PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
10395296-5	1999	Exogenous C16-ceramide (20 microM) and acid sphingomyelinase induced trophoblast apoptosis, an effect abrogated completely by cotreatment with 10 ng/ml EGF.	N-palmitoylsphingosine	10-22	epidermal growth factor	Homo sapiens	152-155
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.	N-palmitoylsphingosine	15-27	phospholipase A2 group IB	Homo sapiens	131-136
34343636-6	2021	Furthermore, CerS6 promoted cell proliferation, colony formation and invasion by producing C16-ceramide and was required for tumor formation.	N-palmitoylsphingosine	91-103	ceramide synthase 6	Homo sapiens	13-18
34343636-8	2021	The AKT1/FOXP3 axis mediated the CerS6 expression and promoted p53 mutant pancreatic tumorigenesis by producing excessive C16-ceramide, which induced the accumulation of mutant p53.	N-palmitoylsphingosine	122-134	AKT serine/threonine kinase 1	Homo sapiens	4-8
34343636-8	2021	The AKT1/FOXP3 axis mediated the CerS6 expression and promoted p53 mutant pancreatic tumorigenesis by producing excessive C16-ceramide, which induced the accumulation of mutant p53.	N-palmitoylsphingosine	122-134	forkhead box P3	Homo sapiens	9-14
34343636-8	2021	The AKT1/FOXP3 axis mediated the CerS6 expression and promoted p53 mutant pancreatic tumorigenesis by producing excessive C16-ceramide, which induced the accumulation of mutant p53.	N-palmitoylsphingosine	122-134	ceramide synthase 6	Homo sapiens	33-38
34343636-8	2021	The AKT1/FOXP3 axis mediated the CerS6 expression and promoted p53 mutant pancreatic tumorigenesis by producing excessive C16-ceramide, which induced the accumulation of mutant p53.	N-palmitoylsphingosine	122-134	tumor protein p53	Homo sapiens	63-66
34343636-8	2021	The AKT1/FOXP3 axis mediated the CerS6 expression and promoted p53 mutant pancreatic tumorigenesis by producing excessive C16-ceramide, which induced the accumulation of mutant p53.	N-palmitoylsphingosine	122-134	tumor protein p53	Homo sapiens	177-180
34062962-5	2021	Instead, our results suggest that ASAH1 activity is important for preventing the accumulation of long chain ceramides such as C16-ceramide.	N-palmitoylsphingosine	126-138	N-acylsphingosine amidohydrolase 1	Homo sapiens	34-39
34482548-8	2021	Exogenous C16 ceramide, dipalmitoyl-phosphatidylcholine, and dipalmitoyl-phosphatidylethanolamine were sufficient to significantly induce Npy expression.	N-palmitoylsphingosine	10-22	neuropeptide Y	Homo sapiens	138-141
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	42-54	ceramide synthase 6	Homo sapiens	71-76
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	42-54	tumor protein p53	Homo sapiens	80-83
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	42-54	ceramide synthase 6	Homo sapiens	125-130
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	139-151	ceramide synthase 6	Homo sapiens	71-76
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	139-151	tumor protein p53	Homo sapiens	80-83
34062962-6	2021	We therefore determined how modulation of C16-ceramide, either through CerS6 or p53, a known PGCC suppressor and enhancer of CerS6-derived C16-ceramide, affected PGCC progeny formation.	N-palmitoylsphingosine	139-151	ceramide synthase 6	Homo sapiens	125-130
35184720-0	2022	Insulin resistance induced by de novo pathway-generated C16-ceramide is associated with type 2 diabetes in an obese population.	N-palmitoylsphingosine	56-68	insulin	Homo sapiens	0-7
35184720-10	2022	CONCLUSIONS: The present study indicates that C16-ceramide plays a pivotal role in inducing insulin resistance.	N-palmitoylsphingosine	46-58	insulin	Homo sapiens	92-99
35184720-11	2022	Overexpression of SPT1 in the obese-diabetic group and its positive correlation with C16-ceramide suggest that C16-ceramide was generated through the de novo pathway.	N-palmitoylsphingosine	85-97	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	18-22
35184720-11	2022	Overexpression of SPT1 in the obese-diabetic group and its positive correlation with C16-ceramide suggest that C16-ceramide was generated through the de novo pathway.	N-palmitoylsphingosine	111-123	serine palmitoyltransferase long chain base subunit 1	Homo sapiens	18-22
33895135-9	2021	The addition of purified acid sphingomyelinase or C16 ceramide restored entry of pp-VSV-SARS-CoV-2 spike into ambroxol-treated epithelial cells.	N-palmitoylsphingosine	50-62	surface glycoprotein	Severe acute respiratory syndrome coronavirus 2	99-104
31744877-10	2020	Furthermore, AC knockdown and exogenous C16-ceramide supplementation induced similar changes in SF3B1 level and Mcl-1S/L ratio.	N-palmitoylsphingosine	40-52	splicing factor 3b subunit 1	Homo sapiens	96-101
31744877-10	2020	Furthermore, AC knockdown and exogenous C16-ceramide supplementation induced similar changes in SF3B1 level and Mcl-1S/L ratio.	N-palmitoylsphingosine	40-52	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	112-118
32045989-7	2020	In contrast, C16 ceramide-enriched HDL3 upregulated the phosphorylation of four intermediates in the mTOR pathway.	N-palmitoylsphingosine	13-25	HDL3	Homo sapiens	35-39
32045989-7	2020	In contrast, C16 ceramide-enriched HDL3 upregulated the phosphorylation of four intermediates in the mTOR pathway.	N-palmitoylsphingosine	13-25	mechanistic target of rapamycin kinase	Homo sapiens	101-105
30836822-0	2019	Expression of the SNAI2 transcriptional repressor is regulated by C16-ceramide.	N-palmitoylsphingosine	66-78	snail family transcriptional repressor 2	Homo sapiens	18-23
31585804-9	2019	Subsequently, we measured the activation of acid sphingomyelinase (ASMase) enzyme by radioenzymatic assay using [14C-methylcholine] sphingomyelin as substrate, and the generation of the proapoptotic C16-ceramide was assessed using the diacylglycerol kinase assay.	N-palmitoylsphingosine	199-211	ASM	Bos taurus	44-65
31585804-9	2019	Subsequently, we measured the activation of acid sphingomyelinase (ASMase) enzyme by radioenzymatic assay using [14C-methylcholine] sphingomyelin as substrate, and the generation of the proapoptotic C16-ceramide was assessed using the diacylglycerol kinase assay.	N-palmitoylsphingosine	199-211	ASM	Bos taurus	67-73
30836822-1	2019	Ceramide synthase 6 (CerS6) is an enzyme that preferentially generates pro-apoptotic C16-ceramide in the sphingolipid metabolic pathway.	N-palmitoylsphingosine	85-97	ceramide synthase 6	Homo sapiens	0-19
30836822-1	2019	Ceramide synthase 6 (CerS6) is an enzyme that preferentially generates pro-apoptotic C16-ceramide in the sphingolipid metabolic pathway.	N-palmitoylsphingosine	85-97	ceramide synthase 6	Homo sapiens	21-26
30836822-7	2019	shRNA against CerS5, which like CerS6 preferentially generates C16-ceramide, also decreased transcriptional activation of SNAI2, suggesting a role for C16-ceramide rather than a specific enzyme in the regulation of this transcription factor.	N-palmitoylsphingosine	63-75	ceramide synthase 5	Homo sapiens	14-19
30836822-7	2019	shRNA against CerS5, which like CerS6 preferentially generates C16-ceramide, also decreased transcriptional activation of SNAI2, suggesting a role for C16-ceramide rather than a specific enzyme in the regulation of this transcription factor.	N-palmitoylsphingosine	63-75	ceramide synthase 6	Homo sapiens	32-37
30836822-7	2019	shRNA against CerS5, which like CerS6 preferentially generates C16-ceramide, also decreased transcriptional activation of SNAI2, suggesting a role for C16-ceramide rather than a specific enzyme in the regulation of this transcription factor.	N-palmitoylsphingosine	151-163	ceramide synthase 5	Homo sapiens	14-19
30836822-7	2019	shRNA against CerS5, which like CerS6 preferentially generates C16-ceramide, also decreased transcriptional activation of SNAI2, suggesting a role for C16-ceramide rather than a specific enzyme in the regulation of this transcription factor.	N-palmitoylsphingosine	151-163	snail family transcriptional repressor 2	Homo sapiens	122-127
30836822-9	2019	In summary, our study identifies SNAI2 as a novel target whose expression can be influenced by C16-ceramide levels.	N-palmitoylsphingosine	95-107	snail family transcriptional repressor 2	Homo sapiens	33-38
30226616-0	2018	C16-ceramide and sphingosine 1-phosphate/S1PR2 have opposite effects on cell growth through mTOR signaling pathway regulation.	N-palmitoylsphingosine	0-12	mechanistic target of rapamycin kinase	Homo sapiens	92-96
30226616-12	2018	Moreover, mTOR activity can be regulated by the balance between S1P and C16-ceramide, which is generated by CerS6.	N-palmitoylsphingosine	72-84	mechanistic target of rapamycin kinase	Homo sapiens	10-14
30226616-12	2018	Moreover, mTOR activity can be regulated by the balance between S1P and C16-ceramide, which is generated by CerS6.	N-palmitoylsphingosine	72-84	ceramide synthase 6	Homo sapiens	108-113
30131496-2	2018	Genetic mouse models have established C16 ceramide as a driver of insulin resistance in liver and adipose tissue.	N-palmitoylsphingosine	38-50	insulin	Homo sapiens	66-73
30297838-0	2018	C16-ceramide is a natural regulatory ligand of p53 in cellular stress response.	N-palmitoylsphingosine	0-12	tumor protein p53	Homo sapiens	47-50
30297838-2	2018	Here we report the mechanism for activation of p53 tumor suppressor by C16-ceramide.	N-palmitoylsphingosine	71-83	tumor protein p53	Homo sapiens	47-50
30297838-3	2018	C16-ceramide tightly binds within the p53 DNA-binding domain (Kd ~ 60 nM), in close vicinity to the Box V motif.	N-palmitoylsphingosine	0-12	tumor protein p53	Homo sapiens	38-41
30297838-8	2018	Our study establishes C16-ceramide as a natural small molecule activating p53 through the direct binding.	N-palmitoylsphingosine	22-34	tumor protein p53	Homo sapiens	74-77
29138469-3	2017	CerS6 preferentially generates C16-ceramide and its mRNA is highly expressed in immune tissues.	N-palmitoylsphingosine	31-43	ceramide synthase 6	Homo sapiens	0-5
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.	N-palmitoylsphingosine	129-141	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.	N-palmitoylsphingosine	129-141	interleukin 1 receptor antagonist	Mus musculus	166-172
29374263-5	2018	CerS6-deficient mice maintained low levels of C16-ceramide after DSS treatment, but the inflammatory lipid sphingosine-1-phosphate was significantly increased in colon tissue.	N-palmitoylsphingosine	46-58	ceramide synthase 6	Mus musculus	0-5
29138469-5	2017	Adoptive transfer of CerS6-deficient splenocytes, which have significantly decreased levels of C16-ceramide, showed that CerS6-deficiency protected against the development of colitis.	N-palmitoylsphingosine	95-107	ceramide synthase 6	Homo sapiens	21-26
28179144-8	2017	We finally showed that irradiation, as well as treatment with exogenous C16-ceramide or bacterial sphingomyelinase, induced in endothelial cells a deep reorganization of the plasma membrane with formation of large lipid platforms at the cell surface, leading to p38 MAPK activation and apoptosis in endothelial cells.	N-palmitoylsphingosine	72-84	mitogen-activated protein kinase 14	Homo sapiens	262-265
26783755-1	2016	We previously reported that ceramide synthase 6 (CerS6) is elevated in response to folate stress in cancer cells, leading to enhanced production of C16-ceramide and apoptosis.	N-palmitoylsphingosine	148-160	ceramide synthase 6	Homo sapiens	28-47
26933996-7	2016	Particularly C16-ceramide and S1P may serve as novel diagnostic markers for the identification of HCC in patients with liver diseases.	N-palmitoylsphingosine	13-25	HCC	Homo sapiens	98-101
27280497-1	2016	Longevity Assurance 5 (LASS5), a member of the LASS/Ceramide Synthases family, synthesizes C16-ceramide and is implicated in tumor biology.	N-palmitoylsphingosine	91-103	ceramide synthase 5	Homo sapiens	0-21
27280497-1	2016	Longevity Assurance 5 (LASS5), a member of the LASS/Ceramide Synthases family, synthesizes C16-ceramide and is implicated in tumor biology.	N-palmitoylsphingosine	91-103	ceramide synthase 5	Homo sapiens	23-28
26783755-1	2016	We previously reported that ceramide synthase 6 (CerS6) is elevated in response to folate stress in cancer cells, leading to enhanced production of C16-ceramide and apoptosis.	N-palmitoylsphingosine	148-160	ceramide synthase 6	Homo sapiens	49-54
26783755-6	2016	The increase in C16-ceramide, however, was eliminated in MTX-treated cells lacking CerS6 through siRNA silencing, while the increase in other ceramides sustained.	N-palmitoylsphingosine	16-28	ceramide synthase 6	Homo sapiens	83-88
26318452-7	2015	Knockdown of individual ceramide synthases identified CerS6 and its product C16-ceramide as the ceramide synthase isoform essential for the regulation of cell death.	N-palmitoylsphingosine	76-88	ceramide synthase 6	Homo sapiens	54-59
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.	N-palmitoylsphingosine	199-212	ceramide synthase 2	Homo sapiens	23-42
27551447-3	2015	In this study, we show here that the elevation of endogenous C16-ceramide levels is a common feature of several known apoptosis-inducing triggers like mmLDL, TNF-alpha, H2O2 and exogenous C6-ceramide.	N-palmitoylsphingosine	61-73	tumor necrosis factor	Homo sapiens	158-167
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.	N-palmitoylsphingosine	129-141	ceramide synthase 6	Homo sapiens	18-23
24632610-7	2015	Furthermore, pharmacological and genetic approaches established that modulation of CerS6 expression/activity in cancer cells altered the level of C16-ceramide, which in turn influenced plasma membrane fluidity and cell motility.	N-palmitoylsphingosine	146-158	ceramide synthase 6	Homo sapiens	83-88
25462172-10	2015	Moreover, mitochondria isolated from cells overexpressing the ceramide synthase responsible for the production of C16-ceramide (CerS5) are permeabilized faster upon the exogenous addition of C16-ceramide whereas they are resistant to permeabilization with added C24-ceramide.	N-palmitoylsphingosine	114-126	ceramide synthase 5	Homo sapiens	128-133
25462172-10	2015	Moreover, mitochondria isolated from cells overexpressing the ceramide synthase responsible for the production of C16-ceramide (CerS5) are permeabilized faster upon the exogenous addition of C16-ceramide whereas they are resistant to permeabilization with added C24-ceramide.	N-palmitoylsphingosine	191-203	ceramide synthase 5	Homo sapiens	128-133
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.	N-palmitoylsphingosine	199-212	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.	N-palmitoylsphingosine	109-122	ceramide synthase 6	Homo sapiens	141-146
24819607-5	2014	We found that C16-ceramide induces EMD phosphorylation on its LEM domain through PRKACA.	N-palmitoylsphingosine	14-26	protein kinase cAMP-activated catalytic subunit alpha	Homo sapiens	81-87
24595304-6	2014	Only TNFalpha treatment of 3T3-L1 cells led to an increase in oxidative stress (as measured by superoxide anion production and protein carbonylation) and C16 ceramide synthesis.	N-palmitoylsphingosine	154-166	tumor necrosis factor	Mus musculus	5-13
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.	N-palmitoylsphingosine	208-221	ceramide synthase 2	Mus musculus	169-174
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.	N-palmitoylsphingosine	96-108	ceramide synthase 2	Mus musculus	2-7
23519469-3	2013	Here we report that the expression of Aldh1l1 in A549 or HCT116 cells results in the elevation of C16-ceramide and a transient up-regulation of ceramide synthase 6 (CerS6) mRNA and protein.	N-palmitoylsphingosine	98-110	aldehyde dehydrogenase 1 family member L1	Homo sapiens	38-45
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.	N-palmitoylsphingosine	112-124	ceramide synthase 6	Homo sapiens	96-101
23283968-4	2013	Significant changes were observed in the sphingolipid profile of CerS2 null mouse liver, including elevated C16-ceramide and sphinganine levels in liver and in isolated mitochondrial fractions.	N-palmitoylsphingosine	108-120	ceramide synthase 2	Mus musculus	65-70
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.	N-palmitoylsphingosine	69-83	ceramide synthase 6	Homo sapiens	109-128
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.	N-palmitoylsphingosine	69-83	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.	N-palmitoylsphingosine	69-83	ceramide synthase 1	Homo sapiens	197-202
22640955-5	2012	The palmitate-induced increase in CD11b and CD36 expression was associated with increased cellular C16 ceramide and sphingomyelin, loss of reduced glutathione, and increased reactive oxygen species (ROS).	N-palmitoylsphingosine	99-111	integrin subunit alpha M	Homo sapiens	34-39
22615346-9	2012	Indeed, PP2Calpha induced the dephosphorylation of p38delta only in the presence of C(16)-ceramide.	N-palmitoylsphingosine	84-98	protein phosphatase, Mg2+/Mn2+ dependent 1A	Homo sapiens	8-17
22615346-9	2012	Indeed, PP2Calpha induced the dephosphorylation of p38delta only in the presence of C(16)-ceramide.	N-palmitoylsphingosine	84-98	mitogen-activated protein kinase 13	Homo sapiens	51-59
20808818-5	2010	Here we show VEGF prevented radiation-induced ASMase activation in cultured endothelium, occurring within minutes after radiation exposure, consequently repressing apoptosis, an event reversible with exogenous C(16)-ceramide.	N-palmitoylsphingosine	210-224	vascular endothelial growth factor A	Mus musculus	13-17
21490809-0	2011	C16-Ceramide Analog Combined with Pc 4 Photodynamic Therapy Evokes Enhanced Total Ceramide Accumulation, Promotion of DEVDase Activation in the Absence of Apoptosis, and Augmented Overall Cell Killing.	N-palmitoylsphingosine	0-12	proprotein convertase subtilisin/kexin type 4	Mus musculus	34-38
20941382-5	2010	Here we show VEGF prevented radiation-induced ASMase activation in cultured endothelium, occurring within minutes after radiation exposure, consequently repressing apoptosis, an event reversible with exogenous C16-ceramide.	N-palmitoylsphingosine	210-222	vascular endothelial growth factor A	Mus musculus	13-17
19723703-0	2010	Antiapoptotic roles of ceramide-synthase-6-generated C16-ceramide via selective regulation of the ATF6/CHOP arm of ER-stress-response pathways.	N-palmitoylsphingosine	53-65	ceramide synthase 6	Homo sapiens	23-42
19723703-0	2010	Antiapoptotic roles of ceramide-synthase-6-generated C16-ceramide via selective regulation of the ATF6/CHOP arm of ER-stress-response pathways.	N-palmitoylsphingosine	53-65	activating transcription factor 6	Homo sapiens	98-102
19723703-0	2010	Antiapoptotic roles of ceramide-synthase-6-generated C16-ceramide via selective regulation of the ATF6/CHOP arm of ER-stress-response pathways.	N-palmitoylsphingosine	53-65	DNA damage inducible transcript 3	Homo sapiens	103-107
19723703-2	2010	Here we report that de novo-generated C(18)- and C(16)-ceramides by ceramide synthases 1 and 6 (CerS1 and CerS6) play opposing proapoptotic and prosurvival roles, respectively, in human head and neck squamous cell carcinomas (HNSCCs).	N-palmitoylsphingosine	49-64	ceramide synthase 1	Homo sapiens	96-101
19723703-2	2010	Here we report that de novo-generated C(18)- and C(16)-ceramides by ceramide synthases 1 and 6 (CerS1 and CerS6) play opposing proapoptotic and prosurvival roles, respectively, in human head and neck squamous cell carcinomas (HNSCCs).	N-palmitoylsphingosine	49-64	ceramide synthase 6	Homo sapiens	106-111
19723703-4	2010	Reconstitution of C(16)-ceramide generation by induced expression of wild-type CerS6, but not its catalytically inactive mutant, protected cells from cell death induced by knockdown of CerS6.	N-palmitoylsphingosine	18-32	ceramide synthase 6	Homo sapiens	79-84
19723703-4	2010	Reconstitution of C(16)-ceramide generation by induced expression of wild-type CerS6, but not its catalytically inactive mutant, protected cells from cell death induced by knockdown of CerS6.	N-palmitoylsphingosine	18-32	ceramide synthase 6	Homo sapiens	185-190
19723703-5	2010	Moreover, using molecular tools coupled with analysis of sphingolipid metabolism showed that generation of C(16)-ceramide, and not dihydro-C(16)-ceramide, by induced expression of CerS6 rescued cells from ER stress and apoptosis.	N-palmitoylsphingosine	107-121	ceramide synthase 6	Homo sapiens	180-185
19137010-1	2009	We have previously shown that the death receptor ligand TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) induces an increase of intracellular C(16)-ceramide in sensitive SW480 but not in resistant SW620 cells.	N-palmitoylsphingosine	157-171	TNF superfamily member 10	Homo sapiens	56-61
19137010-1	2009	We have previously shown that the death receptor ligand TRAIL (tumor necrosis factor-related apoptosis-inducing ligand) induces an increase of intracellular C(16)-ceramide in sensitive SW480 but not in resistant SW620 cells.	N-palmitoylsphingosine	157-171	TNF superfamily member 10	Homo sapiens	63-118
19137010-5	2009	RNAi against CerS6 resulted in a specific and significant decrease of the C(16)-ceramide species, which was sufficient to inhibit TRAIL-induced apoptosis.	N-palmitoylsphingosine	74-88	ceramide synthase 6	Homo sapiens	13-18
19137010-5	2009	RNAi against CerS6 resulted in a specific and significant decrease of the C(16)-ceramide species, which was sufficient to inhibit TRAIL-induced apoptosis.	N-palmitoylsphingosine	74-88	TNF superfamily member 10	Homo sapiens	130-135
18682390-5	2008	In OLs, knockdown of Lyn with small interfering RNA resulted in OL apoptosis with concomitant accumulation of C(16)-ceramide due to activation of acid sphingomyelinase (ASMase) and sphingomyelin hydrolysis.	N-palmitoylsphingosine	110-124	LYN proto-oncogene, Src family tyrosine kinase	Mus musculus	21-24
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.	N-palmitoylsphingosine	145-167	tumor protein p53	Homo sapiens	28-31
17982273-9	2007	This Vav2-siRNA also blocked Rac activation induced by C16-Ceramide (C16-Cer), an intermediate lipid product stimulated by Hcys.	N-palmitoylsphingosine	55-67	vav guanine nucleotide exchange factor 2	Rattus norvegicus	5-9
18400537-0	2008	De novo N-palmitoylsphingosine synthesis is the major biochemical mechanism of ceramide accumulation following p53 up-regulation.	N-palmitoylsphingosine	8-30	tumor protein p53	Homo sapiens	111-114
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.	N-palmitoylsphingosine	190-212	tumor protein p53	Homo sapiens	117-120
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.	N-palmitoylsphingosine	214-226	tumor protein p53	Homo sapiens	117-120
17982273-9	2007	This Vav2-siRNA also blocked Rac activation induced by C16-Ceramide (C16-Cer), an intermediate lipid product stimulated by Hcys.	N-palmitoylsphingosine	55-67	Rac family small GTPase 1	Rattus norvegicus	29-32
17982273-9	2007	This Vav2-siRNA also blocked Rac activation induced by C16-Ceramide (C16-Cer), an intermediate lipid product stimulated by Hcys.	N-palmitoylsphingosine	55-62	vav guanine nucleotide exchange factor 2	Rattus norvegicus	5-9
17982273-9	2007	This Vav2-siRNA also blocked Rac activation induced by C16-Ceramide (C16-Cer), an intermediate lipid product stimulated by Hcys.	N-palmitoylsphingosine	55-62	Rac family small GTPase 1	Rattus norvegicus	29-32
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.	N-palmitoylsphingosine	56-70	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.	N-palmitoylsphingosine	56-70	inorganic pyrophosphatase 1	Homo sapiens	280-283
16636669-5	2006	Further, ASM-deficient splenocytes fail to cluster DR5 in ceramide-enriched membrane domains upon TRAIL stimulation and resist TRAIL-induced apoptosis, events that were restored by addition of natural C(16)-ceramide.	N-palmitoylsphingosine	201-215	TNF superfamily member 10	Homo sapiens	127-132
16170023-8	2005	Upon TRAIL treatment, ceramide (primarily C(16)-ceramide) increased in SW480 but not SW620 cells.	N-palmitoylsphingosine	42-56	TNF superfamily member 10	Homo sapiens	5-10
16118219-7	2005	Overexpression of SphK2 increased incorporation of [(3)H]palmitate, a substrate for both serine palmitoyltransferase and ceramide synthase, into C16-ceramide, whereas SphK1 decreased it.	N-palmitoylsphingosine	145-157	sphingosine kinase 2	Homo sapiens	18-23
15946935-0	2005	Roles for C16-ceramide and sphingosine 1-phosphate in regulating hepatocyte apoptosis in response to tumor necrosis factor-alpha.	N-palmitoylsphingosine	10-22	tumor necrosis factor	Rattus norvegicus	101-128
15946935-3	2005	Endogenous C16-ceramide was elevated during TNF-alpha-induced apoptosis in both rat and mouse primary hepatocytes.	N-palmitoylsphingosine	11-23	tumor necrosis factor	Rattus norvegicus	44-53
15946935-5	2005	Overexpression of neutral CDase (NCDase) inhibited the TNF-alpha-induced increase of C16-ceramide and apoptosis in rat primary hepatocytes.	N-palmitoylsphingosine	85-97	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	18-31
15946935-5	2005	Overexpression of neutral CDase (NCDase) inhibited the TNF-alpha-induced increase of C16-ceramide and apoptosis in rat primary hepatocytes.	N-palmitoylsphingosine	85-97	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	33-39
15946935-5	2005	Overexpression of neutral CDase (NCDase) inhibited the TNF-alpha-induced increase of C16-ceramide and apoptosis in rat primary hepatocytes.	N-palmitoylsphingosine	85-97	tumor necrosis factor	Rattus norvegicus	55-64
15946935-7	2005	This protective effect was abrogated by the sphingosine kinase inhibitor N,N-demethylsphingosine, suggesting that the survival effect of NCDase is due to not only C16-ceramide reduction but also S1P formation.	N-palmitoylsphingosine	163-175	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	137-143
15946935-9	2005	In conclusion, activation of ASMase and generation of C16-ceramide contributed to TNF-alpha-induced hepatocyte apoptosis.	N-palmitoylsphingosine	54-66	tumor necrosis factor	Rattus norvegicus	82-91
15946935-10	2005	NCDase prevented apoptosis both by reducing C16-ceramide and by activation of AKT through S1P formation.	N-palmitoylsphingosine	44-56	N-acylsphingosine amidohydrolase 2	Rattus norvegicus	0-6
15743760-5	2005	Bax conformational change in ASMase(-/-) cells is also caused by synthetic C(16)-ceramide acting on intact cells or isolated mitochondria.	N-palmitoylsphingosine	75-89	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
15743760-5	2005	Bax conformational change in ASMase(-/-) cells is also caused by synthetic C(16)-ceramide acting on intact cells or isolated mitochondria.	N-palmitoylsphingosine	75-89	sphingomyelin phosphodiesterase 1	Homo sapiens	29-35
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.	N-palmitoylsphingosine	147-161	ceramide transporter 1	Homo sapiens	16-20
15596449-7	2005	Among four stereoisomers of C(16)-ceramide, CERT specifically recognized the natural d-erythro isomer.	N-palmitoylsphingosine	28-42	ceramide transporter 1	Homo sapiens	44-48
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.	N-palmitoylsphingosine	40-52	protein kinase C alpha	Homo sapiens	175-183
12829737-6	2003	These results and previously reported effects of short-chain ceramides on phospholipase D activity prompted us to compare the effects of C2-ceramide, C2-dihydroceramide and C16-ceramide on phospholipase D1 and phospholipase D2 activities in vitro.	N-palmitoylsphingosine	173-185	phospholipase D1	Rattus norvegicus	189-205
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.	N-palmitoylsphingosine	145-159	sphingomyelin phosphodiesterase 1	Homo sapiens	0-21
11096096-6	2001	The addition of low nanomolar quantities of natural C16-ceramide, which by itself did not induce apoptosis, completely restored the apoptotic response to anti-Fas in asmase(-/-) hepatocytes.	N-palmitoylsphingosine	52-64	sphingomyelin phosphodiesterase 1, acid lysosomal	Mus musculus	166-172