PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
19706764-3	2009	DBM was found to arrest TRAMP-C1 cells at G(2)-M phase of cell cycle and suppressed phosphorylated retinoblastoma, cyclin D1, and cyclin A.	dibenzoylmethane	0-3	translocating chain-associating membrane protein 1	Mus musculus	24-29
19706764-3	2009	DBM was found to arrest TRAMP-C1 cells at G(2)-M phase of cell cycle and suppressed phosphorylated retinoblastoma, cyclin D1, and cyclin A.	dibenzoylmethane	0-3	cyclin D1	Mus musculus	115-124
19706764-3	2009	DBM was found to arrest TRAMP-C1 cells at G(2)-M phase of cell cycle and suppressed phosphorylated retinoblastoma, cyclin D1, and cyclin A.	dibenzoylmethane	0-3	cyclin A2	Mus musculus	130-138
19706764-4	2009	Importantly, DBM was found to be equally effective in suppression of prostate tumor progression in TRAMP mice.	dibenzoylmethane	13-16	translocating chain-associating membrane protein 1	Mus musculus	99-104
19706764-8	2009	Our findings suggest that DBM blocks the growth and progression of prostate cancer in TRAMP mice via modulation of tumor cell cycle regulation and therefore merits its consideration for future clinical intervention of human prostate cancer.	dibenzoylmethane	26-29	translocating chain-associating membrane protein 1	Mus musculus	86-91
35472330-6	2022	Furthermore, we screened a library of FDA-approved compounds and identified 38 compounds that increased yeast frataxin levels, including the azole Bifonazole, antiparasitic Fipronil, anti-tumor compound Dibenzoylmethane (DBM), antihypertensive 4-hydroxychalcone (4"-OHC), and a non-specific anion channel inhibitor 4,4-diisothiocyanostilbene-2,2-sulfonic acid (DIDS).	dibenzoylmethane	203-219	frataxin	Homo sapiens	110-118
35472330-6	2022	Furthermore, we screened a library of FDA-approved compounds and identified 38 compounds that increased yeast frataxin levels, including the azole Bifonazole, antiparasitic Fipronil, anti-tumor compound Dibenzoylmethane (DBM), antihypertensive 4-hydroxychalcone (4"-OHC), and a non-specific anion channel inhibitor 4,4-diisothiocyanostilbene-2,2-sulfonic acid (DIDS).	dibenzoylmethane	221-224	frataxin	Homo sapiens	110-118
30475214-11	2019	In addition, DBM inhibited NADPH oxidase 2 and 4 expression and oxidative DNA damage.	dibenzoylmethane	13-16	cytochrome b-245, beta polypeptide	Mus musculus	27-48
29709906-0	2018	Dibenzoylmethane Suppresses Lipid Accumulation and Reactive Oxygen Species Production through Regulation of Nuclear Factor (Erythroid-Derived 2)-Like 2 and Insulin Signaling in Adipocytes.	dibenzoylmethane	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	108-151
30068872-4	2018	DBM also significantly inhibited lipopolysaccharide (LPS)-induced nitrite (NO) production through the downregulation of inducible oxide synthase (iNOS) in RAW264.7 cells.	dibenzoylmethane	0-3	nitric oxide synthase 2	Homo sapiens	146-150
30068872-5	2018	The abundance of cyclooxygenase-2 (COX-2), a pro-inflammatory protein, was also effectively decreased by DBM in a dose-dependent manner.	dibenzoylmethane	105-108	prostaglandin-endoperoxide synthase 2	Homo sapiens	17-33
30068872-5	2018	The abundance of cyclooxygenase-2 (COX-2), a pro-inflammatory protein, was also effectively decreased by DBM in a dose-dependent manner.	dibenzoylmethane	105-108	prostaglandin-endoperoxide synthase 2	Homo sapiens	35-40
30068872-6	2018	DBM (50 microM) reduced the levels of COX-2 and iNOS by 81 and 78%, respectively.	dibenzoylmethane	0-3	prostaglandin-endoperoxide synthase 2	Homo sapiens	38-43
30068872-6	2018	DBM (50 microM) reduced the levels of COX-2 and iNOS by 81 and 78%, respectively.	dibenzoylmethane	0-3	nitric oxide synthase 2	Homo sapiens	48-52
30068872-7	2018	DBM significantly inhibited the translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kappaB), an inflammatory transcription factor, into the nucleus.	dibenzoylmethane	0-3	nuclear factor kappa B subunit 1	Homo sapiens	113-122
30068872-8	2018	DBM-mediated increase of NF-kappaB translocation resulted from the DBM-induced suppression of the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha).	dibenzoylmethane	0-3	nuclear factor kappa B subunit 1	Homo sapiens	25-34
30068872-8	2018	DBM-mediated increase of NF-kappaB translocation resulted from the DBM-induced suppression of the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha).	dibenzoylmethane	0-3	NFKB inhibitor alpha	Homo sapiens	117-200
30068872-8	2018	DBM-mediated increase of NF-kappaB translocation resulted from the DBM-induced suppression of the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha).	dibenzoylmethane	0-3	NFKB inhibitor alpha	Homo sapiens	202-214
30068872-8	2018	DBM-mediated increase of NF-kappaB translocation resulted from the DBM-induced suppression of the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha).	dibenzoylmethane	67-70	nuclear factor kappa B subunit 1	Homo sapiens	25-34
30068872-8	2018	DBM-mediated increase of NF-kappaB translocation resulted from the DBM-induced suppression of the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha).	dibenzoylmethane	67-70	NFKB inhibitor alpha	Homo sapiens	117-200
30068872-8	2018	DBM-mediated increase of NF-kappaB translocation resulted from the DBM-induced suppression of the phosphorylation of nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor, alpha (IkappaBalpha).	dibenzoylmethane	67-70	NFKB inhibitor alpha	Homo sapiens	202-214
30068872-9	2018	In contrast, DBM effectively increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its target protein, hemeoxygenase-1 (HO-1).	dibenzoylmethane	13-16	NFE2 like bZIP transcription factor 2	Homo sapiens	57-91
30068872-9	2018	In contrast, DBM effectively increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its target protein, hemeoxygenase-1 (HO-1).	dibenzoylmethane	13-16	NFE2 like bZIP transcription factor 2	Homo sapiens	93-97
30068872-9	2018	In contrast, DBM effectively increased the expression of nuclear factor E2-related factor 2 (Nrf2) and its target protein, hemeoxygenase-1 (HO-1).	dibenzoylmethane	13-16	heme oxygenase 1	Homo sapiens	123-138
30068872-11	2018	Furthermore, DBM effectively inhibited the expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1).	dibenzoylmethane	13-16	tumor necrosis factor	Homo sapiens	92-119
30068872-11	2018	Furthermore, DBM effectively inhibited the expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1).	dibenzoylmethane	13-16	tumor necrosis factor	Homo sapiens	121-130
30068872-11	2018	Furthermore, DBM effectively inhibited the expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1).	dibenzoylmethane	13-16	interleukin 1 beta	Homo sapiens	133-151
30068872-11	2018	Furthermore, DBM effectively inhibited the expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1).	dibenzoylmethane	13-16	interleukin 1 beta	Homo sapiens	153-161
30068872-11	2018	Furthermore, DBM effectively inhibited the expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1).	dibenzoylmethane	13-16	interleukin 6	Homo sapiens	164-168
30068872-11	2018	Furthermore, DBM effectively inhibited the expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1).	dibenzoylmethane	13-16	C-C motif chemokine ligand 2	Homo sapiens	174-208
30068872-11	2018	Furthermore, DBM effectively inhibited the expression of pro-inflammatory cytokines such as tumor necrosis factor alpha (TNF-alpha), interleukin-1 beta (IL-1beta), IL-6, and monocyte chemoattractant protein-1 (MCP-1).	dibenzoylmethane	13-16	C-C motif chemokine ligand 2	Homo sapiens	210-215
30068872-12	2018	These results indicated that the DBM-mediated differential regulation of NF-kappaB and Nrf2, which are major transcription factors involved in inflammation, inhibited the expression of inflammatory cytokines.	dibenzoylmethane	33-36	nuclear factor kappa B subunit 1	Homo sapiens	73-82
30068872-12	2018	These results indicated that the DBM-mediated differential regulation of NF-kappaB and Nrf2, which are major transcription factors involved in inflammation, inhibited the expression of inflammatory cytokines.	dibenzoylmethane	33-36	NFE2 like bZIP transcription factor 2	Homo sapiens	87-91
28828752-0	2017	Dibenzoylmethane Protects Against CCl4-Induced Acute Liver Injury by Activating Nrf2 via JNK, AMPK, and Calcium Signaling.	dibenzoylmethane	0-16	chemokine (C-C motif) ligand 4	Mus musculus	34-38
28828752-0	2017	Dibenzoylmethane Protects Against CCl4-Induced Acute Liver Injury by Activating Nrf2 via JNK, AMPK, and Calcium Signaling.	dibenzoylmethane	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	80-84
28828752-0	2017	Dibenzoylmethane Protects Against CCl4-Induced Acute Liver Injury by Activating Nrf2 via JNK, AMPK, and Calcium Signaling.	dibenzoylmethane	0-16	mitogen-activated protein kinase 8	Mus musculus	89-92
28828752-3	2017	Dibenzoylmethane (DBM) is a minor ingredient in licorice that activates Nrf2 and prevents various cancers and oxidative damage.	dibenzoylmethane	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	72-76
28828752-3	2017	Dibenzoylmethane (DBM) is a minor ingredient in licorice that activates Nrf2 and prevents various cancers and oxidative damage.	dibenzoylmethane	18-21	nuclear factor, erythroid derived 2, like 2	Mus musculus	72-76
28828752-4	2017	In the present study, the mechanisms by which DBM activates Nrf2 signaling were delineated, and its protective effect against carbon tetrachloride (CCl4)-induced liver injury was examined.	dibenzoylmethane	46-49	nuclear factor, erythroid derived 2, like 2	Mus musculus	60-64
28828752-4	2017	In the present study, the mechanisms by which DBM activates Nrf2 signaling were delineated, and its protective effect against carbon tetrachloride (CCl4)-induced liver injury was examined.	dibenzoylmethane	46-49	chemokine (C-C motif) ligand 4	Mus musculus	148-152
28828752-5	2017	DBM potently induced the expression of HO-1 in cells and in the livers of mice, but this induction was diminished in Nrf2-deficient mice and cells.	dibenzoylmethane	0-3	nuclear factor, erythroid derived 2, like 2	Mus musculus	117-121
28828752-6	2017	Overexpression of Nrf2 enhanced DBM-induced HO-1 expression, while overexpression of a dominant-negative fragment of Nrf2 inhibited this induction.	dibenzoylmethane	32-35	nuclear factor, erythroid derived 2, like 2	Mus musculus	18-22
28828752-7	2017	DBM treatment resulted in dissociation from Keap1 and nuclear translocation of Nrf2.	dibenzoylmethane	0-3	kelch-like ECH-associated protein 1	Mus musculus	44-49
28828752-7	2017	DBM treatment resulted in dissociation from Keap1 and nuclear translocation of Nrf2.	dibenzoylmethane	0-3	nuclear factor, erythroid derived 2, like 2	Mus musculus	79-83
28828752-10	2017	Finally, DBM treatment significantly inhibited CCl4-induced acute liver injury in wild-type but not in Nrf2-deficient mice.	dibenzoylmethane	9-12	chemokine (C-C motif) ligand 4	Mus musculus	47-51
28828752-11	2017	Taken together, our results revealed the mechanisms by which DBM activates Nrf2 and induces HO-1 expression, and provide molecular basis for the design and development of DBM and its derivatives for prevention or treatment of liver diseases by targeting Nrf2.	dibenzoylmethane	61-64	nuclear factor, erythroid derived 2, like 2	Mus musculus	75-79
28828752-11	2017	Taken together, our results revealed the mechanisms by which DBM activates Nrf2 and induces HO-1 expression, and provide molecular basis for the design and development of DBM and its derivatives for prevention or treatment of liver diseases by targeting Nrf2.	dibenzoylmethane	61-64	nuclear factor, erythroid derived 2, like 2	Mus musculus	254-258
28430857-7	2017	We identified two compounds, trazodone hydrochloride and dibenzoylmethane, which reversed eIF2α-P-mediated translational attenuation in vitro and in vivo.	dibenzoylmethane	57-73	eukaryotic translation initiation factor 2A	Homo sapiens	90-100
28513720-2	2017	We demonstrate herein, firstly, that the DFT calculated OH 1H NMR chemical shifts of acetylacetone and dibenzoylmethane exhibit a strong linear dependence on the computed OO hydrogen bond length of ~-50 ppm A-1 and as a function of the O-HO bond angle of ~1 ppm per degree, upon the transfer of the hydrogen atom from the ground state toward the transition state.	dibenzoylmethane	103-119	BCL2 related protein A1	Homo sapiens	207-210
25756788-0	2015	Dibenzoylmethane exerts metabolic activity through regulation of AMP-activated protein kinase (AMPK)-mediated glucose uptake and adipogenesis pathways.	dibenzoylmethane	0-16	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	65-93
25756788-0	2015	Dibenzoylmethane exerts metabolic activity through regulation of AMP-activated protein kinase (AMPK)-mediated glucose uptake and adipogenesis pathways.	dibenzoylmethane	0-16	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	95-99
25756788-3	2015	In this study, DBM increased phosphorylation of AMP-activated protein kinase (AMPK) and stimulated glucose uptake in a skeletal muscle cell line.	dibenzoylmethane	15-18	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	48-76
25756788-3	2015	In this study, DBM increased phosphorylation of AMP-activated protein kinase (AMPK) and stimulated glucose uptake in a skeletal muscle cell line.	dibenzoylmethane	15-18	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	78-82
25756788-4	2015	Both knockdown of AMPK with siRNA and inhibition with AMPK inhibitor blocked DBM-induced glucose uptake.	dibenzoylmethane	77-80	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	18-22
25756788-4	2015	Both knockdown of AMPK with siRNA and inhibition with AMPK inhibitor blocked DBM-induced glucose uptake.	dibenzoylmethane	77-80	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	54-58
25756788-6	2015	DBM stimulated phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which was blocked by pretreatment with compound C, an AMPK inhibitor.	dibenzoylmethane	0-3	mitogen-activated protein kinase 14	Homo sapiens	34-70
25756788-6	2015	DBM stimulated phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which was blocked by pretreatment with compound C, an AMPK inhibitor.	dibenzoylmethane	0-3	mitogen-activated protein kinase 14	Homo sapiens	72-80
25756788-6	2015	DBM stimulated phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK), which was blocked by pretreatment with compound C, an AMPK inhibitor.	dibenzoylmethane	0-3	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	137-141
25756788-11	2015	Expression of the adipogenic gene, fatty acid synthase (FAS), was suppressed by DBM in an AMPK-dependent manner.	dibenzoylmethane	80-83	fatty acid synthase	Homo sapiens	35-54
25756788-11	2015	Expression of the adipogenic gene, fatty acid synthase (FAS), was suppressed by DBM in an AMPK-dependent manner.	dibenzoylmethane	80-83	fatty acid synthase	Homo sapiens	56-59
25756788-11	2015	Expression of the adipogenic gene, fatty acid synthase (FAS), was suppressed by DBM in an AMPK-dependent manner.	dibenzoylmethane	80-83	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	90-94
25756788-12	2015	These results showed that the beneficial metabolic effects of DBM might be due to regulation of glucose uptake via AMPK in skeletal muscle and inhibition of adipogenesis in pre-adipocytes.	dibenzoylmethane	62-65	protein kinase AMP-activated catalytic subunit alpha 2	Homo sapiens	115-119
24228838-1	2013	Upon treatment with the K- and Li-enolates of a methylene active compound, such as dimethyl malonate and dibenzoylmethane, D-allal- and D-galactal-derived vinyl N-mesyl aziridines are stereoselectively transformed, in a unique step, into diastereoisomeric, highly functionalized, enantiopure cis-2,5-disubstituted N-mesyl-2,5-dihydropyrroles.	dibenzoylmethane	105-121	suppressor of cytokine signaling 2	Homo sapiens	292-297
23523665-8	2013	In conclusion we identified DBM analogs as a novel class of cytoprotective compounds inhibiting ERK1/2 kinase and protecting from necrotic cell death by a mechanism independent of poly(ADP-ribose) polymerase inhibition.	dibenzoylmethane	28-31	mitogen-activated protein kinase 3	Homo sapiens	96-102
21924245-3	2011	In the current report, we investigated the potency of DBM, DBP, and DBA in relation to curcumin for their ability to suppress TNF-induced NF-kappaB activation, NF-kappaB-regulated gene products, and cell proliferation.	dibenzoylmethane	54-57	tumor necrosis factor	Homo sapiens	126-129
21924245-3	2011	In the current report, we investigated the potency of DBM, DBP, and DBA in relation to curcumin for their ability to suppress TNF-induced NF-kappaB activation, NF-kappaB-regulated gene products, and cell proliferation.	dibenzoylmethane	54-57	nuclear factor kappa B subunit 1	Homo sapiens	138-147
21924245-3	2011	In the current report, we investigated the potency of DBM, DBP, and DBA in relation to curcumin for their ability to suppress TNF-induced NF-kappaB activation, NF-kappaB-regulated gene products, and cell proliferation.	dibenzoylmethane	54-57	nuclear factor kappa B subunit 1	Homo sapiens	160-169
21523861-0	2011	Ornithine decarboxylase prevents dibenzoylmethane-induced apoptosis through repressing reactive oxygen species generation.	dibenzoylmethane	33-49	ornithine decarboxylase 1	Homo sapiens	0-23
21523861-5	2011	Here, we investigated one mechanism of DBM-induced apoptosis and the antiapoptotic effects of ODC during DBM treatment.	dibenzoylmethane	105-108	ornithine decarboxylase 1	Homo sapiens	94-97
21547313-1	2011	In the present work, three dibenzoylmethane derivatives in their beta-diketo form have been selected to investigate their photophysical and photochemical behavior upon interaction with human serum albumin (HSA).	dibenzoylmethane	27-43	albumin	Homo sapiens	191-204
21341276-15	2011	There was an increased systemic plasma exposure of DBM in Nrf2 (-/-) mice, suggesting that the Nrf2 genotype could also play a role in the pharmacokinetic disposition of DBM.	dibenzoylmethane	51-54	nuclear factor, erythroid derived 2, like 2	Mus musculus	58-62
21341276-15	2011	There was an increased systemic plasma exposure of DBM in Nrf2 (-/-) mice, suggesting that the Nrf2 genotype could also play a role in the pharmacokinetic disposition of DBM.	dibenzoylmethane	51-54	nuclear factor, erythroid derived 2, like 2	Mus musculus	95-99
21341276-15	2011	There was an increased systemic plasma exposure of DBM in Nrf2 (-/-) mice, suggesting that the Nrf2 genotype could also play a role in the pharmacokinetic disposition of DBM.	dibenzoylmethane	170-173	nuclear factor, erythroid derived 2, like 2	Mus musculus	58-62
21341276-15	2011	There was an increased systemic plasma exposure of DBM in Nrf2 (-/-) mice, suggesting that the Nrf2 genotype could also play a role in the pharmacokinetic disposition of DBM.	dibenzoylmethane	170-173	nuclear factor, erythroid derived 2, like 2	Mus musculus	95-99
21341276-16	2011	Taken together, the results show that DBM has low oral bioavailability which could be due in part to poor water solubility and this could be overcome by a nanotechnology-based drug delivery system and furthermore the Nrf2 genotype could also play a role in the pharmacokinetics of DBM.	dibenzoylmethane	38-41	NFE2 like bZIP transcription factor 2	Rattus norvegicus	217-221
21341276-16	2011	Taken together, the results show that DBM has low oral bioavailability which could be due in part to poor water solubility and this could be overcome by a nanotechnology-based drug delivery system and furthermore the Nrf2 genotype could also play a role in the pharmacokinetics of DBM.	dibenzoylmethane	281-284	NFE2 like bZIP transcription factor 2	Rattus norvegicus	217-221
19959557-9	2010	Instead, DBM showed increased induction of NF-E2-related factor-2 (Nrf2) transcription factor and phase II detoxifying enzymes, which appears to correlate with in vitro cell lines results that DBM is a more potent Nrf2 activator than PEITC.	dibenzoylmethane	9-12	nuclear factor, erythroid derived 2, like 2	Mus musculus	43-65
19959557-9	2010	Instead, DBM showed increased induction of NF-E2-related factor-2 (Nrf2) transcription factor and phase II detoxifying enzymes, which appears to correlate with in vitro cell lines results that DBM is a more potent Nrf2 activator than PEITC.	dibenzoylmethane	9-12	nuclear factor, erythroid derived 2, like 2	Mus musculus	67-71
19959557-9	2010	Instead, DBM showed increased induction of NF-E2-related factor-2 (Nrf2) transcription factor and phase II detoxifying enzymes, which appears to correlate with in vitro cell lines results that DBM is a more potent Nrf2 activator than PEITC.	dibenzoylmethane	9-12	nuclear factor, erythroid derived 2, like 2	Mus musculus	214-218
21139246-0	2010	Efficacy of dibenzoylmethane derivatives in protecting against endoplasmic reticulum stress and inhibiting nuclear factor kappa B on dextran sulfate sodium induced colitis in mice.	dibenzoylmethane	12-28	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	107-129
21139246-1	2010	We recently reported that some dibenzoylmethane (DBM) derivatives have a protective effect against endoplasmic reticulum (ER) stress and inhibit nuclear factor kappa B (NF-kappaB).	dibenzoylmethane	31-47	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	145-167
21139246-1	2010	We recently reported that some dibenzoylmethane (DBM) derivatives have a protective effect against endoplasmic reticulum (ER) stress and inhibit nuclear factor kappa B (NF-kappaB).	dibenzoylmethane	31-47	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	169-178
21139246-1	2010	We recently reported that some dibenzoylmethane (DBM) derivatives have a protective effect against endoplasmic reticulum (ER) stress and inhibit nuclear factor kappa B (NF-kappaB).	dibenzoylmethane	49-52	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	145-167
21139246-1	2010	We recently reported that some dibenzoylmethane (DBM) derivatives have a protective effect against endoplasmic reticulum (ER) stress and inhibit nuclear factor kappa B (NF-kappaB).	dibenzoylmethane	49-52	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	169-178
21139246-3	2010	The DBM derivatives used in this study were 4,4"-dibromodibenzoylmethane that protects against ER stress, and, 4,4"-dichlorodibenzoylmethane that protects against ER stress and inhibits NF-kappaB.	dibenzoylmethane	4-7	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	186-195
18782044-0	2008	Dibenzoylmethane activates Nrf2-dependent detoxification pathway and inhibits benzo(a)pyrene induced DNA adducts in lungs.	dibenzoylmethane	0-16	nuclear factor, erythroid derived 2, like 2	Mus musculus	27-31
18782044-8	2008	DBM elicited a dose-dependent increase in antioxidant response element (ARE)-driven luciferase reporter activity which correlated with an increase in mRNA expression of NQO1, GSTA2, and GCLC in mouse hepatoma cells, which are well established targets of Nrf2.	dibenzoylmethane	0-3	NAD(P)H dehydrogenase, quinone 1	Mus musculus	169-173
18782044-8	2008	DBM elicited a dose-dependent increase in antioxidant response element (ARE)-driven luciferase reporter activity which correlated with an increase in mRNA expression of NQO1, GSTA2, and GCLC in mouse hepatoma cells, which are well established targets of Nrf2.	dibenzoylmethane	0-3	glutathione S-transferase, alpha 2 (Yc2)	Mus musculus	175-180
18782044-8	2008	DBM elicited a dose-dependent increase in antioxidant response element (ARE)-driven luciferase reporter activity which correlated with an increase in mRNA expression of NQO1, GSTA2, and GCLC in mouse hepatoma cells, which are well established targets of Nrf2.	dibenzoylmethane	0-3	glutamate-cysteine ligase, catalytic subunit	Mus musculus	186-190
18782044-8	2008	DBM elicited a dose-dependent increase in antioxidant response element (ARE)-driven luciferase reporter activity which correlated with an increase in mRNA expression of NQO1, GSTA2, and GCLC in mouse hepatoma cells, which are well established targets of Nrf2.	dibenzoylmethane	0-3	nuclear factor, erythroid derived 2, like 2	Mus musculus	254-258
18782044-11	2008	In conclusion, DBM mediates the induction of phase II enzymes by Nrf2 activation and inhibits benzo[a]pyrene induced DNA adducts by enhancing its detoxification in lungs.	dibenzoylmethane	15-18	nuclear factor, erythroid derived 2, like 2	Mus musculus	65-69
17555355-8	2007	The reactions of benzylic alcohols possessing various substituents on the aromatic ring and dibenzoylmethane (2b) as a diketone were examined in the presence of Hf(OTf)4.	dibenzoylmethane	92-108	POU class 5 homeobox 1	Homo sapiens	164-169
17595765-0	2007	Suppression of androgen receptor expression by dibenzoylmethane as a therapeutic objective in advanced prostate cancer.	dibenzoylmethane	47-63	androgen receptor	Homo sapiens	15-32
17595765-4	2007	MATERIALS AND METHODS: In this study, we attempt to clarify the molecular mechanism by which dibenzoylmethane (DBM), a beta3-diketone, inhibits the growth of androgen-responsive human LNCaP prostate cancer cells and down-regulates expression of the AR.	dibenzoylmethane	93-109	androgen receptor	Homo sapiens	249-251
17595765-4	2007	MATERIALS AND METHODS: In this study, we attempt to clarify the molecular mechanism by which dibenzoylmethane (DBM), a beta3-diketone, inhibits the growth of androgen-responsive human LNCaP prostate cancer cells and down-regulates expression of the AR.	dibenzoylmethane	111-114	androgen receptor	Homo sapiens	249-251
17595765-9	2007	DBM also inhibited the secretion of the AR-regulated tumor marker, prostate-specific antigen (PSA).	dibenzoylmethane	0-3	androgen receptor	Homo sapiens	40-42
17595765-10	2007	Moreover, the relative binding affinity of DBM to AR was lower than that of the synthetic androgen R1881 (methyltrienolone) suggesting that DBM must suppress AR expression independent of an AR-DBM bound interaction.	dibenzoylmethane	43-46	androgen receptor	Homo sapiens	50-52
17595765-10	2007	Moreover, the relative binding affinity of DBM to AR was lower than that of the synthetic androgen R1881 (methyltrienolone) suggesting that DBM must suppress AR expression independent of an AR-DBM bound interaction.	dibenzoylmethane	43-46	androgen receptor	Homo sapiens	158-160
17595765-10	2007	Moreover, the relative binding affinity of DBM to AR was lower than that of the synthetic androgen R1881 (methyltrienolone) suggesting that DBM must suppress AR expression independent of an AR-DBM bound interaction.	dibenzoylmethane	43-46	androgen receptor	Homo sapiens	158-160
17595765-10	2007	Moreover, the relative binding affinity of DBM to AR was lower than that of the synthetic androgen R1881 (methyltrienolone) suggesting that DBM must suppress AR expression independent of an AR-DBM bound interaction.	dibenzoylmethane	140-143	androgen receptor	Homo sapiens	50-52
17595765-10	2007	Moreover, the relative binding affinity of DBM to AR was lower than that of the synthetic androgen R1881 (methyltrienolone) suggesting that DBM must suppress AR expression independent of an AR-DBM bound interaction.	dibenzoylmethane	140-143	androgen receptor	Homo sapiens	158-160
17595765-10	2007	Moreover, the relative binding affinity of DBM to AR was lower than that of the synthetic androgen R1881 (methyltrienolone) suggesting that DBM must suppress AR expression independent of an AR-DBM bound interaction.	dibenzoylmethane	140-143	androgen receptor	Homo sapiens	158-160
17077187-4	2007	In Caco-2 cells, the most pronounced induction of BCRP expression could be observed after treatment with TBHQ (100 microM), dibenzoylmethane (DBM, 50 microM), and quercetin (25 microM), while green tea component (-)-epicatechin (50 microM) decreased BCRP expression.	dibenzoylmethane	124-140	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-54
17077187-4	2007	In Caco-2 cells, the most pronounced induction of BCRP expression could be observed after treatment with TBHQ (100 microM), dibenzoylmethane (DBM, 50 microM), and quercetin (25 microM), while green tea component (-)-epicatechin (50 microM) decreased BCRP expression.	dibenzoylmethane	142-145	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	50-54
17077187-9	2007	Caco-2 cells pretreated with quercetin or DBM showed an enhancement of apically transported benzo[a]pyrene-3-sulfate, indicating that induced BCRP was functionally active.	dibenzoylmethane	42-45	ATP binding cassette subfamily G member 2 (Junior blood group)	Homo sapiens	142-146
16051634-5	2006	Further mechanistic study using chromatin immunoprecipitation assay demonstrated that DBM acts as a pure antagonist by attenuating the binding of estrogen receptor to the estrogen response elements in the regulatory regions of c-myc, hTERT and bcl-2 genes in vivo.	dibenzoylmethane	86-89	MYC proto-oncogene, bHLH transcription factor	Homo sapiens	227-232
16051634-5	2006	Further mechanistic study using chromatin immunoprecipitation assay demonstrated that DBM acts as a pure antagonist by attenuating the binding of estrogen receptor to the estrogen response elements in the regulatory regions of c-myc, hTERT and bcl-2 genes in vivo.	dibenzoylmethane	86-89	telomerase reverse transcriptase	Homo sapiens	234-239
16051634-5	2006	Further mechanistic study using chromatin immunoprecipitation assay demonstrated that DBM acts as a pure antagonist by attenuating the binding of estrogen receptor to the estrogen response elements in the regulatory regions of c-myc, hTERT and bcl-2 genes in vivo.	dibenzoylmethane	86-89	B cell leukemia/lymphoma 2	Mus musculus	244-249
15352255-2	2004	Although DBM, a constituent of licorice, has been shown to induce cell cycle arrest and regulate androgen receptor (AR) expression, the mechanism by which these events occur is unknown.	dibenzoylmethane	9-12	androgen receptor	Homo sapiens	97-114
15352255-2	2004	Although DBM, a constituent of licorice, has been shown to induce cell cycle arrest and regulate androgen receptor (AR) expression, the mechanism by which these events occur is unknown.	dibenzoylmethane	9-12	androgen receptor	Homo sapiens	116-118
12646199-0	2003	Dibenzoylmethane, a natural dietary compound, induces HIF-1 alpha and increases expression of VEGF.	dibenzoylmethane	0-16	hypoxia inducible factor 1 subunit alpha	Homo sapiens	54-65
12646199-0	2003	Dibenzoylmethane, a natural dietary compound, induces HIF-1 alpha and increases expression of VEGF.	dibenzoylmethane	0-16	vascular endothelial growth factor A	Homo sapiens	94-98
12646199-6	2003	In this study, we investigated the effects of dibenzoylmethane (DBM), a natural dietary compound and an iron chelator, on HIF-1 pathway.	dibenzoylmethane	46-62	hypoxia inducible factor 1 subunit alpha	Homo sapiens	122-127
12646199-6	2003	In this study, we investigated the effects of dibenzoylmethane (DBM), a natural dietary compound and an iron chelator, on HIF-1 pathway.	dibenzoylmethane	64-67	hypoxia inducible factor 1 subunit alpha	Homo sapiens	122-127
12646199-10	2003	The effect of DBM on HIF-1 and its low toxicity profile might be therapeutically beneficial in ischemic diseases.	dibenzoylmethane	14-17	hypoxia inducible factor 1 subunit alpha	Homo sapiens	21-26
11358806-0	2001	Dibenzoylmethane modulates aryl hydrocarbon receptor function and expression of cytochromes P50 1A1, 1A2, and 1B1.	dibenzoylmethane	0-16	aryl hydrocarbon receptor	Homo sapiens	27-52
11358806-4	2001	Oral administration of DBM to female Sprague Dawley rats inhibited the increase in hepatic enzyme activity and mRNA levels of CYP1A1, 1A2, and 1B1 caused by the PAH 7,12-dimethylbenz[a]anthracene (DMBA).	dibenzoylmethane	23-26	cytochrome P450, family 1, subfamily a, polypeptide 1	Rattus norvegicus	126-132
11358806-7	2001	In HepG2 human hepatoma cells, DBM inhibited DMBA- and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced enzyme activity and CYP1A1, 1A2, and 1B1 mRNA levels, whereas DBM itself induced activity and mRNA expression.	dibenzoylmethane	31-34	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	126-132
11358806-9	2001	Because the transcription of CYP1A1 is regulated by the aryl hydrocarbon receptor (AhR), we investigated the effect of DBM on AhR activation.	dibenzoylmethane	119-122	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	29-35
11358806-9	2001	Because the transcription of CYP1A1 is regulated by the aryl hydrocarbon receptor (AhR), we investigated the effect of DBM on AhR activation.	dibenzoylmethane	119-122	aryl hydrocarbon receptor	Homo sapiens	126-129
11358806-10	2001	DBM inhibited TCCD-induced DNA-binding of the AhR to the xenobiotic-responsive element (XRE) of CYP1A1 as measured by electrophoretic mobility shift assay.	dibenzoylmethane	0-3	aryl hydrocarbon receptor	Homo sapiens	46-49
11358806-10	2001	DBM inhibited TCCD-induced DNA-binding of the AhR to the xenobiotic-responsive element (XRE) of CYP1A1 as measured by electrophoretic mobility shift assay.	dibenzoylmethane	0-3	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	96-102
10990034-1	2000	Dimethyl malonate and dibenzoylmethane attacked the C-2 position of the title 3-nitro-2-enopyranosides from the side opposite the anomeric methoxyl group to afford the 3-enopyranosides (S(N)2" products).	dibenzoylmethane	22-38	complement C2	Homo sapiens	52-55
10814878-3	2000	The present studies were conducted to examine the capacity of dibenzoylmethane to inhibit the formation of DNA adducts following exposure to benzo[a]pyrene (BP) and 1,6-dinitropyrene (1,6-DNP), and to stimulate the expression of glutathione-S-transferase (GST) and NAD(P)H-quinone reductase (QR) proteins in the human mammary epithelial cell line MCF-10F.	dibenzoylmethane	62-78	glutathione S-transferase kappa 1	Homo sapiens	229-254
10814878-3	2000	The present studies were conducted to examine the capacity of dibenzoylmethane to inhibit the formation of DNA adducts following exposure to benzo[a]pyrene (BP) and 1,6-dinitropyrene (1,6-DNP), and to stimulate the expression of glutathione-S-transferase (GST) and NAD(P)H-quinone reductase (QR) proteins in the human mammary epithelial cell line MCF-10F.	dibenzoylmethane	62-78	glutathione S-transferase kappa 1	Homo sapiens	256-259
10814878-3	2000	The present studies were conducted to examine the capacity of dibenzoylmethane to inhibit the formation of DNA adducts following exposure to benzo[a]pyrene (BP) and 1,6-dinitropyrene (1,6-DNP), and to stimulate the expression of glutathione-S-transferase (GST) and NAD(P)H-quinone reductase (QR) proteins in the human mammary epithelial cell line MCF-10F.	dibenzoylmethane	62-78	crystallin zeta	Homo sapiens	265-290
10814878-3	2000	The present studies were conducted to examine the capacity of dibenzoylmethane to inhibit the formation of DNA adducts following exposure to benzo[a]pyrene (BP) and 1,6-dinitropyrene (1,6-DNP), and to stimulate the expression of glutathione-S-transferase (GST) and NAD(P)H-quinone reductase (QR) proteins in the human mammary epithelial cell line MCF-10F.	dibenzoylmethane	62-78	crystallin zeta	Homo sapiens	292-294
10814878-9	2000	Dibenzoylmethane treatment at the same concentrations did not induce GSTP1-1 expression and significantly stimulated QR expression only at the 2.0 microM concentration.	dibenzoylmethane	0-16	crystallin zeta	Homo sapiens	117-119
9667742-3	1998	Of the beta-diketone compounds initially screened for their capacity to induce quinone-reductase (QR) activity in wild-type Hepa1c1c7 cells and a mutant subclone, curcumin (diferuloylmethane) and dibenzoylmethane were most effective.	dibenzoylmethane	196-212	crystallin, zeta	Mus musculus	79-96
9667742-3	1998	Of the beta-diketone compounds initially screened for their capacity to induce quinone-reductase (QR) activity in wild-type Hepa1c1c7 cells and a mutant subclone, curcumin (diferuloylmethane) and dibenzoylmethane were most effective.	dibenzoylmethane	196-212	crystallin, zeta	Mus musculus	98-100