2021	On the whole, the present study demonstrates that ceramide induces the apoptosis of lung cancer cells by regulating the Txnip/Trx1 complex.	Ceramides	50-58	thioredoxin	Homo sapiens	126-130
33928788-6	2021	Nampt overexpression decreased the GSSG/GSH ratio, oxidation of thioredoxin 1 (Trx1) targets, dityrosine, and the accumulation of toxic lipids, including ceramides and diglycerides, in the presence of HFD consumption.	Ceramides	154-163	nicotinamide phosphoribosyltransferase	Mus musculus	0-5
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.	Ceramides	172-180	glucosylceramidase beta	Homo sapiens	55-78
33914445-11	2021	CONCLUSION: Our study identifies a novel inflammatory pathway in that TLR9 increases the pro-inflammatory cytokine release, such as TNF-alpha, via the induction of a ceramide/S1P imbalance in favor of S1P, adding a novel puzzle piece in TLR9-orchestrated inflammatory pathway and shedding more light on the role of the higher levels of S1P during inflammatory conditions.	Ceramides	166-174	toll like receptor 9	Homo sapiens	70-74
33914445-11	2021	CONCLUSION: Our study identifies a novel inflammatory pathway in that TLR9 increases the pro-inflammatory cytokine release, such as TNF-alpha, via the induction of a ceramide/S1P imbalance in favor of S1P, adding a novel puzzle piece in TLR9-orchestrated inflammatory pathway and shedding more light on the role of the higher levels of S1P during inflammatory conditions.	Ceramides	166-174	tumor necrosis factor	Homo sapiens	132-141
33914445-11	2021	CONCLUSION: Our study identifies a novel inflammatory pathway in that TLR9 increases the pro-inflammatory cytokine release, such as TNF-alpha, via the induction of a ceramide/S1P imbalance in favor of S1P, adding a novel puzzle piece in TLR9-orchestrated inflammatory pathway and shedding more light on the role of the higher levels of S1P during inflammatory conditions.	Ceramides	166-174	toll like receptor 9	Homo sapiens	237-241
33884955-0	2021	UBTD1 regulates ceramide balance and endolysosomal positioning to coordinate EGFR signaling.	Ceramides	16-24	ubiquitin domain containing 1	Homo sapiens	0-5
33923179-7	2021	Sixty-one patient samples over three time points revealed a ceramide metabolite, hexosylceramide (Hex-Cer) was high across all time points (mean 1.63-3.19%; vs. controls 0.22%).	Ceramides	60-68	hematopoietically expressed homeobox	Homo sapiens	98-101
33891387-11	2021	Lipidomic analysis showed that FB1 treatment significantly increased levels of phosphotidylcholines, ceramides, and pheophorbide A, while significantly decreasing the levels of diacylglycerides, sulfoquinovosyl diacylglycerides, and chlorophyll.	Ceramides	101-110	TCF3 fusion partner	Homo sapiens	31-34
33884955-3	2021	On the one hand, by modulating the cellular level of ceramides through ASAH1 (N-Acylsphingosine Amidohydrolase 1) ubiquitination, UBTD1 controls the ligand-independent phosphorylation of EGFR.	Ceramides	53-62	N-acylsphingosine amidohydrolase 1	Homo sapiens	71-76
33884955-3	2021	On the one hand, by modulating the cellular level of ceramides through ASAH1 (N-Acylsphingosine Amidohydrolase 1) ubiquitination, UBTD1 controls the ligand-independent phosphorylation of EGFR.	Ceramides	53-62	N-acylsphingosine amidohydrolase 1	Homo sapiens	78-112
33884955-3	2021	On the one hand, by modulating the cellular level of ceramides through ASAH1 (N-Acylsphingosine Amidohydrolase 1) ubiquitination, UBTD1 controls the ligand-independent phosphorylation of EGFR.	Ceramides	53-62	ubiquitin domain containing 1	Homo sapiens	130-135
33884955-3	2021	On the one hand, by modulating the cellular level of ceramides through ASAH1 (N-Acylsphingosine Amidohydrolase 1) ubiquitination, UBTD1 controls the ligand-independent phosphorylation of EGFR.	Ceramides	53-62	epidermal growth factor receptor	Homo sapiens	187-191
33968145-6	2021	However, PPARD could also activate nitric oxide formation and ceramide synthesis, which was implicated as promoters in the pathogenesis of MDD, indicating the complexity of the relationship between PPARD and MDD.	Ceramides	62-70	peroxisome proliferator activated receptor delta	Homo sapiens	9-14
33895135-1	2021	The acid sphingomyelinase/ceramide system has been shown to be important for cellular infection with at least some viruses, for instance rhinovirus or SARS-CoV-2.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
33895135-6	2021	We found that entry of pp-VSV-SARS-CoV-2 spike required activation of acid sphingomyelinase and release of ceramide, events that were all prevented by pretreatment with ambroxol.	Ceramides	107-115	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	41-46
33968145-6	2021	However, PPARD could also activate nitric oxide formation and ceramide synthesis, which was implicated as promoters in the pathogenesis of MDD, indicating the complexity of the relationship between PPARD and MDD.	Ceramides	62-70	peroxisome proliferator activated receptor delta	Homo sapiens	198-203
33852174-1	2021	LASS2 is a novel tumor-suppressor gene and has been characterized as a ceramide synthase, which synthesizes very-long acyl chain ceramides.	Ceramides	129-138	ceramide synthase 2	Homo sapiens	0-5
33859296-1	2021	Ceramide kinase (CERK) phosphorylates ceramide to produce ceramide-1-phosphate (C1P), which is involved in the development of metabolic inflammation.	Ceramides	38-46	ceramide kinase	Homo sapiens	0-15
33859296-1	2021	Ceramide kinase (CERK) phosphorylates ceramide to produce ceramide-1-phosphate (C1P), which is involved in the development of metabolic inflammation.	Ceramides	38-46	ceramide kinase	Homo sapiens	17-21
33859296-5	2021	Our data show that TNF-alpha upregulates ceramide phosphorylation.	Ceramides	41-49	tumor necrosis factor	Homo sapiens	19-28
33862114-2	2021	This study aimed to explore the role of S100 calcium binding protein B (S100B)/RAGE/ceramide signaling pathway in SAE.	Ceramides	84-92	S100 protein, beta polypeptide, neural	Mus musculus	40-70
33852856-2	2021	The last step of de novo sphingolipid synthesis is the conversion of dihydroceramide to ceramide by dihydroceramide desaturase (human DEGS1; Drosophila Ifc).	Ceramides	76-84	delta 4-desaturase, sphingolipid 1	Homo sapiens	134-139
33852856-2	2021	The last step of de novo sphingolipid synthesis is the conversion of dihydroceramide to ceramide by dihydroceramide desaturase (human DEGS1; Drosophila Ifc).	Ceramides	76-84	infertile crescent	Drosophila melanogaster	152-155
33862114-0	2021	S100B/RAGE/Ceramide signaling pathway is involved in sepsis-associated encephalopathy.	Ceramides	11-19	S100 protein, beta polypeptide, neural	Mus musculus	0-5
33862114-2	2021	This study aimed to explore the role of S100 calcium binding protein B (S100B)/RAGE/ceramide signaling pathway in SAE.	Ceramides	84-92	S100 protein, beta polypeptide, neural	Mus musculus	72-77
33862114-2	2021	This study aimed to explore the role of S100 calcium binding protein B (S100B)/RAGE/ceramide signaling pathway in SAE.	Ceramides	84-92	MOK protein kinase	Mus musculus	79-83
33862114-0	2021	S100B/RAGE/Ceramide signaling pathway is involved in sepsis-associated encephalopathy.	Ceramides	11-19	MOK protein kinase	Mus musculus	6-10
33862114-10	2021	SIGNIFICANCE: This study confirmed that S100B regulates mitochondrial dynamics through RAGE/ceramide pathway, in addition to the role of this pathway in acute brain injury and long-term cognitive impairment during sepsis.	Ceramides	92-100	S100 protein, beta polypeptide, neural	Mus musculus	40-45
33920193-6	2021	The reduction in the levels of very-long-chain ceramides and dihydroceramides could be due to the decrease in the expression of fatty acid elongase 3, as observed in THP-1 monocytes.	Ceramides	47-56	GLI family zinc finger 2	Homo sapiens	166-171
33844153-11	2021	Indeed, RNA data analyses revealed upregulations of genes involved in ceramide synthesis in brain endothelial cells of EAE mice (LASS6/CERS6, LASS3/CERS3, UGCG, ELOVL6, and ELOVL4).	Ceramides	70-78	ceramide synthase 6	Mus musculus	129-134
33844153-11	2021	Indeed, RNA data analyses revealed upregulations of genes involved in ceramide synthesis in brain endothelial cells of EAE mice (LASS6/CERS6, LASS3/CERS3, UGCG, ELOVL6, and ELOVL4).	Ceramides	70-78	elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 4	Mus musculus	173-179
33839155-2	2021	Previous studies have demonstrated a down-regulation of the acid ceramidase in CF epithelial cells resulting in an increase of ceramide and a decrease of sphingosine.	Ceramides	127-135	N-acylsphingosine amidohydrolase 1	Homo sapiens	60-75
33897374-1	2021	The acid sphingomyelinase (ASM) converts sphingomyelin into ceramide.	Ceramides	60-68	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	4-25
33897374-1	2021	The acid sphingomyelinase (ASM) converts sphingomyelin into ceramide.	Ceramides	60-68	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	27-30
33897374-2	2021	Recent work has advanced the ASM/ceramide system as a major player in the pathogenesis of major depressive disorder (MDD).	Ceramides	33-41	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	29-32
33918753-4	2021	C2IIa induces Ca2+-induced lysosomal exocytosis, extracellular release of the acid sphingomyelinase (ASMase), and membrane invagination and endocytosis through generating ceramides in the membrane by ASMase.	Ceramides	171-180	endogenous retrovirus group K member 24	Homo sapiens	0-5
33918753-4	2021	C2IIa induces Ca2+-induced lysosomal exocytosis, extracellular release of the acid sphingomyelinase (ASMase), and membrane invagination and endocytosis through generating ceramides in the membrane by ASMase.	Ceramides	171-180	sphingomyelin phosphodiesterase 1	Homo sapiens	200-206
33839155-6	2021	We report that genetic deficiency or functional inhibition of CFTR/Cftr results in an up-regulation of interferon regulatory factor 8 (IRF8) and a concomitant down-regulation of acid ceramidase expression with CF and an increase of ceramide and a reduction of sphingosine levels in tracheal and bronchial epithelial cells from both human individuals or mice.	Ceramides	232-240	CF transmembrane conductance regulator	Homo sapiens	62-66
33839155-6	2021	We report that genetic deficiency or functional inhibition of CFTR/Cftr results in an up-regulation of interferon regulatory factor 8 (IRF8) and a concomitant down-regulation of acid ceramidase expression with CF and an increase of ceramide and a reduction of sphingosine levels in tracheal and bronchial epithelial cells from both human individuals or mice.	Ceramides	232-240	CF transmembrane conductance regulator	Homo sapiens	67-71
33839155-7	2021	CRISPR/Cas9- or siRNA-mediated down-regulation of IRF8 prevented changes of acid ceramidase, ceramide and sphingosine in CF epithelial cells and restored resistance to Pseudomonas aeruginosa infections, which is one of the most important and common pathogens in lung infection of patients with CF.	Ceramides	93-101	interferon regulatory factor 8	Homo sapiens	50-54
33430631-10	2021	KLF5 ablation suppressed the expression of serine-palmitoyl-transferase-long-chain-base-subunit (SPTLC)1 and SPTLC2, which regulate de novo ceramide biosynthesis.	Ceramides	140-148	serine palmitoyltransferase, long chain base subunit 1	Mus musculus	97-104
33596665-9	2021	Ceramide ratios were significantly associated with MACE independently of LDL-c (low-density lipoprotein cholesterol) and conventional coronary artery disease risk factors.	Ceramides	0-8	component of oligomeric golgi complex 2	Homo sapiens	73-78
33131062-8	2021	Increased total ceramides was associated with STAT3 activation with downstream activation of multiple immune-inflammatory pathways at a transcriptomic level by network analyses.	Ceramides	16-25	signal transducer and activator of transcription 3	Mus musculus	46-51
33504931-9	2021	In addition, a network of 89 metabolites, primarily phosphatidylcholines, plasmalogens, sphingomyelins, and ceramides showed consistent negative correlations with insulin at visit 1 and post-challenge glucose at visit 2, while positive correlation with adiponectin at visit 2.	Ceramides	108-117	insulin	Homo sapiens	163-170
33504931-9	2021	In addition, a network of 89 metabolites, primarily phosphatidylcholines, plasmalogens, sphingomyelins, and ceramides showed consistent negative correlations with insulin at visit 1 and post-challenge glucose at visit 2, while positive correlation with adiponectin at visit 2.	Ceramides	108-117	adiponectin, C1Q and collagen domain containing	Homo sapiens	253-264
33719188-0	2021	Alpha-mangostin improves endothelial dysfunction in db/db mice through inhibition of aSMase/ceramide pathway.	Ceramides	92-100	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	85-91
33785360-6	2021	Accordingly, serum metabolomics of Oat1 knockout mice revealed increased polyunsaturated fatty acids, diacylglycerols, and long chain fatty acids, and decreased ceramides and bile acids when compared to wild type controls.	Ceramides	161-170	solute carrier family 22 (organic anion transporter), member 6	Mus musculus	35-39
33738905-1	2021	Sphingolipids, in particular ceramides, play vital role in pathophysiological processes linked to metabolic syndrome, with implications in the development of insulin resistance, pancreatic ss-cell dysfunction, type 2 diabetes, atherosclerosis, inflammation, nonalcoholic steatohepatitis, and cancer.	Ceramides	29-38	insulin	Homo sapiens	158-165
33738905-2	2021	Ceramides are produced by the hydrolysis of sphingomyelin, catalyzed by different sphingomyelinases, including neutral sphingomyelinase 2 (nSMase2), whose dysregulation appears to underlie many of the inflammation-related pathologies.	Ceramides	0-9	sphingomyelin phosphodiesterase 3	Homo sapiens	111-137
33738905-2	2021	Ceramides are produced by the hydrolysis of sphingomyelin, catalyzed by different sphingomyelinases, including neutral sphingomyelinase 2 (nSMase2), whose dysregulation appears to underlie many of the inflammation-related pathologies.	Ceramides	0-9	sphingomyelin phosphodiesterase 3	Homo sapiens	139-146
33738905-4	2021	nSMase2 contribution to pathogenic processes appears to involve cyclical feed-forward interaction with proinflammatory cytokines, such as TNF-alpha and IL-1ss, which activate nSMase2 and the production of ceramides, that in turn triggers the synthesis and release of inflammatory cytokines.	Ceramides	205-214	sphingomyelin phosphodiesterase 3	Homo sapiens	0-7
33738905-4	2021	nSMase2 contribution to pathogenic processes appears to involve cyclical feed-forward interaction with proinflammatory cytokines, such as TNF-alpha and IL-1ss, which activate nSMase2 and the production of ceramides, that in turn triggers the synthesis and release of inflammatory cytokines.	Ceramides	205-214	tumor necrosis factor	Homo sapiens	138-147
33430631-0	2021	Cardiomyocyte Kruppel-like Factor 5 Promotes De Novo Ceramide Biosynthesis and Contributes to Eccentric Remodeling in Ischemic Cardiomyopathy.	Ceramides	53-61	Kruppel-like factor 5	Mus musculus	14-35
33430631-5	2021	We identified the involvement of KLF5 in regulating lipid metabolism and ceramide accumulation after MI using liquid-chromatography-tandem-mass-spectrometry, and Western Blot and rtPCR analysis of ceramide-metabolism-related genes.	Ceramides	73-81	Kruppel-like factor 5	Mus musculus	33-37
33430631-5	2021	We identified the involvement of KLF5 in regulating lipid metabolism and ceramide accumulation after MI using liquid-chromatography-tandem-mass-spectrometry, and Western Blot and rtPCR analysis of ceramide-metabolism-related genes.	Ceramides	197-205	Kruppel-like factor 5	Mus musculus	33-37
33430631-9	2021	Lipidomic analysis showed that alphaMHC-KLF5-/- mice with MI had lower myocardial ceramide levels compared with littermate control mice with MI although basal ceramide content of alphaMHC-KLF5-/- mice was not different from control mice.	Ceramides	82-90	Kruppel-like factor 5	Mus musculus	40-44
33592537-0	2021	Discovery of novel ceramide analogs with favorable pharmacokinetic properties and combination with AKT inhibitor against colon cancer.	Ceramides	19-27	AKT serine/threonine kinase 1	Rattus norvegicus	99-102
33492757-0	2021	Comprehensive stratum corneum ceramide profiling reveals reduced acylceramides in ichthyosis patient with CERS3 mutations.	Ceramides	30-38	ceramide synthase 3	Homo sapiens	106-111
33492757-3	2021	Ceramide synthase 3 (CERS3) is involved in the synthesis of acylceramides and protein-bound ceramides, and CERS3 mutations cause autosomal recessive congenital ichthyosis.	Ceramides	64-73	ceramide synthase 3	Homo sapiens	0-19
33492757-3	2021	Ceramide synthase 3 (CERS3) is involved in the synthesis of acylceramides and protein-bound ceramides, and CERS3 mutations cause autosomal recessive congenital ichthyosis.	Ceramides	64-73	ceramide synthase 3	Homo sapiens	21-26
33430631-10	2021	KLF5 ablation suppressed the expression of serine-palmitoyl-transferase-long-chain-base-subunit (SPTLC)1 and SPTLC2, which regulate de novo ceramide biosynthesis.	Ceramides	140-148	Kruppel-like factor 5	Mus musculus	0-4
33430631-10	2021	KLF5 ablation suppressed the expression of serine-palmitoyl-transferase-long-chain-base-subunit (SPTLC)1 and SPTLC2, which regulate de novo ceramide biosynthesis.	Ceramides	140-148	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	109-115
33430631-12	2021	Consistently, alphaMHC-rtTA-KLF5 mice showed increased SPTLC1 and SPTLC2 expression, higher myocardial ceramide levels, and systolic dysfunction beginning 2-weeks after KLF5 induction.	Ceramides	103-111	Kruppel-like factor 5	Mus musculus	28-32
33430631-13	2021	Treatment of alphaMHC-rtTA-KLF5 mice with myriocin that inhibits SPT, suppressed myocardial ceramide levels and alleviated systolic dysfunction.	Ceramides	92-100	Kruppel-like factor 5	Mus musculus	27-31
33430631-14	2021	Conclusions: KLF5 is induced during the development of ischemic heart failure in humans and mice and stimulates ceramide biosynthesis.	Ceramides	112-120	Kruppel like factor 5	Homo sapiens	13-17
33430631-15	2021	Genetic or pharmacological inhibition of KLF5 in mice with MI prevents ceramide accumulation, alleviates eccentric remodeling, and increases ejection fraction.	Ceramides	71-79	Kruppel-like factor 5	Mus musculus	41-45
33684145-1	2021	beta-Sitosterol 3-O-d-glucoside (BSG) is known to act as an agonist by binding to estrogen receptors, and estrogen has been reported to enhance the activity of beta-glucocerebrosidase, an epidermal ceramide metabolizing enzyme.	Ceramides	198-206	glucosylceramidase beta	Homo sapiens	160-183
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].	Ceramides	44-52	ceramide synthase 3	Homo sapiens	105-110
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].	Ceramides	44-52	UDP-glucose ceramide glucosyltransferase	Homo sapiens	115-118
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].	Ceramides	210-219	ceramide synthase 3	Homo sapiens	105-110
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].	Ceramides	210-219	UDP-glucose ceramide glucosyltransferase	Homo sapiens	115-118
33665756-1	2021	Acid sphingomyelinase (ASM) and acid beta-glucosidase 1 (GBA1) catalyze ceramide formation through different routes, and both are involved in rheumatoid arthritis (RA) pathogenesis as well as IL-6 production.	Ceramides	72-80	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
33898989-2	2021	We now investigated whether pharmacological targeting of the acid sphingomyelinase, which catalyzes the cleavage of sphingomyelin to ceramide and phosphorylcholine, also allows to manipulate relative CD4+ Foxp3+ regulatory T-cell frequencies in humans.	Ceramides	133-141	sphingomyelin phosphodiesterase 1	Homo sapiens	61-82
33665756-1	2021	Acid sphingomyelinase (ASM) and acid beta-glucosidase 1 (GBA1) catalyze ceramide formation through different routes, and both are involved in rheumatoid arthritis (RA) pathogenesis as well as IL-6 production.	Ceramides	72-80	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
33665756-1	2021	Acid sphingomyelinase (ASM) and acid beta-glucosidase 1 (GBA1) catalyze ceramide formation through different routes, and both are involved in rheumatoid arthritis (RA) pathogenesis as well as IL-6 production.	Ceramides	72-80	glucosylceramidase beta	Homo sapiens	57-61
33658490-2	2021	In this work, we combine molecular dynamics simulations, mutagenesis, and electrophysiology to provide mechanistic insights into how lipophilic molecules (ceramide-sphingolipid probe) alter gating kinetics and K+ currents of hERG1.	Ceramides	155-163	potassium voltage-gated channel subfamily H member 2	Homo sapiens	225-230
33665756-1	2021	Acid sphingomyelinase (ASM) and acid beta-glucosidase 1 (GBA1) catalyze ceramide formation through different routes, and both are involved in rheumatoid arthritis (RA) pathogenesis as well as IL-6 production.	Ceramides	72-80	interleukin 6	Homo sapiens	192-196
33665756-6	2021	GBA1 and ceramide serum levels were negatively and positively correlated with IL-6 serum level in RA patients, respectively.	Ceramides	9-17	interleukin 6	Homo sapiens	78-82
33592213-6	2021	RESULTS: Total and subspecies of serum SMs and globotriaosyl ceramides (Gb3s) were positively related to GIR30, free FAs (FFA 16:1, FFA20:4), some long chain GM3 and complex ceramide GluCers showed strong negative correlations with GIR30.	Ceramides	61-69	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	72-76
33185911-2	2021	Neutral ceramidase (NcDase), highly expressed in the intestinal brush border of the small intestine, plays a critical role in digesting dietary sphingolipids (ceramide) to regulate the balance of sphingosine and free fatty acids (FFAs).	Ceramides	159-167	N-acylsphingosine amidohydrolase 2	Mus musculus	0-18
33583073-2	2021	We identified neutral sphingomyelinase 2 (nSMase2) as the enzyme responsible to generate this bioactive pool of ceramide.	Ceramides	112-120	sphingomyelin phosphodiesterase 3	Homo sapiens	14-40
33583073-2	2021	We identified neutral sphingomyelinase 2 (nSMase2) as the enzyme responsible to generate this bioactive pool of ceramide.	Ceramides	112-120	sphingomyelin phosphodiesterase 3	Homo sapiens	42-49
33583073-5	2021	This led to the identification of several ceramide-PP1 alpha downstream substrates.	Ceramides	42-50	protein phosphatase 1 catalytic subunit alpha	Homo sapiens	51-60
33077892-8	2021	Establishment of the Tlcd3b knockout murine model, an in vivo photoreceptor cell degeneration model due to loss of a ceramide synthase, will provide a unique opportunity in probing the role of ceramide in survival and function of photoreceptor cells.	Ceramides	117-125	TLC domain containing 3B	Homo sapiens	21-27
33077892-8	2021	Establishment of the Tlcd3b knockout murine model, an in vivo photoreceptor cell degeneration model due to loss of a ceramide synthase, will provide a unique opportunity in probing the role of ceramide in survival and function of photoreceptor cells.	Ceramides	193-201	TLC domain containing 3B	Homo sapiens	21-27
33185911-2	2021	Neutral ceramidase (NcDase), highly expressed in the intestinal brush border of the small intestine, plays a critical role in digesting dietary sphingolipids (ceramide) to regulate the balance of sphingosine and free fatty acids (FFAs).	Ceramides	159-167	N-acylsphingosine amidohydrolase 2	Mus musculus	20-26
33352310-3	2021	METHODS: We generated new mouse models allowing for the conditional ablation of genes required for ceramide synthesis (i.e. serine palmitoyltransferase subunit 2, Sptlc2) or degradation (i.e. acid ceramidase 1, Asah1) from mature, thermogenic adipocytes (i.e. from cells expressing uncoupling protein-1).	Ceramides	99-107	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	163-169
33352310-7	2021	Conversely, depletion of Asah1 led to ceramide accumulation, diminution of energy expenditure, and exacerbation of insulin resistance and obesity.	Ceramides	38-46	N-acylsphingosine amidohydrolase 1	Mus musculus	25-30
33507882-2	2021	We performed a comprehensive analysis in human airway epithelial cells, which revealed that tonic IL-33 secretion is dependent on the ceramide biosynthetic enzyme neutral sphingomyelinase 2 (nSMase2).	Ceramides	134-142	sphingomyelin phosphodiesterase 3	Homo sapiens	191-198
33507882-2	2021	We performed a comprehensive analysis in human airway epithelial cells, which revealed that tonic IL-33 secretion is dependent on the ceramide biosynthetic enzyme neutral sphingomyelinase 2 (nSMase2).	Ceramides	134-142	interleukin 33	Homo sapiens	98-103
33507882-2	2021	We performed a comprehensive analysis in human airway epithelial cells, which revealed that tonic IL-33 secretion is dependent on the ceramide biosynthetic enzyme neutral sphingomyelinase 2 (nSMase2).	Ceramides	134-142	sphingomyelin phosphodiesterase 3	Homo sapiens	163-189
33410456-0	2021	Ceramide contributes to pathogenesis and may be targeted for therapy in VCP inclusion body myopathy.	Ceramides	0-8	valosin containing protein	Mus musculus	72-75
33410456-7	2021	RESULTS: Acid ceramidase inhibitor, ARN082, elevated cellular ceramide levels and concomitantly enhanced pathology.	Ceramides	62-70	N-acylsphingosine amidohydrolase 1	Homo sapiens	9-24
33410456-10	2021	CONCLUSION: The ceramide pathway appears to be critical in VCP pathogenesis, and small-molecule inhibitors of ceramide biosynthesis might provide therapeutic benefit in VCP and, related neurodegenerative diseases.	Ceramides	16-24	valosin containing protein	Homo sapiens	59-62
33410456-10	2021	CONCLUSION: The ceramide pathway appears to be critical in VCP pathogenesis, and small-molecule inhibitors of ceramide biosynthesis might provide therapeutic benefit in VCP and, related neurodegenerative diseases.	Ceramides	110-118	valosin containing protein	Homo sapiens	169-172
33627323-5	2021	Metabolomics linked TREM2 deficiency with elevated obesity-instigated serum ceramides that correlated with impaired insulin sensitivity.	Ceramides	76-85	triggering receptor expressed on myeloid cells 2	Mus musculus	20-25
33612104-10	2021	In addition, the pretreatment of cells with sulfo-N-succinimidyl oleate (SSO), an irreversible inhibitor of the scavenger receptor CD36, blocked Cer-induced upregulation of nuclear factor-kappaB (NF-kappaB) activity, TXNIP expression, and NLRP3 inflammasome activation.	Ceramides	145-148	thioredoxin interacting protein	Mus musculus	217-222
33612104-1	2021	BACKGROUND: This study aimed to explore the effects of ceramide (Cer) on NLRP3 inflammasome activation and their underlying mechanisms.	Ceramides	55-63	NLR family, pyrin domain containing 3	Mus musculus	73-78
33612104-10	2021	In addition, the pretreatment of cells with sulfo-N-succinimidyl oleate (SSO), an irreversible inhibitor of the scavenger receptor CD36, blocked Cer-induced upregulation of nuclear factor-kappaB (NF-kappaB) activity, TXNIP expression, and NLRP3 inflammasome activation.	Ceramides	145-148	NLR family, pyrin domain containing 3	Mus musculus	239-244
33612104-1	2021	BACKGROUND: This study aimed to explore the effects of ceramide (Cer) on NLRP3 inflammasome activation and their underlying mechanisms.	Ceramides	65-68	NLR family, pyrin domain containing 3	Mus musculus	73-78
33612104-11	2021	Inhibition of NF-kappaB activation by SN50 prevented Cer-induced upregulation of TXNIP and activation of the NLRP3 inflammasome but did not affect CD36 expression.	Ceramides	53-56	thioredoxin interacting protein	Mus musculus	81-86
33612104-11	2021	Inhibition of NF-kappaB activation by SN50 prevented Cer-induced upregulation of TXNIP and activation of the NLRP3 inflammasome but did not affect CD36 expression.	Ceramides	53-56	NLR family, pyrin domain containing 3	Mus musculus	109-114
33612104-13	2021	The results documented that the CD36-dependent NF-kappaB-TXNIP signaling pathway plays an essential role in the Cer-induced activation of NLRP3 inflammasomes in macrophages.	Ceramides	112-115	thioredoxin interacting protein	Mus musculus	57-62
33612104-13	2021	The results documented that the CD36-dependent NF-kappaB-TXNIP signaling pathway plays an essential role in the Cer-induced activation of NLRP3 inflammasomes in macrophages.	Ceramides	112-115	NLR family, pyrin domain containing 3	Mus musculus	138-143
33604626-3	2021	Here we tested trial separations using various ODS columns and prepared plant ceramide standards generated by human glucocerebrosidase (imiglucerase) using commercially available plant glucosylceramide standards as the substrates.	Ceramides	78-86	glucosylceramidase beta	Homo sapiens	136-148
33479769-6	2021	Silencing of serum- and glucocorticoid-inducible kinase 1 (SGK1) blunted the pro-calcific effects of bacterial sphingomyelinase or ceramide.	Ceramides	131-139	serum/glucocorticoid regulated kinase 1	Mus musculus	13-57
33597019-0	2021	CERTL reduces C16 ceramide, amyloid-beta levels, and inflammation in a model of Alzheimer"s disease.	Ceramides	18-26	ceramide transporter 1	Homo sapiens	0-5
33597019-0	2021	CERTL reduces C16 ceramide, amyloid-beta levels, and inflammation in a model of Alzheimer"s disease.	Ceramides	18-26	c16	None	14-17
33597019-11	2021	Furthermore, we show that intracortical injection of AAV, mediating the expression of CERTL, decreases levels of ceramide d18:1/16:0 and increases sphingomyelin levels in the brain of male 5xFAD mice.	Ceramides	113-121	ceramide transporter 1	Homo sapiens	86-91
33597019-13	2021	CONCLUSION: Our results demonstrate a crucial role of CERTL in regulating ceramide levels in the brain, in amyloid plaque formation and neuroinflammation, thereby opening research avenues for therapeutic targets of AD and other neurodegenerative diseases.	Ceramides	74-82	ceramide transporter 1	Homo sapiens	54-59
33158378-3	2021	Among the numerous lipid subtypes that accumulate, sphingolipids such as ceramides are particularly impactful, as they elicit the selective insulin resistance, dyslipidemia, and ultimately cell death that underlie nearly all metabolic disorders.	Ceramides	73-82	insulin	Homo sapiens	140-147
33633691-2	2020	In the sphingolipid metabolic network, ceramides serve as the central hub that is hydrolyzed to sphingosine, followed by phosphorylation to sphingosine 1-phosphate (S1P) by sphingosine kinase (SphK).	Ceramides	39-48	sphingosine kinase 1	Homo sapiens	173-191
33633691-2	2020	In the sphingolipid metabolic network, ceramides serve as the central hub that is hydrolyzed to sphingosine, followed by phosphorylation to sphingosine 1-phosphate (S1P) by sphingosine kinase (SphK).	Ceramides	39-48	sphingosine kinase 1	Homo sapiens	193-197
33633691-3	2020	SphK is regarded as a "switch" of the sphingolipid rheostat, as it catalyzes the conversion of ceramide/sphingosine to S1P, which often exhibit opposing biological roles in the cell.	Ceramides	95-103	sphingosine kinase 1	Homo sapiens	0-4
33568634-0	2021	Alternative splicing of ceramide synthase 2 alters levels of specific ceramides and modulates cancer cell proliferation and migration in Luminal B breast cancer subtype.	Ceramides	70-79	ceramide synthase 2	Homo sapiens	24-43
33560835-0	2021	Dietary Supplementation with Exogenous Sea-Cucumber-Derived Ceramides and Glucosylceramides Alleviates Insulin Resistance in High-Fructose-Diet-Fed Rats by Upregulating the IRS/PI3K/Akt Signaling Pathway.	Ceramides	60-69	AKT serine/threonine kinase 1	Rattus norvegicus	182-185
33479769-6	2021	Silencing of serum- and glucocorticoid-inducible kinase 1 (SGK1) blunted the pro-calcific effects of bacterial sphingomyelinase or ceramide.	Ceramides	131-139	serum/glucocorticoid regulated kinase 1	Mus musculus	59-63
33479769-10	2021	In conclusion, ASM/ceramide is a critical upstream regulator of vascular calcification, at least partly, through SGK1-dependent signaling.	Ceramides	19-27	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	15-18
33526685-6	2021	Separate metabolite assessments revealed that almost all intermediates of acylcarnitine fatty acid oxidation, ceramides, sphingomyelins, and multiple toxic metabolites were significantly elevated in the predegeneration Rtbdn -/- neural retina.	Ceramides	110-119	retbindin	Homo sapiens	219-224
33479769-10	2021	In conclusion, ASM/ceramide is a critical upstream regulator of vascular calcification, at least partly, through SGK1-dependent signaling.	Ceramides	19-27	serum/glucocorticoid regulated kinase 1	Mus musculus	113-117
33477028-7	2021	Saturated Gb3 isoforms migrated on LiChrospher plate in one of the separated peaks corresponding to the migration zone of ceramide trihexosides standard.	Ceramides	122-130	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	10-13
33221496-11	2021	Moreover, rescue of Aash1 gene expression in podocytes of Asah1fl/fl/PodoCre mice showed normal ceramide metabolism and exosome secretion.	Ceramides	96-104	N-acylsphingosine amidohydrolase 1	Mus musculus	58-63
33539225-12	2021	Pharmacological or genetic KLF5 inhibition alleviated superoxide formation, prevented ceramide accumulation, and improved cardiac function in diabetic mice.	Ceramides	86-94	Kruppel-like factor 5	Mus musculus	27-31
33539225-13	2021	CONCLUSIONS: Diabetes-mediated activation of cardiomyocyte FOXO1 increases KLF5 expression, which stimulates NOX4 expression, ceramide accumulation, and causes DbCM.	Ceramides	126-134	forkhead box O1	Mus musculus	59-64
33539225-13	2021	CONCLUSIONS: Diabetes-mediated activation of cardiomyocyte FOXO1 increases KLF5 expression, which stimulates NOX4 expression, ceramide accumulation, and causes DbCM.	Ceramides	126-134	Kruppel-like factor 5	Mus musculus	75-79
33567768-7	2021	Higher saturated fat intake was associated with higher concentrations of 16:1;O2 sphingolipids including ceramides, monohexosylcermides, dihexosylceramides, sphingomyelins, and sphingosine 1-phosphates.	Ceramides	105-114	FAT atypical cadherin 1	Homo sapiens	17-20
33567768-8	2021	Higher polyunsaturated fat intake was associated with lower plasma long-chain ceramides and long-chain monohexosylcermide concentrations.	Ceramides	78-87	FAT atypical cadherin 1	Homo sapiens	23-26
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.	Ceramides	237-245	sphingomyelin phosphodiesterase 1	Homo sapiens	27-33
33562655-18	2021	These results provide new insights into the essential role of SM deacylase as the beta-subunit aCDase that causes the ceramide deficiency in AD skin.	Ceramides	118-126	N-acylsphingosine amidohydrolase 1	Homo sapiens	95-101
33539341-10	2021	Perturbing EV biogenesis through neutral sphingomyelinase (nSMase), an enzyme important for EV release and ceramide metabolism, enhanced protein aggregation when knocked down in muscle, but did not modify Gba1b mutant protein aggregation when knocked down in neurons.	Ceramides	107-115	neutral sphingomyelinase	Drosophila melanogaster	59-65
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.	Ceramides	42-50	neutral sphingomyelinase	Drosophila melanogaster	22-28
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.	Ceramides	63-71	neutral sphingomyelinase	Drosophila melanogaster	22-28
33612070-0	2021	NF-kappaB pathway play a role in SCD1 deficiency-induced ceramide de novo synthesis.	Ceramides	57-65	nuclear factor kappa B subunit 1	Homo sapiens	0-9
33226447-11	2021	SMS1 inhibition disrupted sphingolipid metabolism via accumulating ceramide and decreasing sphingomyelin, inducing mitochondrial dysfunction and oxidative stress, and decreasing Ras activity in resistant cells.	Ceramides	67-75	sphingomyelin synthase 1	Homo sapiens	0-4
33612070-0	2021	NF-kappaB pathway play a role in SCD1 deficiency-induced ceramide de novo synthesis.	Ceramides	57-65	stearoyl-CoA desaturase	Homo sapiens	33-37
33612070-1	2021	Stearoyl-CoA-desaturase 1 (SCD1) deficiency mediates apoptosis in colorectal cancer cells by promoting ceramide de novo synthesis.	Ceramides	103-111	stearoyl-CoA desaturase	Homo sapiens	0-25
33612070-1	2021	Stearoyl-CoA-desaturase 1 (SCD1) deficiency mediates apoptosis in colorectal cancer cells by promoting ceramide de novo synthesis.	Ceramides	103-111	stearoyl-CoA desaturase	Homo sapiens	27-31
33612070-9	2021	In summary, our data demonstrate that the NF-kappaB pathway plays a role in SCD1 deficiency-induced ceramide de novo synthesis in colorectal cancer cells, and that reduced MUFA levels contribute to the course.	Ceramides	100-108	nuclear factor kappa B subunit 1	Homo sapiens	42-51
33612070-9	2021	In summary, our data demonstrate that the NF-kappaB pathway plays a role in SCD1 deficiency-induced ceramide de novo synthesis in colorectal cancer cells, and that reduced MUFA levels contribute to the course.	Ceramides	100-108	stearoyl-CoA desaturase	Homo sapiens	76-80
32936422-3	2021	Here, we studied the contribution of neutral ceramidase (NC), one of the main enzymes mediating ceramide degradation, in the mechanisms of learning and memory in rats and non-human primates.	Ceramides	96-104	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	37-55
33268241-2	2021	Lipids have long been recognized as contributors to the pathogenesis and pathophysiology of DM and its complications, but recent discoveries have highlighted ceramides, a class of bioactive sphingolipids with cell signaling and second messenger capabilities, as particularly important contributors to insulin resistance and the underlying mechanisms of DM complications.	Ceramides	158-167	insulin	Homo sapiens	301-308
33268241-3	2021	Besides their association with insulin resistance and pathophysiology of type 2 diabetes, evidence is emerging that certain species of ceramides are mediators of cellular mechanisms involved in the initiation and progression of microvascular and macrovascular complications of DM.	Ceramides	135-144	insulin	Homo sapiens	31-38
33181324-1	2021	Lysosome Associated Protein Transmembrane 4B (LAPTM4B) is a four-membrane spanning ceramide interacting protein that regulates mTORC1 signaling.	Ceramides	83-91	lysosomal protein transmembrane 4 beta	Homo sapiens	0-44
33181324-1	2021	Lysosome Associated Protein Transmembrane 4B (LAPTM4B) is a four-membrane spanning ceramide interacting protein that regulates mTORC1 signaling.	Ceramides	83-91	lysosomal protein transmembrane 4 beta	Homo sapiens	46-53
33181324-1	2021	Lysosome Associated Protein Transmembrane 4B (LAPTM4B) is a four-membrane spanning ceramide interacting protein that regulates mTORC1 signaling.	Ceramides	83-91	CREB regulated transcription coactivator 1	Mus musculus	127-133
32374916-4	2021	In present study, we revealed aberrant gene expressions (e.g. SPTLC1 and CERS2) of de novo ceramide biosynthesis and length-specific ceramide production in GBC tissues.	Ceramides	91-99	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	62-68
32374916-4	2021	In present study, we revealed aberrant gene expressions (e.g. SPTLC1 and CERS2) of de novo ceramide biosynthesis and length-specific ceramide production in GBC tissues.	Ceramides	91-99	ceramide synthase 2	Homo sapiens	73-78
32374916-4	2021	In present study, we revealed aberrant gene expressions (e.g. SPTLC1 and CERS2) of de novo ceramide biosynthesis and length-specific ceramide production in GBC tissues.	Ceramides	133-141	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	62-68
32374916-4	2021	In present study, we revealed aberrant gene expressions (e.g. SPTLC1 and CERS2) of de novo ceramide biosynthesis and length-specific ceramide production in GBC tissues.	Ceramides	133-141	ceramide synthase 2	Homo sapiens	73-78
32374916-9	2021	C6-Ceramide, an analogue of natural ceramide, competed with C24-Ceramide for PIP4K2C binding, thereby abrogating C24-Ceramide -mediated mTOR signaling activation and oncogenic activity.	Ceramides	36-44	phosphatidylinositol-5-phosphate 4-kinase type 2 gamma	Homo sapiens	77-84
32374916-9	2021	C6-Ceramide, an analogue of natural ceramide, competed with C24-Ceramide for PIP4K2C binding, thereby abrogating C24-Ceramide -mediated mTOR signaling activation and oncogenic activity.	Ceramides	36-44	mechanistic target of rapamycin kinase	Homo sapiens	136-140
32936422-3	2021	Here, we studied the contribution of neutral ceramidase (NC), one of the main enzymes mediating ceramide degradation, in the mechanisms of learning and memory in rats and non-human primates.	Ceramides	96-104	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	57-59
33515546-3	2021	In many cell types, CerS2, which catalyzes the synthesis of very long chain ceramides, is the major CerS.	Ceramides	76-85	ceramide synthase 2	Homo sapiens	20-25
33515546-5	2021	As expected, we observed that very long chain ceramide, hexosylceramide, and sphingomyelin were reduced in CerS2 knockout cells.	Ceramides	46-54	ceramide synthase 2	Homo sapiens	107-112
33396102-7	2021	Moreover, ceramide was found to function epistatic to pmk-1 and mpk-1 in MAPK pathway to promote radiation-induced apoptosis in Caenorhabditis elegans.	Ceramides	10-18	Mitogen-activated protein kinase pmk-1	Caenorhabditis elegans	54-59
33495212-4	2021	Here, we propose that very-long-chain fatty acid-containing ceramides (VLCFA-Cers) mediate positional signals by stimulating the function of ARABIDOPSIS THALIANA MERISTEM LAYER1 (ATML1), a master regulator of protoderm/epidermis differentiation, during lateral root development.	Ceramides	60-69	Homeobox-leucine zipper family protein / lipid-binding START domain-containing protein	Arabidopsis thaliana	141-177
33495212-4	2021	Here, we propose that very-long-chain fatty acid-containing ceramides (VLCFA-Cers) mediate positional signals by stimulating the function of ARABIDOPSIS THALIANA MERISTEM LAYER1 (ATML1), a master regulator of protoderm/epidermis differentiation, during lateral root development.	Ceramides	60-69	Homeobox-leucine zipper family protein / lipid-binding START domain-containing protein	Arabidopsis thaliana	179-184
33553211-1	2020	Breakdown of the inert and constitutive membrane building block sphingomyelin to the highly active lipid mediator ceramide by extracellularly active acid sphingomyelinase is tightly regulated during stress response and opens the gate for invading pathogens, triggering the immune response, development of remote organ failure, and tissue repair following severe infection.	Ceramides	114-122	sphingomyelin phosphodiesterase 1	Homo sapiens	149-170
33553211-4	2020	When secreted, acid sphingomyelinase (ASM) is able to hydrolyze sphingomyelin present at the outer leaflet of membranes to ceramide.	Ceramides	123-131	sphingomyelin phosphodiesterase 1	Homo sapiens	15-36
33553211-4	2020	When secreted, acid sphingomyelinase (ASM) is able to hydrolyze sphingomyelin present at the outer leaflet of membranes to ceramide.	Ceramides	123-131	sphingomyelin phosphodiesterase 1	Homo sapiens	38-41
33465049-7	2021	Moreover, miR-6784 overexpression caused ceramide accumulation in skin SCC cells.	Ceramides	41-49	microRNA 6784	Homo sapiens	10-18
33396102-7	2021	Moreover, ceramide was found to function epistatic to pmk-1 and mpk-1 in MAPK pathway to promote radiation-induced apoptosis in Caenorhabditis elegans.	Ceramides	10-18	Mitogen-activated protein kinase mpk-1	Caenorhabditis elegans	64-69
33414460-0	2021	Targeting sphingosine kinase 1 (SK1) enhances oncogene-induced senescence through ceramide synthase 2 (CerS2)-mediated generation of very-long-chain ceramides.	Ceramides	149-158	sphingosine kinase 1	Homo sapiens	10-30
33139382-2	2021	Here, we tested whether genetic overexpression of the acid ceramidase rescues cystic fibrosis mice from pulmonary infections with P. aeruginosa We demonstrate that transgenic overexpression of the acid ceramidase in CF mice corresponds to an overexpression of the acid ceramidase in bronchial and tracheal epithelial cells and normalizes ceramide and sphingosine levels in bronchial and tracheal epithelial cells.	Ceramides	338-346	N-acylsphingosine amidohydrolase 1	Mus musculus	54-69
33139382-2	2021	Here, we tested whether genetic overexpression of the acid ceramidase rescues cystic fibrosis mice from pulmonary infections with P. aeruginosa We demonstrate that transgenic overexpression of the acid ceramidase in CF mice corresponds to an overexpression of the acid ceramidase in bronchial and tracheal epithelial cells and normalizes ceramide and sphingosine levels in bronchial and tracheal epithelial cells.	Ceramides	338-346	N-acylsphingosine amidohydrolase 1	Mus musculus	197-212
33139382-2	2021	Here, we tested whether genetic overexpression of the acid ceramidase rescues cystic fibrosis mice from pulmonary infections with P. aeruginosa We demonstrate that transgenic overexpression of the acid ceramidase in CF mice corresponds to an overexpression of the acid ceramidase in bronchial and tracheal epithelial cells and normalizes ceramide and sphingosine levels in bronchial and tracheal epithelial cells.	Ceramides	338-346	N-acylsphingosine amidohydrolase 1	Mus musculus	197-212
33300910-6	2021	Neuraminidase 3 (NEU3) is a key enzyme catalyzing the conversion of ganglioside GM3 to ceramide trihexosides (Gb3), whose expression is increased in drug-resistant HCT-116/L cells.	Ceramides	87-95	neuraminidase 3	Homo sapiens	0-15
33300910-6	2021	Neuraminidase 3 (NEU3) is a key enzyme catalyzing the conversion of ganglioside GM3 to ceramide trihexosides (Gb3), whose expression is increased in drug-resistant HCT-116/L cells.	Ceramides	87-95	neuraminidase 3	Homo sapiens	17-21
33300910-6	2021	Neuraminidase 3 (NEU3) is a key enzyme catalyzing the conversion of ganglioside GM3 to ceramide trihexosides (Gb3), whose expression is increased in drug-resistant HCT-116/L cells.	Ceramides	87-95	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	110-113
33414460-0	2021	Targeting sphingosine kinase 1 (SK1) enhances oncogene-induced senescence through ceramide synthase 2 (CerS2)-mediated generation of very-long-chain ceramides.	Ceramides	149-158	sphingosine kinase 1	Homo sapiens	32-35
33414460-0	2021	Targeting sphingosine kinase 1 (SK1) enhances oncogene-induced senescence through ceramide synthase 2 (CerS2)-mediated generation of very-long-chain ceramides.	Ceramides	149-158	ceramide synthase 2	Homo sapiens	82-101
33414460-0	2021	Targeting sphingosine kinase 1 (SK1) enhances oncogene-induced senescence through ceramide synthase 2 (CerS2)-mediated generation of very-long-chain ceramides.	Ceramides	149-158	ceramide synthase 2	Homo sapiens	103-108
33414460-4	2021	Furthermore, oncogenic K-Ras altered SL metabolism, with an increase of long-chain (LC) C18, C20 ceramides (Cer), and very-long-chain (VLC) C22:1, C24 Cer, and an increase of sphingosine kinase 1 (SK1) expression.	Ceramides	97-106	KRAS proto-oncogene, GTPase	Rattus norvegicus	23-28
33380429-9	2021	Inhibition of S-palmitoylation with 2-bromo palmitic acid or inhibition of ceramide biosynthesis with fumonisin B1 reduces formation of the Arl13b-acetylated tubulin complex and its transport into cilia, concurrent with impairment of ciliogenesis.	Ceramides	75-83	ADP ribosylation factor like GTPase 13B	Homo sapiens	140-146
33691599-6	2021	There was significantly higher abundance of some lipid metabolites in the plasma of ovariectomized HFD-fed ApoE-/- mice than in non-ovariectomized ones, including cholesterol esters, triglycerides, phospholipids, and other types of lipids (free fatty acids, acylcarnitine, sphingomyelins, and ceramides).	Ceramides	293-302	apolipoprotein E	Mus musculus	107-111
32986129-6	2021	The physiological importance of this topological regulation has been demonstrated by the finding that ceramide-induced RAT of TM4SF20 (Transmembrane 4 L6 family member 20) is crucial for the effectiveness of doxorubicin-based chemotherapy, and that dihydroceramide-induced RAT of CCR5 (C-C chemokine receptor type 5), a G protein-coupled receptor, is required for lipopolysaccharide (LPS) to inhibit chemotaxis of macrophages.	Ceramides	102-110	transmembrane 4 L six family member 20	Rattus norvegicus	126-133
32986129-6	2021	The physiological importance of this topological regulation has been demonstrated by the finding that ceramide-induced RAT of TM4SF20 (Transmembrane 4 L6 family member 20) is crucial for the effectiveness of doxorubicin-based chemotherapy, and that dihydroceramide-induced RAT of CCR5 (C-C chemokine receptor type 5), a G protein-coupled receptor, is required for lipopolysaccharide (LPS) to inhibit chemotaxis of macrophages.	Ceramides	102-110	transmembrane 4 L six family member 20	Rattus norvegicus	135-170
32986129-6	2021	The physiological importance of this topological regulation has been demonstrated by the finding that ceramide-induced RAT of TM4SF20 (Transmembrane 4 L6 family member 20) is crucial for the effectiveness of doxorubicin-based chemotherapy, and that dihydroceramide-induced RAT of CCR5 (C-C chemokine receptor type 5), a G protein-coupled receptor, is required for lipopolysaccharide (LPS) to inhibit chemotaxis of macrophages.	Ceramides	102-110	C-C motif chemokine receptor 5	Rattus norvegicus	280-284
32986129-6	2021	The physiological importance of this topological regulation has been demonstrated by the finding that ceramide-induced RAT of TM4SF20 (Transmembrane 4 L6 family member 20) is crucial for the effectiveness of doxorubicin-based chemotherapy, and that dihydroceramide-induced RAT of CCR5 (C-C chemokine receptor type 5), a G protein-coupled receptor, is required for lipopolysaccharide (LPS) to inhibit chemotaxis of macrophages.	Ceramides	102-110	C-C motif chemokine receptor 5	Rattus norvegicus	286-315
32980536-12	2021	Mechanisms of Src-induced resistance to ceramide-induced cytotoxicity are discussed in relation to the Src-induced up-regulation of GCS activity.	Ceramides	40-48	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	14-17
32980536-12	2021	Mechanisms of Src-induced resistance to ceramide-induced cytotoxicity are discussed in relation to the Src-induced up-regulation of GCS activity.	Ceramides	40-48	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	103-106
32615506-0	2021	Somatotropin increases plasma ceramide in relation to enhanced milk yield in cows.	Ceramides	30-38	somatotropin	Bos taurus	0-12
32615506-2	2021	Ceramides inhibit insulin responsiveness in bovine adipocytes and are associated with insulin resistance and milk production in cows.	Ceramides	0-9	insulin	Bos taurus	18-25
32615506-2	2021	Ceramides inhibit insulin responsiveness in bovine adipocytes and are associated with insulin resistance and milk production in cows.	Ceramides	0-9	insulin	Bos taurus	86-93
32615506-12	2021	Somatotropin increased plasma total and very-long-chain (C22:0-, C24:0-, C26:0-) ceramide concentrations (P < 0.01).	Ceramides	81-89	somatotropin	Bos taurus	0-12
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.	Ceramides	26-34	UDP-glucose ceramide glucosyltransferase	Homo sapiens	51-76
33492226-0	2021	[Is obesity-induced insulin resistance mediated by ceramide C18:0 synthesis de novo in skeletal muscles].	Ceramides	51-59	insulin	Homo sapiens	20-27
32770509-2	2021	Certain chemotherapeutic drugs activate the acid sphingomyelinase (ASMase)/ceramide pathway, generating ceramide in the tumor endothelium and this microvascular dysfunction is crucial for the tumor response.	Ceramides	75-83	sphingomyelin phosphodiesterase 1	Homo sapiens	44-65
32770509-2	2021	Certain chemotherapeutic drugs activate the acid sphingomyelinase (ASMase)/ceramide pathway, generating ceramide in the tumor endothelium and this microvascular dysfunction is crucial for the tumor response.	Ceramides	75-83	sphingomyelin phosphodiesterase 1	Homo sapiens	67-73
32770509-2	2021	Certain chemotherapeutic drugs activate the acid sphingomyelinase (ASMase)/ceramide pathway, generating ceramide in the tumor endothelium and this microvascular dysfunction is crucial for the tumor response.	Ceramides	104-112	sphingomyelin phosphodiesterase 1	Homo sapiens	44-65
32770509-2	2021	Certain chemotherapeutic drugs activate the acid sphingomyelinase (ASMase)/ceramide pathway, generating ceramide in the tumor endothelium and this microvascular dysfunction is crucial for the tumor response.	Ceramides	104-112	sphingomyelin phosphodiesterase 1	Homo sapiens	67-73
32770515-2	2021	Here, we describe the fractionation of detergent-resistant membranes and the correlative analysis of the enrichment of T cell receptor (TCR) and omega-azido-modified synthetic ceramide in those fractions upon TCR stimulation.	Ceramides	176-184	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	209-212
33357194-1	2020	Acid ceramidase (AC), the key enzyme of the ceramide metabolic pathway hydrolyzes pro-apoptotic ceramide to sphingosine, which by the action of sphingosine-1-kinase is metabolized to mitogenic sphingosine-1-phosphate.	Ceramides	44-52	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
33290061-1	2020	Acid ceramidase (AC) is a cysteine hydrolase that plays a crucial role in the metabolism of lysosomal ceramides, important members of the sphingolipid family, a diversified class of bioactive molecules that mediate many biological processes ranging from cell structural integrity, signaling, and cell proliferation to cell death.	Ceramides	102-111	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
33290061-1	2020	Acid ceramidase (AC) is a cysteine hydrolase that plays a crucial role in the metabolism of lysosomal ceramides, important members of the sphingolipid family, a diversified class of bioactive molecules that mediate many biological processes ranging from cell structural integrity, signaling, and cell proliferation to cell death.	Ceramides	102-111	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
33357194-1	2020	Acid ceramidase (AC), the key enzyme of the ceramide metabolic pathway hydrolyzes pro-apoptotic ceramide to sphingosine, which by the action of sphingosine-1-kinase is metabolized to mitogenic sphingosine-1-phosphate.	Ceramides	44-52	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
33357194-1	2020	Acid ceramidase (AC), the key enzyme of the ceramide metabolic pathway hydrolyzes pro-apoptotic ceramide to sphingosine, which by the action of sphingosine-1-kinase is metabolized to mitogenic sphingosine-1-phosphate.	Ceramides	96-104	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
33357194-1	2020	Acid ceramidase (AC), the key enzyme of the ceramide metabolic pathway hydrolyzes pro-apoptotic ceramide to sphingosine, which by the action of sphingosine-1-kinase is metabolized to mitogenic sphingosine-1-phosphate.	Ceramides	96-104	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
33357194-2	2020	The intracellular level of AC determines ceramide/sphingosine-1-phosphate rheostat which in turn decides the cell fate.	Ceramides	41-49	N-acylsphingosine amidohydrolase 1	Homo sapiens	27-29
33357194-3	2020	The upregulated AC expression during cancerous condition acts as a "double-edged sword" by converting pro-apoptotic ceramide to anti-apoptotic sphingosine-1-phosphate, wherein on one end, the level of ceramide is decreased and on the other end, the level of sphingosine-1-phosphate is increased, thus altogether aggravating the cancer progression.	Ceramides	116-124	N-acylsphingosine amidohydrolase 1	Homo sapiens	16-18
33357194-3	2020	The upregulated AC expression during cancerous condition acts as a "double-edged sword" by converting pro-apoptotic ceramide to anti-apoptotic sphingosine-1-phosphate, wherein on one end, the level of ceramide is decreased and on the other end, the level of sphingosine-1-phosphate is increased, thus altogether aggravating the cancer progression.	Ceramides	201-209	N-acylsphingosine amidohydrolase 1	Homo sapiens	16-18
33080217-7	2020	Early-onset obesity enhanced PVN expression of SPTLC1, a key enzyme for ceramide synthesis, and advanced the maturation of the ovarian noradrenergic system.	Ceramides	72-80	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	47-53
33374830-6	2020	Furthermore, triple knockout (TKO) cells lacking the whole GABARAP subfamily showed impaired Golgi-dependent vesicular trafficking as assessed by imaging of fluorescently labelled ceramide.	Ceramides	180-188	GABA type A receptor-associated protein	Homo sapiens	59-66
33352865-4	2020	With breast cancer cells, in vitro IGFBP-3 enhanced induced apoptosis, however when GRP78 expression was silenced the actions of IGFBP-3 were switched from increasing to inhibiting ceramide (C2)-induced cell death and promoted cell invasion.	Ceramides	181-189	heat shock protein family A (Hsp70) member 5	Homo sapiens	84-89
33352865-4	2020	With breast cancer cells, in vitro IGFBP-3 enhanced induced apoptosis, however when GRP78 expression was silenced the actions of IGFBP-3 were switched from increasing to inhibiting ceramide (C2)-induced cell death and promoted cell invasion.	Ceramides	181-189	insulin like growth factor binding protein 3	Homo sapiens	129-136
33047409-0	2020	A liposomal FRET assay identifies potent drug-like inhibitors of the ceramide transport protein CERT.	Ceramides	69-77	ceramide transporter 1	Homo sapiens	96-100
33047409-1	2020	Ceramide transfer protein (CERT) mediates non-vesicular transfer of ceramide from endoplasmic reticulum to Golgi apparatus and thus catalyzes the rate-limiting step of sphingomyelin biosynthesis.	Ceramides	68-76	ceramide transporter 1	Homo sapiens	0-25
33047409-1	2020	Ceramide transfer protein (CERT) mediates non-vesicular transfer of ceramide from endoplasmic reticulum to Golgi apparatus and thus catalyzes the rate-limiting step of sphingomyelin biosynthesis.	Ceramides	68-76	ceramide transporter 1	Homo sapiens	27-31
33047409-2	2020	Usually, CERT ligands are evaluated in tedious binding assays or non-homogenous transfer assays using radiolabeled ceramides.	Ceramides	115-124	ceramide transporter 1	Homo sapiens	9-13
33047409-5	2020	By CERT-mediated transfer of fluorescent ceramide, a FRET system was established, which allows readout in 96-well plate format, despite the high hydrophobicity of the components.	Ceramides	41-49	ceramide transporter 1	Homo sapiens	3-7
33303821-9	2020	Using IKK, mTORC1 and ceramide production inhibitors, we were able to blunt IRS1 serine 307 phosphorylation and restore insulin stimulation of Akt.	Ceramides	22-30	insulin receptor substrate 1	Mus musculus	76-80
33303821-9	2020	Using IKK, mTORC1 and ceramide production inhibitors, we were able to blunt IRS1 serine 307 phosphorylation and restore insulin stimulation of Akt.	Ceramides	22-30	thymoma viral proto-oncogene 1	Mus musculus	143-146
33296380-1	2020	BACKGROUND: Animal studies suggest vital roles of sphingolipids, especially ceramides, in the pathogenesis of type 2 diabetes (T2D) via pathways involved in insulin resistance, beta-cell dysfunction, and inflammation, but human studies are limited.	Ceramides	76-85	insulin	Homo sapiens	157-164
33273482-4	2020	Obese NLRP3 deficient mice had lower systemic ceramide levels, potentially resulting attenuating inflammation, altered hepatic expression of fatty acids (FA) with lower mono-saturated FA and higher polyunsaturated FA levels, potentially counteracting development of liver steatosis, downregulated myocardial energy metabolism as assessed by proteomic analyses of LV heart tissue, and different levels of bile acids as compared with WT mice.	Ceramides	46-54	NLR family, pyrin domain containing 3	Mus musculus	6-11
33347465-4	2020	The ceramide transport protein (CERT) encoded by CERT1 mediates inter-organelle trafficking of ceramide for the synthesis of intracellular sphingomyelin.	Ceramides	4-12	ceramide transporter 1	Homo sapiens	32-36
33347465-4	2020	The ceramide transport protein (CERT) encoded by CERT1 mediates inter-organelle trafficking of ceramide for the synthesis of intracellular sphingomyelin.	Ceramides	95-103	ceramide transporter 1	Homo sapiens	32-36
33334892-5	2021	This barrier phenotype in the Ephx3-/- pups was associated with a significant decrease in the covalently bound ceramides in the epidermis (40% reduction, p<0.05), indicating a corresponding structural impairment in the integrity of the water barrier.	Ceramides	111-120	epoxide hydrolase 3	Mus musculus	30-35
32915357-1	2020	Apolipoprotein L1 (APOL1) wild type (G0) plays a role in the metabolism of sphingolipids, glycosphingolipids, sphingomyelin and ceramide, which constitute bioactive components of the lipid rafts (DRM).	Ceramides	128-136	apolipoprotein L1	Homo sapiens	0-17
33090522-0	2020	Lysosomal-associated transmembrane protein 4B regulates ceramide-induced exosome release.	Ceramides	56-64	lysosomal protein transmembrane 4 beta	Homo sapiens	0-45
33090522-3	2020	Here, we found that ceramides, especially those consisting of long fatty acids, were internalized into the endocytic pathway in neuroblastoma SH-SY5Y cells to induce exosome secretion through lysosome-associated protein transmembrane 4B (LAPTM4B).	Ceramides	20-29	lysosomal protein transmembrane 4 beta	Homo sapiens	192-236
33090522-3	2020	Here, we found that ceramides, especially those consisting of long fatty acids, were internalized into the endocytic pathway in neuroblastoma SH-SY5Y cells to induce exosome secretion through lysosome-associated protein transmembrane 4B (LAPTM4B).	Ceramides	20-29	lysosomal protein transmembrane 4 beta	Homo sapiens	238-245
33090522-4	2020	Knockdown of LAPTM4B inhibited the ceramide-mediated increase in exosome release completely.	Ceramides	35-43	lysosomal protein transmembrane 4 beta	Homo sapiens	13-20
33090522-5	2020	Fluorescence microscopy observations indicated that exogenous ceramides promote the transport of multivesicular bodies to the plasma membranes in a LAPTM4B-dependent manner.	Ceramides	62-71	lysosomal protein transmembrane 4 beta	Homo sapiens	148-155
33090522-6	2020	Similarly, inhibition of acid ceramidase, which tends to induce intracellular ceramide accumulation, increased exosome production by SH-SY5Y cells in a LAPTM4B-dependent manner.	Ceramides	78-86	N-acylsphingosine amidohydrolase 1	Homo sapiens	25-40
33090522-6	2020	Similarly, inhibition of acid ceramidase, which tends to induce intracellular ceramide accumulation, increased exosome production by SH-SY5Y cells in a LAPTM4B-dependent manner.	Ceramides	78-86	lysosomal protein transmembrane 4 beta	Homo sapiens	152-159
33090522-7	2020	Furthermore, the level of amyloid-ss protein (Ass) was decreased in neuronal cells following treatment with exogenous ceramide or inhibition of acid ceramidase, and this effect was attributed to the LAPTM4B-dependent efflux of Ass-containing exosomes.	Ceramides	118-126	lysosomal protein transmembrane 4 beta	Homo sapiens	199-206
32632845-4	2020	We observed distinct lipid profiles in brown versus white adipose tissue of Ames dwarf mice that are consistent with increased thermogenesis and insulin sensitivity, such as increased cardiolipin and decreased ceramide concentrations.	Ceramides	210-218	paired like homeodomain factor 1	Mus musculus	76-86
33058843-2	2020	Elevated plasma concentrations of ceramides are associated with multiple risk factors of atherosclerotic cardiovascular diseases and comorbidities including e.g. obesity, insulin resistance and diabetes mellitus.	Ceramides	34-43	insulin	Homo sapiens	171-178
32945898-8	2020	CONCLUSIONS/INTERPRETATION: GH-induced insulin resistance in skeletal muscle is: (1) causally linked to lipolysis; (2) not associated with either accumulation of DAGs and ceramides or impaired insulin signalling; (3) likely to involve substrate competition between glucose and lipid intermediates.	Ceramides	171-180	growth hormone 1	Homo sapiens	28-30
32915357-1	2020	Apolipoprotein L1 (APOL1) wild type (G0) plays a role in the metabolism of sphingolipids, glycosphingolipids, sphingomyelin and ceramide, which constitute bioactive components of the lipid rafts (DRM).	Ceramides	128-136	apolipoprotein L1	Homo sapiens	19-24
32767230-6	2020	Upon irradiation, Noxa was found to translocate to the mitochondria where endogenous ceramide accumulation was observed.	Ceramides	85-93	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	18-22
32767230-7	2020	In contrast, overexpression of Bcl-2, another mitochondrial protein, in Molt-4 cells abolished the endogenous ceramide accumulation and apoptosis.	Ceramides	110-118	BCL2 apoptosis regulator	Homo sapiens	31-36
32767230-0	2020	Crosstalk between Noxa, Bcl-2, and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	35-43	tumor protein p53	Homo sapiens	57-60
32767230-8	2020	In irradiation-induced, p53-dependent pathways of apoptosis, the pro-apoptotic Noxa represents one of several, yet to be identified, pathways simultaneously triggered by p53 to produce mitochondrial ceramide accumulation and apoptosis.	Ceramides	199-207	tumor protein p53	Homo sapiens	24-27
32767230-2	2020	The tumor suppressor p53 stimulates various downstream targets that presumably trigger, individually or in concert, de novo ceramide synthesis and intrinsic apoptosis via mitochondrial outer membrane permeabilization (MOMP).	Ceramides	124-132	tumor protein p53	Homo sapiens	21-24
32767230-3	2020	Among these targets, BH3-only protein Noxa was found to be promptly activated by p53 prior to ceramide accumulation and apoptosis in response to irradiation.	Ceramides	94-102	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	38-42
32767230-8	2020	In irradiation-induced, p53-dependent pathways of apoptosis, the pro-apoptotic Noxa represents one of several, yet to be identified, pathways simultaneously triggered by p53 to produce mitochondrial ceramide accumulation and apoptosis.	Ceramides	199-207	phorbol-12-myristate-13-acetate-induced protein 1	Homo sapiens	79-83
32767230-3	2020	Among these targets, BH3-only protein Noxa was found to be promptly activated by p53 prior to ceramide accumulation and apoptosis in response to irradiation.	Ceramides	94-102	tumor protein p53	Homo sapiens	81-84
32767230-8	2020	In irradiation-induced, p53-dependent pathways of apoptosis, the pro-apoptotic Noxa represents one of several, yet to be identified, pathways simultaneously triggered by p53 to produce mitochondrial ceramide accumulation and apoptosis.	Ceramides	199-207	tumor protein p53	Homo sapiens	170-173
32767230-9	2020	In contrast, Bcl-2 functions as a broader inhibitor of both ceramide accumulation and apoptosis.	Ceramides	60-68	BCL2 apoptosis regulator	Homo sapiens	13-18
32767230-10	2020	Altogether, these results indicate that members of the Bcl-2 family differentially regulate ceramide accumulation and reveal the existence of crosstalk between Bcl-2 family members and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	92-100	BCL2 apoptosis regulator	Homo sapiens	55-60
32767230-10	2020	Altogether, these results indicate that members of the Bcl-2 family differentially regulate ceramide accumulation and reveal the existence of crosstalk between Bcl-2 family members and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	92-100	tumor protein p53	Homo sapiens	207-210
32767230-10	2020	Altogether, these results indicate that members of the Bcl-2 family differentially regulate ceramide accumulation and reveal the existence of crosstalk between Bcl-2 family members and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	185-193	BCL2 apoptosis regulator	Homo sapiens	55-60
32767230-10	2020	Altogether, these results indicate that members of the Bcl-2 family differentially regulate ceramide accumulation and reveal the existence of crosstalk between Bcl-2 family members and ceramide in mediating p53-dependent apoptosis in Molt-4 human T-cell leukemia.	Ceramides	185-193	tumor protein p53	Homo sapiens	207-210
33273368-5	2021	We demonstrate that neutrophil ceramide levels increase after burn injury, and this is associated with decreased expression of CXCR2 and blunted chemotaxis.	Ceramides	31-39	chemokine (C-X-C motif) receptor 2	Mus musculus	127-132
33330630-1	2020	The multi domain ceramide transfer protein (CERT) which contains the domains START and PH, is a protein that allows the transport of ceramide from the endoplasmic reticulum to the Golgi and so it plays a major role in sphingolipid metabolism.	Ceramides	17-25	ceramide transporter 1	Homo sapiens	44-48
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.	Ceramides	32-41	glucosylceramidase beta 2	Homo sapiens	104-108
33273368-6	2021	A major signaling event upon CXCR2 activation is Akt phosphorylation and this was reduced when ceramide was elevated.	Ceramides	95-103	chemokine (C-X-C motif) receptor 2	Mus musculus	29-34
33273368-6	2021	A major signaling event upon CXCR2 activation is Akt phosphorylation and this was reduced when ceramide was elevated.	Ceramides	95-103	thymoma viral proto-oncogene 1	Mus musculus	49-52
33163980-1	2020	The acid sphingomyelinase/ceramide system plays an important role in bacterial and viral infections.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
33313495-3	2020	We demonstrate that elevating endogenous ceramide levels with administration of exogenous ceramide nanoliposomes (CNLs) was efficacious in AR-negative cell lines with limited efficacy in AR-positive cells.	Ceramides	41-49	androgen receptor	Homo sapiens	139-141
33313495-3	2020	We demonstrate that elevating endogenous ceramide levels with administration of exogenous ceramide nanoliposomes (CNLs) was efficacious in AR-negative cell lines with limited efficacy in AR-positive cells.	Ceramides	90-98	androgen receptor	Homo sapiens	139-141
33218173-1	2020	: The acid sphingomyelinase (ASM)/ceramide system exhibits a crucial role in the pathology of major depressive disorder (MDD).	Ceramides	34-42	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	6-27
33218173-1	2020	: The acid sphingomyelinase (ASM)/ceramide system exhibits a crucial role in the pathology of major depressive disorder (MDD).	Ceramides	34-42	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	29-32
33218173-2	2020	ASM hydrolyzes the abundant membrane lipid sphingomyelin to ceramide that regulates the clustering of membrane proteins via microdomain and lipid raft organization.	Ceramides	60-68	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-3
33218173-7	2020	A lipidomic analysis of cortical brain tissue of ASM deficient mice revealed a decrease in ceramide/sphingomyelin molar ratio and an increase in sphingosine.	Ceramides	91-99	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	49-52
33163980-4	2020	Neutralization or consumption of surface ceramide reduces infection with pp-VSV-SARS-CoV-2 spike.	Ceramides	41-49	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	91-96
32998995-8	2020	In concordance with information from melanoma database mining, RNAscope analysis demonstrated a progressive increase of GALC expression from common nevi to stage IV human melanoma samples that was paralleled by increases in microphtalmia transcription factor and tyrosinase immunoreactivity inversely related to SMPD3 and ceramide levels.	Ceramides	322-330	galactosylceramidase	Homo sapiens	120-124
32987010-5	2020	The detailed fragmentation analysis performed by collision-induced dissociation (CID) tandem MS provided information of structural elements related to the glycan core and ceramide moiety, which confirmed the molecular configuration of GD3 (d18:1/24:1) and GD3 (d18:1/24:2) species with potential biomarker role.	Ceramides	171-179	GRDX	Homo sapiens	235-238
32998995-6	2020	Galc-silenced cells displayed altered sphingolipid metabolism and increased intracellular levels of ceramide, paralleled by a non-redundant upregulation of Smpd3, which encodes for the ceramide-generating enzyme neutral sphingomyelinase 2.	Ceramides	100-108	galactosylceramidase b	Danio rerio	0-4
32998995-6	2020	Galc-silenced cells displayed altered sphingolipid metabolism and increased intracellular levels of ceramide, paralleled by a non-redundant upregulation of Smpd3, which encodes for the ceramide-generating enzyme neutral sphingomyelinase 2.	Ceramides	185-193	galactosylceramidase b	Danio rerio	0-4
32998995-9	2020	Overall, these findings indicate that GALC may play an oncogenic role in melanoma by modulating the levels of intracellular ceramide, thus providing novel opportunities for melanoma therapy.	Ceramides	124-132	galactosylceramidase	Homo sapiens	38-42
33168861-1	2020	The metabolism of ceramides is deregulated in the brain of Alzheimer"s disease (AD) patients and is associated with apolipoprotein (APO) APOE4 and amyloid-beta pathology.	Ceramides	18-27	apolipoprotein E	Homo sapiens	137-142
32998995-6	2020	Galc-silenced cells displayed altered sphingolipid metabolism and increased intracellular levels of ceramide, paralleled by a non-redundant upregulation of Smpd3, which encodes for the ceramide-generating enzyme neutral sphingomyelinase 2.	Ceramides	185-193	sphingomyelin phosphodiesterase 3	Danio rerio	156-161
32998995-6	2020	Galc-silenced cells displayed altered sphingolipid metabolism and increased intracellular levels of ceramide, paralleled by a non-redundant upregulation of Smpd3, which encodes for the ceramide-generating enzyme neutral sphingomyelinase 2.	Ceramides	185-193	sphingomyelin phosphodiesterase 3	Homo sapiens	212-238
32998995-7	2020	Accordingly, GALC downregulation caused SMPD3 upregulation, increased ceramide levels, and inhibited the tumorigenic activity of human melanoma A2058 cells, whereas GALC upregulation exerted opposite effects.	Ceramides	70-78	galactosylceramidase	Homo sapiens	13-17
33198218-7	2020	The use of pharmacologic inhibitor strategy suggested the involvement of the lipid ceramide-generating enzyme, acid sphingomyelinase (aSMase) in MVP biogenesis, and observed that regardless of the stimuli used, aSMase inhibition significantly blocked MVP release.	Ceramides	83-91	sphingomyelin phosphodiesterase 1	Homo sapiens	111-132
33198218-7	2020	The use of pharmacologic inhibitor strategy suggested the involvement of the lipid ceramide-generating enzyme, acid sphingomyelinase (aSMase) in MVP biogenesis, and observed that regardless of the stimuli used, aSMase inhibition significantly blocked MVP release.	Ceramides	83-91	sphingomyelin phosphodiesterase 1	Homo sapiens	211-217
33273998-6	2020	Furthermore, Taurisolo  was able to induce autophagic process via increasing the expression of LC3II, a protein marker involved in formation of autophagosome and ex novo synthesis of sphingomyelin, ceramides, and their metabolites both in HG- and THG-H9c2 cells.	Ceramides	198-207	microtubule-associated protein 1 light chain 3 alpha	Rattus norvegicus	95-100
32938759-4	2020	SM biosynthesis starts in the endoplasmic reticulum (ER) and gives rise to ceramide, which is transported from the ER to the Golgi by the action of ceramide transfer protein (CERT), where it can be converted to SM.	Ceramides	75-83	ceramide transporter 1	Homo sapiens	175-179
33168861-1	2020	The metabolism of ceramides is deregulated in the brain of Alzheimer"s disease (AD) patients and is associated with apolipoprotein (APO) APOE4 and amyloid-beta pathology.	Ceramides	18-27	amyloid beta precursor protein	Homo sapiens	147-159
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.	Ceramides	146-154	glucosylceramidase beta	Homo sapiens	0-18
33153050-5	2020	This indicates that the antidepressants paroxetine and amitriptyline reduce social fear via the ASM-ceramide system and that ASM-/- mice represent an appropriate tool to study antidepressant-resistant social fear.	Ceramides	100-108	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	96-99
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.	Ceramides	146-154	glucosylceramidase beta	Homo sapiens	20-25
33219119-0	2020	Role of ceramide-to-dihydroceramide ratios for insulin resistance and non-alcoholic fatty liver disease in humans.	Ceramides	8-16	insulin	Homo sapiens	47-54
33219119-2	2020	A recent study showed that depletion of dihydroceramide desaturase-1 (DES-1) in adipose and/or liver tissue decreases ceramide-to-dihydroceramide ratios (ceramide/dihydroceramide) in several tissues and improves the metabolic profile in mice.	Ceramides	47-55	delta(4)-desaturase, sphingolipid 1	Mus musculus	70-75
33219119-2	2020	A recent study showed that depletion of dihydroceramide desaturase-1 (DES-1) in adipose and/or liver tissue decreases ceramide-to-dihydroceramide ratios (ceramide/dihydroceramide) in several tissues and improves the metabolic profile in mice.	Ceramides	118-126	delta(4)-desaturase, sphingolipid 1	Mus musculus	70-75
33178388-6	2020	The percentage of ceramides and sphingosine was found to be significantly greater in the control cells than in the ATP9A overexpression and ATP9A knockout groups.	Ceramides	18-27	ATPase phospholipid transporting 9A (putative)	Homo sapiens	115-120
32738771-4	2020	Mass spectral analyses showed that B13 treatment significantly raised levels of four types of ceramides in human B-cells.	Ceramides	94-103	NADH:ubiquinone oxidoreductase subunit A5	Homo sapiens	35-38
32918529-9	2020	In regard to other sphingolipids and lysophospholipids, ceramides were similarly modulated by NPC1L1 to S1P, while other lipids were differently influenced by NPC1L1 or ABCG5/8 from S1P.	Ceramides	56-65	NPC1 like intracellular cholesterol transporter 1	Mus musculus	94-100
33058150-1	2020	Mitochondrial translocation of ceramides triggers Bax-dependent apoptosis.	Ceramides	31-40	BCL2 associated X, apoptosis regulator	Homo sapiens	50-53
33058150-2	2020	To elucidate how ceramides activate Bax and commit cells to death, we developed a switchable version of the ceramide transfer protein CERT, sCERT.	Ceramides	17-26	BCL2 associated X, apoptosis regulator	Homo sapiens	36-39
33058150-2	2020	To elucidate how ceramides activate Bax and commit cells to death, we developed a switchable version of the ceramide transfer protein CERT, sCERT.	Ceramides	17-26	ceramide transporter 1	Homo sapiens	134-138
33058150-2	2020	To elucidate how ceramides activate Bax and commit cells to death, we developed a switchable version of the ceramide transfer protein CERT, sCERT.	Ceramides	17-25	BCL2 associated X, apoptosis regulator	Homo sapiens	36-39
33058150-2	2020	To elucidate how ceramides activate Bax and commit cells to death, we developed a switchable version of the ceramide transfer protein CERT, sCERT.	Ceramides	17-25	ceramide transporter 1	Homo sapiens	134-138
33058150-5	2020	The ability of mitochondria-bound sCERT to mediate ceramide import and Bax translocation requires both its START domain and ongoing ceramide biosynthesis.	Ceramides	132-140	BCL2 associated X, apoptosis regulator	Homo sapiens	71-74
32738398-9	2020	Sphk1 knockdown inhibited the hepatic S1P rise while accumulating ceramides in hepatocytes of NAFL mice, leading to aggressive hepatic I/R injury with upregulation of oxidative stress and increase of reactive oxygen species (ROS).	Ceramides	66-75	sphingosine kinase 1	Mus musculus	0-5
33178388-6	2020	The percentage of ceramides and sphingosine was found to be significantly greater in the control cells than in the ATP9A overexpression and ATP9A knockout groups.	Ceramides	18-27	ATPase phospholipid transporting 9A (putative)	Homo sapiens	140-145
33113993-10	2020	The GCE effects could be related to reductions of hepatic (i) mTOR phosphorylation, leading to higher nuclear lipin-1 levels and limiting lipogenic gene expression; (ii) diacylglycerol levels; (iii) hexosylceramide/ceramide ratios; and (iv) very-low-density lipoprotein receptor expression.	Ceramides	206-214	mechanistic target of rapamycin kinase	Rattus norvegicus	62-66
32569477-10	2020	Treatment with recombinant human acid ceramidase, to decrease ceramide, reduced both inflammatory mediator production and susceptibility to infection.	Ceramides	62-70	N-acylsphingosine amidohydrolase 1	Homo sapiens	33-48
33033337-3	2020	Since neutral sphingomyelinase-2 (nSMase2: SMPD3) is a key enzyme for ceramide production involved in inflammation, we investigated whether nSMase2 contributed to the inflammatory changes in the monocytes/macrophages induced by TNF-alpha.	Ceramides	70-78	sphingomyelin phosphodiesterase 3	Homo sapiens	34-41
32687399-0	2020	Membrane Lipids and CFTR: The Ying/Yang of Efficient Ceramide Metabolism.	Ceramides	53-61	CF transmembrane conductance regulator	Homo sapiens	20-24
33057972-1	2020	By cleaving sphingomyelin into ceramide, which is an essential component of plasma membrane microdomains, acid sphingomyelinase (Asm) pivotally controls cell signaling.	Ceramides	31-39	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	106-127
33057972-1	2020	By cleaving sphingomyelin into ceramide, which is an essential component of plasma membrane microdomains, acid sphingomyelinase (Asm) pivotally controls cell signaling.	Ceramides	31-39	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	129-132
33027663-5	2020	Ceramide (a key product of SMPD3) rescues non-inactivating channel behavior.	Ceramides	0-8	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	27-32
33205016-5	2020	Tcb3p and their homologs Tcb1p and Tcb2p are required for formation of ER-Golgi contacts and non-vesicular ceramide transport.	Ceramides	107-115	Tcb3p	Saccharomyces cerevisiae S288C	0-5
33205016-5	2020	Tcb3p and their homologs Tcb1p and Tcb2p are required for formation of ER-Golgi contacts and non-vesicular ceramide transport.	Ceramides	107-115	tricalbin	Saccharomyces cerevisiae S288C	25-30
33205016-5	2020	Tcb3p and their homologs Tcb1p and Tcb2p are required for formation of ER-Golgi contacts and non-vesicular ceramide transport.	Ceramides	107-115	tricalbin	Saccharomyces cerevisiae S288C	35-40
32766878-12	2020	Ceramides may inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways.	Ceramides	0-9	phosphatidylethanolamine N-methyltransferase	Homo sapiens	40-44
33008902-6	2020	Pharmacological inhibition or genetic deletion of nSMase2 in myelinating oligodendrocytes normalized the ceramide content of remyelinated fibers and increased thickness and compaction.	Ceramides	105-113	sphingomyelin phosphodiesterase 3	Homo sapiens	50-57
32766878-12	2020	Ceramides may inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways.	Ceramides	0-9	insulin	Homo sapiens	58-65
32766878-12	2020	Ceramides may inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways.	Ceramides	0-9	phosphatidylethanolamine N-methyltransferase	Homo sapiens	153-157
32766878-12	2020	Ceramides may inhibit the expression of PEMT by increased insulin resistance, thus potentially suggesting a functional pathway that integrates ceramide, PEMT, and glycerolipid biosynthetic pathways.	Ceramides	143-151	phosphatidylethanolamine N-methyltransferase	Homo sapiens	40-44
32860931-9	2020	Furthermore, a synthetic cell-permeable ceramide analog, C2-ceramide, inhibited myotube formation in C2C12 cells and decreased the expressions of MyoD and myogenin, suggesting that accelerated ceramide production is involved in the alpha-toxin-mediated blockage of myogenic differentiation.	Ceramides	40-48	myogenin	Mus musculus	155-163
32860931-9	2020	Furthermore, a synthetic cell-permeable ceramide analog, C2-ceramide, inhibited myotube formation in C2C12 cells and decreased the expressions of MyoD and myogenin, suggesting that accelerated ceramide production is involved in the alpha-toxin-mediated blockage of myogenic differentiation.	Ceramides	60-68	myogenin	Mus musculus	155-163
33090381-9	2020	The upregulation of ceramide accelerated the P1 NP cell degeneration by the reduction of collagen II production and proliferative cells population, increased p16 expression, and apoptotic cells population.	Ceramides	20-28	cyclin dependent kinase inhibitor 2A	Homo sapiens	158-161
33133017-5	2020	Furthermore, the interaction between ceramides and adipokines, most notably adiponectin and leptin, appears to play a role in the pathophysiology of these conditions.	Ceramides	37-46	adiponectin, C1Q and collagen domain containing	Homo sapiens	76-87
33133017-5	2020	Furthermore, the interaction between ceramides and adipokines, most notably adiponectin and leptin, appears to play a role in the pathophysiology of these conditions.	Ceramides	37-46	leptin	Homo sapiens	92-98
33133017-6	2020	Adiponectin appears to counteract the detrimental effects of elevated ceramides, largely through activation of the ceramidase activity of its receptors.	Ceramides	70-79	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
33133017-7	2020	Elevated ceramides appear to worsen leptin resistance, which is an important phenomenon in the pathophysiology of obesity and metabolic syndrome.	Ceramides	9-18	leptin	Homo sapiens	36-42
32902157-4	2020	Under a reduced CERS6 expression condition, the ceramide profile became altered, which was determined to be associated with decreased cell migration and invasion activities in vitro.	Ceramides	48-56	ceramide synthase 6	Mus musculus	16-21
32902157-6	2020	Based on these findings, we consider that ceramide synthesis by CERS6 has important roles in lung cancer migration and metastasis.	Ceramides	42-50	ceramide synthase 6	Mus musculus	64-69
32026462-7	2020	Furthermore, ceramide biosynthesis regulated exosomal-miR-1260b secretion.	Ceramides	13-21	microRNA 1260b	Homo sapiens	54-63
32574624-2	2020	Hepatocytes release ceramide-enriched inflammatory extracellular vesicles (EVs) following activation of IRE1A.	Ceramides	20-28	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	104-109
32574624-14	2020	IRE1A-stimulated EVs were enriched in ceramides.	Ceramides	38-47	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	0-5
32574624-15	2020	Chromatin immunoprecipitation showed that IRE1A activated X-box binding protein 1 (XBP1) to increase transcription of serine palmitoyltransferase genes, which encode the rate-limiting enzyme for ceramide biosynthesis.	Ceramides	195-203	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	42-47
32574624-15	2020	Chromatin immunoprecipitation showed that IRE1A activated X-box binding protein 1 (XBP1) to increase transcription of serine palmitoyltransferase genes, which encode the rate-limiting enzyme for ceramide biosynthesis.	Ceramides	195-203	X-box binding protein 1	Mus musculus	58-81
32574624-15	2020	Chromatin immunoprecipitation showed that IRE1A activated X-box binding protein 1 (XBP1) to increase transcription of serine palmitoyltransferase genes, which encode the rate-limiting enzyme for ceramide biosynthesis.	Ceramides	195-203	X-box binding protein 1	Mus musculus	83-87
32574624-18	2020	CONCLUSIONS: In mouse hepatocytes, activated IRE1A promotes transcription of serine palmitoyltransferase genes via XBP1, resulting in ceramide biosynthesis and release of EVs.	Ceramides	134-142	endoplasmic reticulum (ER) to nucleus signalling 1	Mus musculus	45-50
32574624-18	2020	CONCLUSIONS: In mouse hepatocytes, activated IRE1A promotes transcription of serine palmitoyltransferase genes via XBP1, resulting in ceramide biosynthesis and release of EVs.	Ceramides	134-142	X-box binding protein 1	Mus musculus	115-119
33003449-0	2020	Ceramide-Enriched Membrane Domains Contribute to Targeted and Nontargeted Effects of Radiation through Modulation of PI3K/AKT Signaling in HNSCC Cells.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	122-125
32941570-6	2020	We further demonstrate that this dual drug combination induces a significant increase in the expression of ceramide synthase 1, 4, and 6, thereby increasing the level of ceramides that contribute to the synergistic apoptotic effect.	Ceramides	170-179	ceramide synthase 1	Mus musculus	107-136
32215553-8	2020	Additionally, we found that changes in circulating adiponectin, FGF21 and the 6-minute walk test (6MW) inversely correlated with CV-related circulating ceramides after bed rest.	Ceramides	152-161	adiponectin, C1Q and collagen domain containing	Homo sapiens	51-62
32215553-8	2020	Additionally, we found that changes in circulating adiponectin, FGF21 and the 6-minute walk test (6MW) inversely correlated with CV-related circulating ceramides after bed rest.	Ceramides	152-161	fibroblast growth factor 21	Homo sapiens	64-69
32900381-7	2020	For glycosphingolipids (GSLs), Globo H ceramide, an important tumor-associated GSL which is being actively investigated as a target for new cancer immunotherapies, will be used to demonstrate how glycan structure plays a significant role in enhancing angiogenesis in tumor microenvironments.	Ceramides	39-47	cathepsin A	Homo sapiens	24-27
32973966-0	2020	Small ceramide tames big p53 mutant beast.	Ceramides	6-14	tumor protein p53	Homo sapiens	25-28
33088808-1	2020	Neutral sphingomyelinase-2 (NSM2) is a member of a superfamily of enzymes responsible for conversion of sphingomyelin into phosphocholine and ceramide at the cytosolic leaflet of the plasma membrane.	Ceramides	142-150	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
33088808-1	2020	Neutral sphingomyelinase-2 (NSM2) is a member of a superfamily of enzymes responsible for conversion of sphingomyelin into phosphocholine and ceramide at the cytosolic leaflet of the plasma membrane.	Ceramides	142-150	sphingomyelin phosphodiesterase 3	Homo sapiens	28-32
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	98-122
32885529-7	2021	Ceramide species NS was significantly higher in AD patients compared to healthy volunteers and was also higher in AD patients with a FLG mutation compared to AD patients without a FLG mutation.	Ceramides	0-8	filaggrin	Homo sapiens	133-136
32885529-7	2021	Ceramide species NS was significantly higher in AD patients compared to healthy volunteers and was also higher in AD patients with a FLG mutation compared to AD patients without a FLG mutation.	Ceramides	0-8	filaggrin	Homo sapiens	180-183
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).	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
33205006-3	2020	Previous studies showed that ceramide glycosylation correlates with upregulated expression of p53 hotspot mutant R273H and cancer drug resistance.	Ceramides	29-37	tumor protein p53	Homo sapiens	94-97
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	tumor protein p53	Homo sapiens	230-233
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	62-65
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	tumor protein p53	Homo sapiens	278-281
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	66-70
32691632-10	2020	In line with the proposed role for HSD17B12 in the fatty acid elongation, we observed accumulation of ceramides, dihydroceramides, hexosylceramides and lactosylceramides with shorter than 18-carbon fatty acid side chains in the serum.	Ceramides	102-111	hydroxysteroid (17-beta) dehydrogenase 12	Mus musculus	35-43
33205006-10	2020	Suppression of ceramide glycosylation significantly decreased Gb3-cSrc in GEMs, beta-catenin, and methyltransferase-like 3 for m6A RNA methylation, thus altering pre-mRNA splicing, resulting in upregulated expression of wild-type p53 protein, but not mutants, in cells carrying p53 R273H.	Ceramides	15-23	catenin beta 1	Homo sapiens	80-92
33024732-6	2020	In addition, recent experimental studies utilizing SMS knockout mice and murine disease models provide evidence that SMS-regulated ceramide/SM balance is involved in human diseases.	Ceramides	131-139	spermine synthase	Mus musculus	51-54
32474112-12	2020	Deficiency of Dgat1 in mice resulted in a reduction of 1-OACs to 30% in colon, but not in small intestine and liver, going along with constant free ceramides levels.	Ceramides	148-157	diacylglycerol O-acyltransferase 1	Mus musculus	14-19
33024732-6	2020	In addition, recent experimental studies utilizing SMS knockout mice and murine disease models provide evidence that SMS-regulated ceramide/SM balance is involved in human diseases.	Ceramides	131-139	spermine synthase	Mus musculus	117-120
33024732-9	2020	This review finally presents evidence indicating that the regulation of ceramide/SM balance through SMS could be a therapeutic target for human disorders.	Ceramides	72-80	spermine synthase	Homo sapiens	100-103
32855410-3	2020	Mechanistic studies of the underlying tumor supportive onco-metabolism reveal coordinated activities through which Cav-1 enables rewiring of cancer cell lipid metabolism towards a program of 1) exogenous sphingolipid scavenging independent of cholesterol, 2) increased cancer cell catabolism of sphingomyelins to ceramide derivatives and 3) altered ceramide metabolism that results in increased glycosphingolipid synthesis and efflux of Cav-1-sphingolipid particles containing mitochondrial proteins and lipids.	Ceramides	313-321	caveolin 1	Homo sapiens	115-120
32807460-5	2020	Different studies showed the evidence that sphingomyelinase with Cer production induces expression of interleukin (IL)-6 and have vasoconstrictive proprieties.	Ceramides	65-68	interleukin 6	Homo sapiens	102-120
32855410-3	2020	Mechanistic studies of the underlying tumor supportive onco-metabolism reveal coordinated activities through which Cav-1 enables rewiring of cancer cell lipid metabolism towards a program of 1) exogenous sphingolipid scavenging independent of cholesterol, 2) increased cancer cell catabolism of sphingomyelins to ceramide derivatives and 3) altered ceramide metabolism that results in increased glycosphingolipid synthesis and efflux of Cav-1-sphingolipid particles containing mitochondrial proteins and lipids.	Ceramides	349-357	caveolin 1	Homo sapiens	115-120
32829707-0	2020	Ceramide induces MMP-9 expression through JAK2/STAT3 pathway in airway epithelium.	Ceramides	0-8	matrix metallopeptidase 9	Homo sapiens	17-22
32829707-0	2020	Ceramide induces MMP-9 expression through JAK2/STAT3 pathway in airway epithelium.	Ceramides	0-8	Janus kinase 2	Homo sapiens	42-46
32829707-0	2020	Ceramide induces MMP-9 expression through JAK2/STAT3 pathway in airway epithelium.	Ceramides	0-8	signal transducer and activator of transcription 3	Homo sapiens	47-52
32829707-3	2020	This study was conducted to investigate the effects and underlying mechanisms of ceramide on MMP-9 expression in airway epithelium.	Ceramides	81-89	matrix metallopeptidase 9	Homo sapiens	93-98
32829707-14	2020	CONCLUSIONS: Ceramide could up-regulate MMP-9 expression through the activation of the JAK2/STAT3 pathway in airway epithelium.	Ceramides	13-21	matrix metallopeptidase 9	Mus musculus	40-45
32829707-14	2020	CONCLUSIONS: Ceramide could up-regulate MMP-9 expression through the activation of the JAK2/STAT3 pathway in airway epithelium.	Ceramides	13-21	Janus kinase 2	Mus musculus	87-91
32829707-14	2020	CONCLUSIONS: Ceramide could up-regulate MMP-9 expression through the activation of the JAK2/STAT3 pathway in airway epithelium.	Ceramides	13-21	signal transducer and activator of transcription 3	Mus musculus	92-97
32829707-15	2020	Targeted modulation of the ceramide signaling pathway may offer a potential therapeutic approach for inhibiting MMP-9 expression.	Ceramides	27-35	matrix metallopeptidase 9	Mus musculus	112-117
32641420-2	2020	Inhibition of ceramide biosynthesis has been shown in model systems to antagonize obesity and improve insulin sensitivity.	Ceramides	14-22	insulin	Homo sapiens	102-109
32817366-8	2020	Consistently, a signature of the genes most down-regulated by ceramide identifies patients with advanced fibrosis who could benefit from aCDase targeting.	Ceramides	62-70	N-acylsphingosine amidohydrolase 1	Homo sapiens	137-143
32817366-9	2020	The findings implicate ceramide as a critical regulator of YAP/TAZ signaling and HSC activation and highlight aCDase as a therapeutic target for the treatment of fibrosis.	Ceramides	23-31	Yes1 associated transcriptional regulator	Homo sapiens	59-62
32817366-9	2020	The findings implicate ceramide as a critical regulator of YAP/TAZ signaling and HSC activation and highlight aCDase as a therapeutic target for the treatment of fibrosis.	Ceramides	23-31	tafazzin, phospholipid-lysophospholipid transacylase	Homo sapiens	63-66
32639040-2	2020	In this issue of The EMBO Journal, Martin-Leal et al show that the inflammatory chemokine receptor CCR5, well known for its role in cell migration and HIV infection, regulates ceramide synthesis and TCR nanoclustering to promote memory CD4+ T cell activation.	Ceramides	176-184	C-C motif chemokine receptor 5	Homo sapiens	99-103
32692177-6	2020	Further, the inhibited mRNA expressions of protein phosphatase 2A and protein kinase Czeta involved in blocking Akt phosphorylation connected the controlled ceramides with the restored insulin sensitivity.	Ceramides	157-166	thymoma viral proto-oncogene 1	Mus musculus	112-115
32525588-0	2020	CCR5 deficiency impairs CD4+ T-cell memory responses and antigenic sensitivity through increased ceramide synthesis.	Ceramides	97-105	chemokine (C-C motif) receptor 5	Mus musculus	0-4
32759684-5	2020	Comparing metabolomic profiles between MDM2 higher and lower amplification cells yielded a total of 17 differentially abundant metabolites across both panels (FDR < 0.05, log2 fold change < 0.75), including ceramides, glycosylated ceramides, and sphingomyelins.	Ceramides	207-216	MDM2 proto-oncogene	Homo sapiens	39-43
32639040-2	2020	In this issue of The EMBO Journal, Martin-Leal et al show that the inflammatory chemokine receptor CCR5, well known for its role in cell migration and HIV infection, regulates ceramide synthesis and TCR nanoclustering to promote memory CD4+ T cell activation.	Ceramides	176-184	CD4 molecule	Homo sapiens	236-239
32525588-2	2020	Here, we show that by limiting transcription of specific ceramide synthases, CCR5 signaling reduces ceramide levels and thereby increases T-cell antigen receptor (TCR) nanoclustering in antigen-experienced mouse and human CD4+ T cells.	Ceramides	57-65	chemokine (C-C motif) receptor 5	Mus musculus	77-81
32525588-2	2020	Here, we show that by limiting transcription of specific ceramide synthases, CCR5 signaling reduces ceramide levels and thereby increases T-cell antigen receptor (TCR) nanoclustering in antigen-experienced mouse and human CD4+ T cells.	Ceramides	57-65	T cell receptor alpha variable 6-3	Mus musculus	138-161
32072647-11	2020	CONCLUSION: Uncontrolled asthmatics possess distinct inflammatory phenotypes including increased CD66+ neutrophils and platelet-adherent eosinophils, with an imbalanced ceramide/S1P rheostat, potentially involving ORMDL3 and SGMS1 gene polymorphisms.	Ceramides	169-177	ORMDL sphingolipid biosynthesis regulator 3	Homo sapiens	214-220
32525588-2	2020	Here, we show that by limiting transcription of specific ceramide synthases, CCR5 signaling reduces ceramide levels and thereby increases T-cell antigen receptor (TCR) nanoclustering in antigen-experienced mouse and human CD4+ T cells.	Ceramides	57-65	T cell receptor alpha variable 6-3	Mus musculus	163-166
32525588-2	2020	Here, we show that by limiting transcription of specific ceramide synthases, CCR5 signaling reduces ceramide levels and thereby increases T-cell antigen receptor (TCR) nanoclustering in antigen-experienced mouse and human CD4+ T cells.	Ceramides	57-65	CD4 molecule	Homo sapiens	222-225
32072647-11	2020	CONCLUSION: Uncontrolled asthmatics possess distinct inflammatory phenotypes including increased CD66+ neutrophils and platelet-adherent eosinophils, with an imbalanced ceramide/S1P rheostat, potentially involving ORMDL3 and SGMS1 gene polymorphisms.	Ceramides	169-177	sphingomyelin synthase 1	Homo sapiens	225-230
32650914-0	2020	Effect of Proprotein Convertase Subtilisin/Kexin Type 9 Inhibitors on Plasma Ceramide Levels.	Ceramides	77-85	proprotein convertase subtilisin/kexin type 9	Homo sapiens	10-55
32845565-7	2020	No change in mitochondrial enzyme activity was observed following HFEE, but citrate synthase activity was inversely associated with the increase in the ceramide content (r=-0.52, p = .048).	Ceramides	152-160	citrate synthase	Homo sapiens	76-92
32650914-4	2020	The effect of PCSK9 inhibition on plasma ceramides is not well known.	Ceramides	41-50	proprotein convertase subtilisin/kexin type 9	Homo sapiens	14-19
32650914-5	2020	The study examines the effect of PCSK9 inhibitors on plasma ceramides and CRS in patients with clinical indication for this therapy.	Ceramides	60-69	proprotein convertase subtilisin/kexin type 9	Homo sapiens	33-38
32650914-9	2020	Treatment with PCSK9 inhibitors was associated with significant reduction in mean CRS and individual ceramides levels (p <0.0001).	Ceramides	101-110	proprotein convertase subtilisin/kexin type 9	Homo sapiens	15-20
32650914-13	2020	In conclusion, treatment with PCSK9 inhibitors is associated with significant reduction in CRS and distinct ceramide levels.	Ceramides	108-116	proprotein convertase subtilisin/kexin type 9	Homo sapiens	30-35
32771984-10	2020	Ceramide biosynthesis genes Smpd3, Sptlc2, and Cers4 were decreased in liver and intestine suggesting lower tissue ceramides levels may contribute to improved glucose metabolism.	Ceramides	0-8	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	28-33
32771984-10	2020	Ceramide biosynthesis genes Smpd3, Sptlc2, and Cers4 were decreased in liver and intestine suggesting lower tissue ceramides levels may contribute to improved glucose metabolism.	Ceramides	0-8	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	35-41
32771984-10	2020	Ceramide biosynthesis genes Smpd3, Sptlc2, and Cers4 were decreased in liver and intestine suggesting lower tissue ceramides levels may contribute to improved glucose metabolism.	Ceramides	0-8	ceramide synthase 4	Mus musculus	47-52
32771984-10	2020	Ceramide biosynthesis genes Smpd3, Sptlc2, and Cers4 were decreased in liver and intestine suggesting lower tissue ceramides levels may contribute to improved glucose metabolism.	Ceramides	115-124	ceramide synthase 4	Mus musculus	47-52
31701696-9	2020	Cultured podocytes exposed to agents predicted to be risk factors (high glucose, high free fatty acid, and angiotensin II in combination [GFA]) showed an increase in ceramide accumulation and ROS generation in podocyte mitochondria.	Ceramides	166-174	angiotensinogen	Homo sapiens	107-121
31701696-9	2020	Cultured podocytes exposed to agents predicted to be risk factors (high glucose, high free fatty acid, and angiotensin II in combination [GFA]) showed an increase in ceramide accumulation and ROS generation in podocyte mitochondria.	Ceramides	166-174	glutamine--fructose-6-phosphate transaminase 1	Homo sapiens	138-141
32627931-3	2020	Increasing evidence suggests the farnesoid X receptor (FXR) is involved in ceramide metabolism, as bile acid-FXR crosstalk controls ceramide levels along the gut-liver axis.	Ceramides	75-83	nuclear receptor subfamily 1, group H, member 4	Mus musculus	33-53
32627931-3	2020	Increasing evidence suggests the farnesoid X receptor (FXR) is involved in ceramide metabolism, as bile acid-FXR crosstalk controls ceramide levels along the gut-liver axis.	Ceramides	75-83	nuclear receptor subfamily 1, group H, member 4	Mus musculus	55-58
32627931-3	2020	Increasing evidence suggests the farnesoid X receptor (FXR) is involved in ceramide metabolism, as bile acid-FXR crosstalk controls ceramide levels along the gut-liver axis.	Ceramides	75-83	nuclear receptor subfamily 1, group H, member 4	Mus musculus	109-112
32627931-3	2020	Increasing evidence suggests the farnesoid X receptor (FXR) is involved in ceramide metabolism, as bile acid-FXR crosstalk controls ceramide levels along the gut-liver axis.	Ceramides	132-140	nuclear receptor subfamily 1, group H, member 4	Mus musculus	33-53
32627931-3	2020	Increasing evidence suggests the farnesoid X receptor (FXR) is involved in ceramide metabolism, as bile acid-FXR crosstalk controls ceramide levels along the gut-liver axis.	Ceramides	132-140	nuclear receptor subfamily 1, group H, member 4	Mus musculus	55-58
32627931-3	2020	Increasing evidence suggests the farnesoid X receptor (FXR) is involved in ceramide metabolism, as bile acid-FXR crosstalk controls ceramide levels along the gut-liver axis.	Ceramides	132-140	nuclear receptor subfamily 1, group H, member 4	Mus musculus	109-112
32722909-3	2020	Recently, we showed that a 1h pre-treatment with anti-angiogenic drugs prior to ultra-high single dose radiotherapy and specific chemotherapies transiently de-represses acid sphingomyelinase (ASMase), leading to enhanced cancer therapy-induced, ceramide-mediated vascular injury and tumor response.	Ceramides	245-253	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	169-190
31808525-6	2020	On the contrary, SpA patients had significantly decreased levels of ceramide, in both analyses.	Ceramides	68-76	surfactant protein A2	Homo sapiens	17-20
32722909-3	2020	Recently, we showed that a 1h pre-treatment with anti-angiogenic drugs prior to ultra-high single dose radiotherapy and specific chemotherapies transiently de-represses acid sphingomyelinase (ASMase), leading to enhanced cancer therapy-induced, ceramide-mediated vascular injury and tumor response.	Ceramides	245-253	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	192-198
32849276-3	2020	Recent studies have demonstrated that the acyl-chain is an important determinant of ceramide function, such that a small subset of ceramides (e.g., those containing the C16 or C18 acyl-chain) alter metabolism by inhibiting insulin signaling or inducing mitochondrial fragmentation.	Ceramides	84-92	insulin	Homo sapiens	223-230
32849276-3	2020	Recent studies have demonstrated that the acyl-chain is an important determinant of ceramide function, such that a small subset of ceramides (e.g., those containing the C16 or C18 acyl-chain) alter metabolism by inhibiting insulin signaling or inducing mitochondrial fragmentation.	Ceramides	131-140	insulin	Homo sapiens	223-230
32246947-1	2020	Ceramide kinase (CerK) phosphorylates ceramide to ceramide-1-phosphate (C1P).	Ceramides	38-46	ceramide kinase	Rattus norvegicus	0-15
32487748-9	2020	Remarkably, ceramide-induced RIP of cAMP response element-binding protein 3-like 1 (CREB3L1) also involves RAT.	Ceramides	12-20	cAMP responsive element binding protein 3-like 1	Rattus norvegicus	36-82
32487748-9	2020	Remarkably, ceramide-induced RIP of cAMP response element-binding protein 3-like 1 (CREB3L1) also involves RAT.	Ceramides	12-20	cAMP responsive element binding protein 3-like 1	Rattus norvegicus	84-91
32487748-11	2020	Ceramide inverts the orientation of newly synthesized TM4SF20 in membranes through RAT, converting TM4SF20 from an inhibitor to an activator of RIP of CREB3L1.	Ceramides	0-8	transmembrane 4 L six family member 20	Rattus norvegicus	54-61
32487748-11	2020	Ceramide inverts the orientation of newly synthesized TM4SF20 in membranes through RAT, converting TM4SF20 from an inhibitor to an activator of RIP of CREB3L1.	Ceramides	0-8	transmembrane 4 L six family member 20	Rattus norvegicus	99-106
32487748-11	2020	Ceramide inverts the orientation of newly synthesized TM4SF20 in membranes through RAT, converting TM4SF20 from an inhibitor to an activator of RIP of CREB3L1.	Ceramides	0-8	cAMP responsive element binding protein 3-like 1	Rattus norvegicus	151-158
32707889-10	2020	Ceramide, which is increased by inhibiting choline uptake, also inhibited cell survival and increased caspase-3/7 activity.	Ceramides	0-8	caspase 3	Homo sapiens	102-113
32668665-4	2020	Ceramide is an active lipid that inhibits the insulin signaling pathway as well as inducing pancreatic beta cell death.	Ceramides	0-8	insulin	Homo sapiens	46-53
32135176-4	2020	We demonstrate for the first time that the tumor suppressor lipid, ceramide (Cer), causes Par-4 induction, leading to autophagic cell death in human malignant glioma.	Ceramides	67-75	pro-apoptotic WT1 regulator	Homo sapiens	90-95
32135176-4	2020	We demonstrate for the first time that the tumor suppressor lipid, ceramide (Cer), causes Par-4 induction, leading to autophagic cell death in human malignant glioma.	Ceramides	77-80	pro-apoptotic WT1 regulator	Homo sapiens	90-95
32849291-5	2020	We propose herein that the less abundant ceramides, through evolutionarily-conserved actions intended to help organisms adapt to nutrient excess, drive the cellular events that define NAFL/NASH.	Ceramides	41-50	SAM domain, SH3 domain and nuclear localization signals 1	Homo sapiens	189-193
32573489-6	2020	IGSF3-deficient patient-derived lymphoblastoids exhibited multiple alterations in gene expression, especially in the unfolded protein response and ceramide pathways.	Ceramides	147-155	immunoglobulin superfamily member 3	Homo sapiens	0-5
32573489-7	2020	IGSF3-deficient lymphoblastoids had high ceramide- and sphingosine-1 phosphate-, but low glycosphingolipids- and gangliosides levels; were less apoptotic and more adherent; with marked changes in multiple TNFRSF molecules.	Ceramides	41-49	immunoglobulin superfamily member 3	Homo sapiens	0-5
32573489-8	2020	Similarly, IGSF3 knockdown increased ceramide in lung structural cells, rendering them more adherent, with impaired wound repair and a weakened barrier function.	Ceramides	37-45	immunoglobulin superfamily member 3	Homo sapiens	11-16
32708453-8	2020	Bioactive sphingolipid and glycolipid molecules with reported anti-inflammatory and anti-tumour properties, such as specific ceramides and glucosylcerebrosides with sphingosine, phytosphingosine and dihydrosphingosine bases but also specific monogalactodiglycerides and SM species bearing ALA at their sn-2 position, were identified in the SM subclass, providing a rational for its strong bioactivities against the PAF pathway.	Ceramides	125-134	PCNA clamp associated factor	Homo sapiens	415-418
32246947-1	2020	Ceramide kinase (CerK) phosphorylates ceramide to ceramide-1-phosphate (C1P).	Ceramides	38-46	ceramide kinase	Rattus norvegicus	17-21
32350079-4	2020	Here, we used LC-MS/MS to analyze the presence of key components of the ceramide metabolic pathway in vivo and in vitro in purified endoplasmic reticulum (ER), mitochondria-associated membranes (MAM), and mitochondria.	Ceramides	72-80	sarcoglycan gamma	Homo sapiens	195-198
32630271-1	2020	Ceramide synthase 5 is one of six enzymes that catalyze the production of ceramides from sphingosine or sphinganine.	Ceramides	74-83	ceramide synthase 5	Mus musculus	0-19
32391585-4	2020	Human alkaline ceramidase 2 (ACER2), a key enzyme that regulates hydrolysis of cellular ceramides, affects cancer cell survival, however its role in HCC has not been well characterized.	Ceramides	88-97	alkaline ceramidase 2	Homo sapiens	6-27
32391585-4	2020	Human alkaline ceramidase 2 (ACER2), a key enzyme that regulates hydrolysis of cellular ceramides, affects cancer cell survival, however its role in HCC has not been well characterized.	Ceramides	88-97	alkaline ceramidase 2	Homo sapiens	29-34
32391585-9	2020	Of note, ACER2/SMPDL3B promoted ceramide hydrolysis and S1P production.	Ceramides	32-40	alkaline ceramidase 2	Homo sapiens	9-14
32391585-9	2020	Of note, ACER2/SMPDL3B promoted ceramide hydrolysis and S1P production.	Ceramides	32-40	sphingomyelin phosphodiesterase acid like 3B	Homo sapiens	15-22
32350079-9	2020	We also found that ceramide generation is enhanced in mitochondria when sphingomyelin levels are decreased in the MAM.	Ceramides	19-27	sarcoglycan gamma	Homo sapiens	114-117
32398264-3	2020	Here, we employed a hepatic-specific acid-ceramidase (ASAH) overexpression model to reduce hepatic ceramides in a Lieber-DeCarli model of experimental alcoholic steatosis.	Ceramides	99-108	N-acylsphingosine amidohydrolase 1	Mus musculus	54-58
32398264-5	2020	Our results demonstrate that hepatic ceramide reduction ameliorates the effects of alcohol on hepatic lipid droplet accumulation by promoting VLDL secretion and lipophagy, the latter of which involves ceramide cross-talk between the lysosomal and lipid droplet compartments.	Ceramides	37-45	CD320 antigen	Mus musculus	142-146
32194052-0	2020	Podocytopathy and Nephrotic Syndrome in Mice with Podocyte-Specific Deletion of the Asah1 Gene: Role of Ceramide Accumulation in Glomeruli.	Ceramides	104-112	N-acylsphingosine amidohydrolase 1	Mus musculus	84-89
32430917-0	2020	Plasma Ceramides and Triglycerides Are Elevated during Pregnancy in Association with Markers of Insulin Resistance in Hutterite Women.	Ceramides	7-16	insulin	Homo sapiens	96-103
32430917-2	2020	Although ceramides can cause insulin resistance in mammals, their potential roles during pregnancy and lactation are unknown.	Ceramides	9-18	insulin	Homo sapiens	29-36
32430917-3	2020	We hypothesized that changes in lipids like ceramide and triglycerides could occur across different reproductive states and relate to insulin resistance.	Ceramides	44-52	insulin	Homo sapiens	134-141
32430917-9	2020	Our data support the possibility that ceramides contribute to the development of insulin resistance during pregnancy, and reveal distinct lipid signatures associated with pregnancy and lactation.	Ceramides	38-47	insulin	Homo sapiens	81-88
32636806-7	2020	Notably, recent experimental studies have strongly implicated ceramides in the development of numerous metabolic diseases such as insulin resistance, diabetes, cardiomyopathy, hepatic-steatosis, and atherosclerosis.	Ceramides	62-71	insulin	Homo sapiens	130-137
32291318-3	2020	Here we report that ceramide and its related enzyme acid sphingomyelinase (ASM) are secreted by irradiated endothelial cells and act as bystander factors to enhance the radiotoxicity of intestinal epithelium.	Ceramides	20-28	sphingomyelin phosphodiesterase 1	Homo sapiens	52-73
32298582-1	2020	Neutral sphingomyelinase 2 (nSMase2) catalyzes the cleavage of sphingomyelin to phosphorylcholine and ceramide, an essential step in the formation and release of exosomes from cells that is critical for intracellular communication.	Ceramides	102-110	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
31898284-10	2020	Met-RANTES treatment decreased expressions of CCR1, TPR1, p-ERK, TNF-alpha, and IL-1beta, which was reversed by ceramide C6.	Ceramides	112-120	chemokine (C-C motif) ligand 5	Mus musculus	4-10
31898284-10	2020	Met-RANTES treatment decreased expressions of CCR1, TPR1, p-ERK, TNF-alpha, and IL-1beta, which was reversed by ceramide C6.	Ceramides	112-120	chemokine (C-C motif) receptor 1	Mus musculus	46-50
31898284-10	2020	Met-RANTES treatment decreased expressions of CCR1, TPR1, p-ERK, TNF-alpha, and IL-1beta, which was reversed by ceramide C6.	Ceramides	112-120	tetratricopeptide repeat domain 1	Mus musculus	52-56
31898284-10	2020	Met-RANTES treatment decreased expressions of CCR1, TPR1, p-ERK, TNF-alpha, and IL-1beta, which was reversed by ceramide C6.	Ceramides	112-120	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	58-63
31898284-10	2020	Met-RANTES treatment decreased expressions of CCR1, TPR1, p-ERK, TNF-alpha, and IL-1beta, which was reversed by ceramide C6.	Ceramides	112-120	tumor necrosis factor	Mus musculus	65-74
31898284-10	2020	Met-RANTES treatment decreased expressions of CCR1, TPR1, p-ERK, TNF-alpha, and IL-1beta, which was reversed by ceramide C6.	Ceramides	112-120	interleukin 1 beta	Mus musculus	80-88
33062186-3	2020	We proposed substrate reduction therapy (SRT) as a novel approach to treat this disease, by inhibiting ceramide galactosyltransferase enzyme (UGT8).	Ceramides	103-111	UDP glycosyltransferase 8	Homo sapiens	142-146
32549981-0	2020	PHGDH supports liver ceramide synthesis and sustains lipid homeostasis.	Ceramides	21-29	3-phosphoglycerate dehydrogenase	Mus musculus	0-5
32549981-7	2020	Interestingly, diminished PHGDH expression reduced liver serine and ceramide levels without increasing the levels of deoxysphingolipids.	Ceramides	68-76	3-phosphoglycerate dehydrogenase	Mus musculus	26-31
32549981-9	2020	Conclusions: These results suggest that dietary serine is adequate to support the function of healthy, adult murine tissues, but PHGDH-derived serine supports liver ceramide synthesis and sustains general lipid homeostasis.	Ceramides	165-173	3-phosphoglycerate dehydrogenase	Mus musculus	129-134
32298582-1	2020	Neutral sphingomyelinase 2 (nSMase2) catalyzes the cleavage of sphingomyelin to phosphorylcholine and ceramide, an essential step in the formation and release of exosomes from cells that is critical for intracellular communication.	Ceramides	102-110	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
32194052-1	2020	Lysosomal acid ceramidase (Ac) has been shown to be critical for ceramide hydrolysis and regulation of lysosome function and cellular homeostasis.	Ceramides	65-73	N-acylsphingosine amidohydrolase 1	Mus musculus	10-25
32194052-1	2020	Lysosomal acid ceramidase (Ac) has been shown to be critical for ceramide hydrolysis and regulation of lysosome function and cellular homeostasis.	Ceramides	65-73	N-acylsphingosine amidohydrolase 1	Mus musculus	27-29
32194052-6	2020	Ceramide accumulation determined by LC-MS/MS was demonstrated in isolated glomeruli of Asah1fl/fl/PodoCre mice compared to their littermates.	Ceramides	0-8	N-acylsphingosine amidohydrolase 1	Mus musculus	87-92
32092464-6	2020	More specifically, abnormal localization of GBA and ASM related to an increase in specific ceramide subclasses [AS] and [NS].	Ceramides	91-99	glucosylceramidase beta	Homo sapiens	44-47
32112978-1	2020	Ceramide kinase (CerK) phosphorylates ceramide to ceramide-1-phosphate (C1P), a bioactive sphingolipid.	Ceramides	38-46	ceramide kinase	Mus musculus	0-15
32112978-1	2020	Ceramide kinase (CerK) phosphorylates ceramide to ceramide-1-phosphate (C1P), a bioactive sphingolipid.	Ceramides	38-46	ceramide kinase	Mus musculus	17-21
32092464-6	2020	More specifically, abnormal localization of GBA and ASM related to an increase in specific ceramide subclasses [AS] and [NS].	Ceramides	91-99	sphingomyelin phosphodiesterase 1	Homo sapiens	52-55
32265319-3	2020	We examined two key enzymes involved in epidermal ceramide biosynthesis, glucocerebrosidase (GBA) and acid-sphingomyelinase (ASM).	Ceramides	50-58	glucosylceramidase beta	Homo sapiens	73-91
32156719-1	2020	Inhibition of acid sphingomyelinase (ASM), a lysosomal enzyme that catalyzes the hydrolysis of sphingomyelin into ceramide and phosphorylcholine, may serve as an investigational tool or a therapeutic intervention to control many diseases.	Ceramides	114-122	sphingomyelin phosphodiesterase 1	Homo sapiens	14-35
32156719-1	2020	Inhibition of acid sphingomyelinase (ASM), a lysosomal enzyme that catalyzes the hydrolysis of sphingomyelin into ceramide and phosphorylcholine, may serve as an investigational tool or a therapeutic intervention to control many diseases.	Ceramides	114-122	sphingomyelin phosphodiesterase 1	Homo sapiens	37-40
32307766-5	2020	Neutral sphingomyelinase 2 (nSMase2) was identified as responsible for the generation of plasma membrane ceramide upon chemotherapy treatment, and both ceramide at the plasma membrane and nSMase2 were necessary and sufficient to mediate these "side" effects of chemotherapy on cell adhesion and migration.	Ceramides	105-113	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
32307766-5	2020	Neutral sphingomyelinase 2 (nSMase2) was identified as responsible for the generation of plasma membrane ceramide upon chemotherapy treatment, and both ceramide at the plasma membrane and nSMase2 were necessary and sufficient to mediate these "side" effects of chemotherapy on cell adhesion and migration.	Ceramides	105-113	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
32307766-5	2020	Neutral sphingomyelinase 2 (nSMase2) was identified as responsible for the generation of plasma membrane ceramide upon chemotherapy treatment, and both ceramide at the plasma membrane and nSMase2 were necessary and sufficient to mediate these "side" effects of chemotherapy on cell adhesion and migration.	Ceramides	152-160	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
32307766-5	2020	Neutral sphingomyelinase 2 (nSMase2) was identified as responsible for the generation of plasma membrane ceramide upon chemotherapy treatment, and both ceramide at the plasma membrane and nSMase2 were necessary and sufficient to mediate these "side" effects of chemotherapy on cell adhesion and migration.	Ceramides	152-160	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
32056304-0	2020	MicroRNA-34a causes ceramide accumulation and effects insulin signaling pathway by targeting ceramide kinase (CERK) in aging skeletal muscle.	Ceramides	20-28	microRNA 34a	Mus musculus	0-12
32056304-0	2020	MicroRNA-34a causes ceramide accumulation and effects insulin signaling pathway by targeting ceramide kinase (CERK) in aging skeletal muscle.	Ceramides	93-101	microRNA 34a	Mus musculus	0-12
32056304-0	2020	MicroRNA-34a causes ceramide accumulation and effects insulin signaling pathway by targeting ceramide kinase (CERK) in aging skeletal muscle.	Ceramides	93-101	ceramide kinase	Mus musculus	110-114
32056304-8	2020	Our analyses revealed that miR-34a targets CERK resulting in ceramide accumulation, activation of PP2A and the pJNK pathway in muscle and C2C12 myoblasts.	Ceramides	61-69	microRNA 34a	Homo sapiens	27-34
32056304-8	2020	Our analyses revealed that miR-34a targets CERK resulting in ceramide accumulation, activation of PP2A and the pJNK pathway in muscle and C2C12 myoblasts.	Ceramides	61-69	ceramide kinase	Homo sapiens	43-47
32056304-11	2020	In summary, we, therefore, propose that Mstn levels increase in aging muscle and upregulate miR-34a, which inhibits CERK resulting in increased ceramide levels.	Ceramides	144-152	microRNA 34a	Mus musculus	92-99
32056304-11	2020	In summary, we, therefore, propose that Mstn levels increase in aging muscle and upregulate miR-34a, which inhibits CERK resulting in increased ceramide levels.	Ceramides	144-152	ceramide kinase	Mus musculus	116-120
32056304-12	2020	This ceramide accumulation activates PP2A and pJNK causing hypophosphorylation of AKT and hyperphosphorylation of IRS1 (Ser307), respectively, impairing insulin signaling pathway and eventually inhibiting the sarcolemma localization of GLUT4.	Ceramides	5-13	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	37-41
32056304-12	2020	This ceramide accumulation activates PP2A and pJNK causing hypophosphorylation of AKT and hyperphosphorylation of IRS1 (Ser307), respectively, impairing insulin signaling pathway and eventually inhibiting the sarcolemma localization of GLUT4.	Ceramides	5-13	thymoma viral proto-oncogene 1	Mus musculus	82-85
32056304-12	2020	This ceramide accumulation activates PP2A and pJNK causing hypophosphorylation of AKT and hyperphosphorylation of IRS1 (Ser307), respectively, impairing insulin signaling pathway and eventually inhibiting the sarcolemma localization of GLUT4.	Ceramides	5-13	insulin receptor substrate 1	Mus musculus	114-118
32056304-12	2020	This ceramide accumulation activates PP2A and pJNK causing hypophosphorylation of AKT and hyperphosphorylation of IRS1 (Ser307), respectively, impairing insulin signaling pathway and eventually inhibiting the sarcolemma localization of GLUT4.	Ceramides	5-13	solute carrier family 2 (facilitated glucose transporter), member 4	Mus musculus	236-241
32056304-14	2020	This study is the first to explain the phenomenon of ceramide accrual and impairment of insulin signaling pathway in aging muscle through a miR-34a based mechanism.	Ceramides	53-61	microRNA 34a	Mus musculus	140-147
32056304-15	2020	In conclusion, our results suggest that Mstn and miR-34a antagonism can help ameliorate ceramide accumulation and loss of insulin sensitivity in aging skeletal muscle.	Ceramides	88-96	microRNA 34a	Mus musculus	49-56
32265319-3	2020	We examined two key enzymes involved in epidermal ceramide biosynthesis, glucocerebrosidase (GBA) and acid-sphingomyelinase (ASM).	Ceramides	50-58	glucosylceramidase beta	Homo sapiens	93-96
32265319-3	2020	We examined two key enzymes involved in epidermal ceramide biosynthesis, glucocerebrosidase (GBA) and acid-sphingomyelinase (ASM).	Ceramides	50-58	sphingomyelin phosphodiesterase 1	Homo sapiens	125-128
32265319-4	2020	We compared in situ expression levels and activities of GBA and ASM between NTS patients and controls and correlated the expression and activities with i) stratum corneum ceramide profiles, ii) in situ serine protease activity, and iii) clinical presentation of patients.	Ceramides	171-179	glucosylceramidase beta	Homo sapiens	56-59
32265319-8	2020	They also displayed a stronger increase in stratum corneum ceramides processed via ASM.	Ceramides	59-68	sphingomyelin phosphodiesterase 1	Homo sapiens	83-86
32265319-9	2020	We conclude that changes in the localization of active GBA and ASM correlate with i) altered stratum corneum ceramide composition in NTS patients, ii) local serine protease activity, and iii) the clinical manifestation of NTS.	Ceramides	109-117	glucosylceramidase beta	Homo sapiens	55-58
32265319-9	2020	We conclude that changes in the localization of active GBA and ASM correlate with i) altered stratum corneum ceramide composition in NTS patients, ii) local serine protease activity, and iii) the clinical manifestation of NTS.	Ceramides	109-117	sphingomyelin phosphodiesterase 1	Homo sapiens	63-66
32392908-4	2020	Accumulation of ceramides alters substrate utilization from glucose to lipids, activates triglyceride storage, and results in the development of both insulin resistance and hepatosteatosis, increasing the likelihood of major metabolic diseases.	Ceramides	16-25	insulin	Homo sapiens	150-157
32356173-3	2020	At 3 months of age AbetaPP/Abeta presence upregulated enzymes of ceramide turnover on the salvage pathway: ceramide synthases (CERS2, CERS4, CERS6) and also ceramidase ACER3.	Ceramides	65-73	amyloid beta precursor protein	Homo sapiens	19-24
32356173-3	2020	At 3 months of age AbetaPP/Abeta presence upregulated enzymes of ceramide turnover on the salvage pathway: ceramide synthases (CERS2, CERS4, CERS6) and also ceramidase ACER3.	Ceramides	65-73	ceramide synthase 2	Homo sapiens	127-132
32356173-3	2020	At 3 months of age AbetaPP/Abeta presence upregulated enzymes of ceramide turnover on the salvage pathway: ceramide synthases (CERS2, CERS4, CERS6) and also ceramidase ACER3.	Ceramides	65-73	ceramide synthase 4	Homo sapiens	134-139
32356173-3	2020	At 3 months of age AbetaPP/Abeta presence upregulated enzymes of ceramide turnover on the salvage pathway: ceramide synthases (CERS2, CERS4, CERS6) and also ceramidase ACER3.	Ceramides	65-73	ceramide synthase 6	Homo sapiens	141-146
32356173-5	2020	However, sphingomyelin synthases, which utilize ceramide on the sphingomyelinase pathway, were reduced (SGMS1 at 12 and SGMS2 at 6 months).	Ceramides	48-56	sphingomyelin synthase 1	Homo sapiens	104-109
32356173-9	2020	Moreover, at 12 months, FTY720 increased enzymes of ceramide-sphingosine turnover: CERS4, ASAH1, and ACER3.	Ceramides	52-60	ceramide synthase 4	Homo sapiens	83-88
32273303-2	2020	Ormdl3 gene product has been shown to regulate the biosynthesis of ceramides.	Ceramides	67-76	ORM1-like 3 (S. cerevisiae)	Mus musculus	0-6
32561074-11	2020	There is evidence to suggest that the ceramide or PKC pathway could act as a therapeutic target for tamoxifen or alternative chemotherapeutics and merits further investigation.	Ceramides	38-46	proline rich transmembrane protein 2	Homo sapiens	50-53
32481596-2	2020	We previously demonstrated that activation of acid sphingomyelinase (ASM) is an important early event in the pathogenesis of DR, and recent studies have demonstrated that there is an intricate connection between ceramide and mitochondrial function.	Ceramides	212-220	sphingomyelin phosphodiesterase 1	Homo sapiens	46-67
32481596-10	2020	Our results are consistent with diabetes-induced increase in mitochondrial ceramide through an ASM-dependent pathway leading to impaired mitochondrial function in the RPE cells of the retina.	Ceramides	75-83	sphingomyelin phosphodiesterase 1	Homo sapiens	95-98
32481596-2	2020	We previously demonstrated that activation of acid sphingomyelinase (ASM) is an important early event in the pathogenesis of DR, and recent studies have demonstrated that there is an intricate connection between ceramide and mitochondrial function.	Ceramides	212-220	sphingomyelin phosphodiesterase 1	Homo sapiens	69-72
32481596-3	2020	This study aimed to determine the role of ASM-dependent mitochondrial ceramide accumulation in diabetes-induced RPE cell damage.	Ceramides	70-78	sphingomyelin phosphodiesterase 1	Homo sapiens	42-45
32481596-5	2020	Conversely, the ceramide-to-sphingomyelin ratio was decreased in the mitochondria isolated from ASM-knockout mouse retinas compared to wild-type littermates, confirming the role of ASM in mitochondrial ceramide production.	Ceramides	16-24	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	96-99
32481596-5	2020	Conversely, the ceramide-to-sphingomyelin ratio was decreased in the mitochondria isolated from ASM-knockout mouse retinas compared to wild-type littermates, confirming the role of ASM in mitochondrial ceramide production.	Ceramides	202-210	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	96-99
32481596-5	2020	Conversely, the ceramide-to-sphingomyelin ratio was decreased in the mitochondria isolated from ASM-knockout mouse retinas compared to wild-type littermates, confirming the role of ASM in mitochondrial ceramide production.	Ceramides	202-210	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	181-184
32481596-6	2020	Cellular ceramide was elevated 2.67 +- 1.07-fold in RPE cells derived from diabetic donors compared to control donors, and these changes correlated with increased gene expression of IL-1beta, IL-6, and ASM.	Ceramides	9-17	interleukin 1 alpha	Homo sapiens	182-190
32481596-6	2020	Cellular ceramide was elevated 2.67 +- 1.07-fold in RPE cells derived from diabetic donors compared to control donors, and these changes correlated with increased gene expression of IL-1beta, IL-6, and ASM.	Ceramides	9-17	interleukin 6	Homo sapiens	192-196
32481596-6	2020	Cellular ceramide was elevated 2.67 +- 1.07-fold in RPE cells derived from diabetic donors compared to control donors, and these changes correlated with increased gene expression of IL-1beta, IL-6, and ASM.	Ceramides	9-17	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	202-205
32424203-2	2020	Ceramides, a type of sphingolipid (SL), have been implicated in the development of a range of metabolic disorders from insulin resistance (IR) to hepatic steatosis.	Ceramides	0-9	insulin	Homo sapiens	119-126
32466233-5	2020	Here, we show that DNA damage activates the ceramide synthetic pathway, via the downregulation of sphingomyelin synthase 2 (SMS2) and the upregulation of neutral sphingomyelinase 2 (nSMase2), leading to an increase in senescence-associated EV (SA-EV) biogenesis.	Ceramides	44-52	sphingomyelin synthase 2	Homo sapiens	98-122
32466233-5	2020	Here, we show that DNA damage activates the ceramide synthetic pathway, via the downregulation of sphingomyelin synthase 2 (SMS2) and the upregulation of neutral sphingomyelinase 2 (nSMase2), leading to an increase in senescence-associated EV (SA-EV) biogenesis.	Ceramides	44-52	sphingomyelin synthase 2	Homo sapiens	124-128
32466233-5	2020	Here, we show that DNA damage activates the ceramide synthetic pathway, via the downregulation of sphingomyelin synthase 2 (SMS2) and the upregulation of neutral sphingomyelinase 2 (nSMase2), leading to an increase in senescence-associated EV (SA-EV) biogenesis.	Ceramides	44-52	sphingomyelin phosphodiesterase 3	Homo sapiens	154-180
32466233-5	2020	Here, we show that DNA damage activates the ceramide synthetic pathway, via the downregulation of sphingomyelin synthase 2 (SMS2) and the upregulation of neutral sphingomyelinase 2 (nSMase2), leading to an increase in senescence-associated EV (SA-EV) biogenesis.	Ceramides	44-52	sphingomyelin phosphodiesterase 3	Homo sapiens	182-189
32443534-5	2020	Ceramides in male Asm-tgfb mice were elevated specifically in the dorsal hippocampus.	Ceramides	0-9	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	18-21
32443534-6	2020	mRNA expression analyses indicated that the increase in Asm activity affected other ceramide-generating pathways, which might help to balance ceramide levels in cortical brain regions.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	56-59
32443534-6	2020	mRNA expression analyses indicated that the increase in Asm activity affected other ceramide-generating pathways, which might help to balance ceramide levels in cortical brain regions.	Ceramides	142-150	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	56-59
32455838-4	2020	Two separate but somewhat overlapping models-the diacylglycerol (DAG) model and the ceramide model-have emerged to explain the development of insulin resistance.	Ceramides	84-92	insulin	Homo sapiens	142-149
32455838-5	2020	Studies have shown that lipid deposition in tissues such as muscle and liver inhibit insulin signaling via the toxic molecules DAG and ceramide.	Ceramides	135-143	insulin	Homo sapiens	85-92
32455838-7	2020	Ceramides are sphingolipids with variable acyl group chain length and activate protein phosphatase 2A that dephosphorylates Akt to block insulin signaling.	Ceramides	0-9	AKT serine/threonine kinase 1	Homo sapiens	124-127
32455838-7	2020	Ceramides are sphingolipids with variable acyl group chain length and activate protein phosphatase 2A that dephosphorylates Akt to block insulin signaling.	Ceramides	0-9	insulin	Homo sapiens	137-144
32408599-9	2020	We suppose a ceramide synthesis inhibitor (FB1) effect exerted onto the cell membrane, proven to be toxin dose-dependent and increasing sodium pump activity, with only indirect FA compositional correlations and lack of lipid peroxidation.	Ceramides	13-21	TCF3 fusion partner	Homo sapiens	43-46
32229586-5	2020	Stressed cells increase de novo biosynthesis of ceramides, which return to sub-toxic levels after UGCG-mediate incorporation into GlcCer.	Ceramides	48-57	UDP-glucose ceramide glucosyltransferase	Homo sapiens	98-102
32229586-8	2020	UGCG inhibition with the ceramide analog EtDO-P4 greatly reduced GSL and monosialotetrahexosylganglioside (GM1) levels, and co-treatment with standard chemotherapeutics sensitized cells to mitochondrial membrane potential loss and apoptosis.	Ceramides	25-33	UDP-glucose ceramide glucosyltransferase	Homo sapiens	0-4
32229586-9	2020	ABC subfamily B member 1 (ABCB1) expression was reduced, and ABCC-mediated efflux activity was modulated, by competition with non-glycosylated ceramides.	Ceramides	143-152	ATP binding cassette subfamily B member 1	Homo sapiens	0-24
32229586-9	2020	ABC subfamily B member 1 (ABCB1) expression was reduced, and ABCC-mediated efflux activity was modulated, by competition with non-glycosylated ceramides.	Ceramides	143-152	ATP binding cassette subfamily B member 1	Homo sapiens	26-31
32229586-9	2020	ABC subfamily B member 1 (ABCB1) expression was reduced, and ABCC-mediated efflux activity was modulated, by competition with non-glycosylated ceramides.	Ceramides	143-152	ATP binding cassette subfamily C member 1	Homo sapiens	61-65
31529722-0	2020	Hepatocyte Elovl6 determines ceramide acyl-chain length and hepatic insulin sensitivity in mice.	Ceramides	29-37	ELOVL family member 6, elongation of long chain fatty acids (yeast)	Mus musculus	11-17
32476784-5	2020	The study on the HIF-2alpha-NEU3-ceramide pathway also reveals the role of ceramide in hypoxia and insulin resistance in obese mice.	Ceramides	33-41	neuraminidase 3	Mus musculus	28-32
32476784-6	2020	Under obesity-induced intestinal hypoxia, HIF-2alpha increases the production of ceramide by promoting the expression of the gene Neu3 encoding sialidase 3, which is a key enzyme in ceramide synthesis, resulting in insulin resistance in high-fat diet-induced obese mice.	Ceramides	81-89	endothelial PAS domain protein 1	Mus musculus	42-52
32476784-6	2020	Under obesity-induced intestinal hypoxia, HIF-2alpha increases the production of ceramide by promoting the expression of the gene Neu3 encoding sialidase 3, which is a key enzyme in ceramide synthesis, resulting in insulin resistance in high-fat diet-induced obese mice.	Ceramides	81-89	neuraminidase 3	Mus musculus	130-134
32476784-6	2020	Under obesity-induced intestinal hypoxia, HIF-2alpha increases the production of ceramide by promoting the expression of the gene Neu3 encoding sialidase 3, which is a key enzyme in ceramide synthesis, resulting in insulin resistance in high-fat diet-induced obese mice.	Ceramides	81-89	neuraminidase 3	Mus musculus	144-155
32476784-6	2020	Under obesity-induced intestinal hypoxia, HIF-2alpha increases the production of ceramide by promoting the expression of the gene Neu3 encoding sialidase 3, which is a key enzyme in ceramide synthesis, resulting in insulin resistance in high-fat diet-induced obese mice.	Ceramides	182-190	endothelial PAS domain protein 1	Mus musculus	42-52
32476784-6	2020	Under obesity-induced intestinal hypoxia, HIF-2alpha increases the production of ceramide by promoting the expression of the gene Neu3 encoding sialidase 3, which is a key enzyme in ceramide synthesis, resulting in insulin resistance in high-fat diet-induced obese mice.	Ceramides	182-190	neuraminidase 3	Mus musculus	130-134
32476784-6	2020	Under obesity-induced intestinal hypoxia, HIF-2alpha increases the production of ceramide by promoting the expression of the gene Neu3 encoding sialidase 3, which is a key enzyme in ceramide synthesis, resulting in insulin resistance in high-fat diet-induced obese mice.	Ceramides	182-190	neuraminidase 3	Mus musculus	144-155
31848475-7	2020	Supplementation of ceramide inhibited Ob-Rb expression and STAT3 phosphorylation by inhibiting extracellular signal-regulated kinase 1/2 activation.	Ceramides	19-27	signal transducer and activator of transcription 3	Rattus norvegicus	59-64
31848475-7	2020	Supplementation of ceramide inhibited Ob-Rb expression and STAT3 phosphorylation by inhibiting extracellular signal-regulated kinase 1/2 activation.	Ceramides	19-27	mitogen activated protein kinase 3	Rattus norvegicus	95-136
32181687-4	2020	Herein the authors discuss inhibition of dihydroceramide desaturase-1, the final enzyme in the ceramide biosynthesis pathway, as a potential therapeutic approach to lower ceramides and combat cardiometabolic disease.	Ceramides	171-180	delta 4-desaturase, sphingolipid 1	Homo sapiens	41-69
31529722-12	2020	CONCLUSION: Our study demonstrates the key role of hepatic Elovl6 in the regulation of the acyl-chain composition of ceramide, and that C18:0-ceramide is a potent regulator of hepatic insulin signaling linked to Pnpla3-mediated NAFLD.	Ceramides	117-125	ELOVL family member 6, elongation of long chain fatty acids (yeast)	Mus musculus	59-65
31529722-9	2020	Ceramide(d18:1/18:0) enhances protein phosphatase 2A (PP2A) activity by interfering with the binding of PP2A to its biological inhibitor I2PP2A, leading to Akt dephosphorylation.	Ceramides	0-8	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	38-52
31529722-9	2020	Ceramide(d18:1/18:0) enhances protein phosphatase 2A (PP2A) activity by interfering with the binding of PP2A to its biological inhibitor I2PP2A, leading to Akt dephosphorylation.	Ceramides	0-8	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	54-58
31529722-9	2020	Ceramide(d18:1/18:0) enhances protein phosphatase 2A (PP2A) activity by interfering with the binding of PP2A to its biological inhibitor I2PP2A, leading to Akt dephosphorylation.	Ceramides	0-8	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	104-108
31529722-9	2020	Ceramide(d18:1/18:0) enhances protein phosphatase 2A (PP2A) activity by interfering with the binding of PP2A to its biological inhibitor I2PP2A, leading to Akt dephosphorylation.	Ceramides	0-8	SET nuclear oncogene	Mus musculus	137-143
31529722-11	2020	Consistent with this, liver-specific Elovl6 deletion in ob/ob mice reduced both hepatic ceramide(d18:1/18:0) and PP2A activity, and ameliorated insulin resistance.	Ceramides	88-96	ELOVL family member 6, elongation of long chain fatty acids (yeast)	Mus musculus	37-43
32821738-2	2020	In the present study, we activated de novo ceramide synthesis by inducing the hepatic expression of Sptlc2 to investigate the role of ceramide in glucose and lipid metabolism.	Ceramides	43-51	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	100-106
32821738-6	2020	Results: In HepG2 hepatocytes, adenoviral Sptlc2 expression inhibited insulin signaling and increased ceramide levels via activation of c-Jun N-terminal kinase and serine phosphorylation of insulin receptor substrate 1.	Ceramides	102-110	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	42-48
32821738-9	2020	Conclusion: Hepatic ceramide was found to modulate hepatosteatosis and the insulin response via increased VLDL secretion and inhibition of gluconeogenesis in vivo.	Ceramides	20-28	CD320 antigen	Mus musculus	106-110
32345374-0	2020	Association of Abeta with ceramide-enriched astrosomes mediates Abeta neurotoxicity.	Ceramides	26-34	amyloid beta precursor protein	Homo sapiens	15-20
31665380-8	2020	The RRs for incident diabetes per 1 SD of each log ceramide species (muM) were 1.22 (95% CI: 1.09, 1.37) for Cer-18, 1.18 (95% CI: 1.06, 1.31) for Cer-20, and 1.20 (95% CI: 1.08, 1.32) for Cer-22.	Ceramides	51-59	latexin	Homo sapiens	69-72
32452372-0	2020	[Ceramides, crucial actors in the development of insulin resistance and type 2 diabetes].	Ceramides	1-10	insulin	Homo sapiens	49-56
32452372-6	2020	Numerous studies have shown that ceramides are among the most active lipid second messengers to inhibit insulin signalling.	Ceramides	33-42	insulin	Homo sapiens	104-111
32452372-7	2020	This review describes the major role played by ceramides in the development of insulin resistance in peripheral tissues.	Ceramides	47-56	insulin	Homo sapiens	79-86
32222879-6	2020	Furthermore, Cer and PA attenuated expression levels of IL-10 in colorectal cancer cells co-cultured with M2 macrophages and downregulated STAT3 and NF-kappaB expression.	Ceramides	13-16	interleukin 10	Homo sapiens	56-61
32222879-6	2020	Furthermore, Cer and PA attenuated expression levels of IL-10 in colorectal cancer cells co-cultured with M2 macrophages and downregulated STAT3 and NF-kappaB expression.	Ceramides	13-16	signal transducer and activator of transcription 3	Homo sapiens	139-144
32222879-6	2020	Furthermore, Cer and PA attenuated expression levels of IL-10 in colorectal cancer cells co-cultured with M2 macrophages and downregulated STAT3 and NF-kappaB expression.	Ceramides	13-16	nuclear factor kappa B subunit 1	Homo sapiens	149-158
31916656-2	2020	S1P is generated by sphingosine kinases (SPHK1 and SPHK2) through the phosphorylation of ceramide-derived sphingosine.	Ceramides	89-97	sphingosine-1-phosphate receptor 1	Mus musculus	0-3
31916656-2	2020	S1P is generated by sphingosine kinases (SPHK1 and SPHK2) through the phosphorylation of ceramide-derived sphingosine.	Ceramides	89-97	sphingosine kinase 1	Mus musculus	41-46
31916656-2	2020	S1P is generated by sphingosine kinases (SPHK1 and SPHK2) through the phosphorylation of ceramide-derived sphingosine.	Ceramides	89-97	sphingosine kinase 2	Mus musculus	51-56
31916656-9	2020	Adding exogenous S1P to the medium had no impact, but the cell cycle arrest is partially alleviated by the expression of a ceramide synthase (CERS2), which converts excess sphingosine to ceramide.	Ceramides	123-131	sphingosine-1-phosphate receptor 1	Mus musculus	17-20
31916656-9	2020	Adding exogenous S1P to the medium had no impact, but the cell cycle arrest is partially alleviated by the expression of a ceramide synthase (CERS2), which converts excess sphingosine to ceramide.	Ceramides	123-131	ceramide synthase 2	Mus musculus	142-147
31916656-9	2020	Adding exogenous S1P to the medium had no impact, but the cell cycle arrest is partially alleviated by the expression of a ceramide synthase (CERS2), which converts excess sphingosine to ceramide.	Ceramides	187-195	ceramide synthase 2	Mus musculus	142-147
32425895-5	2020	Sphingomyelinases, including acid sphingomyelinase (ASMase), catalyzes the hydrolysis of membrane SM and consequently transform lipid rafts into ceramide-enriched membrane platforms.	Ceramides	145-153	sphingomyelin phosphodiesterase 1	Homo sapiens	29-50
32425895-5	2020	Sphingomyelinases, including acid sphingomyelinase (ASMase), catalyzes the hydrolysis of membrane SM and consequently transform lipid rafts into ceramide-enriched membrane platforms.	Ceramides	145-153	sphingomyelin phosphodiesterase 1	Homo sapiens	52-58
32345374-3	2020	We show here that brain tissue and serum from the transgenic mouse model of familial AD (5xFAD) and serum from AD patients contains ceramide-enriched and astrocyte-derived exosomes (termed astrosomes) that are associated with Abeta.	Ceramides	132-140	amyloid beta precursor protein	Homo sapiens	226-231
32144204-1	2020	beta-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide.	Ceramides	49-57	glucosidase, beta, acid	Mus musculus	0-23
32325905-8	2020	Importantly, these in vitro data demonstrated that OligoGM1, lacking the hydrophobic ceramide, can advantageously cross the BBB in comparison with GM1, while maintaining its neuroproperties.	Ceramides	85-93	coenzyme Q10A	Mus musculus	56-59
32325909-7	2020	Moreover, we observed a relationship between the amounts of some ceramide species in colorectal cancer tissue and plasma depending on the stage of colorectal cancer according to TNM (tumors, nodes, metastasis) classification.	Ceramides	65-73	teneurin transmembrane protein 1	Homo sapiens	178-181
32144204-1	2020	beta-Glucocerebrosidase (GBA) hydrolyzes glucosylceramide (GlcCer) to generate ceramide.	Ceramides	49-57	glucosidase, beta, acid	Mus musculus	25-28
32176488-3	2020	Acid ceramidase is one of the key enzymes that regulate the metabolism of ceramides and glycosphingolipids, which are important members of the SphL family.	Ceramides	74-83	N-acylsphingosine amidohydrolase 1	Mus musculus	0-15
32277067-0	2020	Correction: Fam57b (family with sequence similarity 57, member B), a novel peroxisome proliferator-activated receptor gamma target gene that regulates adipogenesis through ceramide synthesis.	Ceramides	172-180	TLC domain containing 3B	Homo sapiens	12-18
32277067-0	2020	Correction: Fam57b (family with sequence similarity 57, member B), a novel peroxisome proliferator-activated receptor gamma target gene that regulates adipogenesis through ceramide synthesis.	Ceramides	172-180	peroxisome proliferator activated receptor gamma	Homo sapiens	75-123
32273493-0	2020	Caveolin-1 regulates the ASMase/ceramide-mediated radiation response of endothelial cells in the context of tumor-stroma interactions.	Ceramides	32-40	caveolin 1	Homo sapiens	0-10
32273493-0	2020	Caveolin-1 regulates the ASMase/ceramide-mediated radiation response of endothelial cells in the context of tumor-stroma interactions.	Ceramides	32-40	sphingomyelin phosphodiesterase 1	Homo sapiens	25-31
32273493-4	2020	This study explores the potential impact of differential CAV1 levels in EC on the acid sphingomyelinase (ASMase)/ceramide pathway as a key player in the regulation of EC apoptosis upon irradiation and cancer cell radioresistance.	Ceramides	113-121	caveolin 1	Homo sapiens	57-61
32273493-4	2020	This study explores the potential impact of differential CAV1 levels in EC on the acid sphingomyelinase (ASMase)/ceramide pathway as a key player in the regulation of EC apoptosis upon irradiation and cancer cell radioresistance.	Ceramides	113-121	sphingomyelin phosphodiesterase 1	Homo sapiens	82-103
32273493-4	2020	This study explores the potential impact of differential CAV1 levels in EC on the acid sphingomyelinase (ASMase)/ceramide pathway as a key player in the regulation of EC apoptosis upon irradiation and cancer cell radioresistance.	Ceramides	113-121	sphingomyelin phosphodiesterase 1	Homo sapiens	105-111
32273493-5	2020	Enhanced apoptosis sensitivity of CAV1-deficient EC was associated with increased ASMase activity, ceramide generation, formation of large lipid platforms, and finally an altered p38 mitogen-activated protein kinase (MAPK)/heat-shock protein 27 (HSP27)/AKT (protein kinase B, PKB) signaling.	Ceramides	99-107	caveolin 1	Homo sapiens	34-38
32273493-8	2020	Analysis of the respective ceramide species in PCa cells with increased CAV1 levels like those typically found in radio-resistant advanced prostate tumors further revealed an upregulation of unsaturated C24:1 ceramide that might scavenge the effects of EC-derived apoptosis-inducing C16 ceramide.	Ceramides	27-35	caveolin 1	Homo sapiens	72-76
32273493-9	2020	Higher ASMase as well as ceramide levels could be confirmed by immunohistochemistry in human advanced prostate cancer specimen bearing characteristic CAV1 tumor-stroma alterations.	Ceramides	25-33	caveolin 1	Homo sapiens	150-154
32273493-10	2020	Conclusively, CAV1 critically regulates the generation of ceramide-dependent (re-)organization of the plasma membrane that in turn affects the radiation response of EC and adjacent PCa cells.	Ceramides	58-66	caveolin 1	Homo sapiens	14-18
32221387-1	2020	Activation of acid sphingomyelinase (SMPD1) and the generation of ceramide is a critical regulator of apoptosis in response to cellular stress including radiation.	Ceramides	66-74	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	14-35
32318242-2	2020	We have previously shown that ceramide production contributes to RCD induced by acetic acid and is involved in mitochondrial outer membrane permeabilization and cytochrome c release, especially through hydrolysis of complex sphingolipids catalyzed by Isc1p.	Ceramides	30-38	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	251-256
32055910-9	2020	On the other hand, CD4+ and CD14+ cells contained higher levels of phospholipids and ceramides.	Ceramides	85-94	CD4 molecule	Homo sapiens	19-22
32055910-9	2020	On the other hand, CD4+ and CD14+ cells contained higher levels of phospholipids and ceramides.	Ceramides	85-94	CD14 molecule	Homo sapiens	28-32
31758808-2	2020	The homeostasis between long-chain base (LCB) and ceramide (Cer) seems to play an important role in executions of PCD.	Ceramides	50-58	pterin-4a-carbinolamine dehydratase	Drosophila melanogaster	114-117
31758808-2	2020	The homeostasis between long-chain base (LCB) and ceramide (Cer) seems to play an important role in executions of PCD.	Ceramides	60-63	pterin-4a-carbinolamine dehydratase	Drosophila melanogaster	114-117
31883406-8	2020	Results showed that ASMase deficiency led to increases in not only sphingomyelin, but also ceramide (CER), a bioactive sphingolipid known to promote inflammation.	Ceramides	91-99	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	20-26
31883406-8	2020	Results showed that ASMase deficiency led to increases in not only sphingomyelin, but also ceramide (CER), a bioactive sphingolipid known to promote inflammation.	Ceramides	101-104	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	20-26
31883406-9	2020	Results further showed that ASMase deficiency increased CER de novo synthesis.	Ceramides	56-59	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	28-34
31883406-11	2020	ASMase deficiency leads to an unexpected CER increase by stimulating de novo synthesis CER, which is likely to be involved in the ASMase deficiency-exacerbated periodontitis.	Ceramides	41-44	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
31883406-11	2020	ASMase deficiency leads to an unexpected CER increase by stimulating de novo synthesis CER, which is likely to be involved in the ASMase deficiency-exacerbated periodontitis.	Ceramides	41-44	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	130-136
31883406-11	2020	ASMase deficiency leads to an unexpected CER increase by stimulating de novo synthesis CER, which is likely to be involved in the ASMase deficiency-exacerbated periodontitis.	Ceramides	87-90	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
31883406-11	2020	ASMase deficiency leads to an unexpected CER increase by stimulating de novo synthesis CER, which is likely to be involved in the ASMase deficiency-exacerbated periodontitis.	Ceramides	87-90	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	130-136
32029474-8	2020	The sciatic nerve of Ahr-knockout mice exhibited both reduced ceramide content and reduced myelin thickness.	Ceramides	62-70	aryl-hydrocarbon receptor	Mus musculus	21-24
32273521-0	2020	Comparative lipidomics of 5-Fluorouracil-sensitive and -resistant colorectal cancer cells reveals altered sphingomyelin and ceramide controlled by acid sphingomyelinase (SMPD1).	Ceramides	124-132	sphingomyelin phosphodiesterase 1	Homo sapiens	147-168
32273521-0	2020	Comparative lipidomics of 5-Fluorouracil-sensitive and -resistant colorectal cancer cells reveals altered sphingomyelin and ceramide controlled by acid sphingomyelinase (SMPD1).	Ceramides	124-132	sphingomyelin phosphodiesterase 1	Homo sapiens	170-175
31996991-5	2020	C2 ceramide showed a PKCzeta-mediated tumor-suppressive role in melanoma without exhibiting hepatotoxicity and nephrotoxicity.	Ceramides	3-11	protein kinase C zeta	Homo sapiens	21-28
31996991-6	2020	Moreover, PKCzeta was revealed as one of the key regulators of Akt and ceramide during C2 ceramide-mediated apoptosis.	Ceramides	71-79	protein kinase C zeta	Homo sapiens	10-17
31996991-7	2020	C2 ceramide was effective in repolarization of M2 macrophage phenotype and reduction of angiogenic factors such as VEGF, VEGFR1, VEGFR2, HIF1alpha.	Ceramides	3-11	vascular endothelial growth factor A	Homo sapiens	115-119
31996991-7	2020	C2 ceramide was effective in repolarization of M2 macrophage phenotype and reduction of angiogenic factors such as VEGF, VEGFR1, VEGFR2, HIF1alpha.	Ceramides	3-11	fms related receptor tyrosine kinase 1	Homo sapiens	121-127
31996991-7	2020	C2 ceramide was effective in repolarization of M2 macrophage phenotype and reduction of angiogenic factors such as VEGF, VEGFR1, VEGFR2, HIF1alpha.	Ceramides	3-11	kinase insert domain receptor	Homo sapiens	129-135
31996991-7	2020	C2 ceramide was effective in repolarization of M2 macrophage phenotype and reduction of angiogenic factors such as VEGF, VEGFR1, VEGFR2, HIF1alpha.	Ceramides	3-11	hypoxia inducible factor 1 subunit alpha	Homo sapiens	137-146
31996991-8	2020	Interestingly, PKCzeta knockdown attenuated C2 ceramide-mediated inhibition of melanoma progression.	Ceramides	47-55	protein kinase C zeta	Homo sapiens	15-22
32156385-6	2020	Finally, the Foodomics integration enabled the identification of genes, such as MAD2L1, involved in the polyamine and glutathione metabolism, or the inactivation of the NUPR1 transcription factor, that might be related with the alteration of the intracellular ceramide levels in response to endoplasmic reticulum stress.	Ceramides	260-268	mitotic arrest deficient 2 like 1	Homo sapiens	80-86
32156385-6	2020	Finally, the Foodomics integration enabled the identification of genes, such as MAD2L1, involved in the polyamine and glutathione metabolism, or the inactivation of the NUPR1 transcription factor, that might be related with the alteration of the intracellular ceramide levels in response to endoplasmic reticulum stress.	Ceramides	260-268	nuclear protein 1, transcriptional regulator	Homo sapiens	169-174
31899812-0	2020	Ceramides - a cause of insulin resistance in NAFLD in both murine models and humans.	Ceramides	0-9	insulin	Homo sapiens	23-30
30032721-8	2020	L-cycloserine, OA and EPA all counteracted PA-induced intracellular ceramide accumulation leading to a downregulation of IL-6 and TNFalpha.	Ceramides	68-76	interleukin 6	Mus musculus	121-125
30032721-8	2020	L-cycloserine, OA and EPA all counteracted PA-induced intracellular ceramide accumulation leading to a downregulation of IL-6 and TNFalpha.	Ceramides	68-76	tumor necrosis factor	Mus musculus	130-138
31992066-4	2020	We hypothesized that Acid Ceramidase (AC) overexpression would counteract the negative effects of elevated ceramide and promote cell survival, thereby providing cardioprotection after MI.	Ceramides	107-115	N-acylsphingosine amidohydrolase 1	Mus musculus	21-36
31992066-10	2020	We attributed the improvement in heart function post MI following AC modRNA delivery to decreased ceramide levels, lower cell death rates and changes in the composition of the immune cell population in the LV manifested by lowered abundance of pro-inflammatory detrimental neutrophils.	Ceramides	98-106	N-acylsphingosine amidohydrolase 1	Mus musculus	66-68
31972222-1	2020	There is growing evidence to support a role for the ceramide-metabolizing enzyme, glucosylceramide synthase (GCS), in resistance to a variety of chemotherapeutic agents.	Ceramides	52-60	UDP-glucose ceramide glucosyltransferase	Homo sapiens	82-107
31972222-1	2020	There is growing evidence to support a role for the ceramide-metabolizing enzyme, glucosylceramide synthase (GCS), in resistance to a variety of chemotherapeutic agents.	Ceramides	52-60	UDP-glucose ceramide glucosyltransferase	Homo sapiens	109-112
31972222-7	2020	GlcCer, formed by GCS-mediated ceramide glycosylation, is the precursor to a complex array of glycosphingolipids.	Ceramides	31-39	UDP-glucose ceramide glucosyltransferase	Homo sapiens	18-21
32211403-2	2020	The present study tested whether a lysosomal enzyme, acid ceramidase (AC), plays a critical role in HMGB1-induced alteration in ceramide metabolism and whether such HMGB1-AC interaction is associated with abnormal migration and proliferation of vascular smooth muscle cells (SMCs).	Ceramides	128-136	N-acylsphingosine amidohydrolase 1	Mus musculus	53-68
32164386-5	2020	Interestingly, ASC-exosomes induced the production of ceramides and dihydroceramides.	Ceramides	54-63	PYD and CARD domain containing	Homo sapiens	15-18
32165633-4	2020	In MVBs, acid ceramidase (aCDase) converts ceramide into sphingosine and increases the formation of sphingosine-rich intraluminal vesicles (ILVs).	Ceramides	43-51	N-acylsphingosine amidohydrolase 1	Homo sapiens	9-24
32165633-4	2020	In MVBs, acid ceramidase (aCDase) converts ceramide into sphingosine and increases the formation of sphingosine-rich intraluminal vesicles (ILVs).	Ceramides	43-51	N-acylsphingosine amidohydrolase 1	Mus musculus	26-32
32164386-8	2020	Collectively, our results suggest that ASC-exosomes effectively restore epidermal barrier functions in AD by facilitating the de novo synthesis of ceramides, resulting in a promising cell-free therapeutic option for treating AD.	Ceramides	147-156	PYD and CARD domain containing	Homo sapiens	39-42
32211403-2	2020	The present study tested whether a lysosomal enzyme, acid ceramidase (AC), plays a critical role in HMGB1-induced alteration in ceramide metabolism and whether such HMGB1-AC interaction is associated with abnormal migration and proliferation of vascular smooth muscle cells (SMCs).	Ceramides	128-136	N-acylsphingosine amidohydrolase 1	Mus musculus	70-72
32211403-2	2020	The present study tested whether a lysosomal enzyme, acid ceramidase (AC), plays a critical role in HMGB1-induced alteration in ceramide metabolism and whether such HMGB1-AC interaction is associated with abnormal migration and proliferation of vascular smooth muscle cells (SMCs).	Ceramides	128-136	high mobility group box 1	Mus musculus	100-105
32211403-6	2020	Consistently, HMGB1 significantly induced increases in the levels of long-chain ceramides in CAMs, which were not further enhanced by NOE but blocked by genistein.	Ceramides	80-89	high mobility group box 1	Mus musculus	14-19
32211403-8	2020	Lastly, CAMs isolated from smooth muscle-specific AC knockout mice (AC gene Asah1) exhibited increased ceramide levels and enhanced the migration and proliferation, which resembles the effects of HMGB1 on wild-type CAMs.	Ceramides	103-111	N-acylsphingosine amidohydrolase 1	Mus musculus	50-52
32211403-8	2020	Lastly, CAMs isolated from smooth muscle-specific AC knockout mice (AC gene Asah1) exhibited increased ceramide levels and enhanced the migration and proliferation, which resembles the effects of HMGB1 on wild-type CAMs.	Ceramides	103-111	N-acylsphingosine amidohydrolase 1	Mus musculus	68-70
32211403-8	2020	Lastly, CAMs isolated from smooth muscle-specific AC knockout mice (AC gene Asah1) exhibited increased ceramide levels and enhanced the migration and proliferation, which resembles the effects of HMGB1 on wild-type CAMs.	Ceramides	103-111	N-acylsphingosine amidohydrolase 1	Mus musculus	76-81
32211403-9	2020	Together, these results suggest that HMGB1 promotes SMC migration and proliferation via inhibition of AC expression and ceramide accumulation.	Ceramides	120-128	high mobility group box 1	Mus musculus	37-42
31982233-1	2020	alpha-Galactosylceramide (alpha-GalCer) is recognized by the CD1d proteins on antigen-presenting cells at the ceramide moiety and the galactose moiety is presented to iNKT cells, which stimulates the immune responses.	Ceramides	16-24	CD1d molecule	Homo sapiens	61-65
31994900-0	2020	Pharmacological inhibition of TLR4 ameliorates muscle and liver ceramide content after disuse in previously physically active mice.	Ceramides	64-72	toll-like receptor 4	Mus musculus	30-34
31994900-1	2020	Toll-like receptor 4 (TLR4) is a proposed mediator of ceramide accumulation, muscle atrophy and insulin resistance in skeletal muscle.	Ceramides	54-62	toll-like receptor 4	Mus musculus	0-20
31994900-1	2020	Toll-like receptor 4 (TLR4) is a proposed mediator of ceramide accumulation, muscle atrophy and insulin resistance in skeletal muscle.	Ceramides	54-62	toll-like receptor 4	Mus musculus	22-26
31994900-5	2020	As a result, soleus and liver ceramide abundance was greater (p&lt;0.05) in HS vs WR but was reduced with TLR4 inhibition (HS+TAK242 vs HS).	Ceramides	30-38	toll-like receptor 4	Mus musculus	106-110
31994900-8	2020	Robust decreases in muscle Spt2 and Cd36 mRNA and muscle lipidomic trafficking may partially explain reductions in ceramides with TLR4 inhibition.	Ceramides	115-124	toll-like receptor 4	Mus musculus	130-134
31994900-9	2020	In conclusion, pharmacological TLR4 inhibition in wheel-conditioned mice prevented ceramide accumulation during the early phase of hindlimb suspension (7d) but had little effect on muscle size and insulin sensitivity.	Ceramides	83-91	toll-like receptor 4	Mus musculus	31-35
32072744-4	2020	ABCA12"s action in the pancreas is independent of changes in the abundance of two other cholesterol transporters, ABCA1 and ABCG1, or of changes in cellular cholesterol or ceramide content.	Ceramides	172-180	ATP-binding cassette, sub-family A (ABC1), member 12	Mus musculus	0-6
32072744-4	2020	ABCA12"s action in the pancreas is independent of changes in the abundance of two other cholesterol transporters, ABCA1 and ABCG1, or of changes in cellular cholesterol or ceramide content.	Ceramides	172-180	ATP-binding cassette, sub-family A (ABC1), member 1	Mus musculus	0-5
31970839-2	2020	Sphingomyelin synthase 2 (SMS2) is involved in inflammatory diseases such as obesity and diabetes mellitus by regulation of the SM/ceramide balance.	Ceramides	131-139	sphingomyelin synthase 2	Mus musculus	0-24
32144130-7	2020	As placental ceramide induces mitochondrial fission in pre-eclampsia, we also examined ceramide content in GDM and control placentae and observed a reduction in placental ceramide enrichment in GDM, likely due to an insulin-dependent increase in ceramide-degrading ASAH1 expression.	Ceramides	13-21	insulin	Homo sapiens	216-223
32143184-5	2020	In this context, the ectopic recovery of miR-30b and miR-30c led to significant changes in genes related to FA metabolism, consistent reduction of ceramides, higher mitochondrial activity, and enabled beta-oxidation, redirecting FA metabolism from energy storage to expenditure.	Ceramides	147-156	microRNA 30b	Homo sapiens	41-48
32143184-5	2020	In this context, the ectopic recovery of miR-30b and miR-30c led to significant changes in genes related to FA metabolism, consistent reduction of ceramides, higher mitochondrial activity, and enabled beta-oxidation, redirecting FA metabolism from energy storage to expenditure.	Ceramides	147-156	microRNA 30c-1	Homo sapiens	53-60
31970839-2	2020	Sphingomyelin synthase 2 (SMS2) is involved in inflammatory diseases such as obesity and diabetes mellitus by regulation of the SM/ceramide balance.	Ceramides	131-139	sphingomyelin synthase 2	Mus musculus	26-30
31970839-6	2020	Reduced SM/ceramide balance in SMS2-KO tMEFs suppressed the attachment of EL4 cells through transcriptional reduction of ICAM-1 by the inhibition of NF-kappaB activation.	Ceramides	11-19	sphingomyelin synthase 2	Mus musculus	31-35
31970839-6	2020	Reduced SM/ceramide balance in SMS2-KO tMEFs suppressed the attachment of EL4 cells through transcriptional reduction of ICAM-1 by the inhibition of NF-kappaB activation.	Ceramides	11-19	intercellular adhesion molecule 1	Mus musculus	121-127
31916095-2	2020	Here, we studied DNA damage and repair as a function of male aging and assessed whether sphingosine-1-phosphate (S1P), a ceramide-induced death inhibitor, can prevent sperm aging by enhancing DNA double-strand breaks (DSB) repair.	Ceramides	121-129	sphingosine-1-phosphate receptor 1	Mus musculus	113-116
31489965-4	2020	Reduction of SM by inhibition of the ceramide transfer protein CERT decreased the cholesterol accumulation in NPC cells.	Ceramides	37-45	ceramide transporter 1	Homo sapiens	63-67
31744877-0	2020	Ceramide analog SACLAC modulates sphingolipid levels and Mcl-1 splicing to induce apoptosis in acute myeloid leukemia.	Ceramides	0-8	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	57-62
32111095-1	2020	The ASAH1 gene encodes acid ceramidase (AC), an enzyme that is implicated in the metabolism of ceramide (Cer).	Ceramides	95-103	N-acylsphingosine amidohydrolase 1	Homo sapiens	4-9
32111095-1	2020	The ASAH1 gene encodes acid ceramidase (AC), an enzyme that is implicated in the metabolism of ceramide (Cer).	Ceramides	95-103	N-acylsphingosine amidohydrolase 1	Homo sapiens	23-38
32111095-1	2020	The ASAH1 gene encodes acid ceramidase (AC), an enzyme that is implicated in the metabolism of ceramide (Cer).	Ceramides	105-108	N-acylsphingosine amidohydrolase 1	Homo sapiens	4-9
32111095-1	2020	The ASAH1 gene encodes acid ceramidase (AC), an enzyme that is implicated in the metabolism of ceramide (Cer).	Ceramides	105-108	N-acylsphingosine amidohydrolase 1	Homo sapiens	23-38
32098447-2	2020	A substantial body of evidence has implicated ceramides, a sphingolipid intermediate, as potent antagonists of insulin action that drive insulin resistance.	Ceramides	46-55	insulin	Homo sapiens	111-118
32102436-0	2020	Nrp1 is Activated by Konjac Ceramide Binding-Induced Structural Rigidification of the a1a2 Domain.	Ceramides	28-36	neuropilin 1	Homo sapiens	0-4
31785811-5	2020	Silencing and overexpression of CerS C4M4U4 (the closest homolog of human CerS 2 and 3) demonstrated its involvement in the synthesis of ceramide.	Ceramides	137-145	ceramide synthase 2	Homo sapiens	74-86
31974308-9	2020	The expression levels of the FA elongase Elovl1 were reduced in Fatp4 KO epidermis, partly accounting for the reduction and shortening of saturated, nonacylated ceramides.	Ceramides	161-170	elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 1	Mus musculus	41-47
31974308-9	2020	The expression levels of the FA elongase Elovl1 were reduced in Fatp4 KO epidermis, partly accounting for the reduction and shortening of saturated, nonacylated ceramides.	Ceramides	161-170	solute carrier family 27 (fatty acid transporter), member 4	Mus musculus	64-69
31765623-2	2020	In the present study, we examined whether synaptosomal-associated protein 25 (SNAP-25) is involved in ceramide production and exocytosis.	Ceramides	102-110	synaptosome associated protein 25	Rattus norvegicus	42-76
31765623-2	2020	In the present study, we examined whether synaptosomal-associated protein 25 (SNAP-25) is involved in ceramide production and exocytosis.	Ceramides	102-110	synaptosome associated protein 25	Rattus norvegicus	78-85
31765623-7	2020	A23187-induced ceramide production was concomitantly reduced in SNAP-25 siRNA-transfected PC12 cells compared with that in scrambled siRNA-transfected cells.	Ceramides	15-23	synaptosome associated protein 25	Rattus norvegicus	64-71
31765623-10	2020	Collectively, our results indicate that SNAP-25 interacts with nSMase2 during ceramide production, which mediates exocytosis and neurotransmitter release.	Ceramides	78-86	synaptosome associated protein 25	Rattus norvegicus	40-47
31765623-10	2020	Collectively, our results indicate that SNAP-25 interacts with nSMase2 during ceramide production, which mediates exocytosis and neurotransmitter release.	Ceramides	78-86	sphingomyelin phosphodiesterase 3	Rattus norvegicus	63-70
32082486-1	2020	Neutral sphingomyelinase 2 (nSMase2), the product of the sphingomyelin phosphodiesterase 3 (SMPD3) gene, catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	150-158	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
32082486-1	2020	Neutral sphingomyelinase 2 (nSMase2), the product of the sphingomyelin phosphodiesterase 3 (SMPD3) gene, catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	150-158	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
32082486-1	2020	Neutral sphingomyelinase 2 (nSMase2), the product of the sphingomyelin phosphodiesterase 3 (SMPD3) gene, catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	150-158	sphingomyelin phosphodiesterase 3	Homo sapiens	57-90
32082486-1	2020	Neutral sphingomyelinase 2 (nSMase2), the product of the sphingomyelin phosphodiesterase 3 (SMPD3) gene, catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	150-158	sphingomyelin phosphodiesterase 3	Homo sapiens	92-97
31671075-3	2020	In a patient with SDR9C7 mutation and a mouse Sdr9c7-KO model, we show loss of covalent binding of epidermal ceramides to protein, a structural fault in the barrier.	Ceramides	109-118	short chain dehydrogenase/reductase family 9C member 7	Homo sapiens	18-24
31671075-3	2020	In a patient with SDR9C7 mutation and a mouse Sdr9c7-KO model, we show loss of covalent binding of epidermal ceramides to protein, a structural fault in the barrier.	Ceramides	109-118	4short chain dehydrogenase/reductase family 9C, member 7	Mus musculus	46-52
31821039-1	2020	We reported previously that increased acid sphingomyelinase (ASMase)-catalyzed hydrolysis of sphingomyelin, which leads to increases in ceramide and sphingosine 1 phosphate (S1P), played a key role in the synergistic upregulation of proinflammatory cytokines by palmitic acid (PA), a major saturated fatty acid, and lipopolysaccharide (LPS) in macrophages.	Ceramides	136-144	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	38-59
31821039-1	2020	We reported previously that increased acid sphingomyelinase (ASMase)-catalyzed hydrolysis of sphingomyelin, which leads to increases in ceramide and sphingosine 1 phosphate (S1P), played a key role in the synergistic upregulation of proinflammatory cytokines by palmitic acid (PA), a major saturated fatty acid, and lipopolysaccharide (LPS) in macrophages.	Ceramides	136-144	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	61-67
31166588-7	2020	Plin5-S155A mice showed a substantial increase in cardiac TAG and ceramide levels, which was comparable to mice overexpressing non-mutated Plin5.	Ceramides	66-74	perilipin 5	Mus musculus	0-5
31596951-2	2020	The host ceramide transport protein CERT delivers ceramide from the endoplasmic reticulum to the Golgi complex for the synthesis of sphingomyelin (SM).	Ceramides	9-17	ceramide transporter 1	Homo sapiens	36-40
31596951-2	2020	The host ceramide transport protein CERT delivers ceramide from the endoplasmic reticulum to the Golgi complex for the synthesis of sphingomyelin (SM).	Ceramides	50-58	ceramide transporter 1	Homo sapiens	36-40
31596951-6	2020	These results suggest that C. trachomatis-infected cells can convert ceramide to SM without host SMSs after CERT-mediated transfer of ceramide to the inclusions.	Ceramides	134-142	ceramide transporter 1	Homo sapiens	108-112
32092937-1	2020	Ceramide kinase (CerK) is a lipid kinase that converts the proapoptotic ceramide to ceramide 1-phosphate, which has been proposed to have pro-malignant properties and regulate cell responses such as proliferation, migration, and inflammation.	Ceramides	72-80	ceramide kinase	Homo sapiens	0-15
32092937-1	2020	Ceramide kinase (CerK) is a lipid kinase that converts the proapoptotic ceramide to ceramide 1-phosphate, which has been proposed to have pro-malignant properties and regulate cell responses such as proliferation, migration, and inflammation.	Ceramides	72-80	ceramide kinase	Homo sapiens	17-21
32045989-6	2020	A multiplex analysis of mTOR signaling pathway intermediates showed that the majority (eight) of the pathway phosphorylated proteins measured (eleven) were significantly downregulated in response to C16 ceramide-enriched HDL2 compared to HDL2 alone and hydroxy ceramide-enriched HDL2.	Ceramides	203-211	mechanistic target of rapamycin kinase	Homo sapiens	24-28
32045989-6	2020	A multiplex analysis of mTOR signaling pathway intermediates showed that the majority (eight) of the pathway phosphorylated proteins measured (eleven) were significantly downregulated in response to C16 ceramide-enriched HDL2 compared to HDL2 alone and hydroxy ceramide-enriched HDL2.	Ceramides	203-211	junctophilin 3	Homo sapiens	221-225
32045989-6	2020	A multiplex analysis of mTOR signaling pathway intermediates showed that the majority (eight) of the pathway phosphorylated proteins measured (eleven) were significantly downregulated in response to C16 ceramide-enriched HDL2 compared to HDL2 alone and hydroxy ceramide-enriched HDL2.	Ceramides	253-269	mechanistic target of rapamycin kinase	Homo sapiens	24-28
32045989-6	2020	A multiplex analysis of mTOR signaling pathway intermediates showed that the majority (eight) of the pathway phosphorylated proteins measured (eleven) were significantly downregulated in response to C16 ceramide-enriched HDL2 compared to HDL2 alone and hydroxy ceramide-enriched HDL2.	Ceramides	253-269	junctophilin 3	Homo sapiens	221-225
32028642-7	2020	We next noted that NOX-mediated KC apoptosis is mainly attributable to neutral sphingomyelinase (SMase)-mediated stimulation of ceramides, which is a well-known pro-apoptotic lipid.	Ceramides	128-137	sphingomyelin phosphodiesterase 2	Homo sapiens	71-95
31676440-4	2020	Particularly, lipids with signaling functions such as ceramides and mitochondrial lipids were affected by lipl-5 silencing.	Ceramides	54-63	Lipase lipl-5	Caenorhabditis elegans	106-112
31916624-0	2020	Biosynthesis of the anti-lipid-microdomain sphingoid base 4,14-sphingadiene by the ceramide desaturase FADS3.	Ceramides	83-91	fatty acid desaturase 3	Homo sapiens	103-108
31916624-7	2020	We identified the fatty acid desaturase family protein FADS3 as a ceramide desaturase that produces SPD ceramides by desaturating ceramides containing sphingosine.	Ceramides	104-113	fatty acid desaturase 3	Homo sapiens	55-60
32098447-2	2020	A substantial body of evidence has implicated ceramides, a sphingolipid intermediate, as potent antagonists of insulin action that drive insulin resistance.	Ceramides	46-55	insulin	Homo sapiens	137-144
32098447-3	2020	Indeed, genetic mouse studies that lower ceramides are potently insulin sensitizing.	Ceramides	41-50	insulin	Homo sapiens	64-71
31233888-0	2020	The role of ceramide in regulating endoplasmic reticulum function.	Ceramides	12-20	epiregulin	Homo sapiens	35-56
31645443-4	2020	Our previous works showed that cellular Cer can eradicate cancer cells that carry a p53 deletion-mutation by modulating alternative pre-mRNA splicing, restoring wild-type p53 protein expression.	Ceramides	40-43	transformation related protein 53, pseudogene	Mus musculus	84-87
31645443-4	2020	Our previous works showed that cellular Cer can eradicate cancer cells that carry a p53 deletion-mutation by modulating alternative pre-mRNA splicing, restoring wild-type p53 protein expression.	Ceramides	40-43	transformation related protein 53, pseudogene	Mus musculus	171-174
31645443-5	2020	Here, we report that new Cer-RUB nanomicelles considerably enhance Cer in-vivo bioavailability and restore p53-dependent tumor suppression in cancer cells carrying a p53 missense mutation.	Ceramides	25-28	transformation related protein 53, pseudogene	Mus musculus	107-110
31645443-5	2020	Here, we report that new Cer-RUB nanomicelles considerably enhance Cer in-vivo bioavailability and restore p53-dependent tumor suppression in cancer cells carrying a p53 missense mutation.	Ceramides	25-28	transformation related protein 53, pseudogene	Mus musculus	166-169
31645443-7	2020	Intriguingly, Cer-RUB nanomicelle treatments restored p53-dependent tumor suppression and sensitivity to cisplatin in OVCAR-3 ovarian cancer cells and xenograft tumors carrying p53 R248Q mutation.	Ceramides	14-17	tumor protein p53	Homo sapiens	54-57
31645443-7	2020	Intriguingly, Cer-RUB nanomicelle treatments restored p53-dependent tumor suppression and sensitivity to cisplatin in OVCAR-3 ovarian cancer cells and xenograft tumors carrying p53 R248Q mutation.	Ceramides	14-17	tumor protein p53	Homo sapiens	177-180
31645443-9	2020	Further, Cer-RUB nanomicelles restored p53 phosphorylated protein and downstream function to wild-type levels in p53 R172H/+ transgenic mice.	Ceramides	9-12	transformation related protein 53, pseudogene	Mus musculus	39-42
31645443-9	2020	Further, Cer-RUB nanomicelles restored p53 phosphorylated protein and downstream function to wild-type levels in p53 R172H/+ transgenic mice.	Ceramides	9-12	transformation related protein 53, pseudogene	Mus musculus	113-116
31645443-10	2020	Altogether, this study, for the first time, indicates that natural Cer-RUB nanomicelles offer a feasible approach for efficaciously and safely targeting cancers carrying p53 missense mutations.	Ceramides	67-70	transformation related protein 53, pseudogene	Mus musculus	170-173
31999897-8	2020	Finally, Sptlc1 was transiently silenced and the effect on ceramide content, autophagy and transcriptional activities was evaluated as above mentioned.	Ceramides	59-67	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	9-15
31988398-0	2020	Primary cilia control cell alignment and patterning in bone development via ceramide-PKCzeta-beta-catenin signaling.	Ceramides	76-84	protein kinase C zeta	Homo sapiens	85-92
31988398-0	2020	Primary cilia control cell alignment and patterning in bone development via ceramide-PKCzeta-beta-catenin signaling.	Ceramides	76-84	catenin beta 1	Homo sapiens	93-105
31988398-7	2020	Mechanistically, IFT20 interacts with the ceramide-PKCzeta complex to promote PKCzeta phosphorylation in cilia and induce the apical localization of beta-catenin in osteoblasts, both of which were disrupted in the absence of IFT20.	Ceramides	42-50	intraflagellar transport 20	Homo sapiens	17-22
31988398-7	2020	Mechanistically, IFT20 interacts with the ceramide-PKCzeta complex to promote PKCzeta phosphorylation in cilia and induce the apical localization of beta-catenin in osteoblasts, both of which were disrupted in the absence of IFT20.	Ceramides	42-50	protein kinase C zeta	Homo sapiens	51-58
31988398-7	2020	Mechanistically, IFT20 interacts with the ceramide-PKCzeta complex to promote PKCzeta phosphorylation in cilia and induce the apical localization of beta-catenin in osteoblasts, both of which were disrupted in the absence of IFT20.	Ceramides	42-50	protein kinase C zeta	Homo sapiens	78-85
31988398-7	2020	Mechanistically, IFT20 interacts with the ceramide-PKCzeta complex to promote PKCzeta phosphorylation in cilia and induce the apical localization of beta-catenin in osteoblasts, both of which were disrupted in the absence of IFT20.	Ceramides	42-50	catenin beta 1	Homo sapiens	149-161
31988398-7	2020	Mechanistically, IFT20 interacts with the ceramide-PKCzeta complex to promote PKCzeta phosphorylation in cilia and induce the apical localization of beta-catenin in osteoblasts, both of which were disrupted in the absence of IFT20.	Ceramides	42-50	intraflagellar transport 20	Homo sapiens	225-230
31988398-8	2020	These results reveal that IFT20 regulates polarity and cell alignment via ceramide-pPKCzeta-beta-catenin signaling during bone development.	Ceramides	74-82	intraflagellar transport 20	Homo sapiens	26-31
31988398-8	2020	These results reveal that IFT20 regulates polarity and cell alignment via ceramide-pPKCzeta-beta-catenin signaling during bone development.	Ceramides	74-82	catenin beta 1	Homo sapiens	92-104
32039186-2	2019	It was found that a kind of ceramides analog synthesized from phenylglycinol could inhibit the production of cytokine TNF-alpha.	Ceramides	28-37	tumor necrosis factor	Homo sapiens	118-127
31757669-1	2020	Dysregulation of the ceramide transport protein CERT is associated to diseases such as cancer.	Ceramides	21-29	ceramide transporter 1	Homo sapiens	48-52
31757669-2	2020	In search for new CERT START domain ligands, N-dodecyl-deoxynojirimycin (N-dodecyl-DNJ) iminosugar was found to display, as a ceramide mimic, significant protein recognition.	Ceramides	126-134	ceramide transporter 1	Homo sapiens	18-22
31757669-7	2020	This work opens promising perspectives for the development of new inhibitors of CERT-mediated ceramide trafficking.	Ceramides	94-102	ceramide transporter 1	Homo sapiens	80-84
32010692-5	2019	ASM hydrolyzes sphingomyelin to ceramide, which further fuses to large ceramide-enriched platforms functioning in stabilizing and amplifying molecules and receptors.	Ceramides	32-40	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
32010692-5	2019	ASM hydrolyzes sphingomyelin to ceramide, which further fuses to large ceramide-enriched platforms functioning in stabilizing and amplifying molecules and receptors.	Ceramides	71-79	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
32010692-6	2019	Here, we will discuss the current understanding of the ASM-ceramide system in inflammasome activation, and how it contributes to multiple diseases.	Ceramides	59-67	sphingomyelin phosphodiesterase 1	Homo sapiens	55-58
31896578-8	2020	Furthermore, inhibition of lysosomal exocytosis of ASM, which is required for ceramide production at the apical surface, decreases GII.3 infection.	Ceramides	78-86	sphingomyelin phosphodiesterase 1	Homo sapiens	51-54
31949129-7	2020	Knocking out Acer3 was found to augment PEWD-induced elevation of C18:1-ceramide and alleviate early inflammation and fibrosis but not steatosis in mouse livers with NASH.	Ceramides	72-80	alkaline ceramidase 3	Mus musculus	13-18
31692231-0	2020	A tissue-specific screen of ceramide expression in aged mice identifies ceramide synthase-1 and ceramide synthase-5 as potential regulators of fiber size and strength in skeletal muscle.	Ceramides	28-36	ceramide synthase 5	Mus musculus	96-115
31692231-4	2020	Consistently, the expression of CerS1 and CerS5 mRNA, encoding the ceramide synthases (CerS) with substrate preference for C16:0 and C18:0 acyl chains, respectively, was down-regulated in skeletal muscle of aged mice.	Ceramides	67-75	ceramide synthase 1	Mus musculus	32-37
31692231-4	2020	Consistently, the expression of CerS1 and CerS5 mRNA, encoding the ceramide synthases (CerS) with substrate preference for C16:0 and C18:0 acyl chains, respectively, was down-regulated in skeletal muscle of aged mice.	Ceramides	67-75	ceramide synthase 5	Mus musculus	42-47
31858168-0	2020	Comprehensive characterization and simultaneous analysis of overall lipids in reconstructed human epidermis using NPLC/HR-MSn: 1-O-E (EO) Cer, a new ceramide subclass.	Ceramides	149-157	moesin	Homo sapiens	122-125
31233888-3	2020	The initial steps of sphingolipid synthesis take place in the ER, where the simplest SL, ceramide, is synthesized.	Ceramides	89-97	epiregulin	Homo sapiens	62-64
31233888-5	2020	For this reason and others, ER ceramide levels must be tightly regulated.	Ceramides	31-39	epiregulin	Homo sapiens	28-30
31233888-6	2020	Here, we describe the biological and biophysical properties of ceramide and discuss how this might impact the ER membrane.	Ceramides	63-71	epiregulin	Homo sapiens	110-112
31229410-6	2020	Significant differences regarding triacylglycerols (predominantly identified in RP-LC/MS2) and ceramides (predominantly identified in DI-MS2) indicate experimental- or approach-inherent distinctions.	Ceramides	95-104	MS2	Homo sapiens	137-140
32003689-8	2020	Raised ceramide levels negatively regulate mitochondrial function, both directly and via its negative impact on daytime, arousal-promoting orexin and night-time sleep-promoting pineal gland-derived melatonin.	Ceramides	7-15	hypocretin neuropeptide precursor	Homo sapiens	139-145
31544710-5	2020	RESULTS: HCC is characterised by dysregulation of ceramide metabolism, which could be ascribed to altered activity and expression of ceramide synthases 2, 4 and 6, and acid and alkaline ceramidases 2 and 3, as well as to deregulation of sphingosine kinases (SphK) 1 and 2 and sphingosine-1-phosphate receptors, in particular S1PR1.	Ceramides	50-58	ceramide synthase 2	Homo sapiens	133-162
31544710-5	2020	RESULTS: HCC is characterised by dysregulation of ceramide metabolism, which could be ascribed to altered activity and expression of ceramide synthases 2, 4 and 6, and acid and alkaline ceramidases 2 and 3, as well as to deregulation of sphingosine kinases (SphK) 1 and 2 and sphingosine-1-phosphate receptors, in particular S1PR1.	Ceramides	50-58	sphingosine kinase 1	Homo sapiens	237-271
31544710-5	2020	RESULTS: HCC is characterised by dysregulation of ceramide metabolism, which could be ascribed to altered activity and expression of ceramide synthases 2, 4 and 6, and acid and alkaline ceramidases 2 and 3, as well as to deregulation of sphingosine kinases (SphK) 1 and 2 and sphingosine-1-phosphate receptors, in particular S1PR1.	Ceramides	50-58	sphingosine-1-phosphate receptor 1	Homo sapiens	325-330
30803019-2	2020	Ceramides are primarily recognized as lipid bilayer building blocks, but recent work has shown that these endogenous molecules are important intracellular signalling mediators and may exert some diabetogenic effects via molecular pathways involved in insulin resistance, beta-cell apoptosis and inflammation.	Ceramides	0-9	insulin	Homo sapiens	251-258
30803019-3	2020	In the present review, we consider the available evidence on the possible roles of ceramides in diabetes mellitus and introduce eight different molecular mechanisms mediating the diabetogenic action of ceramides, categorized into those predominantly related to insulin resistance vs those mainly implicated in beta-cell dysfunction.	Ceramides	202-211	insulin	Homo sapiens	261-268
31901865-9	2020	Mechanistically, ceramide accumulation stemming from hydrolysis and the de novo pathway during early adipogenesis is regulated by Sirt1 upon epigenetic alterations of constitutive Histone H3K4 methylation and H3K9 acetylation.	Ceramides	17-25	sirtuin 1	Mus musculus	130-135
31901865-10	2020	INTERPRETATION: The metabolic footprint during adipocyte commitment highlights that apoptosis induced by ceramide is essential for adipogenesis, which is reversed by suppression of Sirt1.	Ceramides	105-113	sirtuin 1	Mus musculus	181-186
31901865-11	2020	Therefore, Sirt1 may constitute a target to treat obesity or other ceramide-associated metabolic syndromes.	Ceramides	67-75	sirtuin 1	Mus musculus	11-16
31836270-3	2020	OBJECTIVE: To clarify the changes of ceramide components in the lesional stratum corneum (SC) and the gene expression profile in the lesional skin of an ARCI patient with a novel frameshift mutation in NIPAL4.	Ceramides	37-45	NIPA like domain containing 4	Homo sapiens	202-208
31743567-0	2020	Medial calcification in the arterial wall of smooth muscle cell-specific Smpd1 transgenic mice: A ceramide-mediated vasculopathy.	Ceramides	98-106	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	73-78
31743567-2	2020	The study was performed to test whether lysosomal acid sphingomyelinase (murine gene code: Smpd1)-derived ceramide contributes to the small extracellular vesicle (sEV) secretion from SMCs and consequently leads to AMC.	Ceramides	106-114	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	50-71
31743567-2	2020	The study was performed to test whether lysosomal acid sphingomyelinase (murine gene code: Smpd1)-derived ceramide contributes to the small extracellular vesicle (sEV) secretion from SMCs and consequently leads to AMC.	Ceramides	106-114	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	91-96
31889854-11	2020	This study suggests that genetic defects in RMND1 gene alters the mitochondrial energy metabolism leading to the accumulation of ceramide, and subsequently promote dysregulated apoptosis and tissue necrosis in kidneys.	Ceramides	129-137	required for meiotic nuclear division 1 homolog	Homo sapiens	44-49
32489964-1	2020	Objective: Total ceramide concentrations are linked with increased insulin resistance and cardiac dysfunction.	Ceramides	17-25	insulin	Homo sapiens	67-74
32489964-8	2020	Nine SNPs, all on chromosome 20 and close to SPTLC3, were significantly associated with C24:0 ceramide concentrations.	Ceramides	94-102	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	45-51
32489964-11	2020	Conclusion: SNPs near the SPTLC3 gene, which encodes serine palmitoyltransferase long chain base subunit 3 (SPTLC3; part of the enzyme that catalyzes the rate-limiting step of de novo sphingolipid synthesis) were associated with plasma C22:0 and C24:0 ceramide concentrations.	Ceramides	252-260	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	26-32
32489964-11	2020	Conclusion: SNPs near the SPTLC3 gene, which encodes serine palmitoyltransferase long chain base subunit 3 (SPTLC3; part of the enzyme that catalyzes the rate-limiting step of de novo sphingolipid synthesis) were associated with plasma C22:0 and C24:0 ceramide concentrations.	Ceramides	252-260	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	53-106
32489964-11	2020	Conclusion: SNPs near the SPTLC3 gene, which encodes serine palmitoyltransferase long chain base subunit 3 (SPTLC3; part of the enzyme that catalyzes the rate-limiting step of de novo sphingolipid synthesis) were associated with plasma C22:0 and C24:0 ceramide concentrations.	Ceramides	252-260	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	108-114
32489964-12	2020	These results are biologically plausible and suggest that SPTLC3 may be a potential therapeutic target for C24:0 and C22:0 ceramide modulation.	Ceramides	123-131	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	58-64
32821721-4	2020	When prolonged, these ceramide actions cause insulin resistance and hepatic steatosis, 2 of the underlying drivers of cardiometabolic diseases.	Ceramides	22-30	insulin	Homo sapiens	45-52
32821721-5	2020	Herein the author discusses the mechanisms linking ceramides to the development of insulin resistance, hepatosteatosis and resultant cardiometabolic disorders.	Ceramides	51-60	insulin	Homo sapiens	83-90
31842461-0	2019	Ceramide Content in Liver Increases Along with Insulin Resistance in Obese Patients.	Ceramides	0-8	insulin	Homo sapiens	47-54
31941852-1	2020	Acid sphingomyelinase (ASM) is a lysosomal hydrolase that degrades sphingomyelin into ceramide and phosphocholine.	Ceramides	86-94	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
31941852-1	2020	Acid sphingomyelinase (ASM) is a lysosomal hydrolase that degrades sphingomyelin into ceramide and phosphocholine.	Ceramides	86-94	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
31880535-3	2019	The mammalian ORMDL proteins (ORMDL1, 2 and 3) mediate feedback inhibition of the de novo synthesis pathway of sphingolipids by inhibiting serine palmitoyl transferase in response to elevated ceramide levels.	Ceramides	192-200	ORMDL sphingolipid biosynthesis regulator 1	Homo sapiens	30-45
31846489-6	2019	Finally, we observed a downregulation of ceramide synthases (hyl-1 and hyl-2) and antioxidant genes (gcs-1 and gst-4), while mitophagy genes (pink-1 and dct-1) were upregulated, probably as part of a mitohormetic mechanism in response to glucose toxicity.	Ceramides	41-49	Ceramide synthase hyl-1;TLC domain-containing protein	Caenorhabditis elegans	61-66
31846489-6	2019	Finally, we observed a downregulation of ceramide synthases (hyl-1 and hyl-2) and antioxidant genes (gcs-1 and gst-4), while mitophagy genes (pink-1 and dct-1) were upregulated, probably as part of a mitohormetic mechanism in response to glucose toxicity.	Ceramides	41-49	Ceramide synthase hyl-2	Caenorhabditis elegans	71-76
31846489-6	2019	Finally, we observed a downregulation of ceramide synthases (hyl-1 and hyl-2) and antioxidant genes (gcs-1 and gst-4), while mitophagy genes (pink-1 and dct-1) were upregulated, probably as part of a mitohormetic mechanism in response to glucose toxicity.	Ceramides	41-49	Glutamate--cysteine ligase	Caenorhabditis elegans	101-106
31846489-6	2019	Finally, we observed a downregulation of ceramide synthases (hyl-1 and hyl-2) and antioxidant genes (gcs-1 and gst-4), while mitophagy genes (pink-1 and dct-1) were upregulated, probably as part of a mitohormetic mechanism in response to glucose toxicity.	Ceramides	41-49	Glutathione S-transferase 4	Caenorhabditis elegans	111-116
32705593-4	2020	Besides neutral lipids, MTP may also help in the transfer of sphingolipids such as ceramides and sphingomyelin to the apoB-containing lipoproteins.	Ceramides	83-92	microsomal triglyceride transfer protein	Homo sapiens	24-27
31842461-3	2019	We sought to explain whether in obese humans, the insulin resistance is associated with hepatic ceramide accumulation.	Ceramides	96-104	insulin	Homo sapiens	50-57
31842461-10	2019	Interestingly, glucose (at 0" and at 120" in OGTT) and HbA1c positively correlated with the ceramide species that most increased in T2D patients (C16:0-Cer, C18:0-Cer, C22:0-Cer, and C24:0-Cer).	Ceramides	92-100	hemoglobin subunit alpha 1	Homo sapiens	55-59
31842461-10	2019	Interestingly, glucose (at 0" and at 120" in OGTT) and HbA1c positively correlated with the ceramide species that most increased in T2D patients (C16:0-Cer, C18:0-Cer, C22:0-Cer, and C24:0-Cer).	Ceramides	152-155	hemoglobin subunit alpha 1	Homo sapiens	55-59
31842461-10	2019	Interestingly, glucose (at 0" and at 120" in OGTT) and HbA1c positively correlated with the ceramide species that most increased in T2D patients (C16:0-Cer, C18:0-Cer, C22:0-Cer, and C24:0-Cer).	Ceramides	163-166	hemoglobin subunit alpha 1	Homo sapiens	55-59
31842461-10	2019	Interestingly, glucose (at 0" and at 120" in OGTT) and HbA1c positively correlated with the ceramide species that most increased in T2D patients (C16:0-Cer, C18:0-Cer, C22:0-Cer, and C24:0-Cer).	Ceramides	163-166	hemoglobin subunit alpha 1	Homo sapiens	55-59
31842461-10	2019	Interestingly, glucose (at 0" and at 120" in OGTT) and HbA1c positively correlated with the ceramide species that most increased in T2D patients (C16:0-Cer, C18:0-Cer, C22:0-Cer, and C24:0-Cer).	Ceramides	163-166	hemoglobin subunit alpha 1	Homo sapiens	55-59
31842461-14	2019	These data indicate ceramide contribution to the induction of hepatic insulin resistance.	Ceramides	20-28	insulin	Homo sapiens	70-77
31797978-5	2019	In macrophages, deficiency of SphK2, a major SphK isoform in this cell type, results in increases in cellular sphingosine and ceramides.	Ceramides	126-135	sphingosine kinase 2	Mus musculus	30-35
31835809-4	2019	Acid sphingomyelinase is the enzyme that generates ceramide upstream of acid ceramidase in the lysosomes.	Ceramides	51-59	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
31835809-8	2019	As a proof-of-concept study, we first cross-bred acid ceramidase deficient mice with acid sphingomyelinase deficient mice in order to prevent ceramide accumulation.	Ceramides	142-150	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	85-106
31330218-0	2019	The ORMDL3 asthma susceptibility gene regulates systemic ceramide levels without altering key asthma features in mice.	Ceramides	57-65	ORM1-like 3 (S. cerevisiae)	Mus musculus	4-10
31487557-3	2019	Mammalian ORMDL proteins are orthologues of the yeast ORM1/2 proteins, which regulate ceramide synthesis in yeast.	Ceramides	86-94	sphingolipid homeostasis protein ORM2	Saccharomyces cerevisiae S288C	54-60
31487557-4	2019	ORMDL proteins inhibit serine palmitoyltransferase (SPT), the enzyme regulating a rate-limiting step of the sphingolipid pathway to control the levels of ceramides and other sphingolipids.	Ceramides	154-163	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	52-55
30661173-2	2019	We, therefore, investigated the role of NADPH oxidase derived O2.--mediated modulation of MMP2-sphingomyeline-ceramide-S1P signalling axis in ET-1 induced increase in proliferation of PASMCs.	Ceramides	110-118	matrix metallopeptidase 2	Bos taurus	90-94
30661173-2	2019	We, therefore, investigated the role of NADPH oxidase derived O2.--mediated modulation of MMP2-sphingomyeline-ceramide-S1P signalling axis in ET-1 induced increase in proliferation of PASMCs.	Ceramides	110-118	endothelin 1	Bos taurus	142-146
31330218-8	2019	Conversely, in liver and serum, levels of total sphingolipids, including ceramides, were increased in Ormdl3-/- mice, whereas they were decreased in Ormdl3Tg/wt mice.	Ceramides	73-82	ORM1-like 3 (S. cerevisiae)	Mus musculus	102-108
31330218-11	2019	CONCLUSION: ORMDL3 regulates systemic ceramide levels, but genetically interfering with Ormdl3 expression does not result in altered experimental asthma.	Ceramides	38-46	ORM1-like 3 (S. cerevisiae)	Mus musculus	12-18
31369090-0	2019	Overeating Saturated Fat Promotes Fatty Liver and Ceramides Compared With Polyunsaturated Fat: A Randomized Trial.	Ceramides	50-59	FAT atypical cadherin 1	Homo sapiens	21-24
31727994-6	2019	Our data showing that plant ceramides prevent Abeta accumulation by promoting EVs-dependent Abeta clearance in vitro and in vivo provide evidence for a protective role of plant ceramides in AD.	Ceramides	28-37	amyloid beta (A4) precursor protein	Mus musculus	46-51
31766565-0	2019	In Human and Mouse Spino-Cerebellar Tissue, Ataxin-2 Expansion Affects Ceramide-Sphingomyelin Metabolism.	Ceramides	71-79	ataxin 2	Mus musculus	44-52
31766565-9	2019	Spinocerebellar expression profiling revealed consistent reductions of CERS protein isoforms, Sptlc2 and Smpd3, but upregulation of Cers2 mRNA, as prominent anomalies in the ceramide-sphingosine metabolism.	Ceramides	174-182	ceramide synthase 2	Mus musculus	132-137
31998000-10	2019	In psoriatic patients with normal body weight, nervonic ceramide (C24:1) correlated with PASI (r = 0.38; p = 0.042) and CRP (C-reactive protein) (r = 0.42; p = 0.023).	Ceramides	56-64	C-reactive protein	Homo sapiens	120-123
31998000-10	2019	In psoriatic patients with normal body weight, nervonic ceramide (C24:1) correlated with PASI (r = 0.38; p = 0.042) and CRP (C-reactive protein) (r = 0.42; p = 0.023).	Ceramides	56-64	C-reactive protein	Homo sapiens	125-143
31998000-11	2019	In overweight patients, the concentration of lignoceric ceramide (C24:0) correlated inversely with the severity of the disease (r = -0.41; p = 0.022) and CRP (r = -0.6; p = 0.0004).	Ceramides	56-64	C-reactive protein	Homo sapiens	154-157
31727994-6	2019	Our data showing that plant ceramides prevent Abeta accumulation by promoting EVs-dependent Abeta clearance in vitro and in vivo provide evidence for a protective role of plant ceramides in AD.	Ceramides	28-37	amyloid beta (A4) precursor protein	Mus musculus	92-97
31727994-6	2019	Our data showing that plant ceramides prevent Abeta accumulation by promoting EVs-dependent Abeta clearance in vitro and in vivo provide evidence for a protective role of plant ceramides in AD.	Ceramides	177-186	amyloid beta (A4) precursor protein	Mus musculus	46-51
31727994-6	2019	Our data showing that plant ceramides prevent Abeta accumulation by promoting EVs-dependent Abeta clearance in vitro and in vivo provide evidence for a protective role of plant ceramides in AD.	Ceramides	177-186	amyloid beta (A4) precursor protein	Mus musculus	92-97
31668872-0	2019	Adipocyte Hypoxia-Inducible Factor 2alpha Suppresses Atherosclerosis by Promoting Adipose Ceramide Catabolism.	Ceramides	90-98	endothelial PAS domain protein 1	Homo sapiens	10-41
31717476-7	2019	Interestingly, when treated with myriocin to inhibit ceramide biosynthesis, these DEP-induced mitochondrial changes were mitigated.	Ceramides	53-61	zinc finger, DHHC domain containing 21	Mus musculus	82-85
31717476-8	2019	Altogether, these data suggest that DEP exposure may compromise macrophage mitochondrial and whole-body function via pathologic alterations in macrophage ceramide metabolism.	Ceramides	154-162	zinc finger, DHHC domain containing 21	Mus musculus	36-39
31668872-4	2019	Adipocyte HIF-2alpha deficiency exacerbated Western-diet-induced atherosclerosis by increasing adipose ceramide levels, which blunted hepatocyte cholesterol elimination and thermogenesis.	Ceramides	103-111	endothelial PAS domain protein 1	Homo sapiens	10-20
31668872-5	2019	Mechanistically, Acer2, the gene encoding alkaline ceramidase 2, was identified as a novel target gene of HIF-2alpha, triggering ceramide catabolism.	Ceramides	129-137	alkaline ceramidase 2	Homo sapiens	17-22
31668872-5	2019	Mechanistically, Acer2, the gene encoding alkaline ceramidase 2, was identified as a novel target gene of HIF-2alpha, triggering ceramide catabolism.	Ceramides	129-137	alkaline ceramidase 2	Homo sapiens	42-63
31668872-5	2019	Mechanistically, Acer2, the gene encoding alkaline ceramidase 2, was identified as a novel target gene of HIF-2alpha, triggering ceramide catabolism.	Ceramides	129-137	endothelial PAS domain protein 1	Homo sapiens	106-116
31668872-7	2019	Furthermore, activation of adipose HIF-2alpha by the HIF prolyl hydroxylase inhibitor FG-4592 had protective effects on atherosclerosis, accompanied by a reduction in adipose and plasma ceramide and plasma cholesterol levels.	Ceramides	186-194	endothelial PAS domain protein 1	Homo sapiens	35-45
31724300-4	2019	We report for the first time that whole-body insulin sensitivity is unchanged in regular chow (RC)-fed Park2 KO mice, and that liver diacylglycerol levels are reduced and very-long-chain ceramides are increased in Park2 KO mice fed HFD for 1 week.	Ceramides	187-196	parkin RBR E3 ubiquitin protein ligase	Mus musculus	214-219
31675352-9	2019	These results suggested that the association of increased ceramides, especially C18:0 and C24:1, with adverse bone phenotypes in elderly people could be explained mainly by the increase in osteoclastogenesis and bone resorption.	Ceramides	58-67	Bardet-Biedl syndrome 9	Homo sapiens	80-83
31393621-12	2019	INTERPRETATION: Galactosylceramide improved behavioral, neuropathological, and biochemical parameters in Cln3 Deltaex7/8 mice, paving the way for effective therapy for CLN3 disease and use of serum ceramide as a potential biomarker to track impact of therapies.	Ceramides	26-34	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	105-109
31676768-0	2019	Hepatic triglyceride accumulation via endoplasmic reticulum stress-induced SREBP-1 activation is regulated by ceramide synthases.	Ceramides	110-118	sterol regulatory element binding transcription factor 1	Mus musculus	75-82
31676768-4	2019	CerS2 generates C22-C24 ceramides, and CerS5 or CerS6 produces C16 ceramide.	Ceramides	24-33	ceramide synthase 2	Mus musculus	0-5
31676768-4	2019	CerS2 generates C22-C24 ceramides, and CerS5 or CerS6 produces C16 ceramide.	Ceramides	24-32	ceramide synthase 2	Mus musculus	0-5
31480861-8	2019	Mechanistically, lipidomics analyses showed that increased ceramides in PKM2-activated T-cell EVs were mainly responsible for enhanced B cell IgG secretion induced by these EVs.	Ceramides	59-68	pyruvate kinase M1/2	Homo sapiens	72-76
30890204-0	2019	Sterol 12alpha-Hydroxylase Aggravates Dyslipidemia by Activating the Ceramide/mTORC1/SREBP-1C Pathway via FGF21 and FGF15.	Ceramides	69-77	cytochrome P450, family 8, subfamily b, polypeptide 1	Mus musculus	0-26
30890204-0	2019	Sterol 12alpha-Hydroxylase Aggravates Dyslipidemia by Activating the Ceramide/mTORC1/SREBP-1C Pathway via FGF21 and FGF15.	Ceramides	69-77	CREB regulated transcription coactivator 1	Mus musculus	78-84
30890204-0	2019	Sterol 12alpha-Hydroxylase Aggravates Dyslipidemia by Activating the Ceramide/mTORC1/SREBP-1C Pathway via FGF21 and FGF15.	Ceramides	69-77	sterol regulatory element binding transcription factor 1	Mus musculus	85-93
30890204-0	2019	Sterol 12alpha-Hydroxylase Aggravates Dyslipidemia by Activating the Ceramide/mTORC1/SREBP-1C Pathway via FGF21 and FGF15.	Ceramides	69-77	fibroblast growth factor 21	Mus musculus	106-111
30890204-0	2019	Sterol 12alpha-Hydroxylase Aggravates Dyslipidemia by Activating the Ceramide/mTORC1/SREBP-1C Pathway via FGF21 and FGF15.	Ceramides	69-77	fibroblast growth factor 15	Mus musculus	116-121
30890204-6	2019	Interestingly, Ad-Cyp8b1 increased ceramide synthesis and activated hepatic mechanistic target of rapamycin complex 1 (mTORC1)-p70S6K signaling cascade and inhibited AKT/insulin signaling in mice.	Ceramides	35-43	cytochrome P450, family 8, subfamily b, polypeptide 1	Mus musculus	18-24
30890204-8	2019	Ceramides stimulated S6K phosphorylation in both mouse and human primary hepatocytes.	Ceramides	0-9	ribosomal protein S6 kinase, polypeptide 1	Mus musculus	21-24
30890204-9	2019	In high-fat diet-fed mice, Ad-Cyp8b1 reduced fibroblast growth factor 21 (FGF21), activated intestinal farnesoid X receptor (FXR) target gene expression, increased serum ceramides, VLDL secretion, and LDL cholesterol.	Ceramides	170-179	cytochrome P450, family 8, subfamily b, polypeptide 1	Mus musculus	30-36
30890204-11	2019	In conclusion, this study unveiled a novel mechanism linking CYP8B1 to ceramide synthesis and mTORC1 signaling in dyslipidemia and insulin resistance, via intestinal FXR-mediated induction of FGF15 and liver FGF21.	Ceramides	71-79	cytochrome P450, family 8, subfamily b, polypeptide 1	Mus musculus	61-67
30890204-11	2019	In conclusion, this study unveiled a novel mechanism linking CYP8B1 to ceramide synthesis and mTORC1 signaling in dyslipidemia and insulin resistance, via intestinal FXR-mediated induction of FGF15 and liver FGF21.	Ceramides	71-79	nuclear receptor subfamily 1, group H, member 4	Mus musculus	166-169
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.	Ceramides	8-16	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.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Mus musculus	99-102
31186544-7	2019	Whole exome sequencing, validated through Sanger sequencing, identified within this locus a single disease-associated homozygous variant in DEGS1, encoding C4-dihydroceramide desaturase, an enzyme of the ceramide synthesis pathway.	Ceramides	166-174	delta 4-desaturase, sphingolipid 1	Homo sapiens	140-145
31585804-11	2019	MAIN OUTCOME MEASURES: Single high-dose radiation therapy induced NADPH oxidases (NOXs) activation and ROS generation via the proapoptotic ASMase/ceramide pathway.	Ceramides	146-154	ASM	Bos taurus	139-145
31585804-17	2019	Sildenafil reduced ROS generation by inhibiting the ASMase/ceramide pathway.	Ceramides	59-67	ASM	Bos taurus	52-58
31660434-7	2019	An enhanced Gba1 activity elevates ceramide levels responsible for apoptosis and decreases glucosylceramides to overcome drug resistance.	Ceramides	35-43	glucosidase, beta, acid	Mus musculus	12-16
31647034-7	2019	RESULTS: Immunohistochemistry showed increased ceramides in the placental villous trophoblasts of the insulin-treated GDM patients.	Ceramides	47-56	insulin	Homo sapiens	102-109
31472960-0	2019	Knockout of neutrophil elastase protects against western diet induced nonalcoholic steatohepatitis in mice by regulating hepatic ceramides metabolism.	Ceramides	129-138	elastase, neutrophil expressed	Mus musculus	12-31
31647034-12	2019	Active caspase was not changed while XIAP protein was increased in trophoblasts treated with ceramide.	Ceramides	93-101	X-linked inhibitor of apoptosis	Homo sapiens	37-41
31647034-14	2019	Furthermore, we conclude that ceramide is increased in the placental trophoblast during insulin treatment and that its upregulation correlates with elevated NFAT5, SMIT, increased apoptosis and decreased trophoblast mitochondrial respiration.	Ceramides	30-38	insulin	Homo sapiens	88-95
31647034-14	2019	Furthermore, we conclude that ceramide is increased in the placental trophoblast during insulin treatment and that its upregulation correlates with elevated NFAT5, SMIT, increased apoptosis and decreased trophoblast mitochondrial respiration.	Ceramides	30-38	nuclear factor of activated T cells 5	Homo sapiens	157-162
31647034-14	2019	Furthermore, we conclude that ceramide is increased in the placental trophoblast during insulin treatment and that its upregulation correlates with elevated NFAT5, SMIT, increased apoptosis and decreased trophoblast mitochondrial respiration.	Ceramides	30-38	solute carrier family 5 member 3	Homo sapiens	164-168
31605240-6	2019	RESULTS: Confirming the link to deteriorated glucose homeostasis, serum ceramides were positively correlated with fasting glucose, but inversely correlated with fasting and OGTT-derived measures of insulin sensitivity and beta-cell function.	Ceramides	72-81	insulin	Homo sapiens	198-205
31648453-1	2019	Objective: To evaluate the clinical values of 4 types of ceramides (Cer1, Cer2, Cer3, Cer4) in the coronary artery stenosis, clinical diagnosis and risk prediction.	Ceramides	57-66	cerberus 1, DAN family BMP antagonist	Homo sapiens	68-72
31681760-1	2019	The activity of neutral sphingomyelinase-2 (NSM2) to catalyze the conversion of sphingomyelin (SM) to ceramide and phosphocholine at the cytosolic leaflet of plasma membrane (PM) is important in T cell receptor (TCR) signaling.	Ceramides	102-110	sphingomyelin phosphodiesterase 3	Homo sapiens	16-42
31681760-1	2019	The activity of neutral sphingomyelinase-2 (NSM2) to catalyze the conversion of sphingomyelin (SM) to ceramide and phosphocholine at the cytosolic leaflet of plasma membrane (PM) is important in T cell receptor (TCR) signaling.	Ceramides	102-110	sphingomyelin phosphodiesterase 3	Homo sapiens	44-48
31681760-1	2019	The activity of neutral sphingomyelinase-2 (NSM2) to catalyze the conversion of sphingomyelin (SM) to ceramide and phosphocholine at the cytosolic leaflet of plasma membrane (PM) is important in T cell receptor (TCR) signaling.	Ceramides	102-110	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	195-210
31681760-1	2019	The activity of neutral sphingomyelinase-2 (NSM2) to catalyze the conversion of sphingomyelin (SM) to ceramide and phosphocholine at the cytosolic leaflet of plasma membrane (PM) is important in T cell receptor (TCR) signaling.	Ceramides	102-110	T cell receptor beta variable 20/OR9-2 (non-functional)	Homo sapiens	212-215
31614447-4	2019	Ceramide elevation by serine palmitoyltransferse (SPT) activation was the primary source of the sphingosine elevation as myriocin, an inhibitor of SPT, prevented sphingosine elevation and protected oligodendrocytes.	Ceramides	0-8	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	50-53
31614447-4	2019	Ceramide elevation by serine palmitoyltransferse (SPT) activation was the primary source of the sphingosine elevation as myriocin, an inhibitor of SPT, prevented sphingosine elevation and protected oligodendrocytes.	Ceramides	0-8	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	147-150
31176039-0	2019	Ceramide regulates interaction of Hsd17b4 with Pex5 and function of peroxisomes.	Ceramides	0-8	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	34-41
31132336-6	2019	We also found that expression of ATP13A2 reduces the ceramide-fluorescence intensity and the content of bis(monoacylglyceryl)phosphate (BMP).	Ceramides	53-61	ATPase cation transporting 13A2	Homo sapiens	33-40
31142470-2	2019	ASM hydrolyzes sphingomyelins to produce ceramides but protein targets of ASM remain largely unclear.	Ceramides	41-50	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
31142470-7	2019	Our studies suggest that ASM, acting at the plasma membrane to produce ceramides, regulates the localization and trafficking of the palmitoylated proteins.	Ceramides	71-80	sphingomyelin phosphodiesterase 1	Homo sapiens	25-28
31290266-7	2019	Similarly, the pro-apoptotic effects of ceramide and thapsigargin were blunted by PGC-1alpha in muscle cells.	Ceramides	40-48	PPARG coactivator 1 alpha	Sus scrofa	82-92
31176039-0	2019	Ceramide regulates interaction of Hsd17b4 with Pex5 and function of peroxisomes.	Ceramides	0-8	peroxisomal biogenesis factor 5	Homo sapiens	47-51
31176039-3	2019	Using affinity chromatography, co-immunoprecipitation, and proximity ligation assays we discovered that ceramide interacts with Hsd17b4, an enzyme critical for peroxisomal VLCFA oxidation and docosahexaenoic acid (DHA) generation.	Ceramides	104-112	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	128-135
31176039-4	2019	Immunocytochemistry showed that Hsd17b4 is distributed to ceramide-enriched mitochondria-associated membranes (CEMAMs).	Ceramides	58-66	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	32-39
31176039-5	2019	Molecular docking and in vitro mutagenesis experiments showed that ceramide binds to the sterol carrier protein 2-like domain in Hsd17b4 adjacent to peroxisome targeting signal 1 (PTS1), the C-terminal signal for interaction with peroxisomal biogenesis factor 5 (Pex5), a peroxin mediating transport of Hsd17b4 into peroxisomes.	Ceramides	67-75	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	129-136
31176039-5	2019	Molecular docking and in vitro mutagenesis experiments showed that ceramide binds to the sterol carrier protein 2-like domain in Hsd17b4 adjacent to peroxisome targeting signal 1 (PTS1), the C-terminal signal for interaction with peroxisomal biogenesis factor 5 (Pex5), a peroxin mediating transport of Hsd17b4 into peroxisomes.	Ceramides	67-75	peroxisomal biogenesis factor 5	Homo sapiens	230-261
31176039-5	2019	Molecular docking and in vitro mutagenesis experiments showed that ceramide binds to the sterol carrier protein 2-like domain in Hsd17b4 adjacent to peroxisome targeting signal 1 (PTS1), the C-terminal signal for interaction with peroxisomal biogenesis factor 5 (Pex5), a peroxin mediating transport of Hsd17b4 into peroxisomes.	Ceramides	67-75	peroxisomal biogenesis factor 5	Homo sapiens	263-267
31176039-5	2019	Molecular docking and in vitro mutagenesis experiments showed that ceramide binds to the sterol carrier protein 2-like domain in Hsd17b4 adjacent to peroxisome targeting signal 1 (PTS1), the C-terminal signal for interaction with peroxisomal biogenesis factor 5 (Pex5), a peroxin mediating transport of Hsd17b4 into peroxisomes.	Ceramides	67-75	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	303-310
31176039-6	2019	Inhibition of ceramide biosynthesis induced translocation of Hsd17b4 from CEMAMs to peroxisomes, interaction of Hsd17b4 with Pex5, and upregulation of DHA.	Ceramides	14-22	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	61-68
31176039-6	2019	Inhibition of ceramide biosynthesis induced translocation of Hsd17b4 from CEMAMs to peroxisomes, interaction of Hsd17b4 with Pex5, and upregulation of DHA.	Ceramides	14-22	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	112-119
31176039-6	2019	Inhibition of ceramide biosynthesis induced translocation of Hsd17b4 from CEMAMs to peroxisomes, interaction of Hsd17b4 with Pex5, and upregulation of DHA.	Ceramides	14-22	peroxisomal biogenesis factor 5	Homo sapiens	125-129
31176039-7	2019	This data indicates a novel role of ceramide as a molecular switch regulating interaction of Hsd17b4 with Pex5 and peroxisomal function.	Ceramides	36-44	hydroxysteroid 17-beta dehydrogenase 4	Homo sapiens	93-100
31176039-7	2019	This data indicates a novel role of ceramide as a molecular switch regulating interaction of Hsd17b4 with Pex5 and peroxisomal function.	Ceramides	36-44	peroxisomal biogenesis factor 5	Homo sapiens	106-110
31519952-0	2019	Fatty acid transport protein 4 is required for incorporation of saturated ultralong-chain fatty acids into epidermal ceramides and monoacylglycerols.	Ceramides	117-126	solute carrier family 27 (fatty acid transporter), member 4	Mus musculus	0-30
31483293-6	2019	Recently, adiponectin was found to enhance exosome biogenesis and secretion, leading to a decrease in cellular ceramides, excess of which is known to cause insulin resistance and cardiovascular disease phenotypes.	Ceramides	111-120	adiponectin, C1Q and collagen domain containing	Homo sapiens	10-21
31453682-5	2019	The apoptosis was induced by activating both sphingomyelin-ceramide signaling pathway and oxidative stress, which included intrinsic (bax and caspase-9) and extrinsic apoptotic pathways (tumor necrosis factor receptor 1, caspase-8, and caspase-3).	Ceramides	59-67	caspase 9	Bos taurus	142-151
31519952-8	2019	Acyl chain length alterations in ceramides also suggested roles for FATP4 in esterifying saturated non-hydroxy and beta-hydroxy FAs with at least 25 carbons and saturated or unsaturated omega-hydroxy FAs with at least 30 carbons to CoA.	Ceramides	33-42	solute carrier family 27 (fatty acid transporter), member 4	Mus musculus	68-73
31514293-7	2019	RESULTS: Analyzing the association between ceramides level and MIB-1, total ceramides and dihydroceramides showed a strong association (r = 0.7257 and r = 0.6733, respectively) with MIB-1 staining (p = 0.0033 and p = 0.0083, respectively).	Ceramides	43-52	MIB E3 ubiquitin protein ligase 1	Homo sapiens	63-68
31514293-7	2019	RESULTS: Analyzing the association between ceramides level and MIB-1, total ceramides and dihydroceramides showed a strong association (r = 0.7257 and r = 0.6733, respectively) with MIB-1 staining (p = 0.0033 and p = 0.0083, respectively).	Ceramides	43-52	MIB E3 ubiquitin protein ligase 1	Homo sapiens	182-187
31514293-7	2019	RESULTS: Analyzing the association between ceramides level and MIB-1, total ceramides and dihydroceramides showed a strong association (r = 0.7257 and r = 0.6733, respectively) with MIB-1 staining (p = 0.0033 and p = 0.0083, respectively).	Ceramides	76-85	MIB E3 ubiquitin protein ligase 1	Homo sapiens	63-68
31535025-4	2019	Cellular stress induces Drp1 nitrosylation/activation, releasing p17/PERMIT to retrieve CerS1 for its OMM trafficking, resulting in mitochondrial ceramide generation, mitophagy and cell death.	Ceramides	146-154	collapsin response mediator protein 1	Mus musculus	24-28
31535025-4	2019	Cellular stress induces Drp1 nitrosylation/activation, releasing p17/PERMIT to retrieve CerS1 for its OMM trafficking, resulting in mitochondrial ceramide generation, mitophagy and cell death.	Ceramides	146-154	ceramide synthase 1	Mus musculus	88-93
31514293-7	2019	RESULTS: Analyzing the association between ceramides level and MIB-1, total ceramides and dihydroceramides showed a strong association (r = 0.7257 and r = 0.6733, respectively) with MIB-1 staining (p = 0.0033 and p = 0.0083, respectively).	Ceramides	76-85	MIB E3 ubiquitin protein ligase 1	Homo sapiens	182-187
31535025-4	2019	Cellular stress induces Drp1 nitrosylation/activation, releasing p17/PERMIT to retrieve CerS1 for its OMM trafficking, resulting in mitochondrial ceramide generation, mitophagy and cell death.	Ceramides	146-154	family with sequence similarity 72, member A	Mus musculus	65-68
31514293-8	2019	Among the single ceramide species, Cer C24:1 (r = 0.8814, p <= 0.0001), DHCer C24:1 (r = 0.8429, p = 0.0002) and DHCer C18:0 (r = 0.9426, p <= 0.0001) showed a significant correlation with MIB-1.	Ceramides	17-25	MIB E3 ubiquitin protein ligase 1	Homo sapiens	189-194
31254056-0	2019	Mass spectrometry imaging reveals ganglioside and ceramide localization patterns during cerebellar degeneration in the Npc1-/- mouse model.	Ceramides	50-58	NPC intracellular cholesterol transporter 1	Mus musculus	119-123
31462128-6	2019	Inhibition of neutral ceramidase, an enzyme responsible for the hydrolysis of ceramide, favored hydrogen peroxide-dependent FID in arterioles from healthy patients.	Ceramides	78-86	N-acylsphingosine amidohydrolase 2	Homo sapiens	14-32
31268777-9	2019	Using a Port-a-Patch planar patch-clamp system, we found that AC-associated sphingolipids, sphingomyelin, ceramide, and sphingosine had different effects on TRPML1 channel activity in podocytes.	Ceramides	106-114	mucolipin 1	Mus musculus	157-163
30546074-2	2019	TNFalpha is also a potent activator of the sphingomyelinase (SMase)/ceramide pathway leading to ceramide synthesis and regulating cell differentiation, proliferation, apoptosis, senescence, and autophagy.	Ceramides	68-76	tumor necrosis factor	Homo sapiens	0-8
31305892-7	2019	The effect of neuronal treatment with CSF from progressive patients was heat stable, thereby prompting us to conduct an unbiased exploratory lipidomic study that identified specific ceramide species as differentially abundant in the CSF of progressive patients compared to relapsing remitting multiple sclerosis.	Ceramides	182-190	colony stimulating factor 2	Homo sapiens	38-41
31305892-7	2019	The effect of neuronal treatment with CSF from progressive patients was heat stable, thereby prompting us to conduct an unbiased exploratory lipidomic study that identified specific ceramide species as differentially abundant in the CSF of progressive patients compared to relapsing remitting multiple sclerosis.	Ceramides	182-190	colony stimulating factor 2	Homo sapiens	233-236
31305892-9	2019	Thus ceramide levels in the CSF of patients with progressive multiple sclerosis not only impaired mitochondrial respiration but also decreased the bioavailability of glucose by increasing its uptake.	Ceramides	5-13	colony stimulating factor 2	Homo sapiens	28-31
31480728-3	2019	In this study, we observed that exogenous ceramide induced two distinct morphologies of cell fate following C2-ceramide treatment between the two breast cancer cell lines MCF-7 (wild type p53) and MDA-MB-231 (mutant p53) cells.	Ceramides	42-50	tumor protein p53	Homo sapiens	188-191
31480728-3	2019	In this study, we observed that exogenous ceramide induced two distinct morphologies of cell fate following C2-ceramide treatment between the two breast cancer cell lines MCF-7 (wild type p53) and MDA-MB-231 (mutant p53) cells.	Ceramides	42-50	tumor protein p53	Homo sapiens	216-219
30546074-10	2019	Autophagy plays an essential role during erythropoiesis and our results demonstrate that the TNFalpha/neutral SMase/ceramide pathway inhibits autophagy in EpoCD34/HSPCs.	Ceramides	116-124	tumor necrosis factor	Homo sapiens	93-101
30546074-14	2019	We demonstrate here that the TNFalpha/neutral SMase/ceramide pathway inhibits erythropoiesis to induce myelopoiesis via modulation of a hematopoietic TF/miR network and inhibition of late steps of autophagy.	Ceramides	52-60	tumor necrosis factor	Homo sapiens	29-37
30546074-2	2019	TNFalpha is also a potent activator of the sphingomyelinase (SMase)/ceramide pathway leading to ceramide synthesis and regulating cell differentiation, proliferation, apoptosis, senescence, and autophagy.	Ceramides	96-104	tumor necrosis factor	Homo sapiens	0-8
30546074-3	2019	Here we evaluated the implication of the TNFalpha/SMase/ceramide pathway on inhibition of erythropoiesis in human CD34+ hematopoietic stem/progenitor cells (CD34/HSPCs) from healthy donors.	Ceramides	56-64	CD34 molecule	Homo sapiens	114-118
30546074-3	2019	Here we evaluated the implication of the TNFalpha/SMase/ceramide pathway on inhibition of erythropoiesis in human CD34+ hematopoietic stem/progenitor cells (CD34/HSPCs) from healthy donors.	Ceramides	56-64	CD34 molecule	Homo sapiens	157-161
30546074-9	2019	Moreover, the expression of microRNAs (miR)-144/451, miR-146a, miR-155, and miR-223 was also modulated by TNFalpha and ceramide treatments, in line with cellular observations.	Ceramides	119-127	microRNA 144	Homo sapiens	28-47
30546074-9	2019	Moreover, the expression of microRNAs (miR)-144/451, miR-146a, miR-155, and miR-223 was also modulated by TNFalpha and ceramide treatments, in line with cellular observations.	Ceramides	119-127	microRNA 146a	Homo sapiens	53-61
30546074-9	2019	Moreover, the expression of microRNAs (miR)-144/451, miR-146a, miR-155, and miR-223 was also modulated by TNFalpha and ceramide treatments, in line with cellular observations.	Ceramides	119-127	microRNA 155	Homo sapiens	63-70
30546074-9	2019	Moreover, the expression of microRNAs (miR)-144/451, miR-146a, miR-155, and miR-223 was also modulated by TNFalpha and ceramide treatments, in line with cellular observations.	Ceramides	119-127	microRNA 223	Homo sapiens	76-83
31254361-0	2019	Structure, functions and regulation of CERT, a lipid-transfer protein for the delivery of ceramide at the ER-Golgi membrane contact sites.	Ceramides	90-98	ceramide transporter 1	Homo sapiens	39-43
31254361-3	2019	Ceramide transport protein (CERT) transports ceramide from the ER to the trans-Golgi regions at the ER-Golgi membrane contact sites (MCS).	Ceramides	45-53	ceramide transporter 1	Homo sapiens	0-26
31254361-3	2019	Ceramide transport protein (CERT) transports ceramide from the ER to the trans-Golgi regions at the ER-Golgi membrane contact sites (MCS).	Ceramides	45-53	ceramide transporter 1	Homo sapiens	28-32
31254361-7	2019	CERT-dependent ceramide transport is also affected by the pool of phosphatidylinositol (PtdIns)-4-phosphate (PtdIns(4)P) in the trans-Golgi regions, while the PtdIns(4)P pool is regulated by PtdIns-4-kinases and oxysterol-binding protein.	Ceramides	15-23	ceramide transporter 1	Homo sapiens	0-4
31227640-0	2019	Rare DEGS1 variant significantly alters de novo ceramide synthesis pathway.	Ceramides	48-56	delta 4-desaturase, sphingolipid 1	Homo sapiens	5-10
31227640-5	2019	We identified a Hispanic ancestry-specific rare functional variant, L175Q, in delta 4-desaturase, sphingolipid 1 (DEGS1), a key enzyme in the pathway that converts dihydroceramide to ceramide.	Ceramides	171-179	delta 4-desaturase, sphingolipid 1	Homo sapiens	114-119
31270131-0	2019	New evidence from plasma ceramides links apoE polymorphism to greater risk of coronary artery disease in Finnish adults.	Ceramides	25-34	apolipoprotein E	Homo sapiens	41-45
31270131-8	2019	apoE associated with seven ceramides that are connected to atherogenically potent macrophages and/or lipoprotein particles; these associations could indicate a plausible linkage between apoE polymorphism and ceramide metabolism, leading to adverse plasma LDL metabolism and atherogenesis.	Ceramides	27-36	apolipoprotein E	Homo sapiens	0-4
31227640-9	2019	Understanding the biological role of DEGS1 variants, such as L175Q, in ceramide synthesis may improve the understanding of metabolic-related disorders and spur ongoing research of drug targets along this pathway.	Ceramides	71-79	delta 4-desaturase, sphingolipid 1	Homo sapiens	37-42
31270131-8	2019	apoE associated with seven ceramides that are connected to atherogenically potent macrophages and/or lipoprotein particles; these associations could indicate a plausible linkage between apoE polymorphism and ceramide metabolism, leading to adverse plasma LDL metabolism and atherogenesis.	Ceramides	27-36	apolipoprotein E	Homo sapiens	186-190
31270131-8	2019	apoE associated with seven ceramides that are connected to atherogenically potent macrophages and/or lipoprotein particles; these associations could indicate a plausible linkage between apoE polymorphism and ceramide metabolism, leading to adverse plasma LDL metabolism and atherogenesis.	Ceramides	27-35	apolipoprotein E	Homo sapiens	0-4
31310676-11	2019	Our data provide evidence that the ASM/ceramide system regulates TRPC6 channels likely by controlling their recruitment to specific lipid subdomains and thereby fine-tuning their physical properties.	Ceramides	39-47	transient receptor potential cation channel, subfamily C, member 6	Rattus norvegicus	65-70
31270131-8	2019	apoE associated with seven ceramides that are connected to atherogenically potent macrophages and/or lipoprotein particles; these associations could indicate a plausible linkage between apoE polymorphism and ceramide metabolism, leading to adverse plasma LDL metabolism and atherogenesis.	Ceramides	27-35	apolipoprotein E	Homo sapiens	186-190
31270131-9	2019	In conclusion, new evidence from plasma ceramides links apoE polymorphism with an increased risk of CAD and extends our understanding of the role of apoE in health and disease.	Ceramides	40-49	apolipoprotein E	Homo sapiens	56-60
31270131-9	2019	In conclusion, new evidence from plasma ceramides links apoE polymorphism with an increased risk of CAD and extends our understanding of the role of apoE in health and disease.	Ceramides	40-49	apolipoprotein E	Homo sapiens	149-153
31162334-15	2019	Induction of cleaved IL-1beta and NLRP2 in DRG neurons was similarly observed after ceramide injection.	Ceramides	84-92	interleukin 1 beta	Mus musculus	21-29
31162334-15	2019	Induction of cleaved IL-1beta and NLRP2 in DRG neurons was similarly observed after ceramide injection.	Ceramides	84-92	NLR family, pyrin domain containing 2	Mus musculus	34-39
31162334-16	2019	NLRP2 siRNA inhibited ceramide-induced pain hypersensitivity.	Ceramides	22-30	NLR family, pyrin domain containing 2	Mus musculus	0-5
31243063-3	2019	In a previous study, we characterized an Arabidopsis (Arabidopsis thaliana) cell-death mutant, accelerated cell death5 (acd5), which accumulates ceramides and exhibits spontaneous cell death late in development.	Ceramides	145-154	Diacylglycerol kinase family protein	Arabidopsis thaliana	120-124
31434754-1	2019	It is caused by loss-of-function mutations in the gene encoding for acid sphingomyelinase (ASM), which hydrolyzes sphingomyelin into ceramide.	Ceramides	133-141	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	68-89
31555088-3	2019	The generation of EVs through the ESCRT-independent pathway depends on the hydrolysis of sphingomyelin by neutral sphingomyelinase 2 (nSMase2) to produce ceramide, which causes the membrane of endosomal multivesicular bodies to bud inward.	Ceramides	154-162	sphingomyelin phosphodiesterase 3	Homo sapiens	106-132
31555088-3	2019	The generation of EVs through the ESCRT-independent pathway depends on the hydrolysis of sphingomyelin by neutral sphingomyelinase 2 (nSMase2) to produce ceramide, which causes the membrane of endosomal multivesicular bodies to bud inward.	Ceramides	154-162	sphingomyelin phosphodiesterase 3	Homo sapiens	134-141
31480447-0	2019	Quantifying Fluorescently Labeled Ceramide Levels in Human Sarcoma Cell Lines in Response to a Sphingomyelin Synthase Inhibitor.	Ceramides	34-42	spermine synthase	Homo sapiens	95-117
31480447-4	2019	Sphingomyelin synthase (SMS) is the enzyme that transfers a phosphatidylcholine to ceramide to generate sphingomyelin.	Ceramides	83-91	spermine synthase	Homo sapiens	0-22
31480447-4	2019	Sphingomyelin synthase (SMS) is the enzyme that transfers a phosphatidylcholine to ceramide to generate sphingomyelin.	Ceramides	83-91	spermine synthase	Homo sapiens	24-27
31480447-5	2019	To test the inhibition of SMS, scientists assess the buildup of ceramide in the cell, which is cytotoxic.	Ceramides	64-72	spermine synthase	Homo sapiens	26-29
31496996-0	2019	The Role of Ceramides in Insulin Resistance.	Ceramides	12-21	insulin	Homo sapiens	25-32
31434754-1	2019	It is caused by loss-of-function mutations in the gene encoding for acid sphingomyelinase (ASM), which hydrolyzes sphingomyelin into ceramide.	Ceramides	133-141	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	91-94
31382484-7	2019	Lipid subclass analyses revealed various oxysterols, sphingomyelins, and ceramides, species uniquely enriched in human plaques were significantly reduced by cholesterol acceptors, especially by apoA-I.	Ceramides	73-82	apolipoprotein A1	Homo sapiens	194-200
31475148-6	2019	PLA1 shows the subcellular localization of a particular CAP that is cross-linked to pacFACer, while PLA2 tests if the cross-linked CAP forms a complex with endogenous ceramide.	Ceramides	167-175	phospholipase A2 group IB	Homo sapiens	100-104
31475148-7	2019	Two proteins, tubulin and voltage-dependent anion channel 1 (VDAC1), were cross-linked to pacFACer and showed PLA signals for a complex with ceramide and pacFACer, which were predominantly colocalized with microtubules and mitochondria, respectively.	Ceramides	141-149	voltage dependent anion channel 1	Homo sapiens	26-59
31475148-7	2019	Two proteins, tubulin and voltage-dependent anion channel 1 (VDAC1), were cross-linked to pacFACer and showed PLA signals for a complex with ceramide and pacFACer, which were predominantly colocalized with microtubules and mitochondria, respectively.	Ceramides	141-149	voltage dependent anion channel 1	Homo sapiens	61-66
31475148-8	2019	Binding of tubulin and VDAC1 to ceramide was confirmed by coimmunoprecipitation assays using anti ceramide antibody.	Ceramides	32-40	voltage dependent anion channel 1	Homo sapiens	23-28
30806093-24	2019	Subsequently liberated ceramides act as intermediaries that regulate TNF-alpha and recruit neutrophils.	Ceramides	23-32	tumor necrosis factor	Mus musculus	69-78
31158401-7	2019	siRNA-knockdown of EMSY in organotypic culture leads to enhanced development of barrier function, reflecting increased expression of structural and functional proteins, including filaggrin and filaggrin-2, as well as long-chain ceramides.	Ceramides	228-237	EMSY transcriptional repressor, BRCA2 interacting	Homo sapiens	19-23
31088855-5	2019	TFAM enhanced muscle glucose uptake despite increased fatty acid (FA) oxidation in concert with higher beta-oxidation capacity to reduce the accumulation of IR-related carnitines and ceramides.	Ceramides	183-192	transcription factor A, mitochondrial	Homo sapiens	0-4
30738053-6	2019	Topical ZAG treatment in AD mice recovered ZAG expression in the skin and improved AD-like symptoms, transepidermal water loss, and ceramide levels.	Ceramides	132-140	alpha-2-glycoprotein 1, zinc	Mus musculus	8-11
33569519-1	2021	The nonlysosomal glucosylceramidase beta2 (GBA2) gene encode an enzyme that catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Ceramides	112-120	glucosylceramidase beta 2	Homo sapiens	17-41
31342535-1	2019	Ceramides (CER) are biologically active sphingolipid precursors that are mechanistically linked to several pathogenic states including cancer, insulin resistance, and neurodegeneration.	Ceramides	0-9	insulin	Homo sapiens	143-150
31342535-1	2019	Ceramides (CER) are biologically active sphingolipid precursors that are mechanistically linked to several pathogenic states including cancer, insulin resistance, and neurodegeneration.	Ceramides	11-14	insulin	Homo sapiens	143-150
33569519-1	2021	The nonlysosomal glucosylceramidase beta2 (GBA2) gene encode an enzyme that catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Ceramides	112-120	glucosylceramidase beta 2	Homo sapiens	43-47
31138648-0	2019	The ceramide moiety of disialoganglioside (GD3) is essential for GD3 recognition by the sialic acid-binding lectin SIGLEC7 on the cell surface.	Ceramides	4-12	GRDX	Homo sapiens	43-46
31273070-2	2019	By genetically engineering mice, we deleted the enzyme dihydroceramide desaturase 1 (DES1), which normally inserts a conserved double bond into the backbone of ceramides and other predominant sphingolipids.	Ceramides	160-169	delta(4)-desaturase, sphingolipid 1	Mus musculus	71-83
31273070-2	2019	By genetically engineering mice, we deleted the enzyme dihydroceramide desaturase 1 (DES1), which normally inserts a conserved double bond into the backbone of ceramides and other predominant sphingolipids.	Ceramides	160-169	delta(4)-desaturase, sphingolipid 1	Mus musculus	85-89
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.	Ceramides	143-151	Aminotran_1_2 domain-containing protein;Serine palmitoyltransferase 1	Caenorhabditis elegans	0-6
31440742-6	2019	In our recent study (Dadsena S et al., 2019, Nat Commun 10:1832), we used a photoactivatable ceramide probe combined with computer simulations and functional studies to identify the voltage-dependent anion channel VDAC2 as a critical effector of ceramide-induced mitochondrial apoptosis.	Ceramides	93-101	voltage dependent anion channel 2	Homo sapiens	214-219
31440742-6	2019	In our recent study (Dadsena S et al., 2019, Nat Commun 10:1832), we used a photoactivatable ceramide probe combined with computer simulations and functional studies to identify the voltage-dependent anion channel VDAC2 as a critical effector of ceramide-induced mitochondrial apoptosis.	Ceramides	246-254	voltage dependent anion channel 2	Homo sapiens	214-219
31138648-3	2019	Because milk-derived GD3 could be recognized by this fusion protein when incorporated onto the surface of DLD-1 cells, we compared the ceramides in DLD-1-generated and milk-derived GD3s to identify the SIGLEC7-specific GD3 structures on the cell membrane, revealing that SIGLEC7 recognizes only GD3-containing regular ceramides but not phytoceramides.	Ceramides	318-327	sialic acid binding Ig like lectin 7	Homo sapiens	202-209
31138648-8	2019	These results indicate that the ceramide structures in glycosphingolipids affect SIGLEC7 binding and distribution on the cell surface and influence cell sensitivity to killing by SIGLEC7-expressing effector cells.	Ceramides	32-40	sialic acid binding Ig like lectin 7	Homo sapiens	81-88
31138648-8	2019	These results indicate that the ceramide structures in glycosphingolipids affect SIGLEC7 binding and distribution on the cell surface and influence cell sensitivity to killing by SIGLEC7-expressing effector cells.	Ceramides	32-40	sialic acid binding Ig like lectin 7	Homo sapiens	179-186
31332167-4	2019	Deletion of MFN1 in oocytes resulted in mitochondrial dysfunction and altered mitochondrial dynamics, as well as accumulation of ceramide, which contributed to increased apoptosis and a reproductive phenotype that was partially rescued by treatment with ceramide synthesis inhibitor myriocin.	Ceramides	129-137	mitofusin 1	Homo sapiens	12-16
31332167-4	2019	Deletion of MFN1 in oocytes resulted in mitochondrial dysfunction and altered mitochondrial dynamics, as well as accumulation of ceramide, which contributed to increased apoptosis and a reproductive phenotype that was partially rescued by treatment with ceramide synthesis inhibitor myriocin.	Ceramides	254-262	mitofusin 1	Homo sapiens	12-16
31332539-3	2019	The skin is modeled as a ceramide (CER2) bilayer.	Ceramides	25-33	DAN domain BMP antagonist family member 5	Homo sapiens	35-39
31138648-0	2019	The ceramide moiety of disialoganglioside (GD3) is essential for GD3 recognition by the sialic acid-binding lectin SIGLEC7 on the cell surface.	Ceramides	4-12	GRDX	Homo sapiens	65-68
31138648-0	2019	The ceramide moiety of disialoganglioside (GD3) is essential for GD3 recognition by the sialic acid-binding lectin SIGLEC7 on the cell surface.	Ceramides	4-12	sialic acid binding Ig like lectin 7	Homo sapiens	115-122
31110049-3	2019	FTY720/fingolimod, a prodrug for the treatment of multiple sclerosis, is phosphorylated in vivo to its active phosphorylated form by sphingosine kinase 2 and has been shown to interfere with the actions of S1P and to inhibit ceramide biosynthesis.	Ceramides	225-233	sphingosine kinase 2	Mus musculus	133-153
31082617-0	2019	GPER1 influences cellular homeostasis and cytostatic drug resistance via influencing long chain ceramide synthesis in breast cancer cells.	Ceramides	96-104	G protein-coupled estrogen receptor 1	Homo sapiens	0-5
31110049-3	2019	FTY720/fingolimod, a prodrug for the treatment of multiple sclerosis, is phosphorylated in vivo to its active phosphorylated form by sphingosine kinase 2 and has been shown to interfere with the actions of S1P and to inhibit ceramide biosynthesis.	Ceramides	225-233	sphingosine-1-phosphate receptor 1	Mus musculus	206-209
30809769-10	2019	The ceramide/S1P ratio correlated with weight loss (r = 0.48, P = 0.08), insulin resistance (r = 0.61, P = 0.02), PGC-1alpha (r = - 0.51, P < 0.06), CS (r = - 0.63, P = 0.01), and SIRT1 (r = - 0.54, P < 0.04).	Ceramides	4-12	PPARG coactivator 1 alpha	Rattus norvegicus	114-124
30809769-10	2019	The ceramide/S1P ratio correlated with weight loss (r = 0.48, P = 0.08), insulin resistance (r = 0.61, P = 0.02), PGC-1alpha (r = - 0.51, P < 0.06), CS (r = - 0.63, P = 0.01), and SIRT1 (r = - 0.54, P < 0.04).	Ceramides	4-12	citrate synthase	Rattus norvegicus	149-151
30809769-10	2019	The ceramide/S1P ratio correlated with weight loss (r = 0.48, P = 0.08), insulin resistance (r = 0.61, P = 0.02), PGC-1alpha (r = - 0.51, P < 0.06), CS (r = - 0.63, P = 0.01), and SIRT1 (r = - 0.54, P < 0.04).	Ceramides	4-12	sirtuin 1	Rattus norvegicus	180-185
31275322-3	2019	In the present study, we determined the impact of acid sphingomyelinase (Asm), which catalyzes the hydrolysis of sphingomyelin to ceramide, on the course of Citrobacter (C.) rodentium-driven colitis.	Ceramides	130-138	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	73-76
31048413-3	2019	We report here that secretagogues (agonists that stimulate secretion) such as the peptide hormone vasoactive intestinal peptide (VIP) and muscarinic agonist carbachol increase CFTR aggregation into cholesterol-dependent clusters, reduce CFTR lateral mobility within and between membrane microdomains, and trigger the fusion of clusters into large (3.0 microm2) ceramide-rich platforms.	Ceramides	361-369	vasoactive intestinal peptide	Homo sapiens	129-132
30909726-12	2019	ACSL1 trafficked LCFA into ceramides without normalizing the reduced triglyceride storage in TAC.	Ceramides	27-36	acyl-CoA synthetase long chain family member 1	Homo sapiens	0-5
30909726-13	2019	ACSL1 prevented de novo synthesis of cardiotoxic C16- and C24-, and C24:1 ceramides and increased potentially cardioprotective C20- and C22-ceramides post-TAC.	Ceramides	74-83	acyl-CoA synthetase long chain family member 1	Homo sapiens	0-5
31053639-3	2019	Angptl4 has also been shown to be required for dexamethasone-induced hepatic ceramide production.	Ceramides	77-85	angiopoietin-like 4	Mus musculus	0-7
31053639-7	2019	Treating mice with myriocin, an inhibitor of the rate-controlling enzyme of de novo ceramide synthesis, serine palmitoyltransferase long-chain base subunit 1 (SPTLC1)/SPTLC2, decreased dexamethasone-induced plasma and liver triglyceride levels in WT but not Angptl4-/- mice.	Ceramides	84-92	serine palmitoyltransferase, long chain base subunit 1	Mus musculus	104-157
31053639-9	2019	Protein phosphatase 2 phosphatase activator (PP2A) and protein kinase Czeta (PKCzeta) are two known downstream effectors of ceramides.	Ceramides	124-133	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	0-43
31053639-9	2019	Protein phosphatase 2 phosphatase activator (PP2A) and protein kinase Czeta (PKCzeta) are two known downstream effectors of ceramides.	Ceramides	124-133	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	45-49
31053639-9	2019	Protein phosphatase 2 phosphatase activator (PP2A) and protein kinase Czeta (PKCzeta) are two known downstream effectors of ceramides.	Ceramides	124-133	protein kinase C, zeta	Mus musculus	55-75
31053639-9	2019	Protein phosphatase 2 phosphatase activator (PP2A) and protein kinase Czeta (PKCzeta) are two known downstream effectors of ceramides.	Ceramides	124-133	protein kinase C zeta	Homo sapiens	77-84
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.	Ceramides	18-26	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-3
31231223-8	2019	Inhibition of mPGES-1 increased the concentration of sphinganine and dihydroceramide (C16:0DhCer), while inhibition of COX-2 caused a general decrease in most ceramides, again suggesting different effects on cell death between the two inhibitors.	Ceramides	159-168	mitochondrially encoded cytochrome c oxidase II	Homo sapiens	119-124
31048413-3	2019	We report here that secretagogues (agonists that stimulate secretion) such as the peptide hormone vasoactive intestinal peptide (VIP) and muscarinic agonist carbachol increase CFTR aggregation into cholesterol-dependent clusters, reduce CFTR lateral mobility within and between membrane microdomains, and trigger the fusion of clusters into large (3.0 microm2) ceramide-rich platforms.	Ceramides	361-369	CF transmembrane conductance regulator	Homo sapiens	176-180
31048413-8	2019	Formation of ceramide-rich platforms containing CFTR enhances transepithelial secretion and likely has other functions related to inflammation and mucosal immunity.	Ceramides	13-21	CF transmembrane conductance regulator	Homo sapiens	48-52
30290227-5	2019	PNPLA1 acts as a unique transacylase that specifically transfers linoleic acid from triglyceride to omega-hydroxy fatty acid in ceramide, thus giving rise to omega-O-acylceramide.	Ceramides	128-136	patatin like phospholipase domain containing 1	Homo sapiens	0-6
30854677-2	2019	Over-activation of acid sphingomyelinase (ASM)/ceramide (Cer) pathway takes centre stage in hepatocyte injury entailed by various stimulus.	Ceramides	47-55	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	19-40
30854677-2	2019	Over-activation of acid sphingomyelinase (ASM)/ceramide (Cer) pathway takes centre stage in hepatocyte injury entailed by various stimulus.	Ceramides	47-55	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	42-45
30854677-2	2019	Over-activation of acid sphingomyelinase (ASM)/ceramide (Cer) pathway takes centre stage in hepatocyte injury entailed by various stimulus.	Ceramides	57-60	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	19-40
30854677-2	2019	Over-activation of acid sphingomyelinase (ASM)/ceramide (Cer) pathway takes centre stage in hepatocyte injury entailed by various stimulus.	Ceramides	57-60	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	42-45
30917007-2	2019	Targeting SET with a sphingolipid analog drug fingolimod (FTY720) or ceramide leads to the reactivation of tumor suppressor PP2A.	Ceramides	69-77	protein phosphatase 2 phosphatase activator	Homo sapiens	124-128
30993698-4	2019	These ceramides are processed by a range of other enzymes, including 12R-lipoxygenase (12R-LOX), before the covalent attachment of the free omega-hydroxyceramides to the CPE surface to form the CLE.	Ceramides	6-15	arachidonate 12-lipoxygenase, 12R type	Homo sapiens	69-85
30993698-4	2019	These ceramides are processed by a range of other enzymes, including 12R-lipoxygenase (12R-LOX), before the covalent attachment of the free omega-hydroxyceramides to the CPE surface to form the CLE.	Ceramides	6-15	arachidonate 12-lipoxygenase, 12R type	Homo sapiens	87-94
30993698-4	2019	These ceramides are processed by a range of other enzymes, including 12R-lipoxygenase (12R-LOX), before the covalent attachment of the free omega-hydroxyceramides to the CPE surface to form the CLE.	Ceramides	6-15	carboxypeptidase E	Homo sapiens	170-173
30876920-8	2019	RESULTS: SR-B1 knockdown resulted in decreased lipid levels in SEs, specifically ceramides, and in decreased transcript levels of LDLR, PPAR-alpha and PPAR-gamma, which are factors involved in regulating ceramide synthesis.	Ceramides	81-90	scavenger receptor class B member 1	Homo sapiens	9-14
31214184-1	2019	The enzyme acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and is thereby involved in several cellular processes such as differentiation, proliferation, and apoptosis in different cell types.	Ceramides	67-75	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	11-32
31214184-1	2019	The enzyme acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and is thereby involved in several cellular processes such as differentiation, proliferation, and apoptosis in different cell types.	Ceramides	67-75	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	34-37
31058489-3	2019	Here, we describe the development of a novel and high-throughput-compatible workflow for the analysis of GSL-derived glycans based on ceramide glycanase digestion, 8-aminopyrene-1,3,6-trisulfonic acid (APTS) labeling, and multiplexed capillary gel electrophoresis coupled to laser-induced fluorescence detection (xCGE-LIF).	Ceramides	134-142	cathepsin A	Homo sapiens	105-108
31101115-1	2019	BACKGROUND: Sphingosine kinase 1 (SPHK1) is an enzyme that converts pro-apoptotic ceramide and sphingosine into anti-apoptotic sphingosine-1-phosphate.	Ceramides	82-90	sphingosine kinase 1	Homo sapiens	12-32
31101115-1	2019	BACKGROUND: Sphingosine kinase 1 (SPHK1) is an enzyme that converts pro-apoptotic ceramide and sphingosine into anti-apoptotic sphingosine-1-phosphate.	Ceramides	82-90	sphingosine kinase 1	Homo sapiens	34-39
31003944-7	2019	Omics analyses additionally confirm the age-related impairment of lipid homeostasis and reveal the accumulation of specific lipid classes, including certain sphingolipids, ceramides, and dolichols in aged brown fat.	Ceramides	172-181	tyrosinase-related protein 1	Mus musculus	205-210
31003944-8	2019	While ceramides as well as enzymes of dolichol metabolism inhibit brown adipogenesis, inhibition of sphingosine 1-phosphate receptor 2 induces brown adipocyte differentiation.	Ceramides	6-15	tyrosinase-related protein 1	Mus musculus	66-71
31159189-7	2019	Release of TNF-alpha, IL-6, and IL-1beta after stimulation with palmitic, oleic, linoleic acid, or C6 ceramide in primary microglia culture were quantified using ELISA.	Ceramides	102-110	tumor necrosis factor	Rattus norvegicus	11-20
31137828-0	2019	Sulforaphane Prevents Hepatic Insulin Resistance by Blocking Serine Palmitoyltransferase 3-Mediated Ceramide Biosynthesis.	Ceramides	100-108	insulin	Homo sapiens	30-37
31137828-0	2019	Sulforaphane Prevents Hepatic Insulin Resistance by Blocking Serine Palmitoyltransferase 3-Mediated Ceramide Biosynthesis.	Ceramides	100-108	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	61-90
31137828-7	2019	In addition, knockdown of serine palmitoyltransferase 3 (SPTLC3) in HepG2 cells prevented ceramide accumulation and alleviated insulin resistance.	Ceramides	90-98	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	26-55
31137828-7	2019	In addition, knockdown of serine palmitoyltransferase 3 (SPTLC3) in HepG2 cells prevented ceramide accumulation and alleviated insulin resistance.	Ceramides	90-98	serine palmitoyltransferase long chain base subunit 3	Homo sapiens	57-63
30876920-8	2019	RESULTS: SR-B1 knockdown resulted in decreased lipid levels in SEs, specifically ceramides, and in decreased transcript levels of LDLR, PPAR-alpha and PPAR-gamma, which are factors involved in regulating ceramide synthesis.	Ceramides	81-89	scavenger receptor class B member 1	Homo sapiens	9-14
30876920-10	2019	CONCLUSION: We conclude that one of the main functions of SR-B1 in the skin is to regulate ceramide levels and thereby maintain the barrier function of the skin, resulting in the protection of cutaneous tissues from outdoor insults.	Ceramides	91-99	scavenger receptor class B member 1	Homo sapiens	58-63
31030513-1	2019	Acid ceramidase (AC) hydrolyzes ceramides into sphingoid bases and fatty acids.	Ceramides	32-41	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
30921693-1	2019	Neutral sphingomyelinase 2 (nSMase2), a key enzyme in ceramide biosynthesis, is a new therapeutic target for the treatment of neurological disorders and cancer.	Ceramides	54-62	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
30921693-1	2019	Neutral sphingomyelinase 2 (nSMase2), a key enzyme in ceramide biosynthesis, is a new therapeutic target for the treatment of neurological disorders and cancer.	Ceramides	54-62	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
30890560-1	2019	Neutral sphingomyelinase 2 (nSMase2) produces the bioactive lipid ceramide and has important roles in neurodegeneration, cancer, and exosome formation.	Ceramides	66-74	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
30928402-2	2019	However, other molecules could participate as signals, such as PLA2 and SMase, which have been proposed to increase PGE2 and ceramides, both involved in the increment of PS externalization due to osmotic stress.	Ceramides	125-134	phospholipase A2 group IIA	Homo sapiens	63-67
30890560-1	2019	Neutral sphingomyelinase 2 (nSMase2) produces the bioactive lipid ceramide and has important roles in neurodegeneration, cancer, and exosome formation.	Ceramides	66-74	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
30771382-7	2019	Moreover, ceramide in podocytes was found elevated upon d-ribose stimulation, and prior treatments of podocyte with acid sphingomyelinase (Asm) inhibitor, amitriptyline, acid ceramidase (AC) inducer, genistein, or AC CRISPR/cas9 activation plasmids were found to decrease d-ribose-induced ceramide accumulation, EVs release and IL-1beta secretion due to reduced interactions of lysosome with MVBs.	Ceramides	10-18	N-acylsphingosine amidohydrolase 1	Homo sapiens	170-185
30771382-7	2019	Moreover, ceramide in podocytes was found elevated upon d-ribose stimulation, and prior treatments of podocyte with acid sphingomyelinase (Asm) inhibitor, amitriptyline, acid ceramidase (AC) inducer, genistein, or AC CRISPR/cas9 activation plasmids were found to decrease d-ribose-induced ceramide accumulation, EVs release and IL-1beta secretion due to reduced interactions of lysosome with MVBs.	Ceramides	10-18	sphingomyelin phosphodiesterase 1	Homo sapiens	116-137
30771382-7	2019	Moreover, ceramide in podocytes was found elevated upon d-ribose stimulation, and prior treatments of podocyte with acid sphingomyelinase (Asm) inhibitor, amitriptyline, acid ceramidase (AC) inducer, genistein, or AC CRISPR/cas9 activation plasmids were found to decrease d-ribose-induced ceramide accumulation, EVs release and IL-1beta secretion due to reduced interactions of lysosome with MVBs.	Ceramides	10-18	interleukin 1 beta	Homo sapiens	328-336
30771382-7	2019	Moreover, ceramide in podocytes was found elevated upon d-ribose stimulation, and prior treatments of podocyte with acid sphingomyelinase (Asm) inhibitor, amitriptyline, acid ceramidase (AC) inducer, genistein, or AC CRISPR/cas9 activation plasmids were found to decrease d-ribose-induced ceramide accumulation, EVs release and IL-1beta secretion due to reduced interactions of lysosome with MVBs.	Ceramides	10-18	sphingomyelin phosphodiesterase 1	Homo sapiens	139-142
31114500-2	2019	In normal cells, de novo synthesized ceramide is mainly converted to sphingomyelin (SM), the most abundant SL, by sphingomyelin synthase 1 (SMS1) and, albeit to a lesser extent, SMS2, encoded by the SGMS1 and SGMS2 genes, respectively.	Ceramides	37-45	sphingomyelin synthase 1	Homo sapiens	114-138
29758301-5	2019	Specifically, lipids and lipid derivatives such as polyunsaturated fatty acids (PUFAs), ceramides and steroids have been shown to directly interact with the lipid facing amino acids in various Kv channels including hERG.	Ceramides	88-97	ETS transcription factor ERG	Homo sapiens	215-219
31114500-2	2019	In normal cells, de novo synthesized ceramide is mainly converted to sphingomyelin (SM), the most abundant SL, by sphingomyelin synthase 1 (SMS1) and, albeit to a lesser extent, SMS2, encoded by the SGMS1 and SGMS2 genes, respectively.	Ceramides	37-45	sphingomyelin synthase 1	Homo sapiens	140-144
31114500-2	2019	In normal cells, de novo synthesized ceramide is mainly converted to sphingomyelin (SM), the most abundant SL, by sphingomyelin synthase 1 (SMS1) and, albeit to a lesser extent, SMS2, encoded by the SGMS1 and SGMS2 genes, respectively.	Ceramides	37-45	sphingomyelin synthase 2	Homo sapiens	178-182
31114500-2	2019	In normal cells, de novo synthesized ceramide is mainly converted to sphingomyelin (SM), the most abundant SL, by sphingomyelin synthase 1 (SMS1) and, albeit to a lesser extent, SMS2, encoded by the SGMS1 and SGMS2 genes, respectively.	Ceramides	37-45	sphingomyelin synthase 1	Homo sapiens	199-204
31114500-2	2019	In normal cells, de novo synthesized ceramide is mainly converted to sphingomyelin (SM), the most abundant SL, by sphingomyelin synthase 1 (SMS1) and, albeit to a lesser extent, SMS2, encoded by the SGMS1 and SGMS2 genes, respectively.	Ceramides	37-45	sphingomyelin synthase 2	Homo sapiens	209-214
31114500-3	2019	Alternatively, ceramide can be converted to glucosylceramide (GlcCer) by the GlcCer synthase (GCS), encoded by the UGCG gene.	Ceramides	15-23	UDP-glucose ceramide glucosyltransferase	Homo sapiens	115-119
31015432-0	2019	Ceramides bind VDAC2 to trigger mitochondrial apoptosis.	Ceramides	0-9	voltage dependent anion channel 2	Homo sapiens	15-20
30910852-5	2019	In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.	Ceramides	263-271	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	13-19
30910852-5	2019	In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.	Ceramides	263-271	nitric oxide synthase 3, endothelial cell	Mus musculus	121-144
30910852-5	2019	In addition, aSMase siRNA or desipramine treatment increased the release of nitric oxide (NO) and the phosphorylation of endothelial NO synthase (eNOS) in diabetic mouse aortas and aortic endothelial cells with HG.These results indicate that inhibition of aSMase/ceramide pathway improves endothelium-dependent vascular relaxation (EDR) largely through regulating the eNOS/NO pathway in diabetic animals.	Ceramides	263-271	nitric oxide synthase 3, endothelial cell	Mus musculus	146-150
30999626-8	2019	Participants who were classified as at "moderate risk" compared to "lower-risk" based on a ceramide risk score had significantly higher body mass index (BMI) values, as well as higher rates of elevated fibrinogen levels, metabolic syndrome, and former smoking status.	Ceramides	91-99	fibrinogen beta chain	Homo sapiens	202-212
30910852-4	2019	High glucose (HG)-induced up-regulation of aSMase activity and ceramide levels were restored by treatment with aSMase siRNA or desipramine in endothelial cells.	Ceramides	63-71	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	111-117
30837168-5	2019	These ceramide analogues decreased xIAP and Bcl-xL level and exhibited significant sensitization activity to overcome human cancer cell resistance to TRAIL, a cancer-selective agent that are being tested in human clinical trials.	Ceramides	6-14	X-linked inhibitor of apoptosis	Homo sapiens	35-39
30837168-5	2019	These ceramide analogues decreased xIAP and Bcl-xL level and exhibited significant sensitization activity to overcome human cancer cell resistance to TRAIL, a cancer-selective agent that are being tested in human clinical trials.	Ceramides	6-14	BCL2 like 1	Homo sapiens	44-50
30837168-5	2019	These ceramide analogues decreased xIAP and Bcl-xL level and exhibited significant sensitization activity to overcome human cancer cell resistance to TRAIL, a cancer-selective agent that are being tested in human clinical trials.	Ceramides	6-14	TNF superfamily member 10	Homo sapiens	150-155
31015432-3	2019	Using a photoactivatable ceramide probe, we here identify the voltage-dependent anion channels VDAC1 and VDAC2 as mitochondrial ceramide binding proteins.	Ceramides	25-33	voltage dependent anion channel 1	Homo sapiens	95-100
31015432-3	2019	Using a photoactivatable ceramide probe, we here identify the voltage-dependent anion channels VDAC1 and VDAC2 as mitochondrial ceramide binding proteins.	Ceramides	25-33	voltage dependent anion channel 2	Homo sapiens	105-110
31015432-3	2019	Using a photoactivatable ceramide probe, we here identify the voltage-dependent anion channels VDAC1 and VDAC2 as mitochondrial ceramide binding proteins.	Ceramides	128-136	voltage dependent anion channel 1	Homo sapiens	95-100
31015432-3	2019	Using a photoactivatable ceramide probe, we here identify the voltage-dependent anion channels VDAC1 and VDAC2 as mitochondrial ceramide binding proteins.	Ceramides	128-136	voltage dependent anion channel 2	Homo sapiens	105-110
31015432-7	2019	Unlike VDAC1 removal, loss of VDAC2 or replacing its membrane-facing glutamate with glutamine renders human colon cancer cells largely resistant to ceramide-induced apoptosis.	Ceramides	148-156	voltage dependent anion channel 2	Homo sapiens	30-35
31015432-8	2019	Collectively, our data support a role of VDAC2 as direct effector of ceramide-mediated cell death, providing a molecular framework for how ceramides exert their anti-neoplastic activity.	Ceramides	69-77	voltage dependent anion channel 2	Homo sapiens	41-46
31015432-8	2019	Collectively, our data support a role of VDAC2 as direct effector of ceramide-mediated cell death, providing a molecular framework for how ceramides exert their anti-neoplastic activity.	Ceramides	139-148	voltage dependent anion channel 2	Homo sapiens	41-46
30974901-3	2019	Moreover, adiponectin potently stimulates ceramidase activity associated with its two receptors and enhances ceramide catabolism and the formation of its anti-apoptotic metabolite, sphingosine 1 phosphate (S1P), independently of AMPK.	Ceramides	109-117	adiponectin, C1Q and collagen domain containing	Homo sapiens	10-21
30513370-0	2019	Oleate increase neutral lipid accumulation, cellular respiration and rescues palmitate-exposed GLP-1 secreting cells by reducing ceramide-induced ROS.	Ceramides	129-137	glucagon like peptide 1 receptor	Homo sapiens	95-100
33911565-9	2019	Results: Treatment with ceramides increased the expression of proteins affecting cell proliferation such as Bcl-2, BAX, phosphorylated-ERK and Cyclin D1.	Ceramides	24-33	BCL2 apoptosis regulator	Homo sapiens	108-113
33911565-9	2019	Results: Treatment with ceramides increased the expression of proteins affecting cell proliferation such as Bcl-2, BAX, phosphorylated-ERK and Cyclin D1.	Ceramides	24-33	BCL2 associated X, apoptosis regulator	Homo sapiens	115-118
33911565-9	2019	Results: Treatment with ceramides increased the expression of proteins affecting cell proliferation such as Bcl-2, BAX, phosphorylated-ERK and Cyclin D1.	Ceramides	24-33	mitogen-activated protein kinase 1	Homo sapiens	135-138
33911565-9	2019	Results: Treatment with ceramides increased the expression of proteins affecting cell proliferation such as Bcl-2, BAX, phosphorylated-ERK and Cyclin D1.	Ceramides	24-33	cyclin D1	Homo sapiens	143-152
33911565-10	2019	Also, ceramides treatment were increased the expression of several growth factors, including epidermal growth factor family, and promote the expression of Wnt/beta-catenin and BMP2/4 signaling.	Ceramides	6-15	catenin beta 1	Homo sapiens	159-171
33911565-10	2019	Also, ceramides treatment were increased the expression of several growth factors, including epidermal growth factor family, and promote the expression of Wnt/beta-catenin and BMP2/4 signaling.	Ceramides	6-15	bone morphogenetic protein 2	Homo sapiens	176-182
33911565-11	2019	Conclusion: Our data suggest that synthetic ceramides stimulates hair growth by induction proliferation of hDPCs via modulation of Wnt/beta-catenin and BMP2/4 signaling.	Ceramides	44-53	catenin beta 1	Homo sapiens	135-147
33911565-11	2019	Conclusion: Our data suggest that synthetic ceramides stimulates hair growth by induction proliferation of hDPCs via modulation of Wnt/beta-catenin and BMP2/4 signaling.	Ceramides	44-53	bone morphogenetic protein 2	Homo sapiens	152-158
30071259-7	2019	An unbalanced ratio between ceramides and terminal metabolic products in the liver and plasma promotes weight gain, inflammation, and insulin resistance.	Ceramides	28-37	insulin	Homo sapiens	134-141
30808712-2	2019	We previously reported that ceramide regulates a transmembrane protein called TM4SF20 (transmembrane 4 L six family member 20) through topological inversion by altering the direction through which the protein is translocated across membranes during translation.	Ceramides	28-36	transmembrane 4 L six family member 20	Rattus norvegicus	78-85
30808712-2	2019	We previously reported that ceramide regulates a transmembrane protein called TM4SF20 (transmembrane 4 L six family member 20) through topological inversion by altering the direction through which the protein is translocated across membranes during translation.	Ceramides	28-36	transmembrane 4 L six family member 20	Rattus norvegicus	87-125
30702345-11	2019	Our study suggests that activation of NSMase3 causes diaphragm weakness in HFREF, presumably through accumulation of ceramide and elevation in mitochondrial ROS.	Ceramides	117-125	sphingomyelin phosphodiesterase 4	Mus musculus	38-45
30513370-8	2019	RESULTS: Generation of intracellular ceramide mediate a detrimental increased in ROS production following long term exposure to SFAs in GLP-1-secreting cells.	Ceramides	37-45	glucagon like peptide 1 receptor	Homo sapiens	136-141
30513370-11	2019	CONCLUSION: This study demonstrates novel data supporting effects of MUFAs on the ceramide biosynthetic pathway, triglyceride storage respiration and secretion in GLP-1 secreting cells.	Ceramides	82-90	glucagon like peptide 1 receptor	Homo sapiens	163-168
30556232-1	2019	Acid sphingomyelinase (ASM) is one of the enzymes that catalyzes the breakdown of sphingomyelin to ceramide and phosphorylcholine.	Ceramides	99-107	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
32265588-2	2019	This study aimed to elucidate dermatological manifestations at different stages of CKD and determine their relationship with interleukin 31 (IL-31), a T-cell cytokine that induces severe pruritus, and uridine diphosphate (UDP)-glucose ceramide glucosyltransferase (UGCG), an enzyme that metabolizes ceramide, which plays an important role in moisturizing epidermis.	Ceramides	235-243	interleukin 31	Homo sapiens	141-146
30818011-1	2019	Niemann-Pick disease type B is a hereditary rare condition caused by deficiency of the acid sphingomyelinase (ASM) that is needed for lysosomal hydrolysis of sphingomyelin to ceramide and phosphocholine.	Ceramides	175-183	sphingomyelin phosphodiesterase 1	Homo sapiens	110-113
30556232-1	2019	Acid sphingomyelinase (ASM) is one of the enzymes that catalyzes the breakdown of sphingomyelin to ceramide and phosphorylcholine.	Ceramides	99-107	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
30700557-0	2019	The ORMDL/Orm-serine palmitoyltransferase (SPT) complex is directly regulated by ceramide: Reconstitution of SPT regulation in isolated membranes.	Ceramides	81-89	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	43-46
31012404-7	2019	These SNPs all lie within the gene encoding ceramide synthase 6 (CERS6) and thus may regulate ceramide synthesis.	Ceramides	44-52	ceramide synthase 6	Homo sapiens	65-70
30444039-1	2019	Sphingosine kinases (SphKs) and ceramide kinase (CerK) phosphorylate sphingosine to sphingosine-1-phosphate (S1P) and ceramide to ceramide-1-phosphate (C1P), respectively.	Ceramides	32-40	ceramide kinase	Homo sapiens	49-53
30776097-7	2019	This underlines that the TrkA-GM1 interaction directly involves the GM1 oligosaccharide, but not the ceramide.	Ceramides	101-109	neurotrophic tyrosine kinase, receptor, type 1	Mus musculus	25-29
30776097-7	2019	This underlines that the TrkA-GM1 interaction directly involves the GM1 oligosaccharide, but not the ceramide.	Ceramides	101-109	coenzyme Q10A	Mus musculus	30-33
30700557-0	2019	The ORMDL/Orm-serine palmitoyltransferase (SPT) complex is directly regulated by ceramide: Reconstitution of SPT regulation in isolated membranes.	Ceramides	81-89	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	109-112
30700557-10	2019	We found that this system is particularly responsive to the pro-apoptotic sphingolipid ceramide and that this response is strictly stereospecific, indicating that ceramide regulates the ORMDL-SPT complex via a specific binding interaction.	Ceramides	87-95	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	192-195
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.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Homo sapiens	27-30
30889865-5	2019	We propose a novel hypothesis that ER-alpha36-GPER signaling initially induces rapid and temporal activation of NADPH oxidase 1 to generate superoxide, which subsequently activates redox-sensitive neutral sphingomyelinase 2 generating the lipid signaling mediator ceramide.	Ceramides	264-272	G protein-coupled estrogen receptor 1	Homo sapiens	46-50
30889865-5	2019	We propose a novel hypothesis that ER-alpha36-GPER signaling initially induces rapid and temporal activation of NADPH oxidase 1 to generate superoxide, which subsequently activates redox-sensitive neutral sphingomyelinase 2 generating the lipid signaling mediator ceramide.	Ceramides	264-272	NADPH oxidase 1	Homo sapiens	112-127
30889865-5	2019	We propose a novel hypothesis that ER-alpha36-GPER signaling initially induces rapid and temporal activation of NADPH oxidase 1 to generate superoxide, which subsequently activates redox-sensitive neutral sphingomyelinase 2 generating the lipid signaling mediator ceramide.	Ceramides	264-272	sphingomyelin phosphodiesterase 3	Homo sapiens	197-223
30326731-10	2019	SMPD1 (sphingomyelin phosphodiesterase 1) was activated by ventilation and stretch, and its inhibition prevented ceramide production, LC3B-II formation, LC3B/first apoptosis signal interaction, caspase-3 activation, and, ultimately, FLRE cell death.	Ceramides	113-121	sphingomyelin phosphodiesterase 1	Rattus norvegicus	0-5
30326731-10	2019	SMPD1 (sphingomyelin phosphodiesterase 1) was activated by ventilation and stretch, and its inhibition prevented ceramide production, LC3B-II formation, LC3B/first apoptosis signal interaction, caspase-3 activation, and, ultimately, FLRE cell death.	Ceramides	113-121	sphingomyelin phosphodiesterase 1	Rattus norvegicus	7-40
30662006-1	2019	The nonlysosomal glucosylceramidase beta2 (GBA2) catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Ceramides	85-93	glucosidase beta 2	Mus musculus	43-47
30231605-0	2019	Development of a Label-Free LC-MS/MS-Based Glucosylceramide Synthase Assay and Its Application to Inhibitors Screening for Ceramide-Related Diseases.	Ceramides	123-131	UDP-glucose ceramide glucosyltransferase	Homo sapiens	43-68
30897694-0	2019	Ceramide Imbalance and Impaired TLR4-Mediated Autophagy in BMDM of an ORMDL3-Overexpressing Mouse Model.	Ceramides	0-8	ORM1-like 3 (S. cerevisiae)	Mus musculus	70-76
30871020-1	2019	Ceramide and diacylglycerol are linked to insulin resistance in rodents, but in humans the data are inconsistent.	Ceramides	0-8	insulin	Homo sapiens	42-49
30871020-11	2019	This study highlights an increased content of saturated ceramides in aging which could be speculated to influence insulin sensitivity.	Ceramides	56-65	insulin	Homo sapiens	114-121
30661200-7	2019	Acid ceramidase (AC) is a promising target protein in the development of multi-targeted anticancer drugs as its inhibition can simultaneously inhibit angiogenesis via the Akt and ERK 1/2 pathway and limit cancer growth through ceramide-induced apoptosis.	Ceramides	227-235	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
30661200-7	2019	Acid ceramidase (AC) is a promising target protein in the development of multi-targeted anticancer drugs as its inhibition can simultaneously inhibit angiogenesis via the Akt and ERK 1/2 pathway and limit cancer growth through ceramide-induced apoptosis.	Ceramides	227-235	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
30231605-8	2019	We also evaluated the inhibition degree of a known GCS inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) on GCS enzymatic activity and proved that this method could be successfully applied to GCS inhibitor screening of preventive and therapeutic drugs for ceramide metabolism diseases, such as atopic dermatitis and Gaucher disease.	Ceramides	272-280	UDP-glucose ceramide glucosyltransferase	Homo sapiens	51-54
30231605-8	2019	We also evaluated the inhibition degree of a known GCS inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) on GCS enzymatic activity and proved that this method could be successfully applied to GCS inhibitor screening of preventive and therapeutic drugs for ceramide metabolism diseases, such as atopic dermatitis and Gaucher disease.	Ceramides	272-280	UDP-glucose ceramide glucosyltransferase	Homo sapiens	124-127
30231605-8	2019	We also evaluated the inhibition degree of a known GCS inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) on GCS enzymatic activity and proved that this method could be successfully applied to GCS inhibitor screening of preventive and therapeutic drugs for ceramide metabolism diseases, such as atopic dermatitis and Gaucher disease.	Ceramides	272-280	UDP-glucose ceramide glucosyltransferase	Homo sapiens	124-127
30487246-16	2019	The mutation abrogated ELOVL1 enzymatic activity and reduced &gt;=C24 ceramides and sphingomyelins in patient cells.	Ceramides	70-79	ELOVL fatty acid elongase 1	Homo sapiens	23-29
30716394-2	2019	A hyperfunction of acid sphingomyelinase (ASM) and resulting ceramide overload were recently identified as one pathway into this comorbidity.	Ceramides	61-69	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	19-40
30716394-2	2019	A hyperfunction of acid sphingomyelinase (ASM) and resulting ceramide overload were recently identified as one pathway into this comorbidity.	Ceramides	61-69	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	42-45
30716394-3	2019	Here we analyzed the involvement of ASM, one of the main enzymes involved in ceramide synthesis, in the molecular control of monoaminergic systems in their basal activity and in response to pharmacological and natural reinforcers.	Ceramides	77-85	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	36-39
30915775-0	2019	Study on ceramide modulates EAAT-2 participation in the immunoinflammatory response in schizophrenia.	Ceramides	9-17	solute carrier family 1 member 2	Homo sapiens	28-34
30915775-10	2019	The NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) reduced the behavioral abnormalities caused by ceramide accumulation, downregulated CONCLUSIONS: The experimental results suggest that ceramide reduces EAAT-2 expression through the NF-kappaB/TNF-alpha pathway and causes neuronal excitotoxicity in the pathogenesis of schizophrenia, leading to neuronal damage.	Ceramides	194-202	solute carrier family 1 member 2	Homo sapiens	211-217
30915775-10	2019	The NF-kappaB inhibitor pyrrolidine dithiocarbamate (PDTC) reduced the behavioral abnormalities caused by ceramide accumulation, downregulated CONCLUSIONS: The experimental results suggest that ceramide reduces EAAT-2 expression through the NF-kappaB/TNF-alpha pathway and causes neuronal excitotoxicity in the pathogenesis of schizophrenia, leading to neuronal damage.	Ceramides	194-202	tumor necrosis factor	Homo sapiens	251-260
30189266-7	2019	Stimulation by BDNF generates the signaling molecule ceramide, which activates PKCzeta leading to induction of the CK2-Nrf2 signaling axis.	Ceramides	53-61	brain derived neurotrophic factor	Homo sapiens	15-19
30189266-7	2019	Stimulation by BDNF generates the signaling molecule ceramide, which activates PKCzeta leading to induction of the CK2-Nrf2 signaling axis.	Ceramides	53-61	protein kinase C zeta	Homo sapiens	79-86
30189266-7	2019	Stimulation by BDNF generates the signaling molecule ceramide, which activates PKCzeta leading to induction of the CK2-Nrf2 signaling axis.	Ceramides	53-61	NFE2 like bZIP transcription factor 2	Homo sapiens	119-123
30189266-9	2019	In contrast, neurons express both TrkB.FL and TrkB.T1, and TrkB.FL tyrosine kinase activity inhibits p75NTR-dependent ceramide generation and internalizes p75NTR.	Ceramides	118-126	nerve growth factor receptor	Homo sapiens	101-107
30620337-8	2019	The enzymatic inhibition of Cer synthase by fingolimod, 1 step prior to DEGS1 in the pathway, reduced the critical DhCer/Cer imbalance and the severe locomotor disability, increasing the number of myelinating oligodendrocytes in a zebrafish model.	Ceramides	28-31	delta(4)-desaturase, sphingolipid 1	Danio rerio	72-77
30620338-4	2019	RESULTS: By whole-exome sequencing in a patient with a multisystem neurological disorder of both the central and peripheral nervous systems, we identified a homozygous p.Ala280Val variant in DEGS1, which catalyzes the last step in the ceramide synthesis pathway.	Ceramides	235-243	delta 4-desaturase, sphingolipid 1	Homo sapiens	191-196
30393086-4	2019	Moreover, significant increases in the levels of ceramide and its downstream metabolites (sphingosine and sphingosine-1-phosphate) following adiponectin stimulation were detected using liquid chromatography-mass spectrometry.	Ceramides	49-57	adiponectin, C1Q and collagen domain containing	Homo sapiens	141-152
30885289-6	2019	SPHK1 knockdown-accelerated cellular senescence was attenuated by co-treatment with sphingosine-1-phosphate and an inhibitor of ceramide synthesis, fumonisin B1, but not by treatment with either one alone.	Ceramides	128-136	sphingosine kinase 1	Homo sapiens	0-5
30655217-2	2019	Recent genetic mouse studies suggest that specific sphingolipid C16:0 ceramide produced by ceramide synthase 6 (CerS6) plays an important role in the development of insulin resistance.	Ceramides	70-78	ceramide synthase 6	Mus musculus	91-110
30655217-2	2019	Recent genetic mouse studies suggest that specific sphingolipid C16:0 ceramide produced by ceramide synthase 6 (CerS6) plays an important role in the development of insulin resistance.	Ceramides	70-78	ceramide synthase 6	Mus musculus	112-117
30655217-11	2019	RESULTS: CerS6 expression were significantly elevated in the liver and brown adipose, this was correlated with significantly elevated C16:0 ceramide concentrations in plasma and liver.	Ceramides	140-148	ceramide synthase 6	Mus musculus	9-14
30655217-12	2019	Treatment with CerS6 ASO selectively reduced CerS6 expression by ~90% predominantly in the liver and this CerS6 KD resulted in a significant reduction of C16:0 ceramide by about 50% in both liver and plasma.	Ceramides	160-168	ceramide synthase 6	Mus musculus	15-20
30655217-17	2019	CerS6 should specifically be targeted for the reduction of C16:0 ceramides, that results in amelioration of insulin resistance, hyperglycemia and obesity.	Ceramides	65-74	ceramide synthase 6	Mus musculus	0-5
30655217-18	2019	CerS6 mediated C16:0 ceramide reduction could be a potentially attractive target for the treatment of insulin resistance, obesity and type 2 diabetes.	Ceramides	21-29	ceramide synthase 6	Mus musculus	0-5
30770781-0	2019	Sphingomyelin synthase 2 promotes an aggressive breast cancer phenotype by disrupting the homoeostasis of ceramide and sphingomyelin.	Ceramides	106-114	sphingomyelin synthase 2	Homo sapiens	0-24
30822302-7	2019	Thus, both synthetic GM3 and GD3 comprising a d18:1-C24:1 ceramide backbone were able to activate iNKT cells in a CD1d-dependent manner.	Ceramides	58-66	CD1d molecule	Homo sapiens	114-118
30837943-0	2019	Developmental Comparison of Ceramide in Wild-Type and Cln3 Deltaex7/8 Mouse Brains and Sera.	Ceramides	28-36	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	54-58
30837943-2	2019	CLN3 pathogenesis has been linked to dysregulation of ceramide, a key intracellular messenger impacting various biological functions.	Ceramides	54-62	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	0-4
30837943-3	2019	Ceramide is upregulated in brains of CLN3 patients and activates apoptosis.	Ceramides	0-8	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	37-41
30837943-9	2019	Increase of ceramide in Cln3 Deltaex7/8 mouse brain at 24 weeks of age precedes neuronal apoptosis.	Ceramides	12-20	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	24-28
30837943-10	2019	The correlation between serum and brain ceramide in WT mice, and dysregulation of ceramide in serum and brain of Cln3 Deltaex7/8 mice, and the significant increase in ceramide in Cln3 Deltaex7/8 mouse brains and sera argue for use of easily accessible serum ceramide levels to track response to novel therapies in human CLN3 disease.	Ceramides	82-90	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	113-117
30837943-10	2019	The correlation between serum and brain ceramide in WT mice, and dysregulation of ceramide in serum and brain of Cln3 Deltaex7/8 mice, and the significant increase in ceramide in Cln3 Deltaex7/8 mouse brains and sera argue for use of easily accessible serum ceramide levels to track response to novel therapies in human CLN3 disease.	Ceramides	82-90	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	113-117
30837943-10	2019	The correlation between serum and brain ceramide in WT mice, and dysregulation of ceramide in serum and brain of Cln3 Deltaex7/8 mice, and the significant increase in ceramide in Cln3 Deltaex7/8 mouse brains and sera argue for use of easily accessible serum ceramide levels to track response to novel therapies in human CLN3 disease.	Ceramides	82-90	ceroid lipofuscinosis, neuronal 3, juvenile (Batten, Spielmeyer-Vogt disease)	Mus musculus	113-117
30623656-6	2019	The increase in the levels of ceramides containing more than 20 C atoms was found in torpor animals, reflecting a higher activity of CerS2 during hibernation, linked to neurofibrillary tangle generation and structural changes in the Golgi apparatus.	Ceramides	30-39	ceramide synthase 2	Mesocricetus auratus	133-138
30822302-0	2019	TLR9-mediated dendritic cell activation uncovers mammalian ganglioside species with specific ceramide backbones that activate invariant natural killer T cells.	Ceramides	93-101	toll like receptor 9	Homo sapiens	0-4
30822302-7	2019	Thus, both synthetic GM3 and GD3 comprising a d18:1-C24:1 ceramide backbone were able to activate iNKT cells in a CD1d-dependent manner.	Ceramides	58-66	granulocyte macrophage antigen 3	Mus musculus	21-24
30822302-7	2019	Thus, both synthetic GM3 and GD3 comprising a d18:1-C24:1 ceramide backbone were able to activate iNKT cells in a CD1d-dependent manner.	Ceramides	58-66	GRDX	Homo sapiens	29-32
30803453-9	2019	Moreover, the observed increase in ceramide in astrocytes correlates with the expression of ceramide synthase 5.	Ceramides	35-43	ceramide synthase 5	Homo sapiens	92-111
30770781-2	2019	Sphingomyelin synthase 2 (SGMS2) is a crucial regulator involved in ceramide (Cer) and sphingomyelin (SM) homoeostasis that is mostly studied for its role in lipid metabolism.	Ceramides	68-76	sphingomyelin synthase 2	Homo sapiens	0-24
30770781-2	2019	Sphingomyelin synthase 2 (SGMS2) is a crucial regulator involved in ceramide (Cer) and sphingomyelin (SM) homoeostasis that is mostly studied for its role in lipid metabolism.	Ceramides	68-76	sphingomyelin synthase 2	Homo sapiens	26-31
30770781-2	2019	Sphingomyelin synthase 2 (SGMS2) is a crucial regulator involved in ceramide (Cer) and sphingomyelin (SM) homoeostasis that is mostly studied for its role in lipid metabolism.	Ceramides	78-81	sphingomyelin synthase 2	Homo sapiens	0-24
30770781-2	2019	Sphingomyelin synthase 2 (SGMS2) is a crucial regulator involved in ceramide (Cer) and sphingomyelin (SM) homoeostasis that is mostly studied for its role in lipid metabolism.	Ceramides	78-81	sphingomyelin synthase 2	Homo sapiens	26-31
30620895-6	2019	Moreover, we showed that BCP exerts its effects through CB2 receptors which overproduction of ceramides by SMase at middle to higher concentrations of BCP reduce the protective activity of BCP and results in the activation of the PPAR-gamma pathway.	Ceramides	94-103	cannabinoid receptor 2	Homo sapiens	56-59
30620895-6	2019	Moreover, we showed that BCP exerts its effects through CB2 receptors which overproduction of ceramides by SMase at middle to higher concentrations of BCP reduce the protective activity of BCP and results in the activation of the PPAR-gamma pathway.	Ceramides	94-103	peroxisome proliferator activated receptor gamma	Homo sapiens	230-240
30578766-2	2019	Previously, we reported that suppression of ceramide glycosylation restored wild-type p53 protein and tumor suppressing function in cancer cells heterozygously carrying p53 R273H, a hot-spot missense mutation; however, the mechanisms underlying the control of mutant protein expression remain elusive.	Ceramides	44-52	tumor protein p53	Homo sapiens	86-89
30774995-9	2019	Perturbing endogenous ceramide generation by fumonisin B1 (FB1) and addition of soluble ceramide (C2-CER) yielded opposite actions on viability of GCs and therefore supported the significance of the ceramide pathway.	Ceramides	88-96	complement C2	Homo sapiens	98-104
30774995-9	2019	Perturbing endogenous ceramide generation by fumonisin B1 (FB1) and addition of soluble ceramide (C2-CER) yielded opposite actions on viability of GCs and therefore supported the significance of the ceramide pathway.	Ceramides	88-96	complement C2	Homo sapiens	98-104
30453012-0	2019	Neuronal ceroid lipofuscinosis related ER membrane protein CLN8 regulates PP2A activity and ceramide levels.	Ceramides	92-100	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	59-63
30453012-3	2019	CLN8 is an ER resident protein with unknown function; however, a role in ceramide metabolism has been suggested.	Ceramides	73-81	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	0-4
30453012-11	2019	A model of how CLN8 along with ceramides affects I2PP2A and PP2A binding and activities is proposed.	Ceramides	31-40	SET nuclear proto-oncogene	Homo sapiens	49-55
30453012-11	2019	A model of how CLN8 along with ceramides affects I2PP2A and PP2A binding and activities is proposed.	Ceramides	31-40	protein phosphatase 2 phosphatase activator	Homo sapiens	51-55
30578766-5	2019	Furthermore, glycosphingolipids (particularly globotriaosylceramide) generated from serial ceramide glycosylation were seen to activate cSrc and beta-catenin signaling so as to upregulate METTL3 expression, in turn promoting expression of p53 R273H mutant protein, with consequent drug resistance.	Ceramides	59-67	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	136-140
30578766-2	2019	Previously, we reported that suppression of ceramide glycosylation restored wild-type p53 protein and tumor suppressing function in cancer cells heterozygously carrying p53 R273H, a hot-spot missense mutation; however, the mechanisms underlying the control of mutant protein expression remain elusive.	Ceramides	44-52	tumor protein p53	Homo sapiens	169-172
30578766-5	2019	Furthermore, glycosphingolipids (particularly globotriaosylceramide) generated from serial ceramide glycosylation were seen to activate cSrc and beta-catenin signaling so as to upregulate METTL3 expression, in turn promoting expression of p53 R273H mutant protein, with consequent drug resistance.	Ceramides	59-67	catenin beta 1	Homo sapiens	145-157
30578766-5	2019	Furthermore, glycosphingolipids (particularly globotriaosylceramide) generated from serial ceramide glycosylation were seen to activate cSrc and beta-catenin signaling so as to upregulate METTL3 expression, in turn promoting expression of p53 R273H mutant protein, with consequent drug resistance.	Ceramides	59-67	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	188-194
30550872-1	2019	Acid sphingomyelinase (ASM) is a membrane lipid hydrolase, acting to generate ceramide and regulate cell functions and inflammatory responses.The roles of ASM in mediating T cell functions are postulated whereas its function in regulation of macrophages remains uncertain.	Ceramides	78-86	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
30578766-5	2019	Furthermore, glycosphingolipids (particularly globotriaosylceramide) generated from serial ceramide glycosylation were seen to activate cSrc and beta-catenin signaling so as to upregulate METTL3 expression, in turn promoting expression of p53 R273H mutant protein, with consequent drug resistance.	Ceramides	59-67	tumor protein p53	Homo sapiens	239-242
30578766-7	2019	Concordantly, suppression of ceramide glycosylation repressed METTL3 expression and m6A formation in p53 pre-mRNA, thus sensitizing cells carrying R273H to anticancer drugs.	Ceramides	29-37	methyltransferase 3, N6-adenosine-methyltransferase complex catalytic subunit	Homo sapiens	62-68
30578766-7	2019	Concordantly, suppression of ceramide glycosylation repressed METTL3 expression and m6A formation in p53 pre-mRNA, thus sensitizing cells carrying R273H to anticancer drugs.	Ceramides	29-37	tumor protein p53	Homo sapiens	101-104
30578766-9	2019	Suppressing both RNA methylation and ceramide glycosylation might constitute an efficacious and specific approach for targeting TP53 missense mutations coding for a G &gt; A transition, thereby improving cancer treatments.	Ceramides	37-45	tumor protein p53	Homo sapiens	128-132
30500419-6	2019	Moreover, CS-induced (sub-chronic) ceramide-accumulation was significantly (p < 0.05) reduced by treatment with TFEB/autophagy-inducing drug, gemfibrozil (GEM), suggesting that autophagy regulates CS-induced ceramide-accumulation.	Ceramides	35-43	transcription factor EB	Homo sapiens	112-116
30500419-6	2019	Moreover, CS-induced (sub-chronic) ceramide-accumulation was significantly (p < 0.05) reduced by treatment with TFEB/autophagy-inducing drug, gemfibrozil (GEM), suggesting that autophagy regulates CS-induced ceramide-accumulation.	Ceramides	208-216	transcription factor EB	Homo sapiens	112-116
30500419-8	2019	In addition to intracellular-accumulation, we found that CSE also induces membrane-ceramide-accumulation by ROS-dependent acid-sphingomyelinase (ASM) activation and plasma-membrane translocation, which was significantly controlled (p < 0.05) by cysteamine (an anti-oxidant) and amitriptyline (AMT, an inhibitor of ASM).	Ceramides	83-91	sphingomyelin phosphodiesterase 1	Homo sapiens	145-148
30500419-9	2019	Cysteamine-mediated and CSE-induced membrane-ceramide regulation was nullified by CFTR-inhibitor-172, demonstrating that CFTR controls redox impaired-autophagy dependent membrane-ceramide accumulation.	Ceramides	45-53	CF transmembrane conductance regulator	Homo sapiens	82-86
30500419-9	2019	Cysteamine-mediated and CSE-induced membrane-ceramide regulation was nullified by CFTR-inhibitor-172, demonstrating that CFTR controls redox impaired-autophagy dependent membrane-ceramide accumulation.	Ceramides	45-53	CF transmembrane conductance regulator	Homo sapiens	121-125
30500419-9	2019	Cysteamine-mediated and CSE-induced membrane-ceramide regulation was nullified by CFTR-inhibitor-172, demonstrating that CFTR controls redox impaired-autophagy dependent membrane-ceramide accumulation.	Ceramides	179-187	CF transmembrane conductance regulator	Homo sapiens	82-86
30500419-9	2019	Cysteamine-mediated and CSE-induced membrane-ceramide regulation was nullified by CFTR-inhibitor-172, demonstrating that CFTR controls redox impaired-autophagy dependent membrane-ceramide accumulation.	Ceramides	179-187	CF transmembrane conductance regulator	Homo sapiens	121-125
30500419-10	2019	In summary, our data shows that CS-mediated autophagy/lipophagy-dysfunction results in intracellular-ceramide-accumulation, while acquired CFTR-dysfunction-induced ASM causes membrane ceramide-accumulation.	Ceramides	184-192	sphingomyelin phosphodiesterase 1	Homo sapiens	164-167
30550872-1	2019	Acid sphingomyelinase (ASM) is a membrane lipid hydrolase, acting to generate ceramide and regulate cell functions and inflammatory responses.The roles of ASM in mediating T cell functions are postulated whereas its function in regulation of macrophages remains uncertain.	Ceramides	78-86	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
30838224-0	2019	IFN-gamma Reduces Epidermal Barrier Function by Affecting Fatty Acid Composition of Ceramide in a Mouse Atopic Dermatitis Model.	Ceramides	84-92	interferon gamma	Mus musculus	0-9
30528460-5	2019	We argue that ceramides may play a critical role in the pathobiology based on the studies of PLA2G6 and VPS35 in Drosophila mutants and human knock-down cells.	Ceramides	14-23	Vacuolar protein sorting 35	Drosophila melanogaster	104-109
30639960-8	2019	Diversion of metabolic fluxes toward synthesis of fatty acids and phospholipids was observed in siRNA-Grx1 treated cells, while siRNA-Trx1 treated cells showed elevated levels of various sphingomyelins and ceramides and signs of increased protein degradation.	Ceramides	206-215	thioredoxin	Homo sapiens	134-138
30838224-3	2019	FA elongases, ELOVL1 and ELOVL4, are essential for the synthesis of these ceramides, together with ceramide synthase 3 (CerS3).	Ceramides	74-83	elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 1	Mus musculus	14-20
30838224-3	2019	FA elongases, ELOVL1 and ELOVL4, are essential for the synthesis of these ceramides, together with ceramide synthase 3 (CerS3).	Ceramides	74-83	elongation of very long chain fatty acids (FEN1/Elo2, SUR4/Elo3, yeast)-like 4	Mus musculus	25-31
30838224-3	2019	FA elongases, ELOVL1 and ELOVL4, are essential for the synthesis of these ceramides, together with ceramide synthase 3 (CerS3).	Ceramides	74-83	ceramide synthase 3	Mus musculus	99-118
30838224-3	2019	FA elongases, ELOVL1 and ELOVL4, are essential for the synthesis of these ceramides, together with ceramide synthase 3 (CerS3).	Ceramides	74-83	ceramide synthase 3	Mus musculus	120-125
30838224-10	2019	These results suggest that IFN-gamma in the lesional skin may reduce ceramides with long-chain FAs by decreasing the expression of ELOVL.	Ceramides	69-78	interferon gamma	Mus musculus	27-36
30678043-9	2019	Ceramides, which are synthetized de novo from saturated FA like palmitate, have been demonstrated to play a critical role in the deterioration of insulin sensitivity in muscle cells.	Ceramides	0-9	insulin	Homo sapiens	146-153
30696906-1	2019	There is a lack of studies which seek to discern disease expression in patients with mutations that alter retinal ceramide metabolism, specifically in the ceramide kinase like (CERKL) gene.	Ceramides	114-122	ceramide kinase like	Homo sapiens	155-175
30696906-1	2019	There is a lack of studies which seek to discern disease expression in patients with mutations that alter retinal ceramide metabolism, specifically in the ceramide kinase like (CERKL) gene.	Ceramides	114-122	ceramide kinase like	Homo sapiens	177-182
30679689-1	2019	Ceramides are sphingolipids with defined acyl chain lengths, which are produced by corresponding ceramide synthases (CerS1-6).	Ceramides	0-9	ceramide synthase 1	Homo sapiens	117-122
30679689-6	2019	In this study we investigated the role of ceramides in G-CSF signaling.	Ceramides	42-51	colony stimulating factor 3	Homo sapiens	55-60
30679689-8	2019	G-CSF also induces downregulation of ceramides in WT and CerS2 null BMCs, as well as upregulation of very long chain lactosylceramides.	Ceramides	37-46	colony stimulating factor 3	Homo sapiens	0-5
30679689-11	2019	In conclusion, very long chain ceramides are important for G-CSF signaling and translocation of G-CSF-R into DRMs.	Ceramides	31-40	colony stimulating factor 3	Homo sapiens	59-64
30679689-11	2019	In conclusion, very long chain ceramides are important for G-CSF signaling and translocation of G-CSF-R into DRMs.	Ceramides	31-40	colony stimulating factor 3 receptor	Homo sapiens	96-103
30678043-10	2019	This review describes the latest progress involving ceramides as major players in the development of muscle insulin-resistance through the targeting of selective actors of the insulin signaling pathway.	Ceramides	52-61	insulin	Homo sapiens	108-115
30678043-10	2019	This review describes the latest progress involving ceramides as major players in the development of muscle insulin-resistance through the targeting of selective actors of the insulin signaling pathway.	Ceramides	52-61	insulin	Homo sapiens	176-183
30420430-3	2019	Here, using the cellular stress model evoked by the sphingolipid analog drug FTY720, we show that formation of ceramide-enriched membrane pores, referred to here as ceramidosomes, is initiated by a receptor-interacting Ser/Thr kinase 1 (RIPK1)-ceramide complex transported to the plasma membrane by nonmuscle myosin IIA-dependent trafficking in human lung cancer cells.	Ceramides	111-119	receptor interacting serine/threonine kinase 1	Homo sapiens	237-242
30669468-4	2019	On the other hand, the ring-expanded C-alkyl piperidine isomers, non-cytotoxic and inactive regarding ceramide glucosylation, revealed to be potent inhibitors of GBA.	Ceramides	102-110	glucosylceramidase beta	Homo sapiens	162-165
30420430-3	2019	Here, using the cellular stress model evoked by the sphingolipid analog drug FTY720, we show that formation of ceramide-enriched membrane pores, referred to here as ceramidosomes, is initiated by a receptor-interacting Ser/Thr kinase 1 (RIPK1)-ceramide complex transported to the plasma membrane by nonmuscle myosin IIA-dependent trafficking in human lung cancer cells.	Ceramides	244-252	receptor interacting serine/threonine kinase 1	Homo sapiens	237-242
30420430-4	2019	Molecular modeling/simulation coupled with site-directed mutagenesis revealed that Asp147 or Asn169 of RIPK1 are key for ceramide binding and that Arg258 or Leu293 residues are involved in the myosin IIA interaction, leading to ceramidosome formation and necroptosis.	Ceramides	121-129	receptor interacting serine/threonine kinase 1	Homo sapiens	103-108
30420430-6	2019	In conclusion, our findings indicate that the RIPK1-ceramide complex forms large membrane pores we named ceramidosomes.	Ceramides	52-60	receptor interacting serine/threonine kinase 1	Homo sapiens	46-51
30623117-1	2019	Previously, we proposed the following mechanism for konjac ceramide (kCer)-mediated neurite outgrowth inhibition: kCer binds to Nrp as a Sema3A agonist, resulting in Nrp1/PlexA complex formation and activation of the Sema3A signaling pathway to induce phosphorylation of CRMP2 and microtubule depolymerization.	Ceramides	59-67	neuropilin 1	Homo sapiens	128-131
30623117-1	2019	Previously, we proposed the following mechanism for konjac ceramide (kCer)-mediated neurite outgrowth inhibition: kCer binds to Nrp as a Sema3A agonist, resulting in Nrp1/PlexA complex formation and activation of the Sema3A signaling pathway to induce phosphorylation of CRMP2 and microtubule depolymerization.	Ceramides	59-67	semaphorin 3A	Homo sapiens	137-143
30623117-1	2019	Previously, we proposed the following mechanism for konjac ceramide (kCer)-mediated neurite outgrowth inhibition: kCer binds to Nrp as a Sema3A agonist, resulting in Nrp1/PlexA complex formation and activation of the Sema3A signaling pathway to induce phosphorylation of CRMP2 and microtubule depolymerization.	Ceramides	59-67	neuropilin 1	Homo sapiens	166-170
30623117-1	2019	Previously, we proposed the following mechanism for konjac ceramide (kCer)-mediated neurite outgrowth inhibition: kCer binds to Nrp as a Sema3A agonist, resulting in Nrp1/PlexA complex formation and activation of the Sema3A signaling pathway to induce phosphorylation of CRMP2 and microtubule depolymerization.	Ceramides	59-67	semaphorin 3A	Homo sapiens	217-223
30623117-1	2019	Previously, we proposed the following mechanism for konjac ceramide (kCer)-mediated neurite outgrowth inhibition: kCer binds to Nrp as a Sema3A agonist, resulting in Nrp1/PlexA complex formation and activation of the Sema3A signaling pathway to induce phosphorylation of CRMP2 and microtubule depolymerization.	Ceramides	59-67	dihydropyrimidinase like 2	Homo sapiens	271-276
30605666-0	2019	CerS1-Derived C18:0 Ceramide in Skeletal Muscle Promotes Obesity-Induced Insulin Resistance.	Ceramides	20-28	ceramide synthase 1	Mus musculus	0-5
30605666-3	2019	Here, ceramide profiling of high-fat diet (HFD)-fed animals revealed increased skeletal muscle C18:0 ceramide content, concomitant with increased expression of ceramide synthase (CerS)1.	Ceramides	6-14	ceramide synthase 1	Mus musculus	179-185
30605666-4	2019	Mice lacking CerS1, either globally or specifically in skeletal muscle (CerS1DeltaSkM), exhibit reduced muscle C18:0 ceramide content and significant improvements in systemic glucose homeostasis.	Ceramides	117-125	ceramide synthase 1	Mus musculus	13-18
31562630-6	2019	In addition, we highlight the main studies describing effects of ceramides in inflammation, specifically in various inflammatory settings including insulin resistance, graft-versus-host disease, immune suppression in cancer, multiple sclerosis, and inflammatory bowel disease.	Ceramides	65-74	insulin	Homo sapiens	148-155
30605666-6	2019	In contrast, muscle-specific deficiency of C16:0 ceramide-producing CerS5 and CerS6 failed to protect mice from obesity-induced insulin resistance.	Ceramides	49-57	ceramide synthase 5	Mus musculus	68-73
30816675-0	2019	Acid Sphingomyelinase-Ceramide System in Bacterial Infections.	Ceramides	22-30	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
30300671-8	2019	We also observed abnormal ceramide metabolism in Pemt-/- mice fed a HFD, with elevation of ceramides and other sphingolipids and higher expression of mRNAs for acid ceramidase (Asah1) and ceramide kinase (Cerk).	Ceramides	26-34	phosphatidylethanolamine N-methyltransferase	Mus musculus	49-53
30300671-8	2019	We also observed abnormal ceramide metabolism in Pemt-/- mice fed a HFD, with elevation of ceramides and other sphingolipids and higher expression of mRNAs for acid ceramidase (Asah1) and ceramide kinase (Cerk).	Ceramides	91-100	phosphatidylethanolamine N-methyltransferase	Mus musculus	49-53
30816675-1	2019	Acid sphingomyelinase hydrolyzes sphingomyelin to ceramide and phosphorylcholine.	Ceramides	50-58	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
30816675-4	2019	Recent studies have suggested several bacteria and bacterial toxins that stimulate the activation and the translocation of acid sphingomyelinase, which leads to the release of ceramide.	Ceramides	176-184	sphingomyelin phosphodiesterase 1	Homo sapiens	123-144
30816675-5	2019	The acid sphingomyelinase/ceramide system also regulates the internalization of bacteria into the host cell, the subsequent cytokine release, inflammatory response, and initiation of host cell apoptosis.	Ceramides	26-34	sphingomyelin phosphodiesterase 1	Homo sapiens	4-25
30827244-3	2019	The conversion of ceramide to sphingosine is mediated by Acid Ceramidase (ASAH1) thus maintaining a rheostat between a tumor suppressor and a tumor promoter.	Ceramides	18-26	N-acylsphingosine amidohydrolase 1	Homo sapiens	57-72
30827244-3	2019	The conversion of ceramide to sphingosine is mediated by Acid Ceramidase (ASAH1) thus maintaining a rheostat between a tumor suppressor and a tumor promoter.	Ceramides	18-26	N-acylsphingosine amidohydrolase 1	Homo sapiens	74-79
31778304-4	2019	In view of the fact that lowering acid sphingomyelinase activity and ceramide level was shown to protect against ischemic injury and ameliorate neurological deficits, the acid sphingomyelinase/ ceramide system might represent a promising target for stroke therapies.	Ceramides	69-77	sphingomyelin phosphodiesterase 1	Homo sapiens	171-192
30243987-2	2019	Elevated levels of SM synthase 1 (SMS1), which catalyzes the synthesis of SM from ceramide and phosphatidylcholine, have been observed in the brains of Alzheimer"s disease (AD), where expression of beta-site APP cleaving enzyme 1 (BACE1), a rate limiting enzyme in amyloid-beta (Abeta) generation, are upregulated.	Ceramides	82-90	sphingomyelin synthase 1	Mus musculus	19-32
30243987-2	2019	Elevated levels of SM synthase 1 (SMS1), which catalyzes the synthesis of SM from ceramide and phosphatidylcholine, have been observed in the brains of Alzheimer"s disease (AD), where expression of beta-site APP cleaving enzyme 1 (BACE1), a rate limiting enzyme in amyloid-beta (Abeta) generation, are upregulated.	Ceramides	82-90	sphingomyelin synthase 1	Mus musculus	34-38
30243987-2	2019	Elevated levels of SM synthase 1 (SMS1), which catalyzes the synthesis of SM from ceramide and phosphatidylcholine, have been observed in the brains of Alzheimer"s disease (AD), where expression of beta-site APP cleaving enzyme 1 (BACE1), a rate limiting enzyme in amyloid-beta (Abeta) generation, are upregulated.	Ceramides	82-90	beta-site APP cleaving enzyme 1	Mus musculus	198-229
30243987-2	2019	Elevated levels of SM synthase 1 (SMS1), which catalyzes the synthesis of SM from ceramide and phosphatidylcholine, have been observed in the brains of Alzheimer"s disease (AD), where expression of beta-site APP cleaving enzyme 1 (BACE1), a rate limiting enzyme in amyloid-beta (Abeta) generation, are upregulated.	Ceramides	82-90	beta-site APP cleaving enzyme 1	Mus musculus	231-236
30243987-2	2019	Elevated levels of SM synthase 1 (SMS1), which catalyzes the synthesis of SM from ceramide and phosphatidylcholine, have been observed in the brains of Alzheimer"s disease (AD), where expression of beta-site APP cleaving enzyme 1 (BACE1), a rate limiting enzyme in amyloid-beta (Abeta) generation, are upregulated.	Ceramides	82-90	amyloid beta (A4) precursor protein	Mus musculus	279-284
30713596-0	2019	Role of acid sphingomyelinase-induced ceramide generation in response to radiation.	Ceramides	38-46	sphingomyelin phosphodiesterase 1	Homo sapiens	8-29
31778304-4	2019	In view of the fact that lowering acid sphingomyelinase activity and ceramide level was shown to protect against ischemic injury and ameliorate neurological deficits, the acid sphingomyelinase/ ceramide system might represent a promising target for stroke therapies.	Ceramides	194-202	sphingomyelin phosphodiesterase 1	Homo sapiens	34-55
31778304-4	2019	In view of the fact that lowering acid sphingomyelinase activity and ceramide level was shown to protect against ischemic injury and ameliorate neurological deficits, the acid sphingomyelinase/ ceramide system might represent a promising target for stroke therapies.	Ceramides	194-202	sphingomyelin phosphodiesterase 1	Homo sapiens	171-192
30564278-10	2018	Instead, pre-treatment with okadaic acid at concentrations that selectively inhibit protein phosphatase 2A (PP2A) blocked both palmitate- and ceramide-induced changes in Tnnt3 alternative splicing, suggesting that palmitate and ceramide act through PP2A to modulate Tnnt3 alternative splicing.	Ceramides	142-150	troponin T3, fast skeletal type	Rattus norvegicus	170-175
30568037-5	2018	In the current study, we found that C3aR/C5aR deficiency enhanced ceramide-dependent lethal mitophagy (CDLM) in DCs.	Ceramides	66-74	complement C3a receptor 1	Homo sapiens	36-40
30568037-5	2018	In the current study, we found that C3aR/C5aR deficiency enhanced ceramide-dependent lethal mitophagy (CDLM) in DCs.	Ceramides	66-74	complement C5a receptor 1	Homo sapiens	41-45
30564278-0	2018	Palmitate- and C6 ceramide-induced Tnnt3 pre-mRNA alternative splicing occurs in a PP2A dependent manner.	Ceramides	18-26	troponin T3, fast skeletal type	Rattus norvegicus	35-40
30564278-8	2018	The effects of palmitate and ceramide on Tnnt3 alternative splicing were accompanied by a 40-50% reduction in phosphorylation of Akt on S473.	Ceramides	29-37	troponin T3, fast skeletal type	Rattus norvegicus	41-46
30564278-8	2018	The effects of palmitate and ceramide on Tnnt3 alternative splicing were accompanied by a 40-50% reduction in phosphorylation of Akt on S473.	Ceramides	29-37	AKT serine/threonine kinase 1	Rattus norvegicus	129-132
30701020-0	2018	TNFalpha mediated ceramide generation triggers cisplatin induced apoptosis in B16F10 melanoma in a PKCdelta independent manner.	Ceramides	18-26	tumor necrosis factor	Mus musculus	0-8
30701020-0	2018	TNFalpha mediated ceramide generation triggers cisplatin induced apoptosis in B16F10 melanoma in a PKCdelta independent manner.	Ceramides	18-26	protein kinase C, delta	Mus musculus	99-107
30701020-2	2018	Although, the PKCdelta-ceramide axis in cancer cells has been an effective target in reduction of cancer, involvement of PKCdelta in inducing nephrotoxicity have become a major questionnaire.	Ceramides	23-31	protein kinase C, delta	Mus musculus	14-22
30701020-3	2018	In the present study, we have elucidated the mechanism by which cisplatin exploits the ceramide to render cancer cell apoptosis leading to the abrogation of malignancy in a PKCdelta independent pathway with lesser toxicity.	Ceramides	87-95	protein kinase C, delta	Mus musculus	173-181
30701020-6	2018	Increased cellular expression of TNFalpha resulted in an elevated ceramide generation by stimulating acid-sphingomyelinase and cPLA2.	Ceramides	66-74	tumor necrosis factor	Mus musculus	33-41
30701020-6	2018	Increased cellular expression of TNFalpha resulted in an elevated ceramide generation by stimulating acid-sphingomyelinase and cPLA2.	Ceramides	66-74	phospholipase A2, group IVA (cytosolic, calcium-dependent)	Mus musculus	127-132
30701020-7	2018	Furthermore, reciprocity in the regulation of sphingosine kinase 1 (Sphk1) and sphingosine kinase 2 (Sphk2) during PKCdelta independent ceramide generation was also observed during cisplatin treatment.	Ceramides	136-144	sphingosine kinase 1	Mus musculus	46-66
30701020-7	2018	Furthermore, reciprocity in the regulation of sphingosine kinase 1 (Sphk1) and sphingosine kinase 2 (Sphk2) during PKCdelta independent ceramide generation was also observed during cisplatin treatment.	Ceramides	136-144	sphingosine kinase 1	Mus musculus	68-73
30701020-7	2018	Furthermore, reciprocity in the regulation of sphingosine kinase 1 (Sphk1) and sphingosine kinase 2 (Sphk2) during PKCdelta independent ceramide generation was also observed during cisplatin treatment.	Ceramides	136-144	sphingosine kinase 2	Mus musculus	79-99
30701020-7	2018	Furthermore, reciprocity in the regulation of sphingosine kinase 1 (Sphk1) and sphingosine kinase 2 (Sphk2) during PKCdelta independent ceramide generation was also observed during cisplatin treatment.	Ceramides	136-144	sphingosine kinase 2	Mus musculus	101-106
30701020-7	2018	Furthermore, reciprocity in the regulation of sphingosine kinase 1 (Sphk1) and sphingosine kinase 2 (Sphk2) during PKCdelta independent ceramide generation was also observed during cisplatin treatment.	Ceramides	136-144	protein kinase C, delta	Mus musculus	115-123
30701020-8	2018	PKCdelta inhibited murine melanoma model showed reduction in nephrotoxicity along with tumor regression by ceramide generation.	Ceramides	107-115	protein kinase C, delta	Mus musculus	0-8
30701020-9	2018	Altogether, the current study emphasized the unexplored signaling cascade of ceramide generation by cisplatin during PKCdelta silenced condition, which is associated with increased TNFalpha generation.	Ceramides	77-85	protein kinase C, delta	Mus musculus	117-125
30701020-9	2018	Altogether, the current study emphasized the unexplored signaling cascade of ceramide generation by cisplatin during PKCdelta silenced condition, which is associated with increased TNFalpha generation.	Ceramides	77-85	tumor necrosis factor	Mus musculus	181-189
30619359-10	2018	Furthermore, CS exposure caused significant upregulation of pro-inflammatory ceramides and related ceramide synthase gene transcripts in SP-D-deficient mice compared to wildtype littermates.	Ceramides	77-86	surfactant associated protein D	Mus musculus	137-141
30619359-13	2018	Our results indicate that SP-D deficiency aggravates CS-induced lung inflammation partly through regulation of ceramide synthesis and that local SP-D enrichment rescues CS-induced inflammation.	Ceramides	111-119	surfactant protein D	Homo sapiens	26-30
30448190-7	2018	A higher dose of LCL521 (10 microM) caused a profound decrease of sphingosine and increase of ceramide, but additionally affected the processing and regeneration of the ACDase protein, with biphasic and reversible effects on the expression of ACDase, which paralleled the long term changes of cellular sphingosine and ceramide.	Ceramides	318-326	N-acylsphingosine amidohydrolase 1	Homo sapiens	169-175
30564278-10	2018	Instead, pre-treatment with okadaic acid at concentrations that selectively inhibit protein phosphatase 2A (PP2A) blocked both palmitate- and ceramide-induced changes in Tnnt3 alternative splicing, suggesting that palmitate and ceramide act through PP2A to modulate Tnnt3 alternative splicing.	Ceramides	142-150	troponin T3, fast skeletal type	Rattus norvegicus	266-271
30550553-9	2018	We have also used a formula for identifying putative FFAT-domains, and we identified several potential VAP-interactors within the ceramide and sphingolipid synthesis pathways that could be candidates for regulation by GLTP.	Ceramides	130-138	glycolipid transfer protein	Homo sapiens	218-222
30251650-7	2018	We also found that the FA elongase ELOVL1 and the ceramide synthase CERS2 were involved in C24:2 ceramide production.	Ceramides	50-58	ceramide synthase 2	Homo sapiens	68-73
30551571-1	2018	By catalyzing the hydrolysis of sphingomyelin into ceramide, acid sphingomyelinase (ASM) changes the local composition of the plasma membrane with effects on receptor-mediated signaling.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	61-82
30551571-1	2018	By catalyzing the hydrolysis of sphingomyelin into ceramide, acid sphingomyelinase (ASM) changes the local composition of the plasma membrane with effects on receptor-mediated signaling.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	84-87
30333154-8	2018	The larger number of CD2-CD2 lipid chain interactions in the LPP than in a symmetrical bilayer structure implied that the ceramide had primarily adopted an extended conformation.	Ceramides	122-130	CD2 molecule	Homo sapiens	21-24
30159588-0	2018	Relation of plasma ceramides to visceral adiposity, insulin resistance and the development of type 2 diabetes mellitus: the Dallas Heart Study.	Ceramides	19-28	insulin	Homo sapiens	52-59
30159588-1	2018	AIMS/HYPOTHESIS: Ceramides are sphingolipids that contribute to insulin resistance in preclinical studies.	Ceramides	17-26	insulin	Homo sapiens	64-71
30159588-2	2018	We hypothesised that plasma ceramides would be associated with body fat distribution, insulin resistance and incident type 2 diabetes in a multi-ethnic cohort.	Ceramides	28-37	insulin	Homo sapiens	86-93
30159588-13	2018	The role of ceramides in a shared pathway of metabolic dysfunction linking visceral adiposity and insulin resistance requires further investigation.	Ceramides	12-21	insulin	Homo sapiens	98-105
30348640-6	2018	This is the first report to demonstrate the reduction of ceramides in the stratum corneum of an NLS patient due to PHGDH mutations.	Ceramides	57-66	phosphoglycerate dehydrogenase	Homo sapiens	115-120
29968910-9	2018	Intriguingly, C6 ceramide downregulated Mcl-1 in HNSCC cells.	Ceramides	17-25	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	40-45
30333154-8	2018	The larger number of CD2-CD2 lipid chain interactions in the LPP than in a symmetrical bilayer structure implied that the ceramide had primarily adopted an extended conformation.	Ceramides	122-130	CD2 molecule	Homo sapiens	25-28
30592185-2	2018	We investigated if insulin-stimulated activation of Rac1 (i.e., Rac1-GTP binding) is impaired by accumulation of diacylglycerols (DAG) and ceramides in cultured muscle cells.	Ceramides	139-148	insulin	Homo sapiens	19-26
30038230-4	2018	ER ceramide stimulates phosphatase 2A and thereby the autophagy proteins Ulk, Beclin, Vps34/Phosphatidylinositol 3-kinase, p62, and Lc3B.	Ceramides	3-11	phosphatidylinositol 3-kinase catalytic subunit type 3	Homo sapiens	86-91
30038230-4	2018	ER ceramide stimulates phosphatase 2A and thereby the autophagy proteins Ulk, Beclin, Vps34/Phosphatidylinositol 3-kinase, p62, and Lc3B.	Ceramides	3-11	nucleoporin 62	Homo sapiens	123-126
30038230-4	2018	ER ceramide stimulates phosphatase 2A and thereby the autophagy proteins Ulk, Beclin, Vps34/Phosphatidylinositol 3-kinase, p62, and Lc3B.	Ceramides	3-11	microtubule associated protein 1 light chain 3 beta	Homo sapiens	132-136
30592185-2	2018	We investigated if insulin-stimulated activation of Rac1 (i.e., Rac1-GTP binding) is impaired by accumulation of diacylglycerols (DAG) and ceramides in cultured muscle cells.	Ceramides	139-148	Rac family small GTPase 1	Homo sapiens	52-56
30279221-7	2018	Tissue-specific ablation studies revealed that hepatic ABCA1 determines plasma HxCer and SM levels; that ablation of MTP and ABCA1 in the liver and intestine reduces plasma HxCer, SM, and ceramide levels; and that hepatic and intestinal MTP contribute to plasma ceramide levels, whereas only hepatic MTP modulates plasma SM levels.	Ceramides	188-196	microsomal triglyceride transfer protein	Homo sapiens	117-120
30224516-6	2018	In contrast to SKi, ABC294640 (25 muM) promotes apoptosis of HEK293T cells via a Degs1-dependent mechanism that is associated with increased de novo synthesis of ceramide.	Ceramides	162-170	delta 4-desaturase, sphingolipid 1	Homo sapiens	81-86
30279221-3	2018	We previously showed that microsomal triglyceride transfer protein (MTP) is critical to determine plasma ceramide and SM, but not HxCer, levels.	Ceramides	105-113	microsomal triglyceride transfer protein	Homo sapiens	26-66
30279221-3	2018	We previously showed that microsomal triglyceride transfer protein (MTP) is critical to determine plasma ceramide and SM, but not HxCer, levels.	Ceramides	105-113	microsomal triglyceride transfer protein	Homo sapiens	68-71
30148701-6	2018	However, blockade of ceramide to S1P metabolic conversion using a specific inhibitor of SPHK1 attenuated the expected Rb1-mediated increase in KC migration.	Ceramides	21-29	sphingosine kinase 1	Homo sapiens	88-93
30148701-6	2018	However, blockade of ceramide to S1P metabolic conversion using a specific inhibitor of SPHK1 attenuated the expected Rb1-mediated increase in KC migration.	Ceramides	21-29	RB transcriptional corepressor 1	Homo sapiens	118-121
30154232-9	2018	Targeting bSMase to the Golgi resulted in increased levels of ceramide that were attenuated by the expression of nCDase, also supporting its ability to metabolize Golgi-generated ceramide.	Ceramides	179-187	N-acylsphingosine amidohydrolase 2	Homo sapiens	113-119
30279221-7	2018	Tissue-specific ablation studies revealed that hepatic ABCA1 determines plasma HxCer and SM levels; that ablation of MTP and ABCA1 in the liver and intestine reduces plasma HxCer, SM, and ceramide levels; and that hepatic and intestinal MTP contribute to plasma ceramide levels, whereas only hepatic MTP modulates plasma SM levels.	Ceramides	188-196	ATP binding cassette subfamily A member 1	Homo sapiens	125-130
30279221-7	2018	Tissue-specific ablation studies revealed that hepatic ABCA1 determines plasma HxCer and SM levels; that ablation of MTP and ABCA1 in the liver and intestine reduces plasma HxCer, SM, and ceramide levels; and that hepatic and intestinal MTP contribute to plasma ceramide levels, whereas only hepatic MTP modulates plasma SM levels.	Ceramides	262-270	microsomal triglyceride transfer protein	Homo sapiens	117-120
30279221-7	2018	Tissue-specific ablation studies revealed that hepatic ABCA1 determines plasma HxCer and SM levels; that ablation of MTP and ABCA1 in the liver and intestine reduces plasma HxCer, SM, and ceramide levels; and that hepatic and intestinal MTP contribute to plasma ceramide levels, whereas only hepatic MTP modulates plasma SM levels.	Ceramides	262-270	ATP binding cassette subfamily A member 1	Homo sapiens	125-130
30386262-0	2018	Chronic Psychosocial Stress in Mice Is Associated With Increased Acid Sphingomyelinase Activity in Liver and Serum and With Hepatic C16:0-Ceramide Accumulation.	Ceramides	138-146	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	65-86
30333512-9	2018	Transcriptome analysis of TM9SF2 knockout cells revealed a potential role for TM9SF2 in cell cycle progression, oxidative phosphorylation, and ceramide signaling.	Ceramides	143-151	transmembrane 9 superfamily member 2	Mus musculus	26-32
30333512-9	2018	Transcriptome analysis of TM9SF2 knockout cells revealed a potential role for TM9SF2 in cell cycle progression, oxidative phosphorylation, and ceramide signaling.	Ceramides	143-151	transmembrane 9 superfamily member 2	Mus musculus	78-84
30326559-0	2018	Acid Sphingomyelinase Inhibition Stabilizes Hepatic Ceramide Content and Improves Hepatic Biotransformation Capacity in a Murine Model of Polymicrobial Sepsis.	Ceramides	52-60	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
30326559-10	2018	In conclusion, partial genetic inhibition of SMPD1 stabilizes hepatic ceramide content and improves hepatic monooxygenase function in the acute phase of polymicrobial sepsis.	Ceramides	70-78	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	45-50
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.	Ceramides	120-128	glucosylceramidase beta 2	Homo sapiens	4-8
30300355-8	2018	These findings suggested that both SSE and tiliroside have a distinct potential to stimulate the level of ceramide [NS, NDS] in the SC by enhancing the expression of GCS and GBA.	Ceramides	106-114	UDP-glucose ceramide glucosyltransferase	Homo sapiens	166-169
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.	Ceramides	120-128	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.	Ceramides	120-128	glucosylceramidase beta 2	Homo sapiens	60-66
30300355-8	2018	These findings suggested that both SSE and tiliroside have a distinct potential to stimulate the level of ceramide [NS, NDS] in the SC by enhancing the expression of GCS and GBA.	Ceramides	106-114	glucosylceramidase beta	Homo sapiens	174-177
30300355-9	2018	The higher stimulatory effect with SSE than tiliroside on SC ceramide synthesis correlates with the significant increase observed with SSE but not tiliroside in the gene expression levels of SPT2 and CerS3.	Ceramides	61-69	serine palmitoyltransferase long chain base subunit 2	Homo sapiens	191-195
30300355-9	2018	The higher stimulatory effect with SSE than tiliroside on SC ceramide synthesis correlates with the significant increase observed with SSE but not tiliroside in the gene expression levels of SPT2 and CerS3.	Ceramides	61-69	ceramide synthase 3	Homo sapiens	200-205
29909971-3	2018	Phospholipases typically hydrolyze glycerol phospholipids, but loss of iPLA2-VIA does not affect the phospholipid composition of brain tissue but rather causes an elevation in ceramides.	Ceramides	176-185	calcium-independent phospholipase A2 VIA	Drosophila melanogaster	71-80
30297838-4	2018	This interaction is highly selective toward the ceramide acyl chain length with its C10 atom being proximal to Ser240 and Ser241.	Ceramides	48-56	homeobox C10	Homo sapiens	84-87
30297838-5	2018	Ceramide binding stabilizes p53 and disrupts its complex with E3 ligase MDM2 leading to the p53 accumulation, nuclear translocation and activation of the downstream targets.	Ceramides	0-8	tumor protein p53	Homo sapiens	28-31
30297838-5	2018	Ceramide binding stabilizes p53 and disrupts its complex with E3 ligase MDM2 leading to the p53 accumulation, nuclear translocation and activation of the downstream targets.	Ceramides	0-8	MDM2 proto-oncogene	Homo sapiens	72-76
30297838-5	2018	Ceramide binding stabilizes p53 and disrupts its complex with E3 ligase MDM2 leading to the p53 accumulation, nuclear translocation and activation of the downstream targets.	Ceramides	0-8	tumor protein p53	Homo sapiens	92-95
29909971-6	2018	Loss of iPLA2-VIA impairs retromer function, leading to a progressive increase in ceramide.	Ceramides	82-90	calcium-independent phospholipase A2 VIA	Drosophila melanogaster	8-17
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Ceramides	156-164	tumor protein p53	Homo sapiens	43-46
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Ceramides	156-164	ceramide synthase 5	Homo sapiens	177-182
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Ceramides	156-164	tumor protein p53	Homo sapiens	261-264
30059758-4	2018	Here, we show that in human wild-type (wt) p53 HCT-116 colon cancer cells treatment with oxaliplatin or 5-fluorouracil (5-FU) leads to a strong increase in ceramide synthase 5 (CerS5) expression and C16:0-ceramide levels, which was not shown in HCT-116 lacking p53 expression (HCT-116 p53-/-).	Ceramides	156-164	tumor protein p53	Homo sapiens	261-264
30059758-6	2018	By contrast, in the p53-deficient cells CerS2 expression and CerS2-related C24:0- and C24:1-ceramide levels were elevated which is possibly related to enhanced polyadenylation of the CerS2 transcript in these cells.	Ceramides	92-100	tumor protein p53	Homo sapiens	20-23
30059758-6	2018	By contrast, in the p53-deficient cells CerS2 expression and CerS2-related C24:0- and C24:1-ceramide levels were elevated which is possibly related to enhanced polyadenylation of the CerS2 transcript in these cells.	Ceramides	92-100	ceramide synthase 2	Homo sapiens	61-66
30059758-6	2018	By contrast, in the p53-deficient cells CerS2 expression and CerS2-related C24:0- and C24:1-ceramide levels were elevated which is possibly related to enhanced polyadenylation of the CerS2 transcript in these cells.	Ceramides	92-100	ceramide synthase 2	Homo sapiens	61-66
29746165-7	2018	The inhibition of beta-glucocerebrosidase and nonlysosomal glucosylceramidase, both involved in ceramide production resulting from glycosphingolipid catabolism on the PM, partially restored cell proliferation.	Ceramides	96-104	glucosylceramidase beta	Homo sapiens	18-41
30106227-0	2018	Exosomal neutral sphingomyelinase 1 suppresses hepatocellular carcinoma via decreasing the ratio of sphingomyelin/ceramide.	Ceramides	114-122	sphingomyelin phosphodiesterase 2	Homo sapiens	9-35
30106227-3	2018	We report that NSMase1, which converts sphingomyelin (SM) to ceramide, was significantly downregulated in HCC tissues.	Ceramides	61-69	sphingomyelin phosphodiesterase 2	Homo sapiens	15-22
30106227-5	2018	NSMase1 downregulation in HCC resulted in increased SM and reduced ceramide (Cer) that led to an increased SM/Cer ratio.	Ceramides	67-75	sphingomyelin phosphodiesterase 2	Homo sapiens	0-7
30106227-5	2018	NSMase1 downregulation in HCC resulted in increased SM and reduced ceramide (Cer) that led to an increased SM/Cer ratio.	Ceramides	77-80	sphingomyelin phosphodiesterase 2	Homo sapiens	0-7
30139741-0	2018	StAR-related lipid transfer domain 11 (STARD11)-mediated ceramide transport mediates extracellular vesicle biogenesis.	Ceramides	57-65	ceramide transporter 1	Mus musculus	0-37
30250535-7	2018	Through bioinformatics, we identified 487 target genes predicted from miR-320a, that were mostly enriched in the bone morphogenetic protein signaling pathway, nicotinamide adenine dinucleotide pathway and de novo ceramide biosynthetic pathway.	Ceramides	213-221	microRNA 320a	Homo sapiens	70-78
30250535-8	2018	In our study, we reported for the first time the circulating miRNA profile of CM patients and suggested that miR-320a may participate in CM development through the ceramide signaling pathway.	Ceramides	164-172	microRNA 320a	Homo sapiens	109-117
30139741-4	2018	Using palmitate as a model of lipotoxic diseases and as a substrate for ceramide biosynthesis in human and murine liver cell lines and primary mouse hepatocytes, we found that STARD11-deficient cells release fewer extracellular vesicles.	Ceramides	72-80	ceramide transporter 1	Mus musculus	176-183
30139741-5	2018	Moreover, STARD11 reciprocally regulated exosome ceramide enrichment and cellular ceramide depletion.	Ceramides	49-57	ceramide transporter 1	Mus musculus	10-17
30139741-0	2018	StAR-related lipid transfer domain 11 (STARD11)-mediated ceramide transport mediates extracellular vesicle biogenesis.	Ceramides	57-65	ceramide transporter 1	Mus musculus	39-46
30139741-5	2018	Moreover, STARD11 reciprocally regulated exosome ceramide enrichment and cellular ceramide depletion.	Ceramides	82-90	ceramide transporter 1	Mus musculus	10-17
30139741-6	2018	We further observed that in STARD11 knockout cells intracellular ceramide accumulates and that this apparent inability to transfer cellular ceramide into extracellular vesicles reduces cellular viability.	Ceramides	65-73	ceramide transporter 1	Mus musculus	28-35
29908119-1	2018	Acid sphingomyelinase (ASM) is the rate-limiting enzyme cleaving sphingomyelin into ceramide and phosphorylcholin.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
30139741-6	2018	We further observed that in STARD11 knockout cells intracellular ceramide accumulates and that this apparent inability to transfer cellular ceramide into extracellular vesicles reduces cellular viability.	Ceramides	140-148	ceramide transporter 1	Mus musculus	28-35
30139741-10	2018	In conclusion, we propose a model of how STARD11 mediates ceramide trafficking in palmitate-treated cells and stimulates exosome biogenesis.	Ceramides	58-66	ceramide transporter 1	Mus musculus	41-48
29908119-1	2018	Acid sphingomyelinase (ASM) is the rate-limiting enzyme cleaving sphingomyelin into ceramide and phosphorylcholin.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
29908122-5	2018	Therefore, this review will address the connection between the hypoxic response and the ASM/ceramide system in the context of inflammatory hypoxia.	Ceramides	92-100	sphingomyelin phosphodiesterase 1	Homo sapiens	88-91
29924727-1	2018	Acid sphingomyelinase (ASM) is a key enzyme in sphingolipid metabolism that converts sphingomyelin to ceramide, thereby modulating membrane structures and signal transduction.	Ceramides	102-110	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
29924727-1	2018	Acid sphingomyelinase (ASM) is a key enzyme in sphingolipid metabolism that converts sphingomyelin to ceramide, thereby modulating membrane structures and signal transduction.	Ceramides	102-110	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
30199530-5	2018	Activated SSAO oppositely regulates uptake of glucose and long-chain fatty acids and remodels the cellular proteome to coordinate changes in fuel availability and related downstream processes, such as glycolysis, de novo lipogenesis, and sphingomyelin/ceramide synthesis.	Ceramides	252-260	amine oxidase copper containing 3	Homo sapiens	10-14
30208901-12	2018	Significant, positive correlation was found between total serum concentration of ceramides and insulin (r = 0.3, p = 0.02) and HOMA-IR (r = 0.28, p = 0.03).	Ceramides	81-90	insulin	Homo sapiens	95-102
30208901-16	2018	CONCLUSION: Elevated ceramide concentrations in obese patients together with their significant correlation with insulin resistance parameters suggest their association with molecular pathways involved in insulin signaling impairment known to be strongly linked to pathogenesis of non-alcoholic fatty liver disease.	Ceramides	21-29	insulin	Homo sapiens	112-119
30344353-3	2018	Herein, we describe C1/C2 lipidation with the biologically active lipid ceramide and a common phospholipid using a cyclopropene scaffold whose reactivity with 1,2,4,5-tetrazines has been caged.	Ceramides	72-80	heterogeneous nuclear ribonucleoprotein C	Homo sapiens	20-25
30031131-2	2018	Among the pleiotropic effects of TNF-alpha within the cell, its binding to TNFR1 receptor has been shown to activate sphingomyelinases leading to the production of ceramides.	Ceramides	164-173	tumor necrosis factor	Homo sapiens	33-42
30031131-2	2018	Among the pleiotropic effects of TNF-alpha within the cell, its binding to TNFR1 receptor has been shown to activate sphingomyelinases leading to the production of ceramides.	Ceramides	164-173	TNF receptor superfamily member 1A	Homo sapiens	75-80
30206207-2	2018	CERS6 is an isoform of ceramide synthases known to generate ceramides with C16 acyl chain (C16-Cer).	Ceramides	60-69	ceramide synthase 6	Homo sapiens	0-5
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.	Ceramides	64-72	UDP-glucose ceramide glucosyltransferase	Homo sapiens	18-21
29906461-8	2018	Molecular docking analysis showed that ASX produced a tight fit in the pocket of sphingomyelin phosphodiesterase 1 (SMPD1), a key enzyme in the production of ceramides.	Ceramides	158-167	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	81-114
29906461-8	2018	Molecular docking analysis showed that ASX produced a tight fit in the pocket of sphingomyelin phosphodiesterase 1 (SMPD1), a key enzyme in the production of ceramides.	Ceramides	158-167	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	116-121
29851147-0	2018	Effects of a ceramide-containing water-in-oil ointment on skin barrier function and allergen penetration in an IL-31 treated 3D model of the disrupted skin barrier.	Ceramides	13-21	interleukin 31	Homo sapiens	111-116
30126999-10	2018	The pivotal role of ceramide in driving EE biogenesis and fusion in the Abca4-/- mice RPE suggests that therapeutic targeting of ceramide could be effective in Stargardt disease and other macular degenerations.	Ceramides	129-137	ATP-binding cassette, sub-family A (ABC1), member 4	Mus musculus	72-77
29509438-2	2018	Ceramides have received special attention since their levels are inversely associated with normal insulin signaling and positively associated with factors that are involved in cardiometabolic disease.	Ceramides	0-9	insulin	Homo sapiens	98-105
29851147-9	2018	In conclusion, our data revealed that topical application of a ceramide-containing skin care ointment reduced IL-31 induced impairments of the physical skin barrier and skin barrier function in an in vitro model of the disrupted skin barrier.	Ceramides	63-71	interleukin 31	Homo sapiens	110-115
29506145-1	2018	Background: High-dose radiotherapy (&gt;8-10 Gy) causes rapid endothelial cell death via acid sphingomyelinase (ASMase)-induced ceramide production, resulting in biologically significant enhancement of tumor responses.	Ceramides	128-136	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	89-110
29863755-6	2018	Enzymes of ceramide metabolism (e.g. beta-glucocerebrosidase or acid sphingomyelinase) as well as proteases (e.g. chymotryptic enzyme or cathepsin D linked to epidermal differentiation and desquamation) are regulated by the pH.	Ceramides	11-19	glucosylceramidase beta	Homo sapiens	37-60
29863755-6	2018	Enzymes of ceramide metabolism (e.g. beta-glucocerebrosidase or acid sphingomyelinase) as well as proteases (e.g. chymotryptic enzyme or cathepsin D linked to epidermal differentiation and desquamation) are regulated by the pH.	Ceramides	11-19	sphingomyelin phosphodiesterase 1	Homo sapiens	64-85
29863755-6	2018	Enzymes of ceramide metabolism (e.g. beta-glucocerebrosidase or acid sphingomyelinase) as well as proteases (e.g. chymotryptic enzyme or cathepsin D linked to epidermal differentiation and desquamation) are regulated by the pH.	Ceramides	11-19	cathepsin D	Homo sapiens	137-148
29506145-1	2018	Background: High-dose radiotherapy (&gt;8-10 Gy) causes rapid endothelial cell death via acid sphingomyelinase (ASMase)-induced ceramide production, resulting in biologically significant enhancement of tumor responses.	Ceramides	128-136	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	112-118
29506145-2	2018	To further augment or solicit similar effects at low radiation doses, we used genetic and chemical approaches to evaluate mechano-acoustic activation of the ASMase-ceramide pathway by ultrasound-stimulated microbubbles (USMB).	Ceramides	164-172	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	157-163
29506145-4	2018	A cohort of wild-type mice received the ASMase-ceramide pathway inhibitor sphingosine-1-phosphate (S1P).	Ceramides	47-55	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	40-46
29506145-11	2018	Conclusions: This work is the first to confirm the involvement of the ASMase-ceramide pathway in mechanotransductive vascular targeting using USMB.	Ceramides	77-85	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	70-76
30250865-3	2018	Ceramide levels were determined in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts before and after treatment.	Ceramides	0-8	tripeptidyl peptidase 1	Homo sapiens	41-45
30072439-9	2018	These results may fit a notion developed in budding yeast stating that Cwh43 conjugates ceramide to glycosylphosphatidylinositol (GPI)-anchored proteins and maintains integrity of membrane organization.	Ceramides	88-96	Cwh43p	Saccharomyces cerevisiae S288C	71-76
30250865-3	2018	Ceramide levels were determined in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts before and after treatment.	Ceramides	0-8	palmitoyl-protein thioesterase 1	Homo sapiens	35-39
30197917-2	2018	Acid ceramidase (ACDase), neutral sphingomyelinase (NSMase) and glucosylceramide synthase (GCS) are critical enzymatic systems in ceramide metabolism.	Ceramides	72-80	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
30197917-2	2018	Acid ceramidase (ACDase), neutral sphingomyelinase (NSMase) and glucosylceramide synthase (GCS) are critical enzymatic systems in ceramide metabolism.	Ceramides	72-80	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-23
30197917-2	2018	Acid ceramidase (ACDase), neutral sphingomyelinase (NSMase) and glucosylceramide synthase (GCS) are critical enzymatic systems in ceramide metabolism.	Ceramides	72-80	sphingomyelin phosphodiesterase 2	Homo sapiens	26-50
30197917-2	2018	Acid ceramidase (ACDase), neutral sphingomyelinase (NSMase) and glucosylceramide synthase (GCS) are critical enzymatic systems in ceramide metabolism.	Ceramides	72-80	sphingomyelin phosphodiesterase 2	Homo sapiens	52-58
30197917-2	2018	Acid ceramidase (ACDase), neutral sphingomyelinase (NSMase) and glucosylceramide synthase (GCS) are critical enzymatic systems in ceramide metabolism.	Ceramides	72-80	UDP-glucose ceramide glucosyltransferase	Homo sapiens	91-94
30150688-5	2018	Further, using both a pharmacologic and siRNA approach to reduce peroxisome proliferator-activated receptors alpha (PPARalpha) gene expression, we demonstrate that C2 ceramide abrogates ethanol-mediated suppression of FA oxidation through an indirect PPARalpha mechanism.	Ceramides	167-175	peroxisome proliferator activated receptor alpha	Homo sapiens	65-114
30150688-5	2018	Further, using both a pharmacologic and siRNA approach to reduce peroxisome proliferator-activated receptors alpha (PPARalpha) gene expression, we demonstrate that C2 ceramide abrogates ethanol-mediated suppression of FA oxidation through an indirect PPARalpha mechanism.	Ceramides	167-175	peroxisome proliferator activated receptor alpha	Homo sapiens	116-125
30150688-5	2018	Further, using both a pharmacologic and siRNA approach to reduce peroxisome proliferator-activated receptors alpha (PPARalpha) gene expression, we demonstrate that C2 ceramide abrogates ethanol-mediated suppression of FA oxidation through an indirect PPARalpha mechanism.	Ceramides	167-175	peroxisome proliferator activated receptor alpha	Homo sapiens	251-260
30072439-0	2018	The putative ceramide-conjugation protein Cwh43 regulates G0 quiescence, nutrient metabolism and lipid homeostasis in fission yeast.	Ceramides	13-21	Cwh43p	Saccharomyces cerevisiae S288C	42-47
30250865-3	2018	Ceramide levels were determined in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts before and after treatment.	Ceramides	0-8	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	47-51
30250865-3	2018	Ceramide levels were determined in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts before and after treatment.	Ceramides	0-8	CLN6 transmembrane ER protein	Homo sapiens	53-57
30250865-3	2018	Ceramide levels were determined in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts before and after treatment.	Ceramides	0-8	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	59-63
30250865-6	2018	All drugs decreased ceramide in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts.	Ceramides	20-28	palmitoyl-protein thioesterase 1	Homo sapiens	32-36
30250865-6	2018	All drugs decreased ceramide in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts.	Ceramides	20-28	tripeptidyl peptidase 1	Homo sapiens	38-42
30250865-6	2018	All drugs decreased ceramide in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts.	Ceramides	20-28	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	44-48
30250865-6	2018	All drugs decreased ceramide in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts.	Ceramides	20-28	CLN6 transmembrane ER protein	Homo sapiens	50-54
30250865-6	2018	All drugs decreased ceramide in CLN1-/CLN2-/CLN3-/CLN6-/CLN8 patient-derived lymphoblasts.	Ceramides	20-28	CLN8 transmembrane ER and ERGIC protein	Homo sapiens	56-60
30250865-7	2018	Increased BCL-2 and decreased ceramide synthesis enzyme expression were established in CLN3-derived PC12 cells treated with the benzyl and allyl carbamate derivatives.	Ceramides	30-38	CLN3 lysosomal/endosomal transmembrane protein, battenin	Rattus norvegicus	87-91
30071029-3	2018	A sensitivity analysis of genetic variants known to be associated with late stage AMD showed that rs1061170 (p.Y402H) in the complement factor H (CFH) gene influences the association of Cer d18:1/16:0 with GA. To understand the possible influence of this genetic variant on ceramide levels, we established a cell-based assay to test the modulation of genes in the ceramide metabolism by factor H-like protein 1 (FHL-1), an alternative splicing variant of CFH that also harbors the 402 residue.	Ceramides	274-282	complement factor H	Homo sapiens	125-144
29945972-8	2018	Conversely, PP2A activation by ceramide or the sphingosine-like compound FTY720 was sufficient to induce TFE3 nuclear translocation.	Ceramides	31-39	protein phosphatase 2 phosphatase activator	Homo sapiens	12-16
29945972-8	2018	Conversely, PP2A activation by ceramide or the sphingosine-like compound FTY720 was sufficient to induce TFE3 nuclear translocation.	Ceramides	31-39	transcription factor binding to IGHM enhancer 3	Homo sapiens	105-109
30071029-3	2018	A sensitivity analysis of genetic variants known to be associated with late stage AMD showed that rs1061170 (p.Y402H) in the complement factor H (CFH) gene influences the association of Cer d18:1/16:0 with GA. To understand the possible influence of this genetic variant on ceramide levels, we established a cell-based assay to test the modulation of genes in the ceramide metabolism by factor H-like protein 1 (FHL-1), an alternative splicing variant of CFH that also harbors the 402 residue.	Ceramides	274-282	complement factor H	Homo sapiens	146-149
30071029-3	2018	A sensitivity analysis of genetic variants known to be associated with late stage AMD showed that rs1061170 (p.Y402H) in the complement factor H (CFH) gene influences the association of Cer d18:1/16:0 with GA. To understand the possible influence of this genetic variant on ceramide levels, we established a cell-based assay to test the modulation of genes in the ceramide metabolism by factor H-like protein 1 (FHL-1), an alternative splicing variant of CFH that also harbors the 402 residue.	Ceramides	364-372	complement factor H	Homo sapiens	125-144
30071029-3	2018	A sensitivity analysis of genetic variants known to be associated with late stage AMD showed that rs1061170 (p.Y402H) in the complement factor H (CFH) gene influences the association of Cer d18:1/16:0 with GA. To understand the possible influence of this genetic variant on ceramide levels, we established a cell-based assay to test the modulation of genes in the ceramide metabolism by factor H-like protein 1 (FHL-1), an alternative splicing variant of CFH that also harbors the 402 residue.	Ceramides	364-372	complement factor H	Homo sapiens	146-149
29906468-5	2018	In addition, our metabolomic analysis revealed the accumulation of bile acids and ceramide (Cer) in the liver of Fech-mut mice.	Ceramides	82-90	ferrochelatase	Mus musculus	113-117
29698625-4	2018	The increase in ceramide mediates an ectopic expression of beta1-integrins in the luminal membrane of CF epithelial cells, which results, via an unknown mechanism, in a down-regulation of acid ceramidase.	Ceramides	16-24	N-acylsphingosine amidohydrolase 1	Mus musculus	188-203
29698625-5	2018	It is predominantly this down-regulation of acid ceramidase that results in the imbalance of ceramide and sphingosine in CF cells.	Ceramides	93-101	N-acylsphingosine amidohydrolase 1	Mus musculus	44-59
29698625-6	2018	Correction of ceramide and sphingosine levels can be achieved by inhalation of functional acid sphingomyelinase inhibitors, recombinant acid ceramidase or by normalization of beta1-integrin expression and subsequent re-expression of endogenous acid ceramidase.	Ceramides	14-22	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	90-111
29698625-6	2018	Correction of ceramide and sphingosine levels can be achieved by inhalation of functional acid sphingomyelinase inhibitors, recombinant acid ceramidase or by normalization of beta1-integrin expression and subsequent re-expression of endogenous acid ceramidase.	Ceramides	14-22	N-acylsphingosine amidohydrolase 1	Mus musculus	136-151
29698625-6	2018	Correction of ceramide and sphingosine levels can be achieved by inhalation of functional acid sphingomyelinase inhibitors, recombinant acid ceramidase or by normalization of beta1-integrin expression and subsequent re-expression of endogenous acid ceramidase.	Ceramides	14-22	N-acylsphingosine amidohydrolase 1	Mus musculus	244-259
29906468-5	2018	In addition, our metabolomic analysis revealed the accumulation of bile acids and ceramide (Cer) in the liver of Fech-mut mice.	Ceramides	92-95	ferrochelatase	Mus musculus	113-117
30169917-4	2018	We identified lipids in plasma from 44 healthy subjects that correlated with CES1 activity as determined by PK parameters of methylphenidate including a ceramide (q value = 0.001) and a phosphatidylcholine (q value = 0.005).	Ceramides	153-161	carboxylesterase 1	Homo sapiens	77-81
29896915-7	2018	Liquid chromatography-tandem mass spectrometry analysis revealed that the levels of OA-containing ceramide, a pro-apoptotic factor, were higher in HepG2 and CAV-1-deficient HLE cells than in HLE cells, suggesting that CAV-1 inhibits apoptosis by decreasing the level of OA-containing ceramide.	Ceramides	98-106	caveolin 1	Homo sapiens	157-162
29588286-1	2018	Experimental studies suggest ceramides may play a role in insulin resistance.	Ceramides	29-38	insulin	Homo sapiens	58-65
29588286-2	2018	However, the relationships of circulating ceramides and related sphingolipids with plasma insulin have been underexplored in humans.	Ceramides	42-51	insulin	Homo sapiens	90-97
29588286-5	2018	Among the 2,086 participants without diabetes, higher levels of plasma ceramides carrying the fatty acids 16:0 (16 carbons, 0 double bond), 18:0, 20:0, or 22:0 were associated with higher plasma insulin and higher HOMA-IR at baseline and at follow-up an average of 5.4 years later.	Ceramides	71-80	insulin	Homo sapiens	195-202
29588286-6	2018	For example, a twofold higher baseline concentration of ceramide 16:0 was associated with 14% higher baseline insulin (P &lt; 0.0001).	Ceramides	56-64	insulin	Homo sapiens	110-117
29462574-0	2018	Adiponectin receptor agonist AdipoRon decreased ceramide, and lipotoxicity, and ameliorated diabetic nephropathy.	Ceramides	48-56	adiponectin, C1Q and collagen domain containing	Mus musculus	0-11
30029679-2	2018	Both disorders are caused by mutations in the ASAH1 gene that encodes the lysosomal hydrolase that breaks down the bioactive lipid ceramide.	Ceramides	131-139	N-acylsphingosine amidohydrolase 1	Homo sapiens	46-51
30030471-3	2018	The method provides the composition and sequence of the glycan, as well as variations in the ceramide portion of the GSL.	Ceramides	93-101	cathepsin A	Homo sapiens	117-120
30018456-4	2018	Here we found that S1P is elevated in BTC with the activation of ceramide-synthetic pathways, suggesting that BTC utilizes SPHK1 to promote lymphatic metastasis.	Ceramides	65-73	sphingosine kinase 1	Homo sapiens	123-128
29848549-2	2018	The ceramide transfer protein (CERT) moves ceramide from the endoplasmic reticulum to the Golgi apparatus in a nonvesicular manner.	Ceramides	4-12	ceramide transporter 1	Homo sapiens	31-35
29759974-4	2018	Ceramides are produced in the endoplasmic reticulum (ER) and transported to the Golgi apparatus through a transporter called CERT, where they are converted into various sphingolipid species.	Ceramides	0-9	ceramide transporter 1	Homo sapiens	125-129
29759974-6	2018	Inhibiting CERT activity in vitro potentiates the deleterious action of lipotoxicity on insulin signaling, whereas overexpression of CERT in vitro or in vivo decreases muscle ceramide content and improves insulin signaling.	Ceramides	175-183	ceramide transporter 1	Homo sapiens	133-137
29794037-6	2018	Palmitate, but not palmitoleate, had mild effects on Akt phosphorylation but significantly inhibited insulin-stimulated GLUT4 translocation and increased expression of pro-inflammatory cytokines Il6 and Ccl2 Ceramides, hexosylceramides, and sphingosine-1-phosphate significantly heightened by palmitate correlated negatively with insulin sensitivity and positively with pro-inflammatory indices.	Ceramides	208-217	C-C motif chemokine ligand 2	Homo sapiens	203-207
29662189-4	2018	These enzymes hydrolyze ceramides into sphingosine (SPH) which in turn is phosphorylated by sphingosine kinases (SK) 1 and 2 to generate sphingosine-1 phosphate (S1P).	Ceramides	24-33	sphingosine kinase 1	Mus musculus	92-124
29662189-5	2018	Importantly, we have recently shown that inhibition of neutral CDase (nCDase) induces an increase of ceramide in colon cancer cells which decreases cellular growth, increases apoptosis and modulates the WNT/beta-catenin pathway.	Ceramides	101-109	N-acylsphingosine amidohydrolase 2	Mus musculus	55-68
29662189-5	2018	Importantly, we have recently shown that inhibition of neutral CDase (nCDase) induces an increase of ceramide in colon cancer cells which decreases cellular growth, increases apoptosis and modulates the WNT/beta-catenin pathway.	Ceramides	101-109	N-acylsphingosine amidohydrolase 2	Mus musculus	70-76
29662189-5	2018	Importantly, we have recently shown that inhibition of neutral CDase (nCDase) induces an increase of ceramide in colon cancer cells which decreases cellular growth, increases apoptosis and modulates the WNT/beta-catenin pathway.	Ceramides	101-109	catenin (cadherin associated protein), beta 1	Mus musculus	207-219
29662189-7	2018	Here, we demonstrate that AKT is a key target for the growth suppressing functions of ceramide.	Ceramides	86-94	thymoma viral proto-oncogene 1	Mus musculus	26-29
29624923-8	2018	RESULTS: There was a significant association between the concentration of active NE and ceramide, sphingomyelin, and monohexosylceramide moieties as well as sphingosine-1-phosphate.	Ceramides	88-96	elastase, neutrophil expressed	Homo sapiens	81-83
29632068-7	2018	Moreover, a chimeric protein, CerS4(291-301 CerS2), based on CerS4 (which normally generates C18-C22 ceramides) displayed significant activity toward C24:1-CoA.	Ceramides	101-110	ceramide synthase 4	Homo sapiens	30-35
29632068-7	2018	Moreover, a chimeric protein, CerS4(291-301 CerS2), based on CerS4 (which normally generates C18-C22 ceramides) displayed significant activity toward C24:1-CoA.	Ceramides	101-110	ceramide synthase 2	Homo sapiens	44-49
29632068-7	2018	Moreover, a chimeric protein, CerS4(291-301 CerS2), based on CerS4 (which normally generates C18-C22 ceramides) displayed significant activity toward C24:1-CoA.	Ceramides	101-110	ceramide synthase 4	Homo sapiens	61-66
29920218-0	2018	Deletion of the stress-response protein REDD1 promotes ceramide-induced retinal cell death and JNK activation.	Ceramides	55-63	DNA-damage-inducible transcript 4	Mus musculus	40-45
29920218-9	2018	The results support a model wherein Cer-induced REDD1 expression attenuates TXNIP-dependent JNK activation and retinal cell death.-Dai, W., Miller, W. P., Toro, A. L., Black, A. J., Dierschke, S. K., Feehan, R. P., Kimball, S. R., Dennis, M. D. Deletion of the stress-response protein REDD1 promotes ceramide-induced retinal cell death and JNK activation.	Ceramides	300-308	DNA-damage-inducible transcript 4	Mus musculus	48-53
29920218-9	2018	The results support a model wherein Cer-induced REDD1 expression attenuates TXNIP-dependent JNK activation and retinal cell death.-Dai, W., Miller, W. P., Toro, A. L., Black, A. J., Dierschke, S. K., Feehan, R. P., Kimball, S. R., Dennis, M. D. Deletion of the stress-response protein REDD1 promotes ceramide-induced retinal cell death and JNK activation.	Ceramides	300-308	thioredoxin interacting protein	Mus musculus	76-81
29978896-6	2018	AdipoR1 and R2 also possesses inherent ceramidase activity, resulting in a decrease in intracellular ceramide, a sphingolipid that has been implicated in insulin resistance, cell death, inflammation, and atherosclerosis.	Ceramides	101-109	adiponectin receptor 1	Homo sapiens	0-7
29889835-6	2018	Adipocyte LPP3 deficiency resulted in blunted ceramide and sphingomyelin accumulation during diet-induced adipose tissue expansion, accumulation of the LPP3 substrate sphingosine 1- phosphate, and reduced expression of serine palmitoyl transferase.	Ceramides	46-54	phospholipid phosphatase 3	Mus musculus	10-14
29546476-1	2018	AIMS/HYPOTHESIS: Ceramide lipids have a role in the development of insulin resistance, diabetes and risk of cardiovascular disease.	Ceramides	17-25	insulin	Homo sapiens	67-74
29579237-6	2018	Inhibition of acid ceramidase by carmofur resulted in increased ceramide levels and decreased glucosylsphingosine levels in GCase-deficient cells, and also reduced oxidized alpha-synuclein and levels of ubiquitinated proteins in GBA1-PD patient-derived dopaminergic neurons.	Ceramides	64-72	N-acylsphingosine amidohydrolase 1	Homo sapiens	14-29
29579237-7	2018	Together, these results suggest that decreased ceramide generation via the catabolic lysosomal salvage pathway in GCase mutant cells contributes to alpha-synuclein accumulation, potentially due to impaired secretory autophagy.	Ceramides	47-55	synuclein alpha	Homo sapiens	148-163
29579237-8	2018	We thus propose that acid ceramidase inhibition which restores ceramide levels may be a potential therapeutic strategy to target synucleinopathies linked to GBA1 mutations including PD and DLB.	Ceramides	63-71	N-acylsphingosine amidohydrolase 1	Homo sapiens	21-36
29621545-3	2018	Further, stable suppression of caspase-2 expression in HEK293T and HeLa cells enabled a systematic investigation of putative novel enzyme functionalities, especially with respect to ceramide production, cell migration, IL-6 production and vesicular homeostasis, all of which have been previously reported to be associated with FAN.	Ceramides	182-190	caspase 2	Homo sapiens	31-40
29806001-0	2018	A Ceramide-Regulated Element in the Late Endosomal Protein LAPTM4B Controls Amino Acid Transporter Interaction.	Ceramides	2-10	lysosomal protein transmembrane 4 beta	Homo sapiens	59-66
29806001-4	2018	Here, we uncover in atomistic detail the ceramide interaction of Lysosome Associated Protein Transmembrane 4B (LAPTM4B), implicated in ceramide-dependent cell death and autophagy, and its functional relevance in lysosomal nutrient signaling.	Ceramides	41-49	lysosomal protein transmembrane 4 beta	Homo sapiens	65-109
29806001-4	2018	Here, we uncover in atomistic detail the ceramide interaction of Lysosome Associated Protein Transmembrane 4B (LAPTM4B), implicated in ceramide-dependent cell death and autophagy, and its functional relevance in lysosomal nutrient signaling.	Ceramides	41-49	lysosomal protein transmembrane 4 beta	Homo sapiens	111-118
29806001-4	2018	Here, we uncover in atomistic detail the ceramide interaction of Lysosome Associated Protein Transmembrane 4B (LAPTM4B), implicated in ceramide-dependent cell death and autophagy, and its functional relevance in lysosomal nutrient signaling.	Ceramides	135-143	lysosomal protein transmembrane 4 beta	Homo sapiens	65-109
29806001-4	2018	Here, we uncover in atomistic detail the ceramide interaction of Lysosome Associated Protein Transmembrane 4B (LAPTM4B), implicated in ceramide-dependent cell death and autophagy, and its functional relevance in lysosomal nutrient signaling.	Ceramides	135-143	lysosomal protein transmembrane 4 beta	Homo sapiens	111-118
29806001-5	2018	The ceramide-mediated regulation of LAPTM4B depends on a sphingolipid interaction motif and an adjacent aspartate residue in the protein"s third transmembrane (TM3) helix.	Ceramides	4-12	lysosomal protein transmembrane 4 beta	Homo sapiens	36-43
29806001-5	2018	The ceramide-mediated regulation of LAPTM4B depends on a sphingolipid interaction motif and an adjacent aspartate residue in the protein"s third transmembrane (TM3) helix.	Ceramides	4-12	tropomyosin 3	Homo sapiens	160-163
29806001-6	2018	The interaction motif provides the preferred contact points for ceramide while the neighboring membrane-embedded acidic residue confers flexibility that is subject to ceramide-induced conformational changes, reducing TM3 bending.	Ceramides	64-72	tropomyosin 3	Homo sapiens	217-220
29806001-6	2018	The interaction motif provides the preferred contact points for ceramide while the neighboring membrane-embedded acidic residue confers flexibility that is subject to ceramide-induced conformational changes, reducing TM3 bending.	Ceramides	167-175	tropomyosin 3	Homo sapiens	217-220
29769046-6	2018	Modulation of ceramide transport by GT3 was studied by immunochemistry of CERT and ARV-1, and the subsequent effects at the cell membrane was analyzed via immunofluorescence of ceramide, caveolin, and DR5.	Ceramides	14-22	ceramide transporter 1	Homo sapiens	74-78
29769046-6	2018	Modulation of ceramide transport by GT3 was studied by immunochemistry of CERT and ARV-1, and the subsequent effects at the cell membrane was analyzed via immunofluorescence of ceramide, caveolin, and DR5.	Ceramides	14-22	ARV1 homolog, fatty acid homeostasis modulator	Homo sapiens	83-88
29769046-8	2018	Additionally, the conversion of newly synthesized ceramide to sphingomyelin and glucosylceramide at the Golgi is prevented by the inhibition of CERT.	Ceramides	50-58	ceramide transporter 1	Homo sapiens	144-148
29751643-7	2018	Thus, the lean-seafood diet decreased circulating isoleucine and valine levels, whereas the non-seafood diet elevated the levels of certain ceramides, metabolites that are associated with insulin-resistance.	Ceramides	140-149	insulin	Homo sapiens	188-195
29229990-0	2018	Tumor suppressor p53 links ceramide metabolism to DNA damage response through alkaline ceramidase 2.	Ceramides	27-35	alkaline ceramidase 2	Homo sapiens	78-99
29229990-5	2018	As ACER2 catalyzes the hydrolysis of ceramides into sphingosine, which in turn is phosphorylated to form sphingosine-1-phosphate (S1P), ACER2 upregulation increased the levels of both sphingosine and S1P while decreasing the levels of ceramides in cells.	Ceramides	37-46	alkaline ceramidase 2	Homo sapiens	3-8
29229990-5	2018	As ACER2 catalyzes the hydrolysis of ceramides into sphingosine, which in turn is phosphorylated to form sphingosine-1-phosphate (S1P), ACER2 upregulation increased the levels of both sphingosine and S1P while decreasing the levels of ceramides in cells.	Ceramides	37-46	alkaline ceramidase 2	Homo sapiens	136-141
29229990-5	2018	As ACER2 catalyzes the hydrolysis of ceramides into sphingosine, which in turn is phosphorylated to form sphingosine-1-phosphate (S1P), ACER2 upregulation increased the levels of both sphingosine and S1P while decreasing the levels of ceramides in cells.	Ceramides	235-244	alkaline ceramidase 2	Homo sapiens	3-8
29229990-5	2018	As ACER2 catalyzes the hydrolysis of ceramides into sphingosine, which in turn is phosphorylated to form sphingosine-1-phosphate (S1P), ACER2 upregulation increased the levels of both sphingosine and S1P while decreasing the levels of ceramides in cells.	Ceramides	235-244	alkaline ceramidase 2	Homo sapiens	136-141
29229990-6	2018	A moderate upregulation of ACER2 inhibited cell cycle arrest and cellular senescence in response to low-level expression of p53 or low-dose IR by elevating S1P, a pro-proliferative and pro-survival bioactive lipid, and/or decreasing ceramides whereas its robust upregulation mediated PCD in response to high-level expression of p53 or high-dose IR likely by accumulating cellular sphingosine, a pro-death bioactive lipid.	Ceramides	233-242	alkaline ceramidase 2	Homo sapiens	27-32
29229990-6	2018	A moderate upregulation of ACER2 inhibited cell cycle arrest and cellular senescence in response to low-level expression of p53 or low-dose IR by elevating S1P, a pro-proliferative and pro-survival bioactive lipid, and/or decreasing ceramides whereas its robust upregulation mediated PCD in response to high-level expression of p53 or high-dose IR likely by accumulating cellular sphingosine, a pro-death bioactive lipid.	Ceramides	233-242	tumor protein p53	Homo sapiens	124-127
29374533-9	2018	In contrast, p75NTR mediates generation of the bioactive lipid ceramide upon stimulation with BDNF and inhibits PKA activation.	Ceramides	63-71	nerve growth factor receptor	Homo sapiens	13-19
29374533-9	2018	In contrast, p75NTR mediates generation of the bioactive lipid ceramide upon stimulation with BDNF and inhibits PKA activation.	Ceramides	63-71	brain derived neurotrophic factor	Homo sapiens	94-98
29374533-10	2018	As ceramide directly activates PKCzeta, we discuss the importance of the TrkB.T1-p75NTR-ceramide-PKCzeta signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA.	Ceramides	3-11	protein kinase C zeta	Homo sapiens	31-38
29374533-10	2018	As ceramide directly activates PKCzeta, we discuss the importance of the TrkB.T1-p75NTR-ceramide-PKCzeta signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA.	Ceramides	3-11	neurotrophic receptor tyrosine kinase 2	Homo sapiens	73-77
29374533-10	2018	As ceramide directly activates PKCzeta, we discuss the importance of the TrkB.T1-p75NTR-ceramide-PKCzeta signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA.	Ceramides	3-11	nerve growth factor receptor	Homo sapiens	81-87
29374533-10	2018	As ceramide directly activates PKCzeta, we discuss the importance of the TrkB.T1-p75NTR-ceramide-PKCzeta signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA.	Ceramides	88-96	neurotrophic receptor tyrosine kinase 2	Homo sapiens	73-77
29374533-10	2018	As ceramide directly activates PKCzeta, we discuss the importance of the TrkB.T1-p75NTR-ceramide-PKCzeta signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA.	Ceramides	88-96	nerve growth factor receptor	Homo sapiens	81-87
29374533-10	2018	As ceramide directly activates PKCzeta, we discuss the importance of the TrkB.T1-p75NTR-ceramide-PKCzeta signaling axis in the stimulation of glycogen and lipid synthesis and activation of RhoA.	Ceramides	88-96	protein kinase C zeta	Homo sapiens	97-104
29374533-11	2018	Ceramide-PKCzeta-casein kinase 2 signaling activates Nrf2 to support oxidative phosphorylation via upregulation of antioxidant enzymes.	Ceramides	0-8	protein kinase C zeta	Homo sapiens	9-16
29374533-11	2018	Ceramide-PKCzeta-casein kinase 2 signaling activates Nrf2 to support oxidative phosphorylation via upregulation of antioxidant enzymes.	Ceramides	0-8	NFE2 like bZIP transcription factor 2	Homo sapiens	53-57
29307520-6	2018	However, ceramides C18:1, C:20, C22, C24 and C24:1 were significantly higher in people with T2DM compared to ND whereas no differences existed for C16 and C18.	Ceramides	9-18	Bardet-Biedl syndrome 9	Homo sapiens	19-22
29522708-10	2018	Taken together, rutin ameliorates CCl4-induced oxidative stress, inflammation and apoptosis through regulating the ceramide, MAPK, p53 and calpain activities and thereby suppressing apoptosis by the mitochondrial pathway.	Ceramides	115-123	chemokine (C-C motif) ligand 4	Mus musculus	34-38
29754287-11	2018	Inhibition of beta cell apoptosis by the ELOVL2/DHA axis was associated with a decrease in ceramide accumulation.	Ceramides	91-99	ELOVL fatty acid elongase 2	Homo sapiens	41-47
29345004-1	2018	Sphingomyelin synthase (SMS) is an enzyme that generates sphingomyelin (SM) from ceramide (CER) and phosphatidylcholine.	Ceramides	81-89	spermine synthase	Mus musculus	24-27
29345004-1	2018	Sphingomyelin synthase (SMS) is an enzyme that generates sphingomyelin (SM) from ceramide (CER) and phosphatidylcholine.	Ceramides	91-94	spermine synthase	Mus musculus	24-27
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.	Ceramides	142-151	apolipoprotein E	Mus musculus	110-114
29653252-3	2018	Thus, very long chain ceramides produced by CerS2 are required for transcriptional regulation of target genes.	Ceramides	22-31	ceramide synthase 2	Mus musculus	44-49
29724781-1	2018	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to produce the biologically active lipid ceramide.	Ceramides	94-102	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
29724781-1	2018	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to produce the biologically active lipid ceramide.	Ceramides	94-102	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
29724781-8	2018	Taken together, these data suggest ASM can produce ceramide which is then converted to C-1-P by CERK, and that C-1-P is required for production of CCL5 and several cytokines and chemokines, with roles in cell migration.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	35-38
30110462-1	2018	This paper considers two models of ceramide-transfer protein (CERT)-mediated ceramide transfer at the trans-Golgi network proposed in the literature, short distance shuttle and neck swinging, and seeks structural (parameter-free) features of the two models, which rely exclusively on the peculiar interaction network and not on specific parameter values.	Ceramides	35-43	ceramide transporter 1	Homo sapiens	62-66
30110462-1	2018	This paper considers two models of ceramide-transfer protein (CERT)-mediated ceramide transfer at the trans-Golgi network proposed in the literature, short distance shuttle and neck swinging, and seeks structural (parameter-free) features of the two models, which rely exclusively on the peculiar interaction network and not on specific parameter values.	Ceramides	77-85	ceramide transporter 1	Homo sapiens	62-66
30110462-3	2018	In the short distance shuttle model, the amount of transferred ceramide is structurally tuned by active protein kinase D (PKD), both directly and indirectly, in a coherent feed-forward loop motif.	Ceramides	63-71	protein kinase D1	Homo sapiens	104-120
30110462-3	2018	In the short distance shuttle model, the amount of transferred ceramide is structurally tuned by active protein kinase D (PKD), both directly and indirectly, in a coherent feed-forward loop motif.	Ceramides	63-71	protein kinase D1	Homo sapiens	122-125
30110462-4	2018	In the neck-swinging model, the amount of transferred ceramide is structurally tuned by active PI4KIIIbeta, while active PKD has an ambivalent effect, due to the presence of an incoherent feed-forward loop motif that directly inhibits ceramide transfer and indirectly promotes it; the structural role of active PKD is to favour CERT mobility in the cytosol.	Ceramides	54-62	phosphatidylinositol 4-kinase beta	Homo sapiens	95-106
30110462-4	2018	In the neck-swinging model, the amount of transferred ceramide is structurally tuned by active PI4KIIIbeta, while active PKD has an ambivalent effect, due to the presence of an incoherent feed-forward loop motif that directly inhibits ceramide transfer and indirectly promotes it; the structural role of active PKD is to favour CERT mobility in the cytosol.	Ceramides	54-62	protein kinase D1	Homo sapiens	311-314
30110462-4	2018	In the neck-swinging model, the amount of transferred ceramide is structurally tuned by active PI4KIIIbeta, while active PKD has an ambivalent effect, due to the presence of an incoherent feed-forward loop motif that directly inhibits ceramide transfer and indirectly promotes it; the structural role of active PKD is to favour CERT mobility in the cytosol.	Ceramides	54-62	ceramide transporter 1	Homo sapiens	328-332
29929540-11	2018	Similar to other neurodegenerative diseases, reduced levels of tryptophan and increased levels of ceramides, di- and triglycerides were observed in SCA3 mouse blood.	Ceramides	98-107	ataxin 3	Mus musculus	148-152
29031494-1	2018	Ceramide generation is involved in signal transduction of cellular stress response, in particular during stress-induced apoptosis in response to stimuli such as minimally modified Low-density lipoproteins, TNFalpha and exogenous C6-ceramide.	Ceramides	0-8	tumor necrosis factor	Homo sapiens	206-214
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.	Ceramides	0-8	sphingosine kinase 1	Mus musculus	72-75
29867196-0	2018	Activation of neutral sphingomyelinase 2 by starvation induces cell-protective autophagy via an increase in Golgi-localized ceramide.	Ceramides	124-132	sphingomyelin phosphodiesterase 3	Homo sapiens	14-40
29867196-4	2018	In this study, we demonstrate that among ceramide-producing enzymes, neutral sphingomyelinase 2 (nSMase2) plays a key role in autophagy during nutrient starvation.	Ceramides	41-49	sphingomyelin phosphodiesterase 3	Homo sapiens	69-95
29867196-4	2018	In this study, we demonstrate that among ceramide-producing enzymes, neutral sphingomyelinase 2 (nSMase2) plays a key role in autophagy during nutrient starvation.	Ceramides	41-49	sphingomyelin phosphodiesterase 3	Homo sapiens	97-104
29867196-7	2018	These findings suggest that nSMase2 is a novel regulator of autophagy and provide evidence that Golgi-localized ceramides participate in cytoprotective autophagy against starvation.	Ceramides	112-121	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
29748132-11	2018	Silencing of the plasma membrane Ca2+ ATPase isoform 1 (PMCA1) was associated with an augmentation in ceramide-induced increases in [Ca2+]CYT and also cell death.	Ceramides	102-110	ATPase plasma membrane Ca2+ transporting 1	Homo sapiens	17-54
29748132-11	2018	Silencing of the plasma membrane Ca2+ ATPase isoform 1 (PMCA1) was associated with an augmentation in ceramide-induced increases in [Ca2+]CYT and also cell death.	Ceramides	102-110	ATPase plasma membrane Ca2+ transporting 1	Homo sapiens	56-61
29579237-1	2018	GBA1 encodes the lysosomal enzyme beta-glucocerebrosidase (GCase) which converts glucosylceramide into ceramide and glucose.	Ceramides	89-97	glucosylceramidase beta	Homo sapiens	0-4
29579237-1	2018	GBA1 encodes the lysosomal enzyme beta-glucocerebrosidase (GCase) which converts glucosylceramide into ceramide and glucose.	Ceramides	89-97	glucosylceramidase beta	Homo sapiens	34-57
29579237-3	2018	In this study, we examined whether decreased ceramide that is observed in GCase-deficient cells contributes to alpha-synuclein accumulation.	Ceramides	45-53	synuclein alpha	Homo sapiens	111-126
29857511-7	2018	Twenty-six significantly changed SPL markers were explored, and the levels of ceramides (Cers) and their metabolites were found to be reversed by IDM treatment.	Ceramides	78-87	sphingosine-1-phosphate lyase 1	Rattus norvegicus	33-36
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.	Ceramides	30-38	delta like canonical Notch ligand 4	Homo sapiens	83-92
29748552-0	2018	Pb(II) Induces Scramblase Activation and Ceramide-Domain Generation in Red Blood Cells.	Ceramides	41-49	submaxillary gland androgen regulated protein 3B	Homo sapiens	0-6
29385411-10	2018	This detrimental effect of ceramide was diminished by AICAR treatment of oocytes.	Ceramides	27-35	5-aminoimidazole-4-carboxamide ribonucleotide formyltransferase/IMP cyclohydrolase	Homo sapiens	54-59
29229990-0	2018	Tumor suppressor p53 links ceramide metabolism to DNA damage response through alkaline ceramidase 2.	Ceramides	27-35	tumor protein p53	Homo sapiens	17-20
29567647-2	2018	Genome-wide studies have identified neutral SMase-2 (nSMase2), an enzyme generating ceramide from SM, as a potential repressor for hepatocellular carcinoma.	Ceramides	84-92	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	36-51
29567647-2	2018	Genome-wide studies have identified neutral SMase-2 (nSMase2), an enzyme generating ceramide from SM, as a potential repressor for hepatocellular carcinoma.	Ceramides	84-92	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	53-60
29567647-9	2018	CD133(+) cells showed strong labeling for SM and ceramide.	Ceramides	49-57	prominin 1	Mus musculus	0-5
29712570-0	2018	IL-1beta suppresses cLTP-induced surface expression of GluA1 and actin polymerization via ceramide-mediated Src activation.	Ceramides	90-98	interleukin 1 beta	Homo sapiens	0-8
29712570-0	2018	IL-1beta suppresses cLTP-induced surface expression of GluA1 and actin polymerization via ceramide-mediated Src activation.	Ceramides	90-98	glutamate ionotropic receptor AMPA type subunit 1	Homo sapiens	55-60
29712570-0	2018	IL-1beta suppresses cLTP-induced surface expression of GluA1 and actin polymerization via ceramide-mediated Src activation.	Ceramides	90-98	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	108-111
29692406-1	2018	Acid ceramidase (aCDase, ASAH1) hydrolyzes lysosomal membrane ceramide into sphingosine, the backbone of all sphingolipids, to regulate many cellular processes.	Ceramides	62-70	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
29692406-1	2018	Acid ceramidase (aCDase, ASAH1) hydrolyzes lysosomal membrane ceramide into sphingosine, the backbone of all sphingolipids, to regulate many cellular processes.	Ceramides	62-70	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-23
29692406-1	2018	Acid ceramidase (aCDase, ASAH1) hydrolyzes lysosomal membrane ceramide into sphingosine, the backbone of all sphingolipids, to regulate many cellular processes.	Ceramides	62-70	N-acylsphingosine amidohydrolase 1	Homo sapiens	25-30
29669945-0	2018	Adiponectin/T-cadherin system enhances exosome biogenesis and decreases cellular ceramides by exosomal release.	Ceramides	81-90	adiponectin, C1Q and collagen domain containing	Mus musculus	0-11
29669945-0	2018	Adiponectin/T-cadherin system enhances exosome biogenesis and decreases cellular ceramides by exosomal release.	Ceramides	81-90	cadherin 13	Mus musculus	12-22
29669945-3	2018	Here, we demonstrate that the adiponectin/T-cadherin system enhances exosome biogenesis and secretion, leading to the decrease of cellular ceramides.	Ceramides	139-148	adiponectin, C1Q and collagen domain containing	Mus musculus	30-41
29669945-3	2018	Here, we demonstrate that the adiponectin/T-cadherin system enhances exosome biogenesis and secretion, leading to the decrease of cellular ceramides.	Ceramides	139-148	cadherin 13	Mus musculus	42-52
29669945-8	2018	Consistently, the ceramide reduction by adiponectin was found in aortas of WT mice treated with angiotensin II, but not in T-cadherin-knockout mice.	Ceramides	18-26	adiponectin, C1Q and collagen domain containing	Mus musculus	40-51
29720981-1	2018	By promoting ceramide release at the cytosolic membrane leaflet, the neutral sphingomyelinase 2 (NSM) is capable of organizing receptor and signalosome segregation.	Ceramides	13-21	sphingomyelin phosphodiesterase 3	Homo sapiens	69-95
29720981-7	2018	Ceramide supplementation rescued PKCzeta membrane recruitment and MTOC translocation in NSM-deficient cells.	Ceramides	0-8	protein kinase C zeta	Homo sapiens	33-40
29325876-3	2018	Unexpectedly, our results show that viability of Nogo-A-overexpressing cells was reduced progressively due to apoptotic cell death following NGF treatment, but only after 24 h. Inhibitors of neutral sphingomyelinase prevented this loss of viability, suggesting that NGF induced the activation of a ceramide-dependent cell death pathway.	Ceramides	298-306	reticulon 4	Rattus norvegicus	49-55
28858294-5	2018	In this study, we showed that C6 ceramide (an exogenous ceramide supplement, 1.25-40 mumol/L) dose-dependently inhibited the proliferation and promoted the apoptosis in human MM OPM2 cell line, which were associated with elevated caspase 3/9 and PARP cleavage.	Ceramides	33-41	caspase 3	Homo sapiens	230-241
28858294-5	2018	In this study, we showed that C6 ceramide (an exogenous ceramide supplement, 1.25-40 mumol/L) dose-dependently inhibited the proliferation and promoted the apoptosis in human MM OPM2 cell line, which were associated with elevated caspase 3/9 and PARP cleavage.	Ceramides	33-41	collagen type XI alpha 2 chain	Homo sapiens	246-250
28858294-10	2018	Taken together, our findings reveal that the ceramide pathway modulates MM survival, probably directly via the caspase pathway and indirectly via exosomal miR mechanisms.	Ceramides	45-53	membrane associated ring-CH-type finger 8	Homo sapiens	155-158
28747072-4	2018	RESULTS: We showed that CD44 activation by S. aureus stimulated Asm via the formation of reactive oxygen species, resulting in ceramide release, clustering of CD44 in ceramide-enriched membrane platforms, CD44/Asm-dependent activation of Rho family GTPases, translocation of phospho-ezrin/radixin/moesin to the plasma-membrane, and a rapid rearrangement of the actin cytoskeleton with cortical actin polymerization.	Ceramides	127-135	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	64-67
28747072-4	2018	RESULTS: We showed that CD44 activation by S. aureus stimulated Asm via the formation of reactive oxygen species, resulting in ceramide release, clustering of CD44 in ceramide-enriched membrane platforms, CD44/Asm-dependent activation of Rho family GTPases, translocation of phospho-ezrin/radixin/moesin to the plasma-membrane, and a rapid rearrangement of the actin cytoskeleton with cortical actin polymerization.	Ceramides	167-175	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	64-67
28747072-7	2018	Innovation and Conclusion: The CD44-Asm-ceramide system plays an important role in the infection of macrophages with S. aureus.	Ceramides	40-48	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	36-39
29472233-7	2018	Mechanistically, IL-1beta treatment of isolated neutrophils induced nuclear localization of ceramide synthase 6 and synthesis of C16-ceramide, which was inhibited by IL-1RA or fumonisin B1, an inhibitor of ceramide synthesis.	Ceramides	92-100	interleukin 1 beta	Mus musculus	17-25
29472233-7	2018	Mechanistically, IL-1beta treatment of isolated neutrophils induced nuclear localization of ceramide synthase 6 and synthesis of C16-ceramide, which was inhibited by IL-1RA or fumonisin B1, an inhibitor of ceramide synthesis.	Ceramides	92-100	interleukin 1 receptor antagonist	Mus musculus	166-172
29325876-3	2018	Unexpectedly, our results show that viability of Nogo-A-overexpressing cells was reduced progressively due to apoptotic cell death following NGF treatment, but only after 24 h. Inhibitors of neutral sphingomyelinase prevented this loss of viability, suggesting that NGF induced the activation of a ceramide-dependent cell death pathway.	Ceramides	298-306	nerve growth factor	Rattus norvegicus	141-144
29470962-7	2018	Results suggested that the ceramide/PP2A/Akt axis is involved in the apoptosis and a possible cyclooxygenase-independent target for indomethacin.	Ceramides	27-35	protein phosphatase 2 phosphatase activator	Homo sapiens	36-40
29362226-0	2018	ELOVL4-Mediated Production of Very Long-Chain Ceramides Stabilizes Tight Junctions and Prevents Diabetes-Induced Retinal Vascular Permeability.	Ceramides	46-55	ELOVL fatty acid elongase 4	Homo sapiens	0-6
29362226-4	2018	VLC fatty acids that incorporate into VLC ceramides are produced by elongase elongation of very long-chain fatty acids protein 4 (ELOVL4).	Ceramides	42-51	ELOVL fatty acid elongase 4	Homo sapiens	130-136
29362226-9	2018	Overall, normalization of retinal ELOVL4 expression could prevent blood-retinal barrier dysregulation in diabetic retinopathy through an increase in VLC ceramides and stabilization of TJs.	Ceramides	153-162	ELOVL fatty acid elongase 4	Homo sapiens	34-40
29470962-7	2018	Results suggested that the ceramide/PP2A/Akt axis is involved in the apoptosis and a possible cyclooxygenase-independent target for indomethacin.	Ceramides	27-35	AKT serine/threonine kinase 1	Homo sapiens	41-44
29378782-1	2018	Activation of the lysosomal ceramide-producing enzyme, acid sphingomyelinase (ASM), by various stresses is centrally involved in cell death and has been implicated in autophagy.	Ceramides	28-36	sphingomyelin phosphodiesterase 1	Homo sapiens	55-76
29395144-0	2018	Hot topic: Ceramide inhibits insulin sensitivity in primary bovine adipocytes.	Ceramides	11-19	insulin	Bos taurus	29-36
29395144-3	2018	We hypothesized that ceramide promotes AKT inactivation and antagonizes insulin sensitivity in primary bovine adipocytes.	Ceramides	21-29	AKT serine/threonine kinase 1	Bos taurus	39-42
29395144-3	2018	We hypothesized that ceramide promotes AKT inactivation and antagonizes insulin sensitivity in primary bovine adipocytes.	Ceramides	21-29	insulin	Bos taurus	72-79
29395144-10	2018	We conclude that ceramide inhibits insulin-stimulated glucose uptake by downregulating AKT activation in primary bovine adipocytes.	Ceramides	17-25	insulin	Bos taurus	35-42
29395144-10	2018	We conclude that ceramide inhibits insulin-stimulated glucose uptake by downregulating AKT activation in primary bovine adipocytes.	Ceramides	17-25	AKT serine/threonine kinase 1	Bos taurus	87-90
29378782-1	2018	Activation of the lysosomal ceramide-producing enzyme, acid sphingomyelinase (ASM), by various stresses is centrally involved in cell death and has been implicated in autophagy.	Ceramides	28-36	sphingomyelin phosphodiesterase 1	Homo sapiens	78-81
29378782-5	2018	Pulse labeling of sphingolipid metabolites revealed that ASM inhibition markedly decreased sphingosine (Sph) and Sph-1-phosphate (S1P) levels at the level of ceramide hydrolysis.	Ceramides	158-166	sphingomyelin phosphodiesterase 1	Homo sapiens	57-60
29242171-2	2018	Although stearoyl-CoA desaturase 1 (SCD1) is expected to relieve palmitic acid (PA)-induced lipotoxicity by regulating diacylglycerol and ceramide, its function is unclear in human trophoblast cells.	Ceramides	138-146	stearoyl-CoA desaturase	Homo sapiens	9-34
29242171-2	2018	Although stearoyl-CoA desaturase 1 (SCD1) is expected to relieve palmitic acid (PA)-induced lipotoxicity by regulating diacylglycerol and ceramide, its function is unclear in human trophoblast cells.	Ceramides	138-146	stearoyl-CoA desaturase	Homo sapiens	36-40
29514098-6	2018	Collectively, these data suggest that high ceramide-associated lipotoxicity is mediated, in part, through altering caspase activation, sarcomeric maintenance, and lipogenesis, thus providing evidence for conserved mechanisms in LCM pathogenesis in mammals.	Ceramides	43-51	Death caspase-1	Drosophila melanogaster	115-122
29536159-11	2018	Our data also suggest that Zpbp2 may act through regulation of ceramide metabolism.	Ceramides	63-71	zona pellucida binding protein 2	Mus musculus	27-32
28042036-8	2018	We confirmed that our SPT inhibitors suppressed ceramide content in non-small-cell lung cancer cell line, HCC4006, by performing a target engagement analysis.	Ceramides	48-56	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	22-25
28042036-9	2018	The potency of ceramide reduction correlated to that observed in a recombinant SPT2 enzyme assay.	Ceramides	15-23	SPT2 chromatin protein domain containing 1	Homo sapiens	79-83
29438993-4	2018	Besides other enzymes involved in sphingolipid synthesis and intermembrane transfer of ceramide, and putative redox partners of FA2H, progesterone receptor membrane component-1 (PGRMC1) and PGRMC2 were identified as putative interaction partners.	Ceramides	87-95	progesterone receptor membrane component 1	Homo sapiens	134-176
29438993-4	2018	Besides other enzymes involved in sphingolipid synthesis and intermembrane transfer of ceramide, and putative redox partners of FA2H, progesterone receptor membrane component-1 (PGRMC1) and PGRMC2 were identified as putative interaction partners.	Ceramides	87-95	progesterone receptor membrane component 2	Homo sapiens	190-196
29438993-7	2018	Moreover, the PGRMC1 inhibitor AG-205 significantly reduced synthesis of hydroxylated ceramide and glucosylceramide in FA2H-expressing cells.	Ceramides	86-94	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.	Ceramides	86-94	fatty acid 2-hydroxylase	Homo sapiens	119-123
29229528-2	2018	In the milk fat globule membrane (MFGM), ceramides are susceptible to affect the lateral packing of polar lipids, especially the milk sphingomyelin (MSM).	Ceramides	41-50	milk fat globule EGF and factor V/VIII domain containing	Homo sapiens	34-38
29229528-7	2018	These results bring new insights on the role of ceramides in the control of biophysical and biological properties of the MFGM.	Ceramides	48-57	milk fat globule EGF and factor V/VIII domain containing	Homo sapiens	121-125
29321137-1	2018	We reported that amyloid beta peptide (Abeta42) activated neutral SMase 2 (nSMase2), thereby increasing the concentration of the sphingolipid ceramide in astrocytes.	Ceramides	142-150	amyloid beta precursor protein	Homo sapiens	17-29
29127192-2	2018	One class of these, the ceramides, constitutes a family of molecules that differ in structure and are synthesized by distinct enzymes, ceramide synthase (CerS)1-CerS6.	Ceramides	24-33	ceramide synthase 1	Mus musculus	154-160
29127192-2	2018	One class of these, the ceramides, constitutes a family of molecules that differ in structure and are synthesized by distinct enzymes, ceramide synthase (CerS)1-CerS6.	Ceramides	24-33	ceramide synthase 6	Mus musculus	161-166
29127192-4	2018	In a mouse model of diabetic cardiomyopathy, sphingolipid profiling revealed increases in not only the CerS5-derived ceramides but also in very long chain (VLC) ceramides derived from CerS2.	Ceramides	117-126	ceramide synthase 5	Mus musculus	103-108
29127192-4	2018	In a mouse model of diabetic cardiomyopathy, sphingolipid profiling revealed increases in not only the CerS5-derived ceramides but also in very long chain (VLC) ceramides derived from CerS2.	Ceramides	161-170	ceramide synthase 2	Mus musculus	184-189
29127192-5	2018	Overexpression of CerS2 elevated VLC ceramides caused insulin resistance, oxidative stress, mitochondrial dysfunction, and mitophagy.	Ceramides	37-46	ceramide synthase 2	Mus musculus	18-23
29133339-4	2018	Here, we show that Hsp27 knockout mice demonstrated decreases in ceramide in peripheral nerve tissue and that the disease-associated Hsp27 S135F mutant demonstrated decreases in mitochondrial ceramide.	Ceramides	65-73	heat shock protein 2	Mus musculus	19-24
29133339-4	2018	Here, we show that Hsp27 knockout mice demonstrated decreases in ceramide in peripheral nerve tissue and that the disease-associated Hsp27 S135F mutant demonstrated decreases in mitochondrial ceramide.	Ceramides	192-200	heat shock protein 2	Mus musculus	133-138
29133339-5	2018	Given that Hsp27 is a chaperone protein, we examined its role in regulating ceramide synthases (CerSs), an enzyme family responsible for catalyzing generation of the sphingolipid ceramide.	Ceramides	76-84	heat shock protein 2	Mus musculus	11-16
29133339-6	2018	We determined that CerSs colocalized with Hsp27, and upon the presence of S135F mutants, CerS1 lost its colocalization with mitochondria suggesting that decreased mitochondrial ceramides result from reduced mitochondrial CerS localization rather than decreased CerS activity.	Ceramides	177-186	ceramide synthase 1	Mus musculus	89-94
29133339-10	2018	These results suggest that mutant Hsp27 decreases mitochondrial ceramide levels, producing structural and functional changes in mitochondria leading to neuronal degeneration.-Schwartz, N. U., Linzer, R. W., Truman, J.-P., Gurevich, M., Hannun, Y.	Ceramides	64-72	heat shock protein 2	Mus musculus	34-39
29343537-0	2018	A search for ceramide binding proteins using bifunctional lipid analogs yields CERT-related protein StarD7.	Ceramides	13-21	ceramide transporter 1	Homo sapiens	79-83
29321137-1	2018	We reported that amyloid beta peptide (Abeta42) activated neutral SMase 2 (nSMase2), thereby increasing the concentration of the sphingolipid ceramide in astrocytes.	Ceramides	142-150	sphingomyelin phosphodiesterase 3	Homo sapiens	58-73
29343537-0	2018	A search for ceramide binding proteins using bifunctional lipid analogs yields CERT-related protein StarD7.	Ceramides	13-21	StAR related lipid transfer domain containing 7	Homo sapiens	100-106
29343537-6	2018	Combining site-directed mutagenesis and photoaffinity labeling experiments, we demonstrate that the steroidogenic acute regulatory transfer domain of StarD7 harbors a common binding site for PC and ceramide.	Ceramides	198-206	StAR related lipid transfer domain containing 7	Homo sapiens	150-156
29321137-1	2018	We reported that amyloid beta peptide (Abeta42) activated neutral SMase 2 (nSMase2), thereby increasing the concentration of the sphingolipid ceramide in astrocytes.	Ceramides	142-150	sphingomyelin phosphodiesterase 3	Homo sapiens	75-82
29343537-7	2018	While StarD7 lacks robust ceramide transfer activity in vitro, we find that its ability to shuttle PC between model membranes is specifically affected by ceramides.	Ceramides	154-163	StAR related lipid transfer domain containing 7	Homo sapiens	6-12
29343537-8	2018	Besides demonstrating the suitability of pacCer as a tool to hunt for ceramide binding proteins, our data point at StarD7 as a candidate effector protein by which ceramides may exert part of their mitochondria-mediated cytotoxic effects.	Ceramides	163-172	StAR related lipid transfer domain containing 7	Homo sapiens	115-121
29321137-6	2018	Ceramide-associated tubulin (CAT) translocated from the perinuclear region to peripheral CEMAMs and mitochondria, which was prevented in nSMase2-deficient or FB1-treated astrocytes.	Ceramides	0-8	sphingomyelin phosphodiesterase 3	Homo sapiens	137-144
29321137-7	2018	Proximity ligation and coimmunoprecipitation assays showed that ceramide depletion reduced association of tubulin with voltage-dependent anion channel 1 (VDAC1), an interaction known to block mitochondrial ADP/ATP transport.	Ceramides	64-72	voltage dependent anion channel 1	Homo sapiens	119-152
29321137-7	2018	Proximity ligation and coimmunoprecipitation assays showed that ceramide depletion reduced association of tubulin with voltage-dependent anion channel 1 (VDAC1), an interaction known to block mitochondrial ADP/ATP transport.	Ceramides	64-72	voltage dependent anion channel 1	Homo sapiens	154-159
29321137-8	2018	Ceramide-depleted astrocytes contained higher levels of ATP, suggesting that ceramide-induced CAT formation leads to VDAC1 closure, thereby reducing mitochondrial ATP release, and potentially motility and resistance to Abeta42 Our data also indicate that inhibiting ceramide generation may protect mitochondria in Alzheimer"s disease.	Ceramides	0-8	voltage dependent anion channel 1	Homo sapiens	117-122
29321137-8	2018	Ceramide-depleted astrocytes contained higher levels of ATP, suggesting that ceramide-induced CAT formation leads to VDAC1 closure, thereby reducing mitochondrial ATP release, and potentially motility and resistance to Abeta42 Our data also indicate that inhibiting ceramide generation may protect mitochondria in Alzheimer"s disease.	Ceramides	77-85	voltage dependent anion channel 1	Homo sapiens	117-122
29321137-8	2018	Ceramide-depleted astrocytes contained higher levels of ATP, suggesting that ceramide-induced CAT formation leads to VDAC1 closure, thereby reducing mitochondrial ATP release, and potentially motility and resistance to Abeta42 Our data also indicate that inhibiting ceramide generation may protect mitochondria in Alzheimer"s disease.	Ceramides	266-274	voltage dependent anion channel 1	Homo sapiens	117-122
29463805-0	2018	Ceramide-induced BOK promotes mitochondrial fission in preeclampsia.	Ceramides	0-8	BCL2 family apoptosis regulator BOK	Homo sapiens	17-20
29359558-3	2018	We find that a C16-PEG(2000 Da)-ceramide causes a 62% fluorescent intensity decrease of the (10,2) chirality nanotube in the presence of 20 mug/mL insulin.	Ceramides	32-40	insulin	Homo sapiens	147-154
29359558-4	2018	The insulin protein has no prior affinity toward the C16-PEG(2000 Da)-ceramide molecules in free solution, verified by isothermal titration calorimetry, and the interaction occurs only upon their adsorption onto the single-walled carbon nanotube scaffolds.	Ceramides	70-78	insulin	Homo sapiens	4-11
29421659-4	2018	We also demonstrate that RIP2 confers TNBC cell resistance against paclitaxel and ceramide-induced apoptosis.	Ceramides	82-90	receptor interacting serine/threonine kinase 2	Homo sapiens	25-29
29415895-7	2018	Sarcolemmal ceramides were inversely related to insulin sensitivity, with a significant relationship found for the C18:0 species.	Ceramides	12-21	insulin	Homo sapiens	48-55
29415895-9	2018	In the mitochondrial/ER and nuclear fractions, 1,2-DAGs were positively related to, while ceramides were inversely related to, insulin sensitivity.	Ceramides	90-99	insulin	Homo sapiens	127-134
28988346-13	2018	Palmitate or C2 ceramide induced ER stress in macrophages as well as increased expression of TXNIP, NLRP3 and IL-1beta.	Ceramides	16-24	thioredoxin interacting protein	Homo sapiens	93-98
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.	Ceramides	122-131	proprotein convertase subtilisin/kexin type 9	Homo sapiens	9-14
29277967-5	2018	Additionally, SM1044 also stimulates the de novo synthesis of ceramide, which in turn activates the CaMKK2-AMPK-ULK1 axis, leading to the initiation of autophagy.	Ceramides	62-70	calcium/calmodulin dependent protein kinase kinase 2	Homo sapiens	100-106
29277967-5	2018	Additionally, SM1044 also stimulates the de novo synthesis of ceramide, which in turn activates the CaMKK2-AMPK-ULK1 axis, leading to the initiation of autophagy.	Ceramides	62-70	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	107-111
29277967-5	2018	Additionally, SM1044 also stimulates the de novo synthesis of ceramide, which in turn activates the CaMKK2-AMPK-ULK1 axis, leading to the initiation of autophagy.	Ceramides	62-70	unc-51 like autophagy activating kinase 1	Homo sapiens	112-116
29437853-9	2018	Immunoblotting analysis indicated that ceramide stretch-induced apoptosis in SMC is accompanied by a decrease in the phosphorylation status of both Fak and Akt, leading to an increase in Bax expression and caspase-3 cleavage.	Ceramides	39-47	protein tyrosine kinase 2	Rattus norvegicus	148-151
29437853-9	2018	Immunoblotting analysis indicated that ceramide stretch-induced apoptosis in SMC is accompanied by a decrease in the phosphorylation status of both Fak and Akt, leading to an increase in Bax expression and caspase-3 cleavage.	Ceramides	39-47	AKT serine/threonine kinase 1	Rattus norvegicus	156-159
29437853-9	2018	Immunoblotting analysis indicated that ceramide stretch-induced apoptosis in SMC is accompanied by a decrease in the phosphorylation status of both Fak and Akt, leading to an increase in Bax expression and caspase-3 cleavage.	Ceramides	39-47	BCL2 associated X, apoptosis regulator	Rattus norvegicus	187-190
29437853-9	2018	Immunoblotting analysis indicated that ceramide stretch-induced apoptosis in SMC is accompanied by a decrease in the phosphorylation status of both Fak and Akt, leading to an increase in Bax expression and caspase-3 cleavage.	Ceramides	39-47	caspase 3	Rattus norvegicus	206-215
28988346-13	2018	Palmitate or C2 ceramide induced ER stress in macrophages as well as increased expression of TXNIP, NLRP3 and IL-1beta.	Ceramides	16-24	NLR family pyrin domain containing 3	Homo sapiens	100-105
28988346-13	2018	Palmitate or C2 ceramide induced ER stress in macrophages as well as increased expression of TXNIP, NLRP3 and IL-1beta.	Ceramides	16-24	interleukin 1 beta	Homo sapiens	110-118
29282302-4	2018	A sphingolipid profile showed elevations of ceramide species and sphingosine that were preventable by inhibiting of an acid sphingomyelinase (ASM) activity.	Ceramides	44-52	sphingomyelin phosphodiesterase 1	Homo sapiens	119-140
29272817-0	2018	Fatty acid transport protein 1 enhances the macrophage inflammatory response by coupling with ceramide and c-Jun N-terminal kinase signaling.	Ceramides	94-102	solute carrier family 27 (fatty acid transporter), member 1	Mus musculus	0-30
29272817-8	2018	Forced expression of FATP1 enhanced production of inflammatory cytokines, such as TNFalpha and IL-6 concomitant with the increased uptake of fatty acids, increased level of ceramide, and increased phosphorylation of c-Jun N-terminal kinase (JNK).	Ceramides	173-181	solute carrier family 27 (fatty acid transporter), member 1	Mus musculus	21-26
29272817-9	2018	The enhancement by FATP1 was abolished by treatment with a JNK inhibitor, NF-kappaB inhibitor, or ceramide synthesis inhibitor.	Ceramides	98-106	solute carrier family 27 (fatty acid transporter), member 1	Mus musculus	19-24
29272817-14	2018	Our findings suggest that ceramide-JNK signaling is important to terminate or sustain inflammation.	Ceramides	26-34	mitogen-activated protein kinase 8	Mus musculus	35-38
29214724-0	2018	CME-1, a novel polysaccharide, suppresses iNOS expression in lipopolysaccharide-stimulated macrophages through ceramide-initiated protein phosphatase 2A activation.	Ceramides	111-119	nitric oxide synthase 2, inducible	Mus musculus	42-46
29214724-0	2018	CME-1, a novel polysaccharide, suppresses iNOS expression in lipopolysaccharide-stimulated macrophages through ceramide-initiated protein phosphatase 2A activation.	Ceramides	111-119	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	138-152
29214724-7	2018	Moreover, CME-1-induced PP2A activation and its subsequent suppression of LPS-activated RAW 264.7 cells were diminished by the inhibition of ceramide signals.	Ceramides	141-149	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	24-28
29214724-10	2018	In conclusion, CME-1 suppressed iNOS expression by up-regulating ceramide-induced PP2A activation and reducing ROS production in LPS-stimulated macrophages.	Ceramides	65-73	nitric oxide synthase 2, inducible	Mus musculus	32-36
29214724-10	2018	In conclusion, CME-1 suppressed iNOS expression by up-regulating ceramide-induced PP2A activation and reducing ROS production in LPS-stimulated macrophages.	Ceramides	65-73	protein phosphatase 2, regulatory subunit A, alpha	Mus musculus	82-86
29282302-4	2018	A sphingolipid profile showed elevations of ceramide species and sphingosine that were preventable by inhibiting of an acid sphingomyelinase (ASM) activity.	Ceramides	44-52	sphingomyelin phosphodiesterase 1	Homo sapiens	142-145
29379059-12	2018	Taken together, targeting a reduction of MCP-1 opens the door to a better understanding of the mechanistic consequences of ceramide accumulation and may even delay the progression of FD in some organ systems.	Ceramides	123-131	C-C motif chemokine ligand 2	Homo sapiens	41-46
28970356-6	2018	The increases in SS C24 ceramides were negatively related to parameters of insulin resistance.	Ceramides	24-33	insulin	Homo sapiens	75-82
28842833-3	2018	The discoveries that plasma Cer concentration increase during depressive episodes in patients and that tricyclic and tetracyclic antidepressants functionally inhibit acid sphingomyelinase (ASM), the enzyme that catalyzes the degradation of sphingomyelin to Cer, have initiated a series of studies on the role of the ASM-Cer system in depressive disorder.	Ceramides	28-31	sphingomyelin phosphodiesterase 1	Homo sapiens	189-192
29610685-7	2018	During the development of IR injury, the initial response of ROS and TNF-alpha production activates two major ceramide generating pathways (sphingomyelin hydrolysis and de novo ceramide synthesis).	Ceramides	110-118	tumor necrosis factor	Homo sapiens	69-78
29610685-7	2018	During the development of IR injury, the initial response of ROS and TNF-alpha production activates two major ceramide generating pathways (sphingomyelin hydrolysis and de novo ceramide synthesis).	Ceramides	177-185	tumor necrosis factor	Homo sapiens	69-78
30060809-8	2018	This complex relationship is based on several molecular mechanisms including the p53-dependent transcriptional regulation of enzymes in sphingolipid pathways, the activation of mutant p53 through ceramide-mediated alternative splicing, as well as modulation of the p53 function through direct and indirect effects on p53 coregulators and downstream targets.	Ceramides	196-204	tumor protein p53	Homo sapiens	184-187
29342149-11	2018	Low levels of muscle IL-18 mRNA correlated to high levels of ceramides (r = -0.31, p = 0.038) and sphingosine-1P (r = -0.29, p = 0.046) in skeletal muscle, whereas such a correlation was not found in healthy controls.	Ceramides	61-70	interleukin 18	Homo sapiens	21-26
30060808-5	2018	Insulin sensitivity, de novo lipogenesis, and the resulting lipotoxicity, fibrosis, and angiogenesis are all seemingly regulated in a manner that involves either ceramide and/or sphingosine-1-phosphate.	Ceramides	162-170	insulin	Homo sapiens	0-7
29507692-4	2018	ASMase activation triggers ceramide-mediated apoptosis, and therein microvascular dysfunction, which increased the vulnerability of tumor cells to lethal damage by radiation.	Ceramides	27-35	sphingomyelin phosphodiesterase 1	Homo sapiens	0-6
28968647-2	2018	Sphingosine kinase 1 (SphK1) is a key metabolic enzyme for the formation of pro-survival S1P from pro-apoptotic ceramide.	Ceramides	112-120	sphingosine kinase 1	Homo sapiens	0-20
28968647-2	2018	Sphingosine kinase 1 (SphK1) is a key metabolic enzyme for the formation of pro-survival S1P from pro-apoptotic ceramide.	Ceramides	112-120	sphingosine kinase 1	Homo sapiens	22-27
28968647-2	2018	Sphingosine kinase 1 (SphK1) is a key metabolic enzyme for the formation of pro-survival S1P from pro-apoptotic ceramide.	Ceramides	112-120	membrane bound transcription factor peptidase, site 1	Homo sapiens	89-92
30060809-1	2018	Ceramides, important players in signal transduction, interact with multiple cellular pathways, including p53 pathways.	Ceramides	0-9	tumor protein p53	Homo sapiens	105-108
30060809-8	2018	This complex relationship is based on several molecular mechanisms including the p53-dependent transcriptional regulation of enzymes in sphingolipid pathways, the activation of mutant p53 through ceramide-mediated alternative splicing, as well as modulation of the p53 function through direct and indirect effects on p53 coregulators and downstream targets.	Ceramides	196-204	tumor protein p53	Homo sapiens	184-187
30060809-2	2018	However, the relationship between ceramide and p53 is very complex, and mechanisms underlying their coregulation are diverse and not fully characterized.	Ceramides	34-42	tumor protein p53	Homo sapiens	47-50
30060809-7	2018	We discuss the recent studies, which underscore the function of p53 in the regulation of ceramide pathways and the reciprocal regulation of p53 by ceramide.	Ceramides	89-97	tumor protein p53	Homo sapiens	64-67
30362095-8	2018	Additionally, expression of acid ceramidase and sphingosine kinase 1 which degrade ceramide into sphingosine and convert sphingosine to sphingosine-1-phosphate (S1P) respectively and expression of S1P receptors S1PR2 and S1PR3 were all upregulated by EtOH and suppressed in the EtOH/SOY group, p &lt; 0.05.	Ceramides	83-91	N-acylsphingosine amidohydrolase 1	Mus musculus	28-43
30362095-8	2018	Additionally, expression of acid ceramidase and sphingosine kinase 1 which degrade ceramide into sphingosine and convert sphingosine to sphingosine-1-phosphate (S1P) respectively and expression of S1P receptors S1PR2 and S1PR3 were all upregulated by EtOH and suppressed in the EtOH/SOY group, p &lt; 0.05.	Ceramides	83-91	sphingosine kinase 1	Mus musculus	48-68
30060809-7	2018	We discuss the recent studies, which underscore the function of p53 in the regulation of ceramide pathways and the reciprocal regulation of p53 by ceramide.	Ceramides	147-155	tumor protein p53	Homo sapiens	140-143
30060809-8	2018	This complex relationship is based on several molecular mechanisms including the p53-dependent transcriptional regulation of enzymes in sphingolipid pathways, the activation of mutant p53 through ceramide-mediated alternative splicing, as well as modulation of the p53 function through direct and indirect effects on p53 coregulators and downstream targets.	Ceramides	196-204	tumor protein p53	Homo sapiens	184-187
29025713-0	2018	Neutrophil elastase increases airway ceramide levels via upregulation of serine palmitoyltransferase.	Ceramides	37-45	elastase, neutrophil expressed	Mus musculus	0-19
29023248-1	2018	Acid ceramidase is the key enzyme of the ceramide metabolic pathway, which plays a vital role in regulating ceramide - sphingosine-1-phosphate rheostat.	Ceramides	41-49	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
29025713-9	2018	Myriocin decreased BAL d18:1/22:0 and d18:1/24:1 ceramide, KC, and HMGB1 induced by NE exposure.	Ceramides	49-57	elastase, neutrophil expressed	Mus musculus	84-86
29025713-10	2018	These results support a feed-forward cycle of NE-generated ceramide and ceramide-driven cytokine signaling that may be a potential target for intervention in lung disease typified by chronic neutrophilic inflammation.	Ceramides	59-67	elastase, neutrophil expressed	Mus musculus	46-48
29023248-1	2018	Acid ceramidase is the key enzyme of the ceramide metabolic pathway, which plays a vital role in regulating ceramide - sphingosine-1-phosphate rheostat.	Ceramides	108-116	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
29709911-6	2018	These results indicated that sphingoid bases and ceramide upregulated caspase-14 mRNA to increase intracellular caspase-14 protein level.	Ceramides	49-57	caspase 14	Homo sapiens	70-80
29709911-6	2018	These results indicated that sphingoid bases and ceramide upregulated caspase-14 mRNA to increase intracellular caspase-14 protein level.	Ceramides	49-57	caspase 14	Homo sapiens	112-122
29709917-2	2018	Ceramide kinase (CerK) catalyzes the phosphorylation of ceramide to ceramide-1-phosphate (C1P).	Ceramides	56-64	ceramide kinase	Mus musculus	0-15
29709917-2	2018	Ceramide kinase (CerK) catalyzes the phosphorylation of ceramide to ceramide-1-phosphate (C1P).	Ceramides	56-64	ceramide kinase	Mus musculus	17-21
30504725-10	2018	CONCLUSION: The findings indicate that the Nsm2/ ceramide system plays an important role in systemic infection of mice with mycobacteria by regulating a signaling cascade via p38K, JNK, b1-integrin and Rac1.	Ceramides	49-57	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	43-47
30504725-10	2018	CONCLUSION: The findings indicate that the Nsm2/ ceramide system plays an important role in systemic infection of mice with mycobacteria by regulating a signaling cascade via p38K, JNK, b1-integrin and Rac1.	Ceramides	49-57	mitogen-activated protein kinase 8	Mus musculus	181-184
30504725-10	2018	CONCLUSION: The findings indicate that the Nsm2/ ceramide system plays an important role in systemic infection of mice with mycobacteria by regulating a signaling cascade via p38K, JNK, b1-integrin and Rac1.	Ceramides	49-57	Rac family small GTPase 1	Mus musculus	202-206
29153923-0	2018	Macrophages sensing oxidized DAMPs reprogram their metabolism to support redox homeostasis and inflammation through a TLR2-Syk-ceramide dependent mechanism.	Ceramides	127-135	toll like receptor 2	Homo sapiens	118-122
29660940-8	2018	However, ceramide, sphingomyelin, and sulfatide content was very significantly correlated with age in the hippocampus of males.	Ceramides	9-17	renin binding protein	Homo sapiens	95-98
29660940-11	2018	Ceramide is a pro-apoptotic lipid, and heavily implicated as a driver of insulin resistance in metabolic tissues.	Ceramides	0-8	insulin	Homo sapiens	73-80
29238029-0	2018	Characterization of Konjac Ceramide (kCer) Binding to Sema3A Receptor Nrp1.	Ceramides	27-35	semaphorin 3A	Homo sapiens	54-60
29238029-0	2018	Characterization of Konjac Ceramide (kCer) Binding to Sema3A Receptor Nrp1.	Ceramides	27-35	neuropilin 1	Homo sapiens	70-74
29079707-0	2018	Ceramide Nanoliposomes as a MLKL-Dependent, Necroptosis-Inducing, Chemotherapeutic Reagent in Ovarian Cancer.	Ceramides	0-8	mixed lineage kinase domain like pseudokinase	Homo sapiens	28-32
29079707-9	2018	Taken together, these results suggest that MLKL is a novel pronecroptotic target for ceramide in ovarian cancer models.	Ceramides	85-93	mixed lineage kinase domain like pseudokinase	Homo sapiens	43-47
28864659-1	2018	Perilipin 2 (PLIN2) is a lipid-droplet protein that is up-regulated in alcoholic steatosis and associated with hepatic accumulation of ceramides, bioactive lipids implicated in alcoholic liver disease pathogenesis.	Ceramides	135-144	perilipin 2	Homo sapiens	0-11
28864659-1	2018	Perilipin 2 (PLIN2) is a lipid-droplet protein that is up-regulated in alcoholic steatosis and associated with hepatic accumulation of ceramides, bioactive lipids implicated in alcoholic liver disease pathogenesis.	Ceramides	135-144	perilipin 2	Homo sapiens	13-18
28864659-2	2018	The specific role of ceramide synthetic enzymes in the regulation of PLIN2 and promotion of hepatocellular lipid accumulation is not well understood.	Ceramides	21-29	perilipin 2	Homo sapiens	69-74
28864659-6	2018	In vivo ceramide reduction by inhibition of de novo ceramide synthesis reduced PLIN2 and hepatic steatosis in alcohol-fed mice, but only de novo synthesis inhibition, not sphingomyelin hydrolysis, improved glucose tolerance and dyslipidemia.	Ceramides	8-16	predicted gene 12551	Mus musculus	79-84
28864659-6	2018	In vivo ceramide reduction by inhibition of de novo ceramide synthesis reduced PLIN2 and hepatic steatosis in alcohol-fed mice, but only de novo synthesis inhibition, not sphingomyelin hydrolysis, improved glucose tolerance and dyslipidemia.	Ceramides	52-60	predicted gene 12551	Mus musculus	79-84
29103713-3	2018	Moreover, elevated circulating FAC and ceramide concentrations are inversely related to insulin action.	Ceramides	39-47	insulin	Bos taurus	88-95
29103713-14	2018	Our results support on-going efforts to determine whether altered mitochondrial FA processing promotes the accumulation of the insulin resistance biomarker ceramide in blood and liver.	Ceramides	156-164	insulin	Bos taurus	127-134
29153923-0	2018	Macrophages sensing oxidized DAMPs reprogram their metabolism to support redox homeostasis and inflammation through a TLR2-Syk-ceramide dependent mechanism.	Ceramides	127-135	spleen associated tyrosine kinase	Homo sapiens	123-126
29153923-7	2018	Mechanistically, we show that OxPL suppress mitochondrial respiration via TLR2-dependent ceramide production, redirecting TCA metabolites to GSH synthesis.	Ceramides	89-97	toll like receptor 2	Homo sapiens	74-78
29153923-8	2018	Finally, we identify spleen tyrosine kinase (Syk) as a critical downstream signaling mediator that translates OxPL-induced effects into ceramide production and inflammatory gene regulation.	Ceramides	136-144	spleen associated tyrosine kinase	Homo sapiens	45-48
29046397-5	2017	Manipulating levels of ceramidase and altering these lipids in spin mutants allowed us to conclude that ceramide homeostasis is the driving force in disease progression and is integral to spin function in the adult nervous system.	Ceramides	104-112	spinster	Drosophila melanogaster	63-67
29147025-5	2018	Moreover, the metabolism of ceramide for S1P biosynthesis, which is mediated by sphingosine kinase 1 and 2, and its role in influencing cancer cell growth, drug resistance and tumour metastasis through S1PR-dependent or receptor-independent signalling are highlighted.	Ceramides	28-36	sphingosine kinase 1	Homo sapiens	80-106
29272311-12	2017	One or more of these altered genes may be involved in p53-dependent ceramide accumulation.	Ceramides	68-76	tumor protein p53	Homo sapiens	54-57
29046397-5	2017	Manipulating levels of ceramidase and altering these lipids in spin mutants allowed us to conclude that ceramide homeostasis is the driving force in disease progression and is integral to spin function in the adult nervous system.	Ceramides	104-112	spinster	Drosophila melanogaster	188-192
28940479-0	2017	Activation of the NLRP3 inflammasome in microglia: the role of ceramide.	Ceramides	63-71	NLR family pyrin domain containing 3	Homo sapiens	18-23
28933423-8	2017	The decrease in hepatic lipid accumulation was mainly due to reduced hepatic levels of ceramides, which was partly the result of the lower expression of ceramide synthesis genes, Sptlc3 and Degs2.	Ceramides	87-96	serine palmitoyltransferase, long chain base subunit 3	Mus musculus	179-185
28933423-8	2017	The decrease in hepatic lipid accumulation was mainly due to reduced hepatic levels of ceramides, which was partly the result of the lower expression of ceramide synthesis genes, Sptlc3 and Degs2.	Ceramides	87-96	delta(4)-desaturase, sphingolipid 2	Mus musculus	190-195
28933423-8	2017	The decrease in hepatic lipid accumulation was mainly due to reduced hepatic levels of ceramides, which was partly the result of the lower expression of ceramide synthesis genes, Sptlc3 and Degs2.	Ceramides	87-95	serine palmitoyltransferase, long chain base subunit 3	Mus musculus	179-185
28933423-8	2017	The decrease in hepatic lipid accumulation was mainly due to reduced hepatic levels of ceramides, which was partly the result of the lower expression of ceramide synthesis genes, Sptlc3 and Degs2.	Ceramides	87-95	delta(4)-desaturase, sphingolipid 2	Mus musculus	190-195
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).	Ceramides	117-126	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).	Ceramides	117-126	glucosylceramidase beta	Homo sapiens	35-39
28806500-2	2017	Acid sphingomyelinase (ASM) catalyzes generation of ceramide (Cer) which if over-activated mediates neuronal disorders in various diseases.	Ceramides	52-60	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
28806500-2	2017	Acid sphingomyelinase (ASM) catalyzes generation of ceramide (Cer) which if over-activated mediates neuronal disorders in various diseases.	Ceramides	52-60	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
28806500-2	2017	Acid sphingomyelinase (ASM) catalyzes generation of ceramide (Cer) which if over-activated mediates neuronal disorders in various diseases.	Ceramides	62-65	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
28806500-2	2017	Acid sphingomyelinase (ASM) catalyzes generation of ceramide (Cer) which if over-activated mediates neuronal disorders in various diseases.	Ceramides	62-65	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
28940479-6	2017	Here, we investigated potential mechanistic links between ceramide as a modulator of NLRP3 inflammasome assembly and the resulting secretion of IL-1beta using small bioactive enzyme stimulators and inhibitors of ceramide signaling in wild-type and apoptosis-associated speck-like protein containing a CARD knockout (ASC-/- ) primary microglia.	Ceramides	58-66	interleukin 1 beta	Homo sapiens	144-152
28940479-8	2017	Treatment with sodium palmitate (PA) induced de novo ceramide synthesis via modulation of its synthesizing protein serine palmitoyl transferase resulting in increased IL-1beta secretion in microglia.	Ceramides	53-61	interleukin 1 beta	Homo sapiens	167-175
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Ceramides	19-27	interleukin 1 beta	Homo sapiens	132-140
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Ceramides	19-27	caspase 1	Homo sapiens	153-162
28940479-10	2017	Application of the ceramide analogue C2 and the sphingosine-1-phosphate-receptor agonist Fingolimod (FTY720) up-regulated levels of IL-1beta and cleaved caspase-1 in wild-type microglia, whereas ASC-/- microglia were unaffected.	Ceramides	19-27	PYD and CARD domain containing	Homo sapiens	195-198
28940479-12	2017	Taken together, our findings reveal a critical role for ceramide as a positive modulator of NLRP3 inflammasome assembly and the resulting release of IL-1beta.	Ceramides	56-64	NLR family pyrin domain containing 3	Homo sapiens	92-97
28940479-12	2017	Taken together, our findings reveal a critical role for ceramide as a positive modulator of NLRP3 inflammasome assembly and the resulting release of IL-1beta.	Ceramides	56-64	interleukin 1 beta	Homo sapiens	149-157
28940479-5	2017	Growing evidence suggests that ceramide plays a critical role in NLRP3 inflammasome assembly, however, the relationship between ceramide and inflammasome activation in microglia remains unknown.	Ceramides	31-39	NLR family pyrin domain containing 3	Homo sapiens	65-70
28940479-6	2017	Here, we investigated potential mechanistic links between ceramide as a modulator of NLRP3 inflammasome assembly and the resulting secretion of IL-1beta using small bioactive enzyme stimulators and inhibitors of ceramide signaling in wild-type and apoptosis-associated speck-like protein containing a CARD knockout (ASC-/- ) primary microglia.	Ceramides	58-66	NLR family pyrin domain containing 3	Homo sapiens	85-90
28939554-2	2017	Sphingosine kinase 2 (SphK2) is a key factor within sphingolipid metabolism, responsible for the conversion of proapoptotic ceramides to antiapoptotic sphingosine-1-phosphate (S1P).	Ceramides	124-133	sphingosine kinase 2	Homo sapiens	0-20
28939554-2	2017	Sphingosine kinase 2 (SphK2) is a key factor within sphingolipid metabolism, responsible for the conversion of proapoptotic ceramides to antiapoptotic sphingosine-1-phosphate (S1P).	Ceramides	124-133	sphingosine kinase 2	Homo sapiens	22-27
28939554-3	2017	We have previously demonstrated that targeting SphK2 using a novel selective inhibitor, ABC294640, leads to the accumulation of intracellular ceramides and induces apoptosis in KSHV-infected primary endothelial cells and PEL tumor cells but not in uninfected cells.	Ceramides	142-151	sphingosine kinase 2	Homo sapiens	47-52
28875582-9	2017	CONCLUSION: Most of the effects of FB1 are mediated by the regulation of ceramide level, which influences protein phosphatase 2 (PP2A) and the phosphoinositide 3-kinase (PI3K)/AKT signaling pathway.	Ceramides	73-81	AKT serine/threonine kinase 1	Sus scrofa	176-179
29071793-6	2017	Overfeeding resulted in inhibition of Akt activity, which correlated with the reductions in smaller, peripherally located lipid droplets and drastic increases in ceramide content.	Ceramides	162-170	AKT serine/threonine kinase 1	Homo sapiens	38-41
29238000-1	2017	Acid sphingomyelinase (ASM) is a lysosomal enzyme that hydrolyzes sphingomyelin into ceramide, a bioactive lipid to regulate cellular physiological functions.	Ceramides	85-93	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
29282180-2	2017	We formulated an itch-relieving moisturizing cream containing 3% menthol and ceramides.	Ceramides	77-86	itchy E3 ubiquitin protein ligase	Homo sapiens	17-21
29238000-1	2017	Acid sphingomyelinase (ASM) is a lysosomal enzyme that hydrolyzes sphingomyelin into ceramide, a bioactive lipid to regulate cellular physiological functions.	Ceramides	85-93	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
29234271-1	2017	The non-lysosomal glucosylceramidase GBA2 catalyzes the hydrolysis of glucosylceramide to glucose and ceramide.	Ceramides	78-86	glucosylceramidase beta 2	Homo sapiens	37-41
28883000-2	2017	In cancer cells, ASM-mediated ceramide production is important for apoptosis, cell proliferation, and immune modulation, highlighting ASM as a potential multimodal therapeutic target.	Ceramides	30-38	sphingomyelin phosphodiesterase 1	Homo sapiens	17-20
29056331-2	2017	With a mouse model deficient in the alkaline ceramidase (Acer1) gene, we demonstrate that ACER1 plays a key role in the homeostasis of the epidermis and its appendages by controlling the metabolism of ceramides.	Ceramides	201-210	alkaline ceramidase 1	Mus musculus	57-62
29056331-2	2017	With a mouse model deficient in the alkaline ceramidase (Acer1) gene, we demonstrate that ACER1 plays a key role in the homeostasis of the epidermis and its appendages by controlling the metabolism of ceramides.	Ceramides	201-210	alkaline ceramidase 1	Mus musculus	90-95
29056331-3	2017	Loss of Acer1 elevated the levels of various ceramides and sphingoid bases in the skin and caused progressive hair loss in mice.	Ceramides	45-54	alkaline ceramidase 1	Mus musculus	8-13
29056331-5	2017	These results suggest that ACER1 plays a key role in maintaining the homeostasis of HFSCs, and thereby the hair follicle structure and function, by regulating the metabolism of ceramides in the epidermis.	Ceramides	177-186	alkaline ceramidase 1	Mus musculus	27-32
29348854-9	2017	We further demonstrate that ASAH1 inhibition increases cellular ceramide level and induces apoptosis.	Ceramides	64-72	N-acylsphingosine amidohydrolase 1	Homo sapiens	28-33
28883000-1	2017	The lipid hydrolase enzyme acid sphingomyelinase (ASM) is required for the conversion of the lipid cell membrane component sphingomyelin into ceramide.	Ceramides	142-150	sphingomyelin phosphodiesterase 1	Homo sapiens	27-48
29156544-10	2017	Conclusions:C. membranaceus uses the ceramide pathway by modulating the SphK1/SphK2 ratio and increasing SPL to generate oxidative stress and consequently apoptosis.	Ceramides	37-45	sphingosine kinase 1	Homo sapiens	72-77
29156544-10	2017	Conclusions:C. membranaceus uses the ceramide pathway by modulating the SphK1/SphK2 ratio and increasing SPL to generate oxidative stress and consequently apoptosis.	Ceramides	37-45	sphingosine kinase 2	Homo sapiens	78-83
29156544-10	2017	Conclusions:C. membranaceus uses the ceramide pathway by modulating the SphK1/SphK2 ratio and increasing SPL to generate oxidative stress and consequently apoptosis.	Ceramides	37-45	sphingosine-1-phosphate lyase 1	Homo sapiens	105-108
28883000-1	2017	The lipid hydrolase enzyme acid sphingomyelinase (ASM) is required for the conversion of the lipid cell membrane component sphingomyelin into ceramide.	Ceramides	142-150	sphingomyelin phosphodiesterase 1	Homo sapiens	50-53
28774589-0	2017	Biallelic Mutations in KDSR Disrupt Ceramide Synthesis and Result in a Spectrum of Keratinization Disorders Associated with Thrombocytopenia.	Ceramides	36-44	3-ketodihydrosphingosine reductase	Homo sapiens	23-27
28938428-0	2017	GLP-1 Receptor Activation Inhibits Palmitate-Induced Apoptosis via Ceramide in Human Cardiac Progenitor Cells.	Ceramides	67-75	glucagon like peptide 1 receptor	Homo sapiens	0-14
28938428-14	2017	GLP1R activation counteracts this lipotoxic damage via inhibition of ceramide generation, and this may represent a cardioprotective mechanism.	Ceramides	69-77	glucagon like peptide 1 receptor	Homo sapiens	0-5
28774589-2	2017	Using whole-exome sequencing in four probands with undiagnosed skin hyperkeratosis/ichthyosis, we identified compound heterozygosity for mutations in KDSR, encoding an enzyme in the de novo synthesis pathway of ceramides.	Ceramides	211-220	3-ketodihydrosphingosine reductase	Homo sapiens	150-154
28774589-5	2017	The mutations in KDSR were associated with reduced ceramide levels in skin and impaired platelet function.	Ceramides	51-59	3-ketodihydrosphingosine reductase	Homo sapiens	17-21
28774589-8	2017	Mutations in KDSR cause defective ceramide biosynthesis, underscoring the importance of ceramide and sphingosine synthesis pathways in skin and platelet biology.	Ceramides	34-42	3-ketodihydrosphingosine reductase	Homo sapiens	13-17
28774589-8	2017	Mutations in KDSR cause defective ceramide biosynthesis, underscoring the importance of ceramide and sphingosine synthesis pathways in skin and platelet biology.	Ceramides	88-96	3-ketodihydrosphingosine reductase	Homo sapiens	13-17
29262618-1	2017	Ceramide synthase 1 (CERS1) is the most highly expressed CERS in the central nervous system, and ceramide with an 18-carbon-containing fatty acid chain (C18-ceramide) in the brain plays important roles in signaling and sphingolipid development.	Ceramides	97-105	ceramide synthase 1	Homo sapiens	0-19
28890071-7	2017	Chitotriosidase activity was similar across the genetic groups, while the levels of key lipids were altered in GBA mutation carriers: Monohexosylceramide, Ceramide and Sphingomyelin were elevated; while Phosphatidic acid (PA), Phosphatidylethanolamine (PE), Plasmalogen phosphatidylethanolamine (PEp) and Acyl Phosphatidylglycerol (AcylPG) were decreased.	Ceramides	155-163	glucosylceramidase beta	Homo sapiens	111-114
29263930-11	2017	Taken together, these findings provide the first body of evidence demonstrating ceramide regulation of STAT3 phosphorylation.	Ceramides	80-88	signal transducer and activator of transcription 3	Mus musculus	103-108
29263930-12	2017	These results are also the first to demonstrate an effect of ceramide on BTK, a critical kinase mediating the B-cell receptor signaling in CLL cells and suggest a novel and synergistic combination of CNL and BTK inhibitors for CLL treatment.	Ceramides	61-69	Bruton agammaglobulinemia tyrosine kinase	Mus musculus	73-76
29263930-12	2017	These results are also the first to demonstrate an effect of ceramide on BTK, a critical kinase mediating the B-cell receptor signaling in CLL cells and suggest a novel and synergistic combination of CNL and BTK inhibitors for CLL treatment.	Ceramides	61-69	Bruton agammaglobulinemia tyrosine kinase	Mus musculus	208-211
29068380-4	2017	In this study we identified Gb3Cer and Gb4Cer lipoforms of serum-free cultivated Caco-2 and HCT-8 cells, chiefly harboring ceramide moieties composed of sphingosine (d18:1) and C16:0, C22:0 or C24:0/C24:1 fatty acid.	Ceramides	123-131	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	28-31
29068380-4	2017	In this study we identified Gb3Cer and Gb4Cer lipoforms of serum-free cultivated Caco-2 and HCT-8 cells, chiefly harboring ceramide moieties composed of sphingosine (d18:1) and C16:0, C22:0 or C24:0/C24:1 fatty acid.	Ceramides	123-131	beta-1,3-N-acetylgalactosaminyltransferase 1 (globoside blood group)	Homo sapiens	39-45
29262618-7	2017	Thus, the combined therapy of CERS1/C18-ceramide and VM-26 may be a novel therapeutic strategy for the treatment of human glioma.	Ceramides	40-48	Bardet-Biedl syndrome 9	Homo sapiens	36-39
28577326-3	2017	SMPD2 increases levels of ceramide and other lipids.	Ceramides	26-34	sphingomyelin phosphodiesterase 2	Homo sapiens	0-5
28577326-4	2017	Confocal immunofluorescence microscopy showed that signals of ceramide overlapped with LC3, suggesting that ceramide might play an important role in the formation of autophagosome.	Ceramides	108-116	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	87-90
29035368-6	2017	Intestine HIF-2alpha inhibition markedly reduced intestine and serum ceramide levels.	Ceramides	69-77	endothelial PAS domain protein 1	Mus musculus	10-20
29035368-7	2017	Mechanistically, intestine HIF-2alpha regulates ceramide metabolism mainly from the salvage pathway, by positively regulating the expression of Neu3, the gene encoding neuraminidase 3.	Ceramides	48-56	endothelial PAS domain protein 1	Mus musculus	27-37
29035368-7	2017	Mechanistically, intestine HIF-2alpha regulates ceramide metabolism mainly from the salvage pathway, by positively regulating the expression of Neu3, the gene encoding neuraminidase 3.	Ceramides	48-56	neuraminidase 3	Mus musculus	144-148
29066540-0	2017	TGF-beta receptor I/II trafficking and signaling at primary cilia are inhibited by ceramide to attenuate cell migration and tumor metastasis.	Ceramides	83-91	transforming growth factor, beta receptor II	Mus musculus	0-22
29066540-3	2017	We investigated whether ceramide metabolism inhibited TbetaRI/II trafficking to primary cilia to attenuate cross-talk between TbetaRI/II and the Shh pathway.	Ceramides	24-32	transforming growth factor, beta receptor I	Mus musculus	54-64
29066540-3	2017	We investigated whether ceramide metabolism inhibited TbetaRI/II trafficking to primary cilia to attenuate cross-talk between TbetaRI/II and the Shh pathway.	Ceramides	24-32	transforming growth factor, beta receptor I	Mus musculus	126-136
29066540-4	2017	We found that ceramide synthase 4 (CerS4)-generated ceramide stabilized the association between TbetaRI and the inhibitory factor Smad7, which limited the trafficking of TbetaRI/II to primary cilia.	Ceramides	14-22	ceramide synthase 4	Mus musculus	35-40
29066540-4	2017	We found that ceramide synthase 4 (CerS4)-generated ceramide stabilized the association between TbetaRI and the inhibitory factor Smad7, which limited the trafficking of TbetaRI/II to primary cilia.	Ceramides	14-22	transforming growth factor, beta receptor I	Mus musculus	96-103
29066540-4	2017	We found that ceramide synthase 4 (CerS4)-generated ceramide stabilized the association between TbetaRI and the inhibitory factor Smad7, which limited the trafficking of TbetaRI/II to primary cilia.	Ceramides	14-22	SMAD family member 7	Mus musculus	130-135
29066540-4	2017	We found that ceramide synthase 4 (CerS4)-generated ceramide stabilized the association between TbetaRI and the inhibitory factor Smad7, which limited the trafficking of TbetaRI/II to primary cilia.	Ceramides	14-22	transforming growth factor, beta receptor I	Mus musculus	170-180
29066540-10	2017	Overall, these data reveal a ceramide-dependent mechanism that suppresses cell migration and invasion by restricting TbetaRI/II-Shh signaling selectively at the plasma membrane of the primary cilium.	Ceramides	29-37	transforming growth factor, beta receptor I	Mus musculus	117-124
29066540-10	2017	Overall, these data reveal a ceramide-dependent mechanism that suppresses cell migration and invasion by restricting TbetaRI/II-Shh signaling selectively at the plasma membrane of the primary cilium.	Ceramides	29-37	sonic hedgehog	Mus musculus	128-131
29262618-1	2017	Ceramide synthase 1 (CERS1) is the most highly expressed CERS in the central nervous system, and ceramide with an 18-carbon-containing fatty acid chain (C18-ceramide) in the brain plays important roles in signaling and sphingolipid development.	Ceramides	97-105	ceramide synthase 1	Homo sapiens	21-26
29262618-1	2017	Ceramide synthase 1 (CERS1) is the most highly expressed CERS in the central nervous system, and ceramide with an 18-carbon-containing fatty acid chain (C18-ceramide) in the brain plays important roles in signaling and sphingolipid development.	Ceramides	97-105	Bardet-Biedl syndrome 9	Homo sapiens	153-156
29076348-1	2017	AIM: ASM, which hydrolyzes sphingomyelin into ceramide, is recognized as a therapeutic target for UV-induced skin damage.	Ceramides	46-54	H19 imprinted maternally expressed transcript	Homo sapiens	5-8
29404440-6	2017	Mass spectrometry-based lipidomics analysis of livers from mice treated with FGF19 or M70 revealed significant reductions in the levels of toxic lipid species (i.e., diacylglycerols, ceramides and free cholesterol) and an increase in levels of unoxidized cardiolipins, an important component of the inner mitochondrial membrane.	Ceramides	183-192	fibroblast growth factor 15	Mus musculus	77-82
28710138-7	2017	We conclude that hypothalamic LPL functions in astrocytes to ensure appropriately balanced nutrient sensing, ceramide distribution, body weight regulation, and glucose metabolism.	Ceramides	109-117	lipoprotein lipase	Mus musculus	30-33
28535204-6	2017	Exposure of primary HRGECs to the ceramide analogon d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP) reduced total Gb3Cer and Gb4Cer content, roughly calculated from two biological replicates, down to half and quarter of its primordial content, respectively, but strengthened their prevalence and cholesterol preponderance in DRMs.	Ceramides	34-42	beta-1,3-N-acetylgalactosaminyltransferase 1 (globoside blood group)	Homo sapiens	143-149
29057873-5	2017	In macrophages, VLDL treatment upregulates intracellular levels of C16:0 ceramides in a VLDLR-dependent manner, which potentiates pro-inflammatory responses and promotes M1-like macrophage polarization.	Ceramides	73-82	CD320 antigen	Mus musculus	16-20
29057873-5	2017	In macrophages, VLDL treatment upregulates intracellular levels of C16:0 ceramides in a VLDLR-dependent manner, which potentiates pro-inflammatory responses and promotes M1-like macrophage polarization.	Ceramides	73-82	very low density lipoprotein receptor	Mus musculus	88-93
28235238-0	2017	Diminished protein-bound omega-hydroxylated ceramides in the skin of patients with ichthyosis with 12R-lipoxygenase (LOX) or eLOX-3 deficiency.	Ceramides	44-53	arachidonate 12-lipoxygenase, 12R type	Homo sapiens	99-115
28235238-0	2017	Diminished protein-bound omega-hydroxylated ceramides in the skin of patients with ichthyosis with 12R-lipoxygenase (LOX) or eLOX-3 deficiency.	Ceramides	44-53	arachidonate 12-lipoxygenase, 12R type	Homo sapiens	117-120
28235238-0	2017	Diminished protein-bound omega-hydroxylated ceramides in the skin of patients with ichthyosis with 12R-lipoxygenase (LOX) or eLOX-3 deficiency.	Ceramides	44-53	arachidonate lipoxygenase 3	Homo sapiens	125-131
28814641-0	2017	Ceramide activation of RhoA/Rho kinase impairs actin polymerization during aggregated LDL catabolism.	Ceramides	0-8	ras homolog family member A	Mus musculus	23-27
28905881-6	2017	ASAH1 is an acid ceramidase known to be involved in tumor formation by controlling the ratio of ceramide and sphingosine.	Ceramides	96-104	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-5
28755941-2	2017	Moreover, ceramide in lipoproteins can mediate the development of insulin resistance.	Ceramides	10-18	insulin	Bos taurus	66-73
28814641-0	2017	Ceramide activation of RhoA/Rho kinase impairs actin polymerization during aggregated LDL catabolism.	Ceramides	0-8	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	28-38
28695226-6	2017	Our results show that restoration of cystic fibrosis conductance regulator (CFTR) expression is associated with normalization of aberrant levels of specific ceramides.	Ceramides	157-166	CF transmembrane conductance regulator	Homo sapiens	37-74
28814641-10	2017	These findings highlight a critical regulatory pathway by which ceramide impairs actin polymerization through increased RhoA/Rho kinase signaling and regulates foam cell formation.	Ceramides	64-72	ras homolog family member A	Mus musculus	120-124
28695226-6	2017	Our results show that restoration of cystic fibrosis conductance regulator (CFTR) expression is associated with normalization of aberrant levels of specific ceramides.	Ceramides	157-166	CF transmembrane conductance regulator	Homo sapiens	76-80
28814641-10	2017	These findings highlight a critical regulatory pathway by which ceramide impairs actin polymerization through increased RhoA/Rho kinase signaling and regulates foam cell formation.	Ceramides	64-72	Rho-associated coiled-coil containing protein kinase 2	Mus musculus	125-135
28695226-7	2017	This demonstrates for the first time a correlation between CFTR protein expression and regulation of specific ceramide levels.	Ceramides	110-118	CF transmembrane conductance regulator	Homo sapiens	59-63
28865931-8	2017	GH reduced thymic levels of TNF-alpha and 4-HNE and increased the number of thymocytes as well as the thymic levels of dihydroceramide, a ceramide precursor and autophagic stimuli for cell survival.	Ceramides	126-134	growth hormone	Mus musculus	0-2
28695226-11	2017	KEY MESSAGES: Long- and very long-chain ceramides (LCCs and VLCCs) are biochemically distinct.	Ceramides	40-49	GLE1 RNA export mediator	Homo sapiens	51-55
28633109-3	2017	The present study tested whether acid sphingomyelinase (ASM) and ceramide associated membrane raft (MR) signaling platforms contribute to the activation of NLRP3 inflammasomes and atherosclerotic lesions during hypercholesterolemia.	Ceramides	65-73	NLR family, pyrin domain containing 3	Mus musculus	156-161
28755941-3	2017	We have previously demonstrated that circulating ceramide increases during the progression of insulin resistance in postpartum dairy cows.	Ceramides	49-57	insulin	Bos taurus	94-101
29169412-0	2017	[TNF-alpha regulates the proliferation of human breast cancer cells via regulation of ceramide content].	Ceramides	86-94	tumor necrosis factor	Homo sapiens	1-10
28733206-8	2017	The increases in ceramide concentrations may induce ER stress and activate the JNK pathway by affecting the expression of the related genes, and eventually trigger the mitochondria-independent apoptosis in hepatocytes.	Ceramides	17-25	mitogen-activated protein kinase 8	Homo sapiens	79-82
28474276-8	2017	TNFalpha and IFNgamma stimulation of oligodendrocytes in culture also led to an accumulation of ceramide with an elevation of sphingosine.	Ceramides	96-104	tumor necrosis factor	Rattus norvegicus	0-8
28474276-8	2017	TNFalpha and IFNgamma stimulation of oligodendrocytes in culture also led to an accumulation of ceramide with an elevation of sphingosine.	Ceramides	96-104	interferon gamma	Rattus norvegicus	13-21
29169412-1	2017	Objective To determine whether tumor necrosis factor alpha (TNF-alpha) regulates the proliferation of MCF-7 and MDA-MB231 cells by modifying ceramide (Cer) production.	Ceramides	141-149	tumor necrosis factor	Homo sapiens	31-58
29169412-1	2017	Objective To determine whether tumor necrosis factor alpha (TNF-alpha) regulates the proliferation of MCF-7 and MDA-MB231 cells by modifying ceramide (Cer) production.	Ceramides	141-149	tumor necrosis factor	Homo sapiens	60-69
29169412-1	2017	Objective To determine whether tumor necrosis factor alpha (TNF-alpha) regulates the proliferation of MCF-7 and MDA-MB231 cells by modifying ceramide (Cer) production.	Ceramides	151-154	tumor necrosis factor	Homo sapiens	31-58
29169412-1	2017	Objective To determine whether tumor necrosis factor alpha (TNF-alpha) regulates the proliferation of MCF-7 and MDA-MB231 cells by modifying ceramide (Cer) production.	Ceramides	151-154	tumor necrosis factor	Homo sapiens	60-69
28827783-6	2017	Interestingly, CCDC3, as a secreted protein, targets liver cancer cells and increases long chain polyunsaturated fatty acids, but decreases ceramide in the cells.	Ceramides	140-148	coiled-coil domain containing 3	Mus musculus	15-20
28894119-5	2017	Ceramides act as a double-edged sword, promoting normal skin homeostasis in the native state, but can be metabolized to sphingosine-1-phosphate (S1P), linked to inflammation and tumorigenesis.	Ceramides	0-9	sphingosine-1-phosphate receptor 1	Mus musculus	145-148
28679588-0	2017	Adipocyte mTORC1 deficiency promotes adipose tissue inflammation and NLRP3 inflammasome activation via oxidative stress and de novo ceramide synthesis.	Ceramides	132-140	CREB regulated transcription coactivator 1	Mus musculus	10-16
28679588-4	2017	Despite reducing adiposity, adipocyte mTORC1 deficiency promoted hepatic steatosis, insulin resistance, and adipose tissue inflammation (increased infiltration of macrophages, neutrophils, and B lymphocytes; crown-like structure density; TNF-alpha, interleukin (IL)-6, and monocyte chemoattractant protein 1 expression; IL-1beta protein content; lipid peroxidation; and de novo ceramide synthesis).	Ceramides	378-386	CREB regulated transcription coactivator 1	Mus musculus	38-44
28679588-5	2017	The anti-oxidant, N-acetylcysteine, partially attenuated, whereas treatment with de novo ceramide synthesis inhibitor, myriocin, completely blocked adipose tissue inflammation and nucleotide oligomerization domain-like receptor pyrin domain-containing 3 (NLRP3)-inflammasome activation, but not hepatic steatosis and insulin resistance induced by adipocyte raptor deletion.	Ceramides	89-97	NLR family, pyrin domain containing 3	Mus musculus	180-253
28679588-7	2017	In conclusion, adipocyte mTORC1 deficiency induces adipose tissue inflammation and NLRP3-inflammasome activation by promoting oxidative stress and de novo ceramide synthesis.	Ceramides	155-163	CREB regulated transcription coactivator 1	Mus musculus	25-31
28797762-0	2017	Ceramide enhances COX-2 expression and VSMC contractile hyperreactivity via ER stress signal activation.	Ceramides	0-8	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	18-23
28797762-4	2017	Ceramide promoted the transcriptional and translational expression of COX-2 and BiP in VSMCs, which were blocked by the ER stress inhibitors, 4-PBA and TUDCA.	Ceramides	0-8	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	70-75
28797762-4	2017	Ceramide promoted the transcriptional and translational expression of COX-2 and BiP in VSMCs, which were blocked by the ER stress inhibitors, 4-PBA and TUDCA.	Ceramides	0-8	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	80-83
28797762-5	2017	These findings show that ceramide enhances PE-induced vascular smooth muscle constriction by mediation of the ER stress/COX-2/PGE2 pathway.	Ceramides	25-33	cytochrome c oxidase II, mitochondrial	Rattus norvegicus	120-125
28674283-1	2017	Neutral ceramidase (NCDase) is a class of ceramidases, a key enzyme in ceramide degradation.	Ceramides	71-79	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	0-18
28674283-1	2017	Neutral ceramidase (NCDase) is a class of ceramidases, a key enzyme in ceramide degradation.	Ceramides	71-79	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	20-26
28674283-2	2017	Recently, it was observed that NCDase activity was suppressed by saturated fatty acids to increase ceramide content in rat muscle.	Ceramides	99-107	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	31-37
28674283-5	2017	In addition, Palm caused a significant accumulation of ceramide, while SPH level remained unchanged, suggesting that inhibition of NCDase activity led to no change of SPH level after treatment with Palm for 24 h. Furthermore, NCDase overexpression significantly reduced Palm-induced apoptosis in INS-1 cells.	Ceramides	55-63	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	226-232
28674283-8	2017	Furthermore, NCDase inhibition was involved in Palm-induced apoptosis by blocking ceramide degradation in INS-1 cells.	Ceramides	82-90	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	13-19
28839270-1	2017	Ceramide, a bioactive lipid and signaling molecule associated with cardiovascular disease, is known to activate extracellular signal regulated kinases 1 and 2 (ERK1/2).	Ceramides	0-8	mitogen-activated protein kinase 1	Homo sapiens	112-158
28839270-1	2017	Ceramide, a bioactive lipid and signaling molecule associated with cardiovascular disease, is known to activate extracellular signal regulated kinases 1 and 2 (ERK1/2).	Ceramides	0-8	mitogen-activated protein kinase 3	Homo sapiens	160-166
28839270-2	2017	Here, we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif containing GTPase activating protein 1 (IQGAP1).	Ceramides	39-47	mitogen-activated protein kinase 3	Homo sapiens	51-57
28839270-2	2017	Here, we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif containing GTPase activating protein 1 (IQGAP1).	Ceramides	39-47	IQ motif containing GTPase activating protein 1	Homo sapiens	120-167
28839270-2	2017	Here, we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif containing GTPase activating protein 1 (IQGAP1).	Ceramides	39-47	IQ motif containing GTPase activating protein 1	Homo sapiens	169-175
28839270-2	2017	Here, we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif containing GTPase activating protein 1 (IQGAP1).	Ceramides	73-81	mitogen-activated protein kinase 3	Homo sapiens	51-57
28839270-2	2017	Here, we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif containing GTPase activating protein 1 (IQGAP1).	Ceramides	73-81	IQ motif containing GTPase activating protein 1	Homo sapiens	120-167
28839270-2	2017	Here, we determined that the effect of ceramide on ERK1/2 is mediated by ceramide signaling on an ERK scaffold protein, IQ motif containing GTPase activating protein 1 (IQGAP1).	Ceramides	73-81	IQ motif containing GTPase activating protein 1	Homo sapiens	169-175
28839270-4	2017	We report here that C6 ceramide increases serum-stimulated ERK1/2 activation in a manner dependent on the ERK1/2 scaffold IQGAP1.	Ceramides	23-31	mitogen-activated protein kinase 3	Homo sapiens	59-65
28839270-4	2017	We report here that C6 ceramide increases serum-stimulated ERK1/2 activation in a manner dependent on the ERK1/2 scaffold IQGAP1.	Ceramides	23-31	mitogen-activated protein kinase 3	Homo sapiens	106-112
28839270-4	2017	We report here that C6 ceramide increases serum-stimulated ERK1/2 activation in a manner dependent on the ERK1/2 scaffold IQGAP1.	Ceramides	23-31	IQ motif containing GTPase activating protein 1	Homo sapiens	122-128
28839270-5	2017	C6 ceramide increases IQGAP1 protein levels by preventing its cleavage.	Ceramides	3-11	IQ motif containing GTPase activating protein 1	Homo sapiens	22-28
28839270-10	2017	Activation of ERK1/2 by ceramide, known to increase lysine acetylation, appears to be mediated by acetylation-dependent stabilization of IQGAP1.	Ceramides	24-32	mitogen-activated protein kinase 3	Homo sapiens	14-20
28839270-10	2017	Activation of ERK1/2 by ceramide, known to increase lysine acetylation, appears to be mediated by acetylation-dependent stabilization of IQGAP1.	Ceramides	24-32	IQ motif containing GTPase activating protein 1	Homo sapiens	137-143
28983319-8	2017	On the other hand, older animals with loss of function mutations in ceramide synthase (hyl-1), which converts sphingosine to ceramide, showed improved neuromuscular function and stress response with age.	Ceramides	68-76	Ceramide synthase hyl-1;TLC domain-containing protein	Caenorhabditis elegans	87-92
28838234-5	2017	Furthermore, isomeric ganglioside species can be differentiated, and the double bond location in the ceramide moiety of the gangliosides can be identified through the MS3 approach involving sequential CID and EID processes.	Ceramides	101-109	MS3	Homo sapiens	167-170
28763689-1	2017	Beta-Glucocerebrosidase (GBA) is a lysosomal protein that is responsible for the hydrolysis of glycosylceramide into glucose and ceramide.	Ceramides	103-111	glucosylceramidase beta	Homo sapiens	0-23
28763689-1	2017	Beta-Glucocerebrosidase (GBA) is a lysosomal protein that is responsible for the hydrolysis of glycosylceramide into glucose and ceramide.	Ceramides	103-111	glucosylceramidase beta	Homo sapiens	25-28
28836149-3	2017	We tested the hypothesis that ceramide accumulates in dairy cows experiencing lipolysis and insulin resistance.	Ceramides	30-38	insulin	Bos taurus	92-99
28544394-3	2017	METHODS AND RESULTS: Diet-induced obesity engendered increased ectopic accumulation of lipotoxic species in skeletal muscle of 4E-BP1 and 4E-BP2 double knockout mice (4E-BP1/2 DKO), namely diacylglycerols and ceramides.	Ceramides	209-218	eukaryotic translation initiation factor 4E binding protein 1	Mus musculus	167-179
28652409-1	2017	De novo synthesis of the sphingolipid sphingomyelin requires non-vesicular transport of ceramide from the endoplasmic reticulum to the Golgi by the multidomain protein ceramide transfer protein (CERT).	Ceramides	88-96	ceramide transporter 1	Homo sapiens	195-199
28652409-2	2017	CERT"s N-terminal pleckstrin homology (PH) domain targets it to the Golgi by binding to phosphatidylinositol 4-phosphate (PtdIns(4)P) in the Golgi membrane, whereas its C-terminal StAR-related lipid transfer domain (START) carries out ceramide transfer.	Ceramides	235-243	ceramide transporter 1	Homo sapiens	0-4
28652409-3	2017	Hyperphosphorylation of a serine-rich motif immediately after the PH domain decreases both PtdIns(4)P binding and ceramide transfer by CERT.	Ceramides	114-122	ceramide transporter 1	Homo sapiens	135-139
28652409-7	2017	We further report that mutations disrupting the PH-START interaction increase both PtdIns(4)P-binding affinity and ceramide transfer activity of a CERT-serine-rich phosphorylation mimic.	Ceramides	115-123	ceramide transporter 1	Homo sapiens	147-151
28749465-2	2017	By generating ceramide, ASM had been reported to have an important role in regulating immune cell functions inclusive of macrophages, NK cells, and CD8+ T cells, whereas the role of ASM bioactivity in regulation of human CD4+ T-cell functions remained uncertain.	Ceramides	14-22	sphingomyelin phosphodiesterase 1	Homo sapiens	24-27
28834722-3	2017	It has been proposed that ceramide forms large and stable channels in the mitochondrial outer membrane that induce cell death through direct release of cytochrome c.	Ceramides	26-34	cytochrome c, somatic	Homo sapiens	152-164
28798382-5	2017	Here we take advantage of the leaky tetracycline promoter system in the Tat-transgenic mouse to show that a chronic very low-level expression of Tat is associated with astrocyte activation, inflammatory cytokine expression, ceramide accumulation, reductions in brain volume, synaptic, and axonal damage that occurs over a time frame of 1 year.	Ceramides	224-232	tyrosine aminotransferase	Mus musculus	145-148
28405720-5	2017	Deletion of CerS2 strongly reduced very long-chain ceramides (Cer24:0, 24:1) but concomitantly increased long-chain ceramides and sphinganine in plasma and colon tissue.	Ceramides	51-60	ceramide synthase 2	Mus musculus	12-17
28405720-5	2017	Deletion of CerS2 strongly reduced very long-chain ceramides (Cer24:0, 24:1) but concomitantly increased long-chain ceramides and sphinganine in plasma and colon tissue.	Ceramides	116-125	ceramide synthase 2	Mus musculus	12-17
28483801-4	2017	We found that HOMA of insulin resistance, plasma insulin, and triglyceride concentrations were positively correlated with SS C16:0 and C18:1 ceramide, but not SS C14:0-Cer, C20:0-Cer, C24:0-Cer, and C24:1-Cer concentrations; IMF ceramide concentrations were not correlated with any metabolic parameters.	Ceramides	141-149	insulin	Homo sapiens	22-29
28483801-4	2017	We found that HOMA of insulin resistance, plasma insulin, and triglyceride concentrations were positively correlated with SS C16:0 and C18:1 ceramide, but not SS C14:0-Cer, C20:0-Cer, C24:0-Cer, and C24:1-Cer concentrations; IMF ceramide concentrations were not correlated with any metabolic parameters.	Ceramides	141-149	insulin	Homo sapiens	49-56
28483801-6	2017	Plasma insulin concentrations correlated positively with the fractional contribution of plasma palmitate to SS 16:0 ceramide.	Ceramides	116-124	insulin	Homo sapiens	7-14
28483801-8	2017	We conclude that skeletal muscle SS ceramides, especially C16 to C18 chain lengths and the de novo synthesis of intramyocellular ceramide from plasma palmitate are associated with markers of insulin resistance.	Ceramides	36-45	insulin	Homo sapiens	191-198
28483801-8	2017	We conclude that skeletal muscle SS ceramides, especially C16 to C18 chain lengths and the de novo synthesis of intramyocellular ceramide from plasma palmitate are associated with markers of insulin resistance.	Ceramides	36-44	insulin	Homo sapiens	191-198
28785021-1	2017	Acid ceramidase (AC) is a lysosomal cysteine hydrolase that catalyzes the conversion of ceramide into fatty acid and sphingosine.	Ceramides	88-96	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
28785021-1	2017	Acid ceramidase (AC) is a lysosomal cysteine hydrolase that catalyzes the conversion of ceramide into fatty acid and sphingosine.	Ceramides	88-96	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
28785021-3	2017	Since increases in ceramide and consequent decreases of S1P reduce proliferation of various cancers, AC might offer a new target for anti-tumor therapy.	Ceramides	19-27	N-acylsphingosine amidohydrolase 1	Homo sapiens	101-103
28785021-6	2017	As seen with administration of exogenous ceramide, AC ablation blocks cell cycle progression and accelerates senescence.	Ceramides	41-49	N-acylsphingosine amidohydrolase 1	Homo sapiens	51-53
28749465-4	2017	Upon stimulation of CD3 and/or CD28, ASM-dependent ceramide signaling mediates intracellular downstream signal cascades of CD3 and CD28, and regulates CD4+ T-cell activation and proliferation.	Ceramides	51-59	CD28 molecule	Homo sapiens	31-35
28749465-4	2017	Upon stimulation of CD3 and/or CD28, ASM-dependent ceramide signaling mediates intracellular downstream signal cascades of CD3 and CD28, and regulates CD4+ T-cell activation and proliferation.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	37-40
28749465-4	2017	Upon stimulation of CD3 and/or CD28, ASM-dependent ceramide signaling mediates intracellular downstream signal cascades of CD3 and CD28, and regulates CD4+ T-cell activation and proliferation.	Ceramides	51-59	CD28 molecule	Homo sapiens	131-135
28749465-4	2017	Upon stimulation of CD3 and/or CD28, ASM-dependent ceramide signaling mediates intracellular downstream signal cascades of CD3 and CD28, and regulates CD4+ T-cell activation and proliferation.	Ceramides	51-59	CD4 molecule	Homo sapiens	151-154
28743803-0	2017	The glucocorticoid-Angptl4-ceramide axis induces insulin resistance through PP2A and PKCzeta.	Ceramides	27-35	angiopoietin-like 4	Mus musculus	19-26
28746357-2	2017	The molecular pathways in this response remain unelucidated, however, previous data has supported a role for cell membrane-metabolism related pathways including an up regulation of UDP glycosyltransferase 8 (UGT8), which catalyzes the transfer of galactose to ceramide, a lipid that is associated with the induction of apoptotic signalling.	Ceramides	260-268	UDP glycosyltransferase 8	Homo sapiens	181-206
28746357-2	2017	The molecular pathways in this response remain unelucidated, however, previous data has supported a role for cell membrane-metabolism related pathways including an up regulation of UDP glycosyltransferase 8 (UGT8), which catalyzes the transfer of galactose to ceramide, a lipid that is associated with the induction of apoptotic signalling.	Ceramides	260-268	UDP glycosyltransferase 8	Homo sapiens	208-212
28746357-6	2017	An increase in the immunolabelling of ceramide was observed in cells where UGT8 was down-regulated as opposed to cells where UGT8 was either not regulated or was up-regulated.	Ceramides	38-46	UDP glycosyltransferase 8	Homo sapiens	75-79
28746357-13	2017	The down regulation of UGT8 led to the accumulation of ceramide resulting in more cell death signalling and therefore, a greater enhancement of radiation effect when vascular disruption takes place through the use of ultrasound-stimulated microbubbles.	Ceramides	55-63	UDP glycosyltransferase 8	Homo sapiens	23-27
28743803-7	2017	Overall, our study demonstrates the key role of Angptl4 in glucocorticoid-augmented hepatic ceramide production that induces whole-body insulin resistance.	Ceramides	92-100	angiopoietin-like 4	Mus musculus	48-55
28743803-0	2017	The glucocorticoid-Angptl4-ceramide axis induces insulin resistance through PP2A and PKCzeta.	Ceramides	27-35	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	76-92
28743803-3	2017	Through metabolomic profiling, we revealed that glucocorticoid treatment increased hepatic ceramide concentrations by inducing enzymes in the ceramide synthetic pathway in an Angptl4-dependent manner.	Ceramides	91-99	angiopoietin-like 4	Mus musculus	175-182
28743803-3	2017	Through metabolomic profiling, we revealed that glucocorticoid treatment increased hepatic ceramide concentrations by inducing enzymes in the ceramide synthetic pathway in an Angptl4-dependent manner.	Ceramides	142-150	angiopoietin-like 4	Mus musculus	175-182
28743803-4	2017	Angptl4 was also required for glucocorticoids to stimulate the activities of the downstream effectors of ceramide, protein phosphatase 2A (PP2A) and protein kinase Czeta (PKCzeta).	Ceramides	105-113	angiopoietin-like 4	Mus musculus	0-7
28495865-0	2017	Ceramide counteracts the effects of ghrelin on the metabolic control of food intake in rainbow trout.	Ceramides	0-8	ghrelin	Oncorhynchus mykiss	36-43
28648781-6	2017	Ceramides synergize with rapamycin, a TORC1 inhibitor, in counteracting the DDR.	Ceramides	0-9	CREB regulated transcription coactivator 1	Homo sapiens	38-43
28659495-2	2017	Previous work revealed that the ER-resident ceramide phosphoethanolamine (CPE) synthase SMSr/SAMD8 is a suppressor of ceramide-mediated apoptosis in cultured cells.	Ceramides	44-52	sterile alpha motif domain containing 8	Homo sapiens	88-92
28659495-2	2017	Previous work revealed that the ER-resident ceramide phosphoethanolamine (CPE) synthase SMSr/SAMD8 is a suppressor of ceramide-mediated apoptosis in cultured cells.	Ceramides	44-52	sterile alpha motif domain containing 8	Homo sapiens	93-98
28659495-2	2017	Previous work revealed that the ER-resident ceramide phosphoethanolamine (CPE) synthase SMSr/SAMD8 is a suppressor of ceramide-mediated apoptosis in cultured cells.	Ceramides	118-126	sterile alpha motif domain containing 8	Homo sapiens	88-92
28659495-2	2017	Previous work revealed that the ER-resident ceramide phosphoethanolamine (CPE) synthase SMSr/SAMD8 is a suppressor of ceramide-mediated apoptosis in cultured cells.	Ceramides	118-126	sterile alpha motif domain containing 8	Homo sapiens	93-98
28714882-2	2017	Particularly, the development of insulin resistance, a major pathophysiological hallmark of Type 2 Diabetes mellitus (T2D), has been linked to ceramide signaling.	Ceramides	143-151	insulin	Homo sapiens	33-40
28659495-7	2017	Our findings underscore a role of SMSr as negative regulator of ceramide-induced cell death and, in view of a prominent expression of the enzyme in brain, raise questions regarding its potential involvement in neurodegenerative disorders.	Ceramides	64-72	sterile alpha motif domain containing 8	Homo sapiens	34-38
28495865-1	2017	In mammals, ceramides are involved in the modulation of the orexigenic effects of ghrelin (GHRL).	Ceramides	12-21	ghrelin	Oncorhynchus mykiss	82-89
28495865-7	2017	The presence of ceramide generally counteracted the effects elicited by GHRL on fatty acid-sensing systems, the capacity of integrative sensors (AMPK, mTOR and SIRT-1), proteins involved in cellular signalling pathways (Akt and FoxO1) and neuropeptides involved in the regulation of food intake (AgRP, NPY, POMC and CART).	Ceramides	16-24	pro-opiomelanocortin A	Oncorhynchus mykiss	307-311
28603987-1	2017	Acid ceramidase (AC) hydrolyzes ceramides, which are central lipid messengers for metabolism and signaling of sphingolipids.	Ceramides	32-41	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
28603987-1	2017	Acid ceramidase (AC) hydrolyzes ceramides, which are central lipid messengers for metabolism and signaling of sphingolipids.	Ceramides	32-41	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
28652336-11	2017	Taken together, these results demonstrate that the DK switch regulates ceramide generation by nSMase2 and is governed by an allosteric interdomain interaction at the membrane interface.	Ceramides	71-79	sphingomyelin phosphodiesterase 3	Homo sapiens	94-101
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.	Ceramides	128-136	glucosylceramidase beta	Homo sapiens	16-20
28652336-0	2017	Structure of human nSMase2 reveals an interdomain allosteric activation mechanism for ceramide generation.	Ceramides	86-94	sphingomyelin phosphodiesterase 3	Homo sapiens	19-26
28652336-1	2017	Neutral sphingomyelinase 2 (nSMase2, product of the SMPD3 gene) is a key enzyme for ceramide generation that is involved in regulating cellular stress responses and exosome-mediated intercellular communication.	Ceramides	84-92	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
28652336-1	2017	Neutral sphingomyelinase 2 (nSMase2, product of the SMPD3 gene) is a key enzyme for ceramide generation that is involved in regulating cellular stress responses and exosome-mediated intercellular communication.	Ceramides	84-92	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
28652336-1	2017	Neutral sphingomyelinase 2 (nSMase2, product of the SMPD3 gene) is a key enzyme for ceramide generation that is involved in regulating cellular stress responses and exosome-mediated intercellular communication.	Ceramides	84-92	sphingomyelin phosphodiesterase 3	Homo sapiens	52-57
28683288-4	2017	The action of T3 depends on AMP-activated protein kinase (AMPK)-induced regulation of two signaling pathways in the ventromedial nucleus of the hypothalamus (VMH): decreased ceramide-induced endoplasmic reticulum (ER) stress, which promotes BAT thermogenesis, and increased c-Jun N-terminal kinase (JNK) activation, which controls hepatic lipid metabolism.	Ceramides	174-182	mitogen-activated protein kinase 8	Homo sapiens	274-297
28683288-4	2017	The action of T3 depends on AMP-activated protein kinase (AMPK)-induced regulation of two signaling pathways in the ventromedial nucleus of the hypothalamus (VMH): decreased ceramide-induced endoplasmic reticulum (ER) stress, which promotes BAT thermogenesis, and increased c-Jun N-terminal kinase (JNK) activation, which controls hepatic lipid metabolism.	Ceramides	174-182	mitogen-activated protein kinase 8	Homo sapiens	299-302
28552668-3	2017	beta1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that trap beta1-integrins on the luminal pole of bronchial epithelial cells.	Ceramides	48-56	integrin subunit beta 1	Homo sapiens	0-14
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.	Ceramides	25-33	UDP-glucose ceramide glucosyltransferase	Mus musculus	146-171
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.	Ceramides	55-64	UDP-glucose ceramide glucosyltransferase	Mus musculus	146-171
28409208-10	2017	We here show that ceramide synthesis is enhanced under treatment with a cigarette smoke mixture correlating with increased expression of inflammatory cytokines and matrix metalloproteinase 9.	Ceramides	18-26	matrix metallopeptidase 9	Homo sapiens	164-190
27077455-2	2017	Neutral sphingomyelinase (N-SMase)/ceramide pathway can regulate NOS2 expression therefore this study determined the role of selective N-SMase inhibition on nitrative and oxidative stress markers following liver IR injury.	Ceramides	35-43	nitric oxide synthase 2	Homo sapiens	65-69
27077455-2	2017	Neutral sphingomyelinase (N-SMase)/ceramide pathway can regulate NOS2 expression therefore this study determined the role of selective N-SMase inhibition on nitrative and oxidative stress markers following liver IR injury.	Ceramides	35-43	sphingomyelin phosphodiesterase 2	Homo sapiens	135-142
27077455-8	2017	Treatment with a specific N-SMase inhibitor significantly decreased all measured ceramides in IR injury.	Ceramides	81-90	sphingomyelin phosphodiesterase 2	Homo sapiens	26-33
28551355-0	2017	Roles of Diacylglycerols and Ceramides in Hepatic Insulin Resistance.	Ceramides	29-38	insulin	Homo sapiens	50-57
28552668-3	2017	beta1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that trap beta1-integrins on the luminal pole of bronchial epithelial cells.	Ceramides	48-56	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	0-5
28552668-3	2017	beta1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that trap beta1-integrins on the luminal pole of bronchial epithelial cells.	Ceramides	78-86	integrin subunit beta 1	Homo sapiens	0-14
28552668-3	2017	beta1-integrin accumulation is due to increased ceramide and the formation of ceramide platforms that trap beta1-integrins on the luminal pole of bronchial epithelial cells.	Ceramides	78-86	potassium calcium-activated channel subfamily M regulatory beta subunit 1	Homo sapiens	0-5
28552668-4	2017	beta1-integrins downregulate acid ceramidase expression, resulting in further accumulation of ceramide and consequent reduction of surface sphingosine, a lipid that kills bacteria.	Ceramides	94-102	hemoglobin, beta adult major chain	Mus musculus	0-5
28614356-1	2017	Acid ceramidase, which catalyzes ceramide hydrolysis to sphingosine and free fatty acid mainly in the lysosome, is being recognized as a potential therapeutic target for cancer.	Ceramides	33-41	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
28288862-6	2017	However, only inhibition of ERK1/2 with PD98059 prevented C2-ceramide-induced autophagy, indicating that the ERK1/2 pathway contributes to ceramide-induced autophagy.	Ceramides	61-69	mitogen-activated protein kinase 3	Homo sapiens	28-34
28288862-6	2017	However, only inhibition of ERK1/2 with PD98059 prevented C2-ceramide-induced autophagy, indicating that the ERK1/2 pathway contributes to ceramide-induced autophagy.	Ceramides	61-69	mitogen-activated protein kinase 3	Homo sapiens	109-115
28592871-0	2017	Incorporation of Fluorescence Ceramide-Based HPLC Assay for Rapidly and Efficiently Assessing Glucosylceramide Synthase In Vivo.	Ceramides	30-38	UDP-glucose ceramide glucosyltransferase	Mus musculus	94-119
28582448-3	2017	Sphingolipids, in particular ceramide and the enzyme acid sphingomyelinase, which generates ceramide from sphingomyelin, seem to be involved in astrocyte activation and neuronal damage in multiple sclerosis.	Ceramides	92-100	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	53-74
28592871-1	2017	Glucosylceramide synthase (GCS) is a rate-limiting enzyme catalyzing ceramide glycosylation, thereby regulating cellular ceramide levels and the synthesis of glycosphingolipids (GSLs) in cellular membranes.	Ceramides	8-16	UDP-glucose ceramide glucosyltransferase	Mus musculus	27-30
28592871-1	2017	Glucosylceramide synthase (GCS) is a rate-limiting enzyme catalyzing ceramide glycosylation, thereby regulating cellular ceramide levels and the synthesis of glycosphingolipids (GSLs) in cellular membranes.	Ceramides	69-77	UDP-glucose ceramide glucosyltransferase	Mus musculus	0-25
28592871-1	2017	Glucosylceramide synthase (GCS) is a rate-limiting enzyme catalyzing ceramide glycosylation, thereby regulating cellular ceramide levels and the synthesis of glycosphingolipids (GSLs) in cellular membranes.	Ceramides	69-77	UDP-glucose ceramide glucosyltransferase	Mus musculus	27-30
28389107-11	2017	A kinetic study of AEA hydrolysis showed that ceramide inhibited the fatty acid amino hydrolase (FAAH) activity in cell extracts.	Ceramides	46-54	fatty acid amide hydrolase	Homo sapiens	69-95
28389107-11	2017	A kinetic study of AEA hydrolysis showed that ceramide inhibited the fatty acid amino hydrolase (FAAH) activity in cell extracts.	Ceramides	46-54	fatty acid amide hydrolase	Homo sapiens	97-101
28434262-5	2017	In particular, acid ceramidase (AC) has emerged as a promising therapeutic target due to its role in neutralizing the pro-death effects of ceramide.	Ceramides	139-147	N-acylsphingosine amidohydrolase 1	Homo sapiens	15-30
28434262-5	2017	In particular, acid ceramidase (AC) has emerged as a promising therapeutic target due to its role in neutralizing the pro-death effects of ceramide.	Ceramides	139-147	N-acylsphingosine amidohydrolase 1	Homo sapiens	32-34
28520810-10	2017	CONCLUSION/INTERPRETATION: Saturated (16:0), but not unsaturated (18:1), fatty acids induce ceramide-mediated apoptosis of GLP-1-producing cells.	Ceramides	92-100	glucagon	Mus musculus	123-128
28238856-3	2017	Acid sphingomyelinase (ASMase) is highly expressed in endothelial cells, converting plasma membrane sphingomyelin to pro-apoptotic ceramide upon activation by diverse stresses.	Ceramides	131-139	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
28238856-3	2017	Acid sphingomyelinase (ASMase) is highly expressed in endothelial cells, converting plasma membrane sphingomyelin to pro-apoptotic ceramide upon activation by diverse stresses.	Ceramides	131-139	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
29069751-0	2017	A peptide antagonist of Prep1-p160 interaction improves ceramide-induced insulin resistance in skeletal muscle cells.	Ceramides	56-64	PBX/knotted 1 homeobox 1	Homo sapiens	24-29
29069751-0	2017	A peptide antagonist of Prep1-p160 interaction improves ceramide-induced insulin resistance in skeletal muscle cells.	Ceramides	56-64	MYB binding protein 1a	Homo sapiens	30-34
29069751-0	2017	A peptide antagonist of Prep1-p160 interaction improves ceramide-induced insulin resistance in skeletal muscle cells.	Ceramides	56-64	insulin	Homo sapiens	73-80
29069751-4	2017	In this study, we show that ceramides (C2cer), a class of lipids antagonizing insulin signalling, increase the levels of Prep1 and p160 in a dose and time-dependent fashion in L6 cells and induce their association by 80%.	Ceramides	28-37	insulin	Homo sapiens	78-85
29069751-4	2017	In this study, we show that ceramides (C2cer), a class of lipids antagonizing insulin signalling, increase the levels of Prep1 and p160 in a dose and time-dependent fashion in L6 cells and induce their association by 80%.	Ceramides	28-37	PBX/knotted 1 homeobox 1	Homo sapiens	121-126
29069751-4	2017	In this study, we show that ceramides (C2cer), a class of lipids antagonizing insulin signalling, increase the levels of Prep1 and p160 in a dose and time-dependent fashion in L6 cells and induce their association by 80%.	Ceramides	28-37	MYB binding protein 1a	Homo sapiens	131-135
28531105-0	2017	High-Mobility Group Box 1 Disrupts Metabolic Function with Cigarette Smoke Exposure in a Ceramide-Dependent Manner.	Ceramides	89-97	high mobility group box 1	Mus musculus	0-25
28531105-7	2017	Further testing revealed that HMGB1 treatment elicited a widespread increase in ceramide species and reduction in myotube mitochondrial respiration, an increase in reactive oxygen species, and reduced insulin-stimulated Akt phosphorylation.	Ceramides	80-88	high mobility group box 1	Mus musculus	30-35
28531105-9	2017	In mice, by comparing treatments of HMGB1 injections with or without myriocin, we found that HMGB1 injections resulted in increased muscle ceramides, especially C16 and C24, which were necessary for reduced muscle mitochondrial respiration and compromised insulin and glucose tolerance.	Ceramides	139-148	high mobility group box 1	Mus musculus	93-98
28531105-10	2017	In conclusion, HMGB1 may be a necessary intermediate in the ceramide-dependent metabolic consequences of cigarette smoke exposure.	Ceramides	60-68	high mobility group box 1	Mus musculus	15-20
29264548-5	2017	The levels of some ceramides were increased by as much as ~eightfold in the livers of Agpat2-/- mice.	Ceramides	19-28	1-acylglycerol-3-phosphate O-acyltransferase 2 (lysophosphatidic acid acyltransferase, beta)	Mus musculus	86-92
29264548-6	2017	Furthermore, several molecular species of ceramides were increased in the plasma of Agpat2-/- mice, specifically ceramide C16:0, which was threefold elevated in the plasma of both the sexes.	Ceramides	42-51	1-acylglycerol-3-phosphate O-acyltransferase 2 (lysophosphatidic acid acyltransferase, beta)	Mus musculus	84-90
29264548-6	2017	Furthermore, several molecular species of ceramides were increased in the plasma of Agpat2-/- mice, specifically ceramide C16:0, which was threefold elevated in the plasma of both the sexes.	Ceramides	42-50	1-acylglycerol-3-phosphate O-acyltransferase 2 (lysophosphatidic acid acyltransferase, beta)	Mus musculus	84-90
28758149-2	2017	As a promoter of ceramide degradation, it works through its cognate receptors, AdipoR1 and AdipoR2, to alter bioactive sphingolipid species.	Ceramides	17-25	adiponectin receptor 1	Homo sapiens	79-86
28758149-2	2017	As a promoter of ceramide degradation, it works through its cognate receptors, AdipoR1 and AdipoR2, to alter bioactive sphingolipid species.	Ceramides	17-25	adiponectin receptor 2	Homo sapiens	91-98
28758149-3	2017	Adiponectin diminishes the accumulation of ceramide, a lipid metabolite which can play a causal role in obesity-induced insulin resistance.	Ceramides	43-51	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
29069751-7	2017	In C2cer-treated L6 cells, 10muM Prep1(54-72) restores insulin signalling impaired by ceramide treatment.	Ceramides	86-94	PBX/knotted 1 homeobox 1	Homo sapiens	33-38
29069751-8	2017	Prep1 overexpressing L6 cells display similar metabolic alterations observed in ceramide-treated L6 cells and the presence of Prep1(54-72) mitigates these events.	Ceramides	80-88	PBX/knotted 1 homeobox 1	Homo sapiens	0-5
29069751-9	2017	All these findings suggest that disruption of the Prep1/p160 molecular interaction enhances insulin sensitivity impaired by ceramides in skeletal muscle cells and indicate this complex as an important target for type 2 diabetes.	Ceramides	124-133	PBX/knotted 1 homeobox 1	Homo sapiens	50-55
29069751-9	2017	All these findings suggest that disruption of the Prep1/p160 molecular interaction enhances insulin sensitivity impaired by ceramides in skeletal muscle cells and indicate this complex as an important target for type 2 diabetes.	Ceramides	124-133	MYB binding protein 1a	Homo sapiens	56-60
29069751-9	2017	All these findings suggest that disruption of the Prep1/p160 molecular interaction enhances insulin sensitivity impaired by ceramides in skeletal muscle cells and indicate this complex as an important target for type 2 diabetes.	Ceramides	124-133	insulin	Homo sapiens	92-99
28320857-3	2017	Here we show that acyl-coenzyme A-binding protein (ACBP) potently facilitates very-long acyl chain ceramide synthesis.	Ceramides	99-107	diazepam binding inhibitor	Mus musculus	18-49
28320857-9	2017	Our data uncover a novel mode of regulation of very-long acyl chain ceramide synthesis by ACBP, which we anticipate is of crucial importance in understanding the regulation of ceramide metabolism in pathogenesis.	Ceramides	176-184	diazepam binding inhibitor	Mus musculus	90-94
28320857-3	2017	Here we show that acyl-coenzyme A-binding protein (ACBP) potently facilitates very-long acyl chain ceramide synthesis.	Ceramides	99-107	diazepam binding inhibitor	Mus musculus	51-55
28320857-7	2017	Consistently, CerS2 and CerS3 activities are significantly reduced in the testes of ACBP-/- mice, concomitant with a significant reduction in long- and very-long-chain ceramide levels.	Ceramides	168-176	ceramide synthase 3	Mus musculus	24-29
28320857-7	2017	Consistently, CerS2 and CerS3 activities are significantly reduced in the testes of ACBP-/- mice, concomitant with a significant reduction in long- and very-long-chain ceramide levels.	Ceramides	168-176	diazepam binding inhibitor	Mus musculus	84-88
28320857-9	2017	Our data uncover a novel mode of regulation of very-long acyl chain ceramide synthesis by ACBP, which we anticipate is of crucial importance in understanding the regulation of ceramide metabolism in pathogenesis.	Ceramides	68-76	diazepam binding inhibitor	Mus musculus	90-94
28179144-0	2017	Plasma membrane reorganization links acid sphingomyelinase/ceramide to p38 MAPK pathways in endothelial cells apoptosis.	Ceramides	59-67	mitogen-activated protein kinase 14	Homo sapiens	71-74
28469091-5	2017	Following myocardial infarction (MI), serine palmitoyl transferase (SPT), the rate-limiting enzyme of the de novo pathway of ceramide synthesis, and ceramides were found increased.	Ceramides	125-133	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	38-66
28469091-5	2017	Following myocardial infarction (MI), serine palmitoyl transferase (SPT), the rate-limiting enzyme of the de novo pathway of ceramide synthesis, and ceramides were found increased.	Ceramides	125-133	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	68-71
28469091-6	2017	Blockade of SPT by the specific inhibitor myriocin reduced ceramide accumulation in ischemic cardiomyopathy and decreased C16, C24:1, and C24 ceramides.	Ceramides	59-67	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	12-15
28469091-6	2017	Blockade of SPT by the specific inhibitor myriocin reduced ceramide accumulation in ischemic cardiomyopathy and decreased C16, C24:1, and C24 ceramides.	Ceramides	142-151	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	12-15
28153611-0	2017	Phosphoglycerol dihydroceramide, a distinctive ceramide produced by Porphyromonas gingivalis, promotes RANKL-induced osteoclastogenesis by acting on non-muscle myosin II-A (Myh9), an osteoclast cell fusion regulatory factor.	Ceramides	23-31	tumor necrosis factor (ligand) superfamily, member 11	Mus musculus	103-108
28153611-0	2017	Phosphoglycerol dihydroceramide, a distinctive ceramide produced by Porphyromonas gingivalis, promotes RANKL-induced osteoclastogenesis by acting on non-muscle myosin II-A (Myh9), an osteoclast cell fusion regulatory factor.	Ceramides	23-31	myosin, heavy polypeptide 9, non-muscle	Mus musculus	173-177
28153611-8	2017	Taken together, our data indicated that PGDHC is a Pg-derived, cell-permeable ceramide that possesses a unique property of promoting osteoclastogenesis via interaction with Myh9 which, in turn, activates a Rac1/DC-STAMP pathway for upregulation of osteoclast cell fusion.	Ceramides	78-86	myosin, heavy polypeptide 9, non-muscle	Mus musculus	173-177
28179144-3	2017	Despite a suggested link between the p38 MAPK and ceramide pathways, the exact molecular events of this connection remain elusive.	Ceramides	50-58	mitogen-activated protein kinase 14	Homo sapiens	37-40
28179144-4	2017	In the present study, by using two different activators of p38 MAPK, namely anisomycin and ionizing radiation, we depicted how ceramide generated by acid sphingomyelinase was involved in p38 MAPK-dependent apoptosis of endothelial cells.	Ceramides	127-135	mitogen-activated protein kinase 14	Homo sapiens	59-62
28179144-4	2017	In the present study, by using two different activators of p38 MAPK, namely anisomycin and ionizing radiation, we depicted how ceramide generated by acid sphingomyelinase was involved in p38 MAPK-dependent apoptosis of endothelial cells.	Ceramides	127-135	mitogen-activated protein kinase 14	Homo sapiens	187-190
28179144-9	2017	Altogether, our results proved that the plasma membrane reorganization leading to ceramide production is essential for stress-induced activation of p38 MAPK and apoptosis in endothelial cells and established the link between the acid sphingomyelinase/ceramide and p38 MAPK pathways.	Ceramides	82-90	mitogen-activated protein kinase 14	Homo sapiens	148-151
28179144-9	2017	Altogether, our results proved that the plasma membrane reorganization leading to ceramide production is essential for stress-induced activation of p38 MAPK and apoptosis in endothelial cells and established the link between the acid sphingomyelinase/ceramide and p38 MAPK pathways.	Ceramides	82-90	mitogen-activated protein kinase 14	Homo sapiens	264-267
28179144-9	2017	Altogether, our results proved that the plasma membrane reorganization leading to ceramide production is essential for stress-induced activation of p38 MAPK and apoptosis in endothelial cells and established the link between the acid sphingomyelinase/ceramide and p38 MAPK pathways.	Ceramides	251-259	mitogen-activated protein kinase 14	Homo sapiens	148-151
28707656-6	2017	The regulation of the main mammalian stress-inducible factor HSF1 and Drosophila melanogaster HSF includes many components, such as a variety of early warning signals indicative of abnormal cell activity (e.g., increases in intracellular ceramide, cytosolic calcium ions, or partly denatured proteins); protein kinases, which phosphorylate HSFs at various Ser residues; acetyltransferases; and regulatory proteins, such as SUMO and HSBP1.	Ceramides	238-246	heat shock transcription factor 1	Homo sapiens	61-65
28357533-8	2017	Mechanistically, ceramide levels were suppressed by chemotherapy via increasing mRNA and protein levels of UDP-glucose ceramide glucosyltransferase (UGCG).	Ceramides	17-25	UDP-glucose ceramide glucosyltransferase	Homo sapiens	107-147
28357533-8	2017	Mechanistically, ceramide levels were suppressed by chemotherapy via increasing mRNA and protein levels of UDP-glucose ceramide glucosyltransferase (UGCG).	Ceramides	17-25	UDP-glucose ceramide glucosyltransferase	Homo sapiens	149-153
28357533-10	2017	CONCLUSIONS: This study clearly demonstrated that the decreased ceramide production via up-regulating UGCG was involved in the resistance of breast cancer cells to chemotherapy.	Ceramides	64-72	UDP-glucose ceramide glucosyltransferase	Homo sapiens	102-106
28336574-2	2017	Its production involves the transfer of phosphocholine from phosphatidylcholine onto ceramide, a reaction catalyzed by SM synthase (SMS)1 in the Golgi and SMS2 at the plasma membrane.	Ceramides	85-93	sphingomyelin synthase 2	Homo sapiens	119-130
28336574-2	2017	Its production involves the transfer of phosphocholine from phosphatidylcholine onto ceramide, a reaction catalyzed by SM synthase (SMS)1 in the Golgi and SMS2 at the plasma membrane.	Ceramides	85-93	sphingomyelin synthase 1	Homo sapiens	132-137
28336574-2	2017	Its production involves the transfer of phosphocholine from phosphatidylcholine onto ceramide, a reaction catalyzed by SM synthase (SMS)1 in the Golgi and SMS2 at the plasma membrane.	Ceramides	85-93	sphingomyelin synthase 2	Homo sapiens	155-159
28322796-3	2017	PTX (20 nM) suppressed cell proliferation and increased various ceramide species in PC3, but not PC3-PR, cells.	Ceramides	64-72	proprotein convertase subtilisin/kexin type 1	Homo sapiens	84-87
28322796-7	2017	Similarly, GCS inhibitors (PDMP and PPMP) increased cellular ceramides and suppressed the proliferation of PC3-PR.	Ceramides	61-70	UDP-glucose ceramide glucosyltransferase	Homo sapiens	11-14
28329765-1	2017	Adiponectin receptors (ADIPORs) are integral membrane proteins that control glucose and lipid metabolism by mediating, at least in part, a cellular ceramidase activity that catalyses the hydrolysis of ceramide to produce sphingosine and a free fatty acid (FFA).	Ceramides	201-209	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
28292932-1	2017	Absorption of dietary sphingomyelin (SM) requires its initial degradation into ceramide, a process catalyzed by the intestinal enzyme alkaline sphingomyelinase (alk-SMase, NPP7, ENPP7).	Ceramides	79-87	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	116-170
28292932-1	2017	Absorption of dietary sphingomyelin (SM) requires its initial degradation into ceramide, a process catalyzed by the intestinal enzyme alkaline sphingomyelinase (alk-SMase, NPP7, ENPP7).	Ceramides	79-87	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	178-183
28189725-0	2017	Role of P-glycoprotein inhibitors in ceramide-based therapeutics for treatment of cancer.	Ceramides	37-45	ATP binding cassette subfamily B member 1	Homo sapiens	8-22
28189725-2	2017	Earlier works using the ceramide analog, C6-ceramide, demonstrated that the antiestrogen tamoxifen, a first generation P-glycoprotein (P-gp) inhibitor, blocked C6-ceramide glycosylation and magnified apoptotic responses.	Ceramides	24-32	ATP binding cassette subfamily B member 1	Homo sapiens	119-133
28189725-2	2017	Earlier works using the ceramide analog, C6-ceramide, demonstrated that the antiestrogen tamoxifen, a first generation P-glycoprotein (P-gp) inhibitor, blocked C6-ceramide glycosylation and magnified apoptotic responses.	Ceramides	24-32	ATP binding cassette subfamily B member 1	Homo sapiens	135-139
28420138-2	2017	Acid sphingomyelinase (SMPD1)-the principal regulator for rapid and transient generation of the lipid mediator ceramide-is involved in both the regulation of host response in sepsis as well as in the pathogenesis of chronic heart failure.	Ceramides	111-119	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
28420138-2	2017	Acid sphingomyelinase (SMPD1)-the principal regulator for rapid and transient generation of the lipid mediator ceramide-is involved in both the regulation of host response in sepsis as well as in the pathogenesis of chronic heart failure.	Ceramides	111-119	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-28
28420138-5	2017	Additionally, ceramide formation in cardiac tissue was dysregulated in SMPD1+/+ as well as SMPD1-/- animals, whereas desipramine pretreatment resulted in stable, but increased ceramide content during host response.	Ceramides	14-22	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	71-76
28420138-5	2017	Additionally, ceramide formation in cardiac tissue was dysregulated in SMPD1+/+ as well as SMPD1-/- animals, whereas desipramine pretreatment resulted in stable, but increased ceramide content during host response.	Ceramides	14-22	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	91-96
28379228-1	2017	Dihydroceramide desaturase 1 (Des1) catalyzes the last step of ceramide synthesis de novo, thus regulating the physiologically relevant balance between dihydrosphingolipids and sphingolipids.	Ceramides	7-15	delta 4-desaturase, sphingolipid 1	Homo sapiens	30-34
28189725-9	2017	In summary, our work details discovery of the link between P-gp inhibitors and the regulation and potentiation of ceramide metabolism in a pro-apoptotic direction in cancer cells.	Ceramides	114-122	ATP binding cassette subfamily B member 1	Homo sapiens	59-63
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.	Ceramides	101-109	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.	Ceramides	101-109	glucosylceramidase beta 2	Homo sapiens	80-84
28329765-5	2017	We also identify a ceramide binding pose and propose a possible mechanism for the hydrolytic activity of ADIPOR2 using computational approaches.	Ceramides	19-27	adiponectin receptor 2	Homo sapiens	105-112
28206952-4	2017	At the signaling level, icaritin inhibited sphingosine kinase 1 (SphK1) activity in HCC cells, which led to pro-apoptotic ceramide production and JNK1 activation.	Ceramides	122-130	sphingosine kinase 1	Homo sapiens	43-63
28206952-4	2017	At the signaling level, icaritin inhibited sphingosine kinase 1 (SphK1) activity in HCC cells, which led to pro-apoptotic ceramide production and JNK1 activation.	Ceramides	122-130	sphingosine kinase 1	Homo sapiens	65-70
27826095-0	2017	Oroscomucoid like protein 3 (ORMDL3) transgenic mice have reduced levels of sphingolipids including sphingosine-1-phosphate and ceramide.	Ceramides	128-136	ORM1-like 3 (S. cerevisiae)	Mus musculus	0-27
28236661-7	2017	Upon depletion of endogenous sphingosine by myriocin treatment, Fam20C activity drops to negligible values both in the lysate and in the conditioned medium; however, it can be partially restored if during myriocin treatment cells are supplemented with either exogenous sphingosine or ceramide, a sphingosine precursor.	Ceramides	284-292	FAM20C golgi associated secretory pathway kinase	Homo sapiens	64-70
27826095-0	2017	Oroscomucoid like protein 3 (ORMDL3) transgenic mice have reduced levels of sphingolipids including sphingosine-1-phosphate and ceramide.	Ceramides	128-136	ORM1-like 3 (S. cerevisiae)	Mus musculus	29-35
28237558-0	2017	Iminosugar-based ceramide mimicry for the design of new CERT START domain ligands.	Ceramides	17-25	ceramide transporter 1	Homo sapiens	56-60
26960947-8	2017	Gene expression analysis showed that neutrophils, mast cells, and T-cells were found to be increased in PVAT compared with AAA as well as cathepsin K and S. The concentration of ceramides in PVAT was determined using mass spectrometry and correlated with content of T-cells in the PVAT.	Ceramides	178-187	cathepsin K	Homo sapiens	138-149
28138018-8	2017	ASMase hydrolyzes sphingomyelin to ceramide on the outer leaflet of the membrane at acidic pH.	Ceramides	35-43	sphingomyelin phosphodiesterase 1	Homo sapiens	0-6
28138018-9	2017	Ceramide was detected in cytoplasmic vesicles containing C2IIa.	Ceramides	0-8	endogenous retrovirus group K member 24	Homo sapiens	57-62
28322247-7	2017	Indeed, TCA treatment of HSCs promoted accumulation of ceramide through inhibition of acid ceramidase (aCDase).	Ceramides	55-63	N-acylsphingosine amidohydrolase 1	Homo sapiens	86-101
28322247-7	2017	Indeed, TCA treatment of HSCs promoted accumulation of ceramide through inhibition of acid ceramidase (aCDase).	Ceramides	55-63	N-acylsphingosine amidohydrolase 1	Homo sapiens	103-109
28322247-8	2017	Depletion of aCDase also promoted accumulation of ceramide and was associated with reduced COL1A1 expression.	Ceramides	50-58	N-acylsphingosine amidohydrolase 1	Homo sapiens	13-19
28223543-1	2017	Acid sphingomyelinase (A-SMase) plays an important role in the initiation of CD95 signaling by forming ceramide-enriched membrane domains that enable clustering and activation of the death receptors.	Ceramides	103-111	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
28223543-1	2017	Acid sphingomyelinase (A-SMase) plays an important role in the initiation of CD95 signaling by forming ceramide-enriched membrane domains that enable clustering and activation of the death receptors.	Ceramides	103-111	sphingomyelin phosphodiesterase 1	Homo sapiens	23-30
28223543-1	2017	Acid sphingomyelinase (A-SMase) plays an important role in the initiation of CD95 signaling by forming ceramide-enriched membrane domains that enable clustering and activation of the death receptors.	Ceramides	103-111	Fas cell surface death receptor	Homo sapiens	77-81
28462076-2	2017	Acid sphingomyelinase (ASM) converts the membrane lipid sphingomyelin to ceramide, thereby affecting membrane composition and domain formation.	Ceramides	73-81	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
28462076-2	2017	Acid sphingomyelinase (ASM) converts the membrane lipid sphingomyelin to ceramide, thereby affecting membrane composition and domain formation.	Ceramides	73-81	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
28273483-2	2017	We demonstrate that ACSL5-generated FA-CoA was utilized with de novo ceramide for the generation of acylceramides, poorly studied ceramide metabolites.	Ceramides	69-77	acyl-CoA synthetase long-chain family member 5	Mus musculus	20-25
28273483-2	2017	We demonstrate that ACSL5-generated FA-CoA was utilized with de novo ceramide for the generation of acylceramides, poorly studied ceramide metabolites.	Ceramides	104-112	acyl-CoA synthetase long-chain family member 5	Mus musculus	20-25
28301620-20	2017	Comparable itch relief to hydrocortisone 1% cream was seen with the ceramide-containing cream over an 8-hour period following a single application.	Ceramides	68-76	itchy E3 ubiquitin protein ligase	Homo sapiens	11-15
28314284-7	2017	RESULTS: In serum of patients with CRC, the levels of C16-, C18-, C18:1-, and C24:1-ceramide, as well as those of sphingosine, were significantly higher than those of controls.	Ceramides	84-92	Bardet-Biedl syndrome 9	Homo sapiens	66-69
28277984-1	2017	Previous studies have revealed the activation of neutral sphingomyelinase (N-SMase)/ceramide pathway in hepatic tissue following warm liver ischemia reperfusion (IR) injury.	Ceramides	84-92	sphingomyelin phosphodiesterase 2	Rattus norvegicus	49-73
28277984-1	2017	Previous studies have revealed the activation of neutral sphingomyelinase (N-SMase)/ceramide pathway in hepatic tissue following warm liver ischemia reperfusion (IR) injury.	Ceramides	84-92	sphingomyelin phosphodiesterase 2	Rattus norvegicus	75-82
28277984-8	2017	Treatment with a specific N-SMase inhibitor significantly decreased all measured ceramides in IR injury.	Ceramides	81-90	sphingomyelin phosphodiesterase 2	Rattus norvegicus	26-33
27158772-4	2017	It is known that both, ceramide and hypericin can significantly influence protein kinase C (PKC) activity.	Ceramides	23-31	protein kinase C delta	Homo sapiens	92-95
28231980-8	2017	The PP1 activator C2 ceramide increased alkaline phosphatase activity, mineralized nodule formation, and mRNA expression of dentin matrix protein 1 and dentin sialophosphoprotein.	Ceramides	21-29	neuropeptide Y receptor Y4	Homo sapiens	4-7
28231980-8	2017	The PP1 activator C2 ceramide increased alkaline phosphatase activity, mineralized nodule formation, and mRNA expression of dentin matrix protein 1 and dentin sialophosphoprotein.	Ceramides	21-29	dentin matrix acidic phosphoprotein 1	Homo sapiens	124-147
28351964-1	2017	Cardiac-specific overexpression of vascular endothelial growth factor (VEGF)-B167 is known to induce left ventricular hypertrophy due to altered lipid metabolism, in which ceramides accumulate to the heart and cause mitochondrial damage.	Ceramides	172-181	vascular endothelial growth factor A	Mus musculus	35-69
28231980-11	2017	C2 ceramide increased levels of bone morphogenetic protein 2, phosphorylation of Smad 1/5/8, and mRNA expression of runt-related transcription factor 2 and osterix.	Ceramides	3-11	bone morphogenetic protein 2	Homo sapiens	32-60
28231980-11	2017	C2 ceramide increased levels of bone morphogenetic protein 2, phosphorylation of Smad 1/5/8, and mRNA expression of runt-related transcription factor 2 and osterix.	Ceramides	3-11	SMAD family member 1	Homo sapiens	81-91
28231980-11	2017	C2 ceramide increased levels of bone morphogenetic protein 2, phosphorylation of Smad 1/5/8, and mRNA expression of runt-related transcription factor 2 and osterix.	Ceramides	3-11	RUNX family transcription factor 2	Homo sapiens	116-151
28231980-11	2017	C2 ceramide increased levels of bone morphogenetic protein 2, phosphorylation of Smad 1/5/8, and mRNA expression of runt-related transcription factor 2 and osterix.	Ceramides	3-11	Sp7 transcription factor	Homo sapiens	156-163
28088541-6	2017	In support of a function in vesicular trafficking at the level of the ER, we provide evidence for altered cellular ceramide composition upon CerS2 knockdown and increased activity of Rab1 in CHO-IgG cells depleted of Tbc1D20.	Ceramides	115-123	ceramide synthase 2	Cricetulus griseus	141-146
28351964-1	2017	Cardiac-specific overexpression of vascular endothelial growth factor (VEGF)-B167 is known to induce left ventricular hypertrophy due to altered lipid metabolism, in which ceramides accumulate to the heart and cause mitochondrial damage.	Ceramides	172-181	vascular endothelial growth factor A	Mus musculus	71-75
27984697-8	2017	Subsequent multivariate statistical analysis of the spectral data revealed significant localization of gangliosides and ceramides species to Abeta positive plaques, which was accompanied by distinct local reduction of sulfatides.	Ceramides	120-129	amyloid beta (A4) precursor protein	Mus musculus	141-146
28424433-0	2017	[Investigating the role of ceramide metabolism-associated CERS5 (LASS5) gene in atherosclerosis pathogenesis in endothelial cells].	Ceramides	27-35	ceramide synthase 5	Homo sapiens	58-63
28424433-0	2017	[Investigating the role of ceramide metabolism-associated CERS5 (LASS5) gene in atherosclerosis pathogenesis in endothelial cells].	Ceramides	27-35	ceramide synthase 5	Homo sapiens	65-70
28424433-3	2017	Ceramide synthase 5 (LASS5 or CERS5) gene has function in de novo synthesis of ceramide, and has indirect effect on AMPK gene.	Ceramides	79-87	ceramide synthase 5	Homo sapiens	0-19
28424433-3	2017	Ceramide synthase 5 (LASS5 or CERS5) gene has function in de novo synthesis of ceramide, and has indirect effect on AMPK gene.	Ceramides	79-87	ceramide synthase 5	Homo sapiens	21-26
28424433-3	2017	Ceramide synthase 5 (LASS5 or CERS5) gene has function in de novo synthesis of ceramide, and has indirect effect on AMPK gene.	Ceramides	79-87	ceramide synthase 5	Homo sapiens	30-35
28424433-3	2017	Ceramide synthase 5 (LASS5 or CERS5) gene has function in de novo synthesis of ceramide, and has indirect effect on AMPK gene.	Ceramides	79-87	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	116-120
28424433-8	2017	Downregulation of LASS5 was found to attenuate ceramide production and increase expression of some AMPK target genes in HUVEC.	Ceramides	47-55	ceramide synthase 5	Homo sapiens	18-23
28073916-12	2017	Thus, ceramide-CD300f binding inhibits LPS-induced skin inflammation, implicating CD300f as a negative regulator of Toll-like receptor 4 (TLR4) signaling in vivo.	Ceramides	6-14	toll-like receptor 4	Mus musculus	116-136
28073916-12	2017	Thus, ceramide-CD300f binding inhibits LPS-induced skin inflammation, implicating CD300f as a negative regulator of Toll-like receptor 4 (TLR4) signaling in vivo.	Ceramides	6-14	toll-like receptor 4	Mus musculus	138-142
28223344-4	2017	Intestinal FXR inhibition decreased ceramide levels by suppressing expression of genes involved in ceramide synthesis specifically in the intestinal ileum epithelial cells.	Ceramides	36-44	nuclear receptor subfamily 1, group H, member 4	Mus musculus	11-14
28223344-4	2017	Intestinal FXR inhibition decreased ceramide levels by suppressing expression of genes involved in ceramide synthesis specifically in the intestinal ileum epithelial cells.	Ceramides	99-107	nuclear receptor subfamily 1, group H, member 4	Mus musculus	11-14
28223344-5	2017	The lower serum ceramides mediated decreased hepatic mitochondrial acetyl-CoA levels and pyruvate carboxylase (PC) activities and attenuated hepatic gluconeogenesis, independent of body weight change and hepatic insulin signaling in vivo; this was reversed by treatment of mice with ceramides or the FXR agonist GW4064.	Ceramides	16-25	pyruvate carboxylase	Mus musculus	89-109
28223344-5	2017	The lower serum ceramides mediated decreased hepatic mitochondrial acetyl-CoA levels and pyruvate carboxylase (PC) activities and attenuated hepatic gluconeogenesis, independent of body weight change and hepatic insulin signaling in vivo; this was reversed by treatment of mice with ceramides or the FXR agonist GW4064.	Ceramides	16-25	nuclear receptor subfamily 1, group H, member 4	Mus musculus	300-303
28223344-6	2017	Ceramides substantially attenuated mitochondrial citrate synthase activities primarily through the induction of endoplasmic reticulum stress, which triggers increased hepatic mitochondrial acetyl-CoA levels and PC activities.	Ceramides	0-9	citrate synthase	Mus musculus	49-65
27894925-6	2017	RESULTS: The compounds activity on autophagy induction took place concomitantly with accumulation of dihydroceramides, which occurred by both stimulation of ceramide synthesis de novo and reduction of Des1 activity.	Ceramides	108-116	delta 4-desaturase, sphingolipid 1	Homo sapiens	201-205
28191815-11	2017	CB2 activation led to ceramide-mediated BC cell apoptosis independently of SL constitutive composition, which instead was modulated by CB2 agonists to reduce cell motility.	Ceramides	22-30	cannabinoid receptor 2	Homo sapiens	0-3
28141794-5	2017	Moreover, DAPK1 overexpression increased neuronal cell death through NDRG2 phosphorylation after ceramide treatment.	Ceramides	97-105	death associated protein kinase 1	Mus musculus	10-15
28141794-5	2017	Moreover, DAPK1 overexpression increased neuronal cell death through NDRG2 phosphorylation after ceramide treatment.	Ceramides	97-105	N-myc downstream regulated gene 2	Mus musculus	69-74
28141794-8	2017	In addition, DAPK1 ablation suppressed ceramide-induced cell death in mouse brain and neuronal cell death in Tg2576 APPswe-overexpressing mice.	Ceramides	39-47	death associated protein kinase 1	Mus musculus	13-18
27836988-8	2017	Interestingly, SMPDL3b-overexpressing podocytes had higher basal levels of sphingosine-1-phosphate and maintained basal ceramide levels after irradiation.	Ceramides	120-128	sphingomyelin phosphodiesterase acid like 3B	Homo sapiens	15-22
28035360-10	2017	Finally, the suppression of ceramide generation via A-SMase inhibition or de novo ceramide synthesis decreased high-fat diet-induced hepatic cytokine production in vivo.	Ceramides	28-36	sphingomyelin phosphodiesterase 1	Homo sapiens	52-59
28120887-1	2017	SMSr/SAMD8 is an ER-resident ceramide phosphoethanolamine synthase with a critical role in controlling ER ceramides and suppressing ceramide-induced apoptosis in cultured cells.	Ceramides	106-115	sterile alpha motif domain containing 8	Homo sapiens	0-4
27866044-2	2017	A recently developed pathogenic model of MDD involves disturbed neurogenesis in the hippocampus, where the acid sphingomyelinase (ASM)/ceramide system plays an important role and is proposed as a molecular target for antidepressant action.	Ceramides	135-143	sphingomyelin phosphodiesterase 1	Homo sapiens	107-128
27866044-2	2017	A recently developed pathogenic model of MDD involves disturbed neurogenesis in the hippocampus, where the acid sphingomyelinase (ASM)/ceramide system plays an important role and is proposed as a molecular target for antidepressant action.	Ceramides	135-143	sphingomyelin phosphodiesterase 1	Homo sapiens	130-133
28001010-9	2017	In contrast, GM3 gangliosides, several ceramides, a triacylglycerol potentially containing arachidonate, and cholesteryl palmitate were downregulated by LBP KD.	Ceramides	39-48	lipopolysaccharide binding protein	Homo sapiens	153-156
26801188-8	2017	Bax interaction with the polar regions of ceramide results in MOM permeabilization through synergy with ceramide.	Ceramides	42-50	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
26801188-8	2017	Bax interaction with the polar regions of ceramide results in MOM permeabilization through synergy with ceramide.	Ceramides	104-112	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
28120887-1	2017	SMSr/SAMD8 is an ER-resident ceramide phosphoethanolamine synthase with a critical role in controlling ER ceramides and suppressing ceramide-induced apoptosis in cultured cells.	Ceramides	106-115	sterile alpha motif domain containing 8	Homo sapiens	5-10
28120887-1	2017	SMSr/SAMD8 is an ER-resident ceramide phosphoethanolamine synthase with a critical role in controlling ER ceramides and suppressing ceramide-induced apoptosis in cultured cells.	Ceramides	29-37	sterile alpha motif domain containing 8	Homo sapiens	0-4
28120887-1	2017	SMSr/SAMD8 is an ER-resident ceramide phosphoethanolamine synthase with a critical role in controlling ER ceramides and suppressing ceramide-induced apoptosis in cultured cells.	Ceramides	29-37	sterile alpha motif domain containing 8	Homo sapiens	5-10
28120887-2	2017	SMSr-mediated ceramide homeostasis relies on the enzyme"s catalytic activity as well as on its N-terminal sterile alpha-motif or SAM domain.	Ceramides	14-22	sterile alpha motif domain containing 8	Homo sapiens	0-4
27888218-0	2017	Diverting CERT-mediated ceramide transport to mitochondria triggers Bax-dependent apoptosis.	Ceramides	24-32	ceramide transporter 1	Homo sapiens	10-14
27888218-0	2017	Diverting CERT-mediated ceramide transport to mitochondria triggers Bax-dependent apoptosis.	Ceramides	24-32	BCL2 associated X, apoptosis regulator	Homo sapiens	68-71
27888218-3	2017	Here, we have analyzed the consequences of targeting the biosynthetic flow of ceramides to mitochondria using a ceramide transfer protein (encoded by COL4A3BP) equipped with an OMM anchor, mitoCERT.	Ceramides	78-87	ceramide transporter 1	Homo sapiens	150-158
27888218-5	2017	Apoptosis induction by mitoCERT was abolished through (i) removal of its ceramide transfer domain, (ii) disruption of its interaction with VAMP-associated proteins (VAPs) in the ER, (iii) addition of antagonistic CERT inhibitor HPA12, (iv) blocking de novo ceramide synthesis and (v) targeting of a bacterial ceramidase to mitochondria.	Ceramides	73-81	ceramide transporter 1	Homo sapiens	27-31
27888218-5	2017	Apoptosis induction by mitoCERT was abolished through (i) removal of its ceramide transfer domain, (ii) disruption of its interaction with VAMP-associated proteins (VAPs) in the ER, (iii) addition of antagonistic CERT inhibitor HPA12, (iv) blocking de novo ceramide synthesis and (v) targeting of a bacterial ceramidase to mitochondria.	Ceramides	257-265	ceramide transporter 1	Homo sapiens	27-31
28011845-4	2017	We find that the yeast protein Nvj2p promotes the nonvesicular transfer of ceramides from the ER to the Golgi complex.	Ceramides	75-84	Nvj2p	Saccharomyces cerevisiae S288C	31-36
28081222-7	2017	Further studies demonstrated that AT7867 inhibited sphingosine kinase 1 (SphK1) activity to promote pro-apoptotic ceramide production in HT-29 cells.	Ceramides	114-122	sphingosine kinase 1	Homo sapiens	51-71
28081222-7	2017	Further studies demonstrated that AT7867 inhibited sphingosine kinase 1 (SphK1) activity to promote pro-apoptotic ceramide production in HT-29 cells.	Ceramides	114-122	sphingosine kinase 1	Homo sapiens	73-78
27876618-0	2017	TLR4/NF-kappaB/Ceramide signaling contributes to Ox-LDL-induced calcification of human vascular smooth muscle cells.	Ceramides	15-23	toll like receptor 4	Homo sapiens	0-4
28268212-0	2017	Inhibition of Ceramide Decreased the Expression of ATP-Binding Cassette Transporter G5/8 mRNA in an Animal Model of Cholesterol Gallstone.	Ceramides	14-22	ATP binding cassette subfamily G member 5	Homo sapiens	51-88
28585211-4	2017	Insulin resistance with the deficiency of insulin receptor substrate-2 (IRS-2)-associated phosphatidylinositol 3-kinase (PI3K) activity causes an increase in intracellular fatty acid-derived metabolites such as diacylglycerol, fatty acyl CoA or ceramides.	Ceramides	245-254	insulin receptor substrate 2	Homo sapiens	42-70
28585211-4	2017	Insulin resistance with the deficiency of insulin receptor substrate-2 (IRS-2)-associated phosphatidylinositol 3-kinase (PI3K) activity causes an increase in intracellular fatty acid-derived metabolites such as diacylglycerol, fatty acyl CoA or ceramides.	Ceramides	245-254	insulin receptor substrate 2	Homo sapiens	72-77
28009749-5	2017	RESULTS: Acid sphingomyelinase activity in pRBCs was associated with the formation of ceramide and the release of microparticles.	Ceramides	86-94	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	9-30
27940403-1	2017	BACKGROUND AND AIMS: Plasma sphingolipids including ceramides, and gangliosides are associated with insulin resistance (IR) through effects on insulin signalling and glucose metabolism.	Ceramides	52-61	insulin	Homo sapiens	100-107
27940403-1	2017	BACKGROUND AND AIMS: Plasma sphingolipids including ceramides, and gangliosides are associated with insulin resistance (IR) through effects on insulin signalling and glucose metabolism.	Ceramides	52-61	insulin	Homo sapiens	143-150
28634575-0	2017	Association between Plasmatic Ceramides Profile and AST/ALT Ratio: C14:0 Ceramide as Predictor of Hepatic Steatosis in Adolescents Independently of Obesity.	Ceramides	30-39	solute carrier family 17 member 5	Homo sapiens	52-55
28634575-0	2017	Association between Plasmatic Ceramides Profile and AST/ALT Ratio: C14:0 Ceramide as Predictor of Hepatic Steatosis in Adolescents Independently of Obesity.	Ceramides	30-38	solute carrier family 17 member 5	Homo sapiens	52-55
28634575-6	2017	RESULTS: All ceramides correlated directly with ALT levels and inversely with ALT/AST ratio; the strongest correlation was observed among C14:0 ceramide (r = 0.41 and r = -0.54, resp.; P &lt; 0.001).	Ceramides	13-22	solute carrier family 17 member 5	Homo sapiens	82-85
28634575-6	2017	RESULTS: All ceramides correlated directly with ALT levels and inversely with ALT/AST ratio; the strongest correlation was observed among C14:0 ceramide (r = 0.41 and r = -0.54, resp.; P &lt; 0.001).	Ceramides	13-21	solute carrier family 17 member 5	Homo sapiens	82-85
27744579-8	2017	These findings indicate a novel pathway in tumor metastasis, i.e., tumor cell mediated activation of P-selectin in platelets, followed by activation and secretion of Asm and in turn release of ceramide and tumor metastasis.	Ceramides	193-201	selectin, platelet	Mus musculus	101-111
27736726-2	2017	The short chain C10:0 ceramide is an asymmetric lipid which consists of an 18 carbon sphingosine base N-acylated with decanoic acid.	Ceramides	22-30	homeobox C10	Homo sapiens	16-19
28214863-7	2017	RESULTS: A 48h CRP treatment significantly increased the percentage of annexin-V-binding cells (&gt;=5microg/ml), [Ca2+]i (&gt;=5microg/ml), ceramide (20microg/ml) and caspase-activity (20microg/ml).	Ceramides	141-149	C-reactive protein	Homo sapiens	15-18
28214863-11	2017	CONCLUSION: C-reactive protein triggers eryptosis, an effect at least partially due to increase of [Ca2+]i, increase of ceramide abundance and caspase activation.	Ceramides	120-128	C-reactive protein	Homo sapiens	12-30
27736726-6	2017	Molecular asymmetry due to the different length of the sphingosine and the N-acyl chains of C10:0 ceramide may explain why this novel phase is formed.	Ceramides	98-106	homeobox C10	Homo sapiens	92-95
28249275-6	2017	This is mediated by FXR modulating in part the expression of genes involved in ceramide synthesis in the small intestine.	Ceramides	79-87	nuclear receptor subfamily 1, group H, member 4	Mus musculus	20-23
28249275-7	2017	In ileum of obese mice due to the presence of endogenous FXR agonists produced in the liver, these genes are activated, while in mice with altered levels of specific gut bacteria, levels of an FXR antagonist, tauro-beta-muricholic acid (T-beta-MCA) increase and FXR signaling and ceramide synthesis are repressed.	Ceramides	280-288	nuclear receptor subfamily 1, group H, member 4	Mus musculus	57-60
28249275-9	2017	These studies reveal that ceramides produced in the ileum under the control of FXR, influence metabolic disease, and suggest that novel FXR antagonist such as Gly-MCA that specifically inhibit intestine FXR, could serve as potential drug for the treatment of metabolic disease.	Ceramides	26-35	nuclear receptor subfamily 1, group H, member 4	Mus musculus	79-82
28249275-9	2017	These studies reveal that ceramides produced in the ileum under the control of FXR, influence metabolic disease, and suggest that novel FXR antagonist such as Gly-MCA that specifically inhibit intestine FXR, could serve as potential drug for the treatment of metabolic disease.	Ceramides	26-35	nuclear receptor subfamily 1, group H, member 4	Mus musculus	136-139
28249275-9	2017	These studies reveal that ceramides produced in the ileum under the control of FXR, influence metabolic disease, and suggest that novel FXR antagonist such as Gly-MCA that specifically inhibit intestine FXR, could serve as potential drug for the treatment of metabolic disease.	Ceramides	26-35	nuclear receptor subfamily 1, group H, member 4	Mus musculus	136-139
28268212-3	2017	We investigated whether ceramide plays a role in cholesterol efflux through the ABC transporters.	Ceramides	24-32	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	80-83
28268212-9	2017	CONCLUSIONS: The inhibition of ceramide biosynthesis by myriocin suppressed gallstone formation and ABCG5/8 mRNA expression.	Ceramides	31-39	ATP binding cassette subfamily G member 5	Homo sapiens	100-107
28268212-10	2017	We expect that ceramide"s role as a regulator of the ABCG5/8 transporter might be linked to cholesterol gallstone formation.	Ceramides	15-23	ATP binding cassette subfamily G member 5	Homo sapiens	53-58
27865938-0	2017	PDMP, a ceramide analogue, acts as an inhibitor of mTORC1 by inducing its translocation from lysosome to endoplasmic reticulum.	Ceramides	8-16	CREB regulated transcription coactivator 1	Mus musculus	51-57
28123341-0	2017	Downregulation of lipin-1 induces insulin resistance by increasing intracellular ceramide accumulation in C2C12 myotubes.	Ceramides	81-89	lipin 1	Mus musculus	18-25
28123341-7	2017	Lipin-1 silencing reduced intracellular DAG and TAG levels, but elevated ceramide accumulation in C2C12 myotubes.	Ceramides	73-81	lipin 1	Mus musculus	0-7
28123341-8	2017	Moreover, the impaired insulin stimulated Akt phosphorylation and glucose uptake caused by lipin-1 silencing could be blocked by the pretreatment with SPT inhibitor myriocin, ceramide synthase inhibitor FB1, or PP2A inhibitor okadaic acid, suggested that the increased ceramide accumulation might be responsible for the development of insulin resistance induced by lipin-1 silencing in C2C12 myotubes.	Ceramides	175-183	thymoma viral proto-oncogene 1	Mus musculus	42-45
28123341-8	2017	Moreover, the impaired insulin stimulated Akt phosphorylation and glucose uptake caused by lipin-1 silencing could be blocked by the pretreatment with SPT inhibitor myriocin, ceramide synthase inhibitor FB1, or PP2A inhibitor okadaic acid, suggested that the increased ceramide accumulation might be responsible for the development of insulin resistance induced by lipin-1 silencing in C2C12 myotubes.	Ceramides	175-183	lipin 1	Mus musculus	91-98
28123341-10	2017	Therefore, our study suggests that lipin-1 plays an important role in lipid metabolism and downregulation of lipin-1 induces insulin resistance by increasing intracellular ceramide accumulation in C2C12 myotubes.	Ceramides	172-180	lipin 1	Mus musculus	35-42
28123341-10	2017	Therefore, our study suggests that lipin-1 plays an important role in lipid metabolism and downregulation of lipin-1 induces insulin resistance by increasing intracellular ceramide accumulation in C2C12 myotubes.	Ceramides	172-180	lipin 1	Mus musculus	109-116
28922150-2	2017	Since the ceramide transporter protein (CERT) is the only known protein able to mediate non-vesicular transfer of ceramide between organelle membranes, the modulation of CERT function may impact on ceramide accumulation.	Ceramides	10-18	ceramide transporter 1	Homo sapiens	40-44
28922150-2	2017	Since the ceramide transporter protein (CERT) is the only known protein able to mediate non-vesicular transfer of ceramide between organelle membranes, the modulation of CERT function may impact on ceramide accumulation.	Ceramides	10-18	ceramide transporter 1	Homo sapiens	170-174
28922150-2	2017	Since the ceramide transporter protein (CERT) is the only known protein able to mediate non-vesicular transfer of ceramide between organelle membranes, the modulation of CERT function may impact on ceramide accumulation.	Ceramides	114-122	ceramide transporter 1	Homo sapiens	10-38
28922150-2	2017	Since the ceramide transporter protein (CERT) is the only known protein able to mediate non-vesicular transfer of ceramide between organelle membranes, the modulation of CERT function may impact on ceramide accumulation.	Ceramides	114-122	ceramide transporter 1	Homo sapiens	40-44
28035926-0	2017	Pleiotropic Effect of Human ApoE4 on Cerebral Ceramide and Saturated Fatty Acid Levels.	Ceramides	46-54	apolipoprotein E	Homo sapiens	28-33
28922150-2	2017	Since the ceramide transporter protein (CERT) is the only known protein able to mediate non-vesicular transfer of ceramide between organelle membranes, the modulation of CERT function may impact on ceramide accumulation.	Ceramides	114-122	ceramide transporter 1	Homo sapiens	170-174
28922150-3	2017	The competitive CERT inhibitor N-(3-hydroxy-1-hydroxymethyl-3-phenylpropyl) dodecanamide (HPA-12) interferes with ceramide trafficking.	Ceramides	114-122	ceramide transporter 1	Homo sapiens	16-20
27358008-8	2017	RESULTS: Level of mRNA encoding ceramide synthase 4 (CERS4), which is one of the enzymes that synthesize ceramide from a sphingoid base and an amide-linked fatty acid, was significantly higher in involved skin than in uninvolved skin (P &lt; 0.01).	Ceramides	32-40	ceramide synthase 4	Homo sapiens	53-58
28035926-3	2017	OBJECTIVE: To determine the specific effects of human ApoE4 (hE4) on cerebral ceramide and FA content during chow or a high fat/high cholesterol (HFHC) diet.	Ceramides	78-86	apolipoprotein E	Homo sapiens	54-59
28035926-3	2017	OBJECTIVE: To determine the specific effects of human ApoE4 (hE4) on cerebral ceramide and FA content during chow or a high fat/high cholesterol (HFHC) diet.	Ceramides	78-86	ubiquitination factor E4A	Homo sapiens	61-64
28035926-6	2017	RESULTS: Similar to E0, hE4 mice displayed lower cerebral total ceramide, Cer16 : 0, and Cer24 : 1 levels than WT mice on both diets.	Ceramides	64-72	ubiquitination factor E4A	Homo sapiens	24-27
28035926-9	2017	Chow-fed hE4 mice showed lower mRNA levels of ceramide synthase (CerS) 6, acid sphingomyelinase, and of most ceramide and FA transporters than WT and E0 mice.	Ceramides	46-54	ubiquitination factor E4A	Homo sapiens	9-12
28035926-11	2017	CONCLUSION: hE4 reduced cerebral ceramide levels to levels observed in E0 mice independent of diet.	Ceramides	33-41	ubiquitination factor E4A	Homo sapiens	12-15
28035926-13	2017	This was associated with alterations in the expression of ceramide and FA transporters specifically in hE4 mice.	Ceramides	58-66	ubiquitination factor E4A	Homo sapiens	103-106
28035934-0	2017	The Association Between Plasma Ceramides and Sphingomyelins and Risk of Alzheimer"s Disease Differs by Sex and APOE in the Baltimore Longitudinal Study of Aging.	Ceramides	31-40	apolipoprotein E	Homo sapiens	111-115
27880732-0	2016	Ceramide activates lysosomal cathepsin B and cathepsin D to attenuate autophagy and induces ER stress to suppress myeloid-derived suppressor cells.	Ceramides	0-8	cathepsin B	Homo sapiens	29-40
29269995-9	2017	Ceramide is the substrate for ceramide kinase (CERK) to yield C1P, and sphingosine is phosphorylated to S1P by sphingosine kinases (SphKs).	Ceramides	0-8	ceramide kinase	Homo sapiens	30-45
28078595-1	2017	Sphingomyelin synthases 1 and 2 convert the anti-oncometabolite ceramide to sphingomyelin, the most abundant sphingolipid in plasma membrane.	Ceramides	64-72	sphingomyelin synthase 1	Homo sapiens	0-31
28078595-2	2017	CD95L-induced ceramide increase is associated with the caspase-dependent inhibition of sphingomyelin synthesis, which enhances the mitochondrial route to apoptosis.	Ceramides	14-22	Fas ligand	Homo sapiens	0-5
28078595-3	2017	Knocking down sphingomyelin synthase 1 or inhibiting sphingomyelin synthesis facilitates ceramide accumulation, cytochrome c release from mitochondria, and caspase-9 activation in cancer cell upon CD95L treatment.	Ceramides	89-97	sphingomyelin synthase 1	Homo sapiens	14-38
27825124-3	2016	Acid ceramidase (AC) catalyzes ceramide breakdown to sphingosine, the precursor for S1P.	Ceramides	31-39	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
29269995-9	2017	Ceramide is the substrate for ceramide kinase (CERK) to yield C1P, and sphingosine is phosphorylated to S1P by sphingosine kinases (SphKs).	Ceramides	0-8	ceramide kinase	Homo sapiens	47-51
29269995-12	2017	Altogether, S1P and C1P are important regulators of ceramide level and cell fate.	Ceramides	52-60	membrane bound transcription factor peptidase, site 1	Homo sapiens	12-23
29131010-0	2017	Blockade of Experimental Multiple Sclerosis by Inhibition of the Acid Sphingomyelinase/Ceramide System.	Ceramides	87-95	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	65-86
29131010-8	2017	CONCLUSION: Activation of the Asm/ceramide system is a central step for the development of EAE.	Ceramides	34-42	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	30-33
27880732-0	2016	Ceramide activates lysosomal cathepsin B and cathepsin D to attenuate autophagy and induces ER stress to suppress myeloid-derived suppressor cells.	Ceramides	0-8	cathepsin D	Homo sapiens	45-56
27418352-8	2016	Restoration of sphingosine levels through direct sphingosine administration or conversion of the increased ceramide to sphingosine by neutral ceramidase reduces mortality and mitigates pulmonary infection after burn injury.	Ceramides	107-115	N-acylsphingosine amidohydrolase 2	Mus musculus	134-152
27765765-1	2016	OBJECTIVE: Ceramides are molecular lipids implicated in apoptosis, inflammation, obesity, and insulin resistance.	Ceramides	11-20	insulin	Homo sapiens	94-101
27751891-4	2016	SCD1 deficiency decreased the intracellular content of free fatty acids, triglycerides, and ceramide in the heart of SCD1-/- and SCD1-/-/PPARalpha-/- mice.	Ceramides	92-100	stearoyl-Coenzyme A desaturase 1	Mus musculus	0-4
27609772-2	2016	Neutral ceramidase (nCDase), a key enzyme in sphingolipid metabolism that hydrolyzes ceramide into sphingosine, is highly expressed in the intestine; however, its role in colon cancer has not been defined.	Ceramides	85-93	N-acylsphingosine amidohydrolase 2	Mus musculus	0-18
27609772-2	2016	Neutral ceramidase (nCDase), a key enzyme in sphingolipid metabolism that hydrolyzes ceramide into sphingosine, is highly expressed in the intestine; however, its role in colon cancer has not been defined.	Ceramides	85-93	N-acylsphingosine amidohydrolase 2	Mus musculus	20-26
27609772-3	2016	Here we show that molecular and pharmacological inhibition of nCDase in colon cancer cells increases ceramide, and this is accompanied by decreased cell survival and increased apoptosis and autophagy, with minimal effects on noncancerous cells.	Ceramides	101-109	N-acylsphingosine amidohydrolase 2	Mus musculus	62-68
27609772-5	2016	Furthermore, inhibition of nCDase in a xenograft model delayed tumor growth and increased ceramide while decreasing proliferation.	Ceramides	90-98	N-acylsphingosine amidohydrolase 2	Mus musculus	27-33
26915736-10	2016	It suggested that ASMase mediated the 50-Hz MF-induced EGFR clustering via ceramide which was produced from hydrolyzation on lipid rafts.	Ceramides	75-83	sphingomyelin phosphodiesterase 1	Homo sapiens	18-24
26915736-10	2016	It suggested that ASMase mediated the 50-Hz MF-induced EGFR clustering via ceramide which was produced from hydrolyzation on lipid rafts.	Ceramides	75-83	epidermal growth factor receptor	Homo sapiens	55-59
27882938-5	2016	SMPD3 deficiency disrupts homeostasis of sphingomyelin (SM), ceramide (Cer) and diacylglycerol (DAG) in the Golgi SMPD3-SMS1 (SM-synthase1) cycle.	Ceramides	61-69	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	0-5
27923879-5	2016	Loss of function of both ORM1 and ORM2 (orm1 amiR-ORM2) stimulated de novo sphingolipid biosynthesis, leading to strong sphingolipid accumulation, especially of long-chain bases and ceramides.	Ceramides	182-191	sphingolipid homeostasis protein ORM2	Saccharomyces cerevisiae S288C	34-38
27923879-5	2016	Loss of function of both ORM1 and ORM2 (orm1 amiR-ORM2) stimulated de novo sphingolipid biosynthesis, leading to strong sphingolipid accumulation, especially of long-chain bases and ceramides.	Ceramides	182-191	sphingolipid homeostasis protein ORM2	Saccharomyces cerevisiae S288C	50-54
27907090-6	2016	Silencing FOXC1 in human normal primary KC undergoing differentiation led to significant down-regulation of late terminal differentiation genes markers including epidermal differentiation complex genes, keratinization genes, sphingolipid/ceramide metabolic process genes and epidermal specific cell-cell adhesion genes.	Ceramides	238-246	forkhead box C1	Homo sapiens	10-15
27882938-5	2016	SMPD3 deficiency disrupts homeostasis of sphingomyelin (SM), ceramide (Cer) and diacylglycerol (DAG) in the Golgi SMPD3-SMS1 (SM-synthase1) cycle.	Ceramides	61-69	sphingomyelin synthase 1	Mus musculus	120-124
27882938-5	2016	SMPD3 deficiency disrupts homeostasis of sphingomyelin (SM), ceramide (Cer) and diacylglycerol (DAG) in the Golgi SMPD3-SMS1 (SM-synthase1) cycle.	Ceramides	71-74	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	0-5
27882938-5	2016	SMPD3 deficiency disrupts homeostasis of sphingomyelin (SM), ceramide (Cer) and diacylglycerol (DAG) in the Golgi SMPD3-SMS1 (SM-synthase1) cycle.	Ceramides	71-74	sphingomyelin synthase 1	Mus musculus	120-124
27857690-0	2016	Interferon-Beta Increases Plasma Ceramides of Specific Chain Length in Multiple Sclerosis Patients, Unlike Fingolimod or Natalizumab.	Ceramides	33-42	interferon beta 1	Homo sapiens	0-15
27870891-16	2016	ApoE in contrast to apoA-I preferentially bound to the ceramide enriched surfaces of oxLDL loaded cells.	Ceramides	55-63	apolipoprotein E	Homo sapiens	0-4
27729449-3	2016	Here, we applied single-molecule photobleaching to analyze the oligomeric state of an endoplasmic reticulum (ER) resident candidate ceramide sensor protein, SMSr/SAMD8.	Ceramides	132-140	sterile alpha motif domain containing 8	Homo sapiens	157-161
27729449-3	2016	Here, we applied single-molecule photobleaching to analyze the oligomeric state of an endoplasmic reticulum (ER) resident candidate ceramide sensor protein, SMSr/SAMD8.	Ceramides	132-140	sterile alpha motif domain containing 8	Homo sapiens	162-167
27729449-4	2016	Co-immunoprecipitation and chemical cross-linking studies previously revealed that the N-terminal sterile alpha motif (or SAM) domain of SMSr drives self-assembly of the protein into oligomers and that SMSr oligomerization is promoted by curcumin, a drug known to perturb ER ceramide and calcium homeostasis.	Ceramides	275-283	sterile alpha motif domain containing 8	Homo sapiens	137-141
27729449-8	2016	Our results document the first successful application of single-molecule photobleaching to resolve drug-induced and domain-dependent changes in the oligomeric state of an ER-resident membrane protein, hence establishing a complementary method to unravel the mechanism by which SMSr controls ceramide levels in the ER.	Ceramides	291-299	sterile alpha motif domain containing 8	Homo sapiens	277-281
27802163-2	2016	We have previously found that acid sphingomyelinase (ASM; also known as SMPD1) regulates the conserved DAF-2 (the ortholog IGF-1R in mammals) RTK signaling pathway in Caenorhabditis elegans How ASM and its catalytic products, ceramides, control RTK signaling pathways remain unclear.	Ceramides	226-235	Insulin-like receptor subunit beta;Protein kinase domain-containing protein;Receptor protein-tyrosine kinase	Caenorhabditis elegans	103-108
27411168-1	2016	Farber disease is a very rare autosomal recessive disease caused by mutation of ASAH1 that results in the accumulation of ceramide in various tissues.	Ceramides	122-130	N-acylsphingosine amidohydrolase 1	Homo sapiens	80-85
27539961-8	2016	The cellular roles for enhanced GlcCer synthesis and increased levels of cholesterol in the trafficking of NBD-ceramide metabolites in NPC1((-/-)) cells have been discussed.	Ceramides	111-119	NPC intracellular cholesterol transporter 1	Homo sapiens	135-139
27581814-0	2016	Intramyocellular ceramides and skeletal muscle mitochondrial respiration are partially regulated by Toll-like receptor 4 during hindlimb unloading.	Ceramides	17-26	toll-like receptor 4	Mus musculus	100-120
27581814-3	2016	Therefore, our goal was to determine whether TLR4 is an underlying mechanism of insulin resistance, mitochondrial dysfunction, and skeletal muscle ceramide accumulation following muscle disuse in mice.	Ceramides	147-155	toll-like receptor 4	Mus musculus	45-49
27581814-7	2016	Importantly, TLR4-/- HU mice were protected from insulin resistance and altered NF-kappaB signaling and were partly resistant to muscle atrophy, ceramide accumulation, and decreased RCR.	Ceramides	145-153	toll-like receptor 4	Mus musculus	13-17
27581814-9	2016	We conclude that TLR4 is an upstream regulator of insulin sensitivity, while partly upregulating muscle ceramides and worsening mitochondrial respiration during 2 wk of HU.	Ceramides	104-113	toll-like receptor 4	Mus musculus	17-21
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.	Ceramides	48-56	ArfGAP with RhoGAP domain, ankyrin repeat and PH domain 2	Mus musculus	14-19
27570113-9	2016	Ceramide released from hepatocytes attracts immune cells and a positive association of the macrophage specific receptor CD163 with NT ceramide was identified.	Ceramides	0-8	CD163 molecule	Homo sapiens	120-125
27570113-9	2016	Ceramide released from hepatocytes attracts immune cells and a positive association of the macrophage specific receptor CD163 with NT ceramide was identified.	Ceramides	134-142	CD163 molecule	Homo sapiens	120-125
27591968-5	2016	Overexpression of CerS2 in primary mouse hepatocytes induced a specific elevation in very long-chain Cer, but despite the overall increase in ceramide abundance, there was a substantial improvement in insulin signal transduction, as well as decreased ER stress and gluconeogenic markers.	Ceramides	142-150	ceramide synthase 2	Mus musculus	18-23
27026573-1	2016	ASAH1 gene encodes for acid ceramidase that is involved in the degradation of ceramide into sphingosine and free fatty acids within lysosomes.	Ceramides	78-86	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-5
27639801-9	2016	Mice lacking FXR in the intestine also have lower serum ceramide levels, and are resistant to HFD-induced metabolic disease, and this was reversed by injection of C16:0 ceramide.	Ceramides	169-177	nuclear receptor subfamily 1, group H, member 4	Mus musculus	13-16
27639801-10	2016	In mouse ileum, because of the presence of endogenous FXR agonists produced in the liver, FXR target genes involved in ceramide synthesis are activated and when Gly-MCA is administered they are repressed, which likely accounts for the decrease in serum ceramides.	Ceramides	119-127	nuclear receptor subfamily 1, group H, member 4	Mus musculus	54-57
27639801-10	2016	In mouse ileum, because of the presence of endogenous FXR agonists produced in the liver, FXR target genes involved in ceramide synthesis are activated and when Gly-MCA is administered they are repressed, which likely accounts for the decrease in serum ceramides.	Ceramides	119-127	nuclear receptor subfamily 1, group H, member 4	Mus musculus	90-93
27639801-10	2016	In mouse ileum, because of the presence of endogenous FXR agonists produced in the liver, FXR target genes involved in ceramide synthesis are activated and when Gly-MCA is administered they are repressed, which likely accounts for the decrease in serum ceramides.	Ceramides	253-262	nuclear receptor subfamily 1, group H, member 4	Mus musculus	54-57
27639801-11	2016	These studies show that ceramides produced in the ileum under control of FXR influence metabolic diseases.	Ceramides	24-33	nuclear receptor subfamily 1, group H, member 4	Mus musculus	73-76
27523779-1	2016	Ceramide is a huge lipid family consisting of diversified structures including various modifications in the fatty acyl chain and the long chain base (LCB).	Ceramides	0-8	clathrin light chain B	Homo sapiens	150-153
27523779-2	2016	In this contribution, negative-ion ESI linear ion-trap multiple-stage mass spectrometric method (LIT MSn) towards complete structural determination of ceramides in ten major families characterized as the [M-H]- ions is described.	Ceramides	151-160	moesin	Homo sapiens	101-104
27523779-4	2016	Thereby, differentiation of ceramide molecules varied by chain length, the LCB (sphingosine, phytosphigosine, 6-hydroxy-sphingosine), and by the modification (alpha-hydroxy-, beta-hydroxy-, omega-hydroxy-FA) can be achieved; and many isomeric structures in the biological specimen can be revealed in detail.	Ceramides	28-36	clathrin light chain B	Homo sapiens	75-78
27639801-9	2016	Mice lacking FXR in the intestine also have lower serum ceramide levels, and are resistant to HFD-induced metabolic disease, and this was reversed by injection of C16:0 ceramide.	Ceramides	56-64	nuclear receptor subfamily 1, group H, member 4	Mus musculus	13-16
27539961-3	2016	We herein demonstrated for the first time that GlcCer synthase activity for the fluorescent ceramide, 4-nitrobenzo-2-oxa-1,3-diazole-labeled C6-ceramide (NBD-ceramide) increased in intact NPC1((-/-)) cells and cell lysates without affecting the protein levels.	Ceramides	92-100	NPC intracellular cholesterol transporter 1	Homo sapiens	188-192
27852416-6	2016	Conclusion: Itraconazole induces apoptosis of PC-3 cell through increasing the intracellular ceramide content, which might relate to upregulation of cleavage-caspase 3 and Bax, downregulation of Bcl-2 and inactivation of Akt-mTORC signal pathway.	Ceramides	93-101	caspase 3	Homo sapiens	158-167
27852416-6	2016	Conclusion: Itraconazole induces apoptosis of PC-3 cell through increasing the intracellular ceramide content, which might relate to upregulation of cleavage-caspase 3 and Bax, downregulation of Bcl-2 and inactivation of Akt-mTORC signal pathway.	Ceramides	93-101	BCL2 associated X, apoptosis regulator	Homo sapiens	172-175
27852416-6	2016	Conclusion: Itraconazole induces apoptosis of PC-3 cell through increasing the intracellular ceramide content, which might relate to upregulation of cleavage-caspase 3 and Bax, downregulation of Bcl-2 and inactivation of Akt-mTORC signal pathway.	Ceramides	93-101	BCL2 apoptosis regulator	Homo sapiens	195-200
27852416-6	2016	Conclusion: Itraconazole induces apoptosis of PC-3 cell through increasing the intracellular ceramide content, which might relate to upregulation of cleavage-caspase 3 and Bax, downregulation of Bcl-2 and inactivation of Akt-mTORC signal pathway.	Ceramides	93-101	AKT serine/threonine kinase 1	Homo sapiens	221-224
27540013-3	2016	Molecular or pharmacologic inhibition of FLT3-ITD reactivated ceramide synthesis, selectively inducing mitophagy and AML cell death.	Ceramides	62-70	fms related receptor tyrosine kinase 3	Homo sapiens	41-45
27833848-5	2016	Moreover, NCDase-enriched exosomes from INS-1 cells rescued PA-induced H4IIEC3 insulin resistance and blocked PA-induced reactive oxygen species production in which ceramide was involved.	Ceramides	165-173	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	10-16
27562715-5	2016	Molecularly, C6 ceramide downregulated Bcl-2 to increase AT406"s sensitivity in pancreatic cancer cells.	Ceramides	16-24	BCL2 apoptosis regulator	Homo sapiens	39-44
27562715-6	2016	Intriguingly, C6 ceramide-mediated AT406 sensitization was nullified with Bcl-2 shRNA knockdown or pretreatment of the Bcl-2 inhibitor ABT-737.	Ceramides	17-25	BCL2 apoptosis regulator	Homo sapiens	74-79
27562715-6	2016	Intriguingly, C6 ceramide-mediated AT406 sensitization was nullified with Bcl-2 shRNA knockdown or pretreatment of the Bcl-2 inhibitor ABT-737.	Ceramides	17-25	BCL2 apoptosis regulator	Homo sapiens	119-124
27562715-10	2016	Together, we demonstrate that C6 ceramide sensitizes AT406-mediated anti-pancreatic cancer cell activity possibly via downregulating Bcl-2.	Ceramides	33-41	BCL2 apoptosis regulator	Homo sapiens	133-138
27507791-2	2016	Caenorhabditis elegans fed a glucose-supplemented diet or with altered ceramide metabolism, due to a hyl-2 mutation, are sensitive to oxygen deprivation (anoxia).	Ceramides	71-79	Ceramide synthase hyl-2	Caenorhabditis elegans	101-106
27540013-0	2016	Targeting FLT3-ITD signaling mediates ceramide-dependent mitophagy and attenuates drug resistance in AML.	Ceramides	38-46	fms related receptor tyrosine kinase 3	Homo sapiens	10-14
27540013-2	2016	Here, we reveal that pro-cell death lipid ceramide generation is suppressed by FLT3-ITD signaling.	Ceramides	42-50	fms related receptor tyrosine kinase 3	Homo sapiens	79-83
27775668-2	2016	Ceramide synthase 2 (CERS2), one of the six ceramide synthase isoforms, is responsible for the synthesis of very long chain fatty acid (C20-26 fatty acids) (VLC)-containing ceramides (VLC-Cer).	Ceramides	173-182	ceramide synthase 2	Homo sapiens	0-19
27775668-2	2016	Ceramide synthase 2 (CERS2), one of the six ceramide synthase isoforms, is responsible for the synthesis of very long chain fatty acid (C20-26 fatty acids) (VLC)-containing ceramides (VLC-Cer).	Ceramides	173-182	ceramide synthase 2	Homo sapiens	21-26
27775668-6	2016	This higher proportion was still maintained even when the proportion of C16-Cer to the total ceramides was increased by disrupting the ceramide transport protein (CERT)-dependent C16-Cer delivery pathway for SM synthesis.	Ceramides	93-102	ceramide transporter 1	Homo sapiens	135-161
27775668-6	2016	This higher proportion was still maintained even when the proportion of C16-Cer to the total ceramides was increased by disrupting the ceramide transport protein (CERT)-dependent C16-Cer delivery pathway for SM synthesis.	Ceramides	93-102	ceramide transporter 1	Homo sapiens	163-167
27590340-6	2016	VPA caused up-regulation of FEN1 and SUR4, encoding fatty acid elongases that catalyze the synthesis of very long chain fatty acids (C24 to C26) required for ceramide synthesis.	Ceramides	158-166	multifunctional nuclease RAD27	Saccharomyces cerevisiae S288C	28-32
27590340-6	2016	VPA caused up-regulation of FEN1 and SUR4, encoding fatty acid elongases that catalyze the synthesis of very long chain fatty acids (C24 to C26) required for ceramide synthesis.	Ceramides	158-166	fatty acid elongase ELO3	Saccharomyces cerevisiae S288C	37-41
27540013-4	2016	Mechanistically, FLT3-ITD targeting induced ceramide accumulation on the outer mitochondrial membrane, which then directly bound autophagy-inducing light chain 3 (LC3), involving its I35 and F52 residues, to recruit autophagosomes for execution of lethal mitophagy.	Ceramides	44-52	fms related receptor tyrosine kinase 3	Homo sapiens	17-21
27540013-4	2016	Mechanistically, FLT3-ITD targeting induced ceramide accumulation on the outer mitochondrial membrane, which then directly bound autophagy-inducing light chain 3 (LC3), involving its I35 and F52 residues, to recruit autophagosomes for execution of lethal mitophagy.	Ceramides	44-52	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	163-166
27540013-5	2016	Short hairpin RNA (shRNA)-mediated knockdown of LC3 prevented AML cell death in response to FLT3-ITD inhibition by crenolanib, which was restored by wild-type (WT)-LC3, but not mutants of LC3 with altered ceramide binding (I35A-LC3 or F52A-LC3).	Ceramides	205-213	microtubule associated protein 1 light chain 3 alpha	Homo sapiens	48-51
27540013-6	2016	Mitochondrial ceramide accumulation and lethal mitophagy induction in response to FLT3-ITD targeting was mediated by dynamin-related protein 1 (Drp1) activation via inhibition of protein kinase A-regulated S637 phosphorylation, resulting in mitochondrial fission.	Ceramides	14-22	fms related receptor tyrosine kinase 3	Homo sapiens	82-86
27540013-6	2016	Mitochondrial ceramide accumulation and lethal mitophagy induction in response to FLT3-ITD targeting was mediated by dynamin-related protein 1 (Drp1) activation via inhibition of protein kinase A-regulated S637 phosphorylation, resulting in mitochondrial fission.	Ceramides	14-22	dynamin 1 like	Homo sapiens	117-142
27540013-6	2016	Mitochondrial ceramide accumulation and lethal mitophagy induction in response to FLT3-ITD targeting was mediated by dynamin-related protein 1 (Drp1) activation via inhibition of protein kinase A-regulated S637 phosphorylation, resulting in mitochondrial fission.	Ceramides	14-22	dynamin 1 like	Homo sapiens	144-148
27540013-7	2016	Inhibition of Drp1 prevented ceramide-dependent lethal mitophagy, and reconstitution of WT-Drp1 or phospho-null S637A-Drp1 but not its inactive phospho-mimic mutant (S637D-Drp1), restored mitochondrial fission and mitophagy in response to crenolanib in FLT3-ITD+ AML cells expressing stable shRNA against endogenous Drp1.	Ceramides	29-37	dynamin 1 like	Homo sapiens	14-18
27540013-8	2016	Moreover, activating FLT3-ITD signaling in crenolanib-resistant AML cells suppressed ceramide-dependent mitophagy and prevented cell death.	Ceramides	85-93	fms related receptor tyrosine kinase 3	Homo sapiens	21-25
27540013-9	2016	FLT3-ITD+ AML drug resistance is attenuated by LCL-461, a mitochondria-targeted ceramide analog drug, in vivo, which also induced lethal mitophagy in human AML blasts with clinically relevant FLT3 mutations.	Ceramides	80-88	fms related receptor tyrosine kinase 3	Homo sapiens	0-4
27540013-10	2016	Thus, these data reveal a novel mechanism which regulates AML cell death by ceramide-dependent mitophagy in response to FLT3-ITD targeting.	Ceramides	76-84	fms related receptor tyrosine kinase 3	Homo sapiens	120-124
27479697-8	2016	These results suggest that mitochondrial nSMase activity contributes to compartmentation and further accumulation of ceramide in mitochondria, deregulating their function during reperfusion.	Ceramides	117-125	sphingomyelin phosphodiesterase 2	Homo sapiens	41-47
27588496-6	2016	Based on these findings, we examined the effect of different levels of cellular SK2 and showed that high-level overexpression reduced cell proliferation and survival, and increased cellular ceramide levels.	Ceramides	190-198	sphingosine kinase 2	Homo sapiens	80-83
27725636-1	2016	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and phosphocholine, essential components of myelin in neurons.	Ceramides	56-64	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
27725636-1	2016	Acid sphingomyelinase (ASM) hydrolyzes sphingomyelin to ceramide and phosphocholine, essential components of myelin in neurons.	Ceramides	56-64	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
27376354-5	2016	Ceramide production in the bronchial epithelial cells and Sphk1 mRNA expression were induced in the lung after the 7-day DE exposure and were partially suppressed by the FB1 treatment.	Ceramides	0-8	defensin beta 1	Mus musculus	121-123
27376354-7	2016	These results suggest that ceramide and Sphk1 may be sensitive biomarkers for low-level DE-induced pulmonary effects.	Ceramides	27-35	defensin beta 1	Mus musculus	88-90
27376354-8	2016	Collectively, ceramide likely contributes to the DE-induced early stage of airway inflammation, which is considered a potential pulmonary target during low-level DE exposure.	Ceramides	14-22	defensin beta 1	Mus musculus	49-51
27376354-8	2016	Collectively, ceramide likely contributes to the DE-induced early stage of airway inflammation, which is considered a potential pulmonary target during low-level DE exposure.	Ceramides	14-22	defensin beta 1	Mus musculus	162-164
27506241-5	2016	Consistent with a role in SPT suppression, AtORM1 and AtORM2 overexpression lines displayed increased resistance to the programmed cell death-inducing mycotoxin fumonisin B1, with an accompanying reduced accumulation of LCBs and C16 fatty acid-containing ceramides relative to wild-type plants.	Ceramides	255-264	long chain base2	Arabidopsis thaliana	26-29
27680501-1	2016	PPM1L, a member of the metal-dependent protein phosphatase (PPM) family, is involved in regulating the stress-activated protein kinase pathway and ceramide trafficking.	Ceramides	147-155	protein phosphatase 1 (formerly 2C)-like	Mus musculus	0-5
27517620-10	2016	Our results further indicate that restoration of p53 through inhibition of ceramide glycosylation might be an effective treatment approach for targeting cancers heterozygously harboring TP53 missense mutations.	Ceramides	75-83	tumor protein p53	Homo sapiens	49-52
27556861-7	2016	Mechanistic approaches revealed WIN 55,212-2 to suppress IL-1beta-induced TF expression via inhibition of ceramide formation and via decreased phosphorylation of p38 mitogen-activated protein kinase (MAPK) and c-Jun N-terminal kinases.	Ceramides	106-114	interleukin 1 beta	Homo sapiens	57-65
27556861-8	2016	Further inhibitor experiments demonstrated neutral sphingomyelinase (nSMase) to confer ceramide generation upon IL-1beta treatment with the parallel IL-1beta-mediated activation of MAPKs occurring via an nSMase-independent pathway.	Ceramides	87-95	sphingomyelin phosphodiesterase 2	Homo sapiens	43-67
27556861-8	2016	Further inhibitor experiments demonstrated neutral sphingomyelinase (nSMase) to confer ceramide generation upon IL-1beta treatment with the parallel IL-1beta-mediated activation of MAPKs occurring via an nSMase-independent pathway.	Ceramides	87-95	sphingomyelin phosphodiesterase 2	Homo sapiens	69-75
27556861-8	2016	Further inhibitor experiments demonstrated neutral sphingomyelinase (nSMase) to confer ceramide generation upon IL-1beta treatment with the parallel IL-1beta-mediated activation of MAPKs occurring via an nSMase-independent pathway.	Ceramides	87-95	interleukin 1 beta	Homo sapiens	112-120
27517620-10	2016	Our results further indicate that restoration of p53 through inhibition of ceramide glycosylation might be an effective treatment approach for targeting cancers heterozygously harboring TP53 missense mutations.	Ceramides	75-83	tumor protein p53	Homo sapiens	186-190
27391427-0	2016	Inhibition of sphingomyelin synthase 1 affects ceramide accumulation and hydrogen peroxide-induced apoptosis in Neuro-2a cells.	Ceramides	47-55	sphingomyelin synthase 1	Mus musculus	14-38
27391427-3	2016	As ceramide, a well-known second messenger of apoptosis, can be metabolized by sphingomyelin synthase 1 (SMS1), recent research has focused on the link between SMS1 and apoptosis in different cells.	Ceramides	3-11	sphingomyelin synthase 1	Mus musculus	79-103
27391427-3	2016	As ceramide, a well-known second messenger of apoptosis, can be metabolized by sphingomyelin synthase 1 (SMS1), recent research has focused on the link between SMS1 and apoptosis in different cells.	Ceramides	3-11	sphingomyelin synthase 1	Mus musculus	105-109
27391427-3	2016	As ceramide, a well-known second messenger of apoptosis, can be metabolized by sphingomyelin synthase 1 (SMS1), recent research has focused on the link between SMS1 and apoptosis in different cells.	Ceramides	3-11	sphingomyelin synthase 1	Mus musculus	160-164
27391427-6	2016	Moreover, pretreatment of N2a cells with D609, an sphingomyelin synthase inhibitor, or SMS1-silencing RNA (siRNA) further increased ceramide and potentiated H2O2-induced apoptosis which could be reversed by SB203580 (a p38 inhibitor).	Ceramides	132-140	sphingomyelin synthase 1	Mus musculus	87-91
27391427-7	2016	Thus, our study has shown that SMS1 regulates ceramide levels in N2a cells and plays a potent protective role in this oxidative stress-induced apoptosis partly through the p38 pathway.	Ceramides	46-54	sphingomyelin synthase 1	Mus musculus	31-35
27391427-7	2016	Thus, our study has shown that SMS1 regulates ceramide levels in N2a cells and plays a potent protective role in this oxidative stress-induced apoptosis partly through the p38 pathway.	Ceramides	46-54	mitogen-activated protein kinase 14	Mus musculus	172-175
27682164-0	2016	Role of Ceramide in Apoptosis and Development of Insulin Resistance.	Ceramides	8-16	insulin	Homo sapiens	49-56
27660431-2	2016	Neutral sphingomyelinase-2 (nSMase-2) and acid SMase (aSMase), which hydrolyze sphingomyelin to produce ceramide, are activated by a range of cellular stresses, including inflammatory cytokines and pathogens, but notably cigarette smoke appears to only activate nSMase-2.	Ceramides	104-112	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
27660431-2	2016	Neutral sphingomyelinase-2 (nSMase-2) and acid SMase (aSMase), which hydrolyze sphingomyelin to produce ceramide, are activated by a range of cellular stresses, including inflammatory cytokines and pathogens, but notably cigarette smoke appears to only activate nSMase-2.	Ceramides	104-112	sphingomyelin phosphodiesterase 3	Homo sapiens	28-36
27660431-2	2016	Neutral sphingomyelinase-2 (nSMase-2) and acid SMase (aSMase), which hydrolyze sphingomyelin to produce ceramide, are activated by a range of cellular stresses, including inflammatory cytokines and pathogens, but notably cigarette smoke appears to only activate nSMase-2.	Ceramides	104-112	sphingomyelin phosphodiesterase 1	Homo sapiens	42-52
27660431-2	2016	Neutral sphingomyelinase-2 (nSMase-2) and acid SMase (aSMase), which hydrolyze sphingomyelin to produce ceramide, are activated by a range of cellular stresses, including inflammatory cytokines and pathogens, but notably cigarette smoke appears to only activate nSMase-2.	Ceramides	104-112	sphingomyelin phosphodiesterase 1	Homo sapiens	54-60
27660431-2	2016	Neutral sphingomyelinase-2 (nSMase-2) and acid SMase (aSMase), which hydrolyze sphingomyelin to produce ceramide, are activated by a range of cellular stresses, including inflammatory cytokines and pathogens, but notably cigarette smoke appears to only activate nSMase-2.	Ceramides	104-112	sphingomyelin phosphodiesterase 3	Homo sapiens	262-270
27660431-11	2016	CONCLUSION: nSMase-2 and aSMase are both increased in COPD alveolar macrophages at the protein level; this may contribute toward the elevated ceramide (C20) detected in alveolar macrophages from COPD patients.	Ceramides	142-150	sphingomyelin phosphodiesterase 3	Homo sapiens	12-31
27155573-2	2016	Acid ceramidase (AC) is one key enzyme that regulates ceramide metabolism.	Ceramides	54-62	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
27647482-11	2016	This finding underlies the essential role of enzymes regulating either the synthesis (CERS1) or degradation (ASAH1) of ceramide, and the link between defects in ceramide metabolism and PME.	Ceramides	119-127	ceramide synthase 1	Homo sapiens	86-91
27647482-11	2016	This finding underlies the essential role of enzymes regulating either the synthesis (CERS1) or degradation (ASAH1) of ceramide, and the link between defects in ceramide metabolism and PME.	Ceramides	119-127	N-acylsphingosine amidohydrolase 1	Homo sapiens	109-114
27278624-0	2016	Macrophages transfer antigens to dendritic cells by releasing exosomes containing dead-cell-associated antigens partially through a ceramide-dependent pathway to enhance CD4(+) T-cell responses.	Ceramides	132-140	CD4 molecule	Homo sapiens	170-173
27364952-0	2016	Dihydroceramide-desaturase-1-mediated caspase 9 activation through ceramide plays a pivotal role in palmitic acid-induced HepG2 cell apoptosis.	Ceramides	7-15	caspase 9	Homo sapiens	38-47
27682164-3	2016	One of the main predispositions for the development of insulin resistance and diabetes is obesity, which is associated with ectopic fat deposition and significant increase in intracellular concentrations of cytotoxic ceramides.	Ceramides	217-226	insulin	Homo sapiens	55-62
27682164-4	2016	A possible approach to the restoration of tissue sensitivity to insulin in type 2 diabetes based on selective reduction of the content of cytotoxic ceramides is discussed.	Ceramides	148-157	insulin	Homo sapiens	64-71
27551720-11	2016	The mechanism utilized by CXCR1 remains elusive, but CXCR2 appears to modulate Nsm activity and resultant production of ceramide to control exosome release.	Ceramides	120-128	C-X-C motif chemokine receptor 2	Homo sapiens	53-58
27341515-1	2016	The pathophysiology of sepsis involves activation of acid sphingomyelinase (SMPD1) with subsequent generation of the bioactive mediator ceramide.	Ceramides	136-144	sphingomyelin phosphodiesterase 1	Homo sapiens	53-74
27341515-1	2016	The pathophysiology of sepsis involves activation of acid sphingomyelinase (SMPD1) with subsequent generation of the bioactive mediator ceramide.	Ceramides	136-144	sphingomyelin phosphodiesterase 1	Homo sapiens	76-81
27341515-11	2016	SMPD1 is involved in the dysregulation of ceramide metabolism in endothelial cells leading to macrodomain formation, cytotoxicity and downregulation of ADAMTS13 expression.	Ceramides	42-50	sphingomyelin phosphodiesterase 1	Homo sapiens	0-5
27341515-11	2016	SMPD1 is involved in the dysregulation of ceramide metabolism in endothelial cells leading to macrodomain formation, cytotoxicity and downregulation of ADAMTS13 expression.	Ceramides	42-50	ADAM metallopeptidase with thrombospondin type 1 motif 13	Homo sapiens	152-160
27551807-7	2016	In cultured wild type keratinocytes, both KALLIKREIN 5 and -7 colocalized with ceramide metabolites following calcium-induced differentiation.	Ceramides	79-87	kallikrein related-peptidase 5	Mus musculus	42-54
26923251-9	2016	ASM was inhibited by siRNA or desipramine (DES), and/or ceramide was degraded by recombinant acid ceramidase (AC).	Ceramides	56-64	N-acylsphingosine amidohydrolase 1	Homo sapiens	93-108
26923251-11	2016	In contrast, recombinant ASM upregulated ceramide and ER stress.	Ceramides	41-49	sphingomyelin phosphodiesterase 1	Homo sapiens	25-28
26923251-14	2016	CONCLUSION: These results indicate that ASM/ceramide signaling pathway is involved in ox-LDL-induced macrophage apoptosis via ER stress pathway.	Ceramides	44-52	sphingomyelin phosphodiesterase 1	Homo sapiens	40-43
27291151-8	2016	Intriguingly, we showed that ceramide (C14), a pro-apoptotic sphingolipid, also induced ATG-7 degradation, and sensitized HNSCC cells to GDC-0349.	Ceramides	29-37	autophagy related 7	Homo sapiens	88-93
27499293-2	2016	Here we report that ceramide stimulates CREB3L1 cleavage by inverting the orientation of TM4SF20 in membranes.	Ceramides	20-28	cAMP responsive element binding protein 3 like 1	Homo sapiens	40-47
27499293-4	2016	This translocation requires TRAM2 (translocating chain-associated membrane protein 2), a membrane protein containing a putative ceramide-interacting domain.	Ceramides	128-136	translocation associated membrane protein 2	Homo sapiens	35-84
27499293-2	2016	Here we report that ceramide stimulates CREB3L1 cleavage by inverting the orientation of TM4SF20 in membranes.	Ceramides	20-28	transmembrane 4 L six family member 20	Homo sapiens	89-96
27499293-4	2016	This translocation requires TRAM2 (translocating chain-associated membrane protein 2), a membrane protein containing a putative ceramide-interacting domain.	Ceramides	128-136	translocation associated membrane protein 2	Homo sapiens	28-33
27499293-5	2016	In the presence of ceramide, the N terminus of the first transmembrane domain of TM4SF20 is exposed to cytosol.	Ceramides	19-27	transmembrane 4 L six family member 20	Homo sapiens	81-88
27499293-7	2016	In the presence of ceramide, translocation of TM4SF20 is TRAM2-independent.	Ceramides	19-27	transmembrane 4 L six family member 20	Homo sapiens	46-53
27535912-10	2016	SIGNIFICANCE STATEMENT: We present for the first time evidence, using Alzheimer"s disease (AD) model mice deficient in neural exosome secretion due to lack of neutral sphingomyelinase-2 function, that ceramide-enriched exosomes exacerbate AD-related pathologies and cognitive deficits.	Ceramides	201-209	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	159-185
27499293-7	2016	In the presence of ceramide, translocation of TM4SF20 is TRAM2-independent.	Ceramides	19-27	translocation associated membrane protein 2	Homo sapiens	57-62
27530098-5	2016	CS-released EMPs and cMPs were ceramide-rich and required the ceramide-synthesis enzyme acid sphingomyelinase (aSMase) for their release, an enzyme which was found to exhibit significantly higher activity in plasma of COPD patients or of CS-exposed mice.	Ceramides	62-70	sphingomyelin phosphodiesterase 1	Homo sapiens	111-117
26970307-8	2016	On the other hand, co-treatment with the glucosylceramide synthase (GCS) inhibitor PDMP or the cell permeable short-chain ceramide (C6) potentiated A-674563"s cytotoxicity against A375 cells.	Ceramides	49-57	UDP-glucose ceramide glucosyltransferase	Homo sapiens	68-71
27302066-8	2016	This study has shown that by direct transcriptional activation of CerS6, p53 can regulate specific ceramide biosynthesis, which contributes to the pro-apoptotic cellular response.	Ceramides	99-107	ceramide synthase 6	Homo sapiens	66-71
27221045-0	2016	Inhibition of ceramide glucosylation sensitizes lung cancer cells to ABC294640, a first-in-class small molecule SphK2 inhibitor.	Ceramides	14-22	sphingosine kinase 2	Homo sapiens	112-117
27221045-4	2016	Inhibition of SphK2 by ABC294640 increased ceramide accumulation, but decreased pro-survival sphingosine-1-phosphate (S1P) content, leading to lung cancer cell apoptosis activation.	Ceramides	43-51	sphingosine kinase 2	Homo sapiens	14-19
27221045-6	2016	The GCS inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) or GCS shRNA/siRNA knockdown facilitated ABC294640-induced ceramide production and lung cancer cell apoptosis.	Ceramides	133-141	UDP-glucose ceramide glucosyltransferase	Homo sapiens	4-7
27221045-6	2016	The GCS inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) or GCS shRNA/siRNA knockdown facilitated ABC294640-induced ceramide production and lung cancer cell apoptosis.	Ceramides	133-141	UDP-glucose ceramide glucosyltransferase	Homo sapiens	77-80
27221045-7	2016	Reversely, forced overexpression of GCS reduced ABC294640"s sensitivity, resulting in decreased ceramide accumulation and apoptosis induction in A549 cells.	Ceramides	96-104	UDP-glucose ceramide glucosyltransferase	Homo sapiens	36-39
27302066-8	2016	This study has shown that by direct transcriptional activation of CerS6, p53 can regulate specific ceramide biosynthesis, which contributes to the pro-apoptotic cellular response.	Ceramides	99-107	tumor protein p53	Homo sapiens	73-76
26897748-0	2016	C6 ceramide sensitizes the anti-hepatocellular carcinoma (HCC) activity by AZD-8055, a novel mTORC1/2 dual inhibitor.	Ceramides	3-11	CREB regulated transcription coactivator 2	Mus musculus	93-101
27382035-6	2016	Because a reduction in skeletal muscle ceramide levels is frequently associated with improvements in insulin sensitivity in humans, the beneficial findings reported for reducing ceramides in preclinical studies may have clinical application in humans.	Ceramides	39-47	insulin	Homo sapiens	101-108
27151272-7	2016	Whereas skeletal muscle sphingolipid content was not clearly affected, plasma levels of very long-chain fatty acid (VLCFA)-containing ceramides were markedly increased in SMS2 KO mice, compared with in WT mice.	Ceramides	134-143	sphingomyelin synthase 2	Mus musculus	171-175
26897748-7	2016	Signaling studies showed that AZD-8055 and C6 ceramide synergistically suppressed Akt-mTOR complex 1/2 cascade activation.	Ceramides	46-54	AKT serine/threonine kinase 1	Homo sapiens	82-85
26897748-7	2016	Signaling studies showed that AZD-8055 and C6 ceramide synergistically suppressed Akt-mTOR complex 1/2 cascade activation.	Ceramides	46-54	mechanistic target of rapamycin kinase	Homo sapiens	86-90
27487939-0	2016	Ceramide mediates FasL-induced caspase 8 activation in colon carcinoma cells to enhance FasL-induced cytotoxicity by tumor-specific cytotoxic T lymphocytes.	Ceramides	0-8	Fas ligand	Homo sapiens	18-22
27487939-0	2016	Ceramide mediates FasL-induced caspase 8 activation in colon carcinoma cells to enhance FasL-induced cytotoxicity by tumor-specific cytotoxic T lymphocytes.	Ceramides	0-8	caspase 8	Homo sapiens	31-40
27487939-0	2016	Ceramide mediates FasL-induced caspase 8 activation in colon carcinoma cells to enhance FasL-induced cytotoxicity by tumor-specific cytotoxic T lymphocytes.	Ceramides	0-8	Fas ligand	Homo sapiens	88-92
27487939-3	2016	We aimed at testing the hypothesis that novel ceramide analogs effectively modulate Fas function to sensitize colon carcinoma cells to FasL-induced apoptosis.	Ceramides	46-54	Fas ligand	Homo sapiens	135-139
27487939-5	2016	Five ceramide analogs, IG4, IG7, IG14, IG17, and IG19, exhibit low toxicity and potent activity in sensitization of human colon carcinoma cells to FasL-induced apoptosis.	Ceramides	5-13	Fas ligand	Homo sapiens	147-151
27487939-7	2016	Ceramide enhances FasL-induced activation of the MAPK, NF-kappaB, and caspase 8 despite induction of potent tumor cell death.	Ceramides	0-8	Fas ligand	Homo sapiens	18-22
27487939-7	2016	Ceramide enhances FasL-induced activation of the MAPK, NF-kappaB, and caspase 8 despite induction of potent tumor cell death.	Ceramides	0-8	caspase 8	Homo sapiens	70-79
27487939-8	2016	Finally, a sublethal dose of several ceramide analogs significantly increased CTL-mediated and FasL-induced apoptosis of colon carcinoma cells.	Ceramides	37-45	Fas ligand	Homo sapiens	95-99
26798039-0	2016	Ceramide inhibits PKCtheta by regulating its phosphorylation and translocation to lipid rafts in Jurkat cells.	Ceramides	0-8	protein kinase C theta	Homo sapiens	18-26
26798039-3	2016	PKCtheta may be regulated by ceramide, a crucial sphingolipid that is known to promote differentiation, growth arrest, and apoptosis.	Ceramides	29-37	protein kinase C theta	Homo sapiens	0-8
26798039-5	2016	Our results suggest that ceramide regulates the PKCtheta pathway through preventing its critical threonine 538 (Thr538) phosphorylation and subsequent activation, thereby inhibiting the kinase"s translocation to lipid rafts.	Ceramides	25-33	protein kinase C theta	Homo sapiens	48-56
26798039-9	2016	Such previously undescribed mechanism of regulation of PKCtheta raises the possibility that ceramide, or one of its derivatives, and may prove valuable in novel therapeutic approaches for disorders involving autoimmunity or excessive inflammation-where PKCtheta plays a critical role.	Ceramides	92-100	protein kinase C theta	Homo sapiens	55-63
26798039-9	2016	Such previously undescribed mechanism of regulation of PKCtheta raises the possibility that ceramide, or one of its derivatives, and may prove valuable in novel therapeutic approaches for disorders involving autoimmunity or excessive inflammation-where PKCtheta plays a critical role.	Ceramides	92-100	protein kinase C theta	Homo sapiens	253-261
27571014-1	2016	PURPOSE: Acid sphingomyelinase (ASMase) catalyzes the hydrolysis of sphingomyelin to ceramide and mediates multiple responses involved in inflammatory and apoptotic signaling.	Ceramides	85-93	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	9-30
27571014-1	2016	PURPOSE: Acid sphingomyelinase (ASMase) catalyzes the hydrolysis of sphingomyelin to ceramide and mediates multiple responses involved in inflammatory and apoptotic signaling.	Ceramides	85-93	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	32-38
27571014-4	2016	METHODS: Changes in ceramide levels and ASMase activity were determined by high performance liquid chromatography-tandem mass spectrometry analysis and ASMase activity.	Ceramides	20-28	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	152-158
27313060-1	2016	The bioactive sphingolipid metabolite, ceramide, regulates physiological processes important for inflammation and elevated levels of ceramide have been implicated in IL-1-mediated events.	Ceramides	39-47	interleukin 1 alpha	Homo sapiens	166-170
27313060-1	2016	The bioactive sphingolipid metabolite, ceramide, regulates physiological processes important for inflammation and elevated levels of ceramide have been implicated in IL-1-mediated events.	Ceramides	133-141	interleukin 1 alpha	Homo sapiens	166-170
27313060-2	2016	Although much has been learned about ceramide generation by activation of sphingomyelinases in response to IL-1, the contribution of the de novo pathway is not completely understood.	Ceramides	37-45	interleukin 1 alpha	Homo sapiens	107-111
27313060-4	2016	In HepG2 liver cells, downregulation of ORMDL3 markedly increased the ceramide precursors, dihydrosphingosine and dihydroceramide, primarily from de novo biosynthesis based on [U-(13)C]palmitate incorporation into base-labeled and dual-labeled dihydroceramides, whereas downregulation of each isoform increased dihydroceramides [(13)C]labeled in only the amide-linked fatty acid.	Ceramides	70-78	ORMDL sphingolipid biosynthesis regulator 3	Homo sapiens	40-46
27313060-5	2016	IL-1 and the IL-6 family cytokine, oncostatin M, increased dihydroceramide and ceramide levels in HepG2 cells and concomitantly decreased ORMDL proteins.	Ceramides	66-74	interleukin 1 alpha	Homo sapiens	0-4
27313060-5	2016	IL-1 and the IL-6 family cytokine, oncostatin M, increased dihydroceramide and ceramide levels in HepG2 cells and concomitantly decreased ORMDL proteins.	Ceramides	66-74	oncostatin M	Homo sapiens	35-47
27313060-6	2016	Moreover, during irritant-induced sterile inflammation in mice leading to induction of the acute-phase response, which is dependent on IL-1, expression of ORMDL proteins in the liver was strongly downregulated and accompanied by increased ceramide levels in the liver and accumulation in the blood.	Ceramides	239-247	interleukin 1 complex	Mus musculus	135-139
27313060-7	2016	Together, our results suggest that ORMDLs may be involved in regulation of ceramides during IL-1-mediated sterile inflammation.	Ceramides	75-84	interleukin 1 alpha	Homo sapiens	92-96
27244255-0	2016	The sensitivity of chronic myeloid leukemia CD34 cells to Bcr-Abl tyrosine kinase inhibitors is modulated by ceramide levels.	Ceramides	109-117	CD34 molecule	Homo sapiens	44-48
27244255-0	2016	The sensitivity of chronic myeloid leukemia CD34 cells to Bcr-Abl tyrosine kinase inhibitors is modulated by ceramide levels.	Ceramides	109-117	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	58-65
27244255-3	2016	In this study, we analyzed ceramide levels in CD34 cells derived from BP-CML patients and healthy donor bone marrow (BM) using liquid chromatography mass spectrometry.	Ceramides	27-35	CD34 molecule	Homo sapiens	46-50
27244255-4	2016	We found that ceramide level was significantly lower in BP-CML CD34 compared with normal BM counterparts.	Ceramides	14-22	CD34 molecule	Homo sapiens	63-67
27244255-5	2016	BP-CML CD34 ceramide(low) were more resistant to BCR-ABL TKIs compared to BP-CML CD34 ceramide(normal).	Ceramides	12-20	CD34 molecule	Homo sapiens	7-11
27244255-5	2016	BP-CML CD34 ceramide(low) were more resistant to BCR-ABL TKIs compared to BP-CML CD34 ceramide(normal).	Ceramides	12-20	ABL proto-oncogene 1, non-receptor tyrosine kinase	Homo sapiens	49-56
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	89-97	sphingomyelin synthase 1	Homo sapiens	33-63
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	89-97	CD34 molecule	Homo sapiens	84-88
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	163-171	sphingomyelin synthase 1	Homo sapiens	33-63
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	163-171	CD34 molecule	Homo sapiens	84-88
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	163-171	CD34 molecule	Homo sapiens	125-129
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	163-171	sphingomyelin synthase 1	Homo sapiens	33-63
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	163-171	CD34 molecule	Homo sapiens	84-88
27244255-6	2016	Both mRNA and proteins levels of sphingomyelin synthase 1 and 2 are lower in BP-CML CD34 ceramide(low) compared to normal BM CD34 cells, suggesting that these two ceramide synthesis enzymes maybe the mechanism of how ceramide level is suppressed.	Ceramides	163-171	CD34 molecule	Homo sapiens	125-129
27244255-7	2016	Importantly, up-regulation of cellular ceramide level induces apoptosis of multiple CML cell lines and BP-CML CD34 progenitors.	Ceramides	39-47	CD34 molecule	Homo sapiens	110-114
27244255-9	2016	Collectively, our work provides evidence that down-regulation of ceramide level is involved in the resistance of BP-CML CD34 progenitors to TKIs treatment.	Ceramides	65-73	CD34 molecule	Homo sapiens	120-124
27349982-1	2016	Acid sphingomyelinase (ASM) is a lysosomal phosphodiesterase that catalyzes the hydrolysis of sphingomyelin to produce ceramide and phosphocholine.	Ceramides	119-127	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
27349982-1	2016	Acid sphingomyelinase (ASM) is a lysosomal phosphodiesterase that catalyzes the hydrolysis of sphingomyelin to produce ceramide and phosphocholine.	Ceramides	119-127	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
26897748-10	2016	Together, these results demonstrate that concurrent targeting mTORC1/2 by AZD-8055 exerts anti-tumor ability in preclinical HCC models, and its activity is further sensitized with co-administration of C6 ceramide.	Ceramides	204-212	CREB regulated transcription coactivator 1	Mus musculus	62-68
27435900-1	2016	Acid sphingomyelinase (ASMase, ASM, SMPD1) converts sphingomyelin into ceramide, modulating membrane properties and signal transduction.	Ceramides	71-79	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
27255710-0	2016	Short Term Palmitate Supply Impairs Intestinal Insulin Signaling via Ceramide Production.	Ceramides	69-77	insulin	Homo sapiens	47-54
27255710-6	2016	We show that palmitic acid or palm oil increases ceramide production in intestinal cells and that treatment with a ceramide analogue partially reproduces the effects of palmitic acid on insulin signaling.	Ceramides	115-123	insulin	Homo sapiens	186-193
27255710-7	2016	In Caco-2/TC7 enterocytes, ceramide effects on insulin-dependent AKT phosphorylation are mediated by protein kinase C but not by protein phosphatase 2A.	Ceramides	27-35	insulin	Homo sapiens	47-54
27255710-8	2016	Finally, inhibiting de novo ceramide synthesis improves the response of palmitic acid-treated Caco-2/TC7 enterocytes to insulin.	Ceramides	28-36	insulin	Homo sapiens	120-127
27462707-5	2016	Biochemical characterization of some other genetic interactions shows that Cst26 is the enzyme mainly responsible for the introduction of saturated very long chain fatty acids into phosphatidylinositol and that the GPI lipid remodelase Cwh43, responsible for introducing ceramides into GPI anchors having a C26:0 fatty acid in sn-2 of the glycerol moiety can also use lyso-GPI protein anchors and various base resistant lipids as substrates.	Ceramides	271-280	putative acyltransferase	Saccharomyces cerevisiae S288C	75-80
27462707-5	2016	Biochemical characterization of some other genetic interactions shows that Cst26 is the enzyme mainly responsible for the introduction of saturated very long chain fatty acids into phosphatidylinositol and that the GPI lipid remodelase Cwh43, responsible for introducing ceramides into GPI anchors having a C26:0 fatty acid in sn-2 of the glycerol moiety can also use lyso-GPI protein anchors and various base resistant lipids as substrates.	Ceramides	271-280	Cwh43p	Saccharomyces cerevisiae S288C	236-241
27435900-1	2016	Acid sphingomyelinase (ASMase, ASM, SMPD1) converts sphingomyelin into ceramide, modulating membrane properties and signal transduction.	Ceramides	71-79	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
27435900-1	2016	Acid sphingomyelinase (ASMase, ASM, SMPD1) converts sphingomyelin into ceramide, modulating membrane properties and signal transduction.	Ceramides	71-79	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
27435900-1	2016	Acid sphingomyelinase (ASMase, ASM, SMPD1) converts sphingomyelin into ceramide, modulating membrane properties and signal transduction.	Ceramides	71-79	sphingomyelin phosphodiesterase 1	Homo sapiens	36-41
27980577-3	2016	Neutral sphingomyelinase (NSMase), acid ceramidase (ACDase) and glucosyl ceramide synthase (GCS) are the main enzymes in ceramide metabolism.	Ceramides	73-81	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
27086873-2	2016	Ceramides are synthesized by six ceramide synthases (CerS1-6).	Ceramides	0-9	ceramide synthase 1	Mus musculus	53-58
27980577-8	2016	Total cell ceramide and the activity of NSMase, the enzyme which elevates ceramide level, increased by silibinin derivatives.	Ceramides	74-82	sphingomyelin phosphodiesterase 2	Homo sapiens	40-46
27980577-3	2016	Neutral sphingomyelinase (NSMase), acid ceramidase (ACDase) and glucosyl ceramide synthase (GCS) are the main enzymes in ceramide metabolism.	Ceramides	73-81	UDP-glucose ceramide glucosyltransferase	Homo sapiens	92-95
27165857-2	2016	Its production involves the transfer of phosphocholine from phosphatidylcholine onto ceramide, a reaction catalyzed by SM synthase (SMS) 1 in the Golgi and SMS2 at the plasma membrane.	Ceramides	85-93	sphingomyelin synthase 1	Homo sapiens	119-138
27165857-2	2016	Its production involves the transfer of phosphocholine from phosphatidylcholine onto ceramide, a reaction catalyzed by SM synthase (SMS) 1 in the Golgi and SMS2 at the plasma membrane.	Ceramides	85-93	sphingomyelin synthase 2	Homo sapiens	156-160
27324416-7	2016	Comparison between AAL toxin treated jai1 and its WT revealed the COI1-dependent JA pathway regulated proteins, including pathways related to redox response, ceramide synthesis, JA, ethylene (ET), salicylic acid (SA) and abscisic acid (ABA) signaling.	Ceramides	158-166	coronatine-insensitive 1	Solanum lycopersicum	66-70
27126290-4	2016	Acer1-deficient (Acer1(-/-) ) mice showed elevated levels of ceramide in the skin, aberrant hair shaft cuticle formation and cyclic alopecia.	Ceramides	61-69	alkaline ceramidase 1	Mus musculus	17-27
27255818-4	2016	The synthesis of very long chain ceramides is catalyzed by ceramide synthase 2 (CERS2).	Ceramides	33-42	ceramide synthase 2	Homo sapiens	59-78
27255818-4	2016	The synthesis of very long chain ceramides is catalyzed by ceramide synthase 2 (CERS2).	Ceramides	33-42	ceramide synthase 2	Homo sapiens	80-85
27173510-0	2016	Compounds of the sphingomyelin-ceramide-glycosphingolipid pathways as secondary messenger molecules: new targets for novel therapies for fatty liver disease and insulin resistance.	Ceramides	31-39	insulin	Homo sapiens	161-168
27163342-1	2016	Sit4p is the catalytic subunit of a ceramide-activated PP2A-like phosphatase that regulates cell cycle, mitochondrial function, oxidative stress resistance and chronological lifespan in yeast.	Ceramides	36-44	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	0-5
27271601-7	2016	We have shown that IL-24 binds to Sigma 1 Receptor and this event induces endoplasmic reticulum stress, calcium mobilization, reactive oxygen species generation, p38MAPK activity, and ceramide production.	Ceramides	184-192	interleukin 24	Homo sapiens	19-24
26996141-0	2016	CrossTalk proposal: Intramyocellular ceramide accumulation does modulate insulin resistance.	Ceramides	37-45	insulin	Homo sapiens	73-80
27173510-1	2016	The compounds of sphingomyelin-ceramide-glycosphingolipid pathways have been studied as potential secondary messenger molecules in various systems, along with liver function and insulin resistance.	Ceramides	31-39	insulin	Homo sapiens	178-185
27055903-13	2016	Lactosylceramide, ceramide, sphingomyelin, and sphingosine-1-phosphate correlated with caspase-3 activity.	Ceramides	8-16	caspase 3	Homo sapiens	87-96
27012437-11	2016	C2 ceramide and SKI606 significantly reversed the rotenone-induced phosphorylation and aggregation of alpha-syn by increasing PP2A activity.	Ceramides	3-11	synuclein alpha	Homo sapiens	102-111
27012437-11	2016	C2 ceramide and SKI606 significantly reversed the rotenone-induced phosphorylation and aggregation of alpha-syn by increasing PP2A activity.	Ceramides	3-11	protein phosphatase 2 catalytic subunit alpha	Homo sapiens	126-130
27085050-4	2016	We discovered that by subjecting SCC19 cells, a human head and neck squamous cell carcinoma cell line, to PDT+HPR resulted in enhanced accumulation of C16-dihydroceramide, not ceramide.	Ceramides	162-170	haptoglobin-related protein	Homo sapiens	110-113
26783265-7	2016	Finally upon the switching on of activated K-Ras expression which induces luminal cell filling, ceramide and LacCer are increased.	Ceramides	96-104	KRAS proto-oncogene, GTPase	Canis lupus familiaris	43-48
27234412-6	2016	Gluco-, galacto-, and lactosylceramide are hydrolyzed to ceramide by lactase-phlorizin hydrolase, which also hydrolyzes lactose.	Ceramides	30-38	lactase	Homo sapiens	69-96
26248324-1	2016	Dihydroceramide desaturase (Des1) is the last enzyme in the de novo synthesis of ceramides (Cer).	Ceramides	81-90	delta 4-desaturase, sphingolipid 1	Homo sapiens	28-32
27162368-5	2016	Here, we ectopically expressed CerS2, a nonneuronal CerS producing C22-C24 ceramides, in neurons of Cers1-deficient mice.	Ceramides	75-84	ceramide synthase 2	Mus musculus	31-36
26511776-8	2016	CONCLUSIONS: It was hypothesized that ethanol promoted ceramide accumulation and increased PP2A activity by activating ASMase, which may be an important mechanism in the inhibitory effect on AMPK phosphorylation and then contributed to the progression of steatosis.	Ceramides	55-63	sphingomyelin phosphodiesterase 1	Homo sapiens	119-125
26511776-9	2016	ASMase, a specific mechanism of ceramide generation, was proved to be a regulator of steatosis, fibrosis, lipotoxicity and endoplasmic reticulum stress.	Ceramides	32-40	sphingomyelin phosphodiesterase 1	Homo sapiens	0-6
26248324-1	2016	Dihydroceramide desaturase (Des1) is the last enzyme in the de novo synthesis of ceramides (Cer).	Ceramides	92-95	delta 4-desaturase, sphingolipid 1	Homo sapiens	28-32
26780287-0	2016	Hepatic ceramides dissociate steatosis and insulin resistance in patients with non-alcoholic fatty liver disease.	Ceramides	8-17	insulin	Homo sapiens	43-50
25673319-2	2016	We have previously shown that CD300f (also called the leucocyte mono-immunoglobulin-like receptor 3 (LMIR3)) suppresses immunoglobulin E-dependent and mast cell-dependent allergic responses by binding to ceramide.	Ceramides	204-212	CD300 molecule like family member F	Mus musculus	54-99
25673319-2	2016	We have previously shown that CD300f (also called the leucocyte mono-immunoglobulin-like receptor 3 (LMIR3)) suppresses immunoglobulin E-dependent and mast cell-dependent allergic responses by binding to ceramide.	Ceramides	204-212	CD300 molecule like family member F	Mus musculus	101-106
25673319-3	2016	The aim of the present study was to clarify the role of ceramide-LMIR3 interaction in the development of IBD.	Ceramides	56-64	CD300 molecule like family member F	Mus musculus	65-70
27098312-1	2016	Gaucher disease, caused by pathological mutations GBA1, encodes the lysosome-resident enzyme glucocerebrosidase, which cleaves glucosylceramide into glucose and ceramide.	Ceramides	135-143	glucosylceramidase beta	Homo sapiens	50-54
25673319-12	2016	Ceramide-LMIR3 interaction inhibited ATP-stimulated activation of BMMCs.	Ceramides	0-8	CD300 molecule like family member F	Mus musculus	9-14
25673319-13	2016	DSS-induced colitis was aggravated by disrupting the ceramide-LMIR3 interaction, whereas it was suppressed by treating with ceramide liposomes.	Ceramides	53-61	CD300 molecule like family member F	Mus musculus	62-67
25673319-15	2016	Ceramide liposomes attenuated DSS-induced colitis by inhibiting ATP-mediated activation of colonic mast cells through ceraimide-LMIR3 binding.	Ceramides	0-8	CD300 molecule like family member F	Mus musculus	128-133
26780287-1	2016	BACKGROUND &amp; AIMS: Recent data in mice have identified de novo ceramide synthesis as the key mediator of hepatic insulin resistance (IR) that in humans characterizes increases in liver fat due to IR ("Metabolic NAFLD" but not that due to the I148M gene variant in PNPLA3 ("PNPLA3 NAFLD").	Ceramides	67-75	insulin	Homo sapiens	117-124
27013100-1	2016	Neutral sphingomyelinase-2 (nSMase2) is a key ceramide-producing enzyme in cellular stress responses.	Ceramides	46-54	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
26780287-1	2016	BACKGROUND &amp; AIMS: Recent data in mice have identified de novo ceramide synthesis as the key mediator of hepatic insulin resistance (IR) that in humans characterizes increases in liver fat due to IR ("Metabolic NAFLD" but not that due to the I148M gene variant in PNPLA3 ("PNPLA3 NAFLD").	Ceramides	67-75	patatin like phospholipase domain containing 3	Homo sapiens	268-274
27013100-1	2016	Neutral sphingomyelinase-2 (nSMase2) is a key ceramide-producing enzyme in cellular stress responses.	Ceramides	46-54	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
26780287-1	2016	BACKGROUND &amp; AIMS: Recent data in mice have identified de novo ceramide synthesis as the key mediator of hepatic insulin resistance (IR) that in humans characterizes increases in liver fat due to IR ("Metabolic NAFLD" but not that due to the I148M gene variant in PNPLA3 ("PNPLA3 NAFLD").	Ceramides	67-75	patatin like phospholipase domain containing 3	Homo sapiens	277-283
26920060-7	2016	Further, A-674563 decreased sphingosine kinase 1 (SphK1) activity in above AML cells to deplete pro-survival sphingosine-1-phosphate (S1P) and boost pro-apoptotic ceramide production.	Ceramides	163-171	sphingosine kinase 1	Homo sapiens	50-55
26364609-0	2016	Ceramide limits phosphatidylinositol-3-kinase C2beta-controlled cell motility in ovarian cancer: potential of ceramide as a metastasis-suppressor lipid.	Ceramides	0-8	secretoglobin family 2B member 3, pseudogene	Homo sapiens	46-52
26364609-6	2016	Mechanistically, ceramide was revealed to interact with the PIK-catalytic domain of PI3KC2beta and affect its compartmentalization, thereby suppressing PI3KC2beta activation and its driven cell motility.	Ceramides	17-25	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta	Homo sapiens	84-94
26851257-5	2016	Thrombin activated acid sphingomyelinase (ASM) and increased ceramide production in HMVEC-L, but not in bovine pulmonary artery cells, which showed little albumin transport in response to thrombin.	Ceramides	61-69	coagulation factor II, thrombin	Bos taurus	0-8
26364609-6	2016	Mechanistically, ceramide was revealed to interact with the PIK-catalytic domain of PI3KC2beta and affect its compartmentalization, thereby suppressing PI3KC2beta activation and its driven cell motility.	Ceramides	17-25	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta	Homo sapiens	152-162
26364609-10	2016	Metastasis of PI3KC2beta knocked-down cells was insensitive to treatment with ceramide liposomes, suggesting specific involvement of ceramide interaction with PI3KC2beta in metastasis suppression.	Ceramides	133-141	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta	Homo sapiens	14-24
26364609-11	2016	Our study identified ceramide as a bioactive lipid that limits PI3KC2beta-governed cell motility, and ceramide is proposed to serve as a metastasis-suppressor lipid in ovarian cancer.	Ceramides	21-29	phosphatidylinositol-4-phosphate 3-kinase catalytic subunit type 2 beta	Homo sapiens	63-73
26884383-7	2016	Inhibition of neutral sphingomyelinase, a key player in the IL-1beta signaling cascade that acts upstream of ERK, also suppressed the IL-1beta effects, while increasing the ceramide, through the addition of C2-ceramide or via treatment with exogenous sphingomyelinase, was sufficient to induce IGFBP1 promoter-driven luciferase activity.	Ceramides	173-181	interleukin 1 beta	Rattus norvegicus	60-68
26884383-8	2016	Studies in primary rat hepatocytes where the levels of neutral sphingomyelinase were either elevated or suppressed using adenoviral constructs affirmed the key role of neutral sphingomyelinase and ceramide (exerted likely through ERK activation) in the IL-1beta-induced IGFBP1 production.	Ceramides	197-205	Eph receptor B1	Rattus norvegicus	230-233
26920060-9	2016	Significantly, K6PC-5, a novel SphK1 activator, or supplement with S1P attenuated A-674563-induced ceramide production, and subsequent U937 cell death and apoptosis.	Ceramides	99-107	sphingosine kinase 1	Homo sapiens	31-36
26739815-8	2016	CONCLUSIONS/INTERPRETATION: These data suggest ceramide and other sphingolipids containing stearate (18:0) are uniquely related to insulin resistance in skeletal muscle.	Ceramides	47-55	insulin	Homo sapiens	131-138
26933996-3	2016	We observed a highly significant upregulation of long and very long chain ceramides (C16-C24) in the serum of patients with HCC as compared to patients with cirrhosis (P &lt; 0.001).	Ceramides	74-83	HCC	Homo sapiens	124-127
26933996-4	2016	Accordingly, dihydro-ceramides, synthetic precursors of ceramides and notably sphingosine, sphingosine-1-phosphate (S1P) and sphinganine-1-phosphate (SA1P) were upregulated in patients with HCC (P &lt; 0.001).	Ceramides	21-30	HCC	Homo sapiens	190-193
26950647-1	2016	Drosophila Ceramide Synthase (CerS) Schlank regulates both ceramide synthesis and fat metabolism.	Ceramides	59-67	schlank	Drosophila melanogaster	36-43
26874430-11	2016	Inhibition of ceramide synthesis with FB1 and ROS production with n-MPG scavenging rescued MMP activity and IL-1beta production in palmitate treated heterophils, but exacerbated monocyte suppression.	Ceramides	14-22	matrix metallopeptidase 2	Gallus gallus	91-94
26874430-11	2016	Inhibition of ceramide synthesis with FB1 and ROS production with n-MPG scavenging rescued MMP activity and IL-1beta production in palmitate treated heterophils, but exacerbated monocyte suppression.	Ceramides	14-22	interleukin 1, beta	Gallus gallus	108-116
26739815-1	2016	AIMS/HYPOTHESES: Ceramides and other sphingolipids comprise a family of lipid molecules that accumulate in skeletal muscle and promote insulin resistance.	Ceramides	17-26	insulin	Homo sapiens	135-142
26739815-9	2016	Recovery from an exercise bout decreased muscle ceramide concentration; this may represent a mechanism promoting the insulin-sensitising effects of acute exercise.	Ceramides	48-56	insulin	Homo sapiens	117-124
26930027-7	2016	Although we showed that cardiac ceramide accumulation was reduced in Smpd1(+/-) mice 24h after an induced myocardial infarction, this reduction was not accompanied by an improvement in heart function or survival.	Ceramides	32-40	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	69-74
26887952-3	2016	Ceramides in mammals vary greatly in their acyl-chain composition: six different ceramide synthase isozymes (CERS1-6) that exhibit distinct substrate specificity and tissue distribution account for this diversity.	Ceramides	0-9	ceramide synthase 1	Mus musculus	109-116
27114850-4	2016	Moreover, many stress-related signaling mechanisms, such as oxidative stress and energy metabolic disturbances, as well as the signaling cascades via ceramide, mTOR, NF-kappaB, and TGF-beta pathways, can also induce the expression of HIF-1alpha protein to facilitate cell survival in normoxia.	Ceramides	150-158	hypoxia inducible factor 1 subunit alpha	Homo sapiens	234-244
26900161-3	2016	Diabetes increased expression of desaturase 1, (dihydro)ceramide synthase (CerS)2, serine palmitoyl transferase 1, and the rate of ceramide formation by mitochondria-resident CerSs, indicating an activation of ceramide biosynthesis.	Ceramides	56-64	ceramide synthase 2	Mus musculus	75-81
26900161-7	2016	Moreover, knocking down the neutral ceramidase (NCDase) resulted in an increase in lactosylceramide level, suggesting a crosstalk between glucosylceramide synthase- and NCDase-mediated ceramide utilization pathways.	Ceramides	91-99	N-acylsphingosine amidohydrolase 2	Mus musculus	28-46
26900161-7	2016	Moreover, knocking down the neutral ceramidase (NCDase) resulted in an increase in lactosylceramide level, suggesting a crosstalk between glucosylceramide synthase- and NCDase-mediated ceramide utilization pathways.	Ceramides	91-99	N-acylsphingosine amidohydrolase 2	Mus musculus	48-54
26900161-7	2016	Moreover, knocking down the neutral ceramidase (NCDase) resulted in an increase in lactosylceramide level, suggesting a crosstalk between glucosylceramide synthase- and NCDase-mediated ceramide utilization pathways.	Ceramides	91-99	N-acylsphingosine amidohydrolase 2	Mus musculus	169-175
26729710-5	2016	Several novel ceramide-binding domains were discovered, including the EF-hand calcium-binding motif, the heat shock chaperonin-binding motif STI1, the SCP2 sterol-binding domain, and the tetratricopeptide repeat region motif.	Ceramides	14-22	Hsp90 cochaperone STI1	Saccharomyces cerevisiae S288C	141-145
26676316-5	2016	ASM upregulation in diabetic CACs caused accumulation of ceramide on their cell membrane, thereby reducing membrane fluidity and impairing CAC migration.	Ceramides	57-65	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
27043542-3	2016	In the present study, we found that exogenous cell-permeable short-chain C2 ceramide inhibits phorbol myristate acetate (PMA)-induced MMP-1, -3, and -9 gene expressions in U87MG and U373MG human astroglioma cells.	Ceramides	76-84	matrix metallopeptidase 1	Homo sapiens	134-151
27043542-4	2016	In addition, C2 ceramide inhibited the protein secretion and enzymatic activities of MMP-1, -3, and -9.	Ceramides	16-24	matrix metallopeptidase 1	Homo sapiens	85-102
27043542-5	2016	The Matrigel invasion assay and wound healing assay showed that C2 ceramide suppresses the in vitro invasion and migration of glioma cells, which appears to be involved in strong inhibition of MMPs by C2 ceramide.	Ceramides	67-75	matrix metallopeptidase 1	Homo sapiens	193-197
27043542-8	2016	The results suggest C2 ceramide inhibits MMP expression and glioma invasion, at least partly, by modulating ROS-p38 MAPK signaling axis and other MAPK signaling pathways.	Ceramides	23-31	mitogen-activated protein kinase 14	Homo sapiens	112-115
26843596-8	2016	IL-1beta accelerated Ca(2+) clearance in a manner blocked by an IL-1beta receptor antagonist or by an inhibitor of neutral sphingomyelinase, the enzyme that produces ceramide.	Ceramides	166-174	interleukin 1 beta	Homo sapiens	0-8
26843596-8	2016	IL-1beta accelerated Ca(2+) clearance in a manner blocked by an IL-1beta receptor antagonist or by an inhibitor of neutral sphingomyelinase, the enzyme that produces ceramide.	Ceramides	166-174	sphingomyelin phosphodiesterase 2	Homo sapiens	115-139
26853464-8	2016	We found a strong impact of CerS5-dependent ceramide synthesis in white adipose tissue after high fat diet feeding.	Ceramides	44-52	ceramide synthase 5	Mus musculus	28-33
26792860-2	2016	ASMase converts sphingomyelin into the signaling lipid, ceramide.	Ceramides	56-64	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
26747710-11	2016	Although nCDase(-/-) cells generated ceramides following 2DG/AA treatment, they did not generate Sph or S1P.	Ceramides	37-46	N-acylsphingosine amidohydrolase 2	Mus musculus	9-15
26886165-7	2016	Moreover, ceramidase Asah1 was highly expressed in aged kidneys, consistent with a decrease in ceramide C16.	Ceramides	95-103	N-acylsphingosine amidohydrolase 1	Mus musculus	21-26
26938296-5	2016	Consistent with these data, we demonstrated that LPS downregulated both Acer3 mRNA levels and its enzymatic activity while elevating C(18:1)-ceramide, a substrate of Acer3, in murine immune cells or CECs.	Ceramides	141-149	alkaline ceramidase 3	Mus musculus	166-171
26938296-6	2016	Knocking out Acer3 enhanced the elevation of C(18:1)-ceramide and the expression of pro-inflammatory cytokines in immune cells and CECs in response to LPS challenge.	Ceramides	53-61	alkaline ceramidase 3	Mus musculus	13-18
26938296-12	2016	Taken together, these results suggest that Acer3 has an important anti-inflammatory role by suppressing cellular or tissue C(18:1)-ceramide, a potent pro-inflammatory bioactive lipid and that dysregulation of ACER3 and C(18:1)-ceramide may contribute to the pathogenesis of inflammatory diseases including cancer.	Ceramides	131-139	alkaline ceramidase 3	Mus musculus	43-48
26938296-12	2016	Taken together, these results suggest that Acer3 has an important anti-inflammatory role by suppressing cellular or tissue C(18:1)-ceramide, a potent pro-inflammatory bioactive lipid and that dysregulation of ACER3 and C(18:1)-ceramide may contribute to the pathogenesis of inflammatory diseases including cancer.	Ceramides	227-235	alkaline ceramidase 3	Mus musculus	43-48
26903652-2	2016	ER stress increases cellular ceramide and one of its distal metabolites, S1P, which activates NF-kappaB followed by C/EBPalpha activation, leading to CAMP production, but in a S1P receptor-independent fashion.	Ceramides	29-37	CCAAT enhancer binding protein alpha	Homo sapiens	116-126
26903652-2	2016	ER stress increases cellular ceramide and one of its distal metabolites, S1P, which activates NF-kappaB followed by C/EBPalpha activation, leading to CAMP production, but in a S1P receptor-independent fashion.	Ceramides	29-37	cathelicidin antimicrobial peptide	Homo sapiens	150-154
26711671-5	2016	For the purpose of clarifying the influence of HA4 on ceramide synthesis, we evaluated both of these factors in keratinocytes in vitro and in vivo.	Ceramides	54-62	keratin 34	Homo sapiens	47-50
26711671-7	2016	In addition, the ceramide increasing effect of HA4 on skin in UVA-irradiated hairless mice was assessed by water content of stratum corneum (SC) and transepidermal water loss (TEWL) methods.	Ceramides	17-25	keratin 33B	Mus musculus	47-50
26711671-8	2016	The mRNA expression of ceramide synthesis-associated enzymes and intracellular ceramide content after HA4 treatment were increased compared with the control.	Ceramides	23-31	keratin 34	Homo sapiens	102-105
26711671-8	2016	The mRNA expression of ceramide synthesis-associated enzymes and intracellular ceramide content after HA4 treatment were increased compared with the control.	Ceramides	79-87	keratin 34	Homo sapiens	102-105
26711671-10	2016	These findings suggest that HA4 affected ceramide synthesis and is involved in the improvement of UV-induced skin damage.	Ceramides	41-49	keratin 34	Homo sapiens	28-31
26635357-2	2016	In Arabidopsis, the varied chemical composition of ceramide is determined by the specificity of three different isoforms of ceramide synthase, denoted LAG one homologue 1, -2 and -3 (LOH1, LOH2 and LOH3), for a range of long-chain base (LCB) and acyl-CoA substrates.	Ceramides	51-59	RNA-binding CRS1 / YhbY (CRM) domain protein	Arabidopsis thaliana	151-181
26873583-0	2016	Short-chain C2 ceramide induces heme oxygenase-1 expression by upregulating AMPK and MAPK signaling pathways in rat primary astrocytes.	Ceramides	15-23	heme oxygenase 1	Rattus norvegicus	32-48
26635357-2	2016	In Arabidopsis, the varied chemical composition of ceramide is determined by the specificity of three different isoforms of ceramide synthase, denoted LAG one homologue 1, -2 and -3 (LOH1, LOH2 and LOH3), for a range of long-chain base (LCB) and acyl-CoA substrates.	Ceramides	51-59	LAG1 homologue 2	Arabidopsis thaliana	189-193
26635357-2	2016	In Arabidopsis, the varied chemical composition of ceramide is determined by the specificity of three different isoforms of ceramide synthase, denoted LAG one homologue 1, -2 and -3 (LOH1, LOH2 and LOH3), for a range of long-chain base (LCB) and acyl-CoA substrates.	Ceramides	51-59	LAG1 longevity assurance-like protein	Arabidopsis thaliana	198-202
26718495-7	2016	Furthermore, SAT ceramide concentrations correlated with the expression of CASP1 and IL1B.	Ceramides	17-25	caspase 1	Homo sapiens	75-80
26718495-7	2016	Furthermore, SAT ceramide concentrations correlated with the expression of CASP1 and IL1B.	Ceramides	17-25	interleukin 1 beta	Homo sapiens	85-89
26873583-5	2016	C2 ceramide increased the expression of phase II antioxidant enzymes, such as heme oxygenase-1 (HO-1), NAD(P)H:quinine oxidoreductase 1 (NQO1), and superoxide dismutase (SOD) that are under the control of Nrf2/ARE signaling pathways.	Ceramides	3-11	heme oxygenase 1	Rattus norvegicus	78-94
26873583-5	2016	C2 ceramide increased the expression of phase II antioxidant enzymes, such as heme oxygenase-1 (HO-1), NAD(P)H:quinine oxidoreductase 1 (NQO1), and superoxide dismutase (SOD) that are under the control of Nrf2/ARE signaling pathways.	Ceramides	3-11	heme oxygenase 1	Rattus norvegicus	96-100
26873583-5	2016	C2 ceramide increased the expression of phase II antioxidant enzymes, such as heme oxygenase-1 (HO-1), NAD(P)H:quinine oxidoreductase 1 (NQO1), and superoxide dismutase (SOD) that are under the control of Nrf2/ARE signaling pathways.	Ceramides	3-11	NFE2 like bZIP transcription factor 2	Rattus norvegicus	205-209
26873583-7	2016	Moreover, C2 ceramide increased the interaction between Nrf2 and c-Jun as shown by antibody co-immunoprecipitation assay.	Ceramides	13-21	NFE2 like bZIP transcription factor 2	Rattus norvegicus	56-60
26916435-6	2016	PP2A is activated by ceramides and dephosphorylates Akt.	Ceramides	21-30	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	0-4
26916435-6	2016	PP2A is activated by ceramides and dephosphorylates Akt.	Ceramides	21-30	thymoma viral proto-oncogene 1	Mus musculus	52-55
27467962-0	2016	Combating rituximab resistance by inducing ceramide/lysosome-involved cell death through initiation of CD20-TNFR1 co-localization.	Ceramides	43-51	keratin 20	Homo sapiens	103-107
27239444-0	2016	mTOR inhibition by rapamycin increases ceramide synthesis by promoting transforming growth factor-beta1/Smad signaling in the skin.	Ceramides	39-47	mechanistic target of rapamycin kinase	Homo sapiens	0-4
27239444-2	2016	In this study, we investigated effects of mTOR inhibition by rapamycin on ceramide synthesis in the skin of rats and human keratinocytes and its regulatory mechanisms.	Ceramides	74-82	mechanistic target of rapamycin kinase	Rattus norvegicus	42-46
27239444-7	2016	These results show that mTOR inhibition by rapamycin increases ceramide synthesis by promoting TGF-beta1/Smad signaling in the skin.	Ceramides	63-71	mechanistic target of rapamycin kinase	Homo sapiens	24-28
27239444-7	2016	These results show that mTOR inhibition by rapamycin increases ceramide synthesis by promoting TGF-beta1/Smad signaling in the skin.	Ceramides	63-71	transforming growth factor beta 1	Homo sapiens	95-104
26809095-8	2016	Desipramine, a functional ASMase inhibitor, prevented RSV-induced ceramide increase.	Ceramides	66-74	sphingomyelin phosphodiesterase 1	Homo sapiens	26-32
26809095-12	2016	These results indicate that increased EGR1/3 and ASMase expression play an important role in cellular ceramide increase by RSV treatment.	Ceramides	102-110	early growth response 1	Homo sapiens	38-44
26809095-12	2016	These results indicate that increased EGR1/3 and ASMase expression play an important role in cellular ceramide increase by RSV treatment.	Ceramides	102-110	sphingomyelin phosphodiesterase 1	Homo sapiens	49-55
27467962-0	2016	Combating rituximab resistance by inducing ceramide/lysosome-involved cell death through initiation of CD20-TNFR1 co-localization.	Ceramides	43-51	TNF receptor superfamily member 1A	Homo sapiens	108-113
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	60-68	keratin 20	Homo sapiens	38-42
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	60-68	keratin 20	Homo sapiens	163-167
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	60-68	TNF receptor superfamily member 1A	Homo sapiens	168-173
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	60-68	keratin 20	Homo sapiens	163-167
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	233-241	keratin 20	Homo sapiens	38-42
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	233-241	keratin 20	Homo sapiens	163-167
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	233-241	TNF receptor superfamily member 1A	Homo sapiens	168-173
27467962-4	2016	Here, we uncover an important role of CD20 in initiation of ceramide/lysosomal membrane permeabilization (LMP)-mediated cell death, showing that colocalization of CD20-TNFR1 after type II CD20 antibody ligation can stimulate de novo ceramide synthesis by ceramide synthase and consequently induce remarkable lysosomal permeabilization (LMP) and lysosome-mediated cell death.	Ceramides	233-241	keratin 20	Homo sapiens	163-167
26522807-12	2016	Monocytes preincubated with C16:0 increased secretion of pro-inflammatory cytokines in response to phorbol myristate acetate-induced differentiation through ceramide-dependent inhibition of PPARgamma activity.	Ceramides	157-165	peroxisome proliferator activated receptor gamma	Homo sapiens	190-199
26698173-0	2016	Sustained Action of Ceramide on the Insulin Signaling Pathway in Muscle Cells: IMPLICATION OF THE DOUBLE-STRANDED RNA-ACTIVATED PROTEIN KINASE.	Ceramides	20-28	insulin	Homo sapiens	36-43
26698173-0	2016	Sustained Action of Ceramide on the Insulin Signaling Pathway in Muscle Cells: IMPLICATION OF THE DOUBLE-STRANDED RNA-ACTIVATED PROTEIN KINASE.	Ceramides	20-28	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	98-142
26698173-2	2016	However, in vitro treatments with saturated fatty acids or their derivative ceramide demonstrate an effect only at the Akt step.	Ceramides	76-84	AKT serine/threonine kinase 1	Homo sapiens	119-122
26698173-6	2016	Short-term treatments of myotubes with palmitate, a ceramide precursor, or directly with ceramide induce an inhibition of Akt, whereas prolonged periods of treatment show an additive inhibition of insulin signaling through increased IRS1 serine 307 phosphorylation.	Ceramides	52-60	AKT serine/threonine kinase 1	Homo sapiens	122-125
26698173-6	2016	Short-term treatments of myotubes with palmitate, a ceramide precursor, or directly with ceramide induce an inhibition of Akt, whereas prolonged periods of treatment show an additive inhibition of insulin signaling through increased IRS1 serine 307 phosphorylation.	Ceramides	52-60	insulin	Homo sapiens	197-204
26698173-6	2016	Short-term treatments of myotubes with palmitate, a ceramide precursor, or directly with ceramide induce an inhibition of Akt, whereas prolonged periods of treatment show an additive inhibition of insulin signaling through increased IRS1 serine 307 phosphorylation.	Ceramides	52-60	insulin receptor substrate 1	Homo sapiens	233-237
26698173-6	2016	Short-term treatments of myotubes with palmitate, a ceramide precursor, or directly with ceramide induce an inhibition of Akt, whereas prolonged periods of treatment show an additive inhibition of insulin signaling through increased IRS1 serine 307 phosphorylation.	Ceramides	89-97	AKT serine/threonine kinase 1	Homo sapiens	122-125
26698173-6	2016	Short-term treatments of myotubes with palmitate, a ceramide precursor, or directly with ceramide induce an inhibition of Akt, whereas prolonged periods of treatment show an additive inhibition of insulin signaling through increased IRS1 serine 307 phosphorylation.	Ceramides	89-97	insulin	Homo sapiens	197-204
26698173-6	2016	Short-term treatments of myotubes with palmitate, a ceramide precursor, or directly with ceramide induce an inhibition of Akt, whereas prolonged periods of treatment show an additive inhibition of insulin signaling through increased IRS1 serine 307 phosphorylation.	Ceramides	89-97	insulin receptor substrate 1	Homo sapiens	233-237
26698173-9	2016	Finally, we show that JNK mediates ceramide-activated PKR inhibitory action on IRS1.	Ceramides	35-43	mitogen-activated protein kinase 8	Homo sapiens	22-25
26698173-9	2016	Finally, we show that JNK mediates ceramide-activated PKR inhibitory action on IRS1.	Ceramides	35-43	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	54-57
26698173-9	2016	Finally, we show that JNK mediates ceramide-activated PKR inhibitory action on IRS1.	Ceramides	35-43	insulin receptor substrate 1	Homo sapiens	79-83
26698173-10	2016	Together, in the long term, our results show that ceramide acts at two distinct levels of the insulin signaling pathway (IRS1 and Akt).	Ceramides	50-58	insulin	Homo sapiens	94-101
26698173-10	2016	Together, in the long term, our results show that ceramide acts at two distinct levels of the insulin signaling pathway (IRS1 and Akt).	Ceramides	50-58	insulin receptor substrate 1	Homo sapiens	121-125
26698173-10	2016	Together, in the long term, our results show that ceramide acts at two distinct levels of the insulin signaling pathway (IRS1 and Akt).	Ceramides	50-58	AKT serine/threonine kinase 1	Homo sapiens	130-133
26698173-11	2016	PKR, which is induced by both inflammation signals and ceramide, could play a major role in the development of insulin resistance in muscle cells.	Ceramides	55-63	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	0-3
26698173-11	2016	PKR, which is induced by both inflammation signals and ceramide, could play a major role in the development of insulin resistance in muscle cells.	Ceramides	55-63	insulin	Homo sapiens	111-118
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.	Ceramides	124-132	synuclein alpha	Homo sapiens	42-51
26811497-4	2016	Our data reveals that ceramide-modifying enzymes, particularly glucosylceramide synthase (GCS), are upregulated during sorafenib treatment in hepatoma cells (HepG2 and Hep3B), and more importantly, in sorafenib-resistant cell lines.	Ceramides	22-30	UDP-glucose ceramide glucosyltransferase	Mus musculus	63-88
26811497-4	2016	Our data reveals that ceramide-modifying enzymes, particularly glucosylceramide synthase (GCS), are upregulated during sorafenib treatment in hepatoma cells (HepG2 and Hep3B), and more importantly, in sorafenib-resistant cell lines.	Ceramides	22-30	UDP-glucose ceramide glucosyltransferase	Mus musculus	90-93
26658266-3	2016	Pharmacological inhibition of ceramidases and more particularly, acid ceramidase (aCDase) is suggestive of a chemotherapeutic approach as it increases the cellular concentration of ceramide inducing apoptosis.	Ceramides	181-189	N-acylsphingosine amidohydrolase 1	Homo sapiens	65-80
26658266-3	2016	Pharmacological inhibition of ceramidases and more particularly, acid ceramidase (aCDase) is suggestive of a chemotherapeutic approach as it increases the cellular concentration of ceramide inducing apoptosis.	Ceramides	181-189	N-acylsphingosine amidohydrolase 1	Homo sapiens	82-88
26863224-6	2016	RESULTS: When examining the differences between transplant stages in each group, C18, C20, C24 ceramides showed significant difference in DBD (p&lt;0.05) and C22 ceramide (p&lt;0.05) were more pronounced for DCD.	Ceramides	95-103	Bardet-Biedl syndrome 9	Homo sapiens	81-84
26849355-7	2016	The results of our analysis suggest the following two prospects about inflammation in AD: (1) ceramide could play important roles in both inflammatory and anti-inflammatory pathways of AD, and (2) several factors such as Sphingomyelinase and Siglec-11 may be associated with ceramide related inflammation and anti-inflammation pathways in AD.	Ceramides	94-102	sialic acid binding Ig like lectin 11	Homo sapiens	242-251
26849355-7	2016	The results of our analysis suggest the following two prospects about inflammation in AD: (1) ceramide could play important roles in both inflammatory and anti-inflammatory pathways of AD, and (2) several factors such as Sphingomyelinase and Siglec-11 may be associated with ceramide related inflammation and anti-inflammation pathways in AD.	Ceramides	275-283	sialic acid binding Ig like lectin 11	Homo sapiens	242-251
26548718-0	2016	The hyaluronic acid inhibitor 4-methylumbelliferone is an NSMase2 activator-role of Ceramide in MU anti-tumor activity.	Ceramides	84-92	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	58-65
26548718-4	2016	In a previous study we demonstrated the regulation of HA synthesis by ceramide, and now show how MU activated neutral sphingomyelinase2 (NSMase2) generates ceramides and mediates MU induced inhibition of HA synthesis, cell migration and invasion, and apoptosis of tumor cells.	Ceramides	70-78	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	110-135
26548718-7	2016	In addition, MU mediated ceramide stimulated activation of p53 and caspase-3, reduced SIRT1 expression and decreased G26-24 viability.	Ceramides	25-33	sirtuin 1	Mus musculus	86-91
26548718-4	2016	In a previous study we demonstrated the regulation of HA synthesis by ceramide, and now show how MU activated neutral sphingomyelinase2 (NSMase2) generates ceramides and mediates MU induced inhibition of HA synthesis, cell migration and invasion, and apoptosis of tumor cells.	Ceramides	70-78	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	137-144
26548718-4	2016	In a previous study we demonstrated the regulation of HA synthesis by ceramide, and now show how MU activated neutral sphingomyelinase2 (NSMase2) generates ceramides and mediates MU induced inhibition of HA synthesis, cell migration and invasion, and apoptosis of tumor cells.	Ceramides	156-165	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	110-135
26548718-4	2016	In a previous study we demonstrated the regulation of HA synthesis by ceramide, and now show how MU activated neutral sphingomyelinase2 (NSMase2) generates ceramides and mediates MU induced inhibition of HA synthesis, cell migration and invasion, and apoptosis of tumor cells.	Ceramides	156-165	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	137-144
26548718-7	2016	In addition, MU mediated ceramide stimulated activation of p53 and caspase-3, reduced SIRT1 expression and decreased G26-24 viability.	Ceramides	25-33	transformation related protein 53, pseudogene	Mus musculus	59-62
26548718-7	2016	In addition, MU mediated ceramide stimulated activation of p53 and caspase-3, reduced SIRT1 expression and decreased G26-24 viability.	Ceramides	25-33	caspase 3	Mus musculus	67-76
26553872-1	2016	Acid ceramidase (AC) is a lysosomal cysteine amidase that controls sphingolipid signaling by lowering the levels of ceramides and concomitantly increasing those of sphingosine and its bioactive metabolite, sphingosine 1-phosphate.	Ceramides	116-125	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
26621917-0	2016	Hepatocytes release ceramide-enriched pro-inflammatory extracellular vesicles in an IRE1alpha-dependent manner.	Ceramides	20-28	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	84-93
26621917-12	2016	PA induces C16:0 ceramide-enriched EV release in an IRE1alpha-dependent manner.	Ceramides	17-25	endoplasmic reticulum to nucleus signaling 1	Homo sapiens	52-61
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.	Ceramides	179-187	glucosylceramidase beta 2	Homo sapiens	42-46
26807955-0	2016	Ceramide Induces Human Hepcidin Gene Transcription through JAK/STAT3 Pathway.	Ceramides	0-8	hepcidin antimicrobial peptide	Homo sapiens	23-31
26807955-0	2016	Ceramide Induces Human Hepcidin Gene Transcription through JAK/STAT3 Pathway.	Ceramides	0-8	signal transducer and activator of transcription 3	Homo sapiens	63-68
26807955-4	2016	We investigated the role of lipid intermediate, ceramide in the regulation of human hepcidin gene, HAMP.	Ceramides	48-56	hepcidin antimicrobial peptide	Homo sapiens	84-92
26807955-4	2016	We investigated the role of lipid intermediate, ceramide in the regulation of human hepcidin gene, HAMP.	Ceramides	48-56	hepcidin antimicrobial peptide	Homo sapiens	99-103
26807955-6	2016	Ceramide induced significant up-regulation of HAMP mRNA expression in HepG2 cells.	Ceramides	0-8	hepcidin antimicrobial peptide	Homo sapiens	46-50
26807955-7	2016	The effect of ceramide on HAMP expression was mediated through transcriptional mechanisms because it was completely blocked with actinomycin D treatment.	Ceramides	14-22	hepcidin antimicrobial peptide	Homo sapiens	26-30
26807955-8	2016	Reporter assays also confirmed the activation of 0.6 kb HAMP promoter by ceramide.	Ceramides	73-81	hepcidin antimicrobial peptide	Homo sapiens	56-60
26807955-9	2016	HepG2 cells treated with ceramide displayed increased phosphorylation of STAT3, JNK, and NF-kappaB proteins.	Ceramides	25-33	signal transducer and activator of transcription 3	Homo sapiens	73-78
26807955-9	2016	HepG2 cells treated with ceramide displayed increased phosphorylation of STAT3, JNK, and NF-kappaB proteins.	Ceramides	25-33	mitogen-activated protein kinase 8	Homo sapiens	80-83
26807955-9	2016	HepG2 cells treated with ceramide displayed increased phosphorylation of STAT3, JNK, and NF-kappaB proteins.	Ceramides	25-33	nuclear factor kappa B subunit 1	Homo sapiens	89-98
26807955-10	2016	However, ceramide induced the binding of STAT3, but not NF-kappaB or c-Jun, to HAMP promoter, as shown by the chromatin immunoprecipitation assays.	Ceramides	9-17	signal transducer and activator of transcription 3	Homo sapiens	41-46
26807955-10	2016	However, ceramide induced the binding of STAT3, but not NF-kappaB or c-Jun, to HAMP promoter, as shown by the chromatin immunoprecipitation assays.	Ceramides	9-17	hepcidin antimicrobial peptide	Homo sapiens	79-83
26807955-11	2016	The mutation of STAT3 response element within 0.6 kb HAMP promoter region significantly inhibited the stimulatory effect of ceramide on HAMP promoter activity.	Ceramides	124-132	signal transducer and activator of transcription 3	Homo sapiens	16-21
26807955-11	2016	The mutation of STAT3 response element within 0.6 kb HAMP promoter region significantly inhibited the stimulatory effect of ceramide on HAMP promoter activity.	Ceramides	124-132	hepcidin antimicrobial peptide	Homo sapiens	53-57
26807955-11	2016	The mutation of STAT3 response element within 0.6 kb HAMP promoter region significantly inhibited the stimulatory effect of ceramide on HAMP promoter activity.	Ceramides	124-132	hepcidin antimicrobial peptide	Homo sapiens	136-140
26807955-12	2016	Similarly, the inhibition of STAT3 with a pan-JAK kinase inhibitor and STAT3 siRNA pool also diminished the induction of both HAMP promoter activity and mRNA expression by ceramide.	Ceramides	172-180	signal transducer and activator of transcription 3	Homo sapiens	29-34
26807955-12	2016	Similarly, the inhibition of STAT3 with a pan-JAK kinase inhibitor and STAT3 siRNA pool also diminished the induction of both HAMP promoter activity and mRNA expression by ceramide.	Ceramides	172-180	signal transducer and activator of transcription 3	Homo sapiens	71-76
26807955-12	2016	Similarly, the inhibition of STAT3 with a pan-JAK kinase inhibitor and STAT3 siRNA pool also diminished the induction of both HAMP promoter activity and mRNA expression by ceramide.	Ceramides	172-180	hepcidin antimicrobial peptide	Homo sapiens	126-130
26807955-13	2016	In conclusion, we have shown a direct role for ceramide in the activation of hepatic HAMP transcription via STAT3.	Ceramides	47-55	hepcidin antimicrobial peptide	Homo sapiens	85-89
26807955-13	2016	In conclusion, we have shown a direct role for ceramide in the activation of hepatic HAMP transcription via STAT3.	Ceramides	47-55	signal transducer and activator of transcription 3	Homo sapiens	108-113
26620563-2	2016	Herein, we report that SIRT3 regulates mitochondrial ceramide biosynthesis via deacetylation of ceramide synthase (CerS) 1, 2, and 6.	Ceramides	53-61	sirtuin 3	Mus musculus	23-28
26620563-2	2016	Herein, we report that SIRT3 regulates mitochondrial ceramide biosynthesis via deacetylation of ceramide synthase (CerS) 1, 2, and 6.	Ceramides	53-61	ceramide synthase 1	Mus musculus	96-132
26620563-5	2016	Investigation of the SIRT3 role in mitochondrial response to brain ischemia/reperfusion (IR) showed that SIRT3-mediated deacetylation of ceramide synthases increased enzyme activity and ceramide accumulation after IR.	Ceramides	137-145	sirtuin 3	Mus musculus	21-26
26620563-5	2016	Investigation of the SIRT3 role in mitochondrial response to brain ischemia/reperfusion (IR) showed that SIRT3-mediated deacetylation of ceramide synthases increased enzyme activity and ceramide accumulation after IR.	Ceramides	137-145	sirtuin 3	Mus musculus	105-110
26620563-8	2016	These data support the hypothesis that IR triggers SIRT3-dependent deacetylation of ceramide synthases and the elevation of ceramide, which could inhibit complex III, leading to increased reactive oxygen species generation and brain injury.	Ceramides	84-92	sirtuin 3	Mus musculus	51-56
26620563-9	2016	The results of these studies highlight a novel mechanism of SIRT3 involvement in modulating mitochondrial ceramide biosynthesis and suggest an important role of SIRT3 in mitochondrial dysfunction and brain injury after experimental stroke.	Ceramides	106-114	sirtuin 3	Mus musculus	60-65
26813308-0	2016	Stearoyl-CoA desaturase-1 mediated cell apoptosis in colorectal cancer by promoting ceramide synthesis.	Ceramides	84-92	stearoyl-Coenzyme A desaturase 1	Mus musculus	0-25
26813308-3	2016	Herein, we reported endo-lipid messenger ceramides played a critical role in tumor fate modulated by SCD1 inhibition.	Ceramides	41-50	stearoyl-Coenzyme A desaturase 1	Mus musculus	101-105
26813308-4	2016	In vitro study in colorectal cancer cells demonstrated inhibition of SCD1 activity promoted apoptosis attributed to mitochondria dysfunctions, upregulation of reaction oxygen species (ROS), alteration of mitochondrial transmembrane potential and translocation of mitochondrial protein cytochrome C. While these effects were mediated by intracellular ceramide signals through induction of ceramide biosynthesis, rather than exclusive SFA accumulation.	Ceramides	350-358	stearoyl-Coenzyme A desaturase 1	Mus musculus	69-73
26813308-4	2016	In vitro study in colorectal cancer cells demonstrated inhibition of SCD1 activity promoted apoptosis attributed to mitochondria dysfunctions, upregulation of reaction oxygen species (ROS), alteration of mitochondrial transmembrane potential and translocation of mitochondrial protein cytochrome C. While these effects were mediated by intracellular ceramide signals through induction of ceramide biosynthesis, rather than exclusive SFA accumulation.	Ceramides	388-396	stearoyl-Coenzyme A desaturase 1	Mus musculus	69-73
26813308-5	2016	In vivo study in xenograft colorectal cancer mice showed pharmacologic administration of SCD1 inhibitor A939 significantly delayed tumor growth, which was reversed by L-cycloserine, an inhibitor of ceramide biosynthesis.	Ceramides	198-206	stearoyl-Coenzyme A desaturase 1	Mus musculus	89-93
26553872-1	2016	Acid ceramidase (AC) is a lysosomal cysteine amidase that controls sphingolipid signaling by lowering the levels of ceramides and concomitantly increasing those of sphingosine and its bioactive metabolite, sphingosine 1-phosphate.	Ceramides	116-125	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-19
26813308-6	2016	These results depicted the cross-talk of SCD1-mediated lipid pathway and endo-ceramide biosynthesis pathway, indicating roles of ceramide signals in SCD1-mediated anti-tumor property.	Ceramides	78-86	stearoyl-Coenzyme A desaturase 1	Mus musculus	149-153
26813308-6	2016	These results depicted the cross-talk of SCD1-mediated lipid pathway and endo-ceramide biosynthesis pathway, indicating roles of ceramide signals in SCD1-mediated anti-tumor property.	Ceramides	129-137	stearoyl-Coenzyme A desaturase 1	Mus musculus	41-45
26553872-9	2016	AC inhibition increased cellular ceramide levels, decreased sphingosine 1-phosphate levels, and acted synergistically with several, albeit not all, antitumoral agents.	Ceramides	33-41	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-2
26813308-6	2016	These results depicted the cross-talk of SCD1-mediated lipid pathway and endo-ceramide biosynthesis pathway, indicating roles of ceramide signals in SCD1-mediated anti-tumor property.	Ceramides	129-137	stearoyl-Coenzyme A desaturase 1	Mus musculus	149-153
26788916-3	2016	We propose that ceramide (mainly C18) production might be responsible for Aldo-mediated damages in HUVECs.	Ceramides	16-24	Bardet-Biedl syndrome 9	Homo sapiens	33-36
26788916-5	2016	On the other hand, the glucosylceramide synthase (GCS) inhibitor PDMP or the ceramide (C6) potentiated Aldo-induced HUVEC apoptosis.	Ceramides	31-39	UDP-glucose ceramide glucosyltransferase	Homo sapiens	50-53
26788916-11	2016	MR and CerS-1 could be the two signaling molecule regulating C18 ceramide production by Aldo.	Ceramides	65-73	ceramide synthase 1	Homo sapiens	7-13
26788916-11	2016	MR and CerS-1 could be the two signaling molecule regulating C18 ceramide production by Aldo.	Ceramides	65-73	Bardet-Biedl syndrome 9	Homo sapiens	61-64
26477382-0	2016	Ceramide signaling targets the PP2A-like protein phosphatase Sit4p to impair vacuolar function, vesicular trafficking and autophagy in Isc1p deficient cells.	Ceramides	0-8	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	61-66
26757638-5	2016	Further examination revealed that PC(O-16:0/2:0) similarly promotes a global increase in ceramide accumulation in human neurons which was associated with mitochondrial-derived reactive oxygen species (ROS) and toxicity.	Ceramides	89-97	pyruvate carboxylase	Homo sapiens	34-36
26752183-1	2016	Ceramide is synthesized in yeast by two redundant acyl-CoA dependent synthases, Lag1 and Lac1.	Ceramides	0-8	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	80-84
26752183-1	2016	Ceramide is synthesized in yeast by two redundant acyl-CoA dependent synthases, Lag1 and Lac1.	Ceramides	0-8	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	89-93
26752183-2	2016	In lag1  lac1  cells, free fatty acids and sphingoid bases are elevated, and ceramides are produced through the redundant alkaline ceramidases Ypc1 and Ydc1, working backwards.	Ceramides	77-86	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	3-7
26752183-2	2016	In lag1  lac1  cells, free fatty acids and sphingoid bases are elevated, and ceramides are produced through the redundant alkaline ceramidases Ypc1 and Ydc1, working backwards.	Ceramides	77-86	sphingosine N-acyltransferase LAC1	Saccharomyces cerevisiae S288C	9-13
26752183-2	2016	In lag1  lac1  cells, free fatty acids and sphingoid bases are elevated, and ceramides are produced through the redundant alkaline ceramidases Ypc1 and Ydc1, working backwards.	Ceramides	77-86	phytoceramidase	Saccharomyces cerevisiae S288C	143-147
26752183-2	2016	In lag1  lac1  cells, free fatty acids and sphingoid bases are elevated, and ceramides are produced through the redundant alkaline ceramidases Ypc1 and Ydc1, working backwards.	Ceramides	77-86	alkaline dihydroceramidase	Saccharomyces cerevisiae S288C	152-156
26752183-5	2016	Indeed, the hextuple lag1  lac1  ypc1  ydc1  ypr114w  yjr116w  mutant still contains ceramides and complex sphingolipids.	Ceramides	85-94	sphingosine N-acyltransferase LAG1	Saccharomyces cerevisiae S288C	21-43
26727592-4	2016	The liposomal C8 (ceramide) potently inhibited HCC cell (HepG2, SMMC-7721 and Huh-7 lines) survival and proliferation, more efficiently than free C8 ceramide.	Ceramides	18-26	MIR7-3 host gene	Homo sapiens	78-83
26501163-6	2016	We demonstrated that: (i) the inflammatory marker IL-6 is upregulated in labored placentas; (ii) IL-6 content inversely correlates with labor duration; (iii) ceramide content and expression of serine palmitoyl transferase (SPT, rate limiting enzyme for de novo ceramide synthesis) are increased in labored placentas; (iv) the expression of SPT directly correlates with inflammation and inversely with labor duration.	Ceramides	158-166	interleukin 6	Homo sapiens	50-54
26501163-6	2016	We demonstrated that: (i) the inflammatory marker IL-6 is upregulated in labored placentas; (ii) IL-6 content inversely correlates with labor duration; (iii) ceramide content and expression of serine palmitoyl transferase (SPT, rate limiting enzyme for de novo ceramide synthesis) are increased in labored placentas; (iv) the expression of SPT directly correlates with inflammation and inversely with labor duration.	Ceramides	261-269	interleukin 6	Homo sapiens	50-54
26727221-0	2016	Glycogen Synthase Kinase-3beta and Caspase-2 Mediate Ceramide- and Etoposide-Induced Apoptosis by Regulating the Lysosomal-Mitochondrial Axis.	Ceramides	53-61	glycogen synthase kinase 3 beta	Homo sapiens	0-30
26727221-0	2016	Glycogen Synthase Kinase-3beta and Caspase-2 Mediate Ceramide- and Etoposide-Induced Apoptosis by Regulating the Lysosomal-Mitochondrial Axis.	Ceramides	53-61	caspase 2	Homo sapiens	35-44
26727221-8	2016	These results demonstrate the importance of GSK-3beta and caspase-2 in ceramide- and etoposide-induced apoptosis through mechanisms involving Mcl-1 destabilization and the lysosomal-mitochondrial axis.	Ceramides	71-79	glycogen synthase kinase 3 beta	Homo sapiens	44-53
26727221-8	2016	These results demonstrate the importance of GSK-3beta and caspase-2 in ceramide- and etoposide-induced apoptosis through mechanisms involving Mcl-1 destabilization and the lysosomal-mitochondrial axis.	Ceramides	71-79	caspase 2	Homo sapiens	58-67
26727221-8	2016	These results demonstrate the importance of GSK-3beta and caspase-2 in ceramide- and etoposide-induced apoptosis through mechanisms involving Mcl-1 destabilization and the lysosomal-mitochondrial axis.	Ceramides	71-79	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	142-147
27651258-6	2016	It became evident that crocin treatment prevents the N-SMase activation resulting in the decrease of ceramide release.	Ceramides	101-109	sphingomyelin phosphodiesterase 2, neutral	Mus musculus	53-60
26477382-0	2016	Ceramide signaling targets the PP2A-like protein phosphatase Sit4p to impair vacuolar function, vesicular trafficking and autophagy in Isc1p deficient cells.	Ceramides	0-8	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	135-140
26477382-8	2016	These results support a model in which Sit4p functions downstream of Isc1p in a TORC1-independent, ceramide-dependent signaling branch that impairs vacuolar function and vesicular trafficking, leading to autophagic defects in yeast.	Ceramides	99-107	type 2A-related serine/threonine-protein phosphatase SIT4	Saccharomyces cerevisiae S288C	39-44
26477382-8	2016	These results support a model in which Sit4p functions downstream of Isc1p in a TORC1-independent, ceramide-dependent signaling branch that impairs vacuolar function and vesicular trafficking, leading to autophagic defects in yeast.	Ceramides	99-107	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	69-74
27475812-11	2016	The release of ceramide is inhibited by concomitant treatment with the antidepressant amitriptyline, which also inhibits the activity of the acid sphingomyelinase.	Ceramides	15-23	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	141-162
26726837-10	2016	Moreover, our studies suggest a third role for ceramide in localizing the mating-specific Ste5 scaffold to the plasma membrane.	Ceramides	47-55	Ste5p	Saccharomyces cerevisiae S288C	90-94
26200920-1	2016	Caged ceramide analogues (C6-, C16-, C18-, C22- and C24-Cer) have been prepared by introducing a hydrophilic coumarin-based cage bearing a short polyethylene glycol (PEG) chain.	Ceramides	6-14	Bardet-Biedl syndrome 9	Homo sapiens	37-40
27512981-4	2016	Acid sphingomyelinase (ASM) is a rate limiting enzyme involved in the production of ceramide by breaking down sphingomyelin.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-21
27512981-4	2016	Acid sphingomyelinase (ASM) is a rate limiting enzyme involved in the production of ceramide by breaking down sphingomyelin.	Ceramides	84-92	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	23-26
26232662-1	2016	Ceramide 1-phosphate (C1P) is a bioactive sphingolipid metabolite that is produced in cells by the action of ceramide kinase (CerK) acting upon ceramide, and is also found in the circulation.	Ceramides	109-117	ceramide kinase	Homo sapiens	126-130
26913518-11	2016	Ku70 is an inhibitor of the proapoptotic Bax, while the product of Lass1, ceramide, operates in both caspase-dependent and -independent pathways of programmed cell death, providing a potential cellular mechanism for the effects of these genes on tissue damage and circulating creatine kinase.	Ceramides	74-82	ceramide synthase 1	Homo sapiens	67-72
26687835-1	2016	BACKGROUND: Acid ceramidase (AC), a key enzyme in ceramide metabolism, plays a role in cancer progression and resistance to therapy.	Ceramides	50-58	N-acylsphingosine amidohydrolase 1	Homo sapiens	12-27
26687835-1	2016	BACKGROUND: Acid ceramidase (AC), a key enzyme in ceramide metabolism, plays a role in cancer progression and resistance to therapy.	Ceramides	50-58	N-acylsphingosine amidohydrolase 1	Homo sapiens	1-3
26709664-9	2016	These findings indicate that the Nsm/ceramide system plays a role in protecting mice against systemic tuberculosis by preventing superoxide-mediated inhibition of autophagy.	Ceramides	37-45	sphingomyelin phosphodiesterase 2	Homo sapiens	33-36
27035458-8	2016	Fourteen molecular species of GM3 and 9 species of GD3, accounting for the variability of the ceramide moiety of the ganglioside molecule, were identified and characterized.	Ceramides	94-102	GRDX	Homo sapiens	51-54
26597010-0	2016	Acid Sphingomyelinase-Derived Ceramide Regulates ICAM-1 Function during T Cell Transmigration across Brain Endothelial Cells.	Ceramides	30-38	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
26597010-0	2016	Acid Sphingomyelinase-Derived Ceramide Regulates ICAM-1 Function during T Cell Transmigration across Brain Endothelial Cells.	Ceramides	30-38	intercellular adhesion molecule 1	Homo sapiens	49-55
26597010-3	2016	In particular, acid sphingomyelinase (ASM), a critical enzyme in the production of the bioactive lipid ceramide, is involved in the pathogenesis of MS; however, its role in the brain vasculature remains unknown.	Ceramides	103-111	sphingomyelin phosphodiesterase 1	Homo sapiens	15-36
26597010-3	2016	In particular, acid sphingomyelinase (ASM), a critical enzyme in the production of the bioactive lipid ceramide, is involved in the pathogenesis of MS; however, its role in the brain vasculature remains unknown.	Ceramides	103-111	sphingomyelin phosphodiesterase 1	Homo sapiens	38-41
26552671-3	2016	This reaction is catalyzed by a family of six ceramide synthases (CERS1-6), each of which preferentially catalyzes the synthesis of ceramides with different fatty acid chain lengths.	Ceramides	132-141	ceramide synthase 1	Homo sapiens	66-71
26552672-3	2016	In mammals, ceramide synthesis from a sphingoid base and a variable length fatty acid is catalyzed by a family of six ceramide synthases (CERS1-6), whose active sites exhibit differential specificity for different length fatty acids.	Ceramides	12-20	ceramide synthase 1	Homo sapiens	138-145
26650179-5	2016	CERS6 knockdown in NSCLC cells altered the ceramide profile, resulting in decreased cell migration and invasion in vitro, and decreased the frequency of RAC1-positive lamellipodia formation while CERS6 overexpression promoted it.	Ceramides	43-51	ceramide synthase 6	Mus musculus	0-5
26650179-8	2016	Together, these results indicate that CERS6-dependent ceramide synthesis and maintenance of ceramide in the cellular membrane are essential for lamellipodia formation and metastasis.	Ceramides	54-62	ceramide synthase 6	Mus musculus	38-43
26650179-8	2016	Together, these results indicate that CERS6-dependent ceramide synthesis and maintenance of ceramide in the cellular membrane are essential for lamellipodia formation and metastasis.	Ceramides	92-100	ceramide synthase 6	Mus musculus	38-43
27777958-1	2016	Ceramide and diacylglycerol (DAG) may be involved in the early phase of insulin resistance but data are inconsistent in man.	Ceramides	0-8	insulin	Homo sapiens	72-79
27965913-5	2016	This was supported by the observations that phosphorylated alpha-syn oligomers entered neurons, rapidly increased accumulated thioflavin S-positive inclusions, and induced a series of metabolic changes that included activation of polo-like kinase 2, inhibition of glucocerebrosidase and protein phosphatase 2A, and reduction of ceramide levels, all of which have been shown to promote alpha-syn phosphorylation and aggregation.	Ceramides	328-336	synuclein alpha	Homo sapiens	59-68
26337769-11	2016	CONCLUSION: This work showed that TMP-I and ceramide SLNs not only significantly enhanced systemic exposure of drug, but also increased antitumor efficacy compared to Taxotere( ) and control SLN.	Ceramides	44-52	sarcolipin	Homo sapiens	53-56
26293898-7	2016	Further studies showed that WYE-132 inhibited sphingosine kinase-1 (SphK1) activity, leading to pro-apoptotic ceramide production in ovarian cancer cells.	Ceramides	110-118	sphingosine kinase 1	Homo sapiens	46-66
27398923-0	2016	Melatonin Acts as an Antidepressant by Inhibition of the Acid Sphingomyelinase/Ceramide System.	Ceramides	79-87	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	57-78
27398923-8	2016	RESULTS: Melatonin treatment inhibited acid sphingomyelinase in vitro in cultured pheochromocytoma cells and in vivo in the hippocampus, which resulted in a reduction of ceramide in vitro and in vivo.	Ceramides	170-178	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	39-60
27398923-9	2016	The inhibition of the acid sphingomyelinase/ceramide system translated into increased neurogenesis in glucocorticosterone-stressed mice after treatment with melatonin, an effect that is abrogated in acid sphingomyelinase-deficient mice.	Ceramides	44-52	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	22-43
26708865-5	2016	The observations that CPT1C binds malonyl-CoA and long-chain acyl-CoA suggest that it is a sensor of lipid metabolism in neurons, where it appears to impact ceramide and triacylglycerol (TAG) metabolism.	Ceramides	157-165	carnitine palmitoyltransferase 1C	Homo sapiens	22-27
26293898-7	2016	Further studies showed that WYE-132 inhibited sphingosine kinase-1 (SphK1) activity, leading to pro-apoptotic ceramide production in ovarian cancer cells.	Ceramides	110-118	sphingosine kinase 1	Homo sapiens	68-73
30191692-2	2016	SGMS1 gene encodes an essential enzyme which is involved in the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide, wich determines its participation in the regulation of intracellular vesicular transport, cholesterol metabolism, cell proliferation, apoptosis and other significant processes.	Ceramides	139-147	sphingomyelin synthase 1	Homo sapiens	0-5
26682540-0	2015	Insulin treatment increases myocardial ceramide accumulation and disrupts cardiometabolic function.	Ceramides	39-47	insulin	Homo sapiens	0-7
26716446-0	2015	Correction: Mitochondrial Ceramide-Rich Macrodomains Functionalize Bax upon Irradiation.	Ceramides	26-34	BCL2 associated X, apoptosis regulator	Homo sapiens	67-70
26682540-3	2015	Considering type 2 diabetics treated with insulin are more likely to suffer from heart complications, we sought to determine the specific effect of insulin on ceramide-dependent cardiometabolic risk factors, including insulin resistance and altered heart mitochondrial physiology.	Ceramides	159-167	insulin	Homo sapiens	148-155
26682540-3	2015	Considering type 2 diabetics treated with insulin are more likely to suffer from heart complications, we sought to determine the specific effect of insulin on ceramide-dependent cardiometabolic risk factors, including insulin resistance and altered heart mitochondrial physiology.	Ceramides	159-167	insulin	Homo sapiens	148-155
26682540-4	2015	METHODS: H9c2 cardiomyocytes and adult mice were treated with insulin with or without myriocin to inhibit ceramide biosynthesis.	Ceramides	106-114	insulin	Homo sapiens	62-69
26682540-10	2015	Second, they identify ceramide as a possible mediator of insulin-related heart disorders.	Ceramides	22-30	insulin	Homo sapiens	57-64
26734030-8	2015	Strikingly, under normal conditions, ctr1-1 mutants contained less ceramides and hydroxyceramides, compared with wild type.	Ceramides	67-76	Protein kinase superfamily protein	Arabidopsis thaliana	37-43
26384245-4	2015	Analysis of the expression of SYT2-GFP fusion protein in the pollen tube indicates that SYT2 was localized to distinct, patchy compartments but could co-localize with the Golgi markers, BODIPY TR C5 ceramide and GmMan1-mCherry.	Ceramides	199-207	Calcium-dependent lipid-binding (CaLB domain) family protein	Arabidopsis thaliana	88-92
26490117-1	2015	Vesicle-associated membrane protein-associated protein (VAP) is an endoplasmic reticulum (ER)-resident integral membrane protein that controls a nonvesicular mode of ceramide and cholesterol transfer from the ER to the Golgi complex by interacting with ceramide transfer protein and oxysterol-binding protein (OSBP), respectively.	Ceramides	253-261	oxysterol binding protein	Homo sapiens	310-314
26515067-9	2015	Examination of the Scs7p structure, coupled with molecular dynamics simulations, allowed for the generation of a model of ceramide binding to Scs7p.	Ceramides	122-130	fatty acid alpha-hydroxylase	Saccharomyces cerevisiae S288C	19-24
26515067-9	2015	Examination of the Scs7p structure, coupled with molecular dynamics simulations, allowed for the generation of a model of ceramide binding to Scs7p.	Ceramides	122-130	fatty acid alpha-hydroxylase	Saccharomyces cerevisiae S288C	142-147
26490117-1	2015	Vesicle-associated membrane protein-associated protein (VAP) is an endoplasmic reticulum (ER)-resident integral membrane protein that controls a nonvesicular mode of ceramide and cholesterol transfer from the ER to the Golgi complex by interacting with ceramide transfer protein and oxysterol-binding protein (OSBP), respectively.	Ceramides	166-174	oxysterol binding protein	Homo sapiens	283-308
26490117-1	2015	Vesicle-associated membrane protein-associated protein (VAP) is an endoplasmic reticulum (ER)-resident integral membrane protein that controls a nonvesicular mode of ceramide and cholesterol transfer from the ER to the Golgi complex by interacting with ceramide transfer protein and oxysterol-binding protein (OSBP), respectively.	Ceramides	166-174	oxysterol binding protein	Homo sapiens	310-314
26490117-1	2015	Vesicle-associated membrane protein-associated protein (VAP) is an endoplasmic reticulum (ER)-resident integral membrane protein that controls a nonvesicular mode of ceramide and cholesterol transfer from the ER to the Golgi complex by interacting with ceramide transfer protein and oxysterol-binding protein (OSBP), respectively.	Ceramides	253-261	oxysterol binding protein	Homo sapiens	283-308
26560855-3	2015	AC inhibitors may be useful in the treatment of pathological conditions, such as cancer, in which ceramide levels are abnormally reduced.	Ceramides	98-106	N-acylsphingosine amidohydrolase 1	Mus musculus	0-2
26438821-5	2015	Here we report that mitochondrial targeted overexpression of catalase, which is established to mitigate oxidative stress, controls ceramide-induced Nlrp3 inflammasome activation but does not affect the ATP-mediated caspase-1 cleavage.	Ceramides	131-139	NLR family, pyrin domain containing 3	Mus musculus	148-153
26438821-4	2015	Given that the metabolic fate of fatty acids in macrophages is not entirely elucidated, we have hypothesized that de novo synthesis of ceramide, through the rate-limiting enzyme serine palmitoyltransferase long chain (Sptlc)-2, is required for saturated fatty acid-driven Nlrp3 inflammasome activation in macrophages.	Ceramides	135-143	serine palmitoyltransferase, long chain base subunit 2	Mus musculus	178-226
26013059-7	2015	As a result, a 24-hr exposure of human erythrocytes to naphthazarin (10 muM) significantly decreased erythrocyte forward scatter, significantly increased the percentage of annexin-V-binding cells, significantly increased ceramide abundance at the erythrocyte surface and significantly increased ROS.	Ceramides	221-229	latexin	Homo sapiens	72-75
26438821-4	2015	Given that the metabolic fate of fatty acids in macrophages is not entirely elucidated, we have hypothesized that de novo synthesis of ceramide, through the rate-limiting enzyme serine palmitoyltransferase long chain (Sptlc)-2, is required for saturated fatty acid-driven Nlrp3 inflammasome activation in macrophages.	Ceramides	135-143	NLR family, pyrin domain containing 3	Mus musculus	272-277
26639035-0	2015	Ceramides And Stress Signalling Intersect With Autophagic Defects In Neurodegenerative Drosophila blue cheese (bchs) Mutants.	Ceramides	0-9	blue cheese	Drosophila melanogaster	98-109
26639035-3	2015	Here, we demonstrate that blue cheese mutant brains exhibit an elevation in total ceramide levels; surprisingly, however, degeneration is ameliorated when the pool of available ceramides is further increased, and exacerbated when ceramide levels are decreased by altering sphingolipid catabolism or blocking de novo synthesis.	Ceramides	82-90	blue cheese	Drosophila melanogaster	26-37
26639035-3	2015	Here, we demonstrate that blue cheese mutant brains exhibit an elevation in total ceramide levels; surprisingly, however, degeneration is ameliorated when the pool of available ceramides is further increased, and exacerbated when ceramide levels are decreased by altering sphingolipid catabolism or blocking de novo synthesis.	Ceramides	177-186	blue cheese	Drosophila melanogaster	26-37
26639035-3	2015	Here, we demonstrate that blue cheese mutant brains exhibit an elevation in total ceramide levels; surprisingly, however, degeneration is ameliorated when the pool of available ceramides is further increased, and exacerbated when ceramide levels are decreased by altering sphingolipid catabolism or blocking de novo synthesis.	Ceramides	177-185	blue cheese	Drosophila melanogaster	26-37
26639035-4	2015	Exogenous ceramide is seen to accumulate in autophagosomes, which are fewer in number and show less efficient clearance in blue cheese mutant neurons.	Ceramides	10-18	blue cheese	Drosophila melanogaster	123-134
26398595-1	2015	Sphingomyelin (SM) is synthesized by SM synthase (SMS) from ceramide (Cer).	Ceramides	60-68	sphingomyelin synthase 2	Homo sapiens	37-48
26398595-1	2015	Sphingomyelin (SM) is synthesized by SM synthase (SMS) from ceramide (Cer).	Ceramides	60-68	sphingomyelin synthase 2	Homo sapiens	50-53
26398595-1	2015	Sphingomyelin (SM) is synthesized by SM synthase (SMS) from ceramide (Cer).	Ceramides	70-73	sphingomyelin synthase 2	Homo sapiens	37-48
26398595-1	2015	Sphingomyelin (SM) is synthesized by SM synthase (SMS) from ceramide (Cer).	Ceramides	70-73	sphingomyelin synthase 2	Homo sapiens	50-53
26432633-4	2015	We found that when Aur1 is gradually depleted by transcriptional downregulation, the accumulation of ceramides becomes a major hindrance to cell survival.	Ceramides	101-110	inositol phosphorylceramide synthase	Saccharomyces cerevisiae S288C	19-23
26404656-5	2015	Loss of MIPC synthesis or an increase in the hydroxylation level of the ceramide moiety of sphingolipids on overexpression of Scs7 and Sur2 sphingolipid hydroxylases enhanced the growth defect of V-ATPase-deleted cells at pH 7.2.	Ceramides	72-80	fatty acid alpha-hydroxylase	Saccharomyces cerevisiae S288C	126-130
26404656-5	2015	Loss of MIPC synthesis or an increase in the hydroxylation level of the ceramide moiety of sphingolipids on overexpression of Scs7 and Sur2 sphingolipid hydroxylases enhanced the growth defect of V-ATPase-deleted cells at pH 7.2.	Ceramides	72-80	sphingosine hydroxylase	Saccharomyces cerevisiae S288C	135-139
26446704-6	2015	Additionally, a ceramide signal was needed for PKR activation to be triggered by glucolipotoxicity and TNFalpha stimulation, and stabilization of P53 required endogenous ceramide accumulation.	Ceramides	16-24	eukaryotic translation initiation factor 2 alpha kinase 2	Homo sapiens	47-50
26739069-0	2015	[Ceramide participates in cell programmed death induced by Type II anti-CD20 mAb].	Ceramides	1-9	keratin 20	Homo sapiens	72-76
26446704-6	2015	Additionally, a ceramide signal was needed for PKR activation to be triggered by glucolipotoxicity and TNFalpha stimulation, and stabilization of P53 required endogenous ceramide accumulation.	Ceramides	16-24	tumor necrosis factor	Homo sapiens	103-111
26446704-6	2015	Additionally, a ceramide signal was needed for PKR activation to be triggered by glucolipotoxicity and TNFalpha stimulation, and stabilization of P53 required endogenous ceramide accumulation.	Ceramides	170-178	tumor protein p53	Homo sapiens	146-149
26446704-7	2015	Glucolipotoxicity and pro-inflammatory cytokines therefore promote the sumoylation-dependent stability of P53 via the ceramide/PKR/Ubc9 signalling pathway that is involved in pancreatic beta-cell proliferation inhibition in the development of type 2 diabetes.	Ceramides	118-126	tumor protein p53	Homo sapiens	106-109
26446842-0	2015	Regulation of Chlamydomonas flagella and ependymal cell motile cilia by ceramide-mediated translocation of GSK3.	Ceramides	72-80	glycogen synthase kinase 3 beta	Mus musculus	107-111
26446842-2	2015	We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively.	Ceramides	109-117	glycogen synthase kinase 3 beta	Mus musculus	49-75
26446842-2	2015	We characterize a novel activation mechanism for glycogen synthase kinase-3 (GSK3) by the sphingolipids phytoceramide and ceramide that is critical for ciliogenesis in Chlamydomonas and murine ependymal cells, respectively.	Ceramides	109-117	glycogen synthase kinase 3 beta	Mus musculus	77-81
26446842-3	2015	We show for the first time that Chlamydomonas expresses serine palmitoyl transferase (SPT), the first enzyme in (phyto)ceramide biosynthesis.	Ceramides	119-127	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	56-84
26446842-3	2015	We show for the first time that Chlamydomonas expresses serine palmitoyl transferase (SPT), the first enzyme in (phyto)ceramide biosynthesis.	Ceramides	119-127	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	86-89
26446842-7	2015	Ceramide depletion, by myriocin or neutral sphingomyelinase deficiency (fro/fro mouse), led to GSK3 dephosphorylation and defective flagella and cilia.	Ceramides	0-8	glycogen synthase kinase 3 beta	Mus musculus	95-99
26739069-12	2015	:  CONCLUSION: Type II but not Type I anti-CD20 mAbs can induce caspase independent PCD in CD20+ NHL cells through the elevation of cellular ceramide levels.	Ceramides	141-149	keratin 20	Homo sapiens	91-95
26455832-5	2015	An overactivation of sphingomyelinase (ASMase) was noted in the treated cells, indicating participation of an extrinsic apoptotic mechanism due to increased ceramide release.	Ceramides	157-165	sphingomyelin phosphodiesterase 1	Homo sapiens	39-45
28955819-0	2016	Chemoenzymatically prepared konjac ceramide inhibits NGF-induced neurite outgrowth by a semaphorin 3A-like action.	Ceramides	35-43	nerve growth factor	Rattus norvegicus	53-56
28955819-0	2016	Chemoenzymatically prepared konjac ceramide inhibits NGF-induced neurite outgrowth by a semaphorin 3A-like action.	Ceramides	35-43	semaphorin 3A	Rattus norvegicus	88-101
26297980-0	2015	CD36 initiated signaling mediates ceramide-induced TXNIP expression in pancreatic beta-cells.	Ceramides	34-42	thioredoxin interacting protein	Rattus norvegicus	51-56
26572827-7	2016	Inhibition of ASM elevates cellular sphingomyelin and reduces cellular ceramide levels.	Ceramides	71-79	sphingomyelin phosphodiesterase 1	Homo sapiens	14-17
26572827-8	2016	Concordantly, delivery of recombinant ASM or exogenous ceramide to fendiline-treated cells rapidly relocalizes K-Ras4B and PtdSer to the plasma membrane.	Ceramides	55-63	KRAS proto-oncogene, GTPase	Homo sapiens	111-118
26253821-0	2015	Regulation of ceramide generation during macrophage apoptosis by ASMase and de novo synthesis.	Ceramides	14-22	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	65-71
26253821-2	2015	We have previously shown that macrophages deprived of macrophage colony stimulating factor (M-CSF) produce ceramide that contributes to apoptosis of these cells, a pathway that is suppressed by exposure to oxidized LDL.	Ceramides	107-115	colony stimulating factor 1 (macrophage)	Mus musculus	54-90
26253821-2	2015	We have previously shown that macrophages deprived of macrophage colony stimulating factor (M-CSF) produce ceramide that contributes to apoptosis of these cells, a pathway that is suppressed by exposure to oxidized LDL.	Ceramides	107-115	colony stimulating factor 1 (macrophage)	Mus musculus	92-97
26297980-4	2015	Using rat islets and the INS-1 beta-cell line, we hypothesized that activation of the redox sensitive protein TXNIP is involved in ceramide-induced beta-cell dysfunction.	Ceramides	131-139	insulin 1	Rattus norvegicus	25-30
26253821-6	2015	Therefore, ceramide production in M-CSF-deprived macrophages arises from a combination of ASMase activity and de novo synthesis.	Ceramides	11-19	colony stimulating factor 1 (macrophage)	Mus musculus	34-39
26253821-6	2015	Therefore, ceramide production in M-CSF-deprived macrophages arises from a combination of ASMase activity and de novo synthesis.	Ceramides	11-19	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	90-96
26297980-4	2015	Using rat islets and the INS-1 beta-cell line, we hypothesized that activation of the redox sensitive protein TXNIP is involved in ceramide-induced beta-cell dysfunction.	Ceramides	131-139	thioredoxin interacting protein	Rattus norvegicus	110-115
26297980-6	2015	Ceramide treatment induced a time dependent increase in TXNIP gene expression accompanied by activation of nuclear factor (NF)-kappaB and reduced mitochondrial thioredoxin (TRX) activity.	Ceramides	0-8	thioredoxin interacting protein	Rattus norvegicus	56-61
26297980-7	2015	Pretreatment with sulfo-N-succinimidyl oleate (SSO), an irreversible inhibitor of the scavenger receptor CD36, blocked ceramide-induced up-regulation of TXNIP expression and activity of NF-kappaB.	Ceramides	119-127	thioredoxin interacting protein	Rattus norvegicus	153-158
26297980-8	2015	Blockade of NF-kappaB nuclear translocation by the peptide SN50 prevented ceramide-mediated TXNIP induction.	Ceramides	74-82	thioredoxin interacting protein	Rattus norvegicus	92-97
26297980-11	2015	These data suggest that CD36 dependent NF-kappaB-TXNIP signaling contributes to the ceramide-induced pathogenesis of pancreatic beta-cell dysfunction and failure.	Ceramides	84-92	thioredoxin interacting protein	Rattus norvegicus	49-54
26253611-1	2015	Prior studies have implicated accumulation of ceramide in blood vessels as a basis for vascular dysfunction in diet-induced obesity via a mechanism involving type 2 protein phosphatase (PP2A) dephosphorylation of endothelial nitric oxide synthase (eNOS).	Ceramides	46-54	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	186-190
26232616-0	2015	Ceramide generation during curcumin-induced apoptosis is controlled by crosstalk among Bcl-2, Bcl-xL, caspases and glutathione.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	87-92
26232616-0	2015	Ceramide generation during curcumin-induced apoptosis is controlled by crosstalk among Bcl-2, Bcl-xL, caspases and glutathione.	Ceramides	0-8	BCL2 like 1	Homo sapiens	94-100
26232616-0	2015	Ceramide generation during curcumin-induced apoptosis is controlled by crosstalk among Bcl-2, Bcl-xL, caspases and glutathione.	Ceramides	0-8	caspase 8	Homo sapiens	102-110
26232616-2	2015	We have demonstrated earlier that apoptosis of HL-60 human leukemia cells induced by curcumin is controlled by ceramide generated by neutral sphingomyelinase (nSMase) which contributes to sphingomyelin synthase (SMS) inhibition favoring accumulation of ceramide in cells.	Ceramides	111-119	sphingomyelin phosphodiesterase 2	Homo sapiens	133-157
26232616-2	2015	We have demonstrated earlier that apoptosis of HL-60 human leukemia cells induced by curcumin is controlled by ceramide generated by neutral sphingomyelinase (nSMase) which contributes to sphingomyelin synthase (SMS) inhibition favoring accumulation of ceramide in cells.	Ceramides	111-119	sphingomyelin phosphodiesterase 2	Homo sapiens	159-165
26232616-2	2015	We have demonstrated earlier that apoptosis of HL-60 human leukemia cells induced by curcumin is controlled by ceramide generated by neutral sphingomyelinase (nSMase) which contributes to sphingomyelin synthase (SMS) inhibition favoring accumulation of ceramide in cells.	Ceramides	253-261	sphingomyelin phosphodiesterase 2	Homo sapiens	133-157
26232616-2	2015	We have demonstrated earlier that apoptosis of HL-60 human leukemia cells induced by curcumin is controlled by ceramide generated by neutral sphingomyelinase (nSMase) which contributes to sphingomyelin synthase (SMS) inhibition favoring accumulation of ceramide in cells.	Ceramides	253-261	sphingomyelin phosphodiesterase 2	Homo sapiens	159-165
26253611-1	2015	Prior studies have implicated accumulation of ceramide in blood vessels as a basis for vascular dysfunction in diet-induced obesity via a mechanism involving type 2 protein phosphatase (PP2A) dephosphorylation of endothelial nitric oxide synthase (eNOS).	Ceramides	46-54	nitric oxide synthase 3, endothelial cell	Mus musculus	213-246
26253611-1	2015	Prior studies have implicated accumulation of ceramide in blood vessels as a basis for vascular dysfunction in diet-induced obesity via a mechanism involving type 2 protein phosphatase (PP2A) dephosphorylation of endothelial nitric oxide synthase (eNOS).	Ceramides	46-54	nitric oxide synthase 3, endothelial cell	Mus musculus	248-252
26253611-3	2015	We show in endothelial cells that ceramide associates with the inhibitor 2 of PP2A (I2PP2A) in the cytosol, which disrupts the association of I2PP2A with PP2A leading to its translocation to the plasma membrane.	Ceramides	34-42	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	78-82
26253611-3	2015	We show in endothelial cells that ceramide associates with the inhibitor 2 of PP2A (I2PP2A) in the cytosol, which disrupts the association of I2PP2A with PP2A leading to its translocation to the plasma membrane.	Ceramides	34-42	SET nuclear oncogene	Mus musculus	84-90
26253611-3	2015	We show in endothelial cells that ceramide associates with the inhibitor 2 of PP2A (I2PP2A) in the cytosol, which disrupts the association of I2PP2A with PP2A leading to its translocation to the plasma membrane.	Ceramides	34-42	SET nuclear oncogene	Mus musculus	142-148
26253611-3	2015	We show in endothelial cells that ceramide associates with the inhibitor 2 of PP2A (I2PP2A) in the cytosol, which disrupts the association of I2PP2A with PP2A leading to its translocation to the plasma membrane.	Ceramides	34-42	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	86-90
26253611-6	2015	These findings reveal a novel mechanism whereby ceramide initiates PP2A colocalization with eNOS and demonstrate that PP2A activation precipitates vascular dysfunction in diet-induced obesity.	Ceramides	48-56	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	67-71
26253611-6	2015	These findings reveal a novel mechanism whereby ceramide initiates PP2A colocalization with eNOS and demonstrate that PP2A activation precipitates vascular dysfunction in diet-induced obesity.	Ceramides	48-56	nitric oxide synthase 3, endothelial cell	Mus musculus	92-96
26194060-1	2015	Oxygen-requiring enzymes, such as Delta4-desaturase (dihydroceramide desaturase), sphingolipid Delta4-desaturase/C-4-hydroxylase, and fatty acid 2-hydroxylase are involved in ceramide synthesis.	Ceramides	60-68	delta 4-desaturase, sphingolipid 2	Homo sapiens	101-128
26386696-10	2015	We conclude: hepatic insulin resistance in human obesity is: advanced; BMI-correlated; and sequentially involves increased aPKC-activating ceramide; increased aPKC levels and activity; decreases in IRS-1 levels, Akt activity, and FoxO1 phosphorylation; and increases in expression/abundance of PGC-1alpha and gluconeogenic and lipogenic genes.	Ceramides	139-147	protein kinase C, zeta	Mus musculus	123-127
26342987-0	2015	Plasma ceramides are elevated in overweight Holstein dairy cows experiencing greater lipolysis and insulin resistance during the transition from late pregnancy to early lactation.	Ceramides	7-16	insulin	Bos taurus	99-106
26342987-3	2015	Mechanisms mediating the development of insulin resistance in overweight peripartal dairy cows may depend on ceramide metabolism.	Ceramides	109-117	insulin	Bos taurus	40-47
26342987-15	2015	Plasma ceramides (e.g., C24:0-ceramide) were positively correlated with plasma NEFA and inversely correlated with insulin sensitivity.	Ceramides	7-16	insulin	Bos taurus	114-121
26342987-15	2015	Plasma ceramides (e.g., C24:0-ceramide) were positively correlated with plasma NEFA and inversely correlated with insulin sensitivity.	Ceramides	7-15	insulin	Bos taurus	114-121
26350457-0	2015	Microsomal Triglyceride Transfer Protein Transfers and Determines Plasma Concentrations of Ceramide and Sphingomyelin but Not Glycosylceramide.	Ceramides	91-99	microsomal triglyceride transfer protein	Homo sapiens	0-40
26512957-1	2015	Neutral sphingomyelinase-2 (nSMase2) is a ceramide-generating enzyme that has been implicated in growth arrest, apoptosis and exosome secretion.	Ceramides	42-50	sphingomyelin phosphodiesterase 3	Homo sapiens	0-26
26512957-1	2015	Neutral sphingomyelinase-2 (nSMase2) is a ceramide-generating enzyme that has been implicated in growth arrest, apoptosis and exosome secretion.	Ceramides	42-50	sphingomyelin phosphodiesterase 3	Homo sapiens	28-35
26350457-6	2015	Abetalipoproteinemia patients with deleterious mutations in MTP and absence of B-lps had significantly lower plasma ceramide and sphingomyelin but normal hexosylceramide, lactosylceramide, and different sphingosines compared with unaffected controls.	Ceramides	116-124	microsomal triglyceride transfer protein	Homo sapiens	60-63
26318452-0	2015	Tumor Necrosis Factor-alpha (TNFalpha)-induced Ceramide Generation via Ceramide Synthases Regulates Loss of Focal Adhesion Kinase (FAK) and Programmed Cell Death.	Ceramides	47-55	tumor necrosis factor	Homo sapiens	0-27
26350457-7	2015	Furthermore, similar differential effects on plasma sphingolipids were seen in liver- and intestine-specific MTP knock-out (L,I-Mttp(-/-)) mice, suggesting that MTP specifically plays a role in the regulation of plasma ceramide and sphingomyelin.	Ceramides	219-227	microsomal triglyceride transfer protein	Mus musculus	161-164
26350457-10	2015	Therefore, MTP is involved in ceramide and sphingomyelin secretion but not in their synthesis.	Ceramides	30-38	microsomal triglyceride transfer protein	Homo sapiens	11-14
26350457-12	2015	Therefore, we propose that MTP might regulate plasma ceramide and sphingomyelin levels by transferring these lipids to B-lps in the liver and intestine and facilitating their secretion.	Ceramides	53-61	microsomal triglyceride transfer protein	Homo sapiens	27-30
26318452-0	2015	Tumor Necrosis Factor-alpha (TNFalpha)-induced Ceramide Generation via Ceramide Synthases Regulates Loss of Focal Adhesion Kinase (FAK) and Programmed Cell Death.	Ceramides	47-55	tumor necrosis factor	Homo sapiens	29-37
26318452-0	2015	Tumor Necrosis Factor-alpha (TNFalpha)-induced Ceramide Generation via Ceramide Synthases Regulates Loss of Focal Adhesion Kinase (FAK) and Programmed Cell Death.	Ceramides	47-55	protein tyrosine kinase 2	Homo sapiens	108-129
26318452-0	2015	Tumor Necrosis Factor-alpha (TNFalpha)-induced Ceramide Generation via Ceramide Synthases Regulates Loss of Focal Adhesion Kinase (FAK) and Programmed Cell Death.	Ceramides	47-55	protein tyrosine kinase 2	Homo sapiens	131-134
26318452-1	2015	Ceramide synthases (CerS1-CerS6), which catalyze the N-acylation of the (dihydro)sphingosine backbone to produce (dihydro)ceramide in both the de novo and the salvage or recycling pathway of ceramide generation, have been implicated in the control of programmed cell death.	Ceramides	122-130	ceramide synthase 1	Homo sapiens	20-25
26318452-1	2015	Ceramide synthases (CerS1-CerS6), which catalyze the N-acylation of the (dihydro)sphingosine backbone to produce (dihydro)ceramide in both the de novo and the salvage or recycling pathway of ceramide generation, have been implicated in the control of programmed cell death.	Ceramides	122-130	ceramide synthase 6	Homo sapiens	26-31
26318452-3	2015	In the current study, we have found that late accumulation of multiple ceramide and dihydroceramide species in MCF-7 cells treated with TNFalpha occurred by up-regulation of both pathways of ceramide synthesis.	Ceramides	71-79	tumor necrosis factor	Homo sapiens	136-144
26318452-3	2015	In the current study, we have found that late accumulation of multiple ceramide and dihydroceramide species in MCF-7 cells treated with TNFalpha occurred by up-regulation of both pathways of ceramide synthesis.	Ceramides	91-99	tumor necrosis factor	Homo sapiens	136-144
26318452-8	2015	In summary, our data suggest a novel role for CerS6/C16-ceramide as an upstream effector of the loss of focal adhesion protein and plasma membrane permeabilization, via the activation of caspase-7, and identify the salvage pathway as the critical mechanism of ceramide generation that controls cell death.	Ceramides	56-64	ceramide synthase 6	Homo sapiens	46-51
26318452-8	2015	In summary, our data suggest a novel role for CerS6/C16-ceramide as an upstream effector of the loss of focal adhesion protein and plasma membrane permeabilization, via the activation of caspase-7, and identify the salvage pathway as the critical mechanism of ceramide generation that controls cell death.	Ceramides	56-64	caspase 7	Homo sapiens	187-196
26318452-8	2015	In summary, our data suggest a novel role for CerS6/C16-ceramide as an upstream effector of the loss of focal adhesion protein and plasma membrane permeabilization, via the activation of caspase-7, and identify the salvage pathway as the critical mechanism of ceramide generation that controls cell death.	Ceramides	260-268	ceramide synthase 6	Homo sapiens	46-51
26446703-5	2015	Furthermore, in silico mutation studies and experimental validations led to a novel finding that concurrently targeting ceramide and PI3K/AKT pathway by chemical probes or marketed drugs achieves synergistic anti-cancer effects.	Ceramides	120-128	AKT serine/threonine kinase 1	Homo sapiens	138-141
26474409-4	2015	Acer3 knockout causes an age-dependent accumulation of various ceramides and C18:1-monohexosylceramide and abolishes the age-related increase in the levels of sphingosine and S1P in the brain; thereby resulting in Purkinje cell degeneration in the cerebellum and deficits in motor coordination and balance.	Ceramides	63-72	alkaline ceramidase 3	Mus musculus	0-5
26474409-5	2015	Our results indicate that Acer3 plays critically protective roles in controlling the homeostasis of various sphingolipids, including ceramides, sphingosine, S1P, and certain complex sphingolipids in the brain and protects Purkinje cells from premature degeneration.	Ceramides	133-142	alkaline ceramidase 3	Mus musculus	26-31
26269384-7	2015	Finally, deletion of YCA1 led to AA-PCD pathway through the activation of ceramides, whereas in the presence of the gene yeast cells underwent an AA-PCD pathway characterized by the shift of the main glycolytic pathway to the pentose phosphate pathway and a proteolytic mechanism to cope with oxidative stress.	Ceramides	74-83	Ca(2+)-dependent cysteine protease MCA1	Saccharomyces cerevisiae S288C	21-25
26269384-8	2015	SIGNIFICANCE: The yeast metacaspase regulates both proteolytic activities through the ubiquitin-proteasome system and ceramide metabolism as revealed by proteome and metabolome profiling of YCA1-knock-out cells during acetic-acid induced programmed cell death.	Ceramides	118-126	Ca(2+)-dependent cysteine protease MCA1	Saccharomyces cerevisiae S288C	190-194
26528430-3	2015	CLN3 protein (CLN3p), deficient in neurodegenerative CLN3 disease is anti-apoptotic, and defects in the CLN3 gene cause accelerated apoptosis of neurons in CLN3 disease and up-regulation of ceramide.	Ceramides	190-198	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
26528430-3	2015	CLN3 protein (CLN3p), deficient in neurodegenerative CLN3 disease is anti-apoptotic, and defects in the CLN3 gene cause accelerated apoptosis of neurons in CLN3 disease and up-regulation of ceramide.	Ceramides	190-198	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	14-19
26528430-3	2015	CLN3 protein (CLN3p), deficient in neurodegenerative CLN3 disease is anti-apoptotic, and defects in the CLN3 gene cause accelerated apoptosis of neurons in CLN3 disease and up-regulation of ceramide.	Ceramides	190-198	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	14-18
26528430-11	2015	CLN3 may be a novel molecular target for cancer drug discovery with the goal of modulation of ceramide pathways.	Ceramides	94-102	CLN3 lysosomal/endosomal transmembrane protein, battenin	Homo sapiens	0-4
25833198-4	2015	Exogenous C6 ceramide also induced secretion of BCRP-associated exosomes, while siRNA-mediated knockdown or GW4869-mediated inhibition of neutral sphingomyelinase 2 (nSMase2), an enzyme generating ceramide, restored cellular BCRP.	Ceramides	13-21	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	48-52
26215742-7	2015	We engineered Bcl-xL point mutations that specifically affect the interaction between ceramide and Bcl-xL to probe the mechanism of ceramide channel regulation and the role of ceramide channels in apoptosis.	Ceramides	86-94	BCL2 like 1	Homo sapiens	14-20
26215742-8	2015	Using these mutants and fluorescently-labeled ceramide, we identified the hydrophobic groove on Bcl-xL as the critical ceramide binding site and regulator of ceramide channel formation.	Ceramides	46-54	BCL2 like 1	Homo sapiens	96-102
26215742-8	2015	Using these mutants and fluorescently-labeled ceramide, we identified the hydrophobic groove on Bcl-xL as the critical ceramide binding site and regulator of ceramide channel formation.	Ceramides	119-127	BCL2 like 1	Homo sapiens	96-102
26215742-8	2015	Using these mutants and fluorescently-labeled ceramide, we identified the hydrophobic groove on Bcl-xL as the critical ceramide binding site and regulator of ceramide channel formation.	Ceramides	119-127	BCL2 like 1	Homo sapiens	96-102
26215742-9	2015	Bcl-xL mutants with weakened interaction with ceramide also have reduced ability to interfere with ceramide channel formation.	Ceramides	46-54	BCL2 like 1	Homo sapiens	0-6
26215742-9	2015	Bcl-xL mutants with weakened interaction with ceramide also have reduced ability to interfere with ceramide channel formation.	Ceramides	99-107	BCL2 like 1	Homo sapiens	0-6
26201515-5	2015	Furthermore, the phosphatase-resistant Akt was refractory to ceramide-dependent dephosphorylation and amplified insulin-dependent Thr(308) phosphorylation in a regulated fashion.	Ceramides	61-69	AKT serine/threonine kinase 1	Homo sapiens	39-42
26486270-12	2015	Overall, Sphingomyeline-Ceramide-Sphingosine-1-phosphate (Spm-Cer-S1P) signalling axis plays an important role in MMP-2 mediated U46619-induced proliferation of PASMCs.	Ceramides	24-32	matrix metallopeptidase 2	Bos taurus	114-119
25833198-4	2015	Exogenous C6 ceramide also induced secretion of BCRP-associated exosomes, while siRNA-mediated knockdown or GW4869-mediated inhibition of neutral sphingomyelinase 2 (nSMase2), an enzyme generating ceramide, restored cellular BCRP.	Ceramides	197-205	sphingomyelin phosphodiesterase 3	Homo sapiens	138-164
25833198-4	2015	Exogenous C6 ceramide also induced secretion of BCRP-associated exosomes, while siRNA-mediated knockdown or GW4869-mediated inhibition of neutral sphingomyelinase 2 (nSMase2), an enzyme generating ceramide, restored cellular BCRP.	Ceramides	197-205	sphingomyelin phosphodiesterase 3	Homo sapiens	166-173
25833198-8	2015	Taken together, our results suggest a novel mechanism by which ceramide induces BCRP secretion and reduces MDR, which may be useful as adjuvant drug treatment for sensitizing breast cancer cells and cancer stem cells to chemotherapy.	Ceramides	63-71	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	80-84
25888580-1	2015	Acid ceramidase (ACDase) metabolizes ceramide to sphingosine, leading to sphingosine 1-phosphate production.	Ceramides	37-45	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
25842287-0	2015	Aberrant ORM (yeast)-like protein isoform 3 (ORMDL3) expression dysregulates ceramide homeostasis in cells and ceramide exacerbates allergic asthma in mice.	Ceramides	77-85	ORM1-like 3 (S. cerevisiae)	Mus musculus	45-51
25842287-0	2015	Aberrant ORM (yeast)-like protein isoform 3 (ORMDL3) expression dysregulates ceramide homeostasis in cells and ceramide exacerbates allergic asthma in mice.	Ceramides	111-119	ORM1-like 3 (S. cerevisiae)	Mus musculus	45-51
25842287-4	2015	OBJECTIVES: We sought to decipher the molecular mechanism for the pathologic functions of ORMDL3 in asthma and the relationship to its evolutionarily conserved role in regulation of ceramide homeostasis.	Ceramides	182-190	ORM1-like 3 (S. cerevisiae)	Mus musculus	90-96
25959529-1	2015	BACKGROUND: Metabolic syndrome (MetS) appears closely linked with ceramide accumulation, inducing insulin resistance and toxicity to multiple cell types.	Ceramides	66-74	insulin	Homo sapiens	98-105
25959529-2	2015	Animal studies demonstrate that thiazolidinediones (TZDs) reduce ceramide concentrations in plasma and skeletal muscle and support lowering of ceramide levels as a potential mediator of TZDs" mechanism of action in reducing insulin resistance; however, studies in humans have yet to be reported.	Ceramides	143-151	insulin	Homo sapiens	224-231
25842287-5	2015	METHODS: We determined the relationship between expression of ORMDL3 and ceramide in epithelial and inflammatory cells and in asthma pathogenesis in mice.	Ceramides	73-81	ORM1-like 3 (S. cerevisiae)	Mus musculus	62-68
25888580-1	2015	Acid ceramidase (ACDase) metabolizes ceramide to sphingosine, leading to sphingosine 1-phosphate production.	Ceramides	37-45	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-23
26286360-2	2015	Previously, we reported on the use of the RBM14 fluorogenic ceramide analogs to determine acidic ceramidase activity.	Ceramides	60-68	RNA binding motif protein 14	Homo sapiens	42-47
25842287-6	2015	RESULTS: Although small increases in ORMDL3 expression decrease ceramide levels, remarkably, higher expression in lung epithelial cells and macrophages in vitro and in vivo increased ceramide production, which promoted chronic inflammation, airway hyperresponsiveness, and mucus production during house dust mite-induced allergic asthma.	Ceramides	64-72	ORM1-like 3 (S. cerevisiae)	Mus musculus	37-43
25842287-6	2015	RESULTS: Although small increases in ORMDL3 expression decrease ceramide levels, remarkably, higher expression in lung epithelial cells and macrophages in vitro and in vivo increased ceramide production, which promoted chronic inflammation, airway hyperresponsiveness, and mucus production during house dust mite-induced allergic asthma.	Ceramides	183-191	ORM1-like 3 (S. cerevisiae)	Mus musculus	37-43
25842287-8	2015	CONCLUSIONS: Our findings demonstrate that overexpression of ORMDL3 regulates ceramide homeostasis in cells in a complex manner and suggest that local FTY720 administration might be a useful therapeutic intervention for the control of allergic asthma.	Ceramides	78-86	ORM1-like 3 (S. cerevisiae)	Mus musculus	61-67
26778897-6	2015	Transcriptomic analysis of mouse kidney tissue revealed expression changes indicative of decreased ceramide synthesis (Degs2, Smpd2) and increased conversion to sphingosine (Acer2) and downstream sphingosine-1-phosphate signaling.	Ceramides	99-107	delta(4)-desaturase, sphingolipid 2	Mus musculus	119-124
26220867-1	2015	Fenretinide, N-(4-hydroxyphenyl)retinamide, (4-HPR), a synthetic retinoid, owes its cancer-toxic effects in part to the generation of ceramide, a potent tumor-suppressing sphingolipid.	Ceramides	134-142	haptoglobin-related protein	Homo sapiens	47-50
26220867-3	2015	Cancer cells, however, via various metabolic routes, inactivate ceramide, and this can limit 4-HPR efficacy.	Ceramides	64-72	haptoglobin-related protein	Homo sapiens	95-98
26220867-4	2015	As relatively little is known regarding 4-HPR-induced ceramide management in acute myelogeneous leukemia (AML), we undertook the present study to evaluate the impact of 4-HPR on ceramide production, metabolism, and cytotoxicity.	Ceramides	54-62	haptoglobin-related protein	Homo sapiens	42-45
26220867-5	2015	In KG-1, HL-60, and HL-60/VCR (multidrug resistant) human leukemia cells, 4-HPR induced 15-, 2-, and 20-fold increases in ceramide (measured using [3H]palmitic acid), respectively.	Ceramides	122-130	haptoglobin-related protein	Homo sapiens	76-79
26220867-6	2015	By use of specific inhibitors we show that ceramide was produced by sphingomyelinase and de novo pathways in response to 4-HPR exposure.	Ceramides	43-51	haptoglobin-related protein	Homo sapiens	123-126
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.	Ceramides	93-101	haptoglobin-related protein	Homo sapiens	71-74
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.	Ceramides	157-165	haptoglobin-related protein	Homo sapiens	71-74
26220867-12	2015	As such, knowledge of these metabolic pathways can provide guidance for enhancing ceramide-driven effects of 4-HPR in treatment of leukemia.	Ceramides	82-90	haptoglobin-related protein	Homo sapiens	111-114
26041663-13	2015	Studies show that in the CNS, CPT1c affects ceramide levels, endocannabionoids, and oxidative processes and may play an important role in various brain functions such as learning.	Ceramides	44-52	carnitine palmitoyltransferase 1C	Homo sapiens	30-35
26280656-0	2015	LAPTM4B facilitates late endosomal ceramide export to control cell death pathways.	Ceramides	35-43	lysosomal protein transmembrane 4 beta	Homo sapiens	0-7
26280656-2	2015	Here we use novel ceramide probes to provide evidence that LAPTM4B interacts with ceramide and facilitates its removal from late endosomal organelles (LEs).	Ceramides	18-26	lysosomal protein transmembrane 4 beta	Homo sapiens	59-66
26280656-2	2015	Here we use novel ceramide probes to provide evidence that LAPTM4B interacts with ceramide and facilitates its removal from late endosomal organelles (LEs).	Ceramides	82-90	lysosomal protein transmembrane 4 beta	Homo sapiens	59-66
26280656-5	2015	However, these cells resist ceramide-driven caspase-3 activation and apoptosis induced by chemotherapeutic agents or gene silencing.	Ceramides	28-36	caspase 3	Homo sapiens	44-53
26280656-6	2015	Conversely, LAPTM4B overexpression reduces LE ceramide and stabilizes lysosomes but sensitizes to drug-induced caspase-3 activation.	Ceramides	46-54	lysosomal protein transmembrane 4 beta	Homo sapiens	12-19
26280656-7	2015	Together, these data uncover a cellular ceramide export route from LEs and identify LAPTM4B as its regulator.	Ceramides	40-48	lysosomal protein transmembrane 4 beta	Homo sapiens	84-91
26280656-8	2015	By compartmentalizing ceramide, LAPTM4B controls key sphingolipid-mediated cell death mechanisms and emerges as a candidate for sphingolipid-targeting cancer therapies.	Ceramides	22-30	lysosomal protein transmembrane 4 beta	Homo sapiens	32-39
26447086-2	2015	Acid sphingomyelinase (ASM) is a lysosomal glycoprotein that hydrolyzes sphingomyelin to ceramide, a lipid, that functions as a second messenger in the regulation of cell functions.	Ceramides	89-97	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
26264277-1	2015	Activation of acid sphingomyelinase (ASM) leads to ceramide accumulation and induces apoptotic cell death in cancer cells.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	14-35
26264277-1	2015	Activation of acid sphingomyelinase (ASM) leads to ceramide accumulation and induces apoptotic cell death in cancer cells.	Ceramides	51-59	sphingomyelin phosphodiesterase 1	Homo sapiens	37-40
26264277-3	2015	Sphingosine kinase 1 (SphK1), a negative regulator of ceramide accumulation with antiapoptotic effects, was markedly elevated in multiple myeloma cells.	Ceramides	54-62	sphingosine kinase 1	Homo sapiens	0-20
26264277-3	2015	Sphingosine kinase 1 (SphK1), a negative regulator of ceramide accumulation with antiapoptotic effects, was markedly elevated in multiple myeloma cells.	Ceramides	54-62	sphingosine kinase 1	Homo sapiens	22-27
26296152-6	2015	Lipids commonly associated with hepatic lipotoxicity, diacylglycerol, and ceramides, were also increased in Ad-PLIN5 liver.	Ceramides	74-83	perilipin 5	Mus musculus	111-116
26447086-2	2015	Acid sphingomyelinase (ASM) is a lysosomal glycoprotein that hydrolyzes sphingomyelin to ceramide, a lipid, that functions as a second messenger in the regulation of cell functions.	Ceramides	89-97	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
26412155-2	2015	Of the myriad lipids that accrue under these conditions, sphingolipids such as ceramide or its metabolites are amongst the most deleterious because they disrupt insulin sensitivity, pancreatic beta cell function, vascular reactivity, and mitochondrial metabolism.	Ceramides	79-87	insulin	Homo sapiens	161-168
26412155-3	2015	Remarkably, inhibiting ceramide biosynthesis or catalyzing ceramide degradation in rodents ameliorates many metabolic disorders including diabetes, cardiomyopathy, insulin resistance, atherosclerosis, and steatohepatitis.	Ceramides	23-31	insulin	Homo sapiens	164-171
26022181-5	2015	Moreover, we show that the palmitate-driven loss in NEU3 protein is mediated, at least in part, by intracellular ceramide synthesis but does not involve the proteasomal pathway.	Ceramides	113-121	neuraminidase 3	Rattus norvegicus	52-56
26379195-0	2015	SGK-1 protects kidney cells against apoptosis induced by ceramide and TNF-alpha.	Ceramides	57-65	serum/glucocorticoid regulated kinase 1	Homo sapiens	0-5
26379195-4	2015	In the present study, since ceramide induces apoptosis by multiple mechanisms in diabetes and its complication such as nephropathy, we aimed to investigate whether SGK-1 may protect even against apoptosis induced by ceramide in kidney cells.	Ceramides	216-224	serum/glucocorticoid regulated kinase 1	Homo sapiens	164-169
26379195-9	2015	SGK-1 and AKT-1 two highly homologous kinases differently reacted to ceramide treatment, since SGK-1 increases in response to apoptotic stimulus while AKT-1 decreases.	Ceramides	69-77	serum/glucocorticoid regulated kinase 1	Homo sapiens	0-5
26379195-9	2015	SGK-1 and AKT-1 two highly homologous kinases differently reacted to ceramide treatment, since SGK-1 increases in response to apoptotic stimulus while AKT-1 decreases.	Ceramides	69-77	AKT serine/threonine kinase 1	Homo sapiens	10-15
26379195-9	2015	SGK-1 and AKT-1 two highly homologous kinases differently reacted to ceramide treatment, since SGK-1 increases in response to apoptotic stimulus while AKT-1 decreases.	Ceramides	69-77	serum/glucocorticoid regulated kinase 1	Homo sapiens	95-100
26379195-9	2015	SGK-1 and AKT-1 two highly homologous kinases differently reacted to ceramide treatment, since SGK-1 increases in response to apoptotic stimulus while AKT-1 decreases.	Ceramides	69-77	AKT serine/threonine kinase 1	Homo sapiens	151-156
26379195-14	2015	In conclusion, we demonstrated that in kidney cells, overexpression of SGK-1 is protective against ceramide-induced apoptosis and the role of SGK-1 can be potentially explored as a therapeutic target in conditions like diabetes, where ceramide levels are increased.	Ceramides	99-107	serum/glucocorticoid regulated kinase 1	Homo sapiens	71-76
26379195-14	2015	In conclusion, we demonstrated that in kidney cells, overexpression of SGK-1 is protective against ceramide-induced apoptosis and the role of SGK-1 can be potentially explored as a therapeutic target in conditions like diabetes, where ceramide levels are increased.	Ceramides	235-243	serum/glucocorticoid regulated kinase 1	Homo sapiens	71-76
26379195-14	2015	In conclusion, we demonstrated that in kidney cells, overexpression of SGK-1 is protective against ceramide-induced apoptosis and the role of SGK-1 can be potentially explored as a therapeutic target in conditions like diabetes, where ceramide levels are increased.	Ceramides	235-243	serum/glucocorticoid regulated kinase 1	Homo sapiens	142-147
26090720-6	2015	SK1-I modulated the balance of ceramide-sphinogosine-S1P and induced CCA apoptosis.	Ceramides	31-39	sphingosine kinase 1	Homo sapiens	0-3
25155190-9	2015	It also interact with CerS1 to enrich liver in d18:1/C18:0 ceramides.	Ceramides	59-68	ceramide synthase 1	Homo sapiens	22-27
26022371-9	2015	Mitochondrial fusion and fission proteins were notably dysregulated by Abeta42 (Mfn1) or Abeta42 plus ceramide (OPA1, Drp1).	Ceramides	102-110	OPA1 mitochondrial dynamin like GTPase	Homo sapiens	112-116
26022371-9	2015	Mitochondrial fusion and fission proteins were notably dysregulated by Abeta42 (Mfn1) or Abeta42 plus ceramide (OPA1, Drp1).	Ceramides	102-110	collapsin response mediator protein 1	Homo sapiens	118-122
26022371-12	2015	Taken together, our data demonstrate that Abeta42 expression and ceramide-induced insulin resistance synergistically interact to exacerbate mitochondrial damage and that therapeutic efforts to reduce insulin resistance could lessen failures of energy production and mitochondrial dynamics.	Ceramides	65-73	insulin	Homo sapiens	82-89
26079297-0	2015	Ceramide signalling impinges on Sit4p and Hog1p to promote mitochondrial fission and mitophagy in Isc1p-deficient cells.	Ceramides	0-8	sphingomyelin phosphodiesterase 2	Homo sapiens	98-103
26079297-3	2015	Yeast cells lacking Isc1p, an orthologue of mammalian neutral sphingomyelinase type 2, exhibit mitochondrial dysfunction and shortened lifespan associated with the accumulation of specific ceramide species and activation of the PP2A-like protein phosphatase Sit4p and of the Hog1p kinase.	Ceramides	189-197	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	20-25
26079297-7	2015	Overall, our work demonstrates that Isc1p-mediated ceramide signalling regulates mitophagy and mitochondrial dynamics in yeast with impact on mitochondrial function and lifespan.	Ceramides	51-59	inositol phosphosphingolipid phospholipase	Saccharomyces cerevisiae S288C	36-41
26405804-10	2015	qRT-PCR analysis showed a reduction in the expression of sphingolipid delta(4)-desaturase (Degs2), an enzyme involved in de novo ceramide synthesis.	Ceramides	129-137	delta(4)-desaturase, sphingolipid 2	Rattus norvegicus	91-96
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.	Ceramides	8-16	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.	Ceramides	8-16	glucosylceramidase beta 2	Homo sapiens	190-194
26022371-0	2015	Synergistic effects of beta-amyloid and ceramide-induced insulin resistance on mitochondrial metabolism in neuronal cells.	Ceramides	40-48	insulin	Homo sapiens	57-64
26022371-3	2015	We investigated the additive and synergistic effects of intracellular Abeta42 and ceramide-induced insulin resistance on mitochondrial metabolism in SH-SY5Y and Neuro-2a cells.	Ceramides	82-90	insulin	Homo sapiens	99-106
26022371-4	2015	In our model, mitochondria take-up Abeta42 expressed through viral-mediated transfection and exposure of the same cells to ceramide produces resistance to insulin signaling.	Ceramides	123-131	insulin	Homo sapiens	155-162
26115843-4	2015	We found that both ceramide analogs D- and L-PDMP (1-phenyl 2-decanoylamino-3-morpholino-1-propanol), which have opposite effects on ganglioside synthesis, selectively inhibited GSK3beta via Ser9 phosphorylation independently of the upstream insulin/Akt pathway.	Ceramides	19-27	glycogen synthase kinase 3 beta	Homo sapiens	178-186
26115843-4	2015	We found that both ceramide analogs D- and L-PDMP (1-phenyl 2-decanoylamino-3-morpholino-1-propanol), which have opposite effects on ganglioside synthesis, selectively inhibited GSK3beta via Ser9 phosphorylation independently of the upstream insulin/Akt pathway.	Ceramides	19-27	AKT serine/threonine kinase 1	Homo sapiens	250-253
26115843-4	2015	We found that both ceramide analogs D- and L-PDMP (1-phenyl 2-decanoylamino-3-morpholino-1-propanol), which have opposite effects on ganglioside synthesis, selectively inhibited GSK3beta via Ser9 phosphorylation independently of the upstream insulin/Akt pathway.	Ceramides	19-27	insulin	Homo sapiens	242-249
26045466-6	2015	(2) Blocking the pathways to germ cell-specific ceramides (CerS3-KO) and further to glycosphingolipids (glucosylceramide synthase-KO) in mice highlights the need for special SLs for spermatid ICB stability.	Ceramides	48-57	ceramide synthase 3	Mus musculus	59-64
26116623-0	2015	C6 ceramide dramatically increases vincristine sensitivity both in vivo and in vitro, involving AMP-activated protein kinase-p53 signaling.	Ceramides	3-11	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	96-124
25975536-7	2015	Melatonin enhanced ceramide levels through both de novo synthesis and acid sphingomyelinase (ASMase) stimulation.	Ceramides	19-27	sphingomyelin phosphodiesterase 1	Homo sapiens	93-99
26116623-0	2015	C6 ceramide dramatically increases vincristine sensitivity both in vivo and in vitro, involving AMP-activated protein kinase-p53 signaling.	Ceramides	3-11	tumor protein p53	Homo sapiens	125-128
26099582-3	2015	We previously developed a recombinant bacterium that expresses a mimic of the Stx receptor globotriaosyl ceramide (Gb3) on its surface through modification of the lipopolysaccharide (A. W. Paton, R. Morona, and J. C. Paton, Nat Med 6:265-270, 2000, http://dx.doi.org/10.1038/73111).	Ceramides	105-113	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	115-118
25975536-10	2015	Findings suggest a crosstalk between SPT-mediated ceramide generation and autophagy in protecting against melatonin, while specific ASMase-induced ceramide production participates in melatonin-mediated cell death.	Ceramides	50-58	alanine--glyoxylate and serine--pyruvate aminotransferase	Homo sapiens	37-40
26189109-2	2015	A marked increase in d18:1/16:0 ceramide was detected in U937 cells treated with TNF in the presence of Z-VAD-fmk (VAD).	Ceramides	32-40	tumor necrosis factor	Homo sapiens	81-84
25975536-10	2015	Findings suggest a crosstalk between SPT-mediated ceramide generation and autophagy in protecting against melatonin, while specific ASMase-induced ceramide production participates in melatonin-mediated cell death.	Ceramides	147-155	sphingomyelin phosphodiesterase 1	Homo sapiens	132-138
26617822-1	2015	Galactocerebrosidase (GALC) is a lysosomal enzyme responsible for glycosphingolipids degradation byproducts of which are important for synthesis of apoptosis mediator ceramide.	Ceramides	167-175	galactosylceramidase	Homo sapiens	0-20
26617822-1	2015	Galactocerebrosidase (GALC) is a lysosomal enzyme responsible for glycosphingolipids degradation byproducts of which are important for synthesis of apoptosis mediator ceramide.	Ceramides	167-175	galactosylceramidase	Homo sapiens	22-26
26189109-7	2015	In contrast with the large increase in ceramide levels in TNF/VAD-treated parental cells, they were only slightly increased in UNR cells.	Ceramides	39-47	tumor necrosis factor	Homo sapiens	58-61
26189109-9	2015	These results implicate that the ROS-induced large increase in ceramide levels may play a role in plasma membrane permeabilization in TNF-induced necroptosis.	Ceramides	63-71	tumor necrosis factor	Homo sapiens	134-137
25985440-0	2015	Ceramide formation mediated by acid sphingomyelinase facilitates endosomal escape of caliciviruses.	Ceramides	0-8	sphingomyelin phosphodiesterase 1	Homo sapiens	31-52
26059452-5	2015	Upon activation of CD39 and CD161, the molecular interactions boost ASM bio-activity, which generates cellular ceramide to further mediate downstream signals inclusive of STAT3 and mTOR.	Ceramides	111-119	ectonucleoside triphosphate diphosphohydrolase 1	Homo sapiens	19-23
26059452-5	2015	Upon activation of CD39 and CD161, the molecular interactions boost ASM bio-activity, which generates cellular ceramide to further mediate downstream signals inclusive of STAT3 and mTOR.	Ceramides	111-119	killer cell lectin like receptor B1	Homo sapiens	28-33
26059452-5	2015	Upon activation of CD39 and CD161, the molecular interactions boost ASM bio-activity, which generates cellular ceramide to further mediate downstream signals inclusive of STAT3 and mTOR.	Ceramides	111-119	sphingomyelin phosphodiesterase 1	Homo sapiens	68-71
26059452-5	2015	Upon activation of CD39 and CD161, the molecular interactions boost ASM bio-activity, which generates cellular ceramide to further mediate downstream signals inclusive of STAT3 and mTOR.	Ceramides	111-119	signal transducer and activator of transcription 3	Homo sapiens	171-176
26059452-5	2015	Upon activation of CD39 and CD161, the molecular interactions boost ASM bio-activity, which generates cellular ceramide to further mediate downstream signals inclusive of STAT3 and mTOR.	Ceramides	111-119	mechanistic target of rapamycin kinase	Homo sapiens	181-185
25985440-3	2015	This endosomal escape by cold treatment or bile acids is associated with ceramide formation by acid sphingomyelinase (ASM).	Ceramides	73-81	sphingomyelin phosphodiesterase 1	Homo sapiens	95-116
25985440-3	2015	This endosomal escape by cold treatment or bile acids is associated with ceramide formation by acid sphingomyelinase (ASM).	Ceramides	73-81	sphingomyelin phosphodiesterase 1	Homo sapiens	118-121
25985440-4	2015	ASM catalyzes hydrolysis of sphingomyelin into ceramide, which is known to destabilize lipid bilayer.	Ceramides	47-55	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
25985440-5	2015	Treatment of LLC-PK cells with bile acids or cold led to ceramide formation, and small molecule antagonists or siRNA of ASM blocked ceramide formation in the endosomes and significantly reduced PEC replication.	Ceramides	132-140	sphingomyelin phosphodiesterase 1	Homo sapiens	120-123
26126684-1	2015	Ceramides and sphingolipids are a family of lipid molecules that circulate in serum and accumulate in skeletal muscle, promoting insulin resistance.	Ceramides	0-9	insulin	Homo sapiens	129-136
26188095-1	2015	The sphingolipid ceramide is a pro apoptotic molecule of ceramide metabolic pathway and is hydrolyzed to proliferative metabolite, sphingosine 1 phosphate by the action of acid ceramidase.	Ceramides	17-25	N-acylsphingosine amidohydrolase 1	Homo sapiens	172-187
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.	Ceramides	21-29	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.	Ceramides	38-46	glucosidase, beta, acid	Mus musculus	0-4
26312487-3	2015	We investigated if the pro-inflammatory kinase p38 is activated in Gaucher"s disease, since ceramide has been proposed to suppress p38 activation.	Ceramides	92-100	mitogen-activated protein kinase 14	Mus musculus	131-134
26126684-2	2015	Plasma ceramide and dihydroceramide are related to insulin resistance, yet less is known regarding other ceramide and sphingolipid species.	Ceramides	7-15	insulin	Homo sapiens	51-58
26126684-2	2015	Plasma ceramide and dihydroceramide are related to insulin resistance, yet less is known regarding other ceramide and sphingolipid species.	Ceramides	27-35	insulin	Homo sapiens	51-58
26071354-4	2015	At the molecular level, miR-101 dramatically down-regulated SphK1 mRNA and protein expression, causing pro-apoptotic ceramide production in above CRC cells.	Ceramides	117-125	microRNA 101a	Mus musculus	24-31
26071354-4	2015	At the molecular level, miR-101 dramatically down-regulated SphK1 mRNA and protein expression, causing pro-apoptotic ceramide production in above CRC cells.	Ceramides	117-125	sphingosine kinase 1	Homo sapiens	60-65
26071354-5	2015	On the other hand, inhibition of miR-101 through expressing antagomiR-101 increased SphK1 expression to down-regulate ceramide level in HT-29 cells.	Ceramides	118-126	microRNA 101a	Mus musculus	33-40
26071354-5	2015	On the other hand, inhibition of miR-101 through expressing antagomiR-101 increased SphK1 expression to down-regulate ceramide level in HT-29 cells.	Ceramides	118-126	sphingosine kinase 1	Homo sapiens	84-89
26071354-7	2015	CRC cells with SphK1-shRNA knockdown showed similar phenotypes as the miR-101-expressed CRC cells, presenting with elevated level of ceramide and high sensitivity to paclitaxel or doxorubicin.	Ceramides	133-141	sphingosine kinase 1	Homo sapiens	15-20
26071354-7	2015	CRC cells with SphK1-shRNA knockdown showed similar phenotypes as the miR-101-expressed CRC cells, presenting with elevated level of ceramide and high sensitivity to paclitaxel or doxorubicin.	Ceramides	133-141	microRNA 101a	Mus musculus	70-77
26244839-3	2015	(2015) present the first crystal structure of human nCDase and show how complexation with phosphate supports a new catalytic mechanism for Zn-dependent amidases while providing a structurally based explanation for ceramide specificity.	Ceramides	214-222	N-acylsphingosine amidohydrolase 2	Homo sapiens	52-58
26190575-0	2015	Structural Basis for Ceramide Recognition and Hydrolysis by Human Neutral Ceramidase.	Ceramides	21-29	N-acylsphingosine amidohydrolase 2	Homo sapiens	66-84
26190575-1	2015	Neutral ceramidase (nCDase) catalyzes conversion of the apoptosis-associated lipid ceramide to sphingosine, the precursor for the proliferative factor sphingosine-1-phosphate.	Ceramides	83-91	N-acylsphingosine amidohydrolase 2	Homo sapiens	0-18
26190575-1	2015	Neutral ceramidase (nCDase) catalyzes conversion of the apoptosis-associated lipid ceramide to sphingosine, the precursor for the proliferative factor sphingosine-1-phosphate.	Ceramides	83-91	N-acylsphingosine amidohydrolase 2	Homo sapiens	20-26
26190575-2	2015	As an enzyme regulating the balance of ceramide and sphingosine-1-phosphate, nCDase is emerging as a therapeutic target for cancer.	Ceramides	39-47	N-acylsphingosine amidohydrolase 2	Homo sapiens	77-83
26190575-5	2015	Our results suggest that nCDase uses a new catalytic strategy for Zn(2+)-dependent amidases, and generates ceramide specificity by sterically excluding sphingolipids with bulky headgroups and specifically recognizing the small hydroxyl head group of ceramide.	Ceramides	107-115	N-acylsphingosine amidohydrolase 2	Homo sapiens	25-31
26190575-5	2015	Our results suggest that nCDase uses a new catalytic strategy for Zn(2+)-dependent amidases, and generates ceramide specificity by sterically excluding sphingolipids with bulky headgroups and specifically recognizing the small hydroxyl head group of ceramide.	Ceramides	250-258	N-acylsphingosine amidohydrolase 2	Homo sapiens	25-31
26190650-2	2015	We have developed transgenic mice inducibly expressing acid ceramidase that display a reduction in ceramides in adult mouse tissues.	Ceramides	99-108	N-acylsphingosine amidohydrolase 1	Mus musculus	55-70
26244926-2	2015	Using a genetic mouse model to acutely degrade ceramides in adipose tissue or the liver (i.e., by conditionally expressing acid ceramidase), in this issue of Cell MetabolismXia et al.	Ceramides	47-56	N-acylsphingosine amidohydrolase 1	Mus musculus	123-138
26142685-7	2015	Ceramides were 23% (p = 0.005) and 24% (borderline significance) lower in HDL2 and HDL3, respectively.	Ceramides	0-9	junctophilin 3	Homo sapiens	74-78
25856778-9	2015	Antiphospholipid antibodies also decreased the expression of protein kinase C-epsilon (PRKCE) in placental explants, possibly due to the disrupted balance between ceramides and diacylglycerols caused by aPL.	Ceramides	163-172	protein kinase C epsilon	Homo sapiens	61-85
25856778-9	2015	Antiphospholipid antibodies also decreased the expression of protein kinase C-epsilon (PRKCE) in placental explants, possibly due to the disrupted balance between ceramides and diacylglycerols caused by aPL.	Ceramides	163-172	protein kinase C epsilon	Homo sapiens	87-92
26142685-7	2015	Ceramides were 23% (p = 0.005) and 24% (borderline significance) lower in HDL2 and HDL3, respectively.	Ceramides	0-9	HDL3	Homo sapiens	83-87
26059977-0	2015	Regulation of mitochondrial ceramide distribution by members of the BCL-2 family.	Ceramides	28-36	B cell leukemia/lymphoma 2	Mus musculus	68-73
25762726-1	2015	Acidic sphingomyelinase (ASMase) catalyses the generation of ceramide from sphingomyelin.	Ceramides	61-69	sphingomyelin phosphodiesterase 1	Homo sapiens	0-23
25762726-1	2015	Acidic sphingomyelinase (ASMase) catalyses the generation of ceramide from sphingomyelin.	Ceramides	61-69	sphingomyelin phosphodiesterase 1	Homo sapiens	25-31
26113602-3	2015	CerS2, one of six mammalian CerS, synthesizes ceramides with very-long (C22-C24) chains.	Ceramides	46-55	ceramide synthase 2	Homo sapiens	0-5
26004871-3	2015	However, a tumour stress activation of glucosylceramide synthase (GCS) follows to eliminate ceramide by formation of glycosphingolipids (GSLs) such as globotriaosylceramide (Gb3), the functional receptor of verotoxin-1.	Ceramides	47-55	UDP-glucose ceramide glucosyltransferase	Homo sapiens	66-69
26004871-3	2015	However, a tumour stress activation of glucosylceramide synthase (GCS) follows to eliminate ceramide by formation of glycosphingolipids (GSLs) such as globotriaosylceramide (Gb3), the functional receptor of verotoxin-1.	Ceramides	47-55	alpha 1,4-galactosyltransferase (P blood group)	Homo sapiens	174-177
26004871-5	2015	GSLs transactivate multidrug resistance 1/P-glycoprotein (MDR1) and multidrug resistance-associated protein 1 (MRP1) expression which further prevents ceramide accumulation and stimulates drug efflux.	Ceramides	151-159	ATP binding cassette subfamily B member 1	Homo sapiens	19-41
26004871-5	2015	GSLs transactivate multidrug resistance 1/P-glycoprotein (MDR1) and multidrug resistance-associated protein 1 (MRP1) expression which further prevents ceramide accumulation and stimulates drug efflux.	Ceramides	151-159	ATP binding cassette subfamily B member 1	Homo sapiens	42-56
26004871-5	2015	GSLs transactivate multidrug resistance 1/P-glycoprotein (MDR1) and multidrug resistance-associated protein 1 (MRP1) expression which further prevents ceramide accumulation and stimulates drug efflux.	Ceramides	151-159	ATP binding cassette subfamily B member 1	Homo sapiens	58-62
26004871-5	2015	GSLs transactivate multidrug resistance 1/P-glycoprotein (MDR1) and multidrug resistance-associated protein 1 (MRP1) expression which further prevents ceramide accumulation and stimulates drug efflux.	Ceramides	151-159	ATP binding cassette subfamily C member 1	Homo sapiens	68-109
26004871-5	2015	GSLs transactivate multidrug resistance 1/P-glycoprotein (MDR1) and multidrug resistance-associated protein 1 (MRP1) expression which further prevents ceramide accumulation and stimulates drug efflux.	Ceramides	151-159	ATP binding cassette subfamily C member 1	Homo sapiens	111-115
26108617-5	2015	Activation of Toll-like receptor 4 (TLR4) raises another lipid class, ceramides (CER), which induce pro-inflammatory pathways and lead to inhibition of Akt phosphorylation.	Ceramides	70-79	toll like receptor 4	Homo sapiens	14-34
26108617-5	2015	Activation of Toll-like receptor 4 (TLR4) raises another lipid class, ceramides (CER), which induce pro-inflammatory pathways and lead to inhibition of Akt phosphorylation.	Ceramides	70-79	toll like receptor 4	Homo sapiens	36-40
26108617-5	2015	Activation of Toll-like receptor 4 (TLR4) raises another lipid class, ceramides (CER), which induce pro-inflammatory pathways and lead to inhibition of Akt phosphorylation.	Ceramides	81-84	toll like receptor 4	Homo sapiens	14-34
26108617-5	2015	Activation of Toll-like receptor 4 (TLR4) raises another lipid class, ceramides (CER), which induce pro-inflammatory pathways and lead to inhibition of Akt phosphorylation.	Ceramides	81-84	toll like receptor 4	Homo sapiens	36-40
26059977-7	2015	Targeted LC/MS analysis revealed elevated levels of additional sphingadiene-containing ceramides (d18:2-Cers) in BAX, BAK-double knockout MEFs.	Ceramides	87-96	BCL2-associated X protein	Mus musculus	113-116
26059977-7	2015	Targeted LC/MS analysis revealed elevated levels of additional sphingadiene-containing ceramides (d18:2-Cers) in BAX, BAK-double knockout MEFs.	Ceramides	87-96	BCL2-antagonist/killer 1	Mus musculus	118-121
25724183-5	2015	Ceramide synthase-1 small hairpin RNA (shRNA)-depletion inhibited cinobufotalin-induced ceramide production and HCC cell apoptosis.	Ceramides	88-96	ceramide synthase 1	Homo sapiens	0-19
26063766-7	2015	Genetic or pharmacologic inhibition of GCS induced accumulation of increased ceramide levels.	Ceramides	77-85	UDP-glucose ceramide glucosyltransferase	Homo sapiens	39-42
25944793-0	2015	Oxidative Stress Increases Surface Toll-Like Receptor 4 Expression in Murine Macrophages Via Ceramide Generation.	Ceramides	93-101	toll-like receptor 4	Mus musculus	35-55
25944793-8	2015	To evaluate the upstream molecules involved in Src activation, we evaluated the ability of oxidative stress to activate the bioactive lipid molecule ceramide.	Ceramides	149-157	Rous sarcoma oncogene	Mus musculus	47-50
25944793-10	2015	Using pharmacological approaches, ceramide was shown to be both necessary and sufficient to mediate TLR4 translocation to the plasma membrane in an Src-dependent manner.	Ceramides	34-42	toll-like receptor 4	Mus musculus	100-104
25944793-10	2015	Using pharmacological approaches, ceramide was shown to be both necessary and sufficient to mediate TLR4 translocation to the plasma membrane in an Src-dependent manner.	Ceramides	34-42	Rous sarcoma oncogene	Mus musculus	148-151
25724183-6	2015	On the other hand, the glucosylceramide synthase (GCS) inhibitor 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (PDMP) facilitated cinobufotalin-induced ceramide production and cell apoptosis.	Ceramides	31-39	UDP-glucose ceramide glucosyltransferase	Homo sapiens	50-53
25724183-7	2015	SphK1 inhibitor II (SKI-II), similar to cinobufotalin, increased cellular ceramide level and promoted HCC cell apoptosis.	Ceramides	74-82	sphingosine kinase 1	Homo sapiens	0-5
26230734-11	2015	In SM-unmodulated adipocytes treated with DL-1-Phenyl-2-Palmitoylamino-3-morpholino-1-propanol (PPMP), where the ceramide level increased, the expression levels of SREBPs and ERK were modulated in an opposite direction relative to the SM-enriched cells.	Ceramides	113-121	mitogen-activated protein kinase 1	Homo sapiens	175-178
25957215-3	2015	Given the role of AGEs and their receptor, RAGE, in activating inflammatory pathways, we sought to determine whether ceramides could be a mediator of RAGE-induced altered heart mitochondrial function.	Ceramides	117-126	advanced glycosylation end product-specific receptor	Mus musculus	150-154
26203857-1	2015	Acid sphingomyelinase (ASM), a lipid hydrolase enzyme, has the potential to modulate various cellular activation responses via the generation of ceramide and by interaction with cellular receptors.	Ceramides	145-153	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
26203857-1	2015	Acid sphingomyelinase (ASM), a lipid hydrolase enzyme, has the potential to modulate various cellular activation responses via the generation of ceramide and by interaction with cellular receptors.	Ceramides	145-153	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
26203857-4	2015	ASM further mediates T-cell proliferation after anti-CD3/CD28 antibody stimulation and alters CD4(+) T-cell activation signals by generating ceramide.	Ceramides	141-149	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
25957215-7	2015	Finally, conditional overexpression of RAGE in the lungs of transgenic mice elicited a robust increase in left ventricular ceramides in the absence of smoke exposure.	Ceramides	123-132	advanced glycosylation end product-specific receptor	Mus musculus	39-43
25968578-0	2015	MyD88 regulates physical inactivity-induced skeletal muscle inflammation, ceramide biosynthesis signaling, and glucose intolerance.	Ceramides	74-82	myeloid differentiation primary response gene 88	Mus musculus	0-5
25968578-2	2015	Elevated inflammation and ceramide biosynthesis have been implicated in metabolic disruption and are linked to Toll-like receptor (TLR)/myeloid differentiation primary response 88 (MyD88) signaling.	Ceramides	26-34	myeloid differentiation primary response gene 88	Mus musculus	181-186
25968578-3	2015	We hypothesize that a physical inactivity stimulus, capable of inducing glucose intolerance, would increase skeletal muscle inflammation and ceramide biosynthesis signaling and that this response would be regulated by the TLR/MyD88 pathway.	Ceramides	141-149	myeloid differentiation primary response gene 88	Mus musculus	226-231
25968578-8	2015	In conclusion, MyD88 signaling is necessary for the increased inflammation, ceramide biosynthesis signaling, and compromised metabolic function that accompanies physical inactivity.	Ceramides	76-84	myeloid differentiation primary response gene 88	Mus musculus	15-20
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.	Ceramides	98-106	sphingosine kinase 2	Mus musculus	26-31
25915851-6	2015	Notable decreases in several glycerolipids after the HFD were reversed by adiponectin, which also corrected elevations in several diacyglycerol and ceramide species.	Ceramides	148-156	adiponectin, C1Q and collagen domain containing	Mus musculus	74-85
25966363-0	2015	Improved insulin sensitivity after exercise training is linked to reduced plasma C14:0 ceramide in obesity and type 2 diabetes.	Ceramides	87-95	insulin	Homo sapiens	9-16
25966363-10	2015	CONCLUSIONS: Ceramides are linked to exercise training-induced improvements in insulin sensitivity, and plasma C14:0 ceramide may provide a specific target for investigating lipid-related insulin resistance in obesity and T2D.	Ceramides	117-125	insulin	Homo sapiens	188-195
25966363-9	2015	Decreases in total (r = -0.51, P = 0.02) and C14:0 (r = -0.56, P = 0.009) ceramide were negatively correlated with the increase in insulin sensitivity.	Ceramides	74-82	insulin	Homo sapiens	131-138
25966363-10	2015	CONCLUSIONS: Ceramides are linked to exercise training-induced improvements in insulin sensitivity, and plasma C14:0 ceramide may provide a specific target for investigating lipid-related insulin resistance in obesity and T2D.	Ceramides	13-22	insulin	Homo sapiens	79-86
26107620-0	2015	Metabolomics Analysis Reveals that AICAR Affects Glycerolipid, Ceramide and Nucleotide Synthesis Pathways in INS-1 Cells.	Ceramides	63-71	insulin 1	Rattus norvegicus	109-114
26056266-5	2015	Increased ceramide, glucosylceramide, GM3, and hexosaminidase activity were also found in SOD1(G93A) mice, a familial model of ALS.	Ceramides	10-18	superoxide dismutase 1, soluble	Mus musculus	90-94
25719313-7	2015	Furthermore, ceramide glycosylation catalyzed by glucosylceramide synthase converts ceramide to glucosylceramide, thus eliminating ceramide and consequently protecting cancer cells from apoptosis.	Ceramides	13-21	UDP-glucose ceramide glucosyltransferase	Homo sapiens	49-74
26070932-8	2015	Yukyung Karne also induced the neutral sphingomyelinase II (nSMNaseII) enzyme activity that is known to hydrolyze sphingomyelins into pro-apoptotic intracellular molecule ceramide.	Ceramides	171-179	sphingomyelin phosphodiesterase 3	Homo sapiens	31-58
26070932-8	2015	Yukyung Karne also induced the neutral sphingomyelinase II (nSMNaseII) enzyme activity that is known to hydrolyze sphingomyelins into pro-apoptotic intracellular molecule ceramide.	Ceramides	171-179	sphingomyelin phosphodiesterase 3	Homo sapiens	60-69
25347576-0	2015	Src regulates cigarette smoke-induced ceramide generation via neutral sphingomyelinase 2 in the airway epithelium.	Ceramides	38-46	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-3
25347576-0	2015	Src regulates cigarette smoke-induced ceramide generation via neutral sphingomyelinase 2 in the airway epithelium.	Ceramides	38-46	sphingomyelin phosphodiesterase 3	Homo sapiens	62-88
25347576-1	2015	We previously demonstrated that the neutral sphingomyelinase (nSMase) 2 is the sole sphingomyelinase activated during cigarette smoke (CS)-induced oxidative stress of human airway epithelial cells, leading to ceramide generation and subsequent apoptosis of affected cells.	Ceramides	209-217	sphingomyelin phosphodiesterase 3	Homo sapiens	36-71
25347576-4	2015	Within this context, we tested and now present Src as a regulator of ceramide generation via modulation of nSMase2 phosphorylation and activity during CS-induced oxidative stress.	Ceramides	69-77	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	47-50
25347576-4	2015	Within this context, we tested and now present Src as a regulator of ceramide generation via modulation of nSMase2 phosphorylation and activity during CS-induced oxidative stress.	Ceramides	69-77	sphingomyelin phosphodiesterase 3	Homo sapiens	107-114
25347576-5	2015	Specifically, we provide evidence that Src activity is necessary for both CS-induced ceramide accumulation in vivo (129/Sv mice) and in vitro (human airway epithelial cells) and for nSMase2 activity during CS-induced oxidative stress.	Ceramides	85-93	Rous sarcoma oncogene	Mus musculus	39-42
25348830-10	2015	Juglone (5 muM) significantly increased ceramide abundance at the erythrocyte surface and decreased erythrocyte ATP concentration.	Ceramides	40-48	latexin	Homo sapiens	11-14
25803076-1	2015	Acid sphingomyelinase (ASM), a key enzyme in sphingolipid metabolism, hydrolyzes sphingomyelin to ceramide and phosphorylcholine.	Ceramides	98-106	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
25720061-3	2015	Ceramide accumulates in the airway epithelium of cystic fibrosis and ceramide synthase 2 (CerS2)-deficient mice, which respond to the lack of very long chain (C22-C24-) ceramides with a profound compensatory increase of long chain (mainly C16-) ceramides.	Ceramides	0-8	ceramide synthase 2	Mus musculus	69-88
25803076-1	2015	Acid sphingomyelinase (ASM), a key enzyme in sphingolipid metabolism, hydrolyzes sphingomyelin to ceramide and phosphorylcholine.	Ceramides	98-106	sphingomyelin phosphodiesterase 1	Homo sapiens	23-26
25938220-1	2015	Acid ceramidase (N-acylsphingosine deacylase, EC 3.5.1.23; AC) is the lipid hydrolase responsible for the degradation of ceramide into sphingosine and free fatty acids within lysosomes.	Ceramides	121-129	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
25720061-3	2015	Ceramide accumulates in the airway epithelium of cystic fibrosis and ceramide synthase 2 (CerS2)-deficient mice, which respond to the lack of very long chain (C22-C24-) ceramides with a profound compensatory increase of long chain (mainly C16-) ceramides.	Ceramides	0-8	ceramide synthase 2	Mus musculus	90-95
25720061-5	2015	Both sphingolipids are crucially involved in the high susceptibility to infection of cystic fibrosis and CerS2-deficient mice, as indicated by findings showing that the normalization of ceramide and sphingosine levels rescue these mice from acute infection with P. aeruginosa.	Ceramides	186-194	ceramide synthase 2	Mus musculus	105-110
25816050-0	2015	Association of Plasma Ceramides and Sphingomyelin With VLDL apoB-100 Fractional Catabolic Rate Before and After Rosuvastatin Treatment.	Ceramides	22-31	apolipoprotein B	Homo sapiens	60-68
25851537-6	2015	Human and mouse melanoma cells triggered activation and release of platelet secretory Asm, in turn leading to ceramide formation, clustering, and activation of alpha5beta1 integrins on melanoma cells finally leading to adhesion of the tumor cells.	Ceramides	110-118	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	86-89
25851537-7	2015	Clustering of integrins by applying purified Asm or C16 ceramide to B16F10 melanoma cells before intravenous injection restored trapping of tumor cells in the lung in Asm-deficient mice.	Ceramides	56-64	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	167-170
25859016-0	2015	A new twist to the emerging functions of ceramides in cancer: novel role for platelet acid sphingomyelinase in cancer metastasis.	Ceramides	41-50	sphingomyelin phosphodiesterase 1	Homo sapiens	86-107
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.	Ceramides	55-63	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.	Ceramides	55-63	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.	Ceramides	55-63	hypoxia inducible factor 1, alpha subunit	Mus musculus	289-299
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.	Ceramides	96-104	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.	Ceramides	96-104	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.	Ceramides	96-104	hypoxia inducible factor 1, alpha subunit	Mus musculus	289-299
25816050-3	2015	RESULTS AND DISCUSSION: Baseline plasma ceramides were associated with very low-density lipoprotein (VLDL) apolipoprotein (apo)-B-100 concentration (r = 0.58, P &lt; .05) and inversely with VLDL apoB-100 fractional catabolic rate (FCR; r = -0.67, P = .02).	Ceramides	40-49	apolipoprotein B	Homo sapiens	195-203
25816050-4	2015	Posttreatment changes with rosuvastatin (40 mg/d) in plasma ceramides were inversely associated with VLDL apoB-100 FCR (r = -0.62, P = .03) independent of changes in plasma triglycerides, cholesterol, and low-density lipoprotein-cholesterol.	Ceramides	60-69	apolipoprotein B	Homo sapiens	106-114
25816050-7	2015	In the metabolic syndrome, the ability of rosuvastatin to increase VLDL apoB-100 FCR may reflect ceramide-specific mechanistic actions and/or sphingolipid exchange.	Ceramides	97-105	apolipoprotein B	Homo sapiens	72-80
25393677-0	2015	Ceramide participates in lysosome-mediated cell death induced by type II anti-CD20 monoclonal antibodies.	Ceramides	0-8	keratin 20	Homo sapiens	78-82
25616357-4	2015	The Asm/ceramide system triggered the formation of superoxide, resulting in degradation of tight junction proteins followed by lung edema.	Ceramides	8-16	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	4-7
25616357-9	2015	S. aureus induces lung edema via the Asm/ceramide system.	Ceramides	41-49	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	37-40
25705848-7	2015	The data indicate that CerS4-directed epidermal ceramide composition is essential to control hair follicle stem and progenitor cell behavior potentially through its regulation of BMP and Wnt signaling.	Ceramides	48-56	ceramide synthase 4	Mus musculus	23-28
25393677-5	2015	The clarification of ceramide involvement in type II anti-CD20 mAb-induced PCD may provide new ideas on CD20-based immunotherapy against NHLs.	Ceramides	21-29	keratin 20	Homo sapiens	58-62
25393677-5	2015	The clarification of ceramide involvement in type II anti-CD20 mAb-induced PCD may provide new ideas on CD20-based immunotherapy against NHLs.	Ceramides	21-29	keratin 20	Homo sapiens	104-108
25797839-2	2015	Nitric oxide (NO) is able to overcome tumor resistance in PTEN mutated rat C6 glioma cells due to its ability to inhibit cell growth by influencing the intracellular distribution of ceramide.	Ceramides	182-190	phosphatase and tensin homolog	Rattus norvegicus	58-62
25797839-3	2015	The aim of this study is to monitor the effects of NO donor PAPANONOate on ceramide trafficking in human glioma cell lines, CCF-STTG1 (PTEN-mutated, p53-wt) and T98G (PTEN-harboring, p53-mutated), together with the assessment of their differential molecular signature by 2D-DIGE and MALDI mass spectrometry.	Ceramides	75-83	phosphatase and tensin homolog	Homo sapiens	135-139
25797839-3	2015	The aim of this study is to monitor the effects of NO donor PAPANONOate on ceramide trafficking in human glioma cell lines, CCF-STTG1 (PTEN-mutated, p53-wt) and T98G (PTEN-harboring, p53-mutated), together with the assessment of their differential molecular signature by 2D-DIGE and MALDI mass spectrometry.	Ceramides	75-83	phosphatase and tensin homolog	Homo sapiens	167-171
25797839-3	2015	The aim of this study is to monitor the effects of NO donor PAPANONOate on ceramide trafficking in human glioma cell lines, CCF-STTG1 (PTEN-mutated, p53-wt) and T98G (PTEN-harboring, p53-mutated), together with the assessment of their differential molecular signature by 2D-DIGE and MALDI mass spectrometry.	Ceramides	75-83	tumor protein p53	Homo sapiens	183-186
26010541-4	2015	Increased nSMase2 activity translates into higher ceramide levels and neuronal cell death, which can be prevented by chemical or genetic inhibition of nSMase2 activity or expression.	Ceramides	50-58	sphingomyelin phosphodiesterase 3	Homo sapiens	10-17
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.	Ceramides	192-200	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.	Ceramides	192-200	glucosylceramidase beta	Homo sapiens	122-125
26010541-4	2015	Increased nSMase2 activity translates into higher ceramide levels and neuronal cell death, which can be prevented by chemical or genetic inhibition of nSMase2 activity or expression.	Ceramides	50-58	sphingomyelin phosphodiesterase 3	Homo sapiens	151-158
26010541-12	2015	Cambinol decreased tumor necrosis factor-alpha or interleukin-1 beta-induced increases of ceramide and cell death in primary neurons.	Ceramides	90-98	interleukin 1 beta	Homo sapiens	50-68
26010541-14	2015	Cambinol and its analogs may be useful as nSMase2 inhibitor tool compounds to prevent ceramide-dependent neurodegeneration.	Ceramides	86-94	sphingomyelin phosphodiesterase 3	Homo sapiens	42-49
25839235-4	2015	Overexpression of CerS6 in HT29 colon cancer cells resulted in increased apoptotic susceptibility and preferential generation of C16-ceramide, which occurred at the expense of very long chain, saturated ceramides.	Ceramides	203-212	ceramide synthase 6	Homo sapiens	18-23
25839235-6	2015	HT-CerS6 cells had increased intracellular levels of sphingosine, which is generated by ceramidases upon hydrolysis of ceramide.	Ceramides	119-127	ceramide synthase 6	Homo sapiens	3-8
25879284-6	2015	The NLRP3 inflammasome is especially relevant to aging as it can get activated in response to structurally diverse damage-associated molecular patterns (DAMPs) such as extracellular ATP, excess glucose, ceramides, amyloids, urate, and cholesterol crystals, all of which increase with age.	Ceramides	203-212	NLR family pyrin domain containing 3	Homo sapiens	4-9
25637185-5	2015	Mechanisms involved in the stimulation eryptosis include ceramide formation which may result from phospholipase A2 dependent formation of platelet activating factor (PAF) with PAF dependent stimulation of sphingomyelinases.	Ceramides	57-65	phospholipase A2 group IB	Homo sapiens	98-114
25637185-5	2015	Mechanisms involved in the stimulation eryptosis include ceramide formation which may result from phospholipase A2 dependent formation of platelet activating factor (PAF) with PAF dependent stimulation of sphingomyelinases.	Ceramides	57-65	PCNA clamp associated factor	Homo sapiens	166-169
25637185-5	2015	Mechanisms involved in the stimulation eryptosis include ceramide formation which may result from phospholipase A2 dependent formation of platelet activating factor (PAF) with PAF dependent stimulation of sphingomyelinases.	Ceramides	57-65	PCNA clamp associated factor	Homo sapiens	176-179
25354938-4	2015	We used nSMase for investigating the signal transduction downstream of ceramide.	Ceramides	71-79	sphingomyelin phosphodiesterase 2	Rattus norvegicus	8-14
25354938-10	2015	In addition, the coexpression of the ceramide with cPLA2, was found in the smooth muscle layer of intrarenal vessels.	Ceramides	37-45	phospholipase A2 group IVA	Rattus norvegicus	51-56
25354938-11	2015	Our results suggest that ANG II stimulates ceramide formation via the activation of nSMase; thus ceramide may indirectly regulate vasoactive processes that modulate the activity of cPLA2 and the release of TxA2.	Ceramides	43-51	angiotensinogen	Rattus norvegicus	25-31
25354938-11	2015	Our results suggest that ANG II stimulates ceramide formation via the activation of nSMase; thus ceramide may indirectly regulate vasoactive processes that modulate the activity of cPLA2 and the release of TxA2.	Ceramides	43-51	sphingomyelin phosphodiesterase 2	Rattus norvegicus	84-90
25354938-11	2015	Our results suggest that ANG II stimulates ceramide formation via the activation of nSMase; thus ceramide may indirectly regulate vasoactive processes that modulate the activity of cPLA2 and the release of TxA2.	Ceramides	97-105	angiotensinogen	Rattus norvegicus	25-31
25354938-11	2015	Our results suggest that ANG II stimulates ceramide formation via the activation of nSMase; thus ceramide may indirectly regulate vasoactive processes that modulate the activity of cPLA2 and the release of TxA2.	Ceramides	97-105	sphingomyelin phosphodiesterase 2	Rattus norvegicus	84-90
25354938-11	2015	Our results suggest that ANG II stimulates ceramide formation via the activation of nSMase; thus ceramide may indirectly regulate vasoactive processes that modulate the activity of cPLA2 and the release of TxA2.	Ceramides	97-105	phospholipase A2 group IVA	Rattus norvegicus	181-186
25964538-3	2015	Several lines of evidence indicate that the expression and increased function of both Pgp and glucosylceramide synthase (GCS, an enzyme responsible for ceramide pathway de-activation in the regulation of apoptosis progression) enhance the resistance of Pgp-positive cells.	Ceramides	102-110	phosphoglycolate phosphatase	Mus musculus	253-256
25964538-6	2015	Consequently, the over-expression of Pgp in Pgp-positive L1210 cells may be associated with reduced ceramide glycosylation.	Ceramides	100-108	phosphoglycolate phosphatase	Mus musculus	37-40
25964538-6	2015	Consequently, the over-expression of Pgp in Pgp-positive L1210 cells may be associated with reduced ceramide glycosylation.	Ceramides	100-108	phosphoglycolate phosphatase	Mus musculus	44-47
25964538-11	2015	The Pgp-positive L1210 variants (R and T) are more sensitive than Pgp-negative S cells to ceramide-induced cell damage, as measured by an fluorescein isothiocyanate-labeled annexin V and propidium iodide apoptosis necrosis kit.	Ceramides	90-98	phosphoglycolate phosphatase	Mus musculus	4-7
25964538-11	2015	The Pgp-positive L1210 variants (R and T) are more sensitive than Pgp-negative S cells to ceramide-induced cell damage, as measured by an fluorescein isothiocyanate-labeled annexin V and propidium iodide apoptosis necrosis kit.	Ceramides	90-98	phosphoglycolate phosphatase	Mus musculus	66-69
25964538-13	2015	CONCLUSION: These evidence indicates that the down-regulation of UDP-glucose contents in Pgp-positive L1210 cells is responsible for their collateral sensitivity to ceramide-induced apoptosis.	Ceramides	165-173	phosphoglycolate phosphatase	Mus musculus	89-92
25748248-1	2015	Acid ceramidase is responsible for the ultimate step in the catabolism of (glyco)sphingolipids by hydrolysis of ceramide into sphingosine and free fatty acid.	Ceramides	112-120	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
25859817-3	2015	This cycloaddition was successfully applied to the synthesis of syn-HPA-12 known as an inhibitor of CERT that mediates the transport of ceramide.	Ceramides	136-144	ceramide transporter 1	Homo sapiens	100-104
25933391-11	2015	A significant increase and accumulation of several species for the lipid classes, ceramides and sphingolipids, was observed in LBD brains carrying GBA mutations compared to controls (p range: p<0.05-p<0.01).	Ceramides	82-91	glucosylceramidase beta	Homo sapiens	147-150
25303541-7	2015	CD95 activation was dependent on nitric oxide and ceramide signaling.	Ceramides	50-58	Fas cell surface death receptor	Homo sapiens	0-4
25853898-4	2015	Placental ceramides were elevated due to greater de novo synthesis via high serine palmitoyltransferase activity and reduced lysosomal breakdown via diminished ASAH1 expression caused by TGFB3-induced E2F4 transcriptional repression.	Ceramides	10-19	N-acylsphingosine amidohydrolase 1	Homo sapiens	160-165
25855965-0	2015	Lysosomal ceramide generated by acid sphingomyelinase triggers cytosolic cathepsin B-mediated degradation of X-linked inhibitor of apoptosis protein in natural killer/T lymphoma cell apoptosis.	Ceramides	10-18	cathepsin B	Homo sapiens	73-84
25855965-0	2015	Lysosomal ceramide generated by acid sphingomyelinase triggers cytosolic cathepsin B-mediated degradation of X-linked inhibitor of apoptosis protein in natural killer/T lymphoma cell apoptosis.	Ceramides	10-18	X-linked inhibitor of apoptosis	Homo sapiens	109-148
25855965-1	2015	We previously reported that IL-2 deprivation induced acid sphingomyelinase-mediated (ASM-mediated) ceramide elevation and apoptosis in an NK/T lymphoma cell line KHYG-1.	Ceramides	99-107	interleukin 2	Homo sapiens	28-32
25855965-1	2015	We previously reported that IL-2 deprivation induced acid sphingomyelinase-mediated (ASM-mediated) ceramide elevation and apoptosis in an NK/T lymphoma cell line KHYG-1.	Ceramides	99-107	H19 imprinted maternally expressed transcript	Homo sapiens	85-88
25855965-5	2015	However, IL-2 deprivation induced ceramide elevation via ASM in lysosomes and activated lysosomal cathepsin B (CTSB) but not cathepsin D.	Ceramides	34-42	interleukin 2	Homo sapiens	9-13
25855965-5	2015	However, IL-2 deprivation induced ceramide elevation via ASM in lysosomes and activated lysosomal cathepsin B (CTSB) but not cathepsin D.	Ceramides	34-42	H19 imprinted maternally expressed transcript	Homo sapiens	57-60
25855965-6	2015	A CTSB inhibitor CA-074 Me and knockdown of CTSB inhibited ceramide-mediated XIAP degradation and apoptosis.	Ceramides	59-67	cathepsin B	Homo sapiens	2-6
25855965-6	2015	A CTSB inhibitor CA-074 Me and knockdown of CTSB inhibited ceramide-mediated XIAP degradation and apoptosis.	Ceramides	59-67	cathepsin B	Homo sapiens	44-48
25855965-6	2015	A CTSB inhibitor CA-074 Me and knockdown of CTSB inhibited ceramide-mediated XIAP degradation and apoptosis.	Ceramides	59-67	X-linked inhibitor of apoptosis	Homo sapiens	77-81
25855965-7	2015	Inhibition of ceramide accumulation in lysosomes using an ASM inhibitor, desipramine, decreased cytosolic activation of CTSB by inhibiting its transfer into cytosol from the lysosome.	Ceramides	14-22	H19 imprinted maternally expressed transcript	Homo sapiens	58-61
25855965-7	2015	Inhibition of ceramide accumulation in lysosomes using an ASM inhibitor, desipramine, decreased cytosolic activation of CTSB by inhibiting its transfer into cytosol from the lysosome.	Ceramides	14-22	cathepsin B	Homo sapiens	120-124
25855965-9	2015	Furthermore, cell permeable N-acetyl sphingosine (C2-ceramide), which increases mainly endogenous d18:1/16:0 and d18:1/24:1 ceramide-like IL-2 deprivation, induced caspase-dependent apoptosis with XIAP degradation through CTSB.	Ceramides	53-61	interleukin 2	Homo sapiens	138-142
25855965-9	2015	Furthermore, cell permeable N-acetyl sphingosine (C2-ceramide), which increases mainly endogenous d18:1/16:0 and d18:1/24:1 ceramide-like IL-2 deprivation, induced caspase-dependent apoptosis with XIAP degradation through CTSB.	Ceramides	53-61	X-linked inhibitor of apoptosis	Homo sapiens	197-201
25855965-9	2015	Furthermore, cell permeable N-acetyl sphingosine (C2-ceramide), which increases mainly endogenous d18:1/16:0 and d18:1/24:1 ceramide-like IL-2 deprivation, induced caspase-dependent apoptosis with XIAP degradation through CTSB.	Ceramides	53-61	cathepsin B	Homo sapiens	222-226
25855965-10	2015	These findings suggest that lysosomal ceramide produced by ASM mediates XIAP degradation by activation of cytosolic CTSB and caspase-dependent apoptosis.	Ceramides	38-46	H19 imprinted maternally expressed transcript	Homo sapiens	59-62
25855965-10	2015	These findings suggest that lysosomal ceramide produced by ASM mediates XIAP degradation by activation of cytosolic CTSB and caspase-dependent apoptosis.	Ceramides	38-46	X-linked inhibitor of apoptosis	Homo sapiens	72-76
25855965-10	2015	These findings suggest that lysosomal ceramide produced by ASM mediates XIAP degradation by activation of cytosolic CTSB and caspase-dependent apoptosis.	Ceramides	38-46	cathepsin B	Homo sapiens	116-120
25855965-11	2015	The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells.	Ceramides	8-16	H19 imprinted maternally expressed transcript	Homo sapiens	4-7
25855965-11	2015	The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells.	Ceramides	8-16	cathepsin B	Homo sapiens	17-21
25855965-11	2015	The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells.	Ceramides	8-16	interleukin 2	Homo sapiens	90-94
25855965-11	2015	The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells.	Ceramides	59-67	H19 imprinted maternally expressed transcript	Homo sapiens	4-7
25855965-11	2015	The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells.	Ceramides	59-67	cathepsin B	Homo sapiens	17-21
25855965-11	2015	The ASM-ceramide-CTSB signaling axis is a novel pathway of ceramide-mediated apoptosis in IL-2-deprived NK/T lymphoma cells.	Ceramides	59-67	interleukin 2	Homo sapiens	90-94
25853898-4	2015	Placental ceramides were elevated due to greater de novo synthesis via high serine palmitoyltransferase activity and reduced lysosomal breakdown via diminished ASAH1 expression caused by TGFB3-induced E2F4 transcriptional repression.	Ceramides	10-19	transforming growth factor beta 3	Homo sapiens	187-192
25853898-4	2015	Placental ceramides were elevated due to greater de novo synthesis via high serine palmitoyltransferase activity and reduced lysosomal breakdown via diminished ASAH1 expression caused by TGFB3-induced E2F4 transcriptional repression.	Ceramides	10-19	E2F transcription factor 4	Homo sapiens	201-205
25853898-8	2015	ASAH1 inhibition or ceramide treatment induced autophagy in human trophoblast cells via a shift of the BOK-MCL1 rheostat toward prodeath BOK.	Ceramides	20-28	BCL2 family apoptosis regulator BOK	Homo sapiens	103-106
25853898-8	2015	ASAH1 inhibition or ceramide treatment induced autophagy in human trophoblast cells via a shift of the BOK-MCL1 rheostat toward prodeath BOK.	Ceramides	20-28	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	107-111
25853898-8	2015	ASAH1 inhibition or ceramide treatment induced autophagy in human trophoblast cells via a shift of the BOK-MCL1 rheostat toward prodeath BOK.	Ceramides	20-28	BCL2 family apoptosis regulator BOK	Homo sapiens	137-140
25853898-9	2015	Pharmacological inhibition of ASAH1 activity in pregnant mice resulted in increased placental ceramide content, abnormal placentation, reduced fetal growth, and increased autophagy via a similar shift in the BOK-MCL1 system.	Ceramides	94-102	N-acylsphingosine amidohydrolase 1	Mus musculus	30-35
25352638-0	2015	Increased dihydroceramide/ceramide ratio mediated by defective expression of degs1 impairs adipocyte differentiation and function.	Ceramides	17-25	delta 4-desaturase, sphingolipid 1	Homo sapiens	77-82
25367746-3	2015	In skeletal muscle, increased ectopic adiposity is linked to insulin resistance through lipid mediators such as ceramide or DAG, inhibiting the insulin receptor signalling pathway.	Ceramides	112-120	insulin	Homo sapiens	61-68
25367746-3	2015	In skeletal muscle, increased ectopic adiposity is linked to insulin resistance through lipid mediators such as ceramide or DAG, inhibiting the insulin receptor signalling pathway.	Ceramides	112-120	insulin	Homo sapiens	144-151
25367746-8	2015	Saturated fatty acids can be regarded as the most detrimental of FFA, being capable of inducing insulin resistance and inflammation through lipid mediators such as ceramide, which can increase risk of developing atherosclerosis.	Ceramides	164-172	insulin	Homo sapiens	96-103
25352638-2	2015	Ceramides are well-known mediators of lipid-induced insulin resistance in peripheral organs such as muscle.	Ceramides	0-9	insulin	Homo sapiens	52-59
25352638-3	2015	DEGS1 is the desaturase catalyzing the last step in the main ceramide biosynthetic pathway.	Ceramides	61-69	delta 4-desaturase, sphingolipid 1	Homo sapiens	0-5
25352638-4	2015	Functional suppression of DEGS1 activity results in substantial changes in ceramide species likely to affect fundamental biological functions such as oxidative stress, cell survival, and proliferation.	Ceramides	75-83	delta 4-desaturase, sphingolipid 1	Homo sapiens	26-31
26046034-2	2015	In this review, we focus on the roles and regulation of N-SMase 1, N-SMase 2, N-SMase 3, an enzyme that generates the bioactive lipid ceramide through the hydrolysis of the membrane lipid sphingomyelin.	Ceramides	134-142	sphingomyelin phosphodiesterase 2	Homo sapiens	56-65
25651930-0	2015	Keratinocyte differentiation and upregulation of ceramide synthesis induced by an oat lipid extract via the activation of PPAR pathways.	Ceramides	49-57	peroxisome proliferator activated receptor alpha	Homo sapiens	122-126
25651930-8	2015	Further, oat oil treatment in keratinocytes significantly increased ceramide levels (70%), suggesting a functional translation of PPAR activation by oat oil in keratinocytes.	Ceramides	68-76	peroxisome proliferator activated receptor alpha	Homo sapiens	130-134
26046034-2	2015	In this review, we focus on the roles and regulation of N-SMase 1, N-SMase 2, N-SMase 3, an enzyme that generates the bioactive lipid ceramide through the hydrolysis of the membrane lipid sphingomyelin.	Ceramides	134-142	sphingomyelin phosphodiesterase 2	Homo sapiens	56-63
26046034-2	2015	In this review, we focus on the roles and regulation of N-SMase 1, N-SMase 2, N-SMase 3, an enzyme that generates the bioactive lipid ceramide through the hydrolysis of the membrane lipid sphingomyelin.	Ceramides	134-142	sphingomyelin phosphodiesterase 2	Homo sapiens	67-74
25667419-4	2015	Acute disruption of SMSr catalytic activity in cultured cells causes a rise in endoplasmic reticulum (ER) ceramides, fragmentation of ER exit sites, and induction of mitochondrial apoptosis.	Ceramides	106-115	sterile alpha motif domain containing 8	Mus musculus	20-24
25822663-7	2015	Consistently, levels of unsaturated very-long-chain (VLC) ceramide species (22:1, 24:1 and 26:1) predominantly declined in the loh1, loh2 and loh3 mutants under dark submergence.	Ceramides	58-66	RNA-binding CRS1 / YhbY (CRM) domain protein	Arabidopsis thaliana	127-131
25809802-2	2015	The underlying factor could be accumulation of certain lipid moieties, such as ceramides (CER) and diacylgycerol (DAG) within muscle tissue, which are known to promote insulin resistance (IR), induce inflammation and oxidative injury, ultimately altering muscle function.	Ceramides	79-88	insulin	Homo sapiens	168-175
25809802-2	2015	The underlying factor could be accumulation of certain lipid moieties, such as ceramides (CER) and diacylgycerol (DAG) within muscle tissue, which are known to promote insulin resistance (IR), induce inflammation and oxidative injury, ultimately altering muscle function.	Ceramides	90-93	insulin	Homo sapiens	168-175
26962194-15	2015	CONCLUSIONS: A healthy Nordic diet transiently modified the plasma lipidomic profile, specifically by increasing the concentrations of antioxidative plasmalogens and decreasing insulin resistance-inducing ceramides.	Ceramides	205-214	insulin	Homo sapiens	177-184
25822663-7	2015	Consistently, levels of unsaturated very-long-chain (VLC) ceramide species (22:1, 24:1 and 26:1) predominantly declined in the loh1, loh2 and loh3 mutants under dark submergence.	Ceramides	58-66	LAG1 homologue 2	Arabidopsis thaliana	133-137
25822663-7	2015	Consistently, levels of unsaturated very-long-chain (VLC) ceramide species (22:1, 24:1 and 26:1) predominantly declined in the loh1, loh2 and loh3 mutants under dark submergence.	Ceramides	58-66	LAG1 longevity assurance-like protein	Arabidopsis thaliana	142-146
25681441-0	2015	Lysosomal degradation of CD44 mediates ceramide nanoliposome-induced anoikis and diminished extravasation in metastatic carcinoma cells.	Ceramides	39-47	CD44 molecule (Indian blood group)	Homo sapiens	25-29
25681441-6	2015	Taken together, our data indicate that ceramide limits CD44-dependent cancer cell migration, suggesting that CNL could be used to prevent and treat solid tumor metastasis.	Ceramides	39-47	CD44 molecule (Indian blood group)	Homo sapiens	55-59
25822663-8	2015	In contrast, significant reduction of VLC ceramides in the loh1-1 loh3-1 knockdown double mutant and lacking of VLC unsaturated ceramides in the ads2 mutants impaired plant tolerance to both dark and light submergences.	Ceramides	42-51	RNA-binding CRS1 / YhbY (CRM) domain protein	Arabidopsis thaliana	59-63
25822663-8	2015	In contrast, significant reduction of VLC ceramides in the loh1-1 loh3-1 knockdown double mutant and lacking of VLC unsaturated ceramides in the ads2 mutants impaired plant tolerance to both dark and light submergences.	Ceramides	42-51	LAG1 longevity assurance-like protein	Arabidopsis thaliana	66-70
25822663-8	2015	In contrast, significant reduction of VLC ceramides in the loh1-1 loh3-1 knockdown double mutant and lacking of VLC unsaturated ceramides in the ads2 mutants impaired plant tolerance to both dark and light submergences.	Ceramides	128-137	16:0delta9 desaturase 2	Arabidopsis thaliana	145-149
25751724-5	2015	Ceramide enhances oligomerization of pro-apoptotic Bcl-2 family proteins, ceramide channel, and reduces anti-apoptotic Bcl-2 proteins in the MOM.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	51-56
25766330-4	2015	The elevated CerS6 activity resulted in accumulation of the pro-apoptotic C16 : 0 ceramide, which facilitates the mitochondrial apoptosis in response to oxidative stress.	Ceramides	82-90	ceramide synthase 6	Homo sapiens	13-18
25627684-7	2015	Pharmacologic inhibition of ceramide synthesis increased cellular sphingosine and S1P but not medium S1P in both apoM(WT) and apoM(Q22A) hepatocytes.	Ceramides	28-36	sphingosine-1-phosphate receptor 1	Mus musculus	82-85
25627684-7	2015	Pharmacologic inhibition of ceramide synthesis increased cellular sphingosine and S1P but not medium S1P in both apoM(WT) and apoM(Q22A) hepatocytes.	Ceramides	28-36	apolipoprotein M	Mus musculus	118-120
25656578-3	2015	Apoptosis, that was suppressed in both cases by inhibition of caspase-9, but not of caspase-8, associated with a higher intracellular accumulation of C6-Cer over C2-Cer, notwithstanding C6-Cer was actively metabolized by direct glucosylation or by conversion to natural ceramide via the sphingosine salvage pathway, whereas C2-Cer was apparently metabolically inhert.	Ceramides	270-278	caspase 9	Homo sapiens	62-71
25751724-5	2015	Ceramide enhances oligomerization of pro-apoptotic Bcl-2 family proteins, ceramide channel, and reduces anti-apoptotic Bcl-2 proteins in the MOM.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	119-124
25751724-9	2015	Crosstalk between Bcl-2 family proteins, ROS, and many signaling pathways regulates ceramide-induced apoptosis.	Ceramides	84-92	BCL2 apoptosis regulator	Homo sapiens	18-23
26045781-8	2015	The activity of SphK1 in resveratrol treated groups was decreased compared to control group with a significant decrease of S1P and increase of ceramide level.	Ceramides	143-151	sphingosine kinase 1	Homo sapiens	16-21
25134969-10	2015	Sulforaphane (100 muM) significantly increased ceramide formation.	Ceramides	47-55	latexin	Homo sapiens	18-21
25424644-8	2015	SMPD3 is localized in the plasma membrane and has been shown to cleave sphingomyelin to generate ceramide, a bioactive lipid second messenger, and phosphocholine, an essential nutrient.	Ceramides	97-105	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	0-5
25576381-1	2015	Here we reported that co-administration of docetaxel and a cell-permeable short-chain ceramide (C6) resulted in a striking increase in growth inhibition and apoptosis in primary and transformed breast cells (MCF-7 and MDA-231), which were associated with mitochondrial permeability transition pore (mPTP) opening, a significant reactive oxygen species (ROS) production and the pro-apoptotic AMP-Protein Kinase (AMPK) as well as c-Jun N-terminal kinases (JNK) activations.	Ceramides	86-94	mitogen-activated protein kinase 8	Homo sapiens	428-452
25576381-1	2015	Here we reported that co-administration of docetaxel and a cell-permeable short-chain ceramide (C6) resulted in a striking increase in growth inhibition and apoptosis in primary and transformed breast cells (MCF-7 and MDA-231), which were associated with mitochondrial permeability transition pore (mPTP) opening, a significant reactive oxygen species (ROS) production and the pro-apoptotic AMP-Protein Kinase (AMPK) as well as c-Jun N-terminal kinases (JNK) activations.	Ceramides	86-94	mitogen-activated protein kinase 8	Homo sapiens	454-457
25576381-5	2015	Significantly, C6 ceramide plus docetaxel caused dramatic human epidermal growth factor receptor (HER)-1/-2 degradation and downstream Akt/Erk inhibition in HER-2 expressing MDA-231 cells.	Ceramides	18-26	epidermal growth factor receptor	Homo sapiens	64-104
25576381-5	2015	Significantly, C6 ceramide plus docetaxel caused dramatic human epidermal growth factor receptor (HER)-1/-2 degradation and downstream Akt/Erk inhibition in HER-2 expressing MDA-231 cells.	Ceramides	18-26	AKT serine/threonine kinase 1	Homo sapiens	135-138
25576381-5	2015	Significantly, C6 ceramide plus docetaxel caused dramatic human epidermal growth factor receptor (HER)-1/-2 degradation and downstream Akt/Erk inhibition in HER-2 expressing MDA-231 cells.	Ceramides	18-26	mitogen-activated protein kinase 1	Homo sapiens	139-142
25576381-5	2015	Significantly, C6 ceramide plus docetaxel caused dramatic human epidermal growth factor receptor (HER)-1/-2 degradation and downstream Akt/Erk inhibition in HER-2 expressing MDA-231 cells.	Ceramides	18-26	erb-b2 receptor tyrosine kinase 2	Homo sapiens	157-162
26045781-10	2015	Resveratrol-induced proliferation inhibition of K562 cells might be mediated through its modulation activity of SphK1 pathway by regulating S1P and ceramide levels, which then affected the proliferation and apoptosis process of leukemia cells.	Ceramides	148-156	sphingosine kinase 1	Homo sapiens	112-117
25603047-0	2015	Type II anti-CD20 mAb-induced lysosome mediated cell death is mediated through a ceramide-dependent pathway.	Ceramides	81-89	keratin 20	Homo sapiens	13-17
25605874-9	2015	Moreover, we measured CPE synthase Km and Vmax for SMS1, SMS2, and SMSr using different NBD ceramides.	Ceramides	92-101	sterile alpha motif domain containing 8	Mus musculus	22-34
25527700-5	2015	METHODS AND RESULTS: We found that CD28(null) T cells in ACS were resistant to apoptosis induction via Fas-ligation or ceramide.	Ceramides	119-127	CD28 molecule	Homo sapiens	35-39
26065260-1	2015	Sphingomyelin synthase 1 (SMS1) is an enzyme of vital importance which is responsible for the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide in eukaryotic cells.	Ceramides	169-177	sphingomyelin synthase 1	Homo sapiens	0-24
26065260-1	2015	Sphingomyelin synthase 1 (SMS1) is an enzyme of vital importance which is responsible for the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide in eukaryotic cells.	Ceramides	169-177	sphingomyelin synthase 1	Homo sapiens	26-30
25889812-2	2015	This process is regulated by a complex molecular network including protein kinase D (PKD), which is directly involved in the fission of transport vesicles, and its interaction with the ceramide transfer protein CERT that transports ceramide from the endoplasmic reticulum to the TGN.	Ceramides	185-193	protein kinase D1	Homo sapiens	67-83
25889812-2	2015	This process is regulated by a complex molecular network including protein kinase D (PKD), which is directly involved in the fission of transport vesicles, and its interaction with the ceramide transfer protein CERT that transports ceramide from the endoplasmic reticulum to the TGN.	Ceramides	185-193	protein kinase D1	Homo sapiens	85-88
25889812-2	2015	This process is regulated by a complex molecular network including protein kinase D (PKD), which is directly involved in the fission of transport vesicles, and its interaction with the ceramide transfer protein CERT that transports ceramide from the endoplasmic reticulum to the TGN.	Ceramides	185-193	ceramide transporter 1	Homo sapiens	211-215
25889812-5	2015	CONCLUSIONS: Our quantitative predictions of absolute molecular concentrations and reaction fluxes have major biological implications: Model comparison provides evidence that PKD and CERT interact in a cooperative manner to regulate ceramide transfer.	Ceramides	233-241	protein kinase D1	Homo sapiens	175-178
25889812-5	2015	CONCLUSIONS: Our quantitative predictions of absolute molecular concentrations and reaction fluxes have major biological implications: Model comparison provides evidence that PKD and CERT interact in a cooperative manner to regulate ceramide transfer.	Ceramides	233-241	ceramide transporter 1	Homo sapiens	183-187
25889812-6	2015	Furthermore, we identify active PKD to be the dominant regulator of the network, especially of CERT-mediated ceramide transfer.	Ceramides	109-117	protein kinase D1	Homo sapiens	32-35
25889812-6	2015	Furthermore, we identify active PKD to be the dominant regulator of the network, especially of CERT-mediated ceramide transfer.	Ceramides	109-117	ceramide transporter 1	Homo sapiens	95-99
25603047-4	2015	Herein, we reveal that the induction of ceramide generation by anti-CD20 mAbs directly correlates with their ability to induce PCD.	Ceramides	40-48	keratin 20	Homo sapiens	68-72
25603047-7	2015	These findings provide further insights into a previously unrecognized role for ceramide generation in mediating PCD evoked by type II anti-CD20 mAbs in Burkitt"s lymphoma cells.	Ceramides	80-88	keratin 20	Homo sapiens	140-144
25168245-8	2015	In addition, the depletion of MAPK8/9 or SMPD2 by RNAi knockdown decreased ceramide generation and stress- and cytokine-induced apoptosis in Jurkat cells.	Ceramides	75-83	mitogen-activated protein kinase 8	Homo sapiens	30-37
25354528-8	2015	To determine whether palmitate-induced ceramide accumulation contributed to this finding, we overexpressed a ceramide-metabolizing enzyme, acid ceramidase.	Ceramides	39-47	N-acylsphingosine amidohydrolase 1	Homo sapiens	139-154
25354528-8	2015	To determine whether palmitate-induced ceramide accumulation contributed to this finding, we overexpressed a ceramide-metabolizing enzyme, acid ceramidase.	Ceramides	109-117	N-acylsphingosine amidohydrolase 1	Homo sapiens	139-154
25168245-0	2015	Stress-induced ceramide generation and apoptosis via the phosphorylation and activation of nSMase1 by JNK signaling.	Ceramides	15-23	sphingomyelin phosphodiesterase 2	Homo sapiens	91-98
25168245-0	2015	Stress-induced ceramide generation and apoptosis via the phosphorylation and activation of nSMase1 by JNK signaling.	Ceramides	15-23	mitogen-activated protein kinase 8	Homo sapiens	102-105
25168245-8	2015	In addition, the depletion of MAPK8/9 or SMPD2 by RNAi knockdown decreased ceramide generation and stress- and cytokine-induced apoptosis in Jurkat cells.	Ceramides	75-83	sphingomyelin phosphodiesterase 2	Homo sapiens	41-46
25168245-1	2015	Neutral sphingomyelinase (nSMase) activation in response to environmental stress or inflammatory cytokine stimuli generates the second messenger ceramide, which mediates the stress-induced apoptosis.	Ceramides	145-153	sphingomyelin phosphodiesterase 2	Homo sapiens	0-24
25168245-1	2015	Neutral sphingomyelinase (nSMase) activation in response to environmental stress or inflammatory cytokine stimuli generates the second messenger ceramide, which mediates the stress-induced apoptosis.	Ceramides	145-153	sphingomyelin phosphodiesterase 2	Homo sapiens	26-32
25168245-3	2015	Here we show that the phosphorylation of nSMase1 (sphingomyelin phosphodiesterase 2, SMPD2) by c-Jun N-terminal kinase (JNK) signaling stimulates ceramide generation and apoptosis and provide evidence for a signaling mechanism that integrates stress- and cytokine-activated apoptosis in vertebrate cells.	Ceramides	146-154	sphingomyelin phosphodiesterase 2	Homo sapiens	41-48
25168245-9	2015	Therefore the phosphorylation of nSMase1 is a pivotal step in JNK signaling, which leads to ceramide generation and apoptosis under stress conditions and in response to cytokine stimulation.	Ceramides	92-100	sphingomyelin phosphodiesterase 2	Homo sapiens	33-40
25168245-3	2015	Here we show that the phosphorylation of nSMase1 (sphingomyelin phosphodiesterase 2, SMPD2) by c-Jun N-terminal kinase (JNK) signaling stimulates ceramide generation and apoptosis and provide evidence for a signaling mechanism that integrates stress- and cytokine-activated apoptosis in vertebrate cells.	Ceramides	146-154	sphingomyelin phosphodiesterase 2	Homo sapiens	50-83
25168245-3	2015	Here we show that the phosphorylation of nSMase1 (sphingomyelin phosphodiesterase 2, SMPD2) by c-Jun N-terminal kinase (JNK) signaling stimulates ceramide generation and apoptosis and provide evidence for a signaling mechanism that integrates stress- and cytokine-activated apoptosis in vertebrate cells.	Ceramides	146-154	sphingomyelin phosphodiesterase 2	Homo sapiens	85-90
25168245-3	2015	Here we show that the phosphorylation of nSMase1 (sphingomyelin phosphodiesterase 2, SMPD2) by c-Jun N-terminal kinase (JNK) signaling stimulates ceramide generation and apoptosis and provide evidence for a signaling mechanism that integrates stress- and cytokine-activated apoptosis in vertebrate cells.	Ceramides	146-154	mitogen-activated protein kinase 8	Homo sapiens	95-118
25168245-9	2015	Therefore the phosphorylation of nSMase1 is a pivotal step in JNK signaling, which leads to ceramide generation and apoptosis under stress conditions and in response to cytokine stimulation.	Ceramides	92-100	mitogen-activated protein kinase 8	Homo sapiens	62-65
25168245-3	2015	Here we show that the phosphorylation of nSMase1 (sphingomyelin phosphodiesterase 2, SMPD2) by c-Jun N-terminal kinase (JNK) signaling stimulates ceramide generation and apoptosis and provide evidence for a signaling mechanism that integrates stress- and cytokine-activated apoptosis in vertebrate cells.	Ceramides	146-154	mitogen-activated protein kinase 8	Homo sapiens	120-123
25168245-6	2015	The JNK inhibitor SP600125 blocked the phosphorylation and activation of nSMase1, which in turn blocked ceramide signaling and apoptosis.	Ceramides	104-112	mitogen-activated protein kinase 8	Homo sapiens	4-7
25168245-10	2015	nSMase1 has a common central role in ceramide signaling during the stress and cytokine responses and apoptosis.	Ceramides	37-45	sphingomyelin phosphodiesterase 2	Homo sapiens	0-7
25168245-6	2015	The JNK inhibitor SP600125 blocked the phosphorylation and activation of nSMase1, which in turn blocked ceramide signaling and apoptosis.	Ceramides	104-112	sphingomyelin phosphodiesterase 2	Homo sapiens	73-80
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.	Ceramides	0-8	glucosylceramidase beta	Homo sapiens	59-62
25168245-7	2015	A variety of stress conditions, including heat shock, UV exposure, hydrogen peroxide treatment, and anti-Fas antibody stimulation, led to the phosphorylation of nSMase1, activated nSMase1, and induced ceramide generation and apoptosis in zebrafish embryonic ZE and human Jurkat T cells.	Ceramides	201-209	sphingomyelin phosphodiesterase 2a	Danio rerio	161-168
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.	Ceramides	0-8	glucosylceramidase beta	Homo sapiens	191-194
25635851-10	2015	We suggest pivotal role of transporters in facilitating fatty acid influx (FATP2), accumulation of ceramides (CERT) and export to the media (MTP and ABCA1).	Ceramides	99-108	microsomal triglyceride transfer protein	Rattus norvegicus	141-144
25465297-2	2015	In this review, we focus on the roles and regulation of neutral sphingomyelinase 2 (nSMase2), an enzyme that generates the bioactive lipid ceramide through the hydrolysis of the membrane lipid sphingomyelin.	Ceramides	139-147	sphingomyelin phosphodiesterase 3	Homo sapiens	56-82
25429105-4	2015	Proper formation of ceramides by CerS has been shown previously to require the Cka2 subunit of casein kinase 2 (CK2), a ubiquitous enzyme with multiple cellular functions, but the precise mechanism involved has remained unidentified.	Ceramides	20-29	casein kinase 2 catalytic subunit CKA2	Saccharomyces cerevisiae S288C	79-83
25395373-2	2015	Ceramide hydrolysis by acid ceramidase (AC) stops the biological activity of these substances and influences survival and function of normal and neoplastic cells.	Ceramides	0-8	N-acylsphingosine amidohydrolase 1	Homo sapiens	23-38
25395373-2	2015	Ceramide hydrolysis by acid ceramidase (AC) stops the biological activity of these substances and influences survival and function of normal and neoplastic cells.	Ceramides	0-8	N-acylsphingosine amidohydrolase 1	Homo sapiens	40-42
25395373-3	2015	Because of its central role in the ceramide metabolism, AC may offer a novel molecular target in disorders with dysfunctional ceramide-mediated signaling.	Ceramides	35-43	N-acylsphingosine amidohydrolase 1	Homo sapiens	56-58
25395373-3	2015	Because of its central role in the ceramide metabolism, AC may offer a novel molecular target in disorders with dysfunctional ceramide-mediated signaling.	Ceramides	126-134	N-acylsphingosine amidohydrolase 1	Homo sapiens	56-58
25300478-9	2015	Cytotoxic effects of DHA were attenuated by co-treatment with myriocin, a selective inhibitor of serine palmitoyl transferase (SPT), preventing de novo ceramide biosynthesis.	Ceramides	152-160	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	97-125
25300478-9	2015	Cytotoxic effects of DHA were attenuated by co-treatment with myriocin, a selective inhibitor of serine palmitoyl transferase (SPT), preventing de novo ceramide biosynthesis.	Ceramides	152-160	alanine--glyoxylate and serine--pyruvate aminotransferase	Rattus norvegicus	127-130
25300478-12	2015	We further demonstrate that CYP oxidase metabolites of DHA, methyl epoxy docosapentaenoate (EDP methyl esters, 1muM) (mix 1:1:1:1:1:1; 4,5-, 7,8-, 10,11-, 13,14-, 16,17- and 19,20-EDP methyl esters) and 19,20-EDP cause cytotoxicity via activation of PPARdelta signaling leading to increased levels of intracellular ceramide.	Ceramides	315-323	cytochrome P450, family 2, subfamily g, polypeptide 1	Rattus norvegicus	28-31
25384187-2	2015	SphK is a key regulator of S1P and the S1P:Sph/ceramide ratio.	Ceramides	47-55	sphingosine kinase 1	Homo sapiens	0-4
25465297-2	2015	In this review, we focus on the roles and regulation of neutral sphingomyelinase 2 (nSMase2), an enzyme that generates the bioactive lipid ceramide through the hydrolysis of the membrane lipid sphingomyelin.	Ceramides	139-147	sphingomyelin phosphodiesterase 3	Homo sapiens	84-91
25380816-0	2015	Akt/eNOS signaling pathway mediates inhibition of endothelial progenitor cells by palmitate-induced ceramide.	Ceramides	100-108	AKT serine/threonine kinase 1	Homo sapiens	0-3
25436917-0	2015	Downregulation of adipose triglyceride lipase promotes cardiomyocyte hypertrophy by triggering the accumulation of ceramides.	Ceramides	115-124	patatin-like phospholipase domain containing 2	Mus musculus	18-45
25436917-6	2015	In addition, ATGL downregulation increased but ATGL overexpression reduced the contents of ceramide, which has been proved to be closely associated with cardiac hypertrophy.	Ceramides	91-99	patatin-like phospholipase domain containing 2	Mus musculus	47-51
25436917-7	2015	Moreover, the accumulation of ceramide was due to elevation of free fatty acids in ATGL-knockdown cardiomyocytes, which could be explained by the reduced activity of peroxisome proliferator-activated receptor (PPAR) alpha leading to imbalance of fatty acid uptake and oxidation.	Ceramides	30-38	patatin-like phospholipase domain containing 2	Mus musculus	83-87
25436917-7	2015	Moreover, the accumulation of ceramide was due to elevation of free fatty acids in ATGL-knockdown cardiomyocytes, which could be explained by the reduced activity of peroxisome proliferator-activated receptor (PPAR) alpha leading to imbalance of fatty acid uptake and oxidation.	Ceramides	30-38	peroxisome proliferator activated receptor alpha	Mus musculus	166-221
25436917-8	2015	These observations suggest that downregulation of ATGL causes the decreased PPARalpha activity which results in the imbalance of FA uptake and oxidation, elevating intracellular FFA contents to promote the accumulation of ceramides, and finally inducing cardiac hypertrophy.	Ceramides	222-231	patatin-like phospholipase domain containing 2	Mus musculus	50-54
25436917-8	2015	These observations suggest that downregulation of ATGL causes the decreased PPARalpha activity which results in the imbalance of FA uptake and oxidation, elevating intracellular FFA contents to promote the accumulation of ceramides, and finally inducing cardiac hypertrophy.	Ceramides	222-231	peroxisome proliferator activated receptor alpha	Mus musculus	76-85
25814122-9	2015	A possible means of counteracting ceramide action would be to prevent the accumulation of the specific ceramide species involved in both insulin resistance and beta-cell apoptosis/dysfunction.	Ceramides	34-42	insulin	Homo sapiens	137-144
24796972-6	2015	Lipidomics analysis identified seven lipid markers including lysophosphatidylcholines, phosphatidylcholines, sphingomyelins and ceramides that were significantly decreased in serum of HFD-fed CYP7A1-tg mice.	Ceramides	128-137	cytochrome P450, family 7, subfamily a, polypeptide 1	Mus musculus	192-198
26488284-9	2015	CONCLUSION: Palmitate-induced alteration in the stoichiometric ratio of mitochondrial CPT isoforms leads to incomplete FAO and enhanced cytosolic ceramide accumulation that lead to insulin resistance.	Ceramides	146-154	insulin	Homo sapiens	181-188
26488284-10	2015	Fenofibrate ameliorated insulin resistance by restoring the altered stoichiometry by upregulating CPT2 and preventing, cytoplasmic ceramide accumulation.	Ceramides	131-139	insulin	Homo sapiens	24-31
26510981-4	2015	We found that ABCA2 overexpression in N2a cells was associated with increased mass of the sphingolipid sphingosine, derived from the catabolism of ceramide.	Ceramides	147-155	ATP-binding cassette, sub-family A (ABC1), member 2	Mus musculus	14-19
26390620-4	2015	N-acetylcysteine as well as specific neutral sphingomyelinase (nSMase) inhibitor--GW4869, decreases ceramide content and increases GSH level, and enhances the insulin-induced [3H-D-glucose uptake in the "aged" tissue.	Ceramides	100-108	sphingomyelin phosphodiesterase 2	Rattus norvegicus	37-61
26390620-4	2015	N-acetylcysteine as well as specific neutral sphingomyelinase (nSMase) inhibitor--GW4869, decreases ceramide content and increases GSH level, and enhances the insulin-induced [3H-D-glucose uptake in the "aged" tissue.	Ceramides	100-108	sphingomyelin phosphodiesterase 2	Rattus norvegicus	63-69
26390620-5	2015	These data indicate that nSMase play important role in the age- and drug-induced ceramide-dependent insuline resistance.	Ceramides	81-89	sphingomyelin phosphodiesterase 2	Rattus norvegicus	25-31
25814122-9	2015	A possible means of counteracting ceramide action would be to prevent the accumulation of the specific ceramide species involved in both insulin resistance and beta-cell apoptosis/dysfunction.	Ceramides	103-111	insulin	Homo sapiens	137-144
25720409-0	2015	The 5XFAD Mouse Model of Alzheimer"s Disease Exhibits an Age-Dependent Increase in Anti-Ceramide IgG and Exogenous Administration of Ceramide Further Increases Anti-Ceramide Titers and Amyloid Plaque Burden.	Ceramides	88-96	renin binding protein	Mus musculus	57-60
26089893-9	2015	Doxorubicin-induced hepatocytes resistance to insulin action could be abolished by inhibition of ceramide production.	Ceramides	97-105	insulin	Homo sapiens	46-53
25720409-1	2015	We present evidence that 5XFAD Alzheimer"s disease model mice develop an age-dependent increase in antibodies against ceramide, suggesting involvement of autoimmunity against ceramide in Alzheimer"s disease pathology.	Ceramides	118-126	renin binding protein	Mus musculus	73-76
26089893-14	2015	PLD is activated downstream of PI3-kinase and Akt and is highly sensitive to ceramide content in the liver cells.	Ceramides	77-85	glycosylphosphatidylinositol specific phospholipase D1	Homo sapiens	0-3
26380311-0	2015	Inhibition of Ceramide De Novo Synthesis Ameliorates Diet Induced Skeletal Muscles Insulin Resistance.	Ceramides	14-22	insulin	Homo sapiens	83-90
25500885-7	2015	The reduction of ceramide levels in the ileum and serum in tempol- or antibiotic-treated mice fed a HFD resulted in downregulation of hepatic SREBP1C and decreased de novo lipogenesis.	Ceramides	17-25	sterol regulatory element binding transcription factor 1	Mus musculus	142-149
25720409-1	2015	We present evidence that 5XFAD Alzheimer"s disease model mice develop an age-dependent increase in antibodies against ceramide, suggesting involvement of autoimmunity against ceramide in Alzheimer"s disease pathology.	Ceramides	175-183	renin binding protein	Mus musculus	73-76
25720409-5	2015	Ceramide-treated mice showed an increase of serum exosomes (up to 3-fold using Alix as marker), suggesting that systemic anti-ceramide IgG and exosome levels are correlated with enhanced plaque formation.	Ceramides	0-8	programmed cell death 6 interacting protein	Mus musculus	79-83
25173968-2	2015	Sortilin trafficking of acid sphingomyelinase (aSMase) may regulate ceramide levels, a major modulator of insulin signalling.	Ceramides	68-76	sortilin 1	Mus musculus	0-8
25173968-2	2015	Sortilin trafficking of acid sphingomyelinase (aSMase) may regulate ceramide levels, a major modulator of insulin signalling.	Ceramides	68-76	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	24-45
25173968-2	2015	Sortilin trafficking of acid sphingomyelinase (aSMase) may regulate ceramide levels, a major modulator of insulin signalling.	Ceramides	68-76	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	47-53
25173968-6	2015	Sortilin deficiency led to attenuated hepatic steatosis, reduced expression of genes involved in lipogenesis, ceramide synthesis and inflammatory cytokine production and reduced activity of ceramide synthase 5/6 (CerS5/6).	Ceramides	110-118	sortilin 1	Mus musculus	0-8
25281863-0	2015	Acid sphingomyelinase-ceramide system in steatohepatitis: a novel target regulating multiple pathways.	Ceramides	22-30	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
25281863-4	2015	Here we discuss emerging data indicating that the acid sphingomyelinase (ASMase), a specific mechanism of ceramide generation, is required for the activation of key pathways that regulate steatosis, fibrosis and lipotoxicity, including endoplasmic reticulum stress, autophagy and lysosomal membrane permeabilization.	Ceramides	106-114	sphingomyelin phosphodiesterase 1	Homo sapiens	50-71
25281863-4	2015	Here we discuss emerging data indicating that the acid sphingomyelinase (ASMase), a specific mechanism of ceramide generation, is required for the activation of key pathways that regulate steatosis, fibrosis and lipotoxicity, including endoplasmic reticulum stress, autophagy and lysosomal membrane permeabilization.	Ceramides	106-114	sphingomyelin phosphodiesterase 1	Homo sapiens	73-79
25403920-3	2015	Ceramides are synthesized by ceramide synthases, of which there are six isoforms in mammals (CERS1-6).	Ceramides	0-9	ceramide synthase 1	Homo sapiens	93-98
25395359-2	2015	In another form of diet-dependent obesity, high-fat-fed mice, hepatic insulin resistance involves ceramide-induced activation of atypical protein kinase C (aPKC), which selectively impairs protein kinase B (Akt)-dependent forkhead box O1 protein (FoxO1) phosphorylation on scaffolding protein, 40 kDa WD(tryp-x-x-asp)-repeat propeller/FYVE protein (WD40/ProF), thereby increasing gluconeogenesis.	Ceramides	98-106	protein kinase C, zeta	Mus musculus	129-154
25395359-2	2015	In another form of diet-dependent obesity, high-fat-fed mice, hepatic insulin resistance involves ceramide-induced activation of atypical protein kinase C (aPKC), which selectively impairs protein kinase B (Akt)-dependent forkhead box O1 protein (FoxO1) phosphorylation on scaffolding protein, 40 kDa WD(tryp-x-x-asp)-repeat propeller/FYVE protein (WD40/ProF), thereby increasing gluconeogenesis.	Ceramides	98-106	protein kinase C, zeta	Mus musculus	156-160
25395359-2	2015	In another form of diet-dependent obesity, high-fat-fed mice, hepatic insulin resistance involves ceramide-induced activation of atypical protein kinase C (aPKC), which selectively impairs protein kinase B (Akt)-dependent forkhead box O1 protein (FoxO1) phosphorylation on scaffolding protein, 40 kDa WD(tryp-x-x-asp)-repeat propeller/FYVE protein (WD40/ProF), thereby increasing gluconeogenesis.	Ceramides	98-106	thymoma viral proto-oncogene 1	Mus musculus	207-210
25395359-2	2015	In another form of diet-dependent obesity, high-fat-fed mice, hepatic insulin resistance involves ceramide-induced activation of atypical protein kinase C (aPKC), which selectively impairs protein kinase B (Akt)-dependent forkhead box O1 protein (FoxO1) phosphorylation on scaffolding protein, 40 kDa WD(tryp-x-x-asp)-repeat propeller/FYVE protein (WD40/ProF), thereby increasing gluconeogenesis.	Ceramides	98-106	forkhead box O1	Mus musculus	222-237
25395359-2	2015	In another form of diet-dependent obesity, high-fat-fed mice, hepatic insulin resistance involves ceramide-induced activation of atypical protein kinase C (aPKC), which selectively impairs protein kinase B (Akt)-dependent forkhead box O1 protein (FoxO1) phosphorylation on scaffolding protein, 40 kDa WD(tryp-x-x-asp)-repeat propeller/FYVE protein (WD40/ProF), thereby increasing gluconeogenesis.	Ceramides	98-106	forkhead box O1	Mus musculus	247-252
25395359-8	2015	In conclusion, hepatic ceramide accumulates in response to CNS-dependent dietary excess irrespective of fat content; hepatic insulin resistance is prominent in ob/ob mice and involves aPKC-dependent displacement of Akt fromWD40/ProF and subsequent impairment of FoxO1 phosphorylation and increased expression of hepatic gluconeogenic and lipogenic enzymes; and hepatic alterations diminish insulin signaling in muscle.	Ceramides	23-31	protein kinase C, zeta	Mus musculus	184-188
25395359-8	2015	In conclusion, hepatic ceramide accumulates in response to CNS-dependent dietary excess irrespective of fat content; hepatic insulin resistance is prominent in ob/ob mice and involves aPKC-dependent displacement of Akt fromWD40/ProF and subsequent impairment of FoxO1 phosphorylation and increased expression of hepatic gluconeogenic and lipogenic enzymes; and hepatic alterations diminish insulin signaling in muscle.	Ceramides	23-31	thymoma viral proto-oncogene 1	Mus musculus	215-218
25395359-8	2015	In conclusion, hepatic ceramide accumulates in response to CNS-dependent dietary excess irrespective of fat content; hepatic insulin resistance is prominent in ob/ob mice and involves aPKC-dependent displacement of Akt fromWD40/ProF and subsequent impairment of FoxO1 phosphorylation and increased expression of hepatic gluconeogenic and lipogenic enzymes; and hepatic alterations diminish insulin signaling in muscle.	Ceramides	23-31	forkhead box O1	Mus musculus	262-267
26226958-6	2015	Here, we report a versatile synthetic method for hexacosanoic acid (1) and the ceramide 2 containing the fatty acid 1.	Ceramides	79-87	mediator complex subunit 25	Homo sapiens	111-117
25403920-10	2015	Using this approach, we show that CERS2 demonstrates a preference for the monounsaturated C24:1 fatty acid substrate compared to the saturated C24:0 substrate, potentially explaining why myelin is enriched in ceramides containing the monounsaturated form of very long chain fatty acids.	Ceramides	209-218	ceramide synthase 2	Homo sapiens	34-39
26684792-6	2015	We have recently discovered that an inhibition of the acid sphingomyelinase/ceramide system mediates the effects of tri- and tetracyclic antidepressants.	Ceramides	76-84	sphingomyelin phosphodiesterase 1	Homo sapiens	54-75
25131496-1	2015	Acid ceramidase (ASAH1) a key enzyme of sphingolipid metabolism converting pro-apoptotic ceramide to sphingosine has been shown to be overexpressed in various cancers.	Ceramides	89-97	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-15
25131496-1	2015	Acid ceramidase (ASAH1) a key enzyme of sphingolipid metabolism converting pro-apoptotic ceramide to sphingosine has been shown to be overexpressed in various cancers.	Ceramides	89-97	N-acylsphingosine amidohydrolase 1	Homo sapiens	17-22
26609196-6	2015	The very long fatty acids C24:0 and C24:1 are the main ceramide components of LacCer in neutrophil plasma membranes and are directly connected with the fatty acids of Lyn and Galphai.	Ceramides	55-63	LYN proto-oncogene, Src family tyrosine kinase	Homo sapiens	167-170
26609196-7	2015	These observations suggest that the very long fatty acid chains of ceramide are critical for GSL-mediated outside-in signaling.	Ceramides	67-75	cathepsin A	Homo sapiens	93-96
25378587-7	2015	ASMase activation increases cellular ceramide, which promotes tubulin acetylation on stabilized microtubules.	Ceramides	37-45	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	0-6
25394686-2	2015	In the present study, we examined the effects of sphingomyelin phosphodiesterase 3 (SMPD3), which generates ceramide from sphingomyelin, on the release of small/microRNAs from intracellular to extracellular spaces.	Ceramides	108-116	sphingomyelin phosphodiesterase 3	Homo sapiens	49-82
25394686-2	2015	In the present study, we examined the effects of sphingomyelin phosphodiesterase 3 (SMPD3), which generates ceramide from sphingomyelin, on the release of small/microRNAs from intracellular to extracellular spaces.	Ceramides	108-116	sphingomyelin phosphodiesterase 3	Homo sapiens	84-89
26090071-0	2015	Ceramides in Alzheimer"s Disease: Key Mediators of Neuronal Apoptosis Induced by Oxidative Stress and Abeta Accumulation.	Ceramides	0-9	amyloid beta precursor protein	Homo sapiens	102-107
26090071-2	2015	Ceramides, the major molecules of sphingolipid metabolism and lipid second messengers, have been associated with AD progression and pathology via Abeta generation.	Ceramides	0-9	amyloid beta precursor protein	Homo sapiens	146-151
26090071-3	2015	Enhanced levels of ceramides directly increase Abeta through stabilization of beta-secretase, the key enzyme in the amyloidogenic processing of Abeta precursor protein (APP).	Ceramides	19-28	amyloid beta precursor protein	Homo sapiens	47-52
26090071-4	2015	As a positive feedback loop, the generated oligomeric and fibrillar Abeta induces a further increase in ceramide levels by activating sphingomyelinases that catalyze the catabolic breakdown of sphingomyelin to ceramide.	Ceramides	104-112	amyloid beta precursor protein	Homo sapiens	68-73
26090071-4	2015	As a positive feedback loop, the generated oligomeric and fibrillar Abeta induces a further increase in ceramide levels by activating sphingomyelinases that catalyze the catabolic breakdown of sphingomyelin to ceramide.	Ceramides	210-218	amyloid beta precursor protein	Homo sapiens	68-73
26090071-6	2015	Ceramides may initiate a cascade of biochemical alterations, which ultimately leads to neuronal death by diverse mechanisms, including depolarization and permeabilization of mitochondria, increased production of reactive oxygen species (ROS), cytochrome c release, Bcl-2 depletion, and caspase-3 activation, mainly by modulating intracellular signalling, particularly along the pathways related to Akt/PKB kinase and mitogen-activated protein kinases (MAPKs).	Ceramides	0-9	cytochrome c, somatic	Homo sapiens	243-255
26090071-6	2015	Ceramides may initiate a cascade of biochemical alterations, which ultimately leads to neuronal death by diverse mechanisms, including depolarization and permeabilization of mitochondria, increased production of reactive oxygen species (ROS), cytochrome c release, Bcl-2 depletion, and caspase-3 activation, mainly by modulating intracellular signalling, particularly along the pathways related to Akt/PKB kinase and mitogen-activated protein kinases (MAPKs).	Ceramides	0-9	BCL2 apoptosis regulator	Homo sapiens	265-270
26090071-6	2015	Ceramides may initiate a cascade of biochemical alterations, which ultimately leads to neuronal death by diverse mechanisms, including depolarization and permeabilization of mitochondria, increased production of reactive oxygen species (ROS), cytochrome c release, Bcl-2 depletion, and caspase-3 activation, mainly by modulating intracellular signalling, particularly along the pathways related to Akt/PKB kinase and mitogen-activated protein kinases (MAPKs).	Ceramides	0-9	caspase 3	Homo sapiens	286-295
26090071-6	2015	Ceramides may initiate a cascade of biochemical alterations, which ultimately leads to neuronal death by diverse mechanisms, including depolarization and permeabilization of mitochondria, increased production of reactive oxygen species (ROS), cytochrome c release, Bcl-2 depletion, and caspase-3 activation, mainly by modulating intracellular signalling, particularly along the pathways related to Akt/PKB kinase and mitogen-activated protein kinases (MAPKs).	Ceramides	0-9	AKT serine/threonine kinase 1	Homo sapiens	398-401
26090071-6	2015	Ceramides may initiate a cascade of biochemical alterations, which ultimately leads to neuronal death by diverse mechanisms, including depolarization and permeabilization of mitochondria, increased production of reactive oxygen species (ROS), cytochrome c release, Bcl-2 depletion, and caspase-3 activation, mainly by modulating intracellular signalling, particularly along the pathways related to Akt/PKB kinase and mitogen-activated protein kinases (MAPKs).	Ceramides	0-9	AKT serine/threonine kinase 1	Homo sapiens	402-405
25482956-5	2015	Furthermore, SCD4, a heart-specific isoform of SCD, is specifically repressed by leptin and the lack of SCD1 function in leptin-deficient ob/ob mice results in a decrease in the accumulation of neutral lipids and ceramide and improves the systolic and diastolic function of a failing heart.	Ceramides	213-221	stearoyl-coenzyme A desaturase 4	Mus musculus	13-17
26605090-3	2015	Besides its well-known property as a selective serotonin reuptake inhibitor, fluoxetine has been reported to inhibit the acid sphingomyelinase (ASM), a key regulator of ceramide levels which derives ceramide from sphingomyelin.	Ceramides	169-177	sphingomyelin phosphodiesterase 1	Homo sapiens	121-142
26605090-3	2015	Besides its well-known property as a selective serotonin reuptake inhibitor, fluoxetine has been reported to inhibit the acid sphingomyelinase (ASM), a key regulator of ceramide levels which derives ceramide from sphingomyelin.	Ceramides	169-177	sphingomyelin phosphodiesterase 1	Homo sapiens	144-147
26605090-3	2015	Besides its well-known property as a selective serotonin reuptake inhibitor, fluoxetine has been reported to inhibit the acid sphingomyelinase (ASM), a key regulator of ceramide levels which derives ceramide from sphingomyelin.	Ceramides	199-207	sphingomyelin phosphodiesterase 1	Homo sapiens	121-142
26605090-3	2015	Besides its well-known property as a selective serotonin reuptake inhibitor, fluoxetine has been reported to inhibit the acid sphingomyelinase (ASM), a key regulator of ceramide levels which derives ceramide from sphingomyelin.	Ceramides	199-207	sphingomyelin phosphodiesterase 1	Homo sapiens	144-147
25482956-5	2015	Furthermore, SCD4, a heart-specific isoform of SCD, is specifically repressed by leptin and the lack of SCD1 function in leptin-deficient ob/ob mice results in a decrease in the accumulation of neutral lipids and ceramide and improves the systolic and diastolic function of a failing heart.	Ceramides	213-221	stearoyl-Coenzyme A desaturase 1	Mus musculus	13-16
25482956-5	2015	Furthermore, SCD4, a heart-specific isoform of SCD, is specifically repressed by leptin and the lack of SCD1 function in leptin-deficient ob/ob mice results in a decrease in the accumulation of neutral lipids and ceramide and improves the systolic and diastolic function of a failing heart.	Ceramides	213-221	stearoyl-Coenzyme A desaturase 1	Mus musculus	104-108
25521388-4	2014	Our study for the first time reveals that transient activation of the neutral sphingomyelinase 2 (NSM2) occurs in physiological co-stimulation of primary T cells where ceramide accumulation is confined to the lamellum (where also NSM2 can be detected) and excluded from IS areas of high actin turnover.	Ceramides	168-176	sphingomyelin phosphodiesterase 3	Homo sapiens	70-96
26274505-1	2015	The human sphingomyelin synthase 1 gene (SGMS1) encodes an essential enzyme that is involved in the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide.	Ceramides	175-183	sphingomyelin synthase 1	Homo sapiens	10-34
26274505-1	2015	The human sphingomyelin synthase 1 gene (SGMS1) encodes an essential enzyme that is involved in the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide.	Ceramides	175-183	sphingomyelin synthase 1	Homo sapiens	41-46
25555205-1	2015	The neutral type 2 sphingomyelinase (nSMase2) hydrolyzes sphingomyelin and generates ceramide, a major bioactive sphingolipid mediator, involved in growth arrest and apoptosis.	Ceramides	85-93	sphingomyelin phosphodiesterase 3	Homo sapiens	37-44
25555205-9	2015	The resistance of fro/fro cells to starvation-induced apoptosis is associated with an increased expression of hyaluronan synthase 2 (HAS2) mRNAs and protein, which is inhibited by ceramide.	Ceramides	180-188	hyaluronan synthase 2	Homo sapiens	110-131
25555205-9	2015	The resistance of fro/fro cells to starvation-induced apoptosis is associated with an increased expression of hyaluronan synthase 2 (HAS2) mRNAs and protein, which is inhibited by ceramide.	Ceramides	180-188	hyaluronan synthase 2	Homo sapiens	133-137
25521388-4	2014	Our study for the first time reveals that transient activation of the neutral sphingomyelinase 2 (NSM2) occurs in physiological co-stimulation of primary T cells where ceramide accumulation is confined to the lamellum (where also NSM2 can be detected) and excluded from IS areas of high actin turnover.	Ceramides	168-176	sphingomyelin phosphodiesterase 3	Homo sapiens	98-102
25521388-6	2014	In line with its suppressive activity, exaggerated, prolonged NSM2 activation as occurring in co-stimulated T cells following MV exposure was associated with aberrant compartmentalization of ceramides, loss of spreading responses, interference with accumulation of tyrosine phosphorylated protein species and expansion.	Ceramides	191-200	sphingomyelin phosphodiesterase 3	Homo sapiens	62-66
25339683-11	2014	Preincubation of vesicles containing SM with acid sphingomyelinase (ASM) (SM phosphodiesterase, EC 3.1.4.12) results in hydrolysis of SM to ceramide (Cer), which enhances cholesterol transfer.	Ceramides	140-148	sphingomyelin phosphodiesterase 1	Homo sapiens	45-66
25240837-11	2014	These data indicate that the early ceramide generation by nSMase2 induced by curcumin intensifies the later ceramide accumulation via inhibition of sphingomyelin synthase, and controls pro-apoptotic signaling.	Ceramides	35-43	sphingomyelin phosphodiesterase 3	Homo sapiens	58-65
25240837-11	2014	These data indicate that the early ceramide generation by nSMase2 induced by curcumin intensifies the later ceramide accumulation via inhibition of sphingomyelin synthase, and controls pro-apoptotic signaling.	Ceramides	108-116	sphingomyelin phosphodiesterase 3	Homo sapiens	58-65
25241943-1	2014	Ceramide synthase 2 (CerS2) null mice cannot synthesize very-long acyl chain (C22-C24) ceramides resulting in significant alterations in the acyl chain composition of sphingolipids.	Ceramides	87-96	ceramide synthase 2	Mus musculus	0-19
25281403-6	2014	Targeting GCS by siRNA also enhanced ceramide accumulation, which is involved in GCS knockdown-induced inhibition of ERK activation and Bcl-2 expression levels.	Ceramides	37-45	UDP-glucose ceramide glucosyltransferase	Homo sapiens	10-13
25281403-6	2014	Targeting GCS by siRNA also enhanced ceramide accumulation, which is involved in GCS knockdown-induced inhibition of ERK activation and Bcl-2 expression levels.	Ceramides	37-45	UDP-glucose ceramide glucosyltransferase	Homo sapiens	81-84
25281403-6	2014	Targeting GCS by siRNA also enhanced ceramide accumulation, which is involved in GCS knockdown-induced inhibition of ERK activation and Bcl-2 expression levels.	Ceramides	37-45	mitogen-activated protein kinase 1	Homo sapiens	117-120
25281403-6	2014	Targeting GCS by siRNA also enhanced ceramide accumulation, which is involved in GCS knockdown-induced inhibition of ERK activation and Bcl-2 expression levels.	Ceramides	37-45	BCL2 apoptosis regulator	Homo sapiens	136-141
25260612-4	2014	Surprisingly, Bco1(-/-) mice had an increase in heart levels of retinol, nonesterified fatty acids, and ceramides and a decrease in heart triglycerides.	Ceramides	104-113	beta-carotene oxygenase 1	Mus musculus	14-18
25240837-10	2014	The early ceramide generation by nSMase was indispensable for the later lipid accumulation, modulation of Bax, Bcl-2 and caspase 3 levels, and for reduction of cell viability in curcumin-treated cells, as all these events were inhibited by GW4869 or nSMase2 depletion.	Ceramides	10-18	sphingomyelin phosphodiesterase 2	Homo sapiens	33-39
25240837-10	2014	The early ceramide generation by nSMase was indispensable for the later lipid accumulation, modulation of Bax, Bcl-2 and caspase 3 levels, and for reduction of cell viability in curcumin-treated cells, as all these events were inhibited by GW4869 or nSMase2 depletion.	Ceramides	10-18	BCL2 associated X, apoptosis regulator	Homo sapiens	106-109
25240837-10	2014	The early ceramide generation by nSMase was indispensable for the later lipid accumulation, modulation of Bax, Bcl-2 and caspase 3 levels, and for reduction of cell viability in curcumin-treated cells, as all these events were inhibited by GW4869 or nSMase2 depletion.	Ceramides	10-18	BCL2 apoptosis regulator	Homo sapiens	111-116
25240837-10	2014	The early ceramide generation by nSMase was indispensable for the later lipid accumulation, modulation of Bax, Bcl-2 and caspase 3 levels, and for reduction of cell viability in curcumin-treated cells, as all these events were inhibited by GW4869 or nSMase2 depletion.	Ceramides	10-18	caspase 3	Homo sapiens	121-130
25240837-10	2014	The early ceramide generation by nSMase was indispensable for the later lipid accumulation, modulation of Bax, Bcl-2 and caspase 3 levels, and for reduction of cell viability in curcumin-treated cells, as all these events were inhibited by GW4869 or nSMase2 depletion.	Ceramides	10-18	sphingomyelin phosphodiesterase 3	Homo sapiens	250-257
24710763-5	2014	In the present study, we show that inhibition of LOX-1 leads to a rearrangement of ceramide from the basal membrane toward the Golgi apparatus.	Ceramides	83-91	oxidized low density lipoprotein receptor 1	Homo sapiens	49-54
25332431-4	2014	Here, we show that blocking autophagy in the liver by deletion of the Atg7 gene, which is essential for autophagosome formation, causes an increase in sphingolipid metabolites including ceramide.	Ceramides	186-194	autophagy related 7	Homo sapiens	70-74
25339683-11	2014	Preincubation of vesicles containing SM with acid sphingomyelinase (ASM) (SM phosphodiesterase, EC 3.1.4.12) results in hydrolysis of SM to ceramide (Cer), which enhances cholesterol transfer.	Ceramides	140-148	sphingomyelin phosphodiesterase 1	Homo sapiens	68-71
25339683-11	2014	Preincubation of vesicles containing SM with acid sphingomyelinase (ASM) (SM phosphodiesterase, EC 3.1.4.12) results in hydrolysis of SM to ceramide (Cer), which enhances cholesterol transfer.	Ceramides	150-153	sphingomyelin phosphodiesterase 1	Homo sapiens	45-66
25339683-11	2014	Preincubation of vesicles containing SM with acid sphingomyelinase (ASM) (SM phosphodiesterase, EC 3.1.4.12) results in hydrolysis of SM to ceramide (Cer), which enhances cholesterol transfer.	Ceramides	150-153	sphingomyelin phosphodiesterase 1	Homo sapiens	68-71
25339683-14	2014	ASM-mediated hydrolysis of liposomal SM was also stimulated by incorporation of diacylglycerol (DAG), Cer, and free fatty acids into the liposomal membranes.	Ceramides	102-105	sphingomyelin phosphodiesterase 1	Homo sapiens	0-3
25312644-2	2014	We recently discovered that a signaling lipid, the ceramide metabolite sphingosine-1-phosphate (S1P), regulates production of a major AMP, cathelicidin antimicrobial peptide (CAMP), in response to a subtoxic level of endoplasmic reticulum (ER) stress that can be induced by external perturbants in keratinocytes.	Ceramides	51-59	cathelicidin antimicrobial peptide	Homo sapiens	139-173
25312644-2	2014	We recently discovered that a signaling lipid, the ceramide metabolite sphingosine-1-phosphate (S1P), regulates production of a major AMP, cathelicidin antimicrobial peptide (CAMP), in response to a subtoxic level of endoplasmic reticulum (ER) stress that can be induced by external perturbants in keratinocytes.	Ceramides	51-59	cathelicidin antimicrobial peptide	Homo sapiens	175-179
25937892-6	2014	RESULTS: RT-PCR, real-time PCR and western blot demonstrated that exogenous ceramide treatment up-regulated GRP78 and p-eIF2alpha expression and XBP1 splicing.	Ceramides	76-84	heat shock protein family A (Hsp70) member 5	Homo sapiens	108-113
25333455-1	2014	Homo sapiens longevity assurance homolog 2 of yeast LAG (Lass2) catalyzes the synthesis of long-chain ceramide which is an essential element of membranous structures.	Ceramides	102-110	ceramide synthase 2	Mus musculus	57-62
25428807-2	2014	Recent evidence suggests that microRNAs can be released through ceramide-dependent secretory machinery regulated by neutral sphingomyelinase 2 (nSMase2) enzyme encoded by the smpd3 gene that triggers exosome secretion.	Ceramides	64-72	sphingomyelin phosphodiesterase 3	Homo sapiens	116-142
25428807-2	2014	Recent evidence suggests that microRNAs can be released through ceramide-dependent secretory machinery regulated by neutral sphingomyelinase 2 (nSMase2) enzyme encoded by the smpd3 gene that triggers exosome secretion.	Ceramides	64-72	sphingomyelin phosphodiesterase 3	Homo sapiens	144-151
25428807-2	2014	Recent evidence suggests that microRNAs can be released through ceramide-dependent secretory machinery regulated by neutral sphingomyelinase 2 (nSMase2) enzyme encoded by the smpd3 gene that triggers exosome secretion.	Ceramides	64-72	sphingomyelin phosphodiesterase 3	Homo sapiens	175-180
25428807-11	2014	In particular, nSMase2 or ceramide promotes the exosome-mediated miR-10b secretion whereas ceramide inhibitor suppresses this secretion.	Ceramides	26-34	microRNA 10b	Homo sapiens	65-72
25937892-6	2014	RESULTS: RT-PCR, real-time PCR and western blot demonstrated that exogenous ceramide treatment up-regulated GRP78 and p-eIF2alpha expression and XBP1 splicing.	Ceramides	76-84	X-box binding protein 1	Homo sapiens	145-149
25937892-7	2014	Moreover, the ceramide synthase inhibitor FB1 abolished ceramide-induced ER stress.	Ceramides	14-22	TCF3 fusion partner	Homo sapiens	42-45
25937892-8	2014	Up-regulation of the ER stress-associated apoptosis promoting transcription factor CHOP and p-JNK suggested that the antitumor activity of ceramide is owing to activation of apoptotic ER stress.	Ceramides	139-147	DNA damage inducible transcript 3	Homo sapiens	83-87
25937892-8	2014	Up-regulation of the ER stress-associated apoptosis promoting transcription factor CHOP and p-JNK suggested that the antitumor activity of ceramide is owing to activation of apoptotic ER stress.	Ceramides	139-147	mitogen-activated protein kinase 8	Homo sapiens	94-97
25256104-0	2014	Identification of novel CERT ligands as potential ceramide trafficking inhibitors.	Ceramides	50-58	ceramide transporter 1	Homo sapiens	24-28
25256104-3	2014	De novo sphingomyelin biosynthesis relies on non-vesicular ceramide trafficking by the CERT (CERamide Transfer) protein.	Ceramides	59-67	ceramide transporter 1	Homo sapiens	87-91
25937892-11	2014	In addition, the downstream metabolite of ceramide, S1P, cannot activate ER stress.	Ceramides	42-50	membrane bound transcription factor peptidase, site 1	Homo sapiens	52-55
25256104-3	2014	De novo sphingomyelin biosynthesis relies on non-vesicular ceramide trafficking by the CERT (CERamide Transfer) protein.	Ceramides	59-67	ceramide transporter 1	Homo sapiens	93-110
25256104-4	2014	Therefore, blocking CERT transfer, thus leading to increased intracellular ceramide availability, represents a potential anticancer strategy.	Ceramides	75-83	ceramide transporter 1	Homo sapiens	20-24
24684526-10	2014	To address this dichotomy in detail, evidence is presented regarding several protein targets, including Src, p38 mitogen-activated protein kinase, and neutral sphingomyelinase 2, the major sphingomyelinase that controls ceramide generation during oxidative stress.	Ceramides	220-228	sphingomyelin phosphodiesterase 3	Homo sapiens	151-177
27499893-1	2015	Ceramide synthase 5 is involved in the de novo synthesis of ceramide, a sphingolipid involved in cell death and proliferation.	Ceramides	60-68	ceramide synthase 5	Homo sapiens	0-19
25195822-0	2014	Ceramide modulates pre-mRNA splicing to restore the expression of wild-type tumor suppressor p53 in deletion-mutant cancer cells.	Ceramides	0-8	tumor protein p53	Homo sapiens	93-96
25384060-1	2014	INTRODUCTION: Acid sphingomyelinase is involved in lipid signalling pathways and regulation of apoptosis by the generation of ceramide and plays an important role during the host response to infectious stimuli.	Ceramides	126-134	sphingomyelin phosphodiesterase 1	Homo sapiens	14-35
25195822-3	2014	Being different from these, we report that ceramide can restore the expression of wild-type p53 and induce p53-dependent apoptosis in deletion-mutant cancer cells.	Ceramides	43-51	tumor protein p53	Homo sapiens	92-95
25195822-6	2014	Furthermore, we elucidate that ceramide activates protein phosphatase-1, and then the dephosphorylated serine/arginine-rich splicing-factor 1 (SRSF1) is translocated to the nucleus, thus promoting pre-mRNA splicing preferentially to wild-type p53 expression.	Ceramides	31-39	serine and arginine rich splicing factor 1	Homo sapiens	103-141
25195822-6	2014	Furthermore, we elucidate that ceramide activates protein phosphatase-1, and then the dephosphorylated serine/arginine-rich splicing-factor 1 (SRSF1) is translocated to the nucleus, thus promoting pre-mRNA splicing preferentially to wild-type p53 expression.	Ceramides	31-39	serine and arginine rich splicing factor 1	Homo sapiens	143-148
25195822-3	2014	Being different from these, we report that ceramide can restore the expression of wild-type p53 and induce p53-dependent apoptosis in deletion-mutant cancer cells.	Ceramides	43-51	tumor protein p53	Homo sapiens	107-110
25195822-6	2014	Furthermore, we elucidate that ceramide activates protein phosphatase-1, and then the dephosphorylated serine/arginine-rich splicing-factor 1 (SRSF1) is translocated to the nucleus, thus promoting pre-mRNA splicing preferentially to wild-type p53 expression.	Ceramides	31-39	tumor protein p53	Homo sapiens	243-246
25195822-8	2014	Ceramide through SRSF1 restores wild-type p53 expression versus deletion-mutant and leads cancer cells to apoptosis.	Ceramides	0-8	serine and arginine rich splicing factor 1	Homo sapiens	17-22
25195822-8	2014	Ceramide through SRSF1 restores wild-type p53 expression versus deletion-mutant and leads cancer cells to apoptosis.	Ceramides	0-8	tumor protein p53	Homo sapiens	42-45
24952994-3	2014	The 18-carbon acyl chain length ceramide species was associated with AbetaX-38 (r = 0.312, p = 0.003), AbetaX-40 (r = 0.327, p = 0.002), and T-tau (r = 0.313, p = 0.003) but not with AbetaX-42 (r = 0.171, p = 0.106) or p-tau (r = 0.086, p = 0.418).	Ceramides	32-40	microtubule associated protein tau	Homo sapiens	143-146
24676687-6	2014	In lymphoblastoid cell lines from pP-7 carriers, transfection of recombinant B55delta or treatment with ceramide led to a partial reconstitution of PP2A activity and dephosphorylation of pP-7 to wtP7.	Ceramides	104-112	protein phosphatase with EF-hand domain 1	Homo sapiens	34-38
24676687-6	2014	In lymphoblastoid cell lines from pP-7 carriers, transfection of recombinant B55delta or treatment with ceramide led to a partial reconstitution of PP2A activity and dephosphorylation of pP-7 to wtP7.	Ceramides	104-112	protein phosphatase 2 phosphatase activator	Homo sapiens	148-152
24676687-6	2014	In lymphoblastoid cell lines from pP-7 carriers, transfection of recombinant B55delta or treatment with ceramide led to a partial reconstitution of PP2A activity and dephosphorylation of pP-7 to wtP7.	Ceramides	104-112	protein phosphatase with EF-hand domain 1	Homo sapiens	187-191
25193995-6	2014	Several hepatic ceramides and acylcarnitines were decreased in the livers of Hint1(-/-) mice.	Ceramides	16-25	histidine triad nucleotide binding protein 1	Mus musculus	77-82
25193995-8	2014	The lipidomic phenotype of the Hint1(-/-) mouse revealed decreased inflammatory eicosanoids with elevated proliferative mediators that, combined with decreased ceramide apoptosis signaling molecules, may contribute to the tumor suppressor activity of Hint1.	Ceramides	160-168	histidine triad nucleotide binding protein 1	Mus musculus	31-36
24952994-3	2014	The 18-carbon acyl chain length ceramide species was associated with AbetaX-38 (r = 0.312, p = 0.003), AbetaX-40 (r = 0.327, p = 0.002), and T-tau (r = 0.313, p = 0.003) but not with AbetaX-42 (r = 0.171, p = 0.106) or p-tau (r = 0.086, p = 0.418).	Ceramides	32-40	microtubule associated protein tau	Homo sapiens	221-224
24952994-6	2014	These results suggest in vivo relationships between cerebrospinal fluid ceramides and sphingomyelins and Abeta and tau levels in cognitively normal individuals at increased risk for Alzheimer"s disease, indicating these sphingolipids may be associated with early pathogenesis.	Ceramides	72-81	amyloid beta precursor protein	Homo sapiens	105-110
24952994-6	2014	These results suggest in vivo relationships between cerebrospinal fluid ceramides and sphingomyelins and Abeta and tau levels in cognitively normal individuals at increased risk for Alzheimer"s disease, indicating these sphingolipids may be associated with early pathogenesis.	Ceramides	72-81	microtubule associated protein tau	Homo sapiens	115-118
25266739-0	2014	Ceramide synthase inhibitor fumonisin B1 inhibits apoptotic cell death in SCC17B human head and neck squamous carcinoma cells after Pc4 photosensitization.	Ceramides	0-8	keratin 6B	Homo sapiens	132-135
25350564-0	2014	Glucolipotoxicity impairs ceramide flow from the endoplasmic reticulum to the Golgi apparatus in INS-1 beta-cells.	Ceramides	26-34	insulin 1	Rattus norvegicus	97-102
25201535-2	2014	Neutral sphingomyelinase (N-SMase)/ceramide pathway can regulate NOS2 expression, hence this study determined the role of selective neutral sphingomyelinase (N-SMase) inhibition on retinal NOS2 levels, ER stress, apoptosis and visual evoked potentials (VEPs) in a rat model of elevated intraocular pressure (EIOP).	Ceramides	35-43	nitric oxide synthase 2	Rattus norvegicus	65-69
25374574-8	2014	The level of complex sphingolipids ceramide d18:0-16:0 and t18:1-16:0 had a twofold increase in pPLAIIIbeta-OE.	Ceramides	35-43	patatin-like protein 6	Arabidopsis thaliana	96-107
25157099-3	2014	In contrast, failing human hearts have severely reduced DGAT1 expression associated with accumulation of DAGs and ceramides.	Ceramides	114-123	diacylglycerol O-acyltransferase 1	Homo sapiens	56-61
25157099-11	2014	Treatment of hDgat1(-/-) mice with the glucagon-like peptide 1 receptor agonist exenatide also improved FS and reduced heart DAG and ceramide content.	Ceramides	133-141	glucagon-like peptide 1 receptor	Mus musculus	39-71
25157099-13	2014	Reduced activation of protein kinase Calpha (PKCalpha), which is increased by DAG and ceramides, paralleled the reductions in these lipids.	Ceramides	86-95	protein kinase C, alpha	Mus musculus	22-43
25157099-13	2014	Reduced activation of protein kinase Calpha (PKCalpha), which is increased by DAG and ceramides, paralleled the reductions in these lipids.	Ceramides	86-95	protein kinase C, alpha	Mus musculus	45-53
25350564-4	2014	Here, we studied the effect of glucolipotoxic conditions on ceramide traffic in INS-1 cells in order to gain insights into the molecular mechanism(s) of glucolipotoxicity.	Ceramides	60-68	insulin 1	Rattus norvegicus	80-85
25350564-6	2014	Glucolipotoxicity impaired both vesicular- and CERT-mediated ceramide transport through (1) the decreasing of phospho-Akt levels which in turn possibly inhibits vesicular traffic, and (2) the reducing of the amount of active CERT mainly due to a lower protein levels and increased protein phosphorylation to prevent its localization to the Golgi.	Ceramides	61-69	AKT serine/threonine kinase 1	Rattus norvegicus	118-121
25295788-0	2014	Obesity-induced CerS6-dependent C16:0 ceramide production promotes weight gain and glucose intolerance.	Ceramides	38-46	ceramide synthase 6	Mus musculus	16-21
25284795-3	2014	Genetic overexpression of the chaperone GRP78/BiP (glucose-regulated protein 78 kDa/binding immunoglobulin protein) in the ventromedial nucleus of the hypothalamus (VMH) abolishes ceramide action by reducing hypothalamic ER stress and increasing BAT thermogenesis, which leads to weight loss and improved glucose homeostasis.	Ceramides	180-188	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	40-45
25284795-3	2014	Genetic overexpression of the chaperone GRP78/BiP (glucose-regulated protein 78 kDa/binding immunoglobulin protein) in the ventromedial nucleus of the hypothalamus (VMH) abolishes ceramide action by reducing hypothalamic ER stress and increasing BAT thermogenesis, which leads to weight loss and improved glucose homeostasis.	Ceramides	180-188	heat shock protein family A (Hsp70) member 5	Rattus norvegicus	46-49
25295788-1	2014	Ceramides increase during obesity and promote insulin resistance.	Ceramides	0-9	insulin	Homo sapiens	46-53
25295788-2	2014	Ceramides vary in acyl-chain lengths from C14:0 to C30:0 and are synthesized by six ceramide synthase enzymes (CerS1-6).	Ceramides	0-9	ceramide synthase 1	Mus musculus	111-116
25295788-5	2014	Conversely, CerS6-deficient (CerS6(Delta/Delta)) mice exhibit reduced C16:0 ceramides and are protected from high-fat-diet-induced obesity and glucose intolerance.	Ceramides	76-85	ceramide synthase 6	Mus musculus	12-17
25295788-8	2014	These experiments highlight CerS6 inhibition as a specific approach for the treatment of obesity and type 2 diabetes mellitus, circumventing the side effects of global ceramide synthesis inhibition.	Ceramides	168-176	ceramide synthase 6	Mus musculus	28-33
25295789-3	2014	Haploinsufficiency for ceramide synthase 2 (CerS2), the dominant isoform in the liver that preferentially makes very-long-chain (C22/C24/C24:1) ceramides, led to compensatory increases in long-chain C16-ceramides and conferred susceptibility to diet-induced steatohepatitis and insulin resistance.	Ceramides	144-153	ceramide synthase 2	Homo sapiens	23-42
25295789-3	2014	Haploinsufficiency for ceramide synthase 2 (CerS2), the dominant isoform in the liver that preferentially makes very-long-chain (C22/C24/C24:1) ceramides, led to compensatory increases in long-chain C16-ceramides and conferred susceptibility to diet-induced steatohepatitis and insulin resistance.	Ceramides	144-153	ceramide synthase 2	Homo sapiens	44-49
25295789-5	2014	Inhibiting global ceramide synthesis negated the effects of CerS2 haploinsufficiency in vivo, and increasing C16-ceramides by overexpressing CerS6 recapitulated the phenotype in isolated, primary hepatocytes.	Ceramides	18-26	ceramide synthase 2	Homo sapiens	60-65
25152399-6	2014	By using pharmacological and siRNA-knockdown strategies, we showed that Akt-mammalian TOR (mTOR) over-activation was an important pemetrexed resistance factor in OS cells, and C6 ceramide-mediated pemetrexed sensitization effect was mediated, at least in part, by Akt-mTOR inhibition.	Ceramides	179-187	AKT serine/threonine kinase 1	Homo sapiens	72-75
25113261-0	2014	Resistance to the antiproliferative effect induced by a short-chain ceramide is associated with an increase of glucosylceramide synthase, P-glycoprotein, and multidrug-resistance gene-1 in cervical cancer cells.	Ceramides	68-76	UDP-glucose ceramide glucosyltransferase	Homo sapiens	111-136
25113261-0	2014	Resistance to the antiproliferative effect induced by a short-chain ceramide is associated with an increase of glucosylceramide synthase, P-glycoprotein, and multidrug-resistance gene-1 in cervical cancer cells.	Ceramides	68-76	ATP binding cassette subfamily B member 1	Homo sapiens	138-152
25113261-0	2014	Resistance to the antiproliferative effect induced by a short-chain ceramide is associated with an increase of glucosylceramide synthase, P-glycoprotein, and multidrug-resistance gene-1 in cervical cancer cells.	Ceramides	68-76	ATP binding cassette subfamily B member 1	Homo sapiens	158-185
25047167-5	2014	SAA-deficient mice exhibited significant aging-associated differences in hepatic GSH, GSH/GSSG, ceramide, and nSMase.	Ceramides	96-104	serum amyloid A cluster	Mus musculus	0-3
25108416-0	2014	Analysis of fluorescent ceramide and sphingomyelin analogs: a novel approach for in vivo monitoring of sphingomyelin synthase activity.	Ceramides	24-32	spermine synthase	Homo sapiens	103-125
25108416-1	2014	A novel sensitive high-performance liquid chromatography-fluorescence detection (HPLC-FLD) method was developed for real-time monitoring of relative sphingomyelin synthase (SMS) activity based on the measurement of a fluorescent ceramide (Cer) analog and its metabolite, a fluorescent sphingomyelin (CerPCho) analog, in plasma.	Ceramides	229-237	spermine synthase	Homo sapiens	149-171
25108416-1	2014	A novel sensitive high-performance liquid chromatography-fluorescence detection (HPLC-FLD) method was developed for real-time monitoring of relative sphingomyelin synthase (SMS) activity based on the measurement of a fluorescent ceramide (Cer) analog and its metabolite, a fluorescent sphingomyelin (CerPCho) analog, in plasma.	Ceramides	229-237	spermine synthase	Homo sapiens	173-176
25108416-1	2014	A novel sensitive high-performance liquid chromatography-fluorescence detection (HPLC-FLD) method was developed for real-time monitoring of relative sphingomyelin synthase (SMS) activity based on the measurement of a fluorescent ceramide (Cer) analog and its metabolite, a fluorescent sphingomyelin (CerPCho) analog, in plasma.	Ceramides	239-242	spermine synthase	Homo sapiens	149-171
25108416-1	2014	A novel sensitive high-performance liquid chromatography-fluorescence detection (HPLC-FLD) method was developed for real-time monitoring of relative sphingomyelin synthase (SMS) activity based on the measurement of a fluorescent ceramide (Cer) analog and its metabolite, a fluorescent sphingomyelin (CerPCho) analog, in plasma.	Ceramides	239-242	spermine synthase	Homo sapiens	173-176
25095742-0	2014	Docosahexanoic acid antagonizes TNF-alpha-induced necroptosis by attenuating oxidative stress, ceramide production, lysosomal dysfunction, and autophagic features.	Ceramides	95-103	tumor necrosis factor	Mus musculus	32-41
25152399-6	2014	By using pharmacological and siRNA-knockdown strategies, we showed that Akt-mammalian TOR (mTOR) over-activation was an important pemetrexed resistance factor in OS cells, and C6 ceramide-mediated pemetrexed sensitization effect was mediated, at least in part, by Akt-mTOR inhibition.	Ceramides	179-187	AKT serine/threonine kinase 1	Homo sapiens	264-267
25152399-6	2014	By using pharmacological and siRNA-knockdown strategies, we showed that Akt-mammalian TOR (mTOR) over-activation was an important pemetrexed resistance factor in OS cells, and C6 ceramide-mediated pemetrexed sensitization effect was mediated, at least in part, by Akt-mTOR inhibition.	Ceramides	179-187	mechanistic target of rapamycin kinase	Homo sapiens	268-272
25152399-9	2014	Together, we conclude that C6 ceramide sensitizes pemetrexed-induced apoptosis and cytotoxicity in OS cells probably through in-activation of Akt-mTOR signaling.	Ceramides	30-38	AKT serine/threonine kinase 1	Homo sapiens	142-145
25152399-9	2014	Together, we conclude that C6 ceramide sensitizes pemetrexed-induced apoptosis and cytotoxicity in OS cells probably through in-activation of Akt-mTOR signaling.	Ceramides	30-38	mechanistic target of rapamycin kinase	Homo sapiens	146-150
25228885-3	2014	The enzyme ASM catalyzes the hydrolysis of sphingomyelin to ceramide.	Ceramides	60-68	sphingomyelin phosphodiesterase 1	Homo sapiens	11-14
25228885-7	2014	The potential to block the generation of ceramide by inhibiting the ASM has opened up new therapeutic approaches for the treatment of these conditions.	Ceramides	41-49	sphingomyelin phosphodiesterase 1	Homo sapiens	68-71
25100243-1	2014	BACKGROUND: Alkaline sphingomyelinase (NPP7) is an ecto-enzyme expressed in intestinal mucosa, which hydrolyses sphingomyelin (SM) to ceramide and inactivates platelet activating factor.	Ceramides	134-142	ectonucleotide pyrophosphatase/phosphodiesterase 7	Homo sapiens	39-43
24953781-4	2014	Interestingly, we found significant differences in representation of various classes of ceramides (especially C16:0, C24:1) between the cancer and normal colon cells treated with DHA and TRAIL, and suggested their potential role in the regulation of the cell response to the drug combination.	Ceramides	88-97	TNF superfamily member 10	Homo sapiens	187-192
25004092-4	2014	We find that the proinflammatory cytokine combination IL-1beta+IFNgamma, induces: a) ER stress, mSREBP-1, and iPLA2beta, b) lysophosphatidylcholine (LPC) generation, c) neutral sphingomyelinase-2 (NSMase2), d) ceramide accumulation, e) mitochondrial membrane decompensation, f) caspase-3 activation, and g) beta-cell apoptosis.	Ceramides	210-218	interleukin 1 beta	Mus musculus	54-62
25004092-4	2014	We find that the proinflammatory cytokine combination IL-1beta+IFNgamma, induces: a) ER stress, mSREBP-1, and iPLA2beta, b) lysophosphatidylcholine (LPC) generation, c) neutral sphingomyelinase-2 (NSMase2), d) ceramide accumulation, e) mitochondrial membrane decompensation, f) caspase-3 activation, and g) beta-cell apoptosis.	Ceramides	210-218	interferon gamma	Mus musculus	63-71
25144372-0	2014	Identification and biochemical characterization of an acid sphingomyelinase-like protein from the bacterial plant pathogen Ralstonia solanacearum that hydrolyzes ATP to AMP but not sphingomyelin to ceramide.	Ceramides	198-206	sphingomyelin phosphodiesterase 1	Homo sapiens	54-75
25144372-1	2014	Acid sphingomyelinase (aSMase) is a human enzyme that catalyzes the hydrolysis of sphingomyelin to generate the bioactive lipid ceramide and phosphocholine.	Ceramides	128-136	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
25144372-1	2014	Acid sphingomyelinase (aSMase) is a human enzyme that catalyzes the hydrolysis of sphingomyelin to generate the bioactive lipid ceramide and phosphocholine.	Ceramides	128-136	sphingomyelin phosphodiesterase 1	Homo sapiens	23-29
25126394-3	2014	It has been suggested that increased amount of lipids inside the skeletal muscle (intramuscular triglyceride, diacylglycerol and ceramides) will impair insulin action in skeletal muscle, but data are not consistent in the human literature.	Ceramides	129-138	insulin	Homo sapiens	152-159
24951586-3	2014	In this work, we sought to define the role of ASM in IL-6 production because our previous work showed that a parallel pathway of ceramide metabolism, acid beta-glucosidase 1, negatively regulates IL-6.	Ceramides	129-137	sphingomyelin phosphodiesterase 1	Homo sapiens	46-49
24951586-3	2014	In this work, we sought to define the role of ASM in IL-6 production because our previous work showed that a parallel pathway of ceramide metabolism, acid beta-glucosidase 1, negatively regulates IL-6.	Ceramides	129-137	interleukin 6	Homo sapiens	53-57
24951586-3	2014	In this work, we sought to define the role of ASM in IL-6 production because our previous work showed that a parallel pathway of ceramide metabolism, acid beta-glucosidase 1, negatively regulates IL-6.	Ceramides	129-137	interleukin 6	Homo sapiens	196-200
24888419-1	2014	HPA-12 is an inhibitor of CERT-mediated non-vesicular transport of ceramide from the ER membranes to the Golgi apparatus.	Ceramides	67-75	ceramide transporter 1	Homo sapiens	26-30
24824073-1	2014	The conversion of sphingomyelin (SM) to a ceramide (Cer) by acid sphingomyelinase (aSMase) is an important event in skin barrier development.	Ceramides	42-50	sphingomyelin phosphodiesterase 1	Homo sapiens	60-81
24824073-1	2014	The conversion of sphingomyelin (SM) to a ceramide (Cer) by acid sphingomyelinase (aSMase) is an important event in skin barrier development.	Ceramides	42-50	sphingomyelin phosphodiesterase 1	Homo sapiens	83-89
24824073-1	2014	The conversion of sphingomyelin (SM) to a ceramide (Cer) by acid sphingomyelinase (aSMase) is an important event in skin barrier development.	Ceramides	52-55	sphingomyelin phosphodiesterase 1	Homo sapiens	60-81
24824073-1	2014	The conversion of sphingomyelin (SM) to a ceramide (Cer) by acid sphingomyelinase (aSMase) is an important event in skin barrier development.	Ceramides	52-55	sphingomyelin phosphodiesterase 1	Homo sapiens	83-89
24866405-6	2014	Ceramides of ypc1 ydc1  remained normal even in presence of aureobasidin A, an inhibitor of inositolphosphorylceramide synthase.	Ceramides	0-9	phytoceramidase	Saccharomyces cerevisiae S288C	13-22
24758915-7	2014	Based on these results demonstrating ceramide regulation of CTGF secretion by HRPE, we suggest that ceramide may have therapeutic potential for the treatment of retinal fibrotic diseases by inhibiting CTGF production.	Ceramides	37-45	cellular communication network factor 2	Homo sapiens	60-64
24758915-7	2014	Based on these results demonstrating ceramide regulation of CTGF secretion by HRPE, we suggest that ceramide may have therapeutic potential for the treatment of retinal fibrotic diseases by inhibiting CTGF production.	Ceramides	100-108	cellular communication network factor 2	Homo sapiens	60-64
24758915-7	2014	Based on these results demonstrating ceramide regulation of CTGF secretion by HRPE, we suggest that ceramide may have therapeutic potential for the treatment of retinal fibrotic diseases by inhibiting CTGF production.	Ceramides	100-108	cellular communication network factor 2	Homo sapiens	201-205
24758915-0	2014	Ceramide inhibits connective tissue growth factor expression by human retinal pigment epithelial cells.	Ceramides	0-8	cellular communication network factor 2	Homo sapiens	18-49
24758915-2	2014	We used human retinal pigment epithelial cells (HRPE), which play critical roles in retinal fibrosis, to examine the expression of CTGF and its regulation by ceramide and TGF-beta.	Ceramides	158-166	cellular communication network factor 2	Homo sapiens	131-135
24758915-4	2014	C2 ceramide also inhibited constitutive and TGF-beta-enhanced CTGF secretion by HRPE cells.	Ceramides	3-11	transforming growth factor beta 1	Homo sapiens	44-52
24758915-4	2014	C2 ceramide also inhibited constitutive and TGF-beta-enhanced CTGF secretion by HRPE cells.	Ceramides	3-11	cellular communication network factor 2	Homo sapiens	62-66
24399507-1	2014	Sphingosine kinases (Sphk1/2) are crucial enzymes in regulation of the biostat between sphingosine-1-phosphate (S1P) and ceramide and play an important role in the pathogenesis/pathomechanism of Alzheimer"s disease (AD).	Ceramides	121-129	sphingosine kinase 1	Homo sapiens	21-28
24875537-2	2014	Dihydroceramide desaturase (Des1), the last enzyme in the de novo synthesis of ceramide (Cer), regulates the balance between dihydroceramides (dhCers) and Cers.	Ceramides	7-15	delta 4-desaturase, sphingolipid 1	Homo sapiens	28-32
24875537-2	2014	Dihydroceramide desaturase (Des1), the last enzyme in the de novo synthesis of ceramide (Cer), regulates the balance between dihydroceramides (dhCers) and Cers.	Ceramides	89-92	delta 4-desaturase, sphingolipid 1	Homo sapiens	28-32
24819540-0	2014	Ceramide and its metabolites modulate time-dependently the activity of the Na+/K+ ATPase in HepG2 cells.	Ceramides	0-8	dynein axonemal heavy chain 8	Homo sapiens	82-88
24819540-1	2014	Ceramide is involved in the regulation of many cellular processes including cell proliferation and apoptosis, which are accompanied respectively with a decrease and an increase in the activity of the Na(+)/K(+) ATPase.	Ceramides	0-8	dynein axonemal heavy chain 8	Homo sapiens	211-217
24819540-3	2014	While we showed previously a ceramide-induced inhibition of the ATPase in HepG2 cells during the first hour, we study here the effect of ceramide thereafter.	Ceramides	29-37	dynein axonemal heavy chain 8	Homo sapiens	64-70
24819540-4	2014	Ceramide stimulated the Na(+)/K(+) ATPase between 1 and 4h with a peak at 2h.	Ceramides	0-8	dynein axonemal heavy chain 8	Homo sapiens	35-41
24420784-4	2014	Our study indicated that ceramide significantly enhanced the level of free radicals and decreased the viability of the human neuroblastoma cell line (SH-SY5Y) through inhibition of the prosurvival PI3-K/Akt pathway.	Ceramides	25-33	AKT serine/threonine kinase 1	Homo sapiens	203-206
24420784-5	2014	Ceramide also decreased anti-apoptotic (Bcl-2) and increased pro-apoptotic (Bax, Hrk) mRNA/protein levels.	Ceramides	0-8	BCL2 apoptosis regulator	Homo sapiens	40-45
24420784-5	2014	Ceramide also decreased anti-apoptotic (Bcl-2) and increased pro-apoptotic (Bax, Hrk) mRNA/protein levels.	Ceramides	0-8	BCL2 associated X, apoptosis regulator	Homo sapiens	76-79
24420784-5	2014	Ceramide also decreased anti-apoptotic (Bcl-2) and increased pro-apoptotic (Bax, Hrk) mRNA/protein levels.	Ceramides	0-8	harakiri, BCL2 interacting protein	Homo sapiens	81-84
24420784-6	2014	Concomitantly, our study indicated that ceramide induced poly(ADP-ribose) polymerase-1 (PARP-1) activation and accumulation of poly(ADP-ribose) PAR, a signalling molecule involved in mitochondria-nucleus cross-talk and mitochondria integrity.	Ceramides	40-48	poly(ADP-ribose) polymerase 1	Homo sapiens	57-86
24420784-6	2014	Concomitantly, our study indicated that ceramide induced poly(ADP-ribose) polymerase-1 (PARP-1) activation and accumulation of poly(ADP-ribose) PAR, a signalling molecule involved in mitochondria-nucleus cross-talk and mitochondria integrity.	Ceramides	40-48	poly(ADP-ribose) polymerase 1	Homo sapiens	88-94
24420784-11	2014	Our data demonstrate that neuronal cell death evoked by ceramide is regulated by PARP/PAR/AIF and by S1P receptor signalling.	Ceramides	56-64	poly(ADP-ribose) polymerase 1	Homo sapiens	81-85
25122154-8	2014	Plants in which IPUT1 was silenced accumulated IPC, the immediate precursor, as well as ceramides and glucosylceramides.	Ceramides	88-97	plant glycogenin-like starch initiation protein 6	Arabidopsis thaliana	16-21
24650793-2	2014	Exosome secretion is prevented by the inhibition of neutral sphingomyelinase 2 (nSMase2), a key regulatory enzyme generating ceramide from sphingomyelin, with GW4869.	Ceramides	125-133	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	52-78
24650793-2	2014	Exosome secretion is prevented by the inhibition of neutral sphingomyelinase 2 (nSMase2), a key regulatory enzyme generating ceramide from sphingomyelin, with GW4869.	Ceramides	125-133	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	80-87
24876379-3	2014	The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.We demonstrate that the development of paclitaxel-induced neuropathic pain was associated with ceramide and S1P formation in the spinal dorsal horn that corresponded with the engagement of S1P receptor subtype 1 (S1PR(1))- dependent neuroinflammatory processes as follows: activation of redox-sensitive transcription factors (NFkappaB) and MAPKs (ERK and p38) as well as enhanced formation of pro-inflammatory and neuroexcitatory cytokines (TNF-alpha and IL-1beta).	Ceramides	4-12	sphingosine-1-phosphate receptor 1	Homo sapiens	489-511
24876379-3	2014	The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.We demonstrate that the development of paclitaxel-induced neuropathic pain was associated with ceramide and S1P formation in the spinal dorsal horn that corresponded with the engagement of S1P receptor subtype 1 (S1PR(1))- dependent neuroinflammatory processes as follows: activation of redox-sensitive transcription factors (NFkappaB) and MAPKs (ERK and p38) as well as enhanced formation of pro-inflammatory and neuroexcitatory cytokines (TNF-alpha and IL-1beta).	Ceramides	4-12	sphingosine-1-phosphate receptor 1	Homo sapiens	513-520
24876379-3	2014	The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.We demonstrate that the development of paclitaxel-induced neuropathic pain was associated with ceramide and S1P formation in the spinal dorsal horn that corresponded with the engagement of S1P receptor subtype 1 (S1PR(1))- dependent neuroinflammatory processes as follows: activation of redox-sensitive transcription factors (NFkappaB) and MAPKs (ERK and p38) as well as enhanced formation of pro-inflammatory and neuroexcitatory cytokines (TNF-alpha and IL-1beta).	Ceramides	4-12	nuclear factor kappa B subunit 1	Homo sapiens	626-634
24876379-3	2014	The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.We demonstrate that the development of paclitaxel-induced neuropathic pain was associated with ceramide and S1P formation in the spinal dorsal horn that corresponded with the engagement of S1P receptor subtype 1 (S1PR(1))- dependent neuroinflammatory processes as follows: activation of redox-sensitive transcription factors (NFkappaB) and MAPKs (ERK and p38) as well as enhanced formation of pro-inflammatory and neuroexcitatory cytokines (TNF-alpha and IL-1beta).	Ceramides	4-12	mitogen-activated protein kinase 14	Homo sapiens	655-658
24876379-3	2014	The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.We demonstrate that the development of paclitaxel-induced neuropathic pain was associated with ceramide and S1P formation in the spinal dorsal horn that corresponded with the engagement of S1P receptor subtype 1 (S1PR(1))- dependent neuroinflammatory processes as follows: activation of redox-sensitive transcription factors (NFkappaB) and MAPKs (ERK and p38) as well as enhanced formation of pro-inflammatory and neuroexcitatory cytokines (TNF-alpha and IL-1beta).	Ceramides	4-12	tumor necrosis factor	Homo sapiens	741-750
24876379-3	2014	The ceramide-to-S1P pathway is also implicated in the development of pain, raising the intriguing possibility that these sphingolipids may contribute to chemotherapy- induced painful peripheral neuropathy, which can be a critical dose-limiting side effect of many widely used chemotherapeutic agents.We demonstrate that the development of paclitaxel-induced neuropathic pain was associated with ceramide and S1P formation in the spinal dorsal horn that corresponded with the engagement of S1P receptor subtype 1 (S1PR(1))- dependent neuroinflammatory processes as follows: activation of redox-sensitive transcription factors (NFkappaB) and MAPKs (ERK and p38) as well as enhanced formation of pro-inflammatory and neuroexcitatory cytokines (TNF-alpha and IL-1beta).	Ceramides	4-12	interleukin 1 beta	Homo sapiens	755-763
25027712-2	2014	Here we report structural results illuminating how LIMP-2 binds and releases beta-GCase according to changes in pH, via a histidine trigger, and suggesting that LIMP-2 localizes the ceramide portion of the substrate adjacent to the beta-GCase catalytic site.	Ceramides	182-190	scavenger receptor class B member 2	Homo sapiens	161-167
25058613-0	2014	Characterising the inhibitory actions of ceramide upon insulin signaling in different skeletal muscle cell models: a mechanistic insight.	Ceramides	41-49	insulin	Homo sapiens	55-62
25058613-1	2014	Ceramides are known to promote insulin resistance in a number of metabolically important tissues including skeletal muscle, the predominant site of insulin-stimulated glucose disposal.	Ceramides	0-9	insulin	Homo sapiens	31-38
25058613-1	2014	Ceramides are known to promote insulin resistance in a number of metabolically important tissues including skeletal muscle, the predominant site of insulin-stimulated glucose disposal.	Ceramides	0-9	insulin	Homo sapiens	148-155
25058613-3	2014	The main aim of this study was to explore the mechanisms by which ceramide inhibits PKB/Akt in three different skeletal muscle-derived cell culture models; rat L6 myotubes, mouse C2C12 myotubes and primary human skeletal muscle cells.	Ceramides	66-74	AKT serine/threonine kinase 1	Homo sapiens	84-91
25058613-4	2014	Our findings indicate that the mechanism by which ceramide acts to repress PKB/Akt is related to the myocellular abundance of caveolin-enriched domains (CEM) present at the plasma membrane.	Ceramides	50-58	AKT serine/threonine kinase 1	Homo sapiens	75-82
25058613-5	2014	Here, we show that ceramide-enriched-CEMs are markedly more abundant in L6 myotubes compared to C2C12 myotubes, consistent with their previously reported role in coordinating aPKC-directed repression of PKB/Akt in L6 muscle cells.	Ceramides	19-27	AKT serine/threonine kinase 1	Homo sapiens	203-210
25058613-6	2014	In contrast, a PP2A-dependent pathway predominantly mediates ceramide-induced inhibition of PKB/Akt in C2C12 myotubes.	Ceramides	61-69	protein phosphatase 2 phosphatase activator	Homo sapiens	15-19
25058613-6	2014	In contrast, a PP2A-dependent pathway predominantly mediates ceramide-induced inhibition of PKB/Akt in C2C12 myotubes.	Ceramides	61-69	AKT serine/threonine kinase 1	Homo sapiens	92-99
25058613-7	2014	In addition, we demonstrate for the first time that ceramide engages an aPKC-dependent pathway to suppress insulin-induced PKB/Akt activation in palmitate-treated cultured human muscle cells as well as in muscle cells from diabetic patients.	Ceramides	52-60	insulin	Homo sapiens	107-114
25058613-7	2014	In addition, we demonstrate for the first time that ceramide engages an aPKC-dependent pathway to suppress insulin-induced PKB/Akt activation in palmitate-treated cultured human muscle cells as well as in muscle cells from diabetic patients.	Ceramides	52-60	AKT serine/threonine kinase 1	Homo sapiens	123-130
25058613-8	2014	Collectively, this work identifies key mechanistic differences, which may be linked to variations in plasma membrane composition, underlying the insulin-desensitising effects of ceramide in different skeletal muscle cell models that are extensively used in signal transduction and metabolic studies.	Ceramides	178-186	insulin	Homo sapiens	145-152
24924631-0	2014	Palmitate induces SHIP2 expression via the ceramide-mediated activation of NF-kappaB, and JNK in skeletal muscle cells.	Ceramides	43-51	inositol polyphosphate phosphatase-like 1	Mus musculus	18-23
24924631-0	2014	Palmitate induces SHIP2 expression via the ceramide-mediated activation of NF-kappaB, and JNK in skeletal muscle cells.	Ceramides	43-51	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	75-84
24924631-8	2014	The results demonstrated that only ceramide synthesis inhibition could prevent palmitate-induced SHIP2 expression in these cells.	Ceramides	35-43	inositol polyphosphate phosphatase-like 1	Mus musculus	97-102
24924631-10	2014	Furthermore, the inhibition of both JNK and NF-kappaB pathways could prevent ceramide-induced SHIP2 expression in myotubes.	Ceramides	77-85	mitogen-activated protein kinase 8	Mus musculus	36-39
24924631-10	2014	Furthermore, the inhibition of both JNK and NF-kappaB pathways could prevent ceramide-induced SHIP2 expression in myotubes.	Ceramides	77-85	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	44-53
24924631-10	2014	Furthermore, the inhibition of both JNK and NF-kappaB pathways could prevent ceramide-induced SHIP2 expression in myotubes.	Ceramides	77-85	inositol polyphosphate phosphatase-like 1	Mus musculus	94-99
24924631-11	2014	SIGNIFICANCE: These findings suggest that palmitate contributes to SHIP2 overexpression in skeletal muscle via the mechanisms involving the activation of ceramide-JNK and NF-kappaB pathways.	Ceramides	154-162	inositol polyphosphate phosphatase-like 1	Mus musculus	67-72
24924631-11	2014	SIGNIFICANCE: These findings suggest that palmitate contributes to SHIP2 overexpression in skeletal muscle via the mechanisms involving the activation of ceramide-JNK and NF-kappaB pathways.	Ceramides	154-162	mitogen-activated protein kinase 8	Mus musculus	163-166
25050888-7	2014	Structural simulation model had also indicated that the direct binding of ceramide to inhibitor 2 of PP2A (I2PP2A) could reactivate PP2A and cause cell death.	Ceramides	74-82	protein phosphatase 2 phosphatase activator	Homo sapiens	101-105
25050888-7	2014	Structural simulation model had also indicated that the direct binding of ceramide to inhibitor 2 of PP2A (I2PP2A) could reactivate PP2A and cause cell death.	Ceramides	74-82	SET nuclear proto-oncogene	Homo sapiens	107-113
25050888-7	2014	Structural simulation model had also indicated that the direct binding of ceramide to inhibitor 2 of PP2A (I2PP2A) could reactivate PP2A and cause cell death.	Ceramides	74-82	protein phosphatase 2 phosphatase activator	Homo sapiens	109-113
25000528-9	2014	The increased intramyocellular ceramide content in the post-myotubes was associated with a significantly higher mRNA expression of Serine Palmitoyltransferase1 (SPT1) after one day of palmitate treatment (p = 0.03) in post-myotubes compared with pre-myotubes.	Ceramides	31-39	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	131-159
25000528-9	2014	The increased intramyocellular ceramide content in the post-myotubes was associated with a significantly higher mRNA expression of Serine Palmitoyltransferase1 (SPT1) after one day of palmitate treatment (p = 0.03) in post-myotubes compared with pre-myotubes.	Ceramides	31-39	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	161-165
24982331-4	2014	RESULTS: Herein we demonstrated that 8a and 8b cause apoptosis with S-phase arrest in lung cancer cells by activating neutral sphingomyelinase with ceramide production.	Ceramides	148-156	sphingomyelin phosphodiesterase 2	Homo sapiens	118-142
24997497-5	2014	The present study showed that CAPE activated neutral sphingomyelinase (N-SMase), which led to the ceramide-mediated activation of MAPKs, including extracellular signal-regulated kinase (ERK), Jun N-terminus kinase (JNK), and p38 MAPK.	Ceramides	98-106	sphingomyelin phosphodiesterase 2	Homo sapiens	45-69
24997497-5	2014	The present study showed that CAPE activated neutral sphingomyelinase (N-SMase), which led to the ceramide-mediated activation of MAPKs, including extracellular signal-regulated kinase (ERK), Jun N-terminus kinase (JNK), and p38 MAPK.	Ceramides	98-106	sphingomyelin phosphodiesterase 2	Homo sapiens	71-78
24997497-5	2014	The present study showed that CAPE activated neutral sphingomyelinase (N-SMase), which led to the ceramide-mediated activation of MAPKs, including extracellular signal-regulated kinase (ERK), Jun N-terminus kinase (JNK), and p38 MAPK.	Ceramides	98-106	mitogen-activated protein kinase 1	Homo sapiens	147-184
24997497-5	2014	The present study showed that CAPE activated neutral sphingomyelinase (N-SMase), which led to the ceramide-mediated activation of MAPKs, including extracellular signal-regulated kinase (ERK), Jun N-terminus kinase (JNK), and p38 MAPK.	Ceramides	98-106	mitogen-activated protein kinase 8	Homo sapiens	215-218
24997497-7	2014	The addition of an N-SMase inhibitor, GW4869, established that NGF/p75NTR was the downstream target of N-SMase/ceramide.	Ceramides	111-119	sphingomyelin phosphodiesterase 2	Homo sapiens	19-26
24997497-7	2014	The addition of an N-SMase inhibitor, GW4869, established that NGF/p75NTR was the downstream target of N-SMase/ceramide.	Ceramides	111-119	nerve growth factor	Homo sapiens	63-66
24997497-7	2014	The addition of an N-SMase inhibitor, GW4869, established that NGF/p75NTR was the downstream target of N-SMase/ceramide.	Ceramides	111-119	nerve growth factor receptor	Homo sapiens	67-73
24997497-7	2014	The addition of an N-SMase inhibitor, GW4869, established that NGF/p75NTR was the downstream target of N-SMase/ceramide.	Ceramides	111-119	sphingomyelin phosphodiesterase 2	Homo sapiens	103-110
24819607-0	2014	New role for EMD (emerin), a key inner nuclear membrane protein, as an enhancer of autophagosome formation in the C16-ceramide autophagy pathway.	Ceramides	118-126	emerin	Homo sapiens	18-24
24819607-6	2014	Upon ceramide treatment, phosphorylated EMD binds MAP1LC3B leading to an increase of autophagosome formation.	Ceramides	5-13	microtubule associated protein 1 light chain 3 beta	Homo sapiens	50-58
24789699-5	2014	Since the -CH=CH- signal encompasses protons from ceramide, this latter difference is consistent with the hypothesis that the GST2 mutation is associated with insulin resistance and apoptosis.	Ceramides	50-58	Glutathione S transferase S1	Drosophila melanogaster	126-130
24650522-0	2014	Ceramide inhibits insulin-stimulated Akt phosphorylation through activation of Rheb/mTORC1/S6K signaling in skeletal muscle.	Ceramides	0-8	insulin	Homo sapiens	18-25
24650522-0	2014	Ceramide inhibits insulin-stimulated Akt phosphorylation through activation of Rheb/mTORC1/S6K signaling in skeletal muscle.	Ceramides	0-8	AKT serine/threonine kinase 1	Homo sapiens	37-40
24650522-0	2014	Ceramide inhibits insulin-stimulated Akt phosphorylation through activation of Rheb/mTORC1/S6K signaling in skeletal muscle.	Ceramides	0-8	Ras homolog, mTORC1 binding	Homo sapiens	79-83
24650522-0	2014	Ceramide inhibits insulin-stimulated Akt phosphorylation through activation of Rheb/mTORC1/S6K signaling in skeletal muscle.	Ceramides	0-8	CREB regulated transcription coactivator 1	Mus musculus	84-90
24650522-0	2014	Ceramide inhibits insulin-stimulated Akt phosphorylation through activation of Rheb/mTORC1/S6K signaling in skeletal muscle.	Ceramides	0-8	ribosomal protein S6 kinase B1	Homo sapiens	91-94
24650522-1	2014	Ceramide is a negative regulator of insulin activity.	Ceramides	0-8	insulin	Homo sapiens	36-43
24742815-2	2014	Previous studies have revealed the sphingomyelinase/ceramide pathway in the regulation of NOS2 induction.	Ceramides	52-60	nitric oxide synthase 2	Homo sapiens	90-94
24622797-5	2014	Lipidomic and microarray analyses revealed accumulation/imbalance of lipid species, including ceramides, in ASKO adipose tissue as well as increased endoplasmic reticulum stress.	Ceramides	94-103	WD and tetratricopeptide repeats 1	Mus musculus	113-120
24789699-5	2014	Since the -CH=CH- signal encompasses protons from ceramide, this latter difference is consistent with the hypothesis that the GST2 mutation is associated with insulin resistance and apoptosis.	Ceramides	50-58	Insulin-like receptor	Drosophila melanogaster	159-166
24687220-0	2014	Arabidopsis Bax inhibitor-1 promotes sphingolipid synthesis during cold stress by interacting with ceramide-modifying enzymes.	Ceramides	99-107	BAX inhibitor 1	Arabidopsis thaliana	12-27
24518171-7	2014	IL-31 increases long chain FFAs in LEMs but decreases relative abundance of EO ceramides.	Ceramides	79-88	interleukin 31	Homo sapiens	0-5
24820416-7	2014	Moreover, diabetic Plin5-KO mice exhibited lower heart levels of lipotoxic molecules, such as diacylglycerol and ceramide, than wild-type mice.	Ceramides	113-121	perilipin 5	Mus musculus	19-24
24804932-5	2014	The major GIPC has one hexose residue, one hexuronic acid residue, inositol phosphate, and a ceramide moiety with a C18 trihydroxylated mono-unsaturated long-chain base and a C24 monohydroxylated saturated fatty acid.	Ceramides	93-101	GIPC PDZ domain containing family member 1	Homo sapiens	10-14
24861084-3	2014	Second, acid sphingomyelinase-like phosphodiesterase 3b encoded by SMPDL3b has a role in the conversion of sphingomyelin to ceramide and its levels are reduced in renal biopsy samples from patients with recurrent FSGS.	Ceramides	124-132	sphingomyelin phosphodiesterase acid like 3B	Homo sapiens	8-55
24861084-3	2014	Second, acid sphingomyelinase-like phosphodiesterase 3b encoded by SMPDL3b has a role in the conversion of sphingomyelin to ceramide and its levels are reduced in renal biopsy samples from patients with recurrent FSGS.	Ceramides	124-132	sphingomyelin phosphodiesterase acid like 3B	Homo sapiens	67-74
24687220-8	2014	In addition, the ceramide-modifying enzymes AtFAH1, sphingolipid base hydroxylase 2 (AtSBH2), acyl lipid desaturase 2 (AtADS2) and AtSLD1 were highly expressed under cold stress, and all are likely to be related to AtBI-1 function.	Ceramides	17-25	BAX inhibitor 1	Arabidopsis thaliana	215-221
24687220-8	2014	In addition, the ceramide-modifying enzymes AtFAH1, sphingolipid base hydroxylase 2 (AtSBH2), acyl lipid desaturase 2 (AtADS2) and AtSLD1 were highly expressed under cold stress, and all are likely to be related to AtBI-1 function.	Ceramides	17-25	fatty acid hydroxylase 1	Arabidopsis thaliana	44-83
24687220-8	2014	In addition, the ceramide-modifying enzymes AtFAH1, sphingolipid base hydroxylase 2 (AtSBH2), acyl lipid desaturase 2 (AtADS2) and AtSLD1 were highly expressed under cold stress, and all are likely to be related to AtBI-1 function.	Ceramides	17-25	sphingoid base hydroxylase 2	Arabidopsis thaliana	85-91
24687220-8	2014	In addition, the ceramide-modifying enzymes AtFAH1, sphingolipid base hydroxylase 2 (AtSBH2), acyl lipid desaturase 2 (AtADS2) and AtSLD1 were highly expressed under cold stress, and all are likely to be related to AtBI-1 function.	Ceramides	17-25	16:0delta9 desaturase 2	Arabidopsis thaliana	119-125
24687220-8	2014	In addition, the ceramide-modifying enzymes AtFAH1, sphingolipid base hydroxylase 2 (AtSBH2), acyl lipid desaturase 2 (AtADS2) and AtSLD1 were highly expressed under cold stress, and all are likely to be related to AtBI-1 function.	Ceramides	17-25	Fatty acid/sphingolipid desaturase	Arabidopsis thaliana	131-137
24936246-0	2014	Defect of insulin signal in peripheral tissues: Important role of ceramide.	Ceramides	66-74	insulin	Homo sapiens	10-17
24936246-7	2014	Several studies suggest that ceramides are among the most active lipid second messengers to inhibit the insulin signaling pathway and this review describes the major role played by ceramide accumulation in the development of insulin resistance of peripherals tissues through the targeting of specific proteins of the insulin signaling pathway.	Ceramides	29-38	insulin	Homo sapiens	104-111
25161888-3	2014	PLIN5 ablation depleted triacylglycerol stores but increased sphingolipids including ceramide, hydroxylceramides and sphingomyelin.	Ceramides	85-93	perilipin 5	Mus musculus	0-5
24936246-7	2014	Several studies suggest that ceramides are among the most active lipid second messengers to inhibit the insulin signaling pathway and this review describes the major role played by ceramide accumulation in the development of insulin resistance of peripherals tissues through the targeting of specific proteins of the insulin signaling pathway.	Ceramides	29-38	insulin	Homo sapiens	225-232
25161888-6	2014	Plin5 (-/-) mice developed skeletal muscle insulin resistance, which was associated with ceramide accumulation.	Ceramides	89-97	perilipin 5	Mus musculus	0-5
24936246-7	2014	Several studies suggest that ceramides are among the most active lipid second messengers to inhibit the insulin signaling pathway and this review describes the major role played by ceramide accumulation in the development of insulin resistance of peripherals tissues through the targeting of specific proteins of the insulin signaling pathway.	Ceramides	29-38	insulin	Homo sapiens	225-232
24936246-7	2014	Several studies suggest that ceramides are among the most active lipid second messengers to inhibit the insulin signaling pathway and this review describes the major role played by ceramide accumulation in the development of insulin resistance of peripherals tissues through the targeting of specific proteins of the insulin signaling pathway.	Ceramides	29-37	insulin	Homo sapiens	104-111
24936246-7	2014	Several studies suggest that ceramides are among the most active lipid second messengers to inhibit the insulin signaling pathway and this review describes the major role played by ceramide accumulation in the development of insulin resistance of peripherals tissues through the targeting of specific proteins of the insulin signaling pathway.	Ceramides	29-37	insulin	Homo sapiens	225-232
24936246-7	2014	Several studies suggest that ceramides are among the most active lipid second messengers to inhibit the insulin signaling pathway and this review describes the major role played by ceramide accumulation in the development of insulin resistance of peripherals tissues through the targeting of specific proteins of the insulin signaling pathway.	Ceramides	29-37	insulin	Homo sapiens	225-232
25050165-4	2014	Using PP2A as the readout, we measured PP2A activity in response to alpha-synuclein, ceramides, and FTY720, and then on the basis of those results, we created new FTY720 compounds.	Ceramides	85-94	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	39-43
24389457-8	2014	Finally, we found that, after Hex alpha subunit transfection, both PC3 and LNCaP were less susceptible to exogenous ceramide treatment.	Ceramides	116-124	hematopoietically expressed homeobox	Homo sapiens	30-33
24389457-8	2014	Finally, we found that, after Hex alpha subunit transfection, both PC3 and LNCaP were less susceptible to exogenous ceramide treatment.	Ceramides	116-124	chromobox 8	Homo sapiens	67-70
24694597-4	2014	Decreasing ceramide levels by inhibiting ceramide synthase or neutral sphingomyelinase 2 leads to translocation of membrane-bound aPKC to the cytosol, concurrent with its activation and the phosphorylation of its substrate Aurora kinase A (AurA).	Ceramides	11-19	sphingomyelin phosphodiesterase 3	Homo sapiens	62-88
24694597-4	2014	Decreasing ceramide levels by inhibiting ceramide synthase or neutral sphingomyelinase 2 leads to translocation of membrane-bound aPKC to the cytosol, concurrent with its activation and the phosphorylation of its substrate Aurora kinase A (AurA).	Ceramides	11-19	aurora kinase A	Homo sapiens	223-238
24694597-4	2014	Decreasing ceramide levels by inhibiting ceramide synthase or neutral sphingomyelinase 2 leads to translocation of membrane-bound aPKC to the cytosol, concurrent with its activation and the phosphorylation of its substrate Aurora kinase A (AurA).	Ceramides	11-19	aurora kinase A	Homo sapiens	240-244
24694597-5	2014	Inhibition of aPKC, AurA, or a downstream target of AurA, HDAC6, restores ciliogenesis in ceramide-depleted cells.	Ceramides	90-98	aurora kinase A	Homo sapiens	20-24
24694597-5	2014	Inhibition of aPKC, AurA, or a downstream target of AurA, HDAC6, restores ciliogenesis in ceramide-depleted cells.	Ceramides	90-98	aurora kinase A	Homo sapiens	52-56
24694597-5	2014	Inhibition of aPKC, AurA, or a downstream target of AurA, HDAC6, restores ciliogenesis in ceramide-depleted cells.	Ceramides	90-98	histone deacetylase 6	Homo sapiens	58-63
24694597-7	2014	Taken together, these results suggest that ceramide prevents activation of HDAC6 by cytosolic aPKC and AurA, which promotes acetylation of tubulin in primary cilia and, potentially, neural processes.	Ceramides	43-51	histone deacetylase 6	Homo sapiens	75-80
24694597-7	2014	Taken together, these results suggest that ceramide prevents activation of HDAC6 by cytosolic aPKC and AurA, which promotes acetylation of tubulin in primary cilia and, potentially, neural processes.	Ceramides	43-51	aurora kinase A	Homo sapiens	103-107
24694597-8	2014	This is the first report on the critical role of ceramide generated by nSMase2 in stem cell ciliogenesis and differentiation.	Ceramides	49-57	sphingomyelin phosphodiesterase 3	Homo sapiens	71-78
24747163-11	2014	Furthermore, pretreatment of BEAS-2B cells with Vam3 or resveratrol significantly suppressed CSC-stimulated intracellular ceramide production, and CSC-induced upregulation of neutral sphingomyelinase 2, the enzyme responsible for ceramide production in bronchial epithelial cells.	Ceramides	230-238	sphingomyelin phosphodiesterase 3	Homo sapiens	175-201
24742988-0	2014	Pharmacological ceramide reduction alleviates alcohol-induced steatosis and hepatomegaly in adiponectin knockout mice.	Ceramides	16-24	adiponectin, C1Q and collagen domain containing	Mus musculus	92-103
24742988-3	2014	Adiponectin can regulate lipid handling in the liver and has been shown to reduce ceramide levels and activate AMPK and PPAR-alpha.	Ceramides	82-90	adiponectin, C1Q and collagen domain containing	Mus musculus	0-11
24742988-10	2014	By contrast, alcohol treatment increased liver ceramide levels in adiponectin KO but not WT mice.	Ceramides	47-55	adiponectin, C1Q and collagen domain containing	Mus musculus	66-77
24742988-11	2014	Importantly, pharmacological inhibition of de novo ceramide synthesis in adiponectin KO mice abrogated alcohol-mediated increases in liver ceramides, steatosis, and hepatomegaly.	Ceramides	51-59	adiponectin, C1Q and collagen domain containing	Mus musculus	73-84
24742988-11	2014	Importantly, pharmacological inhibition of de novo ceramide synthesis in adiponectin KO mice abrogated alcohol-mediated increases in liver ceramides, steatosis, and hepatomegaly.	Ceramides	139-148	adiponectin, C1Q and collagen domain containing	Mus musculus	73-84
24742988-12	2014	These data suggest that adiponectin reduces alcohol-induced steatosis and hepatomegaly through regulation of liver ceramides, but its absence does not exacerbate alcohol-induced liver damage.	Ceramides	115-124	adiponectin, C1Q and collagen domain containing	Mus musculus	24-35
24657936-3	2014	Sphingosine kinase (SphK1) activity can alter the sphingosine-1-phosphate (S1P)/ceramide ratio leading to an imbalance in the sphingolipid rheostat.	Ceramides	80-88	sphingosine kinase 1	Homo sapiens	20-25
24892004-3	2014	Fatty acid induced synthesis of ceramide is considered to be one of the major causes for insulin resistance.	Ceramides	32-40	insulin	Homo sapiens	89-96
24957032-9	2014	Unexpectedly, total ceramide is increased by LMW-APN.	Ceramides	20-28	adiponectin, C1Q and collagen domain containing	Homo sapiens	49-52
24831094-0	2014	Absence of perilipin 2 prevents hepatic steatosis, glucose intolerance and ceramide accumulation in alcohol-fed mice.	Ceramides	75-83	predicted gene 12551	Mus musculus	11-22
24831094-2	2014	An increase in Plin2 in liver is associated with the development of steatosis, glucose intolerance, and ceramide accumulation in alcoholic liver disease.	Ceramides	104-112	predicted gene 12551	Mus musculus	15-20
24831094-9	2014	Most notably, absence of Plin2 prevented hepatic steatosis and ceramide accumulation in alcohol-fed mice.	Ceramides	63-71	predicted gene 12551	Mus musculus	25-30
24831094-11	2014	CONCLUSIONS: Plin2KO mice chronically fed alcohol are protected from hepatic steatosis, glucose intolerance, and hepatic ceramide accumulation, suggesting a critical pathogenic role of Plin2 in experimental alcoholic liver disease.	Ceramides	121-129	predicted gene 12551	Mus musculus	13-18
24892004-6	2014	RESULTS: Treatment of saturated fatty acid (palmitate) but not unsaturated fatty acid (oleate) caused an up-regulation in expression of various nSMase genes which are associated with ceramide synthesis through the salvage pathway.	Ceramides	183-191	sphingomyelin phosphodiesterase 2	Homo sapiens	144-150
23845852-3	2014	In the biosynthesis of SM, ceramide, which is synthesized in the endoplasmic reticulum, is transported to the Golgi region by the ceramide transport protein CERT, probably in a non-vesicular manner, and is then converted to SM by SM synthase, which catalyzes the reaction of phosphocholine transfer from phosphatidylcholine (PtdCho) to ceramide.	Ceramides	130-138	ceramide transporter 1	Homo sapiens	157-161
24606881-10	2014	The findings demonstrate an endothelial VEGF resistance mechanism conferred by PA, which comprises ceramide-induced, PP2A-mediated dephosphorylation of critical activation sites on enzymes central to vascular homeostasis and angiogenesis.	Ceramides	99-107	vascular endothelial growth factor A	Mus musculus	40-44
24606881-10	2014	The findings demonstrate an endothelial VEGF resistance mechanism conferred by PA, which comprises ceramide-induced, PP2A-mediated dephosphorylation of critical activation sites on enzymes central to vascular homeostasis and angiogenesis.	Ceramides	99-107	protein phosphatase 2 (formerly 2A), catalytic subunit, alpha isoform	Mus musculus	117-121
23845852-3	2014	In the biosynthesis of SM, ceramide, which is synthesized in the endoplasmic reticulum, is transported to the Golgi region by the ceramide transport protein CERT, probably in a non-vesicular manner, and is then converted to SM by SM synthase, which catalyzes the reaction of phosphocholine transfer from phosphatidylcholine (PtdCho) to ceramide.	Ceramides	27-35	ceramide transporter 1	Homo sapiens	157-161
23845852-8	2014	CERT may have co-evolved with SM to bypass a competing metabolic reaction at the bifurcated point in the anabolism of ceramide.	Ceramides	118-126	ceramide transporter 1	Homo sapiens	0-4
23845852-3	2014	In the biosynthesis of SM, ceramide, which is synthesized in the endoplasmic reticulum, is transported to the Golgi region by the ceramide transport protein CERT, probably in a non-vesicular manner, and is then converted to SM by SM synthase, which catalyzes the reaction of phosphocholine transfer from phosphatidylcholine (PtdCho) to ceramide.	Ceramides	27-35	sphingomyelin synthase 2	Homo sapiens	230-241
23845852-3	2014	In the biosynthesis of SM, ceramide, which is synthesized in the endoplasmic reticulum, is transported to the Golgi region by the ceramide transport protein CERT, probably in a non-vesicular manner, and is then converted to SM by SM synthase, which catalyzes the reaction of phosphocholine transfer from phosphatidylcholine (PtdCho) to ceramide.	Ceramides	130-138	ceramide transporter 1	Homo sapiens	157-161
24064302-3	2014	Acid CDase catabolizes ceramide in lysosomes and is found only in vertebrates.	Ceramides	23-31	N-acylsphingosine amidohydrolase 1	Homo sapiens	0-10
24630524-0	2014	Ceramide-enriched LDL induces cytokine release through TLR4 and CD14 in monocytes.	Ceramides	0-8	toll like receptor 4	Homo sapiens	55-59
24630524-0	2014	Ceramide-enriched LDL induces cytokine release through TLR4 and CD14 in monocytes.	Ceramides	0-8	CD14 molecule	Homo sapiens	64-68
24650665-6	2014	In addition, DAG enhanced ceramide production by stimulating neutral sphingomyelinase (N-SMase) activity.	Ceramides	26-34	sphingomyelin phosphodiesterase 2	Homo sapiens	61-85
25831888-4	2014	SMS1 enzyme, encoded by this gene, catalyzes the synthesis of sphingomyelin and diacylglycerol from phosphatidylcholine and ceramide.	Ceramides	124-132	sphingomyelin synthase 1	Homo sapiens	0-4
25831888-5	2014	SMS1 may maintain the balance between cell death and survival by regulating the formation of the pro-apoptotic mediator ceramide and anti-apoptotic mediator diacylglycerol.	Ceramides	120-128	sphingomyelin synthase 1	Homo sapiens	0-4
24682752-3	2014	This study was designed to elucidate whether the sphingosine kinase-1 (SPK1), a critical regulator of the ceramide/sphingosine 1-phosphate rheostat, plays a pivotal role in the regulation of death and survival of differentiated neuro-2a cells in response to beta-amyloid peptide fragment 25-35 (Abeta25-35).	Ceramides	106-114	sphingosine kinase 1	Mus musculus	49-69
24682752-3	2014	This study was designed to elucidate whether the sphingosine kinase-1 (SPK1), a critical regulator of the ceramide/sphingosine 1-phosphate rheostat, plays a pivotal role in the regulation of death and survival of differentiated neuro-2a cells in response to beta-amyloid peptide fragment 25-35 (Abeta25-35).	Ceramides	106-114	sphingosine kinase 1	Mus musculus	71-75
24596158-3	2014	Cytokines and angiotensin II are elevated in CHF and stimulate the activity of the enzyme sphingomyelinase (SMase) and accumulation of its reaction product ceramide.	Ceramides	156-164	angiotensinogen	Rattus norvegicus	14-28
24650665-6	2014	In addition, DAG enhanced ceramide production by stimulating neutral sphingomyelinase (N-SMase) activity.	Ceramides	26-34	sphingomyelin phosphodiesterase 2	Homo sapiens	87-94
24448832-3	2014	Here, we investigated the role of ABCB1 in nickel-induced stress signaling mediated by reactive oxygen species (ROS) and ceramides.	Ceramides	121-130	ATP binding cassette subfamily B member 1	Canis lupus familiaris	34-39
24628620-4	2014	This approach can also be used to map the site of a protein-lipid interaction as we identify the peptide in contact with the fatty acid part of ceramide in the START domain of the CERT protein.	Ceramides	144-152	ceramide transporter 1	Homo sapiens	180-184
24569996-0	2014	Phosphoregulation of the ceramide transport protein CERT at serine 315 in the interaction with VAMP-associated protein (VAP) for inter-organelle trafficking of ceramide in mammalian cells.	Ceramides	25-33	ceramide transporter 1	Homo sapiens	52-56
24569996-0	2014	Phosphoregulation of the ceramide transport protein CERT at serine 315 in the interaction with VAMP-associated protein (VAP) for inter-organelle trafficking of ceramide in mammalian cells.	Ceramides	160-168	ceramide transporter 1	Homo sapiens	52-56
24569996-1	2014	The ceramide transport protein CERT mediates the inter-organelle transport of ceramide for the synthesis of sphingomyelin, presumably through endoplasmic reticulum (ER)-Golgi membrane contact sites.	Ceramides	4-12	ceramide transporter 1	Homo sapiens	31-35
24569996-1	2014	The ceramide transport protein CERT mediates the inter-organelle transport of ceramide for the synthesis of sphingomyelin, presumably through endoplasmic reticulum (ER)-Golgi membrane contact sites.	Ceramides	78-86	ceramide transporter 1	Homo sapiens	31-35
24569996-4	2014	The phosphomimetic CERT S315E mutant exhibited higher activity to support the ER-to-Golgi transport of ceramide than the wild-type control in a semi-intact cell system, and this enhanced activity was abrogated when its FFAT motif was deleted.	Ceramides	103-111	ceramide transporter 1	Homo sapiens	19-23
24569996-9	2014	These results demonstrate that the phosphorylation of CERT at the FFAT motif-adjacent serine affected its affinity for VAP, which may regulate the inter-organelle trafficking of ceramide in response to the perturbation of cellular sphingomyelin and/or other sphingolipids.	Ceramides	178-186	ceramide transporter 1	Homo sapiens	54-58
23604129-0	2014	Loss of TSC2 confers resistance to ceramide and nutrient deprivation.	Ceramides	35-43	TSC complex subunit 2	Homo sapiens	8-12
23604129-5	2014	However, murine embryonic fibroblasts (MEFs) lacking TSC2 were highly resistant to ceramide-induced death.	Ceramides	83-91	TSC complex subunit 2	Mus musculus	53-57
23604129-6	2014	Consistent with the observation that ceramide limits access to both amino acids and glucose, TSC2(-/-) MEFs also had a survival advantage when extracellular amino acids and glucose were both reduced.	Ceramides	37-45	TSC complex subunit 2	Homo sapiens	93-97
23604129-8	2014	In low amino acid and glucose medium, and following ceramide-induced nutrient transporter loss, elevated mTORC1 activity significantly enhanced the adaptive upregulation of new transporter proteins for amino acids and glucose.	Ceramides	52-60	CREB regulated transcription coactivator 1	Mus musculus	105-111
23604129-9	2014	Strikingly, the introduction of oncogenic Ras abrogated the survival advantage of TSC2(-/-) MEFs upon ceramide treatment most likely by increasing nutrient demand.	Ceramides	102-110	TSC complex subunit 2	Homo sapiens	82-86
24705014-0	2014	Dynamic GLUT4 sorting through a syntaxin-6 compartment in muscle cells is derailed by insulin resistance-causing ceramide.	Ceramides	113-121	solute carrier family 2 member 4	Homo sapiens	8-13
24705014-0	2014	Dynamic GLUT4 sorting through a syntaxin-6 compartment in muscle cells is derailed by insulin resistance-causing ceramide.	Ceramides	113-121	syntaxin 6	Homo sapiens	32-42
24705014-0	2014	Dynamic GLUT4 sorting through a syntaxin-6 compartment in muscle cells is derailed by insulin resistance-causing ceramide.	Ceramides	113-121	insulin	Homo sapiens	86-93
24705014-11	2014	Our data are consistent with a model where ceramide could cause insulin resistance by altering intracellular GLUT4 sorting.	Ceramides	43-51	insulin	Homo sapiens	64-71
24705014-11	2014	Our data are consistent with a model where ceramide could cause insulin resistance by altering intracellular GLUT4 sorting.	Ceramides	43-51	solute carrier family 2 member 4	Homo sapiens	109-114
24448832-5	2014	Inhibitors of the de novo ceramide synthesis pathway (fumonisin B1, L-cycloserine) and an antioxidant (alpha-tocopherol) attenuated nickel-induced toxicity as well as induction of ABCB1.	Ceramides	26-34	ATP binding cassette subfamily B member 1	Canis lupus familiaris	180-185
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.	Ceramides	36-44	ATP binding cassette subfamily B member 1	Canis lupus familiaris	158-163
24822250-6	2014	This PD-associated change in ceramide acyl chain composition was accompanied by an upregulation of ceramide synthase-1 gene expression, which we consider may represent a response to reduced ceramide levels.	Ceramides	29-37	ceramide synthase 1	Homo sapiens	99-118
24142587-2	2014	We recently reported that the SM metabolite ceramide induces cathepsin D mediated apoptosis in murine intestinal epithelial cells (IECs) and increases inflammation in acute colitis.	Ceramides	44-52	cathepsin D	Mus musculus	61-72
24606127-0	2014	Adiponectin inhibits insulin function in primary trophoblasts by PPARalpha-mediated ceramide synthesis.	Ceramides	84-92	adiponectin, C1Q and collagen domain containing	Homo sapiens	0-11
24606127-0	2014	Adiponectin inhibits insulin function in primary trophoblasts by PPARalpha-mediated ceramide synthesis.	Ceramides	84-92	insulin	Homo sapiens	21-28
24606127-0	2014	Adiponectin inhibits insulin function in primary trophoblasts by PPARalpha-mediated ceramide synthesis.	Ceramides	84-92	peroxisome proliferator activated receptor alpha	Homo sapiens	65-74
24606127-4	2014	We hypothesized that ADN inhibits insulin signaling and insulin-stimulated amino acid transport in primary human trophoblasts by peroxisome proliferator-activated receptor-alpha (PPARalpha)-mediated ceramide synthesis.	Ceramides	199-207	adiponectin, C1Q and collagen domain containing	Mus musculus	21-24
24606127-4	2014	We hypothesized that ADN inhibits insulin signaling and insulin-stimulated amino acid transport in primary human trophoblasts by peroxisome proliferator-activated receptor-alpha (PPARalpha)-mediated ceramide synthesis.	Ceramides	199-207	insulin	Homo sapiens	56-63
24606127-4	2014	We hypothesized that ADN inhibits insulin signaling and insulin-stimulated amino acid transport in primary human trophoblasts by peroxisome proliferator-activated receptor-alpha (PPARalpha)-mediated ceramide synthesis.	Ceramides	199-207	peroxisome proliferator activated receptor alpha	Homo sapiens	129-177
24606127-4	2014	We hypothesized that ADN inhibits insulin signaling and insulin-stimulated amino acid transport in primary human trophoblasts by peroxisome proliferator-activated receptor-alpha (PPARalpha)-mediated ceramide synthesis.	Ceramides	199-207	peroxisome proliferator activated receptor alpha	Homo sapiens	179-188
24606127-9	2014	ADN increased ceramide synthase expression and stimulated ceramide production.	Ceramides	14-22	adiponectin, C1Q and collagen domain containing	Mus musculus	0-3
24606127-11	2014	These findings are consistent with the model that maternal ADN limits fetal growth mediated by activation of placental PPARalpha and ceramide synthesis, which inhibits placental insulin signaling and amino acid transport, resulting in reduced fetal nutrient availability.	Ceramides	133-141	adiponectin, C1Q and collagen domain containing	Mus musculus	59-62
24505141-10	2014	Smpd3 knockdown decreased the apoptosis of terminally matured ATDC5 chondrocytes, probably as a result of decreased ceramide production.	Ceramides	116-124	sphingomyelin phosphodiesterase 3, neutral	Mus musculus	0-5
24037959-1	2014	Neurons contain a mammalian-specific isoform of the enzyme carnitine palmitoyltransferase 1 (CPT1C) that couples malonyl-CoA to ceramide levels thereby contributing to systemic energy homeostasis and feeding behavior.	Ceramides	128-136	carnitine palmitoyltransferase 1C	Homo sapiens	93-98
24753742-7	2014	Since we have shown, previously, that activation of N-SMAse in MgD leads to synthesis and release of ceramide in cardiovascular tissues and cells, we believe this pathway, most likely, helps to result in downregulation of telomerase, upregulation of transcription factors (e.g., p53; NF-kB), cytokine release, mutations, transformations, and dysfunctional growth seen in the cardiac and vascular cells observed in the normal aging process, atherogenesis, hypertension, and cardiac failure.	Ceramides	101-109	sphingomyelin phosphodiesterase 2	Rattus norvegicus	52-59
24642596-1	2014	Ceramide transfer protein (CERT) transfers ceramide from the endoplasmic reticulum (ER) to the Golgi complex.	Ceramides	43-51	ceramide transporter 1	Mus musculus	0-25
24642596-1	2014	Ceramide transfer protein (CERT) transfers ceramide from the endoplasmic reticulum (ER) to the Golgi complex.	Ceramides	43-51	ceramide transporter 1	Mus musculus	27-31
24477431-10	2014	The selective loss of lysosomal glucocerebrosidase was directly related to reduced lysosomal chaperone-mediated autophagy, increased alpha-synuclein and decreased ceramide.	Ceramides	163-171	glucosylceramidase beta	Homo sapiens	22-50
24632809-0	2014	Overexpressed PKCdelta downregulates the expression of PKCalpha in B16F10 melanoma: induction of apoptosis by PKCdelta via ceramide generation.	Ceramides	123-131	protein kinase C, delta	Mus musculus	14-22
24632809-0	2014	Overexpressed PKCdelta downregulates the expression of PKCalpha in B16F10 melanoma: induction of apoptosis by PKCdelta via ceramide generation.	Ceramides	123-131	protein kinase C, delta	Mus musculus	110-118
24632809-3	2014	This in turn promoted cellular proliferation by activating PLD1 expression and subsequent AKT phosphorylation, which eventually resulted in suppressed ceramide generation and apoptosis.	Ceramides	151-159	phospholipase D1	Mus musculus	59-63
24632809-4	2014	On the other hand, B16F10 melanoma tumors preferentially blocked the expression of PKCdelta isotype, which otherwise could exhibit antagonistic effects on PKCalpha-PLD1-AKT signaling and rendered B16F10 cells more sensitive to apoptosis via generating ceramide and subsequently triggering caspase pathway.	Ceramides	252-260	protein kinase C, delta	Mus musculus	83-91
24632809-5	2014	Hence our data suggested a reciprocal PKC signaling operational in B16F10 melanoma cells, which regulates ceramide generation and provide important clues to target melanoma cancer by manipulating the PKCdelta-ceramide axis.	Ceramides	106-114	protein kinase C, alpha	Mus musculus	38-41
24632809-5	2014	Hence our data suggested a reciprocal PKC signaling operational in B16F10 melanoma cells, which regulates ceramide generation and provide important clues to target melanoma cancer by manipulating the PKCdelta-ceramide axis.	Ceramides	106-114	protein kinase C, delta	Mus musculus	200-208
24632809-5	2014	Hence our data suggested a reciprocal PKC signaling operational in B16F10 melanoma cells, which regulates ceramide generation and provide important clues to target melanoma cancer by manipulating the PKCdelta-ceramide axis.	Ceramides	209-217	protein kinase C, alpha	Mus musculus	38-41
24632809-5	2014	Hence our data suggested a reciprocal PKC signaling operational in B16F10 melanoma cells, which regulates ceramide generation and provide important clues to target melanoma cancer by manipulating the PKCdelta-ceramide axis.	Ceramides	209-217	protein kinase C, delta	Mus musculus	200-208
24970218-3	2014	Metabolic alterations that reduce levels of the pro-apoptotic lipid ceramide, particularly its glucosylation by glucosylceramide synthase (GCS), have frequently been associated with cancer drug resistance.	Ceramides	68-76	UDP-glucose ceramide glucosyltransferase	Homo sapiens	112-137
24970218-3	2014	Metabolic alterations that reduce levels of the pro-apoptotic lipid ceramide, particularly its glucosylation by glucosylceramide synthase (GCS), have frequently been associated with cancer drug resistance.	Ceramides	68-76	UDP-glucose ceramide glucosyltransferase	Homo sapiens	139-142
24079644-6	2014	In these cells, caspase-3 was inhibited by ceramide-induced Akt phosphorylation, and by the induction of autophagic microtubule-associated protein-1 light-chain 3 lipidation.	Ceramides	43-51	caspase 3	Homo sapiens	16-25
24079644-6	2014	In these cells, caspase-3 was inhibited by ceramide-induced Akt phosphorylation, and by the induction of autophagic microtubule-associated protein-1 light-chain 3 lipidation.	Ceramides	43-51	AKT serine/threonine kinase 1	Homo sapiens	60-63
24079644-9	2014	In cells from smokers, the prominent up-regulation of Akt pathways inhibited ceramide-triggered apoptosis, and was associated with elevated sphingosine and high-mobility group box 1, skewing the cell"s response toward autophagy and survival.	Ceramides	77-85	AKT serine/threonine kinase 1	Homo sapiens	54-57
24079644-10	2014	In conclusion, the cell responses to ceramide are modulated by an intricate cross-talk between Akt signaling and sphingolipid metabolites, and profoundly modified by previous cigarette smoke exposure, which selects for an apoptosis-resistant phenotype.	Ceramides	37-45	AKT serine/threonine kinase 1	Homo sapiens	95-98
24586752-4	2014	We found that the ceramide metabolite sphingosine-1-phosphate (S1P) stimulated the production of inflammatory mediators such as TNF-alpha and IL-8 from three-dimensionally cultured human primary keratinocytes (termed "3D keratinocytes"), which form a stratum corneum.	Ceramides	18-26	tumor necrosis factor	Homo sapiens	128-137
24518112-3	2014	Further, they demonstrate that interferon gamma decreases the expression of the enzymes required for the synthesis of these ultra long-chain ceramides (ELOVLs and ceramide synthase 3).	Ceramides	141-150	interferon gamma	Homo sapiens	31-47
24518112-3	2014	Further, they demonstrate that interferon gamma decreases the expression of the enzymes required for the synthesis of these ultra long-chain ceramides (ELOVLs and ceramide synthase 3).	Ceramides	141-150	ceramide synthase 3	Homo sapiens	163-182
24518112-4	2014	These results suggest that an increase in interferon gamma by decreasing the key enzymes required for the synthesis of ultra long-chain ceramides could further impair permeability barrier function, thereby exacerbating the pathological changes.	Ceramides	136-145	interferon gamma	Homo sapiens	42-58
24513118-12	2014	Thus, we conclude that PPARbeta/delta protects neural cells against ceramide-induced cell death via induction and activation of CerK.	Ceramides	68-76	peroxisome proliferator-activated receptor delta	Rattus norvegicus	23-31
24513118-12	2014	Thus, we conclude that PPARbeta/delta protects neural cells against ceramide-induced cell death via induction and activation of CerK.	Ceramides	68-76	ceramide kinase	Rattus norvegicus	128-132
24587339-1	2014	BACKGROUND: Sphingosine kinase 1 (SK1) is a key regulator of the dynamic ceramide/sphingosine 1-phosphate rheostat balance and important in the pathological cancer genesis, progression, and metastasis processes.	Ceramides	73-81	sphingosine kinase 1	Homo sapiens	12-32
24587339-1	2014	BACKGROUND: Sphingosine kinase 1 (SK1) is a key regulator of the dynamic ceramide/sphingosine 1-phosphate rheostat balance and important in the pathological cancer genesis, progression, and metastasis processes.	Ceramides	73-81	sphingosine kinase 1	Homo sapiens	34-37
24389129-7	2014	Furthermore, Ang 1-7 treatment decreased cardiac triacylglycerol and ceramide levels in db/db mice, concomitantly with an increase in myocardial adipose triglyceride lipase expression.	Ceramides	69-77	angiogenin, ribonuclease, RNase A family, 5	Mus musculus	13-18
24008422-0	2014	Interferon-gamma decreases ceramides with long-chain fatty acids: possible involvement in atopic dermatitis and psoriasis.	Ceramides	27-36	interferon gamma	Homo sapiens	0-16
24061166-7	2014	Although NHE-1 and sPLA2 were able to compensate the FLG deficiency, maintain the skin surface pH, and ensured ceramide processing (no differences detected), an accumulation of free fatty acids (2-fold increase) led to less ordered intercellular lipid lamellae and higher permeability of the FLG- constructs.	Ceramides	111-119	solute carrier family 9 member A1	Homo sapiens	9-14
24061166-7	2014	Although NHE-1 and sPLA2 were able to compensate the FLG deficiency, maintain the skin surface pH, and ensured ceramide processing (no differences detected), an accumulation of free fatty acids (2-fold increase) led to less ordered intercellular lipid lamellae and higher permeability of the FLG- constructs.	Ceramides	111-119	phospholipase A2 group X	Homo sapiens	19-24
24513118-0	2014	Peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) protects against ceramide-induced cellular toxicity in rat brain astrocytes and neurons by activation of ceramide kinase.	Ceramides	88-96	peroxisome proliferator-activated receptor delta	Rattus norvegicus	0-69
24513118-0	2014	Peroxisome proliferator-activated receptor beta/delta (PPARbeta/delta) protects against ceramide-induced cellular toxicity in rat brain astrocytes and neurons by activation of ceramide kinase.	Ceramides	88-96	ceramide kinase	Rattus norvegicus	176-191
24513118-4	2014	In the present study, we test the hypothesis that neuroprotection induced by PPARbeta/delta could rely on the regulation of ceramide metabolism.	Ceramides	124-132	peroxisome proliferator-activated receptor delta	Rattus norvegicus	77-85
24513118-5	2014	We found that preincubation of neural cells with the PPARbeta/delta agonist L-165041 exerts significant protection against ceramide-induced cell death.	Ceramides	123-131	peroxisome proliferator-activated receptor delta	Rattus norvegicus	53-61
24586752-4	2014	We found that the ceramide metabolite sphingosine-1-phosphate (S1P) stimulated the production of inflammatory mediators such as TNF-alpha and IL-8 from three-dimensionally cultured human primary keratinocytes (termed "3D keratinocytes"), which form a stratum corneum.	Ceramides	18-26	C-X-C motif chemokine ligand 8	Homo sapiens	142-146
24586752-7	2014	Among various ceramide metabolites, sphingosine and S1P enhanced the gene expression of TNF-alpha, endothelin-1, and IL-8.	Ceramides	14-22	tumor necrosis factor	Homo sapiens	88-97
24586752-7	2014	Among various ceramide metabolites, sphingosine and S1P enhanced the gene expression of TNF-alpha, endothelin-1, and IL-8.	Ceramides	14-22	endothelin 1	Homo sapiens	99-111
24586752-7	2014	Among various ceramide metabolites, sphingosine and S1P enhanced the gene expression of TNF-alpha, endothelin-1, and IL-8.	Ceramides	14-22	C-X-C motif chemokine ligand 8	Homo sapiens	117-121
24552349-11	2014	Exercise induces enhanced adiponectin uptake to oxidative skeletal muscles, wherein adiponectin potently lowers ceramide levels.	Ceramides	112-120	adiponectin, C1Q and collagen domain containing	Mus musculus	84-95
24266736-0	2014	c-Src-induced activation of ceramide metabolism impairs membrane microdomains and promotes malignant progression by facilitating the translocation of c-Src to focal adhesions.	Ceramides	28-36	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	0-5
24266736-0	2014	c-Src-induced activation of ceramide metabolism impairs membrane microdomains and promotes malignant progression by facilitating the translocation of c-Src to focal adhesions.	Ceramides	28-36	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	150-155
24266736-3	2014	In the present study we show that c-Src up-regulation perturbs sphingolipid/cholesterol-enriched membrane microdomains by activating ceramide synthesis, resulting in promotion of c-Src translocation.	Ceramides	133-141	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	34-39
24266736-3	2014	In the present study we show that c-Src up-regulation perturbs sphingolipid/cholesterol-enriched membrane microdomains by activating ceramide synthesis, resulting in promotion of c-Src translocation.	Ceramides	133-141	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	179-184
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.	Ceramides	14-22	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	79-84
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.	Ceramides	47-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	79-84
24266736-8	2014	These results suggest that c-Src-induced activation of ceramide synthesis impairs the integrity of microdomains and contributes to malignant progression by promoting the translocation of c-Src to focal adhesions/podosomes.	Ceramides	55-63	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	27-32
24266736-8	2014	These results suggest that c-Src-induced activation of ceramide synthesis impairs the integrity of microdomains and contributes to malignant progression by promoting the translocation of c-Src to focal adhesions/podosomes.	Ceramides	55-63	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	187-192