PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
18337251-5	2008	Nuclear mGlu5-mediated Ca2+ responses could also be blocked by the phospholipase C (PLC) inhibitor, U73122, the phosphatidylinositol (PI) PLC inhibitor 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphorylcholine (ET-18-OCH3), or by using small interfering RNA targeted against PLCbeta1 demonstrating that PI-PLC is involved.	edelfosine	152-207	phospholipase C beta 1	Homo sapiens	273-281
18337251-5	2008	Nuclear mGlu5-mediated Ca2+ responses could also be blocked by the phospholipase C (PLC) inhibitor, U73122, the phosphatidylinositol (PI) PLC inhibitor 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphorylcholine (ET-18-OCH3), or by using small interfering RNA targeted against PLCbeta1 demonstrating that PI-PLC is involved.	edelfosine	152-207	phospholipase C beta 1	Homo sapiens	301-307
17891170-0	2008	Proapoptotic role of Hsp90 by its interaction with c-Jun N-terminal kinase in lipid rafts in edelfosine-mediated antileukemic therapy.	edelfosine	93-103	heat shock protein 90 alpha family class A member 1	Homo sapiens	21-26
17891170-0	2008	Proapoptotic role of Hsp90 by its interaction with c-Jun N-terminal kinase in lipid rafts in edelfosine-mediated antileukemic therapy.	edelfosine	93-103	mitogen-activated protein kinase 8	Homo sapiens	51-74
17891170-4	2008	Following edelfosine treatment, Hsp90 bound to JNK in lipid rafts and Hsp90-JNK clusters were identified at the plasma membrane by immunoelectron microscopy.	edelfosine	10-20	heat shock protein 90 alpha family class A member 1	Homo sapiens	32-37
17891170-4	2008	Following edelfosine treatment, Hsp90 bound to JNK in lipid rafts and Hsp90-JNK clusters were identified at the plasma membrane by immunoelectron microscopy.	edelfosine	10-20	mitogen-activated protein kinase 8	Homo sapiens	47-50
17891170-2	2008	However, we have found that inhibitors of Hsp90 diminished the apoptotic response induced in leukemic cells by the antitumor alkyl-lysophospholipid analog edelfosine, which acts through lipid raft reorganization.	edelfosine	155-165	heat shock protein 90 alpha family class A member 1	Homo sapiens	42-47
17891170-4	2008	Following edelfosine treatment, Hsp90 bound to JNK in lipid rafts and Hsp90-JNK clusters were identified at the plasma membrane by immunoelectron microscopy.	edelfosine	10-20	heat shock protein 90 alpha family class A member 1	Homo sapiens	70-75
17891170-3	2008	Edelfosine treatment recruited Hsp90, c-Jun N-terminal kinase (JNK) and apoptotic molecules in lipid rafts, but not the JNK regulators apoptosis signal-regulating kinase 1 (ASK1) and Daxx, or the survival signaling molecules extracellular signal-regulated kinase (ERK) and Akt.	edelfosine	0-10	heat shock protein 90 alpha family class A member 1	Homo sapiens	31-36
17891170-4	2008	Following edelfosine treatment, Hsp90 bound to JNK in lipid rafts and Hsp90-JNK clusters were identified at the plasma membrane by immunoelectron microscopy.	edelfosine	10-20	mitogen-activated protein kinase 8	Homo sapiens	76-79
17891170-5	2008	Hsp90 inhibition reduced JNK protein level in lipid rafts and turned proapoptotic persistent JNK activation into a transient response in edelfosine-treated cells.	edelfosine	137-147	heat shock protein 90 alpha family class A member 1	Homo sapiens	0-5
17891170-3	2008	Edelfosine treatment recruited Hsp90, c-Jun N-terminal kinase (JNK) and apoptotic molecules in lipid rafts, but not the JNK regulators apoptosis signal-regulating kinase 1 (ASK1) and Daxx, or the survival signaling molecules extracellular signal-regulated kinase (ERK) and Akt.	edelfosine	0-10	mitogen-activated protein kinase 8	Homo sapiens	38-61
17891170-5	2008	Hsp90 inhibition reduced JNK protein level in lipid rafts and turned proapoptotic persistent JNK activation into a transient response in edelfosine-treated cells.	edelfosine	137-147	mitogen-activated protein kinase 8	Homo sapiens	25-28
17891170-3	2008	Edelfosine treatment recruited Hsp90, c-Jun N-terminal kinase (JNK) and apoptotic molecules in lipid rafts, but not the JNK regulators apoptosis signal-regulating kinase 1 (ASK1) and Daxx, or the survival signaling molecules extracellular signal-regulated kinase (ERK) and Akt.	edelfosine	0-10	mitogen-activated protein kinase 8	Homo sapiens	63-66
17891170-5	2008	Hsp90 inhibition reduced JNK protein level in lipid rafts and turned proapoptotic persistent JNK activation into a transient response in edelfosine-treated cells.	edelfosine	137-147	mitogen-activated protein kinase 8	Homo sapiens	93-96
17891170-6	2008	Decrease in edelfosine-induced JNK activation and apoptosis by Hsp90 inhibition was prevented through proteasome inhibition, suggesting that Hsp90 inhibition diminishes apoptosis by promoting JNK protein degradation.	edelfosine	12-22	mitogen-activated protein kinase 8	Homo sapiens	31-34
17891170-3	2008	Edelfosine treatment recruited Hsp90, c-Jun N-terminal kinase (JNK) and apoptotic molecules in lipid rafts, but not the JNK regulators apoptosis signal-regulating kinase 1 (ASK1) and Daxx, or the survival signaling molecules extracellular signal-regulated kinase (ERK) and Akt.	edelfosine	0-10	mitogen-activated protein kinase 1	Homo sapiens	225-262
17891170-6	2008	Decrease in edelfosine-induced JNK activation and apoptosis by Hsp90 inhibition was prevented through proteasome inhibition, suggesting that Hsp90 inhibition diminishes apoptosis by promoting JNK protein degradation.	edelfosine	12-22	heat shock protein 90 alpha family class A member 1	Homo sapiens	63-68
17891170-6	2008	Decrease in edelfosine-induced JNK activation and apoptosis by Hsp90 inhibition was prevented through proteasome inhibition, suggesting that Hsp90 inhibition diminishes apoptosis by promoting JNK protein degradation.	edelfosine	12-22	heat shock protein 90 alpha family class A member 1	Homo sapiens	141-146
17891170-3	2008	Edelfosine treatment recruited Hsp90, c-Jun N-terminal kinase (JNK) and apoptotic molecules in lipid rafts, but not the JNK regulators apoptosis signal-regulating kinase 1 (ASK1) and Daxx, or the survival signaling molecules extracellular signal-regulated kinase (ERK) and Akt.	edelfosine	0-10	mitogen-activated protein kinase 1	Homo sapiens	264-267
17891170-6	2008	Decrease in edelfosine-induced JNK activation and apoptosis by Hsp90 inhibition was prevented through proteasome inhibition, suggesting that Hsp90 inhibition diminishes apoptosis by promoting JNK protein degradation.	edelfosine	12-22	mitogen-activated protein kinase 8	Homo sapiens	192-195
17891170-3	2008	Edelfosine treatment recruited Hsp90, c-Jun N-terminal kinase (JNK) and apoptotic molecules in lipid rafts, but not the JNK regulators apoptosis signal-regulating kinase 1 (ASK1) and Daxx, or the survival signaling molecules extracellular signal-regulated kinase (ERK) and Akt.	edelfosine	0-10	AKT serine/threonine kinase 1	Homo sapiens	273-276
18296338-0	2008	The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets.	edelfosine	26-36	HRas proto-oncogene, GTPase	Homo sapiens	72-77
18296338-0	2008	The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets.	edelfosine	26-36	mitogen-activated protein kinase 3	Homo sapiens	133-139
18296338-0	2008	The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets.	edelfosine	26-36	mitogen-activated protein kinase 1	Homo sapiens	144-147
18296338-0	2008	The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets.	edelfosine	38-49	HRas proto-oncogene, GTPase	Homo sapiens	72-77
18296338-0	2008	The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets.	edelfosine	38-49	mitogen-activated protein kinase 3	Homo sapiens	133-139
18296338-0	2008	The antitumor ether lipid edelfosine (ET-18-O-CH3) induces apoptosis in H-ras transformed human breast epithelial cells: by blocking ERK1/2 and p38 mitogen-activated protein kinases as potential targets.	edelfosine	38-49	mitogen-activated protein kinase 1	Homo sapiens	144-147
18296338-2	2008	ET-18-O-CH3 treatment also enhanced the production of prostaglandin E2 (PGE2), a major COX-2 product.	edelfosine	0-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	87-92
18296338-5	2008	ET-18-O-CH3 also inhibited constitutive activation of ERK1/2, p38 MAPK, and Akt/protein kinase B, which was blunted by a selective COX-2 inhibitor SC58635.	edelfosine	0-11	mitogen-activated protein kinase 3	Homo sapiens	54-60
18296338-5	2008	ET-18-O-CH3 also inhibited constitutive activation of ERK1/2, p38 MAPK, and Akt/protein kinase B, which was blunted by a selective COX-2 inhibitor SC58635.	edelfosine	0-11	mitogen-activated protein kinase 1	Homo sapiens	62-65
18296338-5	2008	ET-18-O-CH3 also inhibited constitutive activation of ERK1/2, p38 MAPK, and Akt/protein kinase B, which was blunted by a selective COX-2 inhibitor SC58635.	edelfosine	0-11	AKT serine/threonine kinase 1	Homo sapiens	76-79
18296338-5	2008	ET-18-O-CH3 also inhibited constitutive activation of ERK1/2, p38 MAPK, and Akt/protein kinase B, which was blunted by a selective COX-2 inhibitor SC58635.	edelfosine	0-11	protein tyrosine kinase 2 beta	Homo sapiens	80-96
18296338-5	2008	ET-18-O-CH3 also inhibited constitutive activation of ERK1/2, p38 MAPK, and Akt/protein kinase B, which was blunted by a selective COX-2 inhibitor SC58635.	edelfosine	0-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	131-136
18296338-6	2008	In addition, ET-18-O-CH3 inhibited DNA binding activity of NF-kappa B in MCF10A-ras cells, and this was again attenuated by SC58635.	edelfosine	13-24	nuclear factor kappa B subunit 1	Homo sapiens	59-69
18296338-7	2008	Based on these findings, it is likely that ET-18-O-CH3 inactivates ERK1/2, Akt, and NF-kappaB signaling via COX-2 induction in MCF10A-ras cells, thereby inducing apoptosis of these cells.	edelfosine	43-54	mitogen-activated protein kinase 3	Homo sapiens	67-73
18296338-7	2008	Based on these findings, it is likely that ET-18-O-CH3 inactivates ERK1/2, Akt, and NF-kappaB signaling via COX-2 induction in MCF10A-ras cells, thereby inducing apoptosis of these cells.	edelfosine	43-54	AKT serine/threonine kinase 1	Homo sapiens	75-78
18296338-7	2008	Based on these findings, it is likely that ET-18-O-CH3 inactivates ERK1/2, Akt, and NF-kappaB signaling via COX-2 induction in MCF10A-ras cells, thereby inducing apoptosis of these cells.	edelfosine	43-54	prostaglandin-endoperoxide synthase 2	Homo sapiens	108-113
18097585-3	2008	Here, we demonstrated that the ether lipid ET-18-OMe induced the translocation of E-cadherin and episialin to membrane microdomains, enriched in glycosphingolipids, known to be involved in cell-cell adhesion and cell signaling.	edelfosine	43-52	cadherin 1	Homo sapiens	82-92
18097585-3	2008	Here, we demonstrated that the ether lipid ET-18-OMe induced the translocation of E-cadherin and episialin to membrane microdomains, enriched in glycosphingolipids, known to be involved in cell-cell adhesion and cell signaling.	edelfosine	43-52	mucin 1, cell surface associated	Homo sapiens	97-106
18097585-4	2008	In addition, it was found that E-cadherin and clusters of episialin colocalized and associated with the glycosphingolipid, MSGb5, upon treatment with ET-18-OMe.	edelfosine	150-159	cadherin 1	Homo sapiens	31-41
18097585-5	2008	Together, these results suggest that ET-18-OMe inhibits cell-cell adhesion by inducing the translocation of E-cadherin and episialin into MSGb5-enriched membrane microdomains, which leads to clustering and colocalization of the pro-adhesive E-cadherin and the anti-adhesive episialin thereby inhibiting cell-cell adhesion.	edelfosine	37-46	mucin 1, cell surface associated	Homo sapiens	274-283
18097585-4	2008	In addition, it was found that E-cadherin and clusters of episialin colocalized and associated with the glycosphingolipid, MSGb5, upon treatment with ET-18-OMe.	edelfosine	150-159	mucin 1, cell surface associated	Homo sapiens	58-67
18097585-5	2008	Together, these results suggest that ET-18-OMe inhibits cell-cell adhesion by inducing the translocation of E-cadherin and episialin into MSGb5-enriched membrane microdomains, which leads to clustering and colocalization of the pro-adhesive E-cadherin and the anti-adhesive episialin thereby inhibiting cell-cell adhesion.	edelfosine	37-46	cadherin 1	Homo sapiens	108-118
18097585-5	2008	Together, these results suggest that ET-18-OMe inhibits cell-cell adhesion by inducing the translocation of E-cadherin and episialin into MSGb5-enriched membrane microdomains, which leads to clustering and colocalization of the pro-adhesive E-cadherin and the anti-adhesive episialin thereby inhibiting cell-cell adhesion.	edelfosine	37-46	mucin 1, cell surface associated	Homo sapiens	123-132
18097585-5	2008	Together, these results suggest that ET-18-OMe inhibits cell-cell adhesion by inducing the translocation of E-cadherin and episialin into MSGb5-enriched membrane microdomains, which leads to clustering and colocalization of the pro-adhesive E-cadherin and the anti-adhesive episialin thereby inhibiting cell-cell adhesion.	edelfosine	37-46	cadherin 1	Homo sapiens	241-251
17974980-5	2007	Edelfosine also induced persistent c-Jun NH(2)-terminal kinase (JNK) activation.	edelfosine	0-10	mitogen-activated protein kinase 8	Homo sapiens	35-62
17974980-5	2007	Edelfosine also induced persistent c-Jun NH(2)-terminal kinase (JNK) activation.	edelfosine	0-10	mitogen-activated protein kinase 8	Homo sapiens	64-67
17974980-6	2007	Gene transfer-mediated overexpression of apoptosis signal-regulating kinase 1, which plays a crucial role in ER stress, enhanced edelfosine-induced JNK activation and apoptosis.	edelfosine	129-139	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	41-77
17974980-6	2007	Gene transfer-mediated overexpression of apoptosis signal-regulating kinase 1, which plays a crucial role in ER stress, enhanced edelfosine-induced JNK activation and apoptosis.	edelfosine	129-139	mitogen-activated protein kinase 8	Homo sapiens	148-151
17974980-7	2007	Inhibition of JNK, caspase-4, or caspase-8 activation diminished edelfosine-induced apoptosis.	edelfosine	65-75	mitogen-activated protein kinase 8	Homo sapiens	14-17
17974980-7	2007	Inhibition of JNK, caspase-4, or caspase-8 activation diminished edelfosine-induced apoptosis.	edelfosine	65-75	caspase 4	Homo sapiens	19-28
17974980-7	2007	Inhibition of JNK, caspase-4, or caspase-8 activation diminished edelfosine-induced apoptosis.	edelfosine	65-75	caspase 8	Homo sapiens	33-42
17974980-8	2007	Edelfosine treatment led to the generation of the p20 caspase-8 cleavage fragment of BAP31, directing proapoptotic signals between the ER and the mitochondria.	edelfosine	0-10	tubulin polymerization promoting protein family member 3	Homo sapiens	50-53
17974980-8	2007	Edelfosine treatment led to the generation of the p20 caspase-8 cleavage fragment of BAP31, directing proapoptotic signals between the ER and the mitochondria.	edelfosine	0-10	caspase 8	Homo sapiens	54-63
17974980-8	2007	Edelfosine treatment led to the generation of the p20 caspase-8 cleavage fragment of BAP31, directing proapoptotic signals between the ER and the mitochondria.	edelfosine	0-10	B cell receptor associated protein 31	Homo sapiens	85-90
17974980-9	2007	bax(-/-)bak(-/-) double-knockout cells fail to undergo edelfosine-induced ER-stored Ca(2+) release and apoptosis.	edelfosine	55-65	BCL2 associated X, apoptosis regulator	Homo sapiens	0-3
17974980-11	2007	Thus, edelfosine-induced apoptosis is dependent on Bax/Bak-mediated ER-stored Ca(2+) release, but phosphatidylcholine and protein synthesis inhibition is not critical.	edelfosine	6-16	BCL2 associated X, apoptosis regulator	Homo sapiens	51-54
17003375-8	2007	Fas/CD95 retrovirus transduction bestowed edelfosine sensitivity in these cells.	edelfosine	42-52	Fas cell surface death receptor	Homo sapiens	4-8
17509155-9	2007	Our data show that the effects of U73122 are indeed via PLC because U73122 and ET-18-OCH3 produced similar effects on cell morphology and actin cytoskeleton organization that were distinct from those caused by NEM.	edelfosine	79-89	small wing	Drosophila melanogaster	56-59
16540473-4	2006	c-Jun amino-terminal kinase (JNK) and caspase-3 were accordingly activated at earlier times in edelfosine-treated Jurkat cells as compared with drug-treated HeLa cells.	edelfosine	95-105	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	0-5
17003375-7	2007	A Fas/CD95-deficient MM subline expressing DR4 and DR5 was resistant to edelfosine.	edelfosine	72-82	TNF receptor superfamily member 10a	Homo sapiens	43-46
16540473-4	2006	c-Jun amino-terminal kinase (JNK) and caspase-3 were accordingly activated at earlier times in edelfosine-treated Jurkat cells as compared with drug-treated HeLa cells.	edelfosine	95-105	mitogen-activated protein kinase 8	Homo sapiens	29-32
16540473-4	2006	c-Jun amino-terminal kinase (JNK) and caspase-3 were accordingly activated at earlier times in edelfosine-treated Jurkat cells as compared with drug-treated HeLa cells.	edelfosine	95-105	caspase 3	Homo sapiens	38-47
16540473-5	2006	Both leukemic and solid tumor cells took up this alkyl-lysophospholipid and expressed the two putative edelfosine targets, namely cell surface Fas death receptor (also known as APO-1 or CD95) and endoplasmic reticulum CTP: phosphocholine cytidylyltransferase.	edelfosine	103-113	Fas cell surface death receptor	Homo sapiens	177-182
16540473-5	2006	Both leukemic and solid tumor cells took up this alkyl-lysophospholipid and expressed the two putative edelfosine targets, namely cell surface Fas death receptor (also known as APO-1 or CD95) and endoplasmic reticulum CTP: phosphocholine cytidylyltransferase.	edelfosine	103-113	Fas cell surface death receptor	Homo sapiens	186-190
16540473-7	2006	Edelfosine induced translocation of Fas, Fas-associated death domain-containing protein, and JNK into membrane rafts in Jurkat cells, but not in HeLa cells.	edelfosine	0-10	mitogen-activated protein kinase 8	Homo sapiens	93-96
16253239-6	2005	ET-18-O-CH3 treatment resulted in elevated release of 15d-PGJ2 and DNA binding and transcriptional activity of PPARgamma.	edelfosine	0-11	peroxisome proliferator activated receptor gamma	Homo sapiens	111-120
16155007-3	2005	Edelfosine addition to yeast resulted in the selective partitioning of the essential plasma membrane protein Pma1p out of lipid rafts.	edelfosine	0-10	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	109-114
16155007-6	2005	Cells with enfeebled endocytosis and vacuolar protease activities prevented edelfosine-mediated (i) mobilization of sterols, (ii) loss of Pma1p from lipid rafts, and (iii) cell death.	edelfosine	76-86	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	138-143
16253239-0	2005	ET-18-O-CH3-induced apoptosis is causally linked to COX-2 upregulation in H-ras transformed human breast epithelial cells.	edelfosine	0-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	52-57
16253239-7	2005	Based on these findings, it is likely that ET-18-O-CH3 induces COX-2 expression and production of 15d-PGJ2 which may mediate the ET-18-O-CH3-induced apoptosis in MCF10A-ras cells.	edelfosine	43-54	prostaglandin-endoperoxide synthase 2	Homo sapiens	63-68
16253239-2	2005	Contrary to this notion, we have found that a novel alkylphospholipid type antitumor agent ET-18-O-CH3 (1-O-octadecyl-2-O-methyl-glycero-3-phosphocholine) induces COX-2 expression in H-ras transformed human breast epithelial cells (MCF10A-ras) while it causes apoptosis at the same concentration range.	edelfosine	91-102	prostaglandin-endoperoxide synthase 2	Homo sapiens	163-168
16253239-4	2005	ET-18-O-CH3 enhanced the transcriptional activities of cyclic AMP response element which is a key regulator of COX-2 expression.	edelfosine	0-11	prostaglandin-endoperoxide synthase 2	Homo sapiens	111-116
15708359-1	2005	The effects of the anti-neoplastic ether lipid ET-18-OCH3 and some structural homologues on the activity of protein kinase C alpha (PKC alpha) were studied and compared with the effects the same had on the activity of PKC epsilon.	edelfosine	47-57	protein kinase C alpha	Homo sapiens	108-130
16138904-8	2005	We exploit the edelfosine resistance phenotype to assess the function of yeast Ncr1 proteins carrying amino acid changes corresponding to human NPC1 patient mutations.	edelfosine	15-25	sphingolipid transporter	Saccharomyces cerevisiae S288C	79-83
16138904-9	2005	We find that one of these amino acid changes severely compromises Ncr1p function as assessed using the edelfosine resistance assay.	edelfosine	103-113	sphingolipid transporter	Saccharomyces cerevisiae S288C	66-71
16138904-6	2005	Here, we identify the first phenotype caused by deletion of NCR1 from the yeast genome, resistance to the ether lipid drug, edelfosine.	edelfosine	124-134	sphingolipid transporter	Saccharomyces cerevisiae S288C	60-64
15708359-2	2005	ET-18-OCH3 progressively inhibited the activity of PKC alpha as the concentration was increased up to 30 mol% of the total lipid, above which the effect was one of activation.	edelfosine	0-10	protein kinase C alpha	Homo sapiens	51-60
15708359-5	2005	The effects were different on PKC epsilon since ET-18-OCH3 had a triphasic effect, activating the enzyme at low concentrations, inhibiting it at slightly higher concentrations and then activating it again at higher concentrations.	edelfosine	48-58	protein kinase C epsilon	Homo sapiens	30-41
15708359-7	2005	Substitution of the phosphocholine group of ET-18-OCH3 by phosphoserine led to a greater activation of PKC alpha, an effect that comes from the Ca(2+)-phospholipid binding site probably because of the specific interaction of this site with the phosphoserine group.	edelfosine	44-54	protein kinase C alpha	Homo sapiens	103-112
15708359-8	2005	The action of ET-18-OCH3 and its homologues, as demonstrated in this paper, may permit the selective inhibition or activation of PKC alpha and PKC epsilon by using the most suitable range of concentrations.	edelfosine	14-24	protein kinase C alpha	Homo sapiens	129-138
15708359-8	2005	The action of ET-18-OCH3 and its homologues, as demonstrated in this paper, may permit the selective inhibition or activation of PKC alpha and PKC epsilon by using the most suitable range of concentrations.	edelfosine	14-24	protein kinase C epsilon	Homo sapiens	143-154
15579006-0	2004	ET-18-OCH3 (edelfosine): a selective antitumour lipid targeting apoptosis through intracellular activation of Fas/CD95 death receptor.	edelfosine	0-10	Fas cell surface death receptor	Homo sapiens	114-118
15816524-0	2005	ET-18-OCH3 inhibits the phosphorylation and activation of p70 S6 kinase in MCF-7 cells.	edelfosine	0-10	ribosomal protein S6 kinase B1	Homo sapiens	58-71
15816524-6	2005	ET-18-OCH3 inhibited insulin-stimulated activation of MCF-7 cells, which is sensitive to the phosphoinositide 3-kinase inhibitor LY294002, and to the m-Tor inhibitor rapamycin.	edelfosine	0-10	RAR related orphan receptor C	Homo sapiens	152-155
15816524-8	2005	Hence the diminished phosphorylation of p70S6K by ET-18-OCH3 is a result of the inhibition of both phosphoinositide 3-kinase-dependent and -independent activation of p70S6K.	edelfosine	50-60	ribosomal protein S6 kinase B1	Homo sapiens	40-46
15816524-8	2005	Hence the diminished phosphorylation of p70S6K by ET-18-OCH3 is a result of the inhibition of both phosphoinositide 3-kinase-dependent and -independent activation of p70S6K.	edelfosine	50-60	ribosomal protein S6 kinase B1	Homo sapiens	166-172
15816524-9	2005	The differential effects of ENE-OCH3, a phosphonocholine analog of ET-18-OCH3, on MCF-7 cell proliferation correlated with its effects on p70S6K activation.	edelfosine	67-77	ribosomal protein S6 kinase B1	Homo sapiens	138-144
15816524-10	2005	The data suggest that the inhibition of p70S6K activation of by ET-18-OCH3 contributes to the antiproliferative effects of ALPs in MCF-7 cells.	edelfosine	64-74	ribosomal protein S6 kinase B1	Homo sapiens	40-46
15579006-0	2004	ET-18-OCH3 (edelfosine): a selective antitumour lipid targeting apoptosis through intracellular activation of Fas/CD95 death receptor.	edelfosine	12-22	Fas cell surface death receptor	Homo sapiens	114-118
15579006-4	2004	Recent progress has unveiled the molecular mechanism underlying the apoptotic action of ET-18-OCH3, involving membrane rafts and Fas/CD95 death receptor, and has led to the proposal of a two-step model for the ET-18-OCH3 selective action on cancer cells, namely: a) ET-18-OCH3 uptake into the tumour cell, but not in normal cells; b) intracellular activation of Fas/CD95 through its translocation and capping into membrane rafts.	edelfosine	88-98	Fas cell surface death receptor	Homo sapiens	133-137
15579006-4	2004	Recent progress has unveiled the molecular mechanism underlying the apoptotic action of ET-18-OCH3, involving membrane rafts and Fas/CD95 death receptor, and has led to the proposal of a two-step model for the ET-18-OCH3 selective action on cancer cells, namely: a) ET-18-OCH3 uptake into the tumour cell, but not in normal cells; b) intracellular activation of Fas/CD95 through its translocation and capping into membrane rafts.	edelfosine	88-98	Fas cell surface death receptor	Homo sapiens	366-370
15579006-4	2004	Recent progress has unveiled the molecular mechanism underlying the apoptotic action of ET-18-OCH3, involving membrane rafts and Fas/CD95 death receptor, and has led to the proposal of a two-step model for the ET-18-OCH3 selective action on cancer cells, namely: a) ET-18-OCH3 uptake into the tumour cell, but not in normal cells; b) intracellular activation of Fas/CD95 through its translocation and capping into membrane rafts.	edelfosine	210-220	Fas cell surface death receptor	Homo sapiens	133-137
15579006-4	2004	Recent progress has unveiled the molecular mechanism underlying the apoptotic action of ET-18-OCH3, involving membrane rafts and Fas/CD95 death receptor, and has led to the proposal of a two-step model for the ET-18-OCH3 selective action on cancer cells, namely: a) ET-18-OCH3 uptake into the tumour cell, but not in normal cells; b) intracellular activation of Fas/CD95 through its translocation and capping into membrane rafts.	edelfosine	210-220	Fas cell surface death receptor	Homo sapiens	366-370
15579006-5	2004	ET-18-OCH3 constitutes the first antitumour drug acting through the intracellular activation of the Fas/CD95 death receptor.	edelfosine	0-10	Fas cell surface death receptor	Homo sapiens	104-108
15579006-6	2004	Computational docking studies have allowed us to propose a molecular model for the putative interaction of ET-18-OCH3 with the intracellular Fas/CD95 death domain.	edelfosine	107-117	Fas cell surface death receptor	Homo sapiens	145-149
14704368-9	2004	A PI-PLC appears to be required for phagocytosis of apoptotic cells, as the PI-PLC inhibitor Et-18-OCH3 and the PLC inhibitor U73122, but not the inactive control U73343, blocked phagocytosis without impairing adhesion.	edelfosine	93-103	protein disulfide isomerase associated 3	Mus musculus	2-8
15289504-1	2004	We have discovered a new and specific cell-killing mechanism mediated by the selective uptake of the antitumor drug 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH(3), Edelfosine) into lipid rafts of tumor cells, followed by its coaggregation with Fas death receptor (also known as APO-1 or CD95) and recruitment of apoptotic molecules into Fas-enriched rafts.	edelfosine	116-169	Fas cell surface death receptor	Homo sapiens	299-304
15289504-1	2004	We have discovered a new and specific cell-killing mechanism mediated by the selective uptake of the antitumor drug 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH(3), Edelfosine) into lipid rafts of tumor cells, followed by its coaggregation with Fas death receptor (also known as APO-1 or CD95) and recruitment of apoptotic molecules into Fas-enriched rafts.	edelfosine	116-169	Fas cell surface death receptor	Homo sapiens	308-312
15158691-10	2004	For comparison, we examined the effect of iNOS transduction on the sensitivity of MCF-7 to edelfosine, a membrane-localizing anticancer drug without direct DNA interaction.	edelfosine	91-101	nitric oxide synthase 2	Homo sapiens	42-46
15102936-8	2004	Pretreatment of all cells expressing wild-type or mutant Rac1 proteins with edelfosine, a phosphatidylinositol-specific PLC inhibitor, or Go 6976, which inhibits conventional protein kinase C (PKC) isoforms, diminishes the M(3) mAChR"s ability to inhibit proliferation.	edelfosine	76-86	Rac family small GTPase 1	Homo sapiens	57-61
14704368-9	2004	A PI-PLC appears to be required for phagocytosis of apoptotic cells, as the PI-PLC inhibitor Et-18-OCH3 and the PLC inhibitor U73122, but not the inactive control U73343, blocked phagocytosis without impairing adhesion.	edelfosine	93-103	protein disulfide isomerase associated 3	Mus musculus	76-82
14704368-9	2004	A PI-PLC appears to be required for phagocytosis of apoptotic cells, as the PI-PLC inhibitor Et-18-OCH3 and the PLC inhibitor U73122, but not the inactive control U73343, blocked phagocytosis without impairing adhesion.	edelfosine	93-103	perlecan (heparan sulfate proteoglycan 2)	Mus musculus	5-8
12894505-0	2003	The antitumor ether lipid 1-Q-octadecyl-2-O-methyl-rac-glycerophosphocholine (ET-18-OCH3) inhibits the association between Ras and Raf-1.	edelfosine	78-88	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	131-136
12842877-0	2003	Lem3p is essential for the uptake and potency of alkylphosphocholine drugs, edelfosine and miltefosine.	edelfosine	76-86	Lem3p	Saccharomyces cerevisiae S288C	0-5
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	41-51	mitogen-activated protein kinase 8	Homo sapiens	182-207
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	41-51	mitogen-activated protein kinase 8	Homo sapiens	209-212
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	41-51	mitogen-activated protein kinase 1	Homo sapiens	255-258
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	41-51	mitogen-activated protein kinase 1	Homo sapiens	261-264
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	41-51	poly(ADP-ribose) polymerase 1	Homo sapiens	277-304
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	41-51	poly(ADP-ribose) polymerase 1	Homo sapiens	306-310
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	110-120	mitogen-activated protein kinase 8	Homo sapiens	182-207
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	110-120	mitogen-activated protein kinase 1	Homo sapiens	255-258
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	110-120	mitogen-activated protein kinase 1	Homo sapiens	261-264
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	110-120	poly(ADP-ribose) polymerase 1	Homo sapiens	277-304
12851688-3	2003	The differential sensitivity of cells to edelfosine"s cytostatic and cytotoxic effects has been attributed to edelfosine-induced changes in the activities of many enzymes, including c-Jun NH2-terminal kinase (JNK), extracellular signal-regulated kinases (ERK), p38 kinase, and poly(ADP-ribose) polymerase (PARP).	edelfosine	110-120	poly(ADP-ribose) polymerase 1	Homo sapiens	306-310
12851688-6	2003	Three out of the four edelfosine-sensitive NSCLC cell lines (NCI-H157, NCI-H520, NCI-H522) exhibit G2/M arrest, significant apoptosis and some degree of JNK activation in response to drug treatment.	edelfosine	22-32	mitogen-activated protein kinase 8	Homo sapiens	153-156
12851688-9	2003	These results demonstrate that edelfosine-induced changes in JNK, ERK, p38, or PARP are not good predictors of cell susceptibility to edelfosine-induced cytotoxicity.	edelfosine	31-41	mitogen-activated protein kinase 8	Homo sapiens	61-64
12851688-9	2003	These results demonstrate that edelfosine-induced changes in JNK, ERK, p38, or PARP are not good predictors of cell susceptibility to edelfosine-induced cytotoxicity.	edelfosine	31-41	mitogen-activated protein kinase 1	Homo sapiens	66-69
12894505-3	2003	ET-18-OCH3 decreased the level of membrane-associated Raf-1 relative to untreated control cells.	edelfosine	0-10	zinc fingers and homeoboxes 2	Homo sapiens	54-57
12894505-4	2003	Since ET-18-OCH3 did not inhibit the activities of the kinases in the cascade, the reduced Raf-1 levels appeared to be the cause for the reduction in the magnitude and duration of MAPK activity.	edelfosine	6-16	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	91-96
12894505-9	2003	RESULTS: In cells preincubated with ET-18-OCH3, the interaction of GST-Ras-GTP-gamma-S with cytosolic Raf was reduced.	edelfosine	36-46	zinc fingers and homeoboxes 2	Homo sapiens	102-105
12894505-10	2003	The addition of ET-18-OCH3 to the cytosolic fraction isolated from untreated cells also reduced the binding of Raf to activated GST-Ras-GTP-gamma-S.	edelfosine	16-26	zinc fingers and homeoboxes 2	Homo sapiens	111-114
12894505-12	2003	CONCLUSION: Our findings suggest that ET-18-OCH3 associates specifically with Raf-1 in the cytosol and interferes in the interaction of Raf-1 with activated Ras, thereby reducing the levels that are translocated to the membrane for activation.	edelfosine	38-48	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	78-83
12894505-12	2003	CONCLUSION: Our findings suggest that ET-18-OCH3 associates specifically with Raf-1 in the cytosol and interferes in the interaction of Raf-1 with activated Ras, thereby reducing the levels that are translocated to the membrane for activation.	edelfosine	38-48	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	136-141
12894505-13	2003	Thus Raf-1 appears to be a molecular target of ET-18-OCH3.	edelfosine	47-57	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	5-10
12655438-1	2003	PURPOSE: This study was undertaken to elucidate the potential mechanism of the antitumor activity of ET-18-O-CH(3), a synthetic analogue of lysophosphatidyl choline, and a known antitumor agent and specific inhibitor of phosphoinositide phospholipase C (PI-PLC).	edelfosine	101-114	phospholipase C, delta 1	Rattus norvegicus	220-252
12655438-1	2003	PURPOSE: This study was undertaken to elucidate the potential mechanism of the antitumor activity of ET-18-O-CH(3), a synthetic analogue of lysophosphatidyl choline, and a known antitumor agent and specific inhibitor of phosphoinositide phospholipase C (PI-PLC).	edelfosine	101-114	phospholipase C, delta 1	Rattus norvegicus	254-260
12655438-7	2003	ET-18-O-CH(3) was also capable of inhibiting both the expression of cdk2 and cdc2 and the activation of ERK1/2, while no effect was found on the expression of p21 ras.	edelfosine	0-13	cyclin dependent kinase 2	Rattus norvegicus	68-72
12655438-7	2003	ET-18-O-CH(3) was also capable of inhibiting both the expression of cdk2 and cdc2 and the activation of ERK1/2, while no effect was found on the expression of p21 ras.	edelfosine	0-13	cyclin-dependent kinase 1	Rattus norvegicus	77-81
12655438-7	2003	ET-18-O-CH(3) was also capable of inhibiting both the expression of cdk2 and cdc2 and the activation of ERK1/2, while no effect was found on the expression of p21 ras.	edelfosine	0-13	mitogen activated protein kinase 3	Rattus norvegicus	104-110
12421819-7	2003	Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases.	edelfosine	13-23	BCL2 apoptosis regulator	Homo sapiens	96-100
12421819-7	2003	Furthermore, ET-18-OCH3, a specific phospholipase C (PLC) inhibitor, blocks nicotine-stimulated Bcl2 phosphorylation and promotes apoptosis, suggesting that PLC may be involved in nicotine activation of Bcl2 kinases.	edelfosine	13-23	BCL2 apoptosis regulator	Homo sapiens	203-207
11739199-0	2001	The antitumor ether lipid ET-18-OCH(3) induces apoptosis through translocation and capping of Fas/CD95 into membrane rafts in human leukemic cells.	edelfosine	26-38	Fas cell surface death receptor	Homo sapiens	98-102
11888912-11	2002	Similar results were obtained with other ALK congeners (miltefosine and edelfosine).	edelfosine	72-82	ALK receptor tyrosine kinase	Homo sapiens	41-44
12167660-6	2002	Our data showed that gat1 and gat2 yeast were resistant and sensitive to lysoplatelet activating factor, platelet activating factor, and the anti-tumor lipid edelfosine, respectively, indicating that their sensitivity to these compounds was not because of differences in rates of phosphatidylcholine deacylation.	edelfosine	158-168	Gat1p	Saccharomyces cerevisiae S288C	21-25
12167660-6	2002	Our data showed that gat1 and gat2 yeast were resistant and sensitive to lysoplatelet activating factor, platelet activating factor, and the anti-tumor lipid edelfosine, respectively, indicating that their sensitivity to these compounds was not because of differences in rates of phosphatidylcholine deacylation.	edelfosine	158-168	Gat2p	Saccharomyces cerevisiae S288C	30-34
11739199-1	2001	The antitumor ether lipid ET-18-OCH(3) promotes apoptosis in tumor cells through intracellular activation of Fas/CD95.	edelfosine	26-38	Fas cell surface death receptor	Homo sapiens	113-117
11737191-7	2001	On the other hand, protein kinase Calpha (PKCalpha) activity progressively decreased when ET-18-OCH3 was incorporated into multilamellar vesicles, reaching a minimum value at 20 mol%, this inhibition being attributed to the modification of the membrane produced by a cone-shaped molecule.	edelfosine	90-100	protein kinase C alpha	Homo sapiens	19-40
11737191-7	2001	On the other hand, protein kinase Calpha (PKCalpha) activity progressively decreased when ET-18-OCH3 was incorporated into multilamellar vesicles, reaching a minimum value at 20 mol%, this inhibition being attributed to the modification of the membrane produced by a cone-shaped molecule.	edelfosine	90-100	protein kinase C alpha	Homo sapiens	42-50
11737191-11	2001	When PKC was assayed using large unilamellar vesicles a slight activation was observed at very low ET-18-OCH3 concentrations.	edelfosine	99-109	protein kinase C alpha	Homo sapiens	5-8
10825148-9	2000	The participation of PLC-beta1 in signaling by SCLC growth factor receptors is indicated by our finding that PLC-beta1 (but not PLC-beta3) coimnunoprecipitates with G(alpha)q/11 upon activation of neurotensin receptors; this association is inhibited by ET-18-OCH3.	edelfosine	253-263	phospholipase C beta 1	Homo sapiens	21-30
11557588-4	2001	Stimulated release of EPO and intracellular Ca(2+) concentration was inhibited by ET-18-OCH(3), a PI-PLC inhibitor, whereas trifluoromethylketone (TFMK), a cPLA(2) blocker, had no inhibitory effect.	edelfosine	82-94	eosinophil peroxidase	Homo sapiens	22-25
11481221-1	2001	The mechanism of induction of apoptosis by the novel anti-cancer drug 1-O-octadecyl-2-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) was investigated in p53-defective SV40 immortalized rat hepatocytes (CWSV1).	edelfosine	123-133	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	155-158
11481221-9	2001	Taken together, these results suggest that the form of p53-independent apoptosis induced by ET-18-OCH3 is mediated by alterations in mitochondrial membrane PC, a loss of mitochondrial membrane potential, and the release of ROS, resulting in completion of apoptosis.	edelfosine	92-102	Wistar clone pR53P1 p53 pseudogene	Rattus norvegicus	55-58
11304687-3	2001	In the present study, we tested the effect of ET-18-OMe on adhesion, invasion and localisation of episialin and E-cadherin in MCF-7/AZ cells expressing a functional E-cadherin/catenin complex.	edelfosine	46-55	mucin 1, cell surface associated	Homo sapiens	98-107
11304687-7	2001	ET-18-OMe inhibited the E-cadherin functions of MCF-7/AZ cells as measured by inhibition of fast and slow aggregation and by the induction of collagen invasion.	edelfosine	0-9	cadherin 1	Homo sapiens	24-34
11304687-11	2001	ET-18-OMe induced finger-like extensions with clustering of episialin together with E-cadherin and carcinoembryonic antigen but not with occludin.	edelfosine	0-9	mucin 1, cell surface associated	Homo sapiens	60-69
11304687-11	2001	ET-18-OMe induced finger-like extensions with clustering of episialin together with E-cadherin and carcinoembryonic antigen but not with occludin.	edelfosine	0-9	cadherin 1	Homo sapiens	84-94
11304687-12	2001	In cells in suspension, ET-18-OMe caused a shift in the flow-cytometric profile of episialin toward a lower intensity for MCF-7/AZ cells.	edelfosine	24-33	mucin 1, cell surface associated	Homo sapiens	83-92
10825148-9	2000	The participation of PLC-beta1 in signaling by SCLC growth factor receptors is indicated by our finding that PLC-beta1 (but not PLC-beta3) coimnunoprecipitates with G(alpha)q/11 upon activation of neurotensin receptors; this association is inhibited by ET-18-OCH3.	edelfosine	253-263	phospholipase C beta 1	Homo sapiens	109-118
10825148-12	2000	These findings indicate that ET-18-OCH3 does not interfere with G(alpha)q/11 activation but rather inhibits the association of G(alpha)q/11 with PLC-beta1.	edelfosine	29-39	G protein subunit alpha q	Homo sapiens	127-136
10825148-12	2000	These findings indicate that ET-18-OCH3 does not interfere with G(alpha)q/11 activation but rather inhibits the association of G(alpha)q/11 with PLC-beta1.	edelfosine	29-39	phospholipase C beta 1	Homo sapiens	145-154
10630309-1	2000	Association of the ether lipid, 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine (ET-18-OCH3) with liposomes (ELL-12) reduces acute toxicity while maintaining or enhancing anticancer activity in experimental tumor models.	edelfosine	32-84	elongation factor for RNA polymerase II	Homo sapiens	114-117
10738248-0	2000	Involvement of mitochondria and caspase-3 in ET-18-OCH(3)-induced apoptosis of human leukemic cells.	edelfosine	45-57	caspase 3	Homo sapiens	32-41
10738248-7	2000	Overexpression of bcl-2 by gene transfer prevented DeltaPsi(m) collapse, ROS generation, caspase activation and apoptosis in ET-18-OCH(3)-treated leukemic T cells.	edelfosine	125-137	BCL2 apoptosis regulator	Homo sapiens	18-23
10679516-8	2000	Calphostin C and ET-18-OCH(3), inhibitors of protein kinase C, reduced the phosphorylation of p38 MAP kinase by AVP.	edelfosine	17-29	mitogen-activated protein kinase 14	Homo sapiens	94-108
10630309-1	2000	Association of the ether lipid, 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine (ET-18-OCH3) with liposomes (ELL-12) reduces acute toxicity while maintaining or enhancing anticancer activity in experimental tumor models.	edelfosine	86-96	elongation factor for RNA polymerase II	Homo sapiens	114-117
10630309-2	2000	ELL-12 has been shown to induce apoptosis by a cytochrome-c-dependent caspase-mediated pathway, which results in proteolytic cleavage of poly(ADP-ribose) polymerase and lamins, but the antitumor effects of ET-18-OCH3 or ELL-12 could result from tumor cell differentiation or activation.	edelfosine	206-216	elongation factor for RNA polymerase II	Homo sapiens	0-3
10630309-5	2000	In contrast, ET-18-OCH3 and ELL-12 up-regulated both CD71 and CD11b and did not have any effect on expression of CD82 in U-937 cells, suggesting that the ELL-12 may activate these cells rather than induce differentiation.	edelfosine	13-23	transferrin receptor	Homo sapiens	53-57
10630309-5	2000	In contrast, ET-18-OCH3 and ELL-12 up-regulated both CD71 and CD11b and did not have any effect on expression of CD82 in U-937 cells, suggesting that the ELL-12 may activate these cells rather than induce differentiation.	edelfosine	13-23	integrin subunit alpha M	Homo sapiens	62-67
10630309-6	2000	Further evidence of activation was that ET-18-OCH3 and ELL-12 strongly induced tumor necrosis factor alpha production by U-937 cells.	edelfosine	40-50	tumor necrosis factor	Homo sapiens	79-106
10542136-8	1999	Furthermore, cholera toxin-induced TNF-alpha production was suppressed by protein kinase C inhibitors H7 and sphingosine and by phospholipase C inhibitors U73122 and ET-18-OCH3, suggesting that PLC and PKC mediate TNF-alpha induction.	edelfosine	166-176	tumor necrosis factor	Homo sapiens	35-44
10552970-0	1999	Liposomal ET-18-OCH(3) induces cytochrome c-mediated apoptosis independently of CD95 (APO-1/Fas) signaling.	edelfosine	10-22	cytochrome c, somatic	Homo sapiens	31-43
10552970-1	1999	ELL-12, a liposome formulation of the ether-lipid 1-O-octadecyl-2-O-methyl-sn-glycero-3-phosphocholine (ET-18-OCH(3)), is a nonmyelosuppressive antiproliferative agent that is more effective and less toxic than the ether lipid itself in tumor model systems.	edelfosine	50-102	elongation factor for RNA polymerase II	Homo sapiens	0-3
10519389-0	1999	Decreased sensitivity to 1-O-octadecyl-2-O-methyl-glycerophosphocholine in MCF-7 cells adapted for serum-free growth correlates with constitutive association of Raf-1 with cellular membranes.	edelfosine	25-71	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	161-166
10519389-1	1999	We have previously shown that inhibition of MCF-7 cell proliferation by 1-O-octadecyl-2-O-methyl-glycerophosphocholine (ET-18-OCH3) is linked to a drug-induced decrease in membrane Raf-1 levels and the subsequent inhibition of mitogen-activated protein (MAP) kinase activation in response to growth factor stimulation.	edelfosine	72-118	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	181-186
10519389-4	1999	ET-18-OCH3 sensitivity could be restored by growing the adapted cells in serum-containing medium, which resulted in the loss of membrane-associated Raf-1.	edelfosine	0-10	zinc fingers and homeoboxes 2	Homo sapiens	148-151
10519389-6	1999	In both cell types, incubation with ET-18-OCH3 had no effect on the membrane-Raf-1 levels, suggesting that ET-18-OCH3-induced reduction of Raf-1 levels in growth factor-stimulated MCF-7 cells is due to inhibition of Raf translocation.	edelfosine	107-117	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	139-144
10519389-8	1999	Because membrane translocation is not required to activate Raf in these cells, inhibition of Raf translocation by ET-18-OCH3 subsequent to cell stimulation has no effect on the activation of the membrane-bound Raf and, consequently, the activation of the MAP kinase pathway.	edelfosine	114-124	zinc fingers and homeoboxes 2	Homo sapiens	93-96
10519389-8	1999	Because membrane translocation is not required to activate Raf in these cells, inhibition of Raf translocation by ET-18-OCH3 subsequent to cell stimulation has no effect on the activation of the membrane-bound Raf and, consequently, the activation of the MAP kinase pathway.	edelfosine	114-124	zinc fingers and homeoboxes 2	Homo sapiens	93-96
10542136-8	1999	Furthermore, cholera toxin-induced TNF-alpha production was suppressed by protein kinase C inhibitors H7 and sphingosine and by phospholipase C inhibitors U73122 and ET-18-OCH3, suggesting that PLC and PKC mediate TNF-alpha induction.	edelfosine	166-176	heparan sulfate proteoglycan 2	Homo sapiens	194-197
10413111-1	1999	ET-18-OCH3, but not ELL-12, blunted the increase in membrane protein kinase C (PKC) activity induced by 12-O-tetradecanoylphorbol 13-myristate (TPA) and markedly reduced levels of PKC alpha in NIH 3T3 fibroblasts.	edelfosine	0-10	protein kinase C alpha	Homo sapiens	79-82
10413111-1	1999	ET-18-OCH3, but not ELL-12, blunted the increase in membrane protein kinase C (PKC) activity induced by 12-O-tetradecanoylphorbol 13-myristate (TPA) and markedly reduced levels of PKC alpha in NIH 3T3 fibroblasts.	edelfosine	0-10	protein kinase C alpha	Homo sapiens	180-189
10089909-0	1999	Synergistic effects of heat and ET-18-OCH3 on membrane expression of hsp70 and lysis of leukemic K562 cells.	edelfosine	32-42	heat shock protein family A (Hsp70) member 4	Homo sapiens	69-74
10455302-6	1999	The [Ca2+]i rise induced by ET-18-OCH3 (25 microM) was not altered when the production of inositol 1,4,5-trisphosphate (IP3) was suppressed by the phospholipase C inhibitor U73122 (2 microM), but was partly inhibited by the phospholipase D inhibitor propranolol (0.1 mM) or the phospholipase A2 inhibitor aristolochic acid (20-40 microM).	edelfosine	28-38	phospholipase A2 group IB	Canis lupus familiaris	278-294
10433487-14	1999	ET-18-OCH3 induced an increase in Fas (APO-1/CD95) ligand mRNA expression in activated T-cells, and incubation with a blocking anti-Fas (APO-1/CD95) antibody partially inhibited the ET-18-OCH3-induced apoptosis of activated T-lymphocytes.	edelfosine	0-10	Fas cell surface death receptor	Homo sapiens	39-44
10433487-14	1999	ET-18-OCH3 induced an increase in Fas (APO-1/CD95) ligand mRNA expression in activated T-cells, and incubation with a blocking anti-Fas (APO-1/CD95) antibody partially inhibited the ET-18-OCH3-induced apoptosis of activated T-lymphocytes.	edelfosine	0-10	Fas cell surface death receptor	Homo sapiens	45-49
10433487-14	1999	ET-18-OCH3 induced an increase in Fas (APO-1/CD95) ligand mRNA expression in activated T-cells, and incubation with a blocking anti-Fas (APO-1/CD95) antibody partially inhibited the ET-18-OCH3-induced apoptosis of activated T-lymphocytes.	edelfosine	0-10	Fas cell surface death receptor	Homo sapiens	137-142
10433487-14	1999	ET-18-OCH3 induced an increase in Fas (APO-1/CD95) ligand mRNA expression in activated T-cells, and incubation with a blocking anti-Fas (APO-1/CD95) antibody partially inhibited the ET-18-OCH3-induced apoptosis of activated T-lymphocytes.	edelfosine	0-10	Fas cell surface death receptor	Homo sapiens	143-147
10433487-14	1999	ET-18-OCH3 induced an increase in Fas (APO-1/CD95) ligand mRNA expression in activated T-cells, and incubation with a blocking anti-Fas (APO-1/CD95) antibody partially inhibited the ET-18-OCH3-induced apoptosis of activated T-lymphocytes.	edelfosine	182-192	Fas cell surface death receptor	Homo sapiens	39-44
10433487-14	1999	ET-18-OCH3 induced an increase in Fas (APO-1/CD95) ligand mRNA expression in activated T-cells, and incubation with a blocking anti-Fas (APO-1/CD95) antibody partially inhibited the ET-18-OCH3-induced apoptosis of activated T-lymphocytes.	edelfosine	182-192	Fas cell surface death receptor	Homo sapiens	137-142
10433487-14	1999	ET-18-OCH3 induced an increase in Fas (APO-1/CD95) ligand mRNA expression in activated T-cells, and incubation with a blocking anti-Fas (APO-1/CD95) antibody partially inhibited the ET-18-OCH3-induced apoptosis of activated T-lymphocytes.	edelfosine	182-192	Fas cell surface death receptor	Homo sapiens	143-147
10432010-7	1999	The potential anti-cancer drug 1-O-octadecyl-2-O-methylglycero-3-phosphocholine (ET-18-OMe, 48 h, 25 microg/ml) belonging to the class of alkyllysophospholipids restored the E-cadherin function in the adhesion-deficient MCF-7/6 cells as evidenced by an increased aggregation.	edelfosine	81-90	cadherin 1	Homo sapiens	174-184
10432010-8	1999	ET-18-OMe caused loss of ST6Gal I mRNA in MCF-7/AZ cells but no changes of sialyltransferase activities or sialic acid moieties on E-cadherin could be observed.	edelfosine	0-9	ST6 beta-galactoside alpha-2,6-sialyltransferase 1	Homo sapiens	25-33
10432010-9	1999	We conclude that Ca2+-dependent, E-cadherin-specific homotypic adhesion of MCF-7/AZ or MCF-7/6 cells treated with ET-18-OMe was not affected by sialylation of E-cadherin.	edelfosine	114-123	cadherin 1	Homo sapiens	33-43
10089909-1	1999	We previously reported that cell surface expression of hsp70, the major stress inducible member of the 70-kDa heat shock protein family, is inducible by nonlethal heat as well as by treatment with the membrane-interactive compound alkyl-lysophospholipid 1-octadecyl-2-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) selectively on human tumor cell lines.	edelfosine	305-315	heat shock protein family A (Hsp70) member 4	Homo sapiens	55-60
10226541-0	1999	Change in the localization of heat shock protein 27 (HSP 27) in BG-1 human ovarian cancer cells following treatment by the ether lipid ET-18-OCH3.	edelfosine	135-145	heat shock protein family B (small) member 1	Homo sapiens	30-51
10075017-7	1999	Addition of the PI-PLC inhibitor, ET 18OCH3, or the PLA2 inhibitor (quinacrine) alone, resulted in secretion of latent TGF-beta and, in the case of ET 18OCH3, active TGF-beta.	edelfosine	34-43	transforming growth factor, beta 1	Mus musculus	119-127
10075017-7	1999	Addition of the PI-PLC inhibitor, ET 18OCH3, or the PLA2 inhibitor (quinacrine) alone, resulted in secretion of latent TGF-beta and, in the case of ET 18OCH3, active TGF-beta.	edelfosine	34-43	transforming growth factor, beta 1	Mus musculus	166-174
10226541-0	1999	Change in the localization of heat shock protein 27 (HSP 27) in BG-1 human ovarian cancer cells following treatment by the ether lipid ET-18-OCH3.	edelfosine	135-145	heat shock protein family B (small) member 1	Homo sapiens	53-59
10226541-4	1999	The partial amino acid sequence of the most dominantly and consistently up-regulated protein spot after ET-18-OCH3 treatment was determined and it was found to be heat shock protein 27 (HSP27).	edelfosine	104-114	heat shock protein family B (small) member 1	Homo sapiens	163-184
10226541-4	1999	The partial amino acid sequence of the most dominantly and consistently up-regulated protein spot after ET-18-OCH3 treatment was determined and it was found to be heat shock protein 27 (HSP27).	edelfosine	104-114	heat shock protein family B (small) member 1	Homo sapiens	186-191
10226541-6	1999	Condensation of HSP27 around the nuclei was observed following treatment by ET-18-OCH3.	edelfosine	76-86	heat shock protein family B (small) member 1	Homo sapiens	16-21
9547349-0	1998	Involvement of c-Jun NH2-terminal kinase activation and c-Jun in the induction of apoptosis by the ether phospholipid 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine.	edelfosine	118-171	mitogen-activated protein kinase 8	Homo sapiens	15-40
9547349-0	1998	Involvement of c-Jun NH2-terminal kinase activation and c-Jun in the induction of apoptosis by the ether phospholipid 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine.	edelfosine	118-171	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	15-20
9547349-2	1998	We show that ET-18-OCH3-induced apoptosis is associated with activation of the c-Jun NH2-terminal kinase (JNK) signaling.	edelfosine	13-23	mitogen-activated protein kinase 8	Homo sapiens	106-109
9547349-2	1998	We show that ET-18-OCH3-induced apoptosis is associated with activation of the c-Jun NH2-terminal kinase (JNK) signaling.	edelfosine	13-23	mitogen-activated protein kinase 8	Homo sapiens	79-104
8932980-2	1996	ET-18-OCH3 significantly increased the release of IL-6, giving the greatest effect at the dose of 2 micrograms/ml.	edelfosine	0-10	interleukin 6	Homo sapiens	50-54
9547349-3	1998	The addition of ET-18-OCH3 to distinct human leukemic cells (HL-60, U937, and Jurkat), which undergo rapid apoptosis on treatment with ET-18-OCH3, induced a dramatic and sustained increase in the of c-jun mRNA level that was associated with activation of activator protein-1 transcription factor.	edelfosine	16-26	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	199-204
9547349-3	1998	The addition of ET-18-OCH3 to distinct human leukemic cells (HL-60, U937, and Jurkat), which undergo rapid apoptosis on treatment with ET-18-OCH3, induced a dramatic and sustained increase in the of c-jun mRNA level that was associated with activation of activator protein-1 transcription factor.	edelfosine	16-26	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	255-274
9547349-4	1998	We found that ET-18-OCH3 induced a persistent activation of JNK in HL-60 cells that was detected before the onset of apoptosis, the latter being assessed by DNA fragmentation and by the appearance of phosphatidylserine on the external leaflet of the plasma membrane.	edelfosine	14-24	mitogen-activated protein kinase 8	Homo sapiens	60-63
9547349-7	1998	ET-18-OCH3-dependent JNK activation was not detected in K562 cells, which did not undergo apoptosis on treatment with ET-18-OCH3.	edelfosine	0-10	mitogen-activated protein kinase 8	Homo sapiens	21-24
9547349-8	1998	Phorbol myristate acetate inhibited both ET-18-OCH3-induced apoptosis and sustained JNK activation; thus, persistent JNK activation by ET-18-OCH3 is associated with the capacity of this ether phospholipid to induce apoptosis.	edelfosine	41-51	mitogen-activated protein kinase 8	Homo sapiens	117-120
9547349-8	1998	Phorbol myristate acetate inhibited both ET-18-OCH3-induced apoptosis and sustained JNK activation; thus, persistent JNK activation by ET-18-OCH3 is associated with the capacity of this ether phospholipid to induce apoptosis.	edelfosine	135-145	mitogen-activated protein kinase 8	Homo sapiens	84-87
9547349-8	1998	Phorbol myristate acetate inhibited both ET-18-OCH3-induced apoptosis and sustained JNK activation; thus, persistent JNK activation by ET-18-OCH3 is associated with the capacity of this ether phospholipid to induce apoptosis.	edelfosine	135-145	mitogen-activated protein kinase 8	Homo sapiens	117-120
9547349-9	1998	Furthermore, antisense oligonucleotides directed against c-jun blocked ET-18-OCH3-induced apoptosis, indicating a role for c-Jun in this apoptotic response.	edelfosine	71-81	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	57-62
9547349-9	1998	Furthermore, antisense oligonucleotides directed against c-jun blocked ET-18-OCH3-induced apoptosis, indicating a role for c-Jun in this apoptotic response.	edelfosine	71-81	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	123-128
9547349-10	1998	These data indicate that JNK activation and c-Jun are involved in the induction of apoptosis by ET-18-OCH3.	edelfosine	96-106	mitogen-activated protein kinase 8	Homo sapiens	25-28
9547349-10	1998	These data indicate that JNK activation and c-Jun are involved in the induction of apoptosis by ET-18-OCH3.	edelfosine	96-106	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	44-49
9295281-11	1997	ET-18-OCH3 also inhibited stimulation of Bcl-2 by TPA and enhanced the decrease in Bcl-2 observed in ara-C-treated cells.	edelfosine	0-10	BCL2 apoptosis regulator	Homo sapiens	41-46
9295281-11	1997	ET-18-OCH3 also inhibited stimulation of Bcl-2 by TPA and enhanced the decrease in Bcl-2 observed in ara-C-treated cells.	edelfosine	0-10	BCL2 apoptosis regulator	Homo sapiens	83-88
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	66-76	phosphoglycolate phosphatase	Mus musculus	127-131
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	66-76	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	190-193
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	66-76	ATP binding cassette subfamily C member 3	Homo sapiens	207-210
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	66-76	ATP-binding cassette a-factor transporter STE6	Saccharomyces cerevisiae S288C	223-227
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	78-88	phosphoglycolate phosphatase	Mus musculus	127-131
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	78-88	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	190-193
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	78-88	ATP binding cassette subfamily C member 3	Homo sapiens	207-210
9201967-5	1997	We report the identification of the synthetic lipid and PC analog ET-18-OCH3 (edelfosine) as a substrate for not only Class II P-gp but also for Class I P-gps and surprisingly for the other ABC transporters MRP, Pgh-1, and STE6.	edelfosine	78-88	ATP-binding cassette a-factor transporter STE6	Saccharomyces cerevisiae S288C	223-227
9201967-8	1997	ET-18-OCH3 was also found capable of blocking a-peptide pheromone transport and STE6 complementation by these ABC proteins.	edelfosine	0-10	ATP-binding cassette a-factor transporter STE6	Saccharomyces cerevisiae S288C	80-84
9201967-8	1997	ET-18-OCH3 was also found capable of blocking a-peptide pheromone transport and STE6 complementation by these ABC proteins.	edelfosine	0-10	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	110-113
9201967-12	1997	Furthermore, the studies with BSA and MAMO suggest that the mechanism of transport of ET-18-OCH3 by these ABC transporters may be related to the flippase mechanism of PC transport by Mdr2.	edelfosine	86-96	ATP binding cassette subfamily B member 6 (Langereis blood group)	Homo sapiens	106-109
9000521-9	1997	The thrombin-dependent recovery of pH(i) is prevented by the phospholipase C inhibitor ET 18 O-CH3 and is mimicked by the addition of the permeable diglyceride dioctanoyl glycerol (DiC8) exogenously supplied.	edelfosine	87-98	coagulation factor II, thrombin	Homo sapiens	4-12
9844614-3	1998	Edelfosine acted directly on cultured capillary endothelial cells, inhibiting their migration toward the angiogenic factor, basic fibroblastic growth factor (bFGF), at doses of 8-200 nM.	edelfosine	0-10	fibroblast growth factor 2	Rattus norvegicus	158-162
9257915-6	1997	ET-18-OCH3 induced an increase in [Ca2+]i mediated through the platelet-activating factor (PAF) receptor in U937, dHL60 cells and PMNs, as shown by cross-desensitization experiments and by prevention of the [Ca2+]i changes by the PAF antagonist WEB-2170.	edelfosine	0-10	platelet activating factor receptor	Homo sapiens	63-104
9182716-3	1997	Preincubation of the cells with 1-O-octadecyl-2-O-methylglycerophosphocholine (Et18-OH3), which blocked the activation of mitogen-activated protein kinase by EGF, also blocked the activation of N-acetylglucosamyltransferase V by this hormone, whereas the activation of N-acetylglucosamyltransferase V by insulin could not be blocked by Et18-OH3.	edelfosine	32-77	epidermal growth factor like 1	Rattus norvegicus	158-161
9136078-7	1997	Inhibitors of protein kinase C, including Et-18-OMe and H-7, dramatically decreased the formation of [3H]inositol phosphates stimulated by either tumor necrosis factor-alpha or A1F4- by 90-100% but did not affect basal formation.	edelfosine	42-51	tumor necrosis factor	Homo sapiens	146-173
9102220-0	1997	Selective induction of apoptosis in cancer cells by the ether lipid ET-18-OCH3 (Edelfosine): molecular structure requirements, cellular uptake, and protection by Bcl-2 and Bcl-X(L).	edelfosine	68-78	BCL2 apoptosis regulator	Homo sapiens	162-167
9102220-0	1997	Selective induction of apoptosis in cancer cells by the ether lipid ET-18-OCH3 (Edelfosine): molecular structure requirements, cellular uptake, and protection by Bcl-2 and Bcl-X(L).	edelfosine	68-78	BCL2 like 1	Homo sapiens	172-180
9102220-0	1997	Selective induction of apoptosis in cancer cells by the ether lipid ET-18-OCH3 (Edelfosine): molecular structure requirements, cellular uptake, and protection by Bcl-2 and Bcl-X(L).	edelfosine	80-90	BCL2 apoptosis regulator	Homo sapiens	162-167
9102220-0	1997	Selective induction of apoptosis in cancer cells by the ether lipid ET-18-OCH3 (Edelfosine): molecular structure requirements, cellular uptake, and protection by Bcl-2 and Bcl-X(L).	edelfosine	80-90	BCL2 like 1	Homo sapiens	172-180
9102220-9	1997	ET-18-OCH3 did not affect the expression of bcl-2, bcl-xL, or bax in HEL and HL-60 human leukemic cells but induced expression of c-myc, an important effector of apoptosis in several systems.	edelfosine	0-10	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	130-135
8770865-6	1996	However, an interference in the association of Raf-1 with membranes and a resultant decrease in Raf-1 kinase activity in membranes of ET18-OCH3-treated cells was observed.	edelfosine	134-143	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	47-52
8770865-6	1996	However, an interference in the association of Raf-1 with membranes and a resultant decrease in Raf-1 kinase activity in membranes of ET18-OCH3-treated cells was observed.	edelfosine	134-143	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	96-101
8770865-8	1996	A direct correlation between ET18-OCH3 accumulation, inhibition of cell proliferation, Raf association with the membrane, and MAPK activation was also established.	edelfosine	29-38	zinc fingers and homeoboxes 2	Homo sapiens	87-90
8770865-9	1996	These results suggest that inhibition of the MAPK cascade by ET18-OCH3 as a result of its effect on Raf-1 activation may be an important mechanism by which ET18-OCH3 inhibits cell proliferation.	edelfosine	61-70	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	100-105
8770865-9	1996	These results suggest that inhibition of the MAPK cascade by ET18-OCH3 as a result of its effect on Raf-1 activation may be an important mechanism by which ET18-OCH3 inhibits cell proliferation.	edelfosine	156-165	Raf-1 proto-oncogene, serine/threonine kinase	Homo sapiens	100-105
8645337-2	1996	Possible interference with mechanisms involving intracellular pH (pHi) regulation was examined by measuring the effect of ET-18-OCH3 on the activity of the Na+/H+ exchanger in the breast cancer-derived cell line MCF-7.	edelfosine	122-132	glucose-6-phosphate isomerase	Homo sapiens	66-69
8598315-5	1996	Similar to the effects induced by nonlethal heat shock, a nontoxic ET-18-OCH3 treatment led to a significant increase in the sensitivity of K562 cells to lysis by interleukin-2 (IL-2) stimulated natural killer (NK) cells.	edelfosine	67-77	interleukin 2	Homo sapiens	163-176
8598315-5	1996	Similar to the effects induced by nonlethal heat shock, a nontoxic ET-18-OCH3 treatment led to a significant increase in the sensitivity of K562 cells to lysis by interleukin-2 (IL-2) stimulated natural killer (NK) cells.	edelfosine	67-77	interleukin 2	Homo sapiens	178-182
8598315-7	1996	ALP treatment does not induce major histocompatibility complex (MHC) expression; however, a significant increase in the cell surface expression of HSP72 was shown by immunoblot analysis of membrane lysates of either untreated or ET-18-OCH3 treated K562 cells.	edelfosine	229-239	heat shock protein family A (Hsp70) member 1A	Homo sapiens	147-152
7707324-1	1995	A series of alkyl lysophospholipid (ALP) analogs of ET-18-OCH3 (1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine) containing modifications in the long C-1 chain has been synthesized and evaluated in human tumor cell line cytotoxicity assays.	edelfosine	64-117	T cell receptor gamma constant 1	Homo sapiens	156-159
7585518-1	1995	1-O-Octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) is a synthetic diether phospholipid that is competitive with phosphatidylserine binding to the regulatory domain of protein kinase C (PKC).	edelfosine	0-53	proline rich transmembrane protein 2	Homo sapiens	183-199
7585518-1	1995	1-O-Octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) is a synthetic diether phospholipid that is competitive with phosphatidylserine binding to the regulatory domain of protein kinase C (PKC).	edelfosine	0-53	proline rich transmembrane protein 2	Homo sapiens	201-204
7585518-1	1995	1-O-Octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) is a synthetic diether phospholipid that is competitive with phosphatidylserine binding to the regulatory domain of protein kinase C (PKC).	edelfosine	55-65	proline rich transmembrane protein 2	Homo sapiens	183-199
7585518-1	1995	1-O-Octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) is a synthetic diether phospholipid that is competitive with phosphatidylserine binding to the regulatory domain of protein kinase C (PKC).	edelfosine	55-65	proline rich transmembrane protein 2	Homo sapiens	201-204
7585518-2	1995	Our previous studies indicate that the selective inhibition of tumor cell growth by ET-18-OCH3 may be due to altered signal transduction mechanisms, including the inhibition of PKC.	edelfosine	84-94	proline rich transmembrane protein 2	Homo sapiens	177-180
7585518-3	1995	To further define the mechanism of action of ET-18-OCH3, we have used it to study the role of PKC in regulation of the transcription factor NF-kappa B, which is activated by diverse stimuli.	edelfosine	45-55	proline rich transmembrane protein 2	Homo sapiens	94-97
7585518-3	1995	To further define the mechanism of action of ET-18-OCH3, we have used it to study the role of PKC in regulation of the transcription factor NF-kappa B, which is activated by diverse stimuli.	edelfosine	45-55	nuclear factor kappa B subunit 1	Homo sapiens	140-150
7585518-8	1995	ET-18-OCH3 markedly inhibits TPA-induced NF-kappa B activation, as measured by HIV long terminal repeat-directed expression of beta-galactosidase.	edelfosine	0-10	nuclear factor kappa B subunit 1	Homo sapiens	41-51
7585518-8	1995	ET-18-OCH3 markedly inhibits TPA-induced NF-kappa B activation, as measured by HIV long terminal repeat-directed expression of beta-galactosidase.	edelfosine	0-10	galactosidase beta 1	Homo sapiens	127-145
7585518-10	1995	Inhibition of TPA-induced NF-kappa B activation was dependent upon preincubation with ET-18-OCH3, and the drug was active at approximately 2 mol% of total cellular phospholipid.	edelfosine	86-96	nuclear factor kappa B subunit 1	Homo sapiens	26-36
7585518-16	1995	Both ET-18-OCH3 and auranofin inhibited cellular induction of the active NF-kappa B complex in response to TPA but not in response to TNF-alpha.	edelfosine	5-15	nuclear factor kappa B subunit 1	Homo sapiens	73-83
7706325-0	1995	Lysophosphatidylcholine and 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine inhibit the CDP-choline pathway of phosphatidylcholine synthesis at the CTP:phosphocholine cytidylyltransferase step.	edelfosine	28-81	cut-like homeobox 1	Mus musculus	94-97
7706325-0	1995	Lysophosphatidylcholine and 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine inhibit the CDP-choline pathway of phosphatidylcholine synthesis at the CTP:phosphocholine cytidylyltransferase step.	edelfosine	28-81	phosphate cytidylyltransferase 1, choline, alpha isoform	Mus musculus	154-193
8092982-10	1994	These data demonstrate that the ether lipid ET-18-OCH3 can affect gene expression by inducing expression of fos and jun proto-oncogenes and by modulating the activity of transcription factor AP-1.	edelfosine	44-54	Fos proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	108-111
8092982-10	1994	These data demonstrate that the ether lipid ET-18-OCH3 can affect gene expression by inducing expression of fos and jun proto-oncogenes and by modulating the activity of transcription factor AP-1.	edelfosine	44-54	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	191-195
8513284-1	1993	In the present paper we analyzed c-fos and zif/268 expression in rat primary astroglial cell cultures after treatment with Platelet-activating Factor (PAF) and its 2-O-methyl-analogue, 1-O-octadecyl-2-O-methoxy-glycero-3-phosphocholine (ET-18-OCH3).	edelfosine	237-247	PCNA clamp associated factor	Rattus norvegicus	151-154
8185658-3	1994	However, membrane-bound PK-C activity in the sensitive HL-60 cells was approximately 3-fold increased in the presence of ET-18-OCH3, whereas in differentiated HL-60 cells and K562 cells PK-C was not influenced by ET-18-OCH3.	edelfosine	121-131	proline rich transmembrane protein 2	Homo sapiens	24-28
8185658-7	1994	Moreover, cells depleted of PK-C activity showed similar sensitivity or resistance to ET-18-OCH3 as cells expressing PK-C activity.	edelfosine	86-96	proline rich transmembrane protein 2	Homo sapiens	28-32
8185658-8	1994	These results suggest that a role of PK-C in the cytotoxic action of ET-18-OCH3 is very unlikely.	edelfosine	69-79	proline rich transmembrane protein 2	Homo sapiens	37-41
8282054-3	1994	ET-18-OCH3 inhibited GM-CSF binding to HL60, U937, and KG-1 cells with a half-maximal inhibitory concentration of 16, 10, and 78 microM, respectively.	edelfosine	0-10	colony stimulating factor 2	Homo sapiens	21-27
8282054-4	1994	ET-18-OCH3 at 10 microM reduced GM-CSF binding sites on HL60, U937, and KG-1, but had little effect on the dissociation constant (Kd).	edelfosine	0-10	colony stimulating factor 2	Homo sapiens	32-38
8282054-5	1994	ET-18-OCH3 at 10 and 30 microM significantly (p < 0.01) decreased, in a dose-dependent manner, the total uptake, surface binding, and internalization of GM-CSF.	edelfosine	0-10	colony stimulating factor 2	Homo sapiens	156-162
8282054-8	1994	Inhibition of GM-CSF binding by a combination of ET-18-OCH3 (10 microM) and TPA (1 or 10 nM) was less than additive, and ET-18-OCH3 partially inhibited TPA-induced protein kinase C (PKC) depletion in the cytosol and translocation to the particulate fractions.	edelfosine	49-59	colony stimulating factor 2	Homo sapiens	14-20
8282054-9	1994	It is suggested that the inhibition of GM-CSF binding by ET-18-OCH3 is due in part to disruption of the plasma membrane and that the inhibition of GM-CSF binding by TPA is due to activation of PKC.	edelfosine	57-67	colony stimulating factor 2	Homo sapiens	39-45
1288731-8	1992	), a peak of IL-6 production was reached 2 h after injection of ET-18-OCH3 [> 1280 U/ml (n = 4, p < 0.001) versus 3.5 +/- 0.2 U/ml (n = 7)], whereas BN 52211 induced a maximum of IL-6 production after 4 h (77 +/- 27 U/ml, n = 5, p < 0.001).	edelfosine	64-74	interleukin 6	Homo sapiens	13-17
1288731-8	1992	), a peak of IL-6 production was reached 2 h after injection of ET-18-OCH3 [> 1280 U/ml (n = 4, p < 0.001) versus 3.5 +/- 0.2 U/ml (n = 7)], whereas BN 52211 induced a maximum of IL-6 production after 4 h (77 +/- 27 U/ml, n = 5, p < 0.001).	edelfosine	64-74	interleukin 6	Homo sapiens	185-189
1627233-0	1992	SRI 62-834, a cyclic ether analogue of the phospholipid ET-18-OCH3, displays long-lasting beneficial effect in chronic relapsing experimental allergic encephalomyelitis in the Lewis rat.	edelfosine	56-66	sorcin	Rattus norvegicus	0-3
2168089-7	1990	When neutrophils had been treated with PAF or ET-18-OCH3 and were subsequently stimulated by fMLP, enhancement of the oxidative response was noted.	edelfosine	46-56	formyl peptide receptor 1	Homo sapiens	93-97
2369723-8	1990	Cells exposed to 5 microM ET-18-OCH3 for 18 h showed no increase in resting [Ca2+]i but there was 95% inhibition of the [Ca2+]i response to platelet-derived growth factor, 63% inhibition of the response to bradykinin, and 55% inhibition of the response to vasopressin.	edelfosine	26-36	kininogen 1	Homo sapiens	206-216
2334912-6	1990	These results suggest that the reduction of estrogen receptor level induced by ET-18-OCH3 resulted in decreases in both the secretion of TGF-alpha and the content of PR in MCF-7, and these effects are specific to ET-18-OCH3.	edelfosine	79-89	transforming growth factor alpha	Homo sapiens	137-146
2334912-6	1990	These results suggest that the reduction of estrogen receptor level induced by ET-18-OCH3 resulted in decreases in both the secretion of TGF-alpha and the content of PR in MCF-7, and these effects are specific to ET-18-OCH3.	edelfosine	213-223	transforming growth factor alpha	Homo sapiens	137-146
2308148-1	1990	Alkylglycerols such as rac-1-O-octadecyl-2-O-methylglycerophosphochocholine (Et-18-OMe) have shown an inhibitory effect on the metastasis and growth of various cancer cell lines.	edelfosine	77-86	Rac family small GTPase 1	Homo sapiens	23-28
2308148-6	1990	The biological testing of these analogues on PKC stimulated with rac-1-O-oleoyl-2-O-acetylglycerol showed several analogues with inhibition comparable to that of Et-18-OMe.	edelfosine	162-171	proline rich transmembrane protein 2	Homo sapiens	45-48
2308148-6	1990	The biological testing of these analogues on PKC stimulated with rac-1-O-oleoyl-2-O-acetylglycerol showed several analogues with inhibition comparable to that of Et-18-OMe.	edelfosine	162-171	Rac family small GTPase 1	Homo sapiens	65-70
3444374-8	1987	Therefore, its selective toxicity to tumor cells cannot be based on the differences in direct detoxification of 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine by AGMO in normal and malignant cells.	edelfosine	112-165	alkylglycerol monooxygenase	Rattus norvegicus	169-173
34885233-6	2021	This correlated with an increase in caspase-3 activity and PARP breakdown, as a major substrate of caspase-3, following PANC-1 CSC treatment with edelfosine.	edelfosine	146-156	caspase 3	Homo sapiens	36-45
34885233-6	2021	This correlated with an increase in caspase-3 activity and PARP breakdown, as a major substrate of caspase-3, following PANC-1 CSC treatment with edelfosine.	edelfosine	146-156	poly(ADP-ribose) polymerase 1	Homo sapiens	59-63
34885233-6	2021	This correlated with an increase in caspase-3 activity and PARP breakdown, as a major substrate of caspase-3, following PANC-1 CSC treatment with edelfosine.	edelfosine	146-156	caspase 3	Homo sapiens	99-108
34885233-7	2021	The antitumor ether lipid edelfosine colocalized with the endoplasmic reticulum in both PANC-1 cells as well as PANC-1 CSCs by using a fluorescent edelfosine analog, and induced an endoplasmic reticulum stress response in both PANC-1 cells and PANC-1 CSCs, with a potent CHOP/GADD153 upregulation.	edelfosine	26-36	DNA damage inducible transcript 3	Homo sapiens	271-275
34885233-7	2021	The antitumor ether lipid edelfosine colocalized with the endoplasmic reticulum in both PANC-1 cells as well as PANC-1 CSCs by using a fluorescent edelfosine analog, and induced an endoplasmic reticulum stress response in both PANC-1 cells and PANC-1 CSCs, with a potent CHOP/GADD153 upregulation.	edelfosine	26-36	DNA damage inducible transcript 3	Homo sapiens	276-283
34445344-10	2021	Furthermore, edelfosine, a phospholipase C (PLC) inhibitor, prevented T3 from acting on (Ca2+)i, UCP1 abundance, Psim, and OCR.	edelfosine	13-23	uncoupling protein 1	Homo sapiens	97-101
34131176-6	2021	Neutrophil-released arginase-1 and arginine deprivation potentiated the antitumor action against pancreatic cancer cells of the ER-targeted antitumor alkylphospholipid analog edelfosine.	edelfosine	175-185	arginase 1	Homo sapiens	20-30
34065546-2	2021	Cumulative evidence shows that edelfosine interacts with cholesterol-rich lipid rafts, endoplasmic reticulum (ER) and mitochondria.	edelfosine	31-41	epiregulin	Homo sapiens	110-112
34065546-4	2021	Edelfosine-induced apoptosis, mediated by lipid rafts and/or ER, requires the involvement of a mitochondrial-dependent step to eventually elicit cell death, leading to the loss of mitochondrial membrane potential, cytochrome c release and the triggering of cell death.	edelfosine	0-10	epiregulin	Homo sapiens	61-63
34065546-4	2021	Edelfosine-induced apoptosis, mediated by lipid rafts and/or ER, requires the involvement of a mitochondrial-dependent step to eventually elicit cell death, leading to the loss of mitochondrial membrane potential, cytochrome c release and the triggering of cell death.	edelfosine	0-10	cytochrome c, somatic	Homo sapiens	214-226
34065546-5	2021	The overexpression of Bcl-2 or Bcl-xL blocks edelfosine-induced apoptosis.	edelfosine	45-55	BCL2 apoptosis regulator	Homo sapiens	22-27
34065546-5	2021	The overexpression of Bcl-2 or Bcl-xL blocks edelfosine-induced apoptosis.	edelfosine	45-55	BCL2 like 1	Homo sapiens	31-37
2785846-2	1989	By pretreatment of the cells with ET-18-OCH3 (10 micrograms/ml) for 12 h, the EGF uptake at 37 degrees C was greatly reduced in both MCF-7 and ZR-75-1 (ET-18-OCH3-susceptible) but not in BT-20 (ET-18-OCH3-resistant) cell lines.	edelfosine	34-44	epidermal growth factor	Homo sapiens	78-81
2785846-7	1989	It is inferrable that the inhibition of the internalization process for EGF may be one of the modes of antitumoral action of ET-18-OCH3.	edelfosine	125-135	epidermal growth factor	Homo sapiens	72-75
2849926-0	1988	Inhibition of Na,K-ATPase and sodium pump by anticancer ether lipids and protein kinase C inhibitors ET-18-OCH3 and BM 41.440.	edelfosine	101-111	dynein axonemal heavy chain 8	Homo sapiens	19-25
2846728-3	1988	The PAF analogue, 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (Et-18-OCH3), did not induce chemiluminescence by itself and desensitized the cells against PAF, like substimulating concentrations of PAF.	edelfosine	18-71	PCNA clamp associated factor	Homo sapiens	4-7
2846728-3	1988	The PAF analogue, 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (Et-18-OCH3), did not induce chemiluminescence by itself and desensitized the cells against PAF, like substimulating concentrations of PAF.	edelfosine	18-71	PCNA clamp associated factor	Homo sapiens	164-167
2846728-3	1988	The PAF analogue, 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (Et-18-OCH3), did not induce chemiluminescence by itself and desensitized the cells against PAF, like substimulating concentrations of PAF.	edelfosine	18-71	PCNA clamp associated factor	Homo sapiens	164-167
2832680-0	1987	Antitumor activity of SRI 62-834, a cyclic ether analog of ET-18-OCH3.	edelfosine	59-69	sorcin	Mus musculus	22-25
2832680-1	1987	SRI 62-834, an analog of the antitumor agent ET-18-OCH3 in which the oxygen atom at carbon atom 2 has been incorporated into a five-membered heterocycle, has been prepared and evaluated as an antitumor agent.	edelfosine	45-55	sorcin	Mus musculus	0-3
34439330-12	2021	The alkylphospholipid analog prototype edelfosine is selectively taken up by tumor cells, accumulates in the ER of a number of human solid tumor cells-including pancreatic cancer cells-and promotes apoptosis through a persistent ER-stress-mediated mechanism both in vitro and in vivo.	edelfosine	39-49	epiregulin	Homo sapiens	109-111
34439330-12	2021	The alkylphospholipid analog prototype edelfosine is selectively taken up by tumor cells, accumulates in the ER of a number of human solid tumor cells-including pancreatic cancer cells-and promotes apoptosis through a persistent ER-stress-mediated mechanism both in vitro and in vivo.	edelfosine	39-49	epiregulin	Homo sapiens	229-231
3444371-1	1987	We have investigated cellular sensitivity to the antitumoral alkyl lysophospholipid (ALP) 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3) in vitro.	edelfosine	145-155	asparaginase and isoaspartyl peptidase 1	Homo sapiens	61-91
3444378-1	1987	The ether phospholipid 1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine (OM-GPC) is known to be a potent inhibitor of cell growth.	edelfosine	23-76	glycophorin C (Gerbich blood group)	Homo sapiens	81-84
27519637-7	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	edelfosine	158-168	cut-like homeobox 1	Mus musculus	26-29
3444389-6	1987	In these experiments, ARA-CDP-D,L-PTBA, ARA-CDP-D,L-PBA, ARA-CDP-L-dipalmitin and ARA-CDP-D,L-PCA were more active than either the parent compounds ARA-C and ET-18-OCH3 alone or their equimolar mixtures.	edelfosine	158-168	cut-like homeobox 1	Mus musculus	26-29
30826858-5	2019	Unexpectedly, CaSR response (high Ca2+-elicited cytosolic [Ca2+] elevation) was unaffected by edelfosine or U73122 but strongly suppressed by SK&F 96365, ruthenium red, and 2-aminoethoxydiphenyl borate (2-APB), suggesting involvement of TRPV and TRPC channels but not Gq-phospholipase C. Acute application of NPS2143, a negative allosteric modulator of CaSR, suppressed CaSR response.	edelfosine	94-104	calcium-sensing receptor	Mus musculus	14-18
3468284-1	1987	The human leukemia cell lines K562, HL60, and Raji and the mouse leukemia cell line L1210 showed a differential susceptibility to the action of the alkyl-lysophospholipid (ALP) 1-octadecyl-2-methyl-rac-glycero-3-phosphocholine (ET-18-OCH3).	edelfosine	228-238	asparaginase like 1	Mus musculus	148-178
3471316-3	1987	When cells were treated with CP-46,665-1 or ET-18-OCH3 (50 micrograms/ml for 1 h), these compounds did not inhibit the growth of normal progenitors, whereas the growth of the clonogenic leukemic cells was inhibited with differences in their sensitivities to the cytotoxic effect of CP-46,665-1 and ET-18-OCH3.	edelfosine	44-54	cytochrome P450 family 46 subfamily A member 1	Homo sapiens	282-293
3471316-3	1987	When cells were treated with CP-46,665-1 or ET-18-OCH3 (50 micrograms/ml for 1 h), these compounds did not inhibit the growth of normal progenitors, whereas the growth of the clonogenic leukemic cells was inhibited with differences in their sensitivities to the cytotoxic effect of CP-46,665-1 and ET-18-OCH3.	edelfosine	298-308	cytochrome P450 family 46 subfamily A member 1	Homo sapiens	29-40
26497035-7	2016	Moreover, thrombin-stimulated PKCalpha/betaII, PKCdelta, p38 MAPK, JNK1/2, or p65 phosphorylation was abrogated by their respective inhibitor of PPACK, GPA2A, D609, ET-18-OCH3, Go6983, Rottlerin, SB202190, SP600125, Bay11-7082, or Helenalin.	edelfosine	165-175	coagulation factor II, thrombin	Homo sapiens	10-18
29567857-5	2018	We further identified and evaluated the efficacy of a known drug, the selective PLC inhibitor edelfosine, in suppressing the PCDH7 signaling pathway to prohibit brain metastases in the animal models.	edelfosine	94-104	heparan sulfate proteoglycan 2	Homo sapiens	80-83
29567857-5	2018	We further identified and evaluated the efficacy of a known drug, the selective PLC inhibitor edelfosine, in suppressing the PCDH7 signaling pathway to prohibit brain metastases in the animal models.	edelfosine	94-104	protocadherin 7	Homo sapiens	125-130
29330349-6	2018	Edelfosine and neomycin, pan-PLC inhibitors, significantly decreased PLC activities in homogenates of the brain tissues.	edelfosine	0-10	1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase classes I and II	Apis mellifera	29-32
29330349-6	2018	Edelfosine and neomycin, pan-PLC inhibitors, significantly decreased PLC activities in homogenates of the brain tissues.	edelfosine	0-10	1-phosphatidylinositol 4,5-bisphosphate phosphodiesterase classes I and II	Apis mellifera	69-72
30229281-7	2018	Edelfosin, an alkyl-lipid blocker of the Abi1 interaction partner SK3, inhibits invasion of urothelial carcinoma cells.	edelfosine	0-9	abl interactor 1	Homo sapiens	41-45
30229281-7	2018	Edelfosin, an alkyl-lipid blocker of the Abi1 interaction partner SK3, inhibits invasion of urothelial carcinoma cells.	edelfosine	0-9	potassium calcium-activated channel subfamily N member 3	Homo sapiens	66-69
26497035-7	2016	Moreover, thrombin-stimulated PKCalpha/betaII, PKCdelta, p38 MAPK, JNK1/2, or p65 phosphorylation was abrogated by their respective inhibitor of PPACK, GPA2A, D609, ET-18-OCH3, Go6983, Rottlerin, SB202190, SP600125, Bay11-7082, or Helenalin.	edelfosine	165-175	protein kinase C alpha	Homo sapiens	30-45
26497035-7	2016	Moreover, thrombin-stimulated PKCalpha/betaII, PKCdelta, p38 MAPK, JNK1/2, or p65 phosphorylation was abrogated by their respective inhibitor of PPACK, GPA2A, D609, ET-18-OCH3, Go6983, Rottlerin, SB202190, SP600125, Bay11-7082, or Helenalin.	edelfosine	165-175	mitogen-activated protein kinase 14	Homo sapiens	57-60
27470549-1	2016	In this study, transferrin (Tf)-conjugated polyethylene glycol (PEG)-poly-l-lysine (PLL)-poly(lactic-co-glycolic acid) (PLGA) (PEG-PLL-PLGA)-based micellar formulations were successfully prepared for the delivery of edelfosine (EDS) in leukemia treatment.	edelfosine	216-226	transferrin	Homo sapiens	15-26
27470549-1	2016	In this study, transferrin (Tf)-conjugated polyethylene glycol (PEG)-poly-l-lysine (PLL)-poly(lactic-co-glycolic acid) (PLGA) (PEG-PLL-PLGA)-based micellar formulations were successfully prepared for the delivery of edelfosine (EDS) in leukemia treatment.	edelfosine	216-226	transferrin	Homo sapiens	28-30
26246489-4	2015	This raft-Fas/CD95 coclustering was first described at the early 2000s as the underlying mechanism for the proapoptotic action of the alkylphospholipid analog edelfosine in leukemic cells, hence facilitating protein-protein interactions and conveying apoptotic signals independently of Fas/CD95 ligand.	edelfosine	159-169	Fas cell surface death receptor	Homo sapiens	14-18
26944919-4	2016	Edelfosine caused a dose-dependent decrease in AKT activity, but did not affect the expression of total AKT in either cell line.	edelfosine	0-10	AKT serine/threonine kinase 1	Homo sapiens	47-50
26944919-5	2016	Furthermore, edelfosine treatment inhibited the expression of androgen receptor (AR) and was associated with an increase in activating transcription factor 3 (ATF3) expression levels, a stress response gene and a negative regulator of AR transactivation.	edelfosine	13-23	androgen receptor	Homo sapiens	62-79
26944919-5	2016	Furthermore, edelfosine treatment inhibited the expression of androgen receptor (AR) and was associated with an increase in activating transcription factor 3 (ATF3) expression levels, a stress response gene and a negative regulator of AR transactivation.	edelfosine	13-23	androgen receptor	Homo sapiens	81-83
26944919-5	2016	Furthermore, edelfosine treatment inhibited the expression of androgen receptor (AR) and was associated with an increase in activating transcription factor 3 (ATF3) expression levels, a stress response gene and a negative regulator of AR transactivation.	edelfosine	13-23	activating transcription factor 3	Homo sapiens	124-157
26944919-5	2016	Furthermore, edelfosine treatment inhibited the expression of androgen receptor (AR) and was associated with an increase in activating transcription factor 3 (ATF3) expression levels, a stress response gene and a negative regulator of AR transactivation.	edelfosine	13-23	activating transcription factor 3	Homo sapiens	159-163
26944919-5	2016	Furthermore, edelfosine treatment inhibited the expression of androgen receptor (AR) and was associated with an increase in activating transcription factor 3 (ATF3) expression levels, a stress response gene and a negative regulator of AR transactivation.	edelfosine	13-23	androgen receptor	Homo sapiens	235-237
26944919-6	2016	ATF3 binds to AR after edelfosine + AD and represses the transcriptional activation of AR as demonstrated by PSA promoter studies.	edelfosine	23-33	activating transcription factor 3	Homo sapiens	0-4
26944919-6	2016	ATF3 binds to AR after edelfosine + AD and represses the transcriptional activation of AR as demonstrated by PSA promoter studies.	edelfosine	23-33	androgen receptor	Homo sapiens	14-16
26944919-7	2016	Knockdown of ATF3 using siRNA-ATF3 reversed the inhibition of PSA promoter activity, suggesting that the growth inhibition effect of edelfosine was ATF3 dependent.	edelfosine	133-143	activating transcription factor 3	Homo sapiens	13-17
26944919-7	2016	Knockdown of ATF3 using siRNA-ATF3 reversed the inhibition of PSA promoter activity, suggesting that the growth inhibition effect of edelfosine was ATF3 dependent.	edelfosine	133-143	activating transcription factor 3	Homo sapiens	30-34
26944919-7	2016	Knockdown of ATF3 using siRNA-ATF3 reversed the inhibition of PSA promoter activity, suggesting that the growth inhibition effect of edelfosine was ATF3 dependent.	edelfosine	133-143	activating transcription factor 3	Homo sapiens	30-34
26944919-8	2016	Moreover, expression of AR variant 7 (ARv7) and TMPRSS2-ERG fusion gene were greatly inhibited after combined treatment with AD and edelfosine in VCaP cells.	edelfosine	132-142	transmembrane serine protease 2	Homo sapiens	48-55
26615420-3	2016	Edelfosine decreased cell viability and induced autophagic death at a moderate concentration (~30 muM), whereas it induced apoptotic cell death at concentrations over 30 muM.	edelfosine	0-10	latexin	Homo sapiens	98-101
26615420-4	2016	Interestingly, low concentrations of edelfosine (5-10 muM) effectively enhanced recombinant human tumor necrosis factor (TNF)-related apoptosis-inducing ligand (rhTRAIL/TNFSF10)-induced apoptosis and clonogenicity in gastric cancer cells, including TRAIL-resistant AGS cells.	edelfosine	37-47	latexin	Homo sapiens	54-57
26615420-4	2016	Interestingly, low concentrations of edelfosine (5-10 muM) effectively enhanced recombinant human tumor necrosis factor (TNF)-related apoptosis-inducing ligand (rhTRAIL/TNFSF10)-induced apoptosis and clonogenicity in gastric cancer cells, including TRAIL-resistant AGS cells.	edelfosine	37-47	TNF superfamily member 10	Homo sapiens	169-176
26615420-4	2016	Interestingly, low concentrations of edelfosine (5-10 muM) effectively enhanced recombinant human tumor necrosis factor (TNF)-related apoptosis-inducing ligand (rhTRAIL/TNFSF10)-induced apoptosis and clonogenicity in gastric cancer cells, including TRAIL-resistant AGS cells.	edelfosine	37-47	TNF superfamily member 10	Homo sapiens	163-168
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	44-60
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	62-65
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	66-75
26615420-5	2016	Edelfosine upregulated the protein level of death receptor 5 (DR5/TNFRSF10B) and/or increased DR5 upregulation in lipid rafts.	edelfosine	0-10	TNF receptor superfamily member 10b	Homo sapiens	94-97
26615420-6	2016	In addition, edelfosine-mediated rhTRAIL sensitization was regulated by the DR5 pathway.	edelfosine	13-23	TNF receptor superfamily member 10b	Homo sapiens	76-79
26615420-7	2016	Edelfosine also activated p38MAPK (MAPK14), and edelfosine-mediated rhTRAIL sensitization was partially regulated by a p38-mediated decrease in mitochondrial membrane potential.	edelfosine	0-10	mitogen-activated protein kinase 14	Homo sapiens	35-41
26711779-0	2016	Erratum to: The small conductance calcium-activated potassium channel 3 (SK3) is a molecular target for Edelfosine to reduce the invasive potential of urothelial carcinoma cells.	edelfosine	104-114	potassium calcium-activated channel subfamily N member 3	Homo sapiens	73-76
26729084-2	2015	Different substitution analogues of the original lipidic ether edelfosine (1-O-octadecyl-2-O-methyl-rac-glycero-3-phosphocholine) are obtained varying the sesterterpenoid in position 1 or 2 of the glycerol or a phosphocholine or PUFA unit in position 3.	edelfosine	75-128	pumilio RNA binding family member 3	Homo sapiens	229-233
26944919-0	2016	Edelfosine Promotes Apoptosis in Androgen-Deprived Prostate Tumors by Increasing ATF3 and Inhibiting Androgen Receptor Activity.	edelfosine	0-10	activating transcription factor 3	Homo sapiens	81-85
26944919-0	2016	Edelfosine Promotes Apoptosis in Androgen-Deprived Prostate Tumors by Increasing ATF3 and Inhibiting Androgen Receptor Activity.	edelfosine	0-10	androgen receptor	Homo sapiens	101-118
26619845-0	2016	The small conductance calcium-activated potassium channel 3 (SK3) is a molecular target for Edelfosine to reduce the invasive potential of urothelial carcinoma cells.	edelfosine	92-102	potassium calcium-activated channel subfamily N member 3	Homo sapiens	61-64
26619845-3	2016	Since Edelfosine, a glycerophospholipid with antitumoral properties, effectively inhibits SK3 channel activity, our goal was to evaluate SK3 as a potential molecular target to inhibit the gain of an invasive phenotype in UC.	edelfosine	6-16	potassium calcium-activated channel subfamily N member 3	Homo sapiens	90-93
26619845-3	2016	Since Edelfosine, a glycerophospholipid with antitumoral properties, effectively inhibits SK3 channel activity, our goal was to evaluate SK3 as a potential molecular target to inhibit the gain of an invasive phenotype in UC.	edelfosine	6-16	potassium calcium-activated channel subfamily N member 3	Homo sapiens	137-140
26619845-9	2016	Edelfosine is able to effectively inhibit migration and invasion of UC cells in vitro and in vivo in an SK3-dependent way, pointing towards a possible role for Edelfosine as an antiinvasive drug to effectively inhibit UC cell invasion and metastasis.	edelfosine	0-10	potassium calcium-activated channel subfamily N member 3	Homo sapiens	104-107
26619845-9	2016	Edelfosine is able to effectively inhibit migration and invasion of UC cells in vitro and in vivo in an SK3-dependent way, pointing towards a possible role for Edelfosine as an antiinvasive drug to effectively inhibit UC cell invasion and metastasis.	edelfosine	160-170	potassium calcium-activated channel subfamily N member 3	Homo sapiens	104-107
26246489-4	2015	This raft-Fas/CD95 coclustering was first described at the early 2000s as the underlying mechanism for the proapoptotic action of the alkylphospholipid analog edelfosine in leukemic cells, hence facilitating protein-protein interactions and conveying apoptotic signals independently of Fas/CD95 ligand.	edelfosine	159-169	Fas cell surface death receptor	Homo sapiens	290-294
25465296-11	2015	Edelfosine also displaced survival PI3K/Akt signaling from lipid rafts, leading to Akt inhibition, in mantle cell lymphoma cells.	edelfosine	0-10	AKT serine/threonine kinase 1	Homo sapiens	40-43
25888510-5	2015	Edelfosine, a specific inhibitor of PI-PLC, did not affect depolarization-induced contractions but modulated myogenic tone.	edelfosine	0-10	protein disulfide isomerase associated 3	Mus musculus	36-42
25749008-3	2015	Preincubation of U118 cells with the selective MEK1/2 inhibitor U0126, which inhibits MEK1/2-mediated activation of ERK1/2, led to a switch from necrosis to caspase-dependent apoptosis following edelfosine treatment.	edelfosine	195-205	mitogen-activated protein kinase kinase 1	Homo sapiens	47-53
25749008-3	2015	Preincubation of U118 cells with the selective MEK1/2 inhibitor U0126, which inhibits MEK1/2-mediated activation of ERK1/2, led to a switch from necrosis to caspase-dependent apoptosis following edelfosine treatment.	edelfosine	195-205	mitogen-activated protein kinase kinase 1	Homo sapiens	86-92
25749008-3	2015	Preincubation of U118 cells with the selective MEK1/2 inhibitor U0126, which inhibits MEK1/2-mediated activation of ERK1/2, led to a switch from necrosis to caspase-dependent apoptosis following edelfosine treatment.	edelfosine	195-205	mitogen-activated protein kinase 3	Homo sapiens	116-122
25749008-4	2015	Combined treatment of U0126 and edelfosine totally inhibited ERK1/2 phosphorylation, and led to RIPK1 and RelA/NF-kappaB degradation, together with a strong activation of caspase-3 and -8.	edelfosine	32-42	mitogen-activated protein kinase 3	Homo sapiens	61-67
25749008-4	2015	Combined treatment of U0126 and edelfosine totally inhibited ERK1/2 phosphorylation, and led to RIPK1 and RelA/NF-kappaB degradation, together with a strong activation of caspase-3 and -8.	edelfosine	32-42	receptor interacting serine/threonine kinase 1	Homo sapiens	96-101
25749008-4	2015	Combined treatment of U0126 and edelfosine totally inhibited ERK1/2 phosphorylation, and led to RIPK1 and RelA/NF-kappaB degradation, together with a strong activation of caspase-3 and -8.	edelfosine	32-42	RELA proto-oncogene, NF-kB subunit	Homo sapiens	106-110
25749008-4	2015	Combined treatment of U0126 and edelfosine totally inhibited ERK1/2 phosphorylation, and led to RIPK1 and RelA/NF-kappaB degradation, together with a strong activation of caspase-3 and -8.	edelfosine	32-42	nuclear factor kappa B subunit 1	Homo sapiens	111-120
25749008-4	2015	Combined treatment of U0126 and edelfosine totally inhibited ERK1/2 phosphorylation, and led to RIPK1 and RelA/NF-kappaB degradation, together with a strong activation of caspase-3 and -8.	edelfosine	32-42	caspase 3	Homo sapiens	171-187
25749008-6	2015	Inhibition of ERK phosphorylation also led to a dramatic increase in edelfosine-induced apoptosis when the alkylphospholipid analog was used at a low micromolar range, suggesting that ERK phosphorylation acts as a potent regulator of apoptotic cell death in edelfosine-treated U118 cells.	edelfosine	69-79	mitogen-activated protein kinase 1	Homo sapiens	14-17
25749008-6	2015	Inhibition of ERK phosphorylation also led to a dramatic increase in edelfosine-induced apoptosis when the alkylphospholipid analog was used at a low micromolar range, suggesting that ERK phosphorylation acts as a potent regulator of apoptotic cell death in edelfosine-treated U118 cells.	edelfosine	69-79	mitogen-activated protein kinase 1	Homo sapiens	184-187
25749008-6	2015	Inhibition of ERK phosphorylation also led to a dramatic increase in edelfosine-induced apoptosis when the alkylphospholipid analog was used at a low micromolar range, suggesting that ERK phosphorylation acts as a potent regulator of apoptotic cell death in edelfosine-treated U118 cells.	edelfosine	258-268	mitogen-activated protein kinase 1	Homo sapiens	14-17
25749008-6	2015	Inhibition of ERK phosphorylation also led to a dramatic increase in edelfosine-induced apoptosis when the alkylphospholipid analog was used at a low micromolar range, suggesting that ERK phosphorylation acts as a potent regulator of apoptotic cell death in edelfosine-treated U118 cells.	edelfosine	258-268	mitogen-activated protein kinase 1	Homo sapiens	184-187
25749008-7	2015	These data show that inhibition of MEK1/2-ERK1/2 signaling pathway highly potentiates edelfosine-induced apoptosis in glioblastoma U118 cells and switches the type of edelfosine-induced cell death from necrosis to apoptosis.	edelfosine	86-96	mitogen-activated protein kinase kinase 1	Homo sapiens	35-41
25749008-7	2015	These data show that inhibition of MEK1/2-ERK1/2 signaling pathway highly potentiates edelfosine-induced apoptosis in glioblastoma U118 cells and switches the type of edelfosine-induced cell death from necrosis to apoptosis.	edelfosine	86-96	mitogen-activated protein kinase 3	Homo sapiens	42-48
25749008-7	2015	These data show that inhibition of MEK1/2-ERK1/2 signaling pathway highly potentiates edelfosine-induced apoptosis in glioblastoma U118 cells and switches the type of edelfosine-induced cell death from necrosis to apoptosis.	edelfosine	167-177	mitogen-activated protein kinase kinase 1	Homo sapiens	35-41
25749008-7	2015	These data show that inhibition of MEK1/2-ERK1/2 signaling pathway highly potentiates edelfosine-induced apoptosis in glioblastoma U118 cells and switches the type of edelfosine-induced cell death from necrosis to apoptosis.	edelfosine	167-177	mitogen-activated protein kinase 3	Homo sapiens	42-48
25465296-11	2015	Edelfosine also displaced survival PI3K/Akt signaling from lipid rafts, leading to Akt inhibition, in mantle cell lymphoma cells.	edelfosine	0-10	AKT serine/threonine kinase 1	Homo sapiens	83-86
24335212-5	2014	Our results indicated that phospholipase Cgamma (PLCgamma) is involved in the CB1 receptor-mediated synaptic effect of BDNF, because the BDNF effect was blocked in the presence of the broad-spectrum PLC inhibitors U-73122 and edelfosine, whereas the inactive analog U-73343 did not alter the suppressive effect of BDNF at inhibitory synapses.	edelfosine	226-236	cannabinoid receptor 1 (brain)	Mus musculus	78-81
25593994-6	2014	The RIPK1-dependent necroptosis inhibitors necrostatin-1 (Nec-1) and Nec-1s as well as siRNA-mediated silencing of RIPK3 inhibited edelfosine-induced necroptosis, resulting in increased caspase-dependent apoptosis in edelfosine-treated glioblastoma U118 cells.	edelfosine	131-141	proprotein convertase subtilisin/kexin type 1	Homo sapiens	43-63
25593994-6	2014	The RIPK1-dependent necroptosis inhibitors necrostatin-1 (Nec-1) and Nec-1s as well as siRNA-mediated silencing of RIPK3 inhibited edelfosine-induced necroptosis, resulting in increased caspase-dependent apoptosis in edelfosine-treated glioblastoma U118 cells.	edelfosine	131-141	receptor interacting serine/threonine kinase 3	Homo sapiens	115-120
25593994-6	2014	The RIPK1-dependent necroptosis inhibitors necrostatin-1 (Nec-1) and Nec-1s as well as siRNA-mediated silencing of RIPK3 inhibited edelfosine-induced necroptosis, resulting in increased caspase-dependent apoptosis in edelfosine-treated glioblastoma U118 cells.	edelfosine	217-227	receptor interacting serine/threonine kinase 1	Homo sapiens	4-9
25593994-6	2014	The RIPK1-dependent necroptosis inhibitors necrostatin-1 (Nec-1) and Nec-1s as well as siRNA-mediated silencing of RIPK3 inhibited edelfosine-induced necroptosis, resulting in increased caspase-dependent apoptosis in edelfosine-treated glioblastoma U118 cells.	edelfosine	217-227	receptor interacting serine/threonine kinase 3	Homo sapiens	115-120
25593994-7	2014	Inhibition of the RIPK3 substrate MLKL with necrosulfonamide also increased apoptosis in edelfosine-treated cells.	edelfosine	89-99	receptor interacting serine/threonine kinase 3	Homo sapiens	18-23
25593994-7	2014	Inhibition of the RIPK3 substrate MLKL with necrosulfonamide also increased apoptosis in edelfosine-treated cells.	edelfosine	89-99	mixed lineage kinase domain like pseudokinase	Homo sapiens	34-38
25593994-8	2014	These data support a major role for RIPK1 and RIPK3 in the induction of necrotic cell death and in the switch from necrosis to apoptosis following edelfosine treatment.	edelfosine	147-157	receptor interacting serine/threonine kinase 1	Homo sapiens	36-41
25593994-8	2014	These data support a major role for RIPK1 and RIPK3 in the induction of necrotic cell death and in the switch from necrosis to apoptosis following edelfosine treatment.	edelfosine	147-157	receptor interacting serine/threonine kinase 3	Homo sapiens	46-51
25304249-8	2014	RESULTS: We determined that cells with suppressed CD74 are more sensitive to FasL-induced apoptosis and Fas signaling-dependent chemotherapies, edelfosine and doxorubicin, than control CD74-expressing cells.	edelfosine	144-154	CD74 molecule	Homo sapiens	50-54
25304249-8	2014	RESULTS: We determined that cells with suppressed CD74 are more sensitive to FasL-induced apoptosis and Fas signaling-dependent chemotherapies, edelfosine and doxorubicin, than control CD74-expressing cells.	edelfosine	144-154	Fas ligand	Homo sapiens	77-81
24628239-5	2014	The subcellular distribution of 1 differed from that reported for a phenyl-polyene analog of ET-18-OCH3; 1 was found to be localized in the endoplasmic reticulum, mitochondria, and lysosomes but not in the plasma membrane or nucleus of PC3 cells.	edelfosine	93-103	chromobox 8	Homo sapiens	236-239
24628241-7	2014	Both raft- and ER-mediated proapoptotic responses require a mitochondrial-related step to eventually promote cell death, and overexpression of Bcl-2 or Bcl-xL prevents edelfosine-induced apoptosis.	edelfosine	168-178	BCL2 apoptosis regulator	Homo sapiens	143-148
24628241-7	2014	Both raft- and ER-mediated proapoptotic responses require a mitochondrial-related step to eventually promote cell death, and overexpression of Bcl-2 or Bcl-xL prevents edelfosine-induced apoptosis.	edelfosine	168-178	BCL2 like 1	Homo sapiens	152-158
26618532-6	2015	RESULTS: A 6 hours exposure of human erythrocytes to edelfosine (5 microM) significantly increased the percentage of annexin-V-binding cells, significantly decreased forward scatter, and significantly increased Fluo3-fluorescence, but did not significantly modify DCFDA fluorescence.	edelfosine	53-63	annexin A5	Homo sapiens	117-126
26618532-7	2015	The effect of edelfosine on annexin-V-binding was significantly blunted, but not abolished by removal of extracellular Ca2+.	edelfosine	14-24	annexin A5	Homo sapiens	28-37
25593994-6	2014	The RIPK1-dependent necroptosis inhibitors necrostatin-1 (Nec-1) and Nec-1s as well as siRNA-mediated silencing of RIPK3 inhibited edelfosine-induced necroptosis, resulting in increased caspase-dependent apoptosis in edelfosine-treated glioblastoma U118 cells.	edelfosine	131-141	receptor interacting serine/threonine kinase 1	Homo sapiens	4-9
25086877-4	2014	Edelfosine improved the disease course and led to reduced frequencies of CD4(+) T cells infiltrating into the central nervous system.	edelfosine	0-10	CD4 molecule	Homo sapiens	73-76
24335212-5	2014	Our results indicated that phospholipase Cgamma (PLCgamma) is involved in the CB1 receptor-mediated synaptic effect of BDNF, because the BDNF effect was blocked in the presence of the broad-spectrum PLC inhibitors U-73122 and edelfosine, whereas the inactive analog U-73343 did not alter the suppressive effect of BDNF at inhibitory synapses.	edelfosine	226-236	brain derived neurotrophic factor	Mus musculus	119-123
24335212-5	2014	Our results indicated that phospholipase Cgamma (PLCgamma) is involved in the CB1 receptor-mediated synaptic effect of BDNF, because the BDNF effect was blocked in the presence of the broad-spectrum PLC inhibitors U-73122 and edelfosine, whereas the inactive analog U-73343 did not alter the suppressive effect of BDNF at inhibitory synapses.	edelfosine	226-236	brain derived neurotrophic factor	Mus musculus	137-141
24335212-5	2014	Our results indicated that phospholipase Cgamma (PLCgamma) is involved in the CB1 receptor-mediated synaptic effect of BDNF, because the BDNF effect was blocked in the presence of the broad-spectrum PLC inhibitors U-73122 and edelfosine, whereas the inactive analog U-73343 did not alter the suppressive effect of BDNF at inhibitory synapses.	edelfosine	226-236	brain derived neurotrophic factor	Mus musculus	137-141
24413065-6	2014	In all three cell lines [Gem+Clo+Ed] decreased the level of phosphorylation of the pro-survival protein AKT and activated the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) stress signaling pathway, which in J45.01 cells resulted in the phosphorylation and heterodimerization of the transcription factors ATF2 and c-Jun.	edelfosine	33-35	AKT serine/threonine kinase 1	Homo sapiens	104-107
24413065-6	2014	In all three cell lines [Gem+Clo+Ed] decreased the level of phosphorylation of the pro-survival protein AKT and activated the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) stress signaling pathway, which in J45.01 cells resulted in the phosphorylation and heterodimerization of the transcription factors ATF2 and c-Jun.	edelfosine	33-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	158-163
24413065-6	2014	In all three cell lines [Gem+Clo+Ed] decreased the level of phosphorylation of the pro-survival protein AKT and activated the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) stress signaling pathway, which in J45.01 cells resulted in the phosphorylation and heterodimerization of the transcription factors ATF2 and c-Jun.	edelfosine	33-35	activating transcription factor 2	Homo sapiens	325-329
24413065-6	2014	In all three cell lines [Gem+Clo+Ed] decreased the level of phosphorylation of the pro-survival protein AKT and activated the stress-activated protein kinase/c-Jun N-terminal kinase (SAPK/JNK) stress signaling pathway, which in J45.01 cells resulted in the phosphorylation and heterodimerization of the transcription factors ATF2 and c-Jun.	edelfosine	33-35	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	334-339
23335509-4	2013	Edelfosine displaced the essential proton pump Pma1p from rafts, inducing its internalization into the vacuole.	edelfosine	0-10	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	47-52
23770096-3	2013	GPR91 agonist-mediated effects detected using dynamic mass redistribution (DMR) were inhibited with PTX, edelfosine and U73122 demonstrating the importance of not only the Galphai pathway but also PLCbeta.	edelfosine	105-115	succinate receptor 1	Homo sapiens	0-5
23786223-7	2013	The phosphatidyl inositol-specific phospholipase C (Pi-PLC) inhibitor ET-18-OCH3 had no effect.	edelfosine	70-80	protein disulfide isomerase associated 3	Mus musculus	52-58
23415083-4	2013	Among the synthesized compounds, 5a, 5b and 6c exhibited potent inhibitory Akt phosphorylation effects with IC50 value of 3.1, 2.0 and 3.0 muM, respectively, and their potencies were better than those of three reference compounds miltefosine, perifosine and edelfosine.	edelfosine	258-268	AKT serine/threonine kinase 1	Homo sapiens	75-78
23344949-8	2013	Significantly, we show that edelfosine selectively reduces lateral segregation of PM proteins like Pma1p and nutrient H(+)-symporters inducing their ubiquitination and internalization.	edelfosine	28-38	H(+)-exporting P2-type ATPase PMA1	Saccharomyces cerevisiae S288C	99-104
21289302-3	2011	Edelfosine is also accumulated by Saccharomyces cerevisiae in a process requiring the membrane protein Lem3p, and the human genome contains a Lem3p homolog TMEM30a.	edelfosine	0-10	Lem3p	Saccharomyces cerevisiae S288C	103-108
21793801-0	2011	Phosphoinositide phosphatase SHIP-1 regulates apoptosis induced by edelfosine, Fas ligation and DNA damage in mouse lymphoma cells.	edelfosine	67-77	inositol polyphosphate-5-phosphatase D	Mus musculus	29-35
21999627-1	2011	Edelfosine is an inhibitor of SK3 channel mediated cell migration.	edelfosine	0-10	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3	Mus musculus	30-33
21999627-3	2011	Using cell SK3 dependent cell-migration assay, patch-clamp, (125)I-apamin binding, and in vivo experiments we tested the ability of 15 lipid derivatives with chemical structures inspired from edelfosine to inhibit SK3 channels.	edelfosine	192-202	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3	Mus musculus	214-217
21999627-4	2011	Using a structure-activity relationship approach we identified an edelfosine analog named Ohmline (1-O-hexadecyl- 2-O-methyl-sn-glycero-3-lactose) with potent inhibitory effects on the SK3 channel.	edelfosine	66-76	potassium intermediate/small conductance calcium-activated channel, subfamily N, member 3	Mus musculus	185-188
21593790-3	2011	Here, we have found that edelfosine induced loss of mitochondrial membrane potential and apoptosis in human cervical carcinoma HeLa cells, both responses being abrogated by Bcl-x(L) overexpression.	edelfosine	25-35	BCL2 like 1	Homo sapiens	173-181
22056873-5	2012	In this study, we found that the anticancer drug edelfosine was the most potent ALP in killing human pancreatic cancer cells, targeting endoplasmic reticulum (ER).	edelfosine	49-59	ATHS	Homo sapiens	80-83
22056873-7	2012	Pancreatic cancer cells show a prominent ER and edelfosine accumulated in this subcellular structure, inducing a potent ER stress response, with caspase-4, BAP31 and c-Jun NH(2)-terminal kinase (JNK) activation, CHOP/GADD153 upregulation and phosphorylation of eukaryotic translation initiation factor 2 alpha-subunit that eventually led to cell death.	edelfosine	48-58	caspase 4, apoptosis-related cysteine peptidase	Mus musculus	145-154
22056873-7	2012	Pancreatic cancer cells show a prominent ER and edelfosine accumulated in this subcellular structure, inducing a potent ER stress response, with caspase-4, BAP31 and c-Jun NH(2)-terminal kinase (JNK) activation, CHOP/GADD153 upregulation and phosphorylation of eukaryotic translation initiation factor 2 alpha-subunit that eventually led to cell death.	edelfosine	48-58	B cell receptor associated protein 31	Mus musculus	156-161
22056873-7	2012	Pancreatic cancer cells show a prominent ER and edelfosine accumulated in this subcellular structure, inducing a potent ER stress response, with caspase-4, BAP31 and c-Jun NH(2)-terminal kinase (JNK) activation, CHOP/GADD153 upregulation and phosphorylation of eukaryotic translation initiation factor 2 alpha-subunit that eventually led to cell death.	edelfosine	48-58	mitogen-activated protein kinase 8	Mus musculus	166-193
22056873-7	2012	Pancreatic cancer cells show a prominent ER and edelfosine accumulated in this subcellular structure, inducing a potent ER stress response, with caspase-4, BAP31 and c-Jun NH(2)-terminal kinase (JNK) activation, CHOP/GADD153 upregulation and phosphorylation of eukaryotic translation initiation factor 2 alpha-subunit that eventually led to cell death.	edelfosine	48-58	mitogen-activated protein kinase 8	Mus musculus	195-198
22056873-7	2012	Pancreatic cancer cells show a prominent ER and edelfosine accumulated in this subcellular structure, inducing a potent ER stress response, with caspase-4, BAP31 and c-Jun NH(2)-terminal kinase (JNK) activation, CHOP/GADD153 upregulation and phosphorylation of eukaryotic translation initiation factor 2 alpha-subunit that eventually led to cell death.	edelfosine	48-58	DNA-damage inducible transcript 3	Mus musculus	212-216
22056873-7	2012	Pancreatic cancer cells show a prominent ER and edelfosine accumulated in this subcellular structure, inducing a potent ER stress response, with caspase-4, BAP31 and c-Jun NH(2)-terminal kinase (JNK) activation, CHOP/GADD153 upregulation and phosphorylation of eukaryotic translation initiation factor 2 alpha-subunit that eventually led to cell death.	edelfosine	48-58	DNA-damage inducible transcript 3	Mus musculus	217-224
22056873-8	2012	Oral administration of edelfosine in xenograft mouse models of pancreatic cancer induced a significant regression in tumor growth and an increase in apoptotic index, as assessed by TUNEL assay and caspase-3 activation in the tumor sections.	edelfosine	23-33	caspase 3	Mus musculus	197-206
22056873-9	2012	The ER stress-associated marker CHOP/GADD153 was visualized in the pancreatic tumor isolated from edelfosine-treated mice, indicating a strong in vivo ER stress response.	edelfosine	98-108	DNA-damage inducible transcript 3	Mus musculus	32-36
22056873-9	2012	The ER stress-associated marker CHOP/GADD153 was visualized in the pancreatic tumor isolated from edelfosine-treated mice, indicating a strong in vivo ER stress response.	edelfosine	98-108	DNA-damage inducible transcript 3	Mus musculus	37-44
21762074-2	2011	The alkyl-lysophospholipid analogue edelfosine was the first antitumor drug reported to induce apoptosis in cancer cells through co-clustering of lipid rafts and Fas/CD95 death receptor.	edelfosine	36-46	Fas cell surface death receptor	Homo sapiens	166-170
21762074-4	2011	The adaptor molecule Fas-associated death domain protein (FADD) and procaspase-8 were also recruited into lipid rafts following edelfosine treatment, forming the death-inducing signaling complex (DISC), and hence these membrane microdomains can act as scaffolds for Fas/CD95 death signaling.	edelfosine	128-138	Fas associated via death domain	Homo sapiens	21-56
21762074-4	2011	The adaptor molecule Fas-associated death domain protein (FADD) and procaspase-8 were also recruited into lipid rafts following edelfosine treatment, forming the death-inducing signaling complex (DISC), and hence these membrane microdomains can act as scaffolds for Fas/CD95 death signaling.	edelfosine	128-138	Fas associated via death domain	Homo sapiens	58-62
21762074-4	2011	The adaptor molecule Fas-associated death domain protein (FADD) and procaspase-8 were also recruited into lipid rafts following edelfosine treatment, forming the death-inducing signaling complex (DISC), and hence these membrane microdomains can act as scaffolds for Fas/CD95 death signaling.	edelfosine	128-138	Fas cell surface death receptor	Homo sapiens	270-274
21681147-7	2011	RESULTS: We found that Ino-C2-PAF has the strongest influence on gene expression in comparison with edelfosine and Glc-PAF.	edelfosine	100-110	PCNA clamp associated factor	Homo sapiens	30-33
21289302-3	2011	Edelfosine is also accumulated by Saccharomyces cerevisiae in a process requiring the membrane protein Lem3p, and the human genome contains a Lem3p homolog TMEM30a.	edelfosine	0-10	ankyrin repeat and LEM domain containing 1	Homo sapiens	142-147
21289302-3	2011	Edelfosine is also accumulated by Saccharomyces cerevisiae in a process requiring the membrane protein Lem3p, and the human genome contains a Lem3p homolog TMEM30a.	edelfosine	0-10	transmembrane protein 30A	Homo sapiens	156-163
20922428-5	2011	The activity was compared with that of standard drugs, edelfosine (IC50 = 0.82 +- 0.13 muM) and miltefosine (IC50 = 2.84 +- 0.10 muM).	edelfosine	55-65	latexin	Homo sapiens	87-90
20955368-4	2011	KEY RESULTS: Edelfosine (1 microM) caused plasma membrane depolarization by substantially inhibiting activity of SK3/K(Ca)2.3 channels, which we had previously demonstrated to play an important role in cancer cell migration.	edelfosine	13-23	potassium calcium-activated channel subfamily N member 3	Homo sapiens	113-116
20955368-5	2011	Edelfosine did not inhibit 125I-Apamin binding to this SK(Ca) channel; rather, it reduced the calcium sensitivity of SK3/K(Ca)2.3 channel and dramatically decreased intracellular Ca2(+) concentration, probably by insertion in the plasma membrane, as suggested by proteinase K experiments.	edelfosine	0-10	potassium calcium-activated channel subfamily N member 3	Homo sapiens	117-129
20955368-8	2011	SK3 protein knockdown decreased cell migration and totally abolished the effect of edelfosine on MDA-MB-435s cell migration.	edelfosine	83-93	potassium calcium-activated channel subfamily N member 3	Homo sapiens	0-3
20955368-9	2011	In contrast, transient expression of SK3/K(Ca)2.3 protein in a SK3/K(Ca)2.3-deficient cell line increased cell migration and made these cells responsive to edelfosine.	edelfosine	156-166	potassium calcium-activated channel subfamily N member 3	Homo sapiens	37-49
20955368-9	2011	In contrast, transient expression of SK3/K(Ca)2.3 protein in a SK3/K(Ca)2.3-deficient cell line increased cell migration and made these cells responsive to edelfosine.	edelfosine	156-166	potassium calcium-activated channel subfamily N member 3	Homo sapiens	37-40
20955368-10	2011	CONCLUSIONS AND IMPLICATIONS: Our data clearly establish edelfosine as an inhibitor of cancer cell migration by acting on SK3/K(Ca)2.3 channels and provide insights into the future development of a new class of migration-targeted, anti-cancer agents.	edelfosine	57-67	potassium calcium-activated channel subfamily N member 3	Homo sapiens	122-125
20955368-0	2011	The SK3/K(Ca)2.3 potassium channel is a new cellular target for edelfosine.	edelfosine	64-74	potassium calcium-activated channel subfamily N member 3	Homo sapiens	4-16
20538604-7	2010	Our results indicate the transcription factors Yap1 and Skn7 as well as the major peroxiredoxin, Tsa1, mediate a response to edelfosine.	edelfosine	125-135	DNA-binding transcription factor YAP1	Saccharomyces cerevisiae S288C	47-51
22096499-7	2011	AmDOP2- and AmOA1-mediated increases in intracellular calcium were inhibited by 10 microM edelfosine indicating a requirement for phospholipase C-beta activity in this signaling pathway.	edelfosine	90-100	dopamine receptor 2	Apis mellifera	0-6
22096499-7	2011	AmDOP2- and AmOA1-mediated increases in intracellular calcium were inhibited by 10 microM edelfosine indicating a requirement for phospholipase C-beta activity in this signaling pathway.	edelfosine	90-100	octopamine receptor	Apis mellifera	12-17
20538604-7	2010	Our results indicate the transcription factors Yap1 and Skn7 as well as the major peroxiredoxin, Tsa1, mediate a response to edelfosine.	edelfosine	125-135	kinase-regulated stress-responsive transcription factor SKN7	Saccharomyces cerevisiae S288C	56-60
20538604-7	2010	Our results indicate the transcription factors Yap1 and Skn7 as well as the major peroxiredoxin, Tsa1, mediate a response to edelfosine.	edelfosine	125-135	thioredoxin peroxidase TSA1	Saccharomyces cerevisiae S288C	97-101
20233887-7	2010	Edelfosine induced coclustering of Fas/CD95 death receptor and rafts in MCL and CLL cells.	edelfosine	0-10	Fas (TNF receptor superfamily member 6)	Mus musculus	39-43
20233887-11	2010	CONCLUSIONS: Our data indicate that edelfosine accumulates and kills MCL and CLL cells in a rather selective way, and set coclustering of Fas/CD95 and lipid rafts as a new framework in MCL and CLL therapy.	edelfosine	36-46	Fas (TNF receptor superfamily member 6)	Mus musculus	142-146
20107083-10	2010	The leptin-induced current was blocked by the Jak2 inhibitor AG490, the PI3 kinase inhibitor wortmannin, and the phospholipase C inhibitors, U73122 and ET-18-OCH3.	edelfosine	152-162	leptin	Mus musculus	4-10
19244550-2	2009	Because L-selectin locates in lipid rafts and plays a crucial role in the recruitment of leukocytes into inflamed tissues, we hypothesized that edelfosine might affect inflammation by modulating L-selectin and inflammatory cell migration.	edelfosine	144-154	selectin L	Rattus norvegicus	8-18
19244550-2	2009	Because L-selectin locates in lipid rafts and plays a crucial role in the recruitment of leukocytes into inflamed tissues, we hypothesized that edelfosine might affect inflammation by modulating L-selectin and inflammatory cell migration.	edelfosine	144-154	selectin L	Rattus norvegicus	195-205
19244550-3	2009	Here, we have found that edelfosine inhibited neutrophil-endothelium interaction through L-selectin shedding.	edelfosine	25-35	selectin L	Rattus norvegicus	89-99
19244550-8	2009	Edelfosine enhanced lipopolysaccharide-induced expression of anti-inflammatory interleukin-10 in mouse macrophages.	edelfosine	0-10	interleukin 10	Mus musculus	79-93
19244550-13	2009	Our data identify edelfosine as a novel anti-inflammatory drug by abating neutrophil infiltration through L-selectin shedding and may provide a new therapeutic approach for inflammatory bowel disease free from toxicity.	edelfosine	18-28	selectin L	Rattus norvegicus	106-116
19352436-0	2009	Involvement of raft aggregates enriched in Fas/CD95 death-inducing signaling complex in the antileukemic action of edelfosine in Jurkat cells.	edelfosine	115-125	Fas cell surface death receptor	Homo sapiens	47-51
19352436-3	2009	Co-immunoprecipitation assays revealed that edelfosine induced the generation of the so-called death-inducing signaling complex (DISC), made up of Fas/CD95, FADD, and procaspase-8, in lipid rafts.	edelfosine	44-54	Fas cell surface death receptor	Homo sapiens	151-155
19352436-3	2009	Co-immunoprecipitation assays revealed that edelfosine induced the generation of the so-called death-inducing signaling complex (DISC), made up of Fas/CD95, FADD, and procaspase-8, in lipid rafts.	edelfosine	44-54	Fas associated via death domain	Homo sapiens	157-161
19352436-4	2009	Electron microscopy analyses allowed to visualize the formation of raft clusters and their co-localization with DISC components Fas/CD95, FADD, and procaspase-8 following edelfosine treatment of Jurkat cells.	edelfosine	171-181	Fas cell surface death receptor	Homo sapiens	132-136
19352436-4	2009	Electron microscopy analyses allowed to visualize the formation of raft clusters and their co-localization with DISC components Fas/CD95, FADD, and procaspase-8 following edelfosine treatment of Jurkat cells.	edelfosine	171-181	Fas associated via death domain	Homo sapiens	138-142
19352436-5	2009	Silencing of Fas/CD95 by RNA interference, transfection with a FADD dominant-negative mutant that blocks Fas/CD95 signaling, and specific inhibition of caspase-8 prevented the apoptotic response triggered by edelfosine, hence demonstrating the functional role of DISC in drug-induced apoptosis.	edelfosine	208-218	Fas cell surface death receptor	Homo sapiens	17-21
19352436-5	2009	Silencing of Fas/CD95 by RNA interference, transfection with a FADD dominant-negative mutant that blocks Fas/CD95 signaling, and specific inhibition of caspase-8 prevented the apoptotic response triggered by edelfosine, hence demonstrating the functional role of DISC in drug-induced apoptosis.	edelfosine	208-218	Fas associated via death domain	Homo sapiens	63-67
19352436-5	2009	Silencing of Fas/CD95 by RNA interference, transfection with a FADD dominant-negative mutant that blocks Fas/CD95 signaling, and specific inhibition of caspase-8 prevented the apoptotic response triggered by edelfosine, hence demonstrating the functional role of DISC in drug-induced apoptosis.	edelfosine	208-218	Fas cell surface death receptor	Homo sapiens	109-113
19352436-5	2009	Silencing of Fas/CD95 by RNA interference, transfection with a FADD dominant-negative mutant that blocks Fas/CD95 signaling, and specific inhibition of caspase-8 prevented the apoptotic response triggered by edelfosine, hence demonstrating the functional role of DISC in drug-induced apoptosis.	edelfosine	208-218	caspase 8	Homo sapiens	152-161