PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
24510625-9	2015	AMR-Me was found to downregulate vascular endothelial growth factor (VEGF)/phosphorylated forms of focal adhesion kinase (pFAK397 )/Jun N-terminus kinase (pJNK)/extracellular signal-regulated kinase (pERK).	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	vascular endothelial growth factor A	Mus musculus	33-67
24510625-9	2015	AMR-Me was found to downregulate vascular endothelial growth factor (VEGF)/phosphorylated forms of focal adhesion kinase (pFAK397 )/Jun N-terminus kinase (pJNK)/extracellular signal-regulated kinase (pERK).	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	vascular endothelial growth factor A	Mus musculus	69-73
24510625-9	2015	AMR-Me was found to downregulate vascular endothelial growth factor (VEGF)/phosphorylated forms of focal adhesion kinase (pFAK397 )/Jun N-terminus kinase (pJNK)/extracellular signal-regulated kinase (pERK).	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	200-204
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	matrix metallopeptidase 14 (membrane-inserted)	Mus musculus	34-41
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	matrix metallopeptidase 2	Mus musculus	43-48
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	matrix metallopeptidase 9	Mus musculus	54-59
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	vascular endothelial growth factor A	Mus musculus	81-85
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	eukaryotic translation initiation factor 2 alpha kinase 3	Mus musculus	100-104
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	105-114
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	tissue inhibitor of metalloproteinase 1	Mus musculus	133-139
24510625-12	2015	AMR-Me suppresses the activity of MT1-MMP, MMP-2, and MMP-9 by downregulation of VEGF/pFAK397 /pJNK/pERK/NF-kappaB and activation of TIMP-1 and TIMP-2 in metastatic melanoma cell line, B16F10.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	tissue inhibitor of metalloproteinase 2	Mus musculus	144-150
24078029-3	2013	As estrogen receptor (ER) and canonical Wnt/b-catenin signaling are involved in the development and progression of breast cancer, the current study was designed to investigate the effects of AMR-Me treatment on the expressions of ER-a, ER-b, b-catenin and cyclin D1 in rat mammary tumors induced by DMBA.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	191-197	estrogen receptor 1	Rattus norvegicus	3-20
23846978-6	2014	AMR-Me downregulated the expression of intratumor COX-2 and HSP90, suppressed the degradation of IkappaB-alpha, and reduced the translocation of NF-kappaB from cytosol to nucleus.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	prostaglandin-endoperoxide synthase 2	Rattus norvegicus	50-55
23846978-6	2014	AMR-Me downregulated the expression of intratumor COX-2 and HSP90, suppressed the degradation of IkappaB-alpha, and reduced the translocation of NF-kappaB from cytosol to nucleus.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	heat shock protein 90 alpha family class A member 1	Rattus norvegicus	60-65
23846978-6	2014	AMR-Me downregulated the expression of intratumor COX-2 and HSP90, suppressed the degradation of IkappaB-alpha, and reduced the translocation of NF-kappaB from cytosol to nucleus.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	NFKB inhibitor alpha	Rattus norvegicus	97-110
23475563-0	2014	AMR-Me inhibits PI3K/Akt signaling in hormone-dependent MCF-7 breast cancer cells and inactivates NF-kappaB in hormone-independent MDA-MB-231 cells.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	AKT serine/threonine kinase 1	Homo sapiens	21-24
23475563-8	2014	EMSA revealed that AMR-Me inhibited nuclear factor-kappaB (NF-kappaB) DNA binding activity in MDA-MB-231 cells in a time-dependent manner and abrogated EGF induced NF-kappaB activation.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	19-25	epidermal growth factor	Homo sapiens	152-155
23475563-9	2014	From these studies we conclude that AMR-Me decreased ERalpha expression and effectively inhibited Akt phosphorylation in MCF-7 cells and inactivate constitutive nuclear NF-kappaB and its regulated proteins in MDA-MB-231 cells.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	36-42	estrogen receptor 1	Homo sapiens	53-60
23475563-9	2014	From these studies we conclude that AMR-Me decreased ERalpha expression and effectively inhibited Akt phosphorylation in MCF-7 cells and inactivate constitutive nuclear NF-kappaB and its regulated proteins in MDA-MB-231 cells.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	36-42	AKT serine/threonine kinase 1	Homo sapiens	98-101
24078029-3	2013	As estrogen receptor (ER) and canonical Wnt/b-catenin signaling are involved in the development and progression of breast cancer, the current study was designed to investigate the effects of AMR-Me treatment on the expressions of ER-a, ER-b, b-catenin and cyclin D1 in rat mammary tumors induced by DMBA.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	191-197	estrogen receptor 1	Rattus norvegicus	22-24
24078029-3	2013	As estrogen receptor (ER) and canonical Wnt/b-catenin signaling are involved in the development and progression of breast cancer, the current study was designed to investigate the effects of AMR-Me treatment on the expressions of ER-a, ER-b, b-catenin and cyclin D1 in rat mammary tumors induced by DMBA.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	191-197	Wnt family member 2	Rattus norvegicus	40-45
24078029-3	2013	As estrogen receptor (ER) and canonical Wnt/b-catenin signaling are involved in the development and progression of breast cancer, the current study was designed to investigate the effects of AMR-Me treatment on the expressions of ER-a, ER-b, b-catenin and cyclin D1 in rat mammary tumors induced by DMBA.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	191-197	cyclin D1	Rattus norvegicus	256-265
24078029-7	2013	AMR-Me also reduced the expression, cytoplasmic accumulation, and nuclear translocation of b-catenin, the essential transcriptional cofactor for Wnt signaling.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	Wnt family member 2	Rattus norvegicus	145-148
23404339-8	2013	AMR-Me dose-dependently suppressed abnormal cell proliferation, induced apoptosis, up-regulated pro-apoptotic protein Bax and down-regulated antiapoptotic protein Bcl-2 in mammary tumors.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	BCL2 associated X, apoptosis regulator	Homo sapiens	118-121
23404339-8	2013	AMR-Me dose-dependently suppressed abnormal cell proliferation, induced apoptosis, up-regulated pro-apoptotic protein Bax and down-regulated antiapoptotic protein Bcl-2 in mammary tumors.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	BCL2 apoptosis regulator	Homo sapiens	163-168
19201082-5	2009	AMR-Me treatment resulted in suppression of hTERT expression and a concomitant inhibition of telomerase activity.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	telomerase reverse transcriptase	Homo sapiens	44-49
19201082-8	2009	Our results suggest that AMR-Me inhibits telomerase activity by decreasing the hTERT expression and induces apoptosis in human lymphoblastic leukemic CEM cells, thus providing the molecular basis for the development of AMR-Me as a novel chemotherapeutic agent against leukemia.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	25-31	telomerase reverse transcriptase	Homo sapiens	79-84
18058803-7	2008	SP600125, a specific inhibitor for JNK and SB203580, a p38 MAPK-specific inhibitor suppressed AMR-Me induced apoptosis indicating that activation of JNK and p38 MAPKs involved in the mitochondrial activation-mediated cell death pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	94-100	mitogen-activated protein kinase 14	Homo sapiens	55-58
18058803-7	2008	SP600125, a specific inhibitor for JNK and SB203580, a p38 MAPK-specific inhibitor suppressed AMR-Me induced apoptosis indicating that activation of JNK and p38 MAPKs involved in the mitochondrial activation-mediated cell death pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	94-100	mitogen-activated protein kinase 8	Homo sapiens	149-152
18058803-4	2008	AMR-Me induced DNA fragmentation and PARP degradation which were preceded by changing Bax/Bcl-2 ratios, cytochrome c release, and subsequent induction of pro-caspase-9 and -7 processing in breast carcinoma MCF-7 cells, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8, suggesting AMR-Me triggered the mitochondrial apoptotic pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	collagen type XI alpha 2 chain	Homo sapiens	37-41
18058803-4	2008	AMR-Me induced DNA fragmentation and PARP degradation which were preceded by changing Bax/Bcl-2 ratios, cytochrome c release, and subsequent induction of pro-caspase-9 and -7 processing in breast carcinoma MCF-7 cells, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8, suggesting AMR-Me triggered the mitochondrial apoptotic pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	BCL2 associated X, apoptosis regulator	Homo sapiens	86-89
18058803-7	2008	SP600125, a specific inhibitor for JNK and SB203580, a p38 MAPK-specific inhibitor suppressed AMR-Me induced apoptosis indicating that activation of JNK and p38 MAPKs involved in the mitochondrial activation-mediated cell death pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	94-100	mitogen-activated protein kinase 14	Homo sapiens	157-160
18058803-4	2008	AMR-Me induced DNA fragmentation and PARP degradation which were preceded by changing Bax/Bcl-2 ratios, cytochrome c release, and subsequent induction of pro-caspase-9 and -7 processing in breast carcinoma MCF-7 cells, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8, suggesting AMR-Me triggered the mitochondrial apoptotic pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	BCL2 apoptosis regulator	Homo sapiens	90-95
18058803-4	2008	AMR-Me induced DNA fragmentation and PARP degradation which were preceded by changing Bax/Bcl-2 ratios, cytochrome c release, and subsequent induction of pro-caspase-9 and -7 processing in breast carcinoma MCF-7 cells, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8, suggesting AMR-Me triggered the mitochondrial apoptotic pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	cytochrome c, somatic	Homo sapiens	104-116
18058803-4	2008	AMR-Me induced DNA fragmentation and PARP degradation which were preceded by changing Bax/Bcl-2 ratios, cytochrome c release, and subsequent induction of pro-caspase-9 and -7 processing in breast carcinoma MCF-7 cells, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8, suggesting AMR-Me triggered the mitochondrial apoptotic pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	Fas ligand	Homo sapiens	245-255
18058803-4	2008	AMR-Me induced DNA fragmentation and PARP degradation which were preceded by changing Bax/Bcl-2 ratios, cytochrome c release, and subsequent induction of pro-caspase-9 and -7 processing in breast carcinoma MCF-7 cells, but it did not act on Fas/Fas ligand pathways and the activation of caspase-8, suggesting AMR-Me triggered the mitochondrial apoptotic pathway.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	caspase 8	Homo sapiens	287-296
18058803-6	2008	AMR-Me stimulated p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase activation during apoptosis.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	mitogen-activated protein kinase 14	Homo sapiens	18-21
18058803-6	2008	AMR-Me stimulated p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase activation during apoptosis.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	mitogen-activated protein kinase 8	Homo sapiens	59-84
18058803-6	2008	AMR-Me stimulated p38 mitogen-activated protein kinase and c-Jun NH2-terminal kinase (JNK), but not extracellular signal-regulated kinase activation during apoptosis.	methyl 25-hydroxy-3-oxoolean-12-en-28-oate	0-6	mitogen-activated protein kinase 8	Homo sapiens	86-89