PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
16235909-0	2005	Studies on the synthesis of the inostamycin natural products: a reductive aldol/reductive Claisen approach to the C10-C24 ketone fragment.	inostamycin	32-43	homeobox C10	Homo sapiens	114-117
16235909-1	2005	[reaction: see text] An approach to the C10-C24 ketone fragment of the inostamycin family of polyether antibiotics is described.	inostamycin	71-82	homeobox C10	Homo sapiens	40-43
15672866-0	2004	Inostamycin suppresses vascular endothelial growth factor-stimulated growth and migration of human umbilical vein endothelial cells.	inostamycin	0-11	vascular endothelial growth factor A	Homo sapiens	23-57
15672866-2	2004	In the present study, we determined the effect of inostamycin (an inhibitor of phosphatidylinositol synthesis) on vascular endothelial growth factor (VEGF)-induced proliferation and migration of human umbilical vein endothelial cells (HUVECs).	inostamycin	50-61	vascular endothelial growth factor A	Homo sapiens	114-148
15672866-2	2004	In the present study, we determined the effect of inostamycin (an inhibitor of phosphatidylinositol synthesis) on vascular endothelial growth factor (VEGF)-induced proliferation and migration of human umbilical vein endothelial cells (HUVECs).	inostamycin	50-61	vascular endothelial growth factor A	Homo sapiens	150-154
15672866-3	2004	Inostamycin significantly attenuated both VEGF-induced proliferation and migration of HUVECs.	inostamycin	0-11	vascular endothelial growth factor A	Homo sapiens	42-46
15672866-4	2004	Inostamycin inhibited activation of mitogen-activated kinases (ERK and p38) and elevation of cyclin D1 induced by VEGF.	inostamycin	0-11	mitogen-activated protein kinase 1	Homo sapiens	63-66
15672866-4	2004	Inostamycin inhibited activation of mitogen-activated kinases (ERK and p38) and elevation of cyclin D1 induced by VEGF.	inostamycin	0-11	mitogen-activated protein kinase 14	Homo sapiens	71-74
15672866-4	2004	Inostamycin inhibited activation of mitogen-activated kinases (ERK and p38) and elevation of cyclin D1 induced by VEGF.	inostamycin	0-11	cyclin D1	Homo sapiens	93-102
15672866-4	2004	Inostamycin inhibited activation of mitogen-activated kinases (ERK and p38) and elevation of cyclin D1 induced by VEGF.	inostamycin	0-11	vascular endothelial growth factor A	Homo sapiens	114-118
15672866-5	2004	These data suggest that inostamycin reduced both proliferation and migration of HUVECs by targeting ERK-cyclin D1 and p38, respectively.	inostamycin	24-35	mitogen-activated protein kinase 1	Homo sapiens	100-103
15672866-5	2004	These data suggest that inostamycin reduced both proliferation and migration of HUVECs by targeting ERK-cyclin D1 and p38, respectively.	inostamycin	24-35	cyclin D1	Homo sapiens	104-113
15672866-5	2004	These data suggest that inostamycin reduced both proliferation and migration of HUVECs by targeting ERK-cyclin D1 and p38, respectively.	inostamycin	24-35	mitogen-activated protein kinase 14	Homo sapiens	118-121
10964506-3	2000	In the present study, we examined the possible involvement of protein kinase C (PKC) and ceramide generation in caspase-3(-like) protease activation induced by inostamycin, a phosphatidylinositol synthesis inhibitor.	inostamycin	160-171	caspase 3	Homo sapiens	112-127
10964506-4	2000	Treatment of cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA), an activator of PKC, suppressed the release of cytochrome c from mitochondria and the activation of caspase-3(-like) proteases in inostamycin-treated cells, but not in other anticancer drug-treated cells.	inostamycin	199-210	caspase 3	Homo sapiens	169-184
12729794-0	2003	Transmembrane domain of Bcl-2 is required for inhibition of ceramide synthesis, but not cytochrome c release in the pathway of inostamycin-induced apoptosis.	inostamycin	127-138	BCL2 apoptosis regulator	Homo sapiens	24-29
12729794-3	2003	In the present study, we found that overexpression of Bcl-2 in human small cell lung carcinoma Ms-1 cells inhibited not only the release of cytochrome c from mitochondria into cytosol but also de novo ceramide synthesis induced by inostamycin, a phosphatidylinositol turnover inhibitor.	inostamycin	231-242	BCL2 apoptosis regulator	Homo sapiens	54-59
12729794-4	2003	To investigate the correlation between the structure of Bcl-2 and its inhibitory function in inostamycin-induced apoptosis, Ms-1 cells that stably overexpress domain-deletional mutants of Bcl-2 were established.	inostamycin	93-104	BCL2 apoptosis regulator	Homo sapiens	56-61
12729794-5	2003	Transmembrane domain-deleted Bcl-2 failed to inhibit inostamycin-induced de novo ceramide synthesis, whereas it inhibited inostamycin-induced cytochrome c release, indicating that anchoring of Bcl-2 to membrane was a requirement for its inhibitory effect on inostamycin-induced ceramide synthesis, but not cytochrome c release.	inostamycin	122-133	cytochrome c, somatic	Homo sapiens	142-154
12729794-5	2003	Transmembrane domain-deleted Bcl-2 failed to inhibit inostamycin-induced de novo ceramide synthesis, whereas it inhibited inostamycin-induced cytochrome c release, indicating that anchoring of Bcl-2 to membrane was a requirement for its inhibitory effect on inostamycin-induced ceramide synthesis, but not cytochrome c release.	inostamycin	122-133	cytochrome c, somatic	Homo sapiens	142-154
12729794-6	2003	Thus, the deletion mutant of tarnsmembrane domain of Bcl-2 can suppress inostamycin-induced apoptosis by inhibiting cytochrome c release, a downstream event of ceramide synthesis in the pathway of inostamycin-induced apoptosis.	inostamycin	72-83	BCL2 apoptosis regulator	Homo sapiens	53-58
12729794-6	2003	Thus, the deletion mutant of tarnsmembrane domain of Bcl-2 can suppress inostamycin-induced apoptosis by inhibiting cytochrome c release, a downstream event of ceramide synthesis in the pathway of inostamycin-induced apoptosis.	inostamycin	72-83	cytochrome c, somatic	Homo sapiens	116-128
12729794-6	2003	Thus, the deletion mutant of tarnsmembrane domain of Bcl-2 can suppress inostamycin-induced apoptosis by inhibiting cytochrome c release, a downstream event of ceramide synthesis in the pathway of inostamycin-induced apoptosis.	inostamycin	197-208	BCL2 apoptosis regulator	Homo sapiens	53-58
12729794-7	2003	We also found that the BH3 and BH4 domains of Bcl-2 were necessary for inhibition of inostamycin-induced apoptosis, and deletion of BH1 or BH2 did not affect the inhibitory effect of Bcl-2 to inostamycin-induced apoptotic events.	inostamycin	85-96	BCL2 apoptosis regulator	Homo sapiens	46-51
12729794-7	2003	We also found that the BH3 and BH4 domains of Bcl-2 were necessary for inhibition of inostamycin-induced apoptosis, and deletion of BH1 or BH2 did not affect the inhibitory effect of Bcl-2 to inostamycin-induced apoptotic events.	inostamycin	192-203	BCL2 apoptosis regulator	Homo sapiens	46-51
10964506-5	2000	Inostamycin induced the elevation of intracellular ceramide levels, and fumonisin B1, an inhibitor of ceramide synthase, inhibited inostamycin-induced cytochrome c release, caspase-3(-like) protease activation, and apoptosis.	inostamycin	131-142	cytochrome c, somatic	Homo sapiens	151-163
10964506-4	2000	Treatment of cells with 12-O-tetradecanoyl phorbol-13-acetate (TPA), an activator of PKC, suppressed the release of cytochrome c from mitochondria and the activation of caspase-3(-like) proteases in inostamycin-treated cells, but not in other anticancer drug-treated cells.	inostamycin	199-210	cytochrome c, somatic	Homo sapiens	116-128
11315101-0	2000	Inostamycin, an inhibitor of cytidine 5"-diphosphate 1,2-diacyl-sn-glycerol (CDP-DG): inositol transferase, suppresses invasion ability by reducing productions of matrix metalloproteinase-2 and -9 and cell motility in HSC-4 tongue carcinoma cell line.	inostamycin	0-11	matrix metallopeptidase 2	Homo sapiens	163-196
11315101-4	2000	Zymographic analysis showed that inostamycin suppressed pro-MMP-2 and pro-MMP-9 levels at a dose-dependent fashion, while MMP-2 activity was not significantly affected.	inostamycin	33-44	matrix metallopeptidase 2	Homo sapiens	60-65
11315101-5	2000	By reverse transcription-polymerase chain reaction, it was found that inostamycin diminished steady state levels of MMP-2 and -9 but not membrane type 1-MMP mRNA expressions.	inostamycin	70-81	matrix metallopeptidase 2	Homo sapiens	116-128
11315101-6	2000	Inostamycin partially blocked both EGF- and phorbol 12-myristate 13-acetate-stimulated pro-MMP-9 production.	inostamycin	0-11	epidermal growth factor	Homo sapiens	35-38
11315101-8	2000	EGF-stimulated motility of HSC-4 cells was suppressed by inostamycin treatment along with reduction of actin cytoskeletal reorganisation, filopodia formation and cdc42 expression.	inostamycin	57-68	epidermal growth factor	Homo sapiens	0-3
9309157-6	1997	We previously isolated inostamycin from Streptomyces as an inhibitor of PI synthase.	inostamycin	23-34	CDP-diacylglycerol--inositol 3-phosphatidyltransferase	Homo sapiens	72-83
9756937-5	1998	Anticancer drugs such as camptothecin, vinblastine, inostamycin, and adriamycin induced activation of caspase-3(-like) proteases and apoptosis.	inostamycin	52-63	caspase 3	Homo sapiens	102-117
9600126-1	1998	Previously, we demonstrated that inostamycin, an inhibitor of phosphatidylinositol turnover, caused cell cycle arrest at the G1 phase, inhibiting the expression of cyclins D1 and E in normal cells.	inostamycin	33-44	cyclin D1	Homo sapiens	164-180
9600126-4	1998	We found that inostamycin decreased cyclin D1, and increased cyclin-dependent kinase inhibitors such as p21WAF1 and p27KIP1 in Ms-1 cells.	inostamycin	14-25	cyclin D1	Homo sapiens	36-45
9600126-4	1998	We found that inostamycin decreased cyclin D1, and increased cyclin-dependent kinase inhibitors such as p21WAF1 and p27KIP1 in Ms-1 cells.	inostamycin	14-25	cyclin dependent kinase inhibitor 1B	Homo sapiens	116-123
9600126-6	1998	Inostamycin-induced apoptosis was suppressed by an inhibitor of caspase-3, and a 17 kDa fragment of activated caspase-3 was detected following inostamycin treatment.	inostamycin	0-11	caspase 3	Homo sapiens	64-73
9600126-6	1998	Inostamycin-induced apoptosis was suppressed by an inhibitor of caspase-3, and a 17 kDa fragment of activated caspase-3 was detected following inostamycin treatment.	inostamycin	0-11	caspase 3	Homo sapiens	110-119
9600126-6	1998	Inostamycin-induced apoptosis was suppressed by an inhibitor of caspase-3, and a 17 kDa fragment of activated caspase-3 was detected following inostamycin treatment.	inostamycin	143-154	caspase 3	Homo sapiens	110-119
9600126-7	1998	Therefore, caspase-3(-like) would appear to be involved in inostamycin-induced apoptosis.	inostamycin	59-70	caspase 3	Homo sapiens	11-26
9010759-5	1996	However, in the inostamycin-treated cell, cyclin-dependent kinase 2 (CDK2) failed to be activated after serum stimulation.	inostamycin	16-27	cyclin dependent kinase 2	Rattus norvegicus	42-67
9010759-5	1996	However, in the inostamycin-treated cell, cyclin-dependent kinase 2 (CDK2) failed to be activated after serum stimulation.	inostamycin	16-27	cyclin dependent kinase 2	Rattus norvegicus	69-73
9010759-6	1996	Since serum-induced expression of cyclin E was also suppressed by inostamycin, this inhibitor would appear to block CDK2 activation by inhibiting cyclin E expression.	inostamycin	66-77	cyclin E1	Rattus norvegicus	34-42
9010759-6	1996	Since serum-induced expression of cyclin E was also suppressed by inostamycin, this inhibitor would appear to block CDK2 activation by inhibiting cyclin E expression.	inostamycin	66-77	cyclin dependent kinase 2	Rattus norvegicus	116-120
9010759-6	1996	Since serum-induced expression of cyclin E was also suppressed by inostamycin, this inhibitor would appear to block CDK2 activation by inhibiting cyclin E expression.	inostamycin	66-77	cyclin E1	Rattus norvegicus	146-154
9010759-7	1996	Furthermore, inostamycin also inhibited cyclin D1 expression induced by serum; and consequently, hyperphosphorylation of retinoblastoma protein (pRB) by RB-kinases such as CDK4 and CDK2 was abolished, which would result in elimination of functional inactivation of pRB.	inostamycin	13-24	cyclin D1	Rattus norvegicus	40-49
9010759-7	1996	Furthermore, inostamycin also inhibited cyclin D1 expression induced by serum; and consequently, hyperphosphorylation of retinoblastoma protein (pRB) by RB-kinases such as CDK4 and CDK2 was abolished, which would result in elimination of functional inactivation of pRB.	inostamycin	13-24	RB transcriptional corepressor 1	Rattus norvegicus	145-148
9010759-7	1996	Furthermore, inostamycin also inhibited cyclin D1 expression induced by serum; and consequently, hyperphosphorylation of retinoblastoma protein (pRB) by RB-kinases such as CDK4 and CDK2 was abolished, which would result in elimination of functional inactivation of pRB.	inostamycin	13-24	cyclin-dependent kinase 4	Rattus norvegicus	172-176
9010759-7	1996	Furthermore, inostamycin also inhibited cyclin D1 expression induced by serum; and consequently, hyperphosphorylation of retinoblastoma protein (pRB) by RB-kinases such as CDK4 and CDK2 was abolished, which would result in elimination of functional inactivation of pRB.	inostamycin	13-24	cyclin dependent kinase 2	Rattus norvegicus	181-185
9010759-7	1996	Furthermore, inostamycin also inhibited cyclin D1 expression induced by serum; and consequently, hyperphosphorylation of retinoblastoma protein (pRB) by RB-kinases such as CDK4 and CDK2 was abolished, which would result in elimination of functional inactivation of pRB.	inostamycin	13-24	RB transcriptional corepressor 1	Rattus norvegicus	265-268
9010759-8	1996	Thus, early G1 arrest in NRK cells by inostamycin is due to the inhibition of cyclin D1 and E expressions.	inostamycin	38-49	cyclin D1	Rattus norvegicus	78-87
7591966-3	1995	Inostamycin inhibited azidopine binding to P-glycoprotein, even after KB plasma membranes had been preincubated with inostamycin and washed.	inostamycin	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	43-57
7591966-6	1995	These results suggest that inostamycin can inhibit P-glycoprotein irreversibly by binding to plasma membranes irreversibly through phosphatidylethanolamine.	inostamycin	27-38	ATP binding cassette subfamily B member 1	Homo sapiens	51-65
1328172-1	1992	Inostamycin, a novel microbial secondary metabolite, inhibited [3H]inositol and 32P1 incorporation into phosphatidylinositol (PtdIns) induced by epidermal growth factor (EGF) in cultured A431 cells, the IC50 being 0.5 micrograms/ml, without inhibiting macromolecular synthesis.	inostamycin	0-11	epidermal growth factor	Homo sapiens	145-168
1328172-1	1992	Inostamycin, a novel microbial secondary metabolite, inhibited [3H]inositol and 32P1 incorporation into phosphatidylinositol (PtdIns) induced by epidermal growth factor (EGF) in cultured A431 cells, the IC50 being 0.5 micrograms/ml, without inhibiting macromolecular synthesis.	inostamycin	0-11	epidermal growth factor	Homo sapiens	170-173
22472572-0	2012	Inostamycin enhanced TRAIL-induced apoptosis through DR5 upregulation on the cell surface.	inostamycin	0-11	TNF superfamily member 10	Homo sapiens	21-26
22472572-0	2012	Inostamycin enhanced TRAIL-induced apoptosis through DR5 upregulation on the cell surface.	inostamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	53-56
22472572-6	2012	Inostamycin upregulated DR5, and a knockdown of DR5 suppressed the apoptosis that was synergistically induced by co-treatment with inostamycin and TRAIL.	inostamycin	0-11	TNF receptor superfamily member 10b	Homo sapiens	24-27
22472572-6	2012	Inostamycin upregulated DR5, and a knockdown of DR5 suppressed the apoptosis that was synergistically induced by co-treatment with inostamycin and TRAIL.	inostamycin	0-11	TNF superfamily member 10	Homo sapiens	147-152
22472572-6	2012	Inostamycin upregulated DR5, and a knockdown of DR5 suppressed the apoptosis that was synergistically induced by co-treatment with inostamycin and TRAIL.	inostamycin	131-142	TNF receptor superfamily member 10b	Homo sapiens	48-51
22472572-7	2012	Moreover, inostamycin increased the expression of DR5 on the cell surface.	inostamycin	10-21	TNF receptor superfamily member 10b	Homo sapiens	50-53
22472572-8	2012	Therefore, inostamycin-increased cell surface expression of DR5 may have contributed to the enhancement of TRAIL-induced apoptosis.	inostamycin	11-22	TNF receptor superfamily member 10b	Homo sapiens	60-63
22472572-8	2012	Therefore, inostamycin-increased cell surface expression of DR5 may have contributed to the enhancement of TRAIL-induced apoptosis.	inostamycin	11-22	TNF superfamily member 10	Homo sapiens	107-112
22472572-9	2012	Our study suggests that combined treatment with inostamycin and TRAIL may offer a strategy to overcome TRAIL resistance in tumor cells.	inostamycin	48-59	TNF superfamily member 10	Homo sapiens	103-108
7591966-0	1995	Inostamycin, an inhibitor of P-glycoprotein function, interacts specifically with phosphatidylethanolamine.	inostamycin	0-11	ATP binding cassette subfamily B member 1	Homo sapiens	29-43