PMID-sentid	Pub_year	Sent_text	compound_name	comp_offset	prot_official_name	organism	prot_offset
15961392-0	2005	Checkpoint kinase 1 regulates diallyl trisulfide-induced mitotic arrest in human prostate cancer cells.	diallyl trisulfide	30-48	checkpoint kinase 1	Homo sapiens	0-19
15961392-1	2005	We have shown previously that diallyl trisulfide (DATS), a constituent of processed garlic, inhibits proliferation of PC-3 and DU145 human prostate cancer cells by causing G(2)-M phase cell cycle arrest in association with inhibition of cyclin-dependent kinase 1 activity and hyperphosphorylation of Cdc25C at Ser(216).	diallyl trisulfide	30-48	cyclin dependent kinase 1	Homo sapiens	237-262
15961392-1	2005	We have shown previously that diallyl trisulfide (DATS), a constituent of processed garlic, inhibits proliferation of PC-3 and DU145 human prostate cancer cells by causing G(2)-M phase cell cycle arrest in association with inhibition of cyclin-dependent kinase 1 activity and hyperphosphorylation of Cdc25C at Ser(216).	diallyl trisulfide	30-48	cell division cycle 25C	Homo sapiens	300-306
15961392-1	2005	We have shown previously that diallyl trisulfide (DATS), a constituent of processed garlic, inhibits proliferation of PC-3 and DU145 human prostate cancer cells by causing G(2)-M phase cell cycle arrest in association with inhibition of cyclin-dependent kinase 1 activity and hyperphosphorylation of Cdc25C at Ser(216).	diallyl trisulfide	50-54	cyclin dependent kinase 1	Homo sapiens	237-262
15961392-1	2005	We have shown previously that diallyl trisulfide (DATS), a constituent of processed garlic, inhibits proliferation of PC-3 and DU145 human prostate cancer cells by causing G(2)-M phase cell cycle arrest in association with inhibition of cyclin-dependent kinase 1 activity and hyperphosphorylation of Cdc25C at Ser(216).	diallyl trisulfide	50-54	cell division cycle 25C	Homo sapiens	300-306
15961392-7	2005	In conclusion, the results of the present study suggest existence of a checkpoint kinase 1-dependent mechanism for diallyl trisulfide-induced mitotic arrest in human prostate cancer cells.	diallyl trisulfide	115-133	checkpoint kinase 1	Homo sapiens	71-90
16110831-1	2005	The present study aimed to investigate the effect of diallyl trisulfide (DATS) on tumor necrosis factor (TNF)-alpha expression in inflammed mucosa of ulcerative colitis and its possible mechanism.	diallyl trisulfide	53-71	tumor necrosis factor	Homo sapiens	82-115
16110831-1	2005	The present study aimed to investigate the effect of diallyl trisulfide (DATS) on tumor necrosis factor (TNF)-alpha expression in inflammed mucosa of ulcerative colitis and its possible mechanism.	diallyl trisulfide	73-77	tumor necrosis factor	Homo sapiens	82-115
16110831-6	2005	Concentrations of TNF-alpha in supernatants of biopsies treated with 5 and 10 microM DATS were lower than those of untreated biopsies.	diallyl trisulfide	85-89	tumor necrosis factor	Homo sapiens	18-27
16110831-7	2005	There were fewer lamina propria mononuclear cells whose NF-kappaB P65 expression in nuclei was positive, and less mRNA expression of TNF-alpha in biopsies treated with 10 microM DATS than in untreated biopsies.	diallyl trisulfide	178-182	RELA proto-oncogene, NF-kB subunit	Homo sapiens	56-69
16110831-7	2005	There were fewer lamina propria mononuclear cells whose NF-kappaB P65 expression in nuclei was positive, and less mRNA expression of TNF-alpha in biopsies treated with 10 microM DATS than in untreated biopsies.	diallyl trisulfide	178-182	tumor necrosis factor	Homo sapiens	133-142
15184882-0	2004	Diallyl trisulfide-induced apoptosis in human prostate cancer cells involves c-Jun N-terminal kinase and extracellular-signal regulated kinase-mediated phosphorylation of Bcl-2.	diallyl trisulfide	0-18	BCL2 apoptosis regulator	Homo sapiens	171-176
15477009-7	2004	DATS-induced ARE activity was inhibited by dominant-negative Nrf2 Kelch-like ECH-associating protein 1 and constructs.	diallyl trisulfide	0-4	NFE2 like bZIP transcription factor 2	Homo sapiens	61-65
15477009-8	2004	Cotreatment with thiol antioxidants decreased the ARE activity and Nrf2 protein level induced by DATS.	diallyl trisulfide	97-101	NFE2 like bZIP transcription factor 2	Homo sapiens	67-71
15854348-9	2005	CONCLUSIONS: The combination of HSV-TK/GCV system with allitride can inhibit the proliferation of BIU87 cells congenerously through apoptosis, which may be correlated with S- and G(2)-phase arrest, down-regulation of bcl-2 and increased caspase-3 expression and its activity.	diallyl trisulfide	55-64	BCL2 apoptosis regulator	Homo sapiens	217-222
15854348-9	2005	CONCLUSIONS: The combination of HSV-TK/GCV system with allitride can inhibit the proliferation of BIU87 cells congenerously through apoptosis, which may be correlated with S- and G(2)-phase arrest, down-regulation of bcl-2 and increased caspase-3 expression and its activity.	diallyl trisulfide	55-64	caspase 3	Homo sapiens	237-246
15500931-5	2004	According to the Western blot analysis, DATS decreased cyclin-dependent kinase (Cdks)-Cdk7 (i.e. Cdc2 activate kinase) protein levels in J5 cells but increased cyclin B1 protein level.	diallyl trisulfide	40-44	cyclin dependent kinase 1	Homo sapiens	80-84
15500931-5	2004	According to the Western blot analysis, DATS decreased cyclin-dependent kinase (Cdks)-Cdk7 (i.e. Cdc2 activate kinase) protein levels in J5 cells but increased cyclin B1 protein level.	diallyl trisulfide	40-44	cyclin dependent kinase 7	Homo sapiens	86-90
15500931-5	2004	According to the Western blot analysis, DATS decreased cyclin-dependent kinase (Cdks)-Cdk7 (i.e. Cdc2 activate kinase) protein levels in J5 cells but increased cyclin B1 protein level.	diallyl trisulfide	40-44	cyclin dependent kinase 1	Homo sapiens	97-101
15500931-5	2004	According to the Western blot analysis, DATS decreased cyclin-dependent kinase (Cdks)-Cdk7 (i.e. Cdc2 activate kinase) protein levels in J5 cells but increased cyclin B1 protein level.	diallyl trisulfide	40-44	cyclin B1	Homo sapiens	160-169
15500931-6	2004	The modulation potency to cyclin B1 and Cdk7 expressions was in the order of DATS > DADS > DAS.	diallyl trisulfide	77-81	cyclin B1	Homo sapiens	26-35
15500931-6	2004	The modulation potency to cyclin B1 and Cdk7 expressions was in the order of DATS > DADS > DAS.	diallyl trisulfide	77-81	cyclin dependent kinase 7	Homo sapiens	40-44
15500931-7	2004	The modulation potency to cyclin B1 and Cdk7 protein levels increased with increasing in DATS concentration and culture time.	diallyl trisulfide	89-93	cyclin B1	Homo sapiens	26-35
15500931-7	2004	The modulation potency to cyclin B1 and Cdk7 protein levels increased with increasing in DATS concentration and culture time.	diallyl trisulfide	89-93	cyclin dependent kinase 7	Homo sapiens	40-44
15500931-8	2004	In conclusion, DATS might affect cell viability and cell morphological changes in J5 cells and lead cells to be arrested in G2/M phase via controlling the expression of cyclin B1 and Cdk7 in J5 cells, and the controlling action might relate to the sulfuric atom numbers in the structures of all these allyl sulfides.	diallyl trisulfide	15-19	cyclin B1	Homo sapiens	169-178
15500931-8	2004	In conclusion, DATS might affect cell viability and cell morphological changes in J5 cells and lead cells to be arrested in G2/M phase via controlling the expression of cyclin B1 and Cdk7 in J5 cells, and the controlling action might relate to the sulfuric atom numbers in the structures of all these allyl sulfides.	diallyl trisulfide	15-19	cyclin dependent kinase 7	Homo sapiens	183-187
15184882-4	2004	DATS-induced apoptosis in PC-3 cells was associated with phosphorylation of Bcl-2, reduced Bcl-2 : Bax interaction, and cleavage of procaspase-9 and -3.	diallyl trisulfide	0-4	BCL2 apoptosis regulator	Homo sapiens	76-81
15184882-4	2004	DATS-induced apoptosis in PC-3 cells was associated with phosphorylation of Bcl-2, reduced Bcl-2 : Bax interaction, and cleavage of procaspase-9 and -3.	diallyl trisulfide	0-4	BCL2 apoptosis regulator	Homo sapiens	91-96
15184882-4	2004	DATS-induced apoptosis in PC-3 cells was associated with phosphorylation of Bcl-2, reduced Bcl-2 : Bax interaction, and cleavage of procaspase-9 and -3.	diallyl trisulfide	0-4	BCL2 associated X, apoptosis regulator	Homo sapiens	99-102
15184882-4	2004	DATS-induced apoptosis in PC-3 cells was associated with phosphorylation of Bcl-2, reduced Bcl-2 : Bax interaction, and cleavage of procaspase-9 and -3.	diallyl trisulfide	0-4	caspase 3	Homo sapiens	132-151
15184882-8	2004	Moreover, JNK inhibitor afforded significant protection against DATS-induced apoptosis in both cells.	diallyl trisulfide	64-68	mitogen-activated protein kinase 8	Homo sapiens	10-13
15184882-9	2004	DATS-induced Bcl-2 phosphorylation and apoptosis were partially attenuated by pharmacological inhibition of ERK1/2 using PD98059 or U0126.	diallyl trisulfide	0-4	BCL2 apoptosis regulator	Homo sapiens	13-18
15184882-9	2004	DATS-induced Bcl-2 phosphorylation and apoptosis were partially attenuated by pharmacological inhibition of ERK1/2 using PD98059 or U0126.	diallyl trisulfide	0-4	mitogen-activated protein kinase 3	Homo sapiens	108-114
15184882-11	2004	In conclusion, our data point towards important roles for Bcl-2, JNK and ERK in DATS-induced apoptosis in human prostate cancer cells.	diallyl trisulfide	80-84	BCL2 apoptosis regulator	Homo sapiens	58-63
15184882-11	2004	In conclusion, our data point towards important roles for Bcl-2, JNK and ERK in DATS-induced apoptosis in human prostate cancer cells.	diallyl trisulfide	80-84	mitogen-activated protein kinase 8	Homo sapiens	65-68
15184882-11	2004	In conclusion, our data point towards important roles for Bcl-2, JNK and ERK in DATS-induced apoptosis in human prostate cancer cells.	diallyl trisulfide	80-84	mitogen-activated protein kinase 1	Homo sapiens	73-76
15046820-6	2004	With respect to the phase II enzymes, DATS (10 micromol/kg) and DADS at a 10-fold higher dose (100 micromol/kg) significantly increased the activities of glutathione S-transferase, quinone reductase, and antioxidative enzyme glutathione peroxidase; whereas DAS did not.	diallyl trisulfide	38-42	hematopoietic prostaglandin D synthase	Rattus norvegicus	154-179
15046820-7	2004	In the carbon tetrachloride (CCl4)-induced acute liver injury model of rats, either DATS (10 micromol/kg) or DADS (100 micromol/kg) significantly reduced the injury caused by the induction of phase II enzymes with CCl4.	diallyl trisulfide	84-88	C-C motif chemokine ligand 4	Rattus norvegicus	29-33
15046820-7	2004	In the carbon tetrachloride (CCl4)-induced acute liver injury model of rats, either DATS (10 micromol/kg) or DADS (100 micromol/kg) significantly reduced the injury caused by the induction of phase II enzymes with CCl4.	diallyl trisulfide	84-88	C-C motif chemokine ligand 4	Rattus norvegicus	214-218
11758911-5	2001	Immunoblot results indicated that the B[a]P inducible CYP1A2 protein was suppressed by 100-1,000 microM of DADS and 10-100 microM of DATS, but CYP1A1 and 1B1 were not detectable in any microsomes.	diallyl trisulfide	133-137	cytochrome P450 family 1 subfamily A member 2	Homo sapiens	54-60
15051817-7	2004	The activity of glutathione reductase (GRd) was higher than in the control cells at 24 h (P < 0.05) when the hepatocytes were treated with 0.025 mmol/L DATS.	diallyl trisulfide	155-159	glutathione-disulfide reductase	Rattus norvegicus	16-37
15051817-7	2004	The activity of glutathione reductase (GRd) was higher than in the control cells at 24 h (P < 0.05) when the hepatocytes were treated with 0.025 mmol/L DATS.	diallyl trisulfide	155-159	glutathione-disulfide reductase	Rattus norvegicus	39-42
15051817-8	2004	When the hepatocytes were treated with 0.025 mmol/L DATS, the activity of glutathione S-transferase (GST) was higher than in the control cells at 48 h (P < 0.05).	diallyl trisulfide	52-56	hematopoietic prostaglandin D synthase	Rattus norvegicus	74-99
15051817-8	2004	When the hepatocytes were treated with 0.025 mmol/L DATS, the activity of glutathione S-transferase (GST) was higher than in the control cells at 48 h (P < 0.05).	diallyl trisulfide	52-56	hematopoietic prostaglandin D synthase	Rattus norvegicus	101-104
15051817-9	2004	In hepatocytes treated with 0.05 mmol/L DATS, the activity of GST and glutathione peroxidase (GPx) was higher than in the control cells (P < 0.05) at 24 and 48 h of incubation.	diallyl trisulfide	40-44	hematopoietic prostaglandin D synthase	Rattus norvegicus	62-65
15051817-10	2004	The results indicate that 0.025 or 0.05 mmol/L DATS could enhance antioxidation and detoxification capabilities by increasing the intracellular GSH level and the activity of GPx, GRd, or GST in rat primary hepatocytes.	diallyl trisulfide	47-51	glutathione-disulfide reductase	Rattus norvegicus	179-182
15051817-10	2004	The results indicate that 0.025 or 0.05 mmol/L DATS could enhance antioxidation and detoxification capabilities by increasing the intracellular GSH level and the activity of GPx, GRd, or GST in rat primary hepatocytes.	diallyl trisulfide	47-51	hematopoietic prostaglandin D synthase	Rattus norvegicus	187-190
15630193-6	2004	In the CCl4-induced acute liver injury model of rats, DATS (10 micromol/kg) significantly suppressed the increase in plasma lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activities.	diallyl trisulfide	54-58	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	184-187
15630193-8	2004	DATS significantly reduced the liver injury caused by CCl4.	diallyl trisulfide	0-4	C-C motif chemokine ligand 4	Rattus norvegicus	54-58
15630193-5	2004	DATS (10 micromol/kg) and DADS at a 10-fold higher dose (100 micromol/kg) significantly increased the activities of glutathione S-transferase (GST) and quinone reductase (QR); whereas DAS did not.	diallyl trisulfide	0-4	hematopoietic prostaglandin D synthase	Rattus norvegicus	116-141
15630193-5	2004	DATS (10 micromol/kg) and DADS at a 10-fold higher dose (100 micromol/kg) significantly increased the activities of glutathione S-transferase (GST) and quinone reductase (QR); whereas DAS did not.	diallyl trisulfide	0-4	hematopoietic prostaglandin D synthase	Rattus norvegicus	143-146
15630193-6	2004	In the CCl4-induced acute liver injury model of rats, DATS (10 micromol/kg) significantly suppressed the increase in plasma lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activities.	diallyl trisulfide	54-58	C-C motif chemokine ligand 4	Rattus norvegicus	7-11
15630193-6	2004	In the CCl4-induced acute liver injury model of rats, DATS (10 micromol/kg) significantly suppressed the increase in plasma lactate dehydrogenase (LDH) and aspartate aminotransferase (AST) activities.	diallyl trisulfide	54-58	glutamic-oxaloacetic transaminase 2	Rattus norvegicus	156-182
15203378-5	2004	IC50 for depentylation of 40 microM MPN by rat CYP2E1 was 5-12 microM for diallyl sulfide (DAS), diallyl disulfide (DADS), and PEITC and 10-20 microM for diallyl sulfone, allyl mercaptan, and diallyl trisulfide.	diallyl trisulfide	192-210	cytochrome P450, family 2, subfamily e, polypeptide 1	Rattus norvegicus	47-53
34558885-0	2021	Diallyl Trisulfide Suppresses High-Glucose-Induced Cardiomyocyte Apoptosis by Targeting Reactive Oxygen Species-Mediated Hypoxia-Inducible Factor-1alpha/Insulin-like Growth Factor Binding Protein 3 Activation.	diallyl trisulfide	0-18	insulin like growth factor binding protein 3	Homo sapiens	153-197
34848446-0	2021	Effect of Diallyl Trisulfide on TNF-alpha-induced CCL2/MCP-1 Release in Genetically Different Triple-negative Breast Cancer Cells.	diallyl trisulfide	10-28	C-C motif chemokine ligand 2	Homo sapiens	50-54
26056963-0	2015	Diallyl trisulfide protects against high glucose-induced cardiac apoptosis by stimulating the production of cystathionine gamma-lyase-derived hydrogen sulfide.	diallyl trisulfide	0-18	cystathionine gamma-lyase	Rattus norvegicus	108-133
26056963-2	2015	We investigated the effects of diallyl trisulfide (DATS) on CSE expression and H2S generation in myocardium and examined whether DATS-mediated H2S generation effectively protects rat heart from diabetes-induced cardiac damage.	diallyl trisulfide	51-55	cystathionine gamma-lyase	Rattus norvegicus	60-63
2843330-1	1988	Cytotoxic effects of allyl trisulfide (Alt, a synthetic chemical identical with one of the main active principles of garlic), 5 FU, MMC and DDP on SGC 7901 ( a moderately differentiated human gastric adenocarcinoma cell line) and MGC 803 (a poorly differentiated human gastric mucoadenocarcinoma cell line) had been reported before.	diallyl trisulfide	21-37	glutamic pyruvic transaminase, soluble	Mus musculus	39-42
35512572-0	2022	Monocarboxylate transporter 1 is a novel target for breast cancer stem like-cell inhibition by diallyl trisulfide.	diallyl trisulfide	95-113	solute carrier family 16 member 1	Homo sapiens	0-29
35512572-11	2022	In conclusion, the present study reveals that MCT1 is a novel target for bCSC inhibition by DATS treatment.	diallyl trisulfide	92-96	solute carrier family 16 member 1	Homo sapiens	46-50
33372687-0	2020	Diallyl trisulfide regulates cell apoptosis and invasion in human Osteosarcoma U2OS cells through regulating PI3K/AKT/GSK3beta signaling pathway.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	114-117
33854440-1	2021	Aim: The aim was to study the effect of Allitridum (Allicin) on the heterologous expression of the late sodium current on the DeltaKPQ-SCN5A mutations in HEK293 cells, with a view to screening new drugs for the treatment of long QT syndrome type 3 (LQT3).	diallyl trisulfide	40-50	sodium voltage-gated channel alpha subunit 5	Homo sapiens	135-140
33751676-0	2021	Diallyl trisulphide, a H2 S donor, compromises the stem cell phenotype and restores thyroid-specific gene expression in anaplastic thyroid carcinoma cells by targeting AKT-SOX2 axis.	diallyl trisulfide	0-19	AKT serine/threonine kinase 1	Homo sapiens	168-171
33751676-0	2021	Diallyl trisulphide, a H2 S donor, compromises the stem cell phenotype and restores thyroid-specific gene expression in anaplastic thyroid carcinoma cells by targeting AKT-SOX2 axis.	diallyl trisulfide	0-19	SRY-box transcription factor 2	Homo sapiens	172-176
33310503-7	2021	Rescuing H2S signaling in CSE-KO mice by Diallyl trisulfide (DATS) supplementation or reconstitution with endothelial cell specific CSE over-expression significantly reduced atrial superoxide, increased sulfide levels, and lowered AF inducibility.	diallyl trisulfide	41-59	cystathionase (cystathionine gamma-lyase)	Mus musculus	26-29
33310503-7	2021	Rescuing H2S signaling in CSE-KO mice by Diallyl trisulfide (DATS) supplementation or reconstitution with endothelial cell specific CSE over-expression significantly reduced atrial superoxide, increased sulfide levels, and lowered AF inducibility.	diallyl trisulfide	61-65	cystathionase (cystathionine gamma-lyase)	Mus musculus	26-29
33310503-8	2021	Lastly, low H2S levels in CSE KO mice was associated with atrial electrical remodeling including longer effective refractory periods, slower conduction velocity, increased myocyte calcium sparks, and increased myocyte action potential duration that were reversed by DATS supplementation or endothelial CSE overexpression.	diallyl trisulfide	266-270	cystathionase (cystathionine gamma-lyase)	Mus musculus	26-29
33310503-8	2021	Lastly, low H2S levels in CSE KO mice was associated with atrial electrical remodeling including longer effective refractory periods, slower conduction velocity, increased myocyte calcium sparks, and increased myocyte action potential duration that were reversed by DATS supplementation or endothelial CSE overexpression.	diallyl trisulfide	266-270	cystathionase (cystathionine gamma-lyase)	Mus musculus	302-305
33372687-0	2020	Diallyl trisulfide regulates cell apoptosis and invasion in human Osteosarcoma U2OS cells through regulating PI3K/AKT/GSK3beta signaling pathway.	diallyl trisulfide	0-18	glycogen synthase kinase 3 alpha	Homo sapiens	118-126
32745770-5	2020	Our results showed that DATS treatment led to a decrease in plasma levels of tumor necrosis factor-alpha (TNF-alpha) induced by DOX.	diallyl trisulfide	24-28	tumor necrosis factor	Rattus norvegicus	77-104
32745770-5	2020	Our results showed that DATS treatment led to a decrease in plasma levels of tumor necrosis factor-alpha (TNF-alpha) induced by DOX.	diallyl trisulfide	24-28	tumor necrosis factor	Rattus norvegicus	106-115
32853959-0	2020	Diallyl trisulfide potentiates chemotherapeutic efficacy of doxorubicin in experimentally induced mammary carcinoma: Role of Notch signaling.	diallyl trisulfide	0-18	notch 1	Mus musculus	125-130
32283691-0	2020	Diallyl Trisulfide (DATS) Suppresses AGE-Induced Cardiomyocyte Apoptosis by Targeting ROS-Mediated PKCdelta Activation.	diallyl trisulfide	0-18	renin binding protein	Rattus norvegicus	37-40
32606266-10	2020	Coadministration of ANA-12 (BDNF blocker) abolished pain attenuating actions as well as BDNF and the Nrf2 restorative actions of diallyl disulfide and diallyl trisulfide, without modulating H2S levels.	diallyl trisulfide	151-169	brain-derived neurotrophic factor	Rattus norvegicus	28-32
32606266-10	2020	Coadministration of ANA-12 (BDNF blocker) abolished pain attenuating actions as well as BDNF and the Nrf2 restorative actions of diallyl disulfide and diallyl trisulfide, without modulating H2S levels.	diallyl trisulfide	151-169	NFE2 like bZIP transcription factor 2	Rattus norvegicus	101-105
32606266-11	2020	Conclusions: Diallyl disulfide and diallyl trisulfide have the potential to attenuate neuropathic pain in CCI-subjected rats possibly through activation of H2S-BDNF-Nrf2 signaling pathway.	diallyl trisulfide	35-53	brain-derived neurotrophic factor	Rattus norvegicus	160-164
32606266-11	2020	Conclusions: Diallyl disulfide and diallyl trisulfide have the potential to attenuate neuropathic pain in CCI-subjected rats possibly through activation of H2S-BDNF-Nrf2 signaling pathway.	diallyl trisulfide	35-53	NFE2 like bZIP transcription factor 2	Rattus norvegicus	165-169
31984539-6	2020	Specifically, DATS treatment significantly upregulated the expression and enzymatic activity of cystathionine gamma-lyase (CTH), one of H2 S-producing enzymes, which was responsible for endogenous H2 S generation.	diallyl trisulfide	14-18	cystathionine gamma-lyase	Homo sapiens	96-121
31984539-6	2020	Specifically, DATS treatment significantly upregulated the expression and enzymatic activity of cystathionine gamma-lyase (CTH), one of H2 S-producing enzymes, which was responsible for endogenous H2 S generation.	diallyl trisulfide	14-18	cystathionine gamma-lyase	Homo sapiens	123-126
31984539-7	2020	After DATS treatment, H2 S quickly permeated cell membranes and activated NF-kappaBeta/p65 signaling pathway in KTC-1 cells.	diallyl trisulfide	6-10	nuclear factor kappa B subunit 1	Homo sapiens	74-86
32467084-0	2020	Retraction notice to "Diallyl trisulfide, a garlic polysulfide protects against As-induced renal oxidative nephrotoxicity, apoptosis and inflammation in rats by activating the Nrf2/ARE signaling pathway" [Int.	diallyl trisulfide	22-40	NFE2 like bZIP transcription factor 2	Rattus norvegicus	176-180
32283691-0	2020	Diallyl Trisulfide (DATS) Suppresses AGE-Induced Cardiomyocyte Apoptosis by Targeting ROS-Mediated PKCdelta Activation.	diallyl trisulfide	20-24	renin binding protein	Rattus norvegicus	37-40
31540440-0	2019	Diallyl Trisulfide Protects Rat Brain Tissue against the Damage Induced by Ischemia-Reperfusion through the Nrf2 Pathway.	diallyl trisulfide	0-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	108-112
32266174-0	2020	Diallyl Trisulfide Inhibits Leptin-induced Oncogenic Signaling in Human Breast Cancer Cells but Fails to Prevent Chemically-induced Luminal-type Cancer in Rats.	diallyl trisulfide	0-18	leptin	Homo sapiens	28-34
31927886-6	2020	Compared with DPTS, DATS potently inhibited platelet aggregation induced by thrombin, U46619, and collagen.	diallyl trisulfide	20-24	coagulation factor II	Mus musculus	76-84
31115753-0	2019	Diallyl trisulfide attenuates hyperglycemia-induced endothelial apoptosis by inhibition of Drp1-mediated mitochondrial fission.	diallyl trisulfide	0-18	dynamin 1 like	Homo sapiens	91-95
31115753-4	2019	RESULTS: DATS treatment significantly inhibited high glucose-induced HUVEC apoptosis by blockage of intracellular and mitochondrial ROS generation, maintenance of the mitochondrial membrane potential, and suppression of high glucose-induced dynamin-related protein 1 (Drp1) expression.	diallyl trisulfide	9-13	dynamin 1 like	Homo sapiens	241-266
31115753-4	2019	RESULTS: DATS treatment significantly inhibited high glucose-induced HUVEC apoptosis by blockage of intracellular and mitochondrial ROS generation, maintenance of the mitochondrial membrane potential, and suppression of high glucose-induced dynamin-related protein 1 (Drp1) expression.	diallyl trisulfide	9-13	dynamin 1 like	Homo sapiens	268-272
31115753-6	2019	CONCLUSIONS: DATS demonstrated the ability to inhibit high glucose-induced HUVEC apoptosis via suppression of Drp1-mediated mitochondrial fission in an AMPK-dependent fashion.	diallyl trisulfide	13-17	dynamin 1 like	Homo sapiens	110-114
31617531-6	2019	The phosphorylation of H2A.X, which is a DNA damage marker, was induced by DATS both in a dose- and time-dependent manner.	diallyl trisulfide	75-79	H2A.X variant histone	Homo sapiens	23-28
31617531-8	2019	DATS also induced G2/M cell-cycle arrest followed by the translocation of Cdc25C from the nucleus to the cytoplasm.	diallyl trisulfide	0-4	cell division cycle 25C	Homo sapiens	74-80
31617531-9	2019	Further results showed that DATS induced mitochondrial apoptosis in 8505C cells, evidenced by Hoechst/PI double staining, PI-Annexin V assay and western blot.	diallyl trisulfide	28-32	annexin A5	Homo sapiens	125-134
31540440-3	2019	Different compounds, such as diallyl trisulfide (DATS), have the ability to activate Nrf2.	diallyl trisulfide	29-47	NFE2 like bZIP transcription factor 2	Rattus norvegicus	85-89
31540440-3	2019	Different compounds, such as diallyl trisulfide (DATS), have the ability to activate Nrf2.	diallyl trisulfide	49-53	NFE2 like bZIP transcription factor 2	Rattus norvegicus	85-89
30378099-6	2019	On the other hand, after GJ function and Cx43 expression were increased by allicin, diallyl disulfide, or diallyl trisulfide, the impairment of NRK-52E cells by NaOx or other GJ inhibitors and the adhesion between CaOx crystals and renal cells decreased significantly.	diallyl trisulfide	106-124	gap junction protein, alpha 1	Rattus norvegicus	41-45
30682720-0	2019	Preventive effect of Diallyl Trisulfide on cutaneous toxicities induced by EGFR inhibitor.	diallyl trisulfide	21-39	epidermal growth factor receptor	Mus musculus	75-79
31092429-0	2019	Diallyl Trisulfide Enhances Benzo[a]pyrene-induced CYP1A1 Expression and Metabolic Activation in Hepatic HepG2 Cells.	diallyl trisulfide	0-18	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	51-57
31092429-5	2019	RESULTS: DATS enhanced BaP-induced CYP1A1 and CYP1B1 mRNA expression, BaP hydroxylation and BaP-DNA adduct formation.	diallyl trisulfide	9-13	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	35-41
31092429-5	2019	RESULTS: DATS enhanced BaP-induced CYP1A1 and CYP1B1 mRNA expression, BaP hydroxylation and BaP-DNA adduct formation.	diallyl trisulfide	9-13	cytochrome P450 family 1 subfamily B member 1	Homo sapiens	46-52
31092429-7	2019	DATS enhanced BaP-induced AHR recruitment and histone H3 acetylation on the CYP1A1 promoter.	diallyl trisulfide	0-4	aryl hydrocarbon receptor	Homo sapiens	26-29
31092429-7	2019	DATS enhanced BaP-induced AHR recruitment and histone H3 acetylation on the CYP1A1 promoter.	diallyl trisulfide	0-4	cytochrome P450 family 1 subfamily A member 1	Homo sapiens	76-82
31092429-8	2019	CONCLUSION: DATS combined treatment enhances BaP metabolic activation through an AHR-modulating mechanism.	diallyl trisulfide	12-16	aryl hydrocarbon receptor	Homo sapiens	81-84
30682720-11	2019	The release of TNF-alpha, IL-6 and other inflammatory factors was reduced by DATS.	diallyl trisulfide	77-81	tumor necrosis factor	Mus musculus	15-24
30682720-11	2019	The release of TNF-alpha, IL-6 and other inflammatory factors was reduced by DATS.	diallyl trisulfide	77-81	interleukin 6	Mus musculus	26-30
30863778-8	2019	In addition, Srx expression, MDA levels, and ROS levels in BGC823 cells were markedly inhibited upon treatment with diallyl trisulfide (DATS), a major constituent of garlic oil with proven anticancer effects.	diallyl trisulfide	116-134	sulfiredoxin 1	Homo sapiens	13-16
30863778-8	2019	In addition, Srx expression, MDA levels, and ROS levels in BGC823 cells were markedly inhibited upon treatment with diallyl trisulfide (DATS), a major constituent of garlic oil with proven anticancer effects.	diallyl trisulfide	136-140	sulfiredoxin 1	Homo sapiens	13-16
30301827-9	2019	Mechanistically, MZF1 was upregulated in both GC and GES-1 cells by MT2A ectopically expressed or induced upon treatment with a garlic-derived compound, diallyl trisulfide (DATS).	diallyl trisulfide	153-171	myeloid zinc finger 1	Homo sapiens	17-21
30301827-9	2019	Mechanistically, MZF1 was upregulated in both GC and GES-1 cells by MT2A ectopically expressed or induced upon treatment with a garlic-derived compound, diallyl trisulfide (DATS).	diallyl trisulfide	153-171	metallothionein 2A	Homo sapiens	68-72
30301827-9	2019	Mechanistically, MZF1 was upregulated in both GC and GES-1 cells by MT2A ectopically expressed or induced upon treatment with a garlic-derived compound, diallyl trisulfide (DATS).	diallyl trisulfide	173-177	myeloid zinc finger 1	Homo sapiens	17-21
30725425-6	2019	A deficiency of dietary sulfur amino acids downregulates cystathionine synthase, causing hyperhomocysteinemia.The organic sulfur compound diallyl trisulfide increases hydrogen sulfide production from homocysteine in animal models, inhibits Stat3 signaling in cancer stem cells, and produces apoptosis of malignant cells.	diallyl trisulfide	138-156	signal transducer and activator of transcription 3	Homo sapiens	240-245
30209569-9	2018	Western blotting showed that DATS was associated with increases in histone acetylation (Ac-Histone H3/H4) and activated caspase-3 in this novel preclinical model.	diallyl trisulfide	29-33	caspase 3	Homo sapiens	120-129
30370258-0	2018	Diallyl Trisulfide Suppresses the Production of Lipopolysaccharide-induced Inflammatory Mediators in BV2 Microglia by Decreasing the NF-kappaB Pathway Activity Associated With Toll-like Receptor 4 and CXCL12/CXCR4 Pathway Blockade.	diallyl trisulfide	0-18	toll-like receptor 4	Mus musculus	176-196
30317421-0	2018	Diallyl Trisulfide Protects Motor Neurons from the Neurotoxic Protein TDP-43 via Activating Lysosomal Degradation and the Antioxidant Response.	diallyl trisulfide	0-18	TAR DNA binding protein	Mus musculus	70-76
30317421-5	2018	Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments.	diallyl trisulfide	90-108	TAR DNA binding protein	Mus musculus	78-84
30317421-5	2018	Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments.	diallyl trisulfide	90-108	TAR DNA binding protein	Mus musculus	170-176
30317421-5	2018	Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments.	diallyl trisulfide	90-108	TAR DNA binding protein	Mus musculus	170-176
30317421-5	2018	Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments.	diallyl trisulfide	110-114	TAR DNA binding protein	Mus musculus	78-84
30317421-5	2018	Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments.	diallyl trisulfide	110-114	TAR DNA binding protein	Mus musculus	170-176
30317421-5	2018	Here we report that treatment of motor neuron-like NSC34 cells overexpressing TDP-43 with diallyl trisulfide (DATS) induced neuronal autophagy and lysosomal clearance of TDP-43 and C-terminal TDP-43 fragments.	diallyl trisulfide	110-114	TAR DNA binding protein	Mus musculus	170-176
30317421-7	2018	Consequently, DATS suppressed the increase in the levels of reactive oxygen species induced by TDP-43 expression.	diallyl trisulfide	14-18	TAR DNA binding protein	Mus musculus	95-101
30370258-0	2018	Diallyl Trisulfide Suppresses the Production of Lipopolysaccharide-induced Inflammatory Mediators in BV2 Microglia by Decreasing the NF-kappaB Pathway Activity Associated With Toll-like Receptor 4 and CXCL12/CXCR4 Pathway Blockade.	diallyl trisulfide	0-18	chemokine (C-X-C motif) ligand 12	Mus musculus	201-207
30370258-0	2018	Diallyl Trisulfide Suppresses the Production of Lipopolysaccharide-induced Inflammatory Mediators in BV2 Microglia by Decreasing the NF-kappaB Pathway Activity Associated With Toll-like Receptor 4 and CXCL12/CXCR4 Pathway Blockade.	diallyl trisulfide	0-18	chemokine (C-X-C motif) receptor 4	Mus musculus	208-213
30370258-10	2018	Conclusions: These results indicate that DATS inhibits the activation of the CXCL12/CXCR4 axis associated with antagonizing effect on TLR4 and blocks NF-kappaB signaling, thus demonstrating anti-inflammatory effects against LPS stimulation.	diallyl trisulfide	41-45	chemokine (C-X-C motif) ligand 12	Mus musculus	77-83
30370258-10	2018	Conclusions: These results indicate that DATS inhibits the activation of the CXCL12/CXCR4 axis associated with antagonizing effect on TLR4 and blocks NF-kappaB signaling, thus demonstrating anti-inflammatory effects against LPS stimulation.	diallyl trisulfide	41-45	chemokine (C-X-C motif) receptor 4	Mus musculus	84-89
30370258-10	2018	Conclusions: These results indicate that DATS inhibits the activation of the CXCL12/CXCR4 axis associated with antagonizing effect on TLR4 and blocks NF-kappaB signaling, thus demonstrating anti-inflammatory effects against LPS stimulation.	diallyl trisulfide	41-45	toll-like receptor 4	Mus musculus	134-138
28680385-9	2017	Through microarray gene expression analysis, ANGPTL4, PLCXD1, and MMP3 were identified as candidates of molecular targets of DATS.	diallyl trisulfide	125-129	angiopoietin like 4	Homo sapiens	45-52
29786427-0	2018	Induction of Apoptosis in Human Papillary-Thyroid-Carcinoma BCPAP Cells by Diallyl Trisulfide through Activation of the MAPK Signaling Pathway.	diallyl trisulfide	75-93	mitogen-activated protein kinase 1	Homo sapiens	120-124
29786427-6	2018	Moreover, ERK and JNK inhibitors partially reversed apoptosis in BCPAP cells induced by DATS treatment.	diallyl trisulfide	88-92	mitogen-activated protein kinase 1	Homo sapiens	10-13
29786427-6	2018	Moreover, ERK and JNK inhibitors partially reversed apoptosis in BCPAP cells induced by DATS treatment.	diallyl trisulfide	88-92	mitogen-activated protein kinase 8	Homo sapiens	18-21
29786427-7	2018	Taken together, our results demonstrated that DATS exerted an apoptosis-inducing effect on papillary-thyroid-cancer cells via activation of the MAPK signaling pathway, which shed light on a prospective therapeutic target for thyroid-cancer treatment.	diallyl trisulfide	46-50	mitogen-activated protein kinase 1	Homo sapiens	144-148
29594332-0	2018	Wnt/beta-catenin signaling mediates the suppressive effects of diallyl trisulfide on colorectal cancer stem cells.	diallyl trisulfide	63-81	catenin beta 1	Homo sapiens	4-16
29844798-0	2018	Treatment of Saos-2 osteosarcoma cells with diallyl trisulfide is associated with an increase in calreticulin expression.	diallyl trisulfide	44-62	calreticulin	Homo sapiens	97-109
29844798-8	2018	The levels of CRT mRNA and protein in the Saos-2 cells were significantly upregulated following exposure to DATS.	diallyl trisulfide	108-112	calreticulin	Homo sapiens	14-17
29844798-9	2018	The upregulation of CRT expression by DATS may be a mechanism underlying the ability of DATS to inhibit the growth of human osteosarcoma Saos-2 cells.	diallyl trisulfide	38-42	calreticulin	Homo sapiens	20-23
29844798-9	2018	The upregulation of CRT expression by DATS may be a mechanism underlying the ability of DATS to inhibit the growth of human osteosarcoma Saos-2 cells.	diallyl trisulfide	88-92	calreticulin	Homo sapiens	20-23
30396169-0	2018	Targeting Thioredoxin System with an Organosulfur Compound, Diallyl Trisulfide (DATS), Attenuates Progression and Metastasis of Triple-Negative Breast Cancer (TNBC).	diallyl trisulfide	60-78	thioredoxin	Homo sapiens	10-21
30396169-0	2018	Targeting Thioredoxin System with an Organosulfur Compound, Diallyl Trisulfide (DATS), Attenuates Progression and Metastasis of Triple-Negative Breast Cancer (TNBC).	diallyl trisulfide	80-84	thioredoxin	Homo sapiens	10-21
30396169-3	2018	Here, we identified an organosulfur compound named DATS isolated from garlic, that inhibits the expression of Trx-1 and the enzyme activity of Trx reductase in breast cancer cells.	diallyl trisulfide	51-55	thioredoxin	Homo sapiens	110-115
30396169-3	2018	Here, we identified an organosulfur compound named DATS isolated from garlic, that inhibits the expression of Trx-1 and the enzyme activity of Trx reductase in breast cancer cells.	diallyl trisulfide	51-55	thioredoxin	Homo sapiens	110-113
28810199-12	2017	In summary, we demonstrated that benzene-induced cytopenia was related to the apoptosis of PBMCs and BMCs, and DATS treatment could prevent benzene-induced cytopenia by suppressing oxidative stress-mediated cell apoptosis via the PI3K/Akt pathway.	diallyl trisulfide	111-115	AKT serine/threonine kinase 1	Rattus norvegicus	235-238
28741790-9	2017	Subsequently, DATS induced a strong decrease in total FAK, phosphorylated FAK Tyr-397,-576, -577, and disorganized F-actin stress fibers, resulting in a nonmigratory phenotype.	diallyl trisulfide	14-18	protein tyrosine kinase 2	Homo sapiens	54-57
28741790-9	2017	Subsequently, DATS induced a strong decrease in total FAK, phosphorylated FAK Tyr-397,-576, -577, and disorganized F-actin stress fibers, resulting in a nonmigratory phenotype.	diallyl trisulfide	14-18	protein tyrosine kinase 2	Homo sapiens	74-77
28753455-7	2017	Moreover, DATS provoked intracellular ROS generation and the loss of mitochondrial membrane potential, and in particular, when ROS production was blocked by antioxidant N-acety-l-cysteine, both AMPK activation and growth inhibition by DATS were completely abolished.	diallyl trisulfide	10-14	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	194-198
28753455-7	2017	Moreover, DATS provoked intracellular ROS generation and the loss of mitochondrial membrane potential, and in particular, when ROS production was blocked by antioxidant N-acety-l-cysteine, both AMPK activation and growth inhibition by DATS were completely abolished.	diallyl trisulfide	235-239	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	194-198
28753455-8	2017	Collectively, these findings suggest that DATS inhibited growth of AGS cells, which was mediated by complex interplay between cellular mechanisms governing redox homeostasis, apoptosis, and cell cycle arrest, through a ROS-dependent activation of AMPK pathway.	diallyl trisulfide	42-46	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	247-251
28648972-0	2017	Diallyl trisulfide, a garlic polysulfide protects against As-induced renal oxidative nephrotoxicity, apoptosis and inflammation in rats by activating the Nrf2/ARE signaling pathway.	diallyl trisulfide	0-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	154-158
28992023-10	2017	Based on the results from the current study, DADS + DATS can ameliorate oxidative effects of hydrogen peroxide, as well as alter IL-8 secretion in LPS-treated IPEC-J2 cells.	diallyl trisulfide	52-56	C-X-C motif chemokine ligand 8	Sus scrofa	129-133
29088824-0	2017	Diallyl trisulfide exerts cardioprotection against myocardial ischemia-reperfusion injury in diabetic state, role of AMPK-mediated AKT/GSK-3beta/HIF-1alpha activation.	diallyl trisulfide	0-18	protein kinase AMP-activated catalytic subunit alpha 2	Rattus norvegicus	117-121
29088824-0	2017	Diallyl trisulfide exerts cardioprotection against myocardial ischemia-reperfusion injury in diabetic state, role of AMPK-mediated AKT/GSK-3beta/HIF-1alpha activation.	diallyl trisulfide	0-18	glycogen synthase kinase 3 beta	Rattus norvegicus	135-144
29088824-0	2017	Diallyl trisulfide exerts cardioprotection against myocardial ischemia-reperfusion injury in diabetic state, role of AMPK-mediated AKT/GSK-3beta/HIF-1alpha activation.	diallyl trisulfide	0-18	hypoxia inducible factor 1 subunit alpha	Rattus norvegicus	145-155
28344324-5	2017	DATS (50-200 mumol/L) induced cell cycle arrest at G2/M phase in BGC-823 cells, which correlated with significant accumulation of cyclin A2 and B1.	diallyl trisulfide	0-4	cyclin A2	Homo sapiens	130-139
28344324-9	2017	We showed that treatment of BGC-823 cells with DATS in vitro and in vivo significantly activated kinases such as p38 and JNK/MAPK and attenuated the Nrf2/Akt pathway.	diallyl trisulfide	47-51	mitogen-activated protein kinase 14	Homo sapiens	113-116
28344324-9	2017	We showed that treatment of BGC-823 cells with DATS in vitro and in vivo significantly activated kinases such as p38 and JNK/MAPK and attenuated the Nrf2/Akt pathway.	diallyl trisulfide	47-51	mitogen-activated protein kinase 8	Homo sapiens	121-124
28344324-9	2017	We showed that treatment of BGC-823 cells with DATS in vitro and in vivo significantly activated kinases such as p38 and JNK/MAPK and attenuated the Nrf2/Akt pathway.	diallyl trisulfide	47-51	NFE2 like bZIP transcription factor 2	Homo sapiens	149-153
28344324-9	2017	We showed that treatment of BGC-823 cells with DATS in vitro and in vivo significantly activated kinases such as p38 and JNK/MAPK and attenuated the Nrf2/Akt pathway.	diallyl trisulfide	47-51	AKT serine/threonine kinase 1	Homo sapiens	154-157
29594332-11	2018	Moreover, DATS suppressed the activity of Wnt/beta-catenin pathway, while upregulation of Wnt/beta-catenin diminished the inhibitory effect of DATS on colorectal CSCs.	diallyl trisulfide	10-14	catenin beta 1	Homo sapiens	46-58
29594332-12	2018	CONCLUSIONS: Wnt/beta-catenin pathway mediates DATS-induced colorectal CSCs suppression.	diallyl trisulfide	47-51	catenin beta 1	Homo sapiens	17-29
29713750-0	2018	Correction to: Wnt/beta-catenin signaling mediates the suppressive effects of diallyl trisulfide on colorectal cancer stem cells.	diallyl trisulfide	78-96	catenin beta 1	Homo sapiens	19-31
29386905-0	2018	Experimental study of inhibitory effects of diallyl trisulfide on the growth of human osteosarcoma Saos-2 cells by downregulating expression of glucose-regulated protein 78.	diallyl trisulfide	44-62	heat shock protein family A (Hsp70) member 5	Homo sapiens	144-172
29386905-2	2018	There are many studies pointing out that DATS can downregulate expression of the glucose-regulated protein 78 (GRP78), which is associated with poor prognosis and drug resistance in various types of human cancers.	diallyl trisulfide	41-45	heat shock protein family A (Hsp70) member 5	Homo sapiens	81-109
29386905-2	2018	There are many studies pointing out that DATS can downregulate expression of the glucose-regulated protein 78 (GRP78), which is associated with poor prognosis and drug resistance in various types of human cancers.	diallyl trisulfide	41-45	heat shock protein family A (Hsp70) member 5	Homo sapiens	111-116
29386905-8	2018	Results: The expression level of GRP78 mRNA and proteins was significantly downregulated due to the increased concentration and effective times of DATS (P<0.05).	diallyl trisulfide	147-151	heat shock protein family A (Hsp70) member 5	Homo sapiens	33-38
29386905-9	2018	In addition, there were significant associations between GRP78 silencing and cell proliferation (P<0.05) of DATS treatment.	diallyl trisulfide	111-115	heat shock protein family A (Hsp70) member 5	Homo sapiens	57-62
29386905-10	2018	Conclusion: These results indicate that DATS inhibits the growth of human osteosarcoma Saos-2 cells by downregulating the expression of GRP78.	diallyl trisulfide	40-44	heat shock protein family A (Hsp70) member 5	Homo sapiens	136-141
30396169-6	2018	Western blot, immunofluorescence, redox state assessment and detection of enzyme activity were employed to determine the effect of DATS on thioredoxin system.	diallyl trisulfide	131-135	thioredoxin	Homo sapiens	139-150
30396169-7	2018	Trx-1 siRNA interference was used to investigate the conclusive evidence that Trx-1 was the target of DATS.	diallyl trisulfide	102-106	thioredoxin	Homo sapiens	0-5
30396169-7	2018	Trx-1 siRNA interference was used to investigate the conclusive evidence that Trx-1 was the target of DATS.	diallyl trisulfide	102-106	thioredoxin	Homo sapiens	78-83
30396169-8	2018	RESULTS: In agreement with reduced Trx-1 nuclear translocation from cytoplasm by DATS, the production of reduced form of Trx-1 was dramatically decreased.	diallyl trisulfide	81-85	thioredoxin	Homo sapiens	35-40
30396169-11	2018	Notably, the effects of DATS on the expression of downstream metastasis-associated genes were mediated by Trx-1, as demonstrated by the combination use of DATS and Trx-1 siRNA.	diallyl trisulfide	24-28	thioredoxin	Homo sapiens	106-111
30396169-11	2018	Notably, the effects of DATS on the expression of downstream metastasis-associated genes were mediated by Trx-1, as demonstrated by the combination use of DATS and Trx-1 siRNA.	diallyl trisulfide	24-28	thioredoxin	Homo sapiens	164-169
30396169-11	2018	Notably, the effects of DATS on the expression of downstream metastasis-associated genes were mediated by Trx-1, as demonstrated by the combination use of DATS and Trx-1 siRNA.	diallyl trisulfide	155-159	thioredoxin	Homo sapiens	106-111
30396169-12	2018	CONCLUSION: Collectively, this present study indicates that targeting Trx system with DATS may provide a promising strategy for treating metastasis of TNBC.	diallyl trisulfide	86-90	thioredoxin	Homo sapiens	70-73
28815294-0	2017	Diallyl trisulfide inhibits proliferation, invasion and angiogenesis of glioma cells by inactivating Wnt/beta-catenin signaling.	diallyl trisulfide	0-18	catenin beta 1	Homo sapiens	105-117
28815294-7	2017	Consistent with the previous results, diallyl trisulfide inhibited proliferation, invasion and angiogenesis in glioma cells by suppressing Wnt/beta-catenin signaling.	diallyl trisulfide	38-56	catenin beta 1	Homo sapiens	143-155
28852876-3	2017	The inhibition of proliferation of the investigated cells by DATS was correlated with an increase in the inactivated form of Bcl-2.	diallyl trisulfide	61-65	BCL2 apoptosis regulator	Homo sapiens	125-130
28852876-6	2017	MPST and rhodanese, the level of which is increased in the presence of DATS, can serve as antioxidant proteins.	diallyl trisulfide	71-75	mercaptopyruvate sulfurtransferase	Homo sapiens	0-4
29056905-7	2017	Diallyl trisulfide and napabucasin inhibit the signaling by the signal transducer and activator of transcription 3 (Stat3), potentially enhancing immune function by effects on T helper lymphocytes and promotion of apoptosis.	diallyl trisulfide	0-18	signal transducer and activator of transcription 3	Homo sapiens	64-114
29056905-7	2017	Diallyl trisulfide and napabucasin inhibit the signaling by the signal transducer and activator of transcription 3 (Stat3), potentially enhancing immune function by effects on T helper lymphocytes and promotion of apoptosis.	diallyl trisulfide	0-18	signal transducer and activator of transcription 3	Homo sapiens	116-121
28753455-0	2017	Diallyl trisulfide induces apoptosis and mitotic arrest in AGS human gastric carcinoma cells through reactive oxygen species-mediated activation of AMP-activated protein kinase.	diallyl trisulfide	0-18	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	148-176
28753455-3	2017	In this study, we investigated the role of ROS on the activation of AMP-activated protein kinase (AMPK) in DATS-induced apoptosis and cell cycle arrest in AGS human gastric carcinoma cells.	diallyl trisulfide	107-111	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	68-96
28753455-3	2017	In this study, we investigated the role of ROS on the activation of AMP-activated protein kinase (AMPK) in DATS-induced apoptosis and cell cycle arrest in AGS human gastric carcinoma cells.	diallyl trisulfide	107-111	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	98-102
28753455-4	2017	The results of the present study indicate that DATS inhibited proliferation of AGS cells by promoting apoptosis, and accumulating cellular portion of G2/M phase via the induction of cyclin B1 and cyclin-dependent kinase p21(WAF1/CIP1).	diallyl trisulfide	47-51	cyclin B1	Homo sapiens	182-191
28753455-4	2017	The results of the present study indicate that DATS inhibited proliferation of AGS cells by promoting apoptosis, and accumulating cellular portion of G2/M phase via the induction of cyclin B1 and cyclin-dependent kinase p21(WAF1/CIP1).	diallyl trisulfide	47-51	cyclin dependent kinase inhibitor 1A	Homo sapiens	196-233
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	27-31	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	72-76
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	27-31	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	27-31	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	27-31	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	72-76
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	72-76
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28753455-6	2017	Furthermore, we found that DATS concurrently induced phosphorylation of AMPK; however, chemical inhibition of AMPK by compound C, an AMPK inhibitor, significantly blocked apoptosis induced by DATS, suggesting that DATS induces cytotoxicity of AGS cells through the AMPK-dependent pathway.	diallyl trisulfide	192-196	protein kinase AMP-activated catalytic subunit alpha 1	Homo sapiens	110-114
28574600-0	2017	Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF-1alpha synthesis, and decreases breast cancer metastasis.	diallyl trisulfide	0-19	histone deacetylase 9	Homo sapiens	31-50
28574600-0	2017	Diallyl trisulfides, a natural histone deacetylase inhibitor, attenuate HIF-1alpha synthesis, and decreases breast cancer metastasis.	diallyl trisulfide	0-19	hypoxia inducible factor 1 subunit alpha	Homo sapiens	72-82
28574600-9	2017	The expressions of L1CAM, VEGF-A, and EMT-related proteins (Slug, Snail, MMP-2) were inhibited by DATS.	diallyl trisulfide	98-102	L1 cell adhesion molecule	Homo sapiens	19-24
28574600-9	2017	The expressions of L1CAM, VEGF-A, and EMT-related proteins (Slug, Snail, MMP-2) were inhibited by DATS.	diallyl trisulfide	98-102	vascular endothelial growth factor A	Homo sapiens	26-32
28574600-9	2017	The expressions of L1CAM, VEGF-A, and EMT-related proteins (Slug, Snail, MMP-2) were inhibited by DATS.	diallyl trisulfide	98-102	snail family transcriptional repressor 2	Homo sapiens	60-64
28574600-9	2017	The expressions of L1CAM, VEGF-A, and EMT-related proteins (Slug, Snail, MMP-2) were inhibited by DATS.	diallyl trisulfide	98-102	snail family transcriptional repressor 1	Homo sapiens	66-71
28574600-9	2017	The expressions of L1CAM, VEGF-A, and EMT-related proteins (Slug, Snail, MMP-2) were inhibited by DATS.	diallyl trisulfide	98-102	matrix metallopeptidase 2	Homo sapiens	73-78
28574600-10	2017	DATS dose-dependently inhibited HIF-1alpha transcriptional activity and hypoxia-induced hematogenous metastasis of MDA-MB-231 cells.	diallyl trisulfide	0-4	hypoxia inducible factor 1 subunit alpha	Homo sapiens	32-42
28571773-3	2017	Here we present that in combination with diallyl trisulfide (DATS), exposure to TRAIL induced apoptosis in TRAIL-resistant glioma cells.	diallyl trisulfide	41-59	TNF superfamily member 10	Homo sapiens	80-85
28571773-3	2017	Here we present that in combination with diallyl trisulfide (DATS), exposure to TRAIL induced apoptosis in TRAIL-resistant glioma cells.	diallyl trisulfide	41-59	TNF superfamily member 10	Homo sapiens	107-112
28571773-3	2017	Here we present that in combination with diallyl trisulfide (DATS), exposure to TRAIL induced apoptosis in TRAIL-resistant glioma cells.	diallyl trisulfide	61-65	TNF superfamily member 10	Homo sapiens	80-85
28571773-3	2017	Here we present that in combination with diallyl trisulfide (DATS), exposure to TRAIL induced apoptosis in TRAIL-resistant glioma cells.	diallyl trisulfide	61-65	TNF superfamily member 10	Homo sapiens	107-112
28571773-4	2017	Surprisingly, we found that subtoxic concentrations of DATS significantly potentiated TRAIL-induced cytotoxicity and apoptosis in glioma cells.	diallyl trisulfide	55-59	TNF superfamily member 10	Homo sapiens	86-91
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	diallyl trisulfide	13-17	TNF superfamily member 10	Homo sapiens	27-32
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	diallyl trisulfide	13-17	MCL1 apoptosis regulator, BCL2 family member	Homo sapiens	105-110
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	diallyl trisulfide	13-17	TNF receptor superfamily member 10b	Homo sapiens	136-139
28571773-6	2017	In addition, DATS enhances TRAIL-induced apoptosis through the downregulation of anti-apoptotic protein (Mcl-1) and the upregulation of DR5 receptors through actions on the ROS- induced-p53.	diallyl trisulfide	13-17	tumor protein p53	Homo sapiens	186-189
28344324-0	2017	Diallyl trisulfide suppresses tumor growth through the attenuation of Nrf2/Akt and activation of p38/JNK and potentiates cisplatin efficacy in gastric cancer treatment.	diallyl trisulfide	0-18	NFE2 like bZIP transcription factor 2	Homo sapiens	70-74
28344324-0	2017	Diallyl trisulfide suppresses tumor growth through the attenuation of Nrf2/Akt and activation of p38/JNK and potentiates cisplatin efficacy in gastric cancer treatment.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	75-78
28344324-0	2017	Diallyl trisulfide suppresses tumor growth through the attenuation of Nrf2/Akt and activation of p38/JNK and potentiates cisplatin efficacy in gastric cancer treatment.	diallyl trisulfide	0-18	mitogen-activated protein kinase 14	Homo sapiens	97-100
28344324-0	2017	Diallyl trisulfide suppresses tumor growth through the attenuation of Nrf2/Akt and activation of p38/JNK and potentiates cisplatin efficacy in gastric cancer treatment.	diallyl trisulfide	0-18	mitogen-activated protein kinase 8	Homo sapiens	101-104
28455824-0	2017	Diallyl trisulfide ameliorates myocardial ischemia-reperfusion injury by reducing oxidative stress and endoplasmic reticulum stress-mediated apoptosis in type 1 diabetic rats: role of SIRT1 activation.	diallyl trisulfide	0-18	sirtuin 1	Rattus norvegicus	184-189
28455824-3	2017	We hypothesize that DATS reduces diabetic MI/R injury by activating SIRT1 signaling.	diallyl trisulfide	20-24	sirtuin 1	Rattus norvegicus	68-73
28455824-9	2017	Additionally, PERK/eIF2alpha/ATF4/CHOP-mediated ER stress-induced apoptosis was suppressed by DATS treatment.	diallyl trisulfide	94-98	eukaryotic translation initiation factor 2A	Rattus norvegicus	19-28
28455824-9	2017	Additionally, PERK/eIF2alpha/ATF4/CHOP-mediated ER stress-induced apoptosis was suppressed by DATS treatment.	diallyl trisulfide	94-98	activating transcription factor 4	Rattus norvegicus	29-33
28455824-9	2017	Additionally, PERK/eIF2alpha/ATF4/CHOP-mediated ER stress-induced apoptosis was suppressed by DATS treatment.	diallyl trisulfide	94-98	DNA-damage inducible transcript 3	Rattus norvegicus	34-38
28455824-12	2017	Taken together, these data suggest that perioperative DATS treatment effectively ameliorates MI/R injury in type 1 diabetic setting by enhancing cardiac SIRT1 signaling.	diallyl trisulfide	54-58	sirtuin 1	Rattus norvegicus	153-158
28501767-6	2017	Besides, activation of JNK, ERK and p38 phosphorylation in DATS-treated cells suggested that mitogen-activated protein kinase (MAPKs) pathways were involved in DATS-induced apoptosis.	diallyl trisulfide	59-63	mitogen-activated protein kinase 8	Homo sapiens	23-26
28501767-6	2017	Besides, activation of JNK, ERK and p38 phosphorylation in DATS-treated cells suggested that mitogen-activated protein kinase (MAPKs) pathways were involved in DATS-induced apoptosis.	diallyl trisulfide	59-63	mitogen-activated protein kinase 14	Homo sapiens	36-39
28501767-7	2017	Meanwhile, DATS significantly inhibited tumor growth and promoted tumor apoptosis in a xenograft model of gastric cancer cell SGC-7901.	diallyl trisulfide	11-15	sarcoglycan beta	Homo sapiens	126-129
28501767-8	2017	DATS inhibited tumor migration and invasion by modulating MMP9 and E-cadherin protein expressions.	diallyl trisulfide	0-4	matrix metallopeptidase 9	Homo sapiens	58-62
28501767-8	2017	DATS inhibited tumor migration and invasion by modulating MMP9 and E-cadherin protein expressions.	diallyl trisulfide	0-4	cadherin 1	Homo sapiens	67-77
28501767-9	2017	In addition, DATS treatment evidently increased the cytokine secretions of IL-12, TNF-alpha and IFN-gamma (p<0.05).	diallyl trisulfide	13-17	tumor necrosis factor	Homo sapiens	82-91
28501767-9	2017	In addition, DATS treatment evidently increased the cytokine secretions of IL-12, TNF-alpha and IFN-gamma (p<0.05).	diallyl trisulfide	13-17	interferon gamma	Homo sapiens	96-105
28680385-10	2017	Introduction of each gene to EJ cells revealed that ANGPTL4 was associated with the DATS-induced inhibition of cell growth, migration, and invasion.	diallyl trisulfide	84-88	angiopoietin like 4	Homo sapiens	52-59
28680385-11	2017	Conclusions: ANGPTL4 regulates DATS-mediated inhibition of proliferation, migration, and invasion of EJ cells, and thus, has potential as a prognostic marker for bladder cancer patients.	diallyl trisulfide	31-35	angiopoietin like 4	Homo sapiens	13-20
28440392-5	2017	It was also found that DATS suppressed the migration and invasion of MDA-MB-231 cells in the presence of platelets activated by PAF in vitro in a dose-dependent manner.	diallyl trisulfide	23-27	PCNA clamp associated factor	Homo sapiens	128-131
28440392-6	2017	Furthermore, our results revealed thaat the release of activated TGF-beta1 in the platelet-tumor cell system was markedly attenuated by DATS.	diallyl trisulfide	136-140	transforming growth factor beta 1	Homo sapiens	65-74
28255269-9	2017	In addition, increased E-cadherin and decreased MMP-9 expression levels were observed in DATS-treated tumor tissues.	diallyl trisulfide	89-93	cadherin 1	Homo sapiens	23-33
28216514-0	2017	Diallyl Trisulfide Augments Ischemia-Induced Angiogenesis via an Endothelial Nitric Oxide Synthase-Dependent Mechanism.	diallyl trisulfide	0-18	nitric oxide synthase 3, endothelial cell	Mus musculus	65-98
28216514-7	2017	DATS also increased the phosphorylation of Akt and eNOS in ischemic muscles.	diallyl trisulfide	0-4	thymoma viral proto-oncogene 1	Mus musculus	43-46
28216514-9	2017	In cultured human umbilical vein endothelium cells, DATS decreased apoptotic activity and oxidative stress under hypoxic conditions, and stimulated the phosphorylation of Akt and eNOS.	diallyl trisulfide	52-56	AKT serine/threonine kinase 1	Homo sapiens	171-174
28216514-10	2017	Inhibition of Akt or NOS signaling reversed DATS-stimulated eNOS phosphorylation and blocked the effects of DATS on apoptosis and oxidative stress.	diallyl trisulfide	44-48	thymoma viral proto-oncogene 1	Mus musculus	14-17
28216514-10	2017	Inhibition of Akt or NOS signaling reversed DATS-stimulated eNOS phosphorylation and blocked the effects of DATS on apoptosis and oxidative stress.	diallyl trisulfide	108-112	thymoma viral proto-oncogene 1	Mus musculus	14-17
28216514-11	2017	CONCLUSIONS: These observations suggest that DATS promotes revascularization in response to HLI through its ability to stimulate the Akt-eNOS signaling pathway.	diallyl trisulfide	45-49	thymoma viral proto-oncogene 1	Mus musculus	133-136
28161636-8	2017	Furthermore, we show that DATS inhibits the Notch ligands Jagged-1 and Jagged-2 involved in activation of Notch signaling pathway.	diallyl trisulfide	26-30	jagged canonical Notch ligand 1	Homo sapiens	58-66
28161636-8	2017	Furthermore, we show that DATS inhibits the Notch ligands Jagged-1 and Jagged-2 involved in activation of Notch signaling pathway.	diallyl trisulfide	26-30	jagged canonical Notch ligand 2	Homo sapiens	71-79
27566995-4	2017	Here, we show that the action of DATS is associated with downregulation of lactate dehydrogenase A (LDHA), an essential protein of the Warburg effect whose upregulation is closely related to tumorigenesis.	diallyl trisulfide	33-37	lactate dehydrogenase A	Homo sapiens	75-98
27566995-4	2017	Here, we show that the action of DATS is associated with downregulation of lactate dehydrogenase A (LDHA), an essential protein of the Warburg effect whose upregulation is closely related to tumorigenesis.	diallyl trisulfide	33-37	lactate dehydrogenase A	Homo sapiens	100-104
28218609-0	2017	Antioxidative effects of diallyl trisulfide on hydrogen peroxide-induced cytotoxicity through regulation of nuclear factor-E2-related factor-mediated thioredoxin reductase 1 expression in C2C12 skeletal muscle myoblast cells.	diallyl trisulfide	25-43	thioredoxin reductase 1	Mus musculus	150-173
28218609-4	2017	Treatment with DATS alone effectively upregulated the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and thioredoxin reductase 1 (TrxR1), which was associated with the increased phosphorylation of Nrf2.	diallyl trisulfide	15-19	nuclear factor, erythroid derived 2, like 2	Mus musculus	68-111
28218609-4	2017	Treatment with DATS alone effectively upregulated the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and thioredoxin reductase 1 (TrxR1), which was associated with the increased phosphorylation of Nrf2.	diallyl trisulfide	15-19	nuclear factor, erythroid derived 2, like 2	Mus musculus	113-117
28218609-4	2017	Treatment with DATS alone effectively upregulated the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and thioredoxin reductase 1 (TrxR1), which was associated with the increased phosphorylation of Nrf2.	diallyl trisulfide	15-19	thioredoxin reductase 1	Mus musculus	123-146
28218609-4	2017	Treatment with DATS alone effectively upregulated the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and thioredoxin reductase 1 (TrxR1), which was associated with the increased phosphorylation of Nrf2.	diallyl trisulfide	15-19	thioredoxin reductase 1	Mus musculus	148-153
28218609-4	2017	Treatment with DATS alone effectively upregulated the expression of nuclear factor-erythroid 2-related factor 2 (Nrf2) and thioredoxin reductase 1 (TrxR1), which was associated with the increased phosphorylation of Nrf2.	diallyl trisulfide	15-19	nuclear factor, erythroid derived 2, like 2	Mus musculus	215-219
28218609-6	2017	Moreover, DATS-mediated phosphorylation of Nrf2 and induction of TrxR1 were markedly reduced by genetic silencing of Nrf2.	diallyl trisulfide	10-14	nuclear factor, erythroid derived 2, like 2	Mus musculus	43-47
28218609-6	2017	Moreover, DATS-mediated phosphorylation of Nrf2 and induction of TrxR1 were markedly reduced by genetic silencing of Nrf2.	diallyl trisulfide	10-14	thioredoxin reductase 1	Mus musculus	65-70
28218609-6	2017	Moreover, DATS-mediated phosphorylation of Nrf2 and induction of TrxR1 were markedly reduced by genetic silencing of Nrf2.	diallyl trisulfide	10-14	nuclear factor, erythroid derived 2, like 2	Mus musculus	117-121
28218609-7	2017	DATS treatment also induced the phosphorylation extracellular signal-regulating kinase (ERK), and analysis using specific inhibitors of cellular signaling pathways demonstrated that only ERK activation was involved in Nrf2 phosphorylation and TrxR1 induction.	diallyl trisulfide	0-4	mitogen-activated protein kinase 1	Mus musculus	48-86
28218609-7	2017	DATS treatment also induced the phosphorylation extracellular signal-regulating kinase (ERK), and analysis using specific inhibitors of cellular signaling pathways demonstrated that only ERK activation was involved in Nrf2 phosphorylation and TrxR1 induction.	diallyl trisulfide	0-4	mitogen-activated protein kinase 1	Mus musculus	88-91
28218609-7	2017	DATS treatment also induced the phosphorylation extracellular signal-regulating kinase (ERK), and analysis using specific inhibitors of cellular signaling pathways demonstrated that only ERK activation was involved in Nrf2 phosphorylation and TrxR1 induction.	diallyl trisulfide	0-4	mitogen-activated protein kinase 1	Mus musculus	187-190
28218609-7	2017	DATS treatment also induced the phosphorylation extracellular signal-regulating kinase (ERK), and analysis using specific inhibitors of cellular signaling pathways demonstrated that only ERK activation was involved in Nrf2 phosphorylation and TrxR1 induction.	diallyl trisulfide	0-4	nuclear factor, erythroid derived 2, like 2	Mus musculus	218-222
28218609-7	2017	DATS treatment also induced the phosphorylation extracellular signal-regulating kinase (ERK), and analysis using specific inhibitors of cellular signaling pathways demonstrated that only ERK activation was involved in Nrf2 phosphorylation and TrxR1 induction.	diallyl trisulfide	0-4	thioredoxin reductase 1	Mus musculus	243-248
28218609-9	2017	The results demonstrate that DATS protects against oxidative stress-induced DNA damage and apoptosis in C2C12 cells in part through the activation of Nrf2-mediated TrxR1 induction via the ERK signaling pathway.	diallyl trisulfide	29-33	nuclear factor, erythroid derived 2, like 2	Mus musculus	150-154
28218609-9	2017	The results demonstrate that DATS protects against oxidative stress-induced DNA damage and apoptosis in C2C12 cells in part through the activation of Nrf2-mediated TrxR1 induction via the ERK signaling pathway.	diallyl trisulfide	29-33	thioredoxin reductase 1	Mus musculus	164-169
28218609-9	2017	The results demonstrate that DATS protects against oxidative stress-induced DNA damage and apoptosis in C2C12 cells in part through the activation of Nrf2-mediated TrxR1 induction via the ERK signaling pathway.	diallyl trisulfide	29-33	mitogen-activated protein kinase 1	Mus musculus	188-191
28255269-9	2017	In addition, increased E-cadherin and decreased MMP-9 expression levels were observed in DATS-treated tumor tissues.	diallyl trisulfide	89-93	matrix metallopeptidase 9	Homo sapiens	48-53
27044810-6	2016	Our results demonstrated that DATS prevented ethanol-induced injury, as indicated by the reduced activities of aspartate transaminase (AST) and alanine aminotransferase (ALT) in the serum and culture medium, and inhibition of cell apoptosis.	diallyl trisulfide	30-34	solute carrier family 17 member 5	Homo sapiens	111-133
26801633-0	2016	Epigenetic Upregulation of Metallothionein 2A by Diallyl Trisulfide Enhances Chemosensitivity of Human Gastric Cancer Cells to Docetaxel Through Attenuating NF-kappaB Activation.	diallyl trisulfide	49-67	metallothionein 2A	Homo sapiens	27-45
26801633-3	2016	The present study investigated the effect of diallyl trisulfide (DATS), a garlic-derived compound, and docetaxel (DOC) on regulation of MT2A in relation to NF-kappaB in GC cells.	diallyl trisulfide	45-63	metallothionein 2A	Homo sapiens	136-140
26801633-3	2016	The present study investigated the effect of diallyl trisulfide (DATS), a garlic-derived compound, and docetaxel (DOC) on regulation of MT2A in relation to NF-kappaB in GC cells.	diallyl trisulfide	65-69	metallothionein 2A	Homo sapiens	136-140
26801633-5	2016	The anti-GC effect of DATS was attributable to its capacity to epigenetically upregulate MT2A, which in turn enhanced transcription of IkappaB-alpha to suppress NF-kappaB activation in GC cells.	diallyl trisulfide	22-26	metallothionein 2A	Homo sapiens	89-93
26801633-5	2016	The anti-GC effect of DATS was attributable to its capacity to epigenetically upregulate MT2A, which in turn enhanced transcription of IkappaB-alpha to suppress NF-kappaB activation in GC cells.	diallyl trisulfide	22-26	NFKB inhibitor alpha	Homo sapiens	135-148
26801633-9	2016	INNOVATION AND CONCLUSION: We conclude that DATS exerts its anti-GC activity and enhances chemosensitivity of GC to DOC by epigenetic upregulation of MT2A to attenuate NF-kappaB signaling.	diallyl trisulfide	44-48	metallothionein 2A	Homo sapiens	150-154
27929399-5	2016	Moreover, DADS and DATS increased the total sulfane sulfur level and CSE activity in the normal mouse kidney.	diallyl trisulfide	19-23	cystathionase (cystathionine gamma-lyase)	Mus musculus	69-72
27929399-6	2016	ALDH activity was inhibited in the kidney after DATS administration.	diallyl trisulfide	48-52	aldehyde dehydrogenase family 3, subfamily A1	Mus musculus	0-4
27486324-3	2016	Mesoporous silica nanoparticles (MSNs) were synthesized using the sol-gel method and loaded with diallyl trisulfide (DATS), an H2S-releasing agent named DATS-MSN.	diallyl trisulfide	97-115	moesin	Homo sapiens	33-36
27486324-3	2016	Mesoporous silica nanoparticles (MSNs) were synthesized using the sol-gel method and loaded with diallyl trisulfide (DATS), an H2S-releasing agent named DATS-MSN.	diallyl trisulfide	117-121	moesin	Homo sapiens	33-36
27486324-3	2016	Mesoporous silica nanoparticles (MSNs) were synthesized using the sol-gel method and loaded with diallyl trisulfide (DATS), an H2S-releasing agent named DATS-MSN.	diallyl trisulfide	153-157	moesin	Homo sapiens	33-36
27486324-5	2016	In vivo experiments demonstrated that the apoptosis of graft endothelium was mitigated in the presence of DATS-MSN.	diallyl trisulfide	106-110	moesin	Homo sapiens	111-114
27107369-9	2016	Lastly, we found DATS could increase the expressions of cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS), the major H2S-producing enzymes.	diallyl trisulfide	17-21	cystathionine gamma-lyase	Homo sapiens	56-81
27107369-9	2016	Lastly, we found DATS could increase the expressions of cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS), the major H2S-producing enzymes.	diallyl trisulfide	17-21	cystathionine gamma-lyase	Homo sapiens	83-86
27107369-9	2016	Lastly, we found DATS could increase the expressions of cystathionine gamma-lyase (CSE) and cystathionine beta-synthase (CBS), the major H2S-producing enzymes.	diallyl trisulfide	17-21	cystathionine beta-synthase	Homo sapiens	92-119
27129776-0	2016	Forkhead Box Q1 Is a Novel Target of Breast Cancer Stem Cell Inhibition by Diallyl Trisulfide.	diallyl trisulfide	75-93	forkhead box Q1	Homo sapiens	0-15
27129776-5	2016	Inhibition of ALDH1 activity and/or mammosphere formation upon DATS treatment was significantly attenuated by overexpression of FoxQ1.	diallyl trisulfide	63-67	aldehyde dehydrogenase 1 family member A1	Homo sapiens	14-19
27129776-5	2016	Inhibition of ALDH1 activity and/or mammosphere formation upon DATS treatment was significantly attenuated by overexpression of FoxQ1.	diallyl trisulfide	63-67	forkhead box Q1	Homo sapiens	128-133
27129776-9	2016	Moreover, inducible expression of DACH1 augmented DATS-mediated inhibition of bCSC.	diallyl trisulfide	50-54	dachshund family transcription factor 1	Homo sapiens	34-39
27129776-12	2016	DATS administration inhibited ALDH1 activity in vivo in SUM159 xenografts.	diallyl trisulfide	0-4	aldehyde dehydrogenase 1 family member A1	Homo sapiens	30-35
27035545-0	2016	Diallyl trisulfide induces osteosarcoma cell apoptosis through reactive oxygen species-mediated downregulation of the PI3K/Akt pathway.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	123-126
27035545-6	2016	DATS induced apoptosis in the MG63 and MNNG/HOS cells via inhibition of the PI3K/Akt signaling pathway and through the mitochondrial apoptotic pathway.	diallyl trisulfide	0-4	AKT serine/threonine kinase 1	Homo sapiens	81-84
27035545-8	2016	However, N-acetylcysteine (NAC), a general ROS scavenger, completely blocked the DATS-induced ROS increase, inhibition of the PI3K/Akt pathway and cell apoptosis.	diallyl trisulfide	81-85	AKT serine/threonine kinase 1	Homo sapiens	131-134
27044810-6	2016	Our results demonstrated that DATS prevented ethanol-induced injury, as indicated by the reduced activities of aspartate transaminase (AST) and alanine aminotransferase (ALT) in the serum and culture medium, and inhibition of cell apoptosis.	diallyl trisulfide	30-34	solute carrier family 17 member 5	Homo sapiens	135-138
27044810-6	2016	Our results demonstrated that DATS prevented ethanol-induced injury, as indicated by the reduced activities of aspartate transaminase (AST) and alanine aminotransferase (ALT) in the serum and culture medium, and inhibition of cell apoptosis.	diallyl trisulfide	30-34	glutamic--pyruvic transaminase	Homo sapiens	144-168
26647777-0	2016	Diallyl trisulfide induces apoptosis by suppressing NF-kappaB signaling through destabilization of TRAF6 in primary effusion lymphoma.	diallyl trisulfide	0-18	TNF receptor associated factor 6	Homo sapiens	99-104
30090404-7	2016	Results: DATS co-administration significantly inhibited the increase of liver index and elevation of serum ALT, AST and T.Bili levels induced by INH&RFP, as well as improved the hepatocellular structure.	diallyl trisulfide	9-13	glutamic pyruvic transaminase, soluble	Mus musculus	107-110
30090404-7	2016	Results: DATS co-administration significantly inhibited the increase of liver index and elevation of serum ALT, AST and T.Bili levels induced by INH&RFP, as well as improved the hepatocellular structure.	diallyl trisulfide	9-13	solute carrier family 17 (anion/sugar transporter), member 5	Mus musculus	112-115
30090404-9	2016	Furthermore, DATS co-administration reactivated the KCs inhibited by INH&RFP, which was illustrated by the increase of carbon phagocytosis, and the restoration of the number of activated KCs and IL-1-beta levels in the liver.	diallyl trisulfide	13-17	interleukin 1 beta	Mus musculus	199-208
24890016-3	2015	In in vitro study, DATS induced apoptosis of WEHI-3 cells through the G0/G1 phase arrest and induction of caspase-3 activation.	diallyl trisulfide	19-23	caspase 3	Mus musculus	106-115
26548347-6	2015	The mechanistic study showed that the DATS-mediated inhibition of naphthalene-induced oxidative injury and the production of inflammatory responses (i.e., TNF-alpha, IL-6, and IL-8) were attributed to inhibiting the activity of nuclear factor-kappa B (NF-kappaB).	diallyl trisulfide	38-42	tumor necrosis factor	Mus musculus	155-164
26548347-6	2015	The mechanistic study showed that the DATS-mediated inhibition of naphthalene-induced oxidative injury and the production of inflammatory responses (i.e., TNF-alpha, IL-6, and IL-8) were attributed to inhibiting the activity of nuclear factor-kappa B (NF-kappaB).	diallyl trisulfide	38-42	interleukin 6	Mus musculus	166-170
26548347-6	2015	The mechanistic study showed that the DATS-mediated inhibition of naphthalene-induced oxidative injury and the production of inflammatory responses (i.e., TNF-alpha, IL-6, and IL-8) were attributed to inhibiting the activity of nuclear factor-kappa B (NF-kappaB).	diallyl trisulfide	38-42	chemokine (C-X-C motif) ligand 15	Mus musculus	176-180
26548347-6	2015	The mechanistic study showed that the DATS-mediated inhibition of naphthalene-induced oxidative injury and the production of inflammatory responses (i.e., TNF-alpha, IL-6, and IL-8) were attributed to inhibiting the activity of nuclear factor-kappa B (NF-kappaB).	diallyl trisulfide	38-42	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	228-250
26548347-6	2015	The mechanistic study showed that the DATS-mediated inhibition of naphthalene-induced oxidative injury and the production of inflammatory responses (i.e., TNF-alpha, IL-6, and IL-8) were attributed to inhibiting the activity of nuclear factor-kappa B (NF-kappaB).	diallyl trisulfide	38-42	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	252-261
26548347-7	2015	In addition, DATS inhibited the production of serum nitric oxide NO and myeloperoxidase (MPO) in the lungs of Kunming mice.	diallyl trisulfide	13-17	myeloperoxidase	Mus musculus	72-87
26548347-7	2015	In addition, DATS inhibited the production of serum nitric oxide NO and myeloperoxidase (MPO) in the lungs of Kunming mice.	diallyl trisulfide	13-17	myeloperoxidase	Mus musculus	89-92
25500681-0	2015	Diallyl trisulfide exerts anti-inflammatory effects in lipopolysaccharide-stimulated RAW 264.7 macrophages by suppressing the Toll-like receptor 4/nuclear factor-kappaB pathway.	diallyl trisulfide	0-18	toll-like receptor 4	Mus musculus	126-146
26194202-7	2015	Treatment of CSE KO mice with the polysulfide donor diallyl trisulfide restored ischaemic vascular remodelling, monocyte infiltration, and cytokine expression.	diallyl trisulfide	52-70	cystathionase (cystathionine gamma-lyase)	Mus musculus	13-16
25927362-0	2015	Antimetastatic Therapies of the Polysulfide Diallyl Trisulfide against Triple-Negative Breast Cancer (TNBC) via Suppressing MMP2/9 by Blocking NF-kappaB and ERK/MAPK Signaling Pathways.	diallyl trisulfide	44-62	matrix metallopeptidase 2	Homo sapiens	124-130
25927362-0	2015	Antimetastatic Therapies of the Polysulfide Diallyl Trisulfide against Triple-Negative Breast Cancer (TNBC) via Suppressing MMP2/9 by Blocking NF-kappaB and ERK/MAPK Signaling Pathways.	diallyl trisulfide	44-62	mitogen-activated protein kinase 1	Homo sapiens	157-160
25927362-0	2015	Antimetastatic Therapies of the Polysulfide Diallyl Trisulfide against Triple-Negative Breast Cancer (TNBC) via Suppressing MMP2/9 by Blocking NF-kappaB and ERK/MAPK Signaling Pathways.	diallyl trisulfide	44-62	mitogen-activated protein kinase 1	Homo sapiens	161-165
25927362-7	2015	Moreover, DATS inhibited the mRNA/protein/ enzymes activities of MMP2/9 via attenuating the NF-kappaB pathway.	diallyl trisulfide	10-14	matrix metallopeptidase 2	Homo sapiens	65-71
25927362-8	2015	DATS also inhibited ERK/MAPK rather than p38 and JNK.	diallyl trisulfide	0-4	mitogen-activated protein kinase 1	Homo sapiens	20-23
25927362-8	2015	DATS also inhibited ERK/MAPK rather than p38 and JNK.	diallyl trisulfide	0-4	mitogen-activated protein kinase 1	Homo sapiens	24-28
25500681-4	2015	At non-toxic concentrations, DATS inhibited the production of nitric oxide (NO) and prostaglandin E2 by inhibiting inducible NO synthase and cyclooxygenase-2 expression at the transcriptional level in lipopolysaccharide (LPS)-activated RAW 264.7 macrophages.	diallyl trisulfide	29-33	prostaglandin-endoperoxide synthase 2	Mus musculus	141-157
25500681-7	2015	In addition, DATS was observed to significantly suppress LPS-induced Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 expression and the binding of LPS to macrophages, indicating the antagonistic effect of DATS against TLR4.	diallyl trisulfide	13-17	toll-like receptor 4	Mus musculus	69-89
25500681-7	2015	In addition, DATS was observed to significantly suppress LPS-induced Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 expression and the binding of LPS to macrophages, indicating the antagonistic effect of DATS against TLR4.	diallyl trisulfide	13-17	toll-like receptor 4	Mus musculus	91-95
25500681-7	2015	In addition, DATS was observed to significantly suppress LPS-induced Toll-like receptor 4 (TLR4) and myeloid differentiation factor 88 expression and the binding of LPS to macrophages, indicating the antagonistic effect of DATS against TLR4.	diallyl trisulfide	13-17	toll-like receptor 4	Mus musculus	236-240
25974998-6	2015	Also, Western blot was performed to detect the activation of ERK1/2 and AKT1 responds to DATS.	diallyl trisulfide	89-93	mitogen-activated protein kinase 3	Mus musculus	61-67
25403643-3	2015	In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases-2, -7 and -9 and VEGF.	diallyl trisulfide	15-19	protein tyrosine kinase 2	Homo sapiens	79-100
25403643-3	2015	In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases-2, -7 and -9 and VEGF.	diallyl trisulfide	15-19	protein tyrosine kinase 2	Homo sapiens	102-105
25403643-3	2015	In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases-2, -7 and -9 and VEGF.	diallyl trisulfide	15-19	mitogen-activated protein kinase 14	Homo sapiens	175-178
25403643-3	2015	In HT29 cells, DATS inhibited migration and invasion through the inhibition of focal adhesion kinase (FAK), extracellular signal-regulated kinase, c-Jun N-terminal kinase and p38 which was associated with inhibition of matrix metalloproteinases-2, -7 and -9 and VEGF.	diallyl trisulfide	15-19	vascular endothelial growth factor A	Homo sapiens	262-266
25403643-4	2015	In human umbilical vein endothelial cells (HUVEC), DATS inhibited the migration and angiogenesis through FAK, Src and Ras.	diallyl trisulfide	51-55	protein tyrosine kinase 2	Homo sapiens	105-108
25403643-4	2015	In human umbilical vein endothelial cells (HUVEC), DATS inhibited the migration and angiogenesis through FAK, Src and Ras.	diallyl trisulfide	51-55	SRC proto-oncogene, non-receptor tyrosine kinase	Homo sapiens	110-113
25403643-5	2015	DATS also inhibited the secretion of VEGF.	diallyl trisulfide	0-4	vascular endothelial growth factor A	Homo sapiens	37-41
25974998-6	2015	Also, Western blot was performed to detect the activation of ERK1/2 and AKT1 responds to DATS.	diallyl trisulfide	89-93	thymoma viral proto-oncogene 1	Mus musculus	72-76
25974998-10	2015	Suppression of ERK1/2 activation with PD9805 also completely blocked DATS-inhibited ESCC cell proliferation.	diallyl trisulfide	69-73	mitogen-activated protein kinase 3	Mus musculus	15-21
25974998-12	2015	CONCLUSIONS: Our finding demonstrated that DATS inhibits the proliferation of ESCC cells by activation of ERK1/2 in vitro and in vivo.	diallyl trisulfide	43-47	mitogen-activated protein kinase 3	Mus musculus	106-112
24487688-0	2014	Diallyl trisulfide inhibits estrogen receptor-alpha activity in human breast cancer cells.	diallyl trisulfide	0-18	estrogen receptor 1	Homo sapiens	28-51
24788927-0	2014	Reversion of P-glycoprotein-mediated multidrug resistance by diallyl trisulfide in a human osteosarcoma cell line.	diallyl trisulfide	61-79	ATP binding cassette subfamily B member 1	Homo sapiens	13-27
24788927-9	2014	Moreover, P-gp expression was decreased and the apoptosis rate was increased in a concentration-dependent manner following treatment of DATS.	diallyl trisulfide	136-140	ATP binding cassette subfamily B member 1	Homo sapiens	10-14
24487688-10	2014	DATS treatment caused a decrease in protein levels of peptidyl-prolyl cis-trans isomerase (Pin1), and overexpression of Pin1 partially attenuated ER-alpha downregulation by DATS.	diallyl trisulfide	173-177	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	120-124
24487688-3	2014	This study reports, for the first time, that garlic organosulfide diallyl trisulfide (DATS) inhibits estrogen receptor-alpha (ER-alpha) activity in human breast cancer cells.	diallyl trisulfide	66-84	estrogen receptor 1	Homo sapiens	101-124
24487688-10	2014	DATS treatment caused a decrease in protein levels of peptidyl-prolyl cis-trans isomerase (Pin1), and overexpression of Pin1 partially attenuated ER-alpha downregulation by DATS.	diallyl trisulfide	173-177	estrogen receptor 1	Homo sapiens	146-154
24487688-11	2014	DATS-induced apoptosis was modestly but significantly augmented by overexpression of Pin1.	diallyl trisulfide	0-4	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	85-89
24487688-3	2014	This study reports, for the first time, that garlic organosulfide diallyl trisulfide (DATS) inhibits estrogen receptor-alpha (ER-alpha) activity in human breast cancer cells.	diallyl trisulfide	66-84	estrogen receptor 1	Homo sapiens	126-134
24487688-3	2014	This study reports, for the first time, that garlic organosulfide diallyl trisulfide (DATS) inhibits estrogen receptor-alpha (ER-alpha) activity in human breast cancer cells.	diallyl trisulfide	86-90	estrogen receptor 1	Homo sapiens	101-124
24487688-3	2014	This study reports, for the first time, that garlic organosulfide diallyl trisulfide (DATS) inhibits estrogen receptor-alpha (ER-alpha) activity in human breast cancer cells.	diallyl trisulfide	86-90	estrogen receptor 1	Homo sapiens	126-134
24487688-4	2014	Exposure of MCF-7 and T47D cells to DATS resulted in downregulation of ER-alpha protein, which peaked between 12- and 24-h post-treatment.	diallyl trisulfide	36-40	estrogen receptor 1	Homo sapiens	71-79
24487688-5	2014	DATS was relatively more effective in suppressing ER-alpha protein expression compared with its mono and disulfide analogs.	diallyl trisulfide	0-4	estrogen receptor 1	Homo sapiens	50-58
24487688-6	2014	The 17beta-estradiol (E2)-induced expression of pS2 and cyclin D1, ER-alpha target gene products, was also decreased in the presence of DATS.	diallyl trisulfide	136-140	trefoil factor 1	Homo sapiens	48-51
24487688-6	2014	The 17beta-estradiol (E2)-induced expression of pS2 and cyclin D1, ER-alpha target gene products, was also decreased in the presence of DATS.	diallyl trisulfide	136-140	cyclin D1	Homo sapiens	56-65
24487688-6	2014	The 17beta-estradiol (E2)-induced expression of pS2 and cyclin D1, ER-alpha target gene products, was also decreased in the presence of DATS.	diallyl trisulfide	136-140	estrogen receptor 1	Homo sapiens	67-75
24487688-7	2014	Downregulation of ER-alpha protein expression resulting from DATS treatment was accompanied by a decrease in nuclear levels of ER-alpha protein, ER-alpha mRNA suppression, and inhibition of ERE2e1b-luciferase reporter activity.	diallyl trisulfide	61-65	estrogen receptor 1	Homo sapiens	18-26
24487688-7	2014	Downregulation of ER-alpha protein expression resulting from DATS treatment was accompanied by a decrease in nuclear levels of ER-alpha protein, ER-alpha mRNA suppression, and inhibition of ERE2e1b-luciferase reporter activity.	diallyl trisulfide	61-65	estrogen receptor 1	Homo sapiens	127-135
24487688-7	2014	Downregulation of ER-alpha protein expression resulting from DATS treatment was accompanied by a decrease in nuclear levels of ER-alpha protein, ER-alpha mRNA suppression, and inhibition of ERE2e1b-luciferase reporter activity.	diallyl trisulfide	61-65	estrogen receptor 1	Homo sapiens	127-135
24487688-10	2014	DATS treatment caused a decrease in protein levels of peptidyl-prolyl cis-trans isomerase (Pin1), and overexpression of Pin1 partially attenuated ER-alpha downregulation by DATS.	diallyl trisulfide	0-4	peptidylprolyl cis/trans isomerase, NIMA-interacting 1	Homo sapiens	91-95
24504171-1	2014	OBJECTIVES: To investigate the effects of allitridin on human ether-a-go-go-related gene (hERG) channels.	diallyl trisulfide	42-52	ETS transcription factor ERG	Homo sapiens	90-94
24489685-0	2014	Keap1 cysteine 288 as a potential target for diallyl trisulfide-induced Nrf2 activation.	diallyl trisulfide	45-63	kelch-like ECH-associated protein 1	Mus musculus	0-5
24489685-0	2014	Keap1 cysteine 288 as a potential target for diallyl trisulfide-induced Nrf2 activation.	diallyl trisulfide	45-63	nuclear factor, erythroid derived 2, like 2	Mus musculus	72-76
25130746-2	2014	A unique protein spot appeared by DATS treatment was identified to be heat shock protein 27 (HSP27).	diallyl trisulfide	34-38	heat shock protein family B (small) member 1	Homo sapiens	70-91
25130746-2	2014	A unique protein spot appeared by DATS treatment was identified to be heat shock protein 27 (HSP27).	diallyl trisulfide	34-38	heat shock protein family B (small) member 1	Homo sapiens	93-98
25130747-0	2014	Diallyl trisulfide induces apoptosis in Jurkat cells by the modification of cysteine residues in thioredoxin.	diallyl trisulfide	0-18	thioredoxin	Homo sapiens	97-108
25130747-2	2014	In this study, we examined if DATS modifies the cysteine residue of thioredoxin (Trx) by urea-polyacryl amide gel electrophoresis.	diallyl trisulfide	30-34	thioredoxin	Homo sapiens	68-79
25130747-2	2014	In this study, we examined if DATS modifies the cysteine residue of thioredoxin (Trx) by urea-polyacryl amide gel electrophoresis.	diallyl trisulfide	30-34	thioredoxin	Homo sapiens	81-84
25130747-3	2014	DATS modified two specific cysteine residues in Trx and this oxidative modification of cysteine residues would be sole causative of the apoptosis induced by DATS in leukemic cells.	diallyl trisulfide	0-4	thioredoxin	Homo sapiens	48-51
24504171-2	2014	METHODS: We used whole-cell patch clamping and laser confocal scanning microscopy to evaluate the effects of allitridin on hERG currents and the membrane expression of the hERG protein expressed in HEK 293 cells.	diallyl trisulfide	109-119	ETS transcription factor ERG	Homo sapiens	123-127
23064375-0	2012	Diallyl trisulfide sensitizes human melanoma cells to TRAIL-induced             cell death by promoting endoplasmic reticulum-mediated apoptosis.	diallyl trisulfide	0-18	TNF superfamily member 10	Homo sapiens	54-59
24309133-0	2014	Diallyl trisulfide-induced apoptosis of bladder cancer cells is caspase-dependent and regulated by PI3K/Akt and JNK pathways.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	104-107
24309133-0	2014	Diallyl trisulfide-induced apoptosis of bladder cancer cells is caspase-dependent and regulated by PI3K/Akt and JNK pathways.	diallyl trisulfide	0-18	mitogen-activated protein kinase 8	Homo sapiens	112-115
24309133-9	2014	The study further investigated the roles of the phosphatidylinositol 3-kinase (PI3K)/Akt and mitogen-activated protein kinases (MAPKs) pathways with respect to the apoptotic effect of DATS, and showed that DATS deactivates Akt.	diallyl trisulfide	184-188	phosphatidylinositol-4,5-bisphosphate 3-kinase catalytic subunit delta	Homo sapiens	48-77
24309133-9	2014	The study further investigated the roles of the phosphatidylinositol 3-kinase (PI3K)/Akt and mitogen-activated protein kinases (MAPKs) pathways with respect to the apoptotic effect of DATS, and showed that DATS deactivates Akt.	diallyl trisulfide	184-188	AKT serine/threonine kinase 1	Homo sapiens	85-88
24309133-10	2014	Additionally, DATS activates extracellular signal-regulated kinase (ERK) and c-Jun N-terminal protein kinase (JNK), but not p38 MAPK, in T24 cells.	diallyl trisulfide	14-18	mitogen-activated protein kinase 8	Homo sapiens	77-108
24309133-10	2014	Additionally, DATS activates extracellular signal-regulated kinase (ERK) and c-Jun N-terminal protein kinase (JNK), but not p38 MAPK, in T24 cells.	diallyl trisulfide	14-18	mitogen-activated protein kinase 8	Homo sapiens	110-113
24309133-11	2014	Unlike ERK, JNK inhibitors reversed DATS-induced apoptosis and growth inhibition; however, inhibition of PI3K/Akt notably enhanced the apoptotic action of DATS.	diallyl trisulfide	155-159	AKT serine/threonine kinase 1	Homo sapiens	110-113
23158927-0	2013	Diallyl trisufide (DATS) suppresses high glucose-induced cardiomyocyte apoptosis by inhibiting JNK/NFkappaB signaling via attenuating ROS generation.	diallyl trisulfide	19-23	mitogen-activated protein kinase 8	Rattus norvegicus	95-98
23158927-6	2013	RESULTS: We found that DATS treatment led to a dose-dependent decrease in ROS levels as well as protein levels of p22phox, gp91phox, phosphorylated JNK, and phosphorylated c-Jun.	diallyl trisulfide	23-27	cytochrome b-245 alpha chain	Rattus norvegicus	114-121
23158927-6	2013	RESULTS: We found that DATS treatment led to a dose-dependent decrease in ROS levels as well as protein levels of p22phox, gp91phox, phosphorylated JNK, and phosphorylated c-Jun.	diallyl trisulfide	23-27	cytochrome b-245 beta chain	Rattus norvegicus	123-131
23158927-6	2013	RESULTS: We found that DATS treatment led to a dose-dependent decrease in ROS levels as well as protein levels of p22phox, gp91phox, phosphorylated JNK, and phosphorylated c-Jun.	diallyl trisulfide	23-27	mitogen-activated protein kinase 8	Rattus norvegicus	148-151
23158927-7	2013	In addition, DATS inhibited the HG-induced activation of caspase 3 as well as the nuclear translocation of NF-kappaB.	diallyl trisulfide	13-17	caspase 3	Rattus norvegicus	57-66
23158927-10	2013	CONCLUSION: DATS appears to suppress high glucose-induced cardiomyocyte apoptosis by inhibiting NADPH oxidase-related ROS and its downstream JNK/NF-kappaB signaling, and may possess the potential on the therapy of diabetic cardiomyopathy.	diallyl trisulfide	12-16	mitogen-activated protein kinase 8	Rattus norvegicus	141-144
23754639-10	2013	Our data also demonstrated an increase in p21Waf1 expression, which correlated with increased p53 expression and MDM2 degradation following DATS treatment.	diallyl trisulfide	140-144	transformation related protein 53, pseudogene	Mus musculus	94-97
23754639-10	2013	Our data also demonstrated an increase in p21Waf1 expression, which correlated with increased p53 expression and MDM2 degradation following DATS treatment.	diallyl trisulfide	140-144	transformed mouse 3T3 cell double minute 2	Mus musculus	113-117
23811270-0	2013	Diallyl trisulfide suppresses dextran sodium sulfate-induced mouse colitis: NF-kappaB and STAT3 as potential targets.	diallyl trisulfide	0-18	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	76-85
23811270-0	2013	Diallyl trisulfide suppresses dextran sodium sulfate-induced mouse colitis: NF-kappaB and STAT3 as potential targets.	diallyl trisulfide	0-18	signal transducer and activator of transcription 3	Mus musculus	90-95
23811270-5	2013	Likewise, DSS-induced phosphorylation of extracellular signal-regulated kinase 1/2 was suppressed by DATS treatment.	diallyl trisulfide	101-105	mitogen-activated protein kinase 3	Mus musculus	41-82
23811270-6	2013	In conclusion, DATS ameliorates the DSS-induced mouse colitis presumably by blocking inflammatory signaling mediated by NF-kappaB and STAT3.	diallyl trisulfide	15-19	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	120-129
23811270-6	2013	In conclusion, DATS ameliorates the DSS-induced mouse colitis presumably by blocking inflammatory signaling mediated by NF-kappaB and STAT3.	diallyl trisulfide	15-19	signal transducer and activator of transcription 3	Mus musculus	134-139
23430952-0	2013	Diallyl trisulfide inhibits proliferation, invasion and angiogenesis of osteosarcoma cells by switching on suppressor microRNAs and inactivating of Notch-1 signaling.	diallyl trisulfide	0-18	notch receptor 1	Homo sapiens	148-155
23341371-1	2013	This study investigated the effects of allitridin compound on murine cytomegalovirus (MCMV)-induced regulatory T cell (Treg; CD4(+) CD25(+) Foxp3(+) ) amplification in vivo and in vitro.	diallyl trisulfide	39-49	forkhead box P3	Mus musculus	140-145
23341371-11	2013	In vitro treatment with allitridin also increased significantly the percentages of Tc1, Tc2, and Th1, reduced the secreted levels of IL-10 and TGF-beta1, and significantly suppressed viral loads.	diallyl trisulfide	24-34	transcobalamin 1	Homo sapiens	83-86
23341371-11	2013	In vitro treatment with allitridin also increased significantly the percentages of Tc1, Tc2, and Th1, reduced the secreted levels of IL-10 and TGF-beta1, and significantly suppressed viral loads.	diallyl trisulfide	24-34	transcobalamin 2	Homo sapiens	88-91
23341371-11	2013	In vitro treatment with allitridin also increased significantly the percentages of Tc1, Tc2, and Th1, reduced the secreted levels of IL-10 and TGF-beta1, and significantly suppressed viral loads.	diallyl trisulfide	24-34	negative elongation factor complex member C/D	Homo sapiens	97-100
23341371-11	2013	In vitro treatment with allitridin also increased significantly the percentages of Tc1, Tc2, and Th1, reduced the secreted levels of IL-10 and TGF-beta1, and significantly suppressed viral loads.	diallyl trisulfide	24-34	interleukin 10	Homo sapiens	133-138
23341371-11	2013	In vitro treatment with allitridin also increased significantly the percentages of Tc1, Tc2, and Th1, reduced the secreted levels of IL-10 and TGF-beta1, and significantly suppressed viral loads.	diallyl trisulfide	24-34	transforming growth factor beta 1	Homo sapiens	143-152
23412769-6	2013	Overexpression of Cu,Zn-superoxide dismutase (Cu,Zn-SOD) as well as Mn-SOD conferred significant protection against DATS-induced ROS production and apoptotic cell death in MDA-MB-231 and MCF-7 cells.	diallyl trisulfide	116-120	superoxide dismutase 1	Homo sapiens	18-44
23412769-6	2013	Overexpression of Cu,Zn-superoxide dismutase (Cu,Zn-SOD) as well as Mn-SOD conferred significant protection against DATS-induced ROS production and apoptotic cell death in MDA-MB-231 and MCF-7 cells.	diallyl trisulfide	116-120	superoxide dismutase 1	Homo sapiens	46-55
23412769-6	2013	Overexpression of Cu,Zn-superoxide dismutase (Cu,Zn-SOD) as well as Mn-SOD conferred significant protection against DATS-induced ROS production and apoptotic cell death in MDA-MB-231 and MCF-7 cells.	diallyl trisulfide	116-120	superoxide dismutase 2	Homo sapiens	68-74
23412769-7	2013	Activation of Bak, but not Bax, resulting from DATS treatment was markedly suppressed by overexpression of Mn-SOD.	diallyl trisulfide	47-51	BCL2 antagonist/killer 1	Homo sapiens	14-17
23412769-7	2013	Activation of Bak, but not Bax, resulting from DATS treatment was markedly suppressed by overexpression of Mn-SOD.	diallyl trisulfide	47-51	superoxide dismutase 2	Homo sapiens	107-113
24084732-5	2013	DATS treatment up-regulated expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 in 5637 cells.	diallyl trisulfide	0-4	TIMP metallopeptidase inhibitor 1	Homo sapiens	42-88
24084732-5	2013	DATS treatment up-regulated expression of tissue inhibitor of metalloproteinase (TIMP)-1 and TIMP-2 in 5637 cells.	diallyl trisulfide	0-4	TIMP metallopeptidase inhibitor 2	Homo sapiens	93-99
23453443-0	2013	Antioxidant effects of diallyl trisulfide on high glucose-induced apoptosis are mediated by the PI3K/Akt-dependent activation of Nrf2 in cardiomyocytes.	diallyl trisulfide	23-41	AKT serine/threonine kinase 1	Rattus norvegicus	101-104
23453443-0	2013	Antioxidant effects of diallyl trisulfide on high glucose-induced apoptosis are mediated by the PI3K/Akt-dependent activation of Nrf2 in cardiomyocytes.	diallyl trisulfide	23-41	NFE2 like bZIP transcription factor 2	Rattus norvegicus	129-133
23453443-5	2013	METHODS AND RESULTS: Treatment of H9c2 cells with HG resulted in an increase in intracellular ROS level and caspase-3 activity, which were markedly reduced by the administration of DATS (10 muM).	diallyl trisulfide	181-185	caspase 3	Rattus norvegicus	108-117
23453443-6	2013	DATS treatment significantly increased Nrf2 protein stability and nuclear translocation, upregulated downstream gene HO-1, and suppressed its repressor Keap1.	diallyl trisulfide	0-4	NFE2 like bZIP transcription factor 2	Rattus norvegicus	39-43
23453443-6	2013	DATS treatment significantly increased Nrf2 protein stability and nuclear translocation, upregulated downstream gene HO-1, and suppressed its repressor Keap1.	diallyl trisulfide	0-4	Kelch-like ECH-associated protein 1	Rattus norvegicus	152-157
23453443-8	2013	Inhibition of PI3K/Akt signaling by LY294002 (PI3K inhibitor) or PI3K-specific siRNA not only decreased the level of DATS-induced Nrf2-mediated HO-1 expression, but also diminished the protective effects of DATS.	diallyl trisulfide	117-121	AKT serine/threonine kinase 1	Rattus norvegicus	19-22
23453443-8	2013	Inhibition of PI3K/Akt signaling by LY294002 (PI3K inhibitor) or PI3K-specific siRNA not only decreased the level of DATS-induced Nrf2-mediated HO-1 expression, but also diminished the protective effects of DATS.	diallyl trisulfide	117-121	NFE2 like bZIP transcription factor 2	Rattus norvegicus	130-134
23453443-8	2013	Inhibition of PI3K/Akt signaling by LY294002 (PI3K inhibitor) or PI3K-specific siRNA not only decreased the level of DATS-induced Nrf2-mediated HO-1 expression, but also diminished the protective effects of DATS.	diallyl trisulfide	207-211	AKT serine/threonine kinase 1	Rattus norvegicus	19-22
23453443-8	2013	Inhibition of PI3K/Akt signaling by LY294002 (PI3K inhibitor) or PI3K-specific siRNA not only decreased the level of DATS-induced Nrf2-mediated HO-1 expression, but also diminished the protective effects of DATS.	diallyl trisulfide	207-211	NFE2 like bZIP transcription factor 2	Rattus norvegicus	130-134
23453443-10	2013	CONCLUSIONS: Our findings indicate that DATS protects against hyperglycemia-induced ROS-mediated apoptosis by upregulating the PI3K/Akt/Nrf2 pathway, which further activates Nrf2-regulated antioxidant enzymes in cardiomyocytes exposed to HG.	diallyl trisulfide	40-44	AKT serine/threonine kinase 1	Rattus norvegicus	132-135
23453443-10	2013	CONCLUSIONS: Our findings indicate that DATS protects against hyperglycemia-induced ROS-mediated apoptosis by upregulating the PI3K/Akt/Nrf2 pathway, which further activates Nrf2-regulated antioxidant enzymes in cardiomyocytes exposed to HG.	diallyl trisulfide	40-44	NFE2 like bZIP transcription factor 2	Rattus norvegicus	136-140
23453443-10	2013	CONCLUSIONS: Our findings indicate that DATS protects against hyperglycemia-induced ROS-mediated apoptosis by upregulating the PI3K/Akt/Nrf2 pathway, which further activates Nrf2-regulated antioxidant enzymes in cardiomyocytes exposed to HG.	diallyl trisulfide	40-44	NFE2 like bZIP transcription factor 2	Rattus norvegicus	174-178
23064375-3	2012	Here, we show that diallyl trisulfide (DATS), a garlic             organosulfur compound, sensitizes melanoma cells to TRAIL-induced apoptosis while             sparing normal cells.	diallyl trisulfide	19-37	TNF superfamily member 10	Homo sapiens	119-124
23064375-3	2012	Here, we show that diallyl trisulfide (DATS), a garlic             organosulfur compound, sensitizes melanoma cells to TRAIL-induced apoptosis while             sparing normal cells.	diallyl trisulfide	39-43	TNF superfamily member 10	Homo sapiens	119-124
23064375-11	2012	The present findings raise the possibility             that DATS may be combined with death ligands to treat TRAIL-resistance melanoma             cells without impairing its tumor selectivity.	diallyl trisulfide	60-64	TNF superfamily member 10	Homo sapiens	109-114
22020565-0	2012	Diallyl trisulfide-induced prostate cancer cell death is associated with Akt/PKB dephosphorylation mediated by P-p66shc.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	73-76
22981381-0	2012	Diallyl trisulfide induces apoptosis in human breast cancer cells through ROS-mediated activation of JNK and AP-1.	diallyl trisulfide	0-18	mitogen-activated protein kinase 8	Homo sapiens	101-104
22981381-6	2012	DATS treatment activated c-Jun N-terminal kinase (JNK).	diallyl trisulfide	0-4	mitogen-activated protein kinase 8	Homo sapiens	25-48
22981381-6	2012	DATS treatment activated c-Jun N-terminal kinase (JNK).	diallyl trisulfide	0-4	mitogen-activated protein kinase 8	Homo sapiens	50-53
22981381-9	2012	DATS-induced apoptosis as well as activation of JNK was abrogated by N-acetyl-l-cysteine (NAC).	diallyl trisulfide	0-4	X-linked Kx blood group	Homo sapiens	90-93
22981381-10	2012	Furthermore, DATS induced phosphorylation and expression of c-Jun, which were attenuated by NAC.	diallyl trisulfide	13-17	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	60-65
22981381-10	2012	Furthermore, DATS induced phosphorylation and expression of c-Jun, which were attenuated by NAC.	diallyl trisulfide	13-17	X-linked Kx blood group	Homo sapiens	92-95
22981381-12	2012	Proteolytic cleavage of PARP induced by DATS was abrogated in the cells transfected with c-jun siRNA.	diallyl trisulfide	40-44	poly(ADP-ribose) polymerase 1	Homo sapiens	24-28
22981381-12	2012	Proteolytic cleavage of PARP induced by DATS was abrogated in the cells transfected with c-jun siRNA.	diallyl trisulfide	40-44	Jun proto-oncogene, AP-1 transcription factor subunit	Homo sapiens	89-94
22981381-14	2012	These results suggest that DATS-induced apoptosis is mediated through ROS generation and subsequent activation of JNK and AP-1.	diallyl trisulfide	27-31	mitogen-activated protein kinase 8	Homo sapiens	114-117
22020565-13	2012	In such cells, DATS-induced Akt dephosphorylation was significantly reduced.	diallyl trisulfide	15-19	AKT serine/threonine kinase 1	Homo sapiens	28-31
22020565-15	2012	CONCLUSIONS: Our results uncover a novel signaling pathway with p66Shc being indispensable for DATS-induced inactivation of Akt due to hypophosphorylation.	diallyl trisulfide	95-99	AKT serine/threonine kinase 1	Homo sapiens	124-127
22578287-5	2012	In U937 cells, DATS-induced apoptosis was correlated with down-regulation of Bcl-2, XIAP, and cIAP-1 protein levels, cleavage of Bid proteins, activation of caspases, and collapse of mitochondrial membrane potential.	diallyl trisulfide	15-19	BCL2 apoptosis regulator	Homo sapiens	77-82
23073793-9	2012	After DATS treatment, the levels of c-fos and c-jun and MDA in the hepatic tissues were significantly lower in group D than in group C (P<0.05).	diallyl trisulfide	6-10	Fos proto-oncogene, AP-1 transcription factor subunit	Rattus norvegicus	36-41
22736270-8	2012	The mitochondria-dependent apoptotic signaling pathway             was shown to be involved as determined by increase in the levels of cytochrome             c, Apaf-1, AIF and caspase-3 and caspase-9 in DATS-treated primary colorectal             cancer cells.	diallyl trisulfide	204-208	cytochrome c, somatic	Homo sapiens	135-159
22397993-5	2012	In vitro experiments indicated that DATS promoted gene expression of multidrug resistant 1 (Mdr1) (p<0.05), and DAS and DADS promoted MRP3 gene expression and DATS alone stimulated gene expression of multidrug resistance-associated protein-1 (MRP1) (p<0.05) in colo 205 cells.	diallyl trisulfide	36-40	ATP binding cassette subfamily B member 1	Homo sapiens	92-96
22397993-6	2012	In vivo studies demonstrated that DADS and DATS induced Mdr1 and MRP1 gene expression (p<0.05).	diallyl trisulfide	43-47	ATP binding cassette subfamily B member 1	Homo sapiens	56-60
22397993-6	2012	In vivo studies demonstrated that DADS and DATS induced Mdr1 and MRP1 gene expression (p<0.05).	diallyl trisulfide	43-47	ATP binding cassette subfamily C member 1	Homo sapiens	65-69
22736270-8	2012	The mitochondria-dependent apoptotic signaling pathway             was shown to be involved as determined by increase in the levels of cytochrome             c, Apaf-1, AIF and caspase-3 and caspase-9 in DATS-treated primary colorectal             cancer cells.	diallyl trisulfide	204-208	apoptotic peptidase activating factor 1	Homo sapiens	161-167
22736270-8	2012	The mitochondria-dependent apoptotic signaling pathway             was shown to be involved as determined by increase in the levels of cytochrome             c, Apaf-1, AIF and caspase-3 and caspase-9 in DATS-treated primary colorectal             cancer cells.	diallyl trisulfide	204-208	apoptosis inducing factor mitochondria associated 1	Homo sapiens	169-172
22736270-8	2012	The mitochondria-dependent apoptotic signaling pathway             was shown to be involved as determined by increase in the levels of cytochrome             c, Apaf-1, AIF and caspase-3 and caspase-9 in DATS-treated primary colorectal             cancer cells.	diallyl trisulfide	204-208	caspase 3	Homo sapiens	177-186
22736270-8	2012	The mitochondria-dependent apoptotic signaling pathway             was shown to be involved as determined by increase in the levels of cytochrome             c, Apaf-1, AIF and caspase-3 and caspase-9 in DATS-treated primary colorectal             cancer cells.	diallyl trisulfide	204-208	caspase 9	Homo sapiens	191-200
22578287-5	2012	In U937 cells, DATS-induced apoptosis was correlated with down-regulation of Bcl-2, XIAP, and cIAP-1 protein levels, cleavage of Bid proteins, activation of caspases, and collapse of mitochondrial membrane potential.	diallyl trisulfide	15-19	X-linked inhibitor of apoptosis	Homo sapiens	84-88
22578287-5	2012	In U937 cells, DATS-induced apoptosis was correlated with down-regulation of Bcl-2, XIAP, and cIAP-1 protein levels, cleavage of Bid proteins, activation of caspases, and collapse of mitochondrial membrane potential.	diallyl trisulfide	15-19	baculoviral IAP repeat containing 2	Homo sapiens	94-100
22578287-5	2012	In U937 cells, DATS-induced apoptosis was correlated with down-regulation of Bcl-2, XIAP, and cIAP-1 protein levels, cleavage of Bid proteins, activation of caspases, and collapse of mitochondrial membrane potential.	diallyl trisulfide	15-19	BH3 interacting domain death agonist	Homo sapiens	129-132
22578287-6	2012	The data further demonstrated that DATS increased intracellular reactive oxygen species (ROS) generation, which was attenuated by pretreatment with antioxidant N-acetyl-l-cysteine (NAC), a scavenger of ROS.	diallyl trisulfide	35-39	X-linked Kx blood group	Homo sapiens	181-184
22578287-7	2012	In addition, administration of NAC resulted in significant inhibition of DATS-induced apoptosis by inhibiting activation of caspases.	diallyl trisulfide	73-77	X-linked Kx blood group	Homo sapiens	31-34
22138247-7	2012	DATS did not ameliorate the endotoxin-induced serum level of sICAM-1 or CINC-1 but suppressed intestinal IL-1beta at both doses.	diallyl trisulfide	0-4	interleukin 1 beta	Rattus norvegicus	105-113
22143535-6	2012	All of the evidences above indicate that DATS derivatives suppressed proliferation of PC-3 cells which was associated with the induction of apoptosis regulated by Bax/Bcl-2.	diallyl trisulfide	41-45	BCL2 associated X, apoptosis regulator	Homo sapiens	163-166
22143535-6	2012	All of the evidences above indicate that DATS derivatives suppressed proliferation of PC-3 cells which was associated with the induction of apoptosis regulated by Bax/Bcl-2.	diallyl trisulfide	41-45	BCL2 apoptosis regulator	Homo sapiens	167-172
22138247-8	2012	The low but not the high dose of DATS also ameliorated the intestinal contents of ICAM-1 and TNF-alpha (p<0.05).	diallyl trisulfide	33-37	intercellular adhesion molecule 1	Rattus norvegicus	82-88
22138247-8	2012	The low but not the high dose of DATS also ameliorated the intestinal contents of ICAM-1 and TNF-alpha (p<0.05).	diallyl trisulfide	33-37	tumor necrosis factor	Rattus norvegicus	93-102
22919419-0	2012	Reversion of p-glycoprotein-mediated multidrug resistance in human leukemic cell line by diallyl trisulfide.	diallyl trisulfide	89-107	ATP binding cassette subfamily B member 1	Homo sapiens	13-27
22919419-7	2012	The expression of NF-kappaB/p65 (downregulation) was significantly linked to the drug-resistance mechanism of DATS, whereas the expression of IkappaBalpha was not affected by DATS.	diallyl trisulfide	110-114	nuclear factor kappa B subunit 1	Homo sapiens	18-27
22919419-7	2012	The expression of NF-kappaB/p65 (downregulation) was significantly linked to the drug-resistance mechanism of DATS, whereas the expression of IkappaBalpha was not affected by DATS.	diallyl trisulfide	110-114	RELA proto-oncogene, NF-kB subunit	Homo sapiens	28-31
22919419-9	2012	More importantly, we proved for the first time that the suppression of NF-kappaB possibly involves the molecular mechanism in the course of reversion by DATS.	diallyl trisulfide	153-157	nuclear factor kappa B subunit 1	Homo sapiens	71-80
21296648-0	2011	The garlic constituent diallyl trisulfide increases the lifespan of C. elegans via skn-1 activation.	diallyl trisulfide	23-41	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	83-88
22519436-7	2012	Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2+ mobilization, upregulation of Bip/GRP78 and CHOP/GADD153, and activation of caspase-4.	diallyl trisulfide	12-16	heat shock protein family A (Hsp70) member 5	Homo sapiens	139-142
22519436-7	2012	Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2+ mobilization, upregulation of Bip/GRP78 and CHOP/GADD153, and activation of caspase-4.	diallyl trisulfide	12-16	heat shock protein family A (Hsp70) member 5	Homo sapiens	143-148
22519436-7	2012	Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2+ mobilization, upregulation of Bip/GRP78 and CHOP/GADD153, and activation of caspase-4.	diallyl trisulfide	12-16	DNA damage inducible transcript 3	Homo sapiens	153-157
22519436-7	2012	Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2+ mobilization, upregulation of Bip/GRP78 and CHOP/GADD153, and activation of caspase-4.	diallyl trisulfide	12-16	DNA damage inducible transcript 3	Homo sapiens	158-165
22519436-7	2012	Exposure to DATS additionally induced endogenous endoplasmic reticulum stress markers and intracellular Ca2+ mobilization, upregulation of Bip/GRP78 and CHOP/GADD153, and activation of caspase-4.	diallyl trisulfide	12-16	caspase 4	Homo sapiens	185-194
21616139-3	2011	In this paper we demonstrate that DATS-induced ROS formation depends on p66Shc.	diallyl trisulfide	34-38	src homology 2 domain-containing transforming protein C1	Mus musculus	72-78
21616139-4	2011	In cells stably expressing a dominant negative mutant of p66Shc (p66ShcS36A), DATS did not induce ROS formation.	diallyl trisulfide	78-82	src homology 2 domain-containing transforming protein C1	Mus musculus	57-63
21616139-7	2011	Moreover, DATS-induced G2/M arrest is completely abrogated in cells expressing p66ShcS36A.	diallyl trisulfide	10-14	src homology 2 domain-containing transforming protein C1	Mus musculus	79-89
21616139-10	2011	Moreover, increases in LIP and ROS formation were significantly attenuated in p66Shc(-/-) MEFs treated with DATS.	diallyl trisulfide	108-112	src homology 2 domain-containing transforming protein C1	Mus musculus	78-84
21411500-0	2011	Garlic constituent diallyl trisulfide suppresses x-linked inhibitor of apoptosis protein in prostate cancer cells in culture and in vivo.	diallyl trisulfide	19-37	X-linked inhibitor of apoptosis	Homo sapiens	49-80
21411500-3	2011	Level of X-linked inhibitor of apoptosis (XIAP) protein was decreased on 8-hour treatment with 20 and 40 mumol/L DATS, but this effect was partially attenuated at the 16-hour time point.	diallyl trisulfide	113-117	X-linked inhibitor of apoptosis	Homo sapiens	9-40
21411500-3	2011	Level of X-linked inhibitor of apoptosis (XIAP) protein was decreased on 8-hour treatment with 20 and 40 mumol/L DATS, but this effect was partially attenuated at the 16-hour time point.	diallyl trisulfide	113-117	X-linked inhibitor of apoptosis	Homo sapiens	42-46
21411500-5	2011	In contrast, DATS-treated PC-3 and LNCaP cells exhibited marked induction of survivin and cellular inhibitor of apoptosis protein 1 (cIAP1) proteins.	diallyl trisulfide	13-17	baculoviral IAP repeat-containing 5	Mus musculus	77-85
21411500-5	2011	In contrast, DATS-treated PC-3 and LNCaP cells exhibited marked induction of survivin and cellular inhibitor of apoptosis protein 1 (cIAP1) proteins.	diallyl trisulfide	13-17	baculoviral IAP repeat containing 2	Homo sapiens	90-131
21411500-5	2011	In contrast, DATS-treated PC-3 and LNCaP cells exhibited marked induction of survivin and cellular inhibitor of apoptosis protein 1 (cIAP1) proteins.	diallyl trisulfide	13-17	baculoviral IAP repeat containing 2	Homo sapiens	133-138
21411500-6	2011	Induction of survivin protein expression resulting from DATS exposure was associated with an increase in its mRNA level.	diallyl trisulfide	56-60	baculoviral IAP repeat-containing 5	Mus musculus	13-21
21411500-7	2011	Dorsolateral prostates from DATS-treated TRAMP mice exhibited statistically significant downregulation of XIAP and induction of survivin protein compared with those of control mice.	diallyl trisulfide	28-32	tumor necrosis factor receptor superfamily, member 25	Mus musculus	41-46
21411500-7	2011	Dorsolateral prostates from DATS-treated TRAMP mice exhibited statistically significant downregulation of XIAP and induction of survivin protein compared with those of control mice.	diallyl trisulfide	28-32	X-linked inhibitor of apoptosis	Mus musculus	106-110
21411500-7	2011	Dorsolateral prostates from DATS-treated TRAMP mice exhibited statistically significant downregulation of XIAP and induction of survivin protein compared with those of control mice.	diallyl trisulfide	28-32	baculoviral IAP repeat-containing 5	Mus musculus	128-136
21411500-8	2011	Ectopic expression of XIAP conferred partial but significant protection against DATS-induced apoptosis.	diallyl trisulfide	80-84	X-linked inhibitor of apoptosis	Homo sapiens	22-26
21411500-9	2011	On the other hand, DATS-induced apoptosis was only marginally affected by RNA interference of survivin or cIAP1.	diallyl trisulfide	19-23	baculoviral IAP repeat-containing 5	Mus musculus	94-102
21411500-9	2011	On the other hand, DATS-induced apoptosis was only marginally affected by RNA interference of survivin or cIAP1.	diallyl trisulfide	19-23	baculoviral IAP repeat containing 2	Homo sapiens	106-111
21411500-10	2011	In conclusion, the present study indicates that the DATS-induced apoptosis in prostate cancer cells is mediated in part by suppression of XIAP protein expression, and that XIAP represents a viable biomarker of DATS response for future clinical investigations.	diallyl trisulfide	52-56	X-linked inhibitor of apoptosis	Homo sapiens	138-142
21296648-2	2011	We now demonstrate that garlic constituent diallyl trisulfide (DATS) increases longevity of Caenorhabditis elegans by affecting the skn-1 pathway.	diallyl trisulfide	43-61	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	132-137
21296648-2	2011	We now demonstrate that garlic constituent diallyl trisulfide (DATS) increases longevity of Caenorhabditis elegans by affecting the skn-1 pathway.	diallyl trisulfide	63-67	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	132-137
21296648-5	2011	Microarray experiments demonstrated that a number of genes regulated by oxidative stress and the skn-1 transcription factor were also changed by DATS treatment.	diallyl trisulfide	145-149	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	97-102
21296648-7	2011	We also found that the effects of DATS on worm lifespan depend on skn-1 activity in both in the intestine and ASI neurons.	diallyl trisulfide	34-38	BZIP domain-containing protein;Protein skinhead-1	Caenorhabditis elegans	66-71
19748259-0	2010	Diallyl trisulfide induces Bcl-2 and caspase-3-dependent apoptosis via downregulation of Akt phosphorylation in human T24 bladder cancer cells.	diallyl trisulfide	0-18	BCL2 apoptosis regulator	Homo sapiens	27-32
21053278-0	2011	Role of Bim in diallyl trisulfide-induced cytotoxicity in human cancer cells.	diallyl trisulfide	15-33	BCL2 like 11	Homo sapiens	8-11
21053278-5	2011	DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1).	diallyl trisulfide	0-4	glutaredoxin	Homo sapiens	51-63
21053278-5	2011	DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1).	diallyl trisulfide	0-4	glutaredoxin	Homo sapiens	65-68
21053278-5	2011	DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1).	diallyl trisulfide	0-4	glutaredoxin	Homo sapiens	114-117
21053278-5	2011	DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1).	diallyl trisulfide	0-4	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	139-175
21053278-5	2011	DATS-induced oxidative stress was detected through glutaredoxin (GRX), a redox-sensing molecule, and subsequently GRX was dissociated from apoptosis signal-regulating kinase 1 (ASK1).	diallyl trisulfide	0-4	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	177-181
21053278-8	2011	SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity.	diallyl trisulfide	37-41	mitogen-activated protein kinase 8	Homo sapiens	12-15
21053278-8	2011	SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity.	diallyl trisulfide	37-41	BCL2 like 11	Homo sapiens	50-53
21053278-8	2011	SP600125, a JNK inhibitor, inhibited DATS-induced Bim phosphorylation and protected cells from DATS-induced cytotoxicity.	diallyl trisulfide	95-99	mitogen-activated protein kinase 8	Homo sapiens	12-15
21053278-9	2011	Our results indicate that the cytotoxicity caused by DATS is mediated by the generation of ROS and subsequent activation of the ASK1-JNK-Bim signal transduction pathway in human breast carcinoma MDA-MB-231 cells.	diallyl trisulfide	53-57	mitogen-activated protein kinase kinase kinase 5	Homo sapiens	128-132
21053278-9	2011	Our results indicate that the cytotoxicity caused by DATS is mediated by the generation of ROS and subsequent activation of the ASK1-JNK-Bim signal transduction pathway in human breast carcinoma MDA-MB-231 cells.	diallyl trisulfide	53-57	mitogen-activated protein kinase 8	Homo sapiens	133-136
21053278-9	2011	Our results indicate that the cytotoxicity caused by DATS is mediated by the generation of ROS and subsequent activation of the ASK1-JNK-Bim signal transduction pathway in human breast carcinoma MDA-MB-231 cells.	diallyl trisulfide	53-57	BCL2 like 11	Homo sapiens	137-140
20959517-0	2010	Diallyl trisulfide inhibits activation of signal transducer and activator of transcription 3 in prostate cancer cells in culture and in vivo.	diallyl trisulfide	0-18	signal transducer and activator of transcription 3	Homo sapiens	42-92
20959517-2	2010	The present study shows that diallyl trisulfide (DATS), a promising cancer-chemopreventive constituent of processed garlic, inhibits phosphorylation of STAT3 in prostate cancer cells in culture and in vivo.	diallyl trisulfide	29-47	signal transducer and activator of transcription 3	Homo sapiens	152-157
20959517-2	2010	The present study shows that diallyl trisulfide (DATS), a promising cancer-chemopreventive constituent of processed garlic, inhibits phosphorylation of STAT3 in prostate cancer cells in culture and in vivo.	diallyl trisulfide	49-53	signal transducer and activator of transcription 3	Homo sapiens	152-157
20959517-8	2010	In conclusion, the present study indicates that DATS treatment suppresses STAT3 phosphorylation in prostate cancer cells in culture and in vivo, but activation of this oncogenic transcription factor is largely dispensable for cellular responses to DATS.	diallyl trisulfide	48-52	signal transducer and activator of transcription 3	Homo sapiens	74-79
20143254-0	2010	Diallyl trisulfide-induced G2/M phase cell cycle arrest in DU145 cells is associated with delayed nuclear translocation of cyclin-dependent kinase 1.	diallyl trisulfide	0-18	cyclin dependent kinase 1	Homo sapiens	123-148
20143254-9	2010	CONCLUSION: The present study indicates that the DATS-mediated G2/M phase cell cycle arrest in DU145 cells results from differential kinetics of nuclear localization of cdk1 and cyclin B1.	diallyl trisulfide	49-53	cyclin dependent kinase 1	Homo sapiens	169-173
20143254-9	2010	CONCLUSION: The present study indicates that the DATS-mediated G2/M phase cell cycle arrest in DU145 cells results from differential kinetics of nuclear localization of cdk1 and cyclin B1.	diallyl trisulfide	49-53	cyclin B1	Homo sapiens	178-187
20237067-6	2010	The increase in GSTP enzyme activity in cells treated with 5 micromol/L SFN, 50 micromol/L DATS, and 600 micromol/L LA and DHLA was 172, 75, 122, and 117%, respectively (P < 0.05).	diallyl trisulfide	91-95	glutathione S-transferase pi 1	Rattus norvegicus	16-20
21147075-0	2011	Neuroprotective effects of diallyl trisulfide in SOD1-G93A transgenic mouse model of amyotrophic lateral sclerosis.	diallyl trisulfide	27-45	superoxide dismutase 1, soluble	Mus musculus	49-53
20802973-0	2010	Caspase-8 and p38MAPK in DATS-induced apoptosis of human CNE2 cells.	diallyl trisulfide	25-29	caspase 8	Homo sapiens	0-9
20802973-3	2010	In this study, we investigated the function of p38 mitogen-activated protein kinase (MAPK) and caspase-8 in DATS-induced apoptosis of human CNE2 cells using MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide], flow cytometry assay, and Western blotting.	diallyl trisulfide	108-112	mitogen-activated protein kinase 14	Homo sapiens	47-83
20802973-3	2010	In this study, we investigated the function of p38 mitogen-activated protein kinase (MAPK) and caspase-8 in DATS-induced apoptosis of human CNE2 cells using MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide], flow cytometry assay, and Western blotting.	diallyl trisulfide	108-112	caspase 8	Homo sapiens	95-104
20802973-9	2010	The results indicated that DATS activates p38MAPK and caspase-8, but both inhibitors have an effect on P38MAPK and caspase-8 activity.	diallyl trisulfide	27-31	caspase 8	Homo sapiens	54-63
20802973-10	2010	In conclusion, our data indicate that p38MAPK and caspase-8 are involved in the process of DATS-induced apoptosis in human CNE2 cells and interact with each other.	diallyl trisulfide	91-95	caspase 8	Homo sapiens	50-59
19748259-0	2010	Diallyl trisulfide induces Bcl-2 and caspase-3-dependent apoptosis via downregulation of Akt phosphorylation in human T24 bladder cancer cells.	diallyl trisulfide	0-18	caspase 3	Homo sapiens	37-46
19748259-0	2010	Diallyl trisulfide induces Bcl-2 and caspase-3-dependent apoptosis via downregulation of Akt phosphorylation in human T24 bladder cancer cells.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	89-92
19748259-4	2010	Mechanistically, DATS inhibits phosphatidylinositol 3"-kinase/Akt activation that, in turn, results in modulation of Bcl-2 family proteins, leading to enhanced apoptosis of T24 cells.	diallyl trisulfide	17-21	AKT serine/threonine kinase 1	Homo sapiens	62-65
19748259-4	2010	Mechanistically, DATS inhibits phosphatidylinositol 3"-kinase/Akt activation that, in turn, results in modulation of Bcl-2 family proteins, leading to enhanced apoptosis of T24 cells.	diallyl trisulfide	17-21	BCL2 apoptosis regulator	Homo sapiens	117-122
20179211-0	2010	Diallyl trisulfide inhibits phorbol ester-induced tumor promotion, activation of AP-1, and expression of COX-2 in mouse skin by blocking JNK and Akt signaling.	diallyl trisulfide	0-18	jun proto-oncogene	Mus musculus	81-85
20179211-0	2010	Diallyl trisulfide inhibits phorbol ester-induced tumor promotion, activation of AP-1, and expression of COX-2 in mouse skin by blocking JNK and Akt signaling.	diallyl trisulfide	0-18	mitogen-activated protein kinase 8	Mus musculus	137-140
20179211-0	2010	Diallyl trisulfide inhibits phorbol ester-induced tumor promotion, activation of AP-1, and expression of COX-2 in mouse skin by blocking JNK and Akt signaling.	diallyl trisulfide	0-18	thymoma viral proto-oncogene 1	Mus musculus	145-148
20055834-0	2009	Diallyl trisulphide-induced apoptosis in human melanoma cells involves downregulation of Bcl-2 and Bcl-xL expression and activation of caspases.	diallyl trisulfide	0-19	BCL2 apoptosis regulator	Homo sapiens	89-94
20055834-0	2009	Diallyl trisulphide-induced apoptosis in human melanoma cells involves downregulation of Bcl-2 and Bcl-xL expression and activation of caspases.	diallyl trisulfide	0-19	BCL2 like 1	Homo sapiens	99-105
20055834-0	2009	Diallyl trisulphide-induced apoptosis in human melanoma cells involves downregulation of Bcl-2 and Bcl-xL expression and activation of caspases.	diallyl trisulfide	0-19	caspase 9	Homo sapiens	135-143
20055834-4	2009	Apoptosis induction in DATS-treated cells was assessed by staining with 4",6-diamidino-2-phenylindole (DAPI) and double staining with annexin V and propidium iodide.	diallyl trisulfide	23-27	annexin A5	Homo sapiens	134-143
19459175-0	2009	Diallyl trisulfide-induced apoptosis in human cancer cells is linked to checkpoint kinase 1-mediated mitotic arrest.	diallyl trisulfide	0-18	checkpoint kinase 1	Homo sapiens	72-91
19823037-6	2009	DATS-induced apoptosis was markedly elevated in MCF-7 cells compared with MCF-12a cells and this was correlated with elevated levels of cyclin B1.	diallyl trisulfide	0-4	cyclin B1	Homo sapiens	136-145
19823037-7	2009	The results from semi-quantitative and real-time RT-PCR indicated that DATS-enhanced the expression levels of FAS and cyclin D1, but in contrast, downregulated the expression levels of Akt and Bcl-2.	diallyl trisulfide	71-75	cyclin D1	Homo sapiens	118-127
19823037-7	2009	The results from semi-quantitative and real-time RT-PCR indicated that DATS-enhanced the expression levels of FAS and cyclin D1, but in contrast, downregulated the expression levels of Akt and Bcl-2.	diallyl trisulfide	71-75	AKT serine/threonine kinase 1	Homo sapiens	185-188
19823037-7	2009	The results from semi-quantitative and real-time RT-PCR indicated that DATS-enhanced the expression levels of FAS and cyclin D1, but in contrast, downregulated the expression levels of Akt and Bcl-2.	diallyl trisulfide	71-75	BCL2 apoptosis regulator	Homo sapiens	193-198
19459175-8	2009	Even though DATS treatment resulted in stabilization and Ser15 phosphorylation of p53, the knockdown of p53 protein failed to rescue DATS-induced mitotic arrest.	diallyl trisulfide	12-16	tumor protein p53	Homo sapiens	82-85
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	29-47	checkpoint kinase 1	Homo sapiens	166-185
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	29-47	checkpoint kinase 1	Homo sapiens	187-191
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	49-53	checkpoint kinase 1	Homo sapiens	166-185
19459175-1	2009	Growth suppressive effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, against cultured human cancer cells correlates with checkpoint kinase 1 (Chk1)-mediated mitotic arrest, but the fate of the cells arrested in mitosis remains elusive.	diallyl trisulfide	49-53	checkpoint kinase 1	Homo sapiens	187-191
19622577-0	2009	Transcriptional repression and inhibition of nuclear translocation of androgen receptor by diallyl trisulfide in human prostate cancer cells.	diallyl trisulfide	91-109	androgen receptor	Homo sapiens	70-87
19622577-1	2009	PURPOSE: The present study was undertaken to determine the effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, on androgen receptor (AR) protein expression and function using prostate cancer cells.	diallyl trisulfide	69-87	androgen receptor	Homo sapiens	157-174
19622577-1	2009	PURPOSE: The present study was undertaken to determine the effect of diallyl trisulfide (DATS), a promising cancer chemopreventive constituent of garlic, on androgen receptor (AR) protein expression and function using prostate cancer cells.	diallyl trisulfide	89-93	androgen receptor	Homo sapiens	157-174
19622577-3	2009	The effect of DATS treatment on AR mRNA level and AR promoter activity was determined by quantitative reverse transcription-PCR and luciferase reporter assay, respectively.	diallyl trisulfide	14-18	androgen receptor	Homo sapiens	32-34
19622577-3	2009	The effect of DATS treatment on AR mRNA level and AR promoter activity was determined by quantitative reverse transcription-PCR and luciferase reporter assay, respectively.	diallyl trisulfide	14-18	androgen receptor	Homo sapiens	50-52
19622577-7	2009	RESULTS: Exposure of prostate cancer cells (LNCaP, C4-2, and TRAMP-C1) to DATS resulted in a concentration-dependent decrease in protein level of AR, which was accompanied by suppression of intracellular and secreted levels of PSA.	diallyl trisulfide	74-78	tumor necrosis factor receptor superfamily, member 25	Mus musculus	61-66
19622577-7	2009	RESULTS: Exposure of prostate cancer cells (LNCaP, C4-2, and TRAMP-C1) to DATS resulted in a concentration-dependent decrease in protein level of AR, which was accompanied by suppression of intracellular and secreted levels of PSA.	diallyl trisulfide	74-78	androgen receptor	Homo sapiens	146-148
19622577-7	2009	RESULTS: Exposure of prostate cancer cells (LNCaP, C4-2, and TRAMP-C1) to DATS resulted in a concentration-dependent decrease in protein level of AR, which was accompanied by suppression of intracellular and secreted levels of PSA.	diallyl trisulfide	74-78	kallikrein related peptidase 3	Homo sapiens	227-230
19622577-8	2009	Structure-activity studies revealed critical roles for allyl groups and the oligosulfide chain length in DATS-mediated down-modulation of AR protein.	diallyl trisulfide	105-109	androgen receptor	Homo sapiens	138-140
19622577-11	2009	Oral gavage of 2 mg/day DATS (three times per week for 13 weeks) markedly suppressed AR protein level in poorly differentiated prostate cancer in TRAMP mice.	diallyl trisulfide	24-28	tumor necrosis factor receptor superfamily, member 25	Mus musculus	146-151
19622577-12	2009	CONCLUSION: The present study shows, for the first time, that DATS treatment suppresses AR function in prostate cancer cells.	diallyl trisulfide	62-66	androgen receptor	Homo sapiens	88-90
21475820-0	2009	Diallyl trisulfide reverses drug resistance and lowers the ratio of CD133+ cells in conjunction with methotrexate in a human osteosarcoma drug-resistant cell subline.	diallyl trisulfide	0-18	prominin 1	Homo sapiens	68-73
18800351-10	2009	In conclusion, the present study indicates that Bax and Bak proteins are critical targets of DATS-induced apoptosis in human lung cancer cells.	diallyl trisulfide	93-97	BCL2 associated X, apoptosis regulator	Homo sapiens	48-51
18800351-10	2009	In conclusion, the present study indicates that Bax and Bak proteins are critical targets of DATS-induced apoptosis in human lung cancer cells.	diallyl trisulfide	93-97	BCL2 antagonist/killer 1	Homo sapiens	56-59
19197990-8	2009	Further investigation revealed that the specific JNK inhibitor SP600125 and the antioxidant NAC blocked DADS and DATS-induced apoptosis, whereas ERK inhibitors did not.	diallyl trisulfide	113-117	mitogen-activated protein kinase 8	Homo sapiens	49-52
19298793-8	2009	We conclude that DAS, DADS, and DATS are agonist of both TRPA1 and TRPV1 but with high affinity for TRPA1.	diallyl trisulfide	32-36	LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily A member 1	Cricetulus griseus	57-62
19298793-8	2009	We conclude that DAS, DADS, and DATS are agonist of both TRPA1 and TRPV1 but with high affinity for TRPA1.	diallyl trisulfide	32-36	LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily V member 1	Cricetulus griseus	67-72
19298793-8	2009	We conclude that DAS, DADS, and DATS are agonist of both TRPA1 and TRPV1 but with high affinity for TRPA1.	diallyl trisulfide	32-36	LOW QUALITY PROTEIN: transient receptor potential cation channel subfamily A member 1	Cricetulus griseus	100-105
18800351-0	2009	Diallyl trisulfide selectively causes Bax- and Bak-mediated apoptosis in human lung cancer cells.	diallyl trisulfide	0-18	BCL2 associated X, apoptosis regulator	Homo sapiens	38-41
18800351-0	2009	Diallyl trisulfide selectively causes Bax- and Bak-mediated apoptosis in human lung cancer cells.	diallyl trisulfide	0-18	BCL2 antagonist/killer 1	Homo sapiens	47-50
18800351-8	2009	Knockdown of Bax and Bak proteins conferred significant protection against DATS-induced apoptotic cytoplasmic histone-associated DNA fragmentation.	diallyl trisulfide	75-79	BCL2 associated X, apoptosis regulator	Homo sapiens	13-16
18800351-8	2009	Knockdown of Bax and Bak proteins conferred significant protection against DATS-induced apoptotic cytoplasmic histone-associated DNA fragmentation.	diallyl trisulfide	75-79	BCL2 antagonist/killer 1	Homo sapiens	21-24
21475820-3	2009	In the present study, we demonstrated that DATS down-regulated P-gp expression and reversed drug resistance.	diallyl trisulfide	43-47	ATP binding cassette subfamily B member 1	Homo sapiens	63-67
21475820-4	2009	DATS and methotrexate (MTX) decreased the ratio of drug-resistant human osteosarcoma cells positive for CD133 (a tumor stem cell marker).	diallyl trisulfide	0-4	prominin 1	Homo sapiens	104-109
21475820-5	2009	To the best of our knowledge, this is the first evidence that DATS can reverse drug resistance and lower the ratio of CD133+ cells in human osteosarcoma cells in conjunction with MTX.	diallyl trisulfide	62-66	prominin 1	Homo sapiens	118-123
18768114-6	2009	Diallyl trisulfide (DATS) was previously shown to induce many Nrf2 target genes in non-nervous cells.	diallyl trisulfide	0-18	NFE2 like bZIP transcription factor 2	Rattus norvegicus	62-66
18768114-6	2009	Diallyl trisulfide (DATS) was previously shown to induce many Nrf2 target genes in non-nervous cells.	diallyl trisulfide	20-24	NFE2 like bZIP transcription factor 2	Rattus norvegicus	62-66
18768114-7	2009	Our studies have shown that DATS at 50 microM caused activation of Nrf2 and Nrf2 target gene in rat spinal cord explants.	diallyl trisulfide	28-32	NFE2 like bZIP transcription factor 2	Rattus norvegicus	67-71
18768114-7	2009	Our studies have shown that DATS at 50 microM caused activation of Nrf2 and Nrf2 target gene in rat spinal cord explants.	diallyl trisulfide	28-32	NFE2 like bZIP transcription factor 2	Rattus norvegicus	76-80
18768114-9	2009	These have identified DATS as a promising neuroprotective agent and suggest that the activation of Nrf2 signal pathway may be a new strategy in neurodegeneration disease.	diallyl trisulfide	22-26	NFE2 like bZIP transcription factor 2	Rattus norvegicus	99-103
18492825-8	2008	The protein kinase A (PKA) inhibitor H89 reversed the suppression of VCAM-1 by DADS and DATS, but the phosphoinositide 3-kinase (PI3K) inhibitor wortmannin had no effect.	diallyl trisulfide	88-92	vascular cell adhesion molecule 1	Homo sapiens	69-75
18723480-0	2008	Diallyl trisulfide increases the effectiveness of TRAIL and inhibits prostate cancer growth in an orthotopic model: molecular mechanisms.	diallyl trisulfide	0-18	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	50-55
18723480-2	2008	The objectives of this study were to investigate the molecular mechanisms by which diallyl trisulfide (DATS) enhanced the therapeutic potential of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in prostate cancer cells in vitro and on orthotopically transplanted PC-3 prostate carcinoma in nude mice.	diallyl trisulfide	83-101	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	147-202
18723480-2	2008	The objectives of this study were to investigate the molecular mechanisms by which diallyl trisulfide (DATS) enhanced the therapeutic potential of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in prostate cancer cells in vitro and on orthotopically transplanted PC-3 prostate carcinoma in nude mice.	diallyl trisulfide	83-101	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	204-209
18723480-2	2008	The objectives of this study were to investigate the molecular mechanisms by which diallyl trisulfide (DATS) enhanced the therapeutic potential of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in prostate cancer cells in vitro and on orthotopically transplanted PC-3 prostate carcinoma in nude mice.	diallyl trisulfide	103-107	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	147-202
18723480-2	2008	The objectives of this study were to investigate the molecular mechanisms by which diallyl trisulfide (DATS) enhanced the therapeutic potential of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in prostate cancer cells in vitro and on orthotopically transplanted PC-3 prostate carcinoma in nude mice.	diallyl trisulfide	103-107	tumor necrosis factor (ligand) superfamily, member 10	Mus musculus	204-209
18723480-4	2008	DATS enhanced the apoptosis-inducing potential of TRAIL in PC-3 cells and sensitized TRAIL-resistant LNCaP cells.	diallyl trisulfide	0-4	TNF superfamily member 10	Homo sapiens	50-55
18723480-4	2008	DATS enhanced the apoptosis-inducing potential of TRAIL in PC-3 cells and sensitized TRAIL-resistant LNCaP cells.	diallyl trisulfide	0-4	TNF superfamily member 10	Homo sapiens	85-90
18723480-5	2008	Dominant-negative FADD inhibited the synergistic interaction between DATS and TRAIL on apoptosis.	diallyl trisulfide	69-73	Fas (TNFRSF6)-associated via death domain	Mus musculus	18-22
18492825-0	2008	Diallyl disulfide and diallyl trisulfide suppress oxidized LDL-induced vascular cell adhesion molecule and E-selectin expression through protein kinase A- and B-dependent signaling pathways.	diallyl trisulfide	22-40	selectin E	Homo sapiens	107-117
18492825-0	2008	Diallyl disulfide and diallyl trisulfide suppress oxidized LDL-induced vascular cell adhesion molecule and E-selectin expression through protein kinase A- and B-dependent signaling pathways.	diallyl trisulfide	22-40	protein tyrosine kinase 2 beta	Homo sapiens	137-160
18624451-5	2008	In addition, tea polyphenols and diallyl trisulfide could increase glutathione S-transferase activity remarkably.	diallyl trisulfide	33-51	glutathione S-transferase kappa 1	Homo sapiens	67-92
18492825-9	2008	In contrast, wortmannin abolished DADS- and DATS-induced suppression of ox-LDL-induced E-selectin expression.	diallyl trisulfide	44-48	selectin E	Homo sapiens	87-97
17513609-0	2007	Mitochondria-mediated apoptosis by diallyl trisulfide in human prostate cancer cells is associated with generation of reactive oxygen species and regulated by Bax/Bak.	diallyl trisulfide	35-53	BCL2 associated X, apoptosis regulator	Homo sapiens	159-162
17513609-0	2007	Mitochondria-mediated apoptosis by diallyl trisulfide in human prostate cancer cells is associated with generation of reactive oxygen species and regulated by Bax/Bak.	diallyl trisulfide	35-53	BCL2 antagonist/killer 1	Homo sapiens	163-166
17513609-8	2007	In conclusion, the present study reveals that the mitochondria-mediated cell death by DATS is associated with ROS generation and regulated by Bax/Bak but independent of Bcl-2 or Bcl-xL.	diallyl trisulfide	86-90	BCL2 associated X, apoptosis regulator	Homo sapiens	142-145
17513609-8	2007	In conclusion, the present study reveals that the mitochondria-mediated cell death by DATS is associated with ROS generation and regulated by Bax/Bak but independent of Bcl-2 or Bcl-xL.	diallyl trisulfide	86-90	BCL2 antagonist/killer 1	Homo sapiens	146-149
17406033-9	2007	In conclusion, the present study describes a novel signaling pathway involving ATR/Chk1 in the regulation of DATS-induced prometaphase arrest.	diallyl trisulfide	109-113	ATR serine/threonine kinase	Homo sapiens	79-82
17045015-0	2006	[Effect of allitridum on expression of the gamma-glutamyl-cysteine synthetase in rat lung epithelial L2 cells].	diallyl trisulfide	11-21	glutamate-cysteine ligase, catalytic subunit	Rattus norvegicus	43-77
17059769-2	2006	This study was to investigate the changes and significance of caspase-3 activity in diallyl trisulfide (DATS)-induced apoptosis of human gastric cancer cell line MGC803.	diallyl trisulfide	104-108	caspase 3	Homo sapiens	62-71
17059769-6	2006	Moreover, pro-caspase-3 was hydrolyzed and activated in DATS-treated MGC803 cells.	diallyl trisulfide	56-60	caspase 3	Homo sapiens	10-23
17059769-7	2006	CONCLUSION: DATS induces apoptosis in MGC803 cells which may be through the activation of caspase-3 pathway.	diallyl trisulfide	12-16	caspase 3	Homo sapiens	90-99
17448272-0	2007	[Effect of diallyl trisulfide on tumor necrosis factor-alpha expression and nuclear factor-KappaB activity in mice with acute lung injury induced by lipopolysaccharide].	diallyl trisulfide	11-29	tumor necrosis factor	Mus musculus	33-60
17448272-1	2007	OBJECTIVE: To investigate the effect of diallyl trisulfide (DATS) on tumor necrosis factor-alpha (TNF-alpha) expression and nuclear factor-KappaB (NF-KappaB) activity in mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS).	diallyl trisulfide	40-58	tumor necrosis factor	Mus musculus	69-96
17448272-1	2007	OBJECTIVE: To investigate the effect of diallyl trisulfide (DATS) on tumor necrosis factor-alpha (TNF-alpha) expression and nuclear factor-KappaB (NF-KappaB) activity in mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS).	diallyl trisulfide	60-64	tumor necrosis factor	Mus musculus	69-96
17448272-1	2007	OBJECTIVE: To investigate the effect of diallyl trisulfide (DATS) on tumor necrosis factor-alpha (TNF-alpha) expression and nuclear factor-KappaB (NF-KappaB) activity in mice with acute lung injury (ALI) induced by lipopolysaccharide (LPS).	diallyl trisulfide	60-64	tumor necrosis factor	Mus musculus	98-107
17448272-9	2007	The expression of TNF-alpha mRNA in the lung tissues of ALI group increased markedly at 2 hours compared with those of control groups (both P<0.01), and it could be down-regulated by pretreatment with DATS (P<0.05).	diallyl trisulfide	204-208	tumor necrosis factor	Mus musculus	18-27
17448272-12	2007	CONCLUSION: Pretreatment of DATS for ALI in mice could inhibit NF-KappaB activity, TNF-alpha mRNA expression in lung tissues, and decrease the release of TNF-alpha in the serum and the lung homogenates, and they might be the underlying mechanisms of prevention of the occurrence of ALI by DATS.	diallyl trisulfide	28-32	nuclear factor of kappa light polypeptide gene enhancer in B cells 1, p105	Mus musculus	63-72
17448272-12	2007	CONCLUSION: Pretreatment of DATS for ALI in mice could inhibit NF-KappaB activity, TNF-alpha mRNA expression in lung tissues, and decrease the release of TNF-alpha in the serum and the lung homogenates, and they might be the underlying mechanisms of prevention of the occurrence of ALI by DATS.	diallyl trisulfide	28-32	tumor necrosis factor	Mus musculus	83-92
17448272-12	2007	CONCLUSION: Pretreatment of DATS for ALI in mice could inhibit NF-KappaB activity, TNF-alpha mRNA expression in lung tissues, and decrease the release of TNF-alpha in the serum and the lung homogenates, and they might be the underlying mechanisms of prevention of the occurrence of ALI by DATS.	diallyl trisulfide	28-32	tumor necrosis factor	Mus musculus	154-163
17121905-0	2006	Diallyl trisulfide suppresses growth of PC-3 human prostate cancer xenograft in vivo in association with Bax and Bak induction.	diallyl trisulfide	0-18	BCL2 associated X, apoptosis regulator	Homo sapiens	105-108
17121905-0	2006	Diallyl trisulfide suppresses growth of PC-3 human prostate cancer xenograft in vivo in association with Bax and Bak induction.	diallyl trisulfide	0-18	BCL2 antagonist/killer 1	Homo sapiens	113-116
17121905-11	2006	CONCLUSIONS: The present study indicates that DATS administration inhibits growth of PC-3 xenografts in vivo in association with induction of Bax and Bak.	diallyl trisulfide	46-50	BCL2-associated X protein	Mus musculus	142-145
17121905-11	2006	CONCLUSIONS: The present study indicates that DATS administration inhibits growth of PC-3 xenografts in vivo in association with induction of Bax and Bak.	diallyl trisulfide	46-50	BCL2-antagonist/killer 1	Mus musculus	150-153
17059769-0	2006	[Diallyl trisulfide induces apoptosis of human gastric cancer cell line MGC803 through caspase-3 pathway].	diallyl trisulfide	1-19	caspase 3	Homo sapiens	87-96
17059769-2	2006	This study was to investigate the changes and significance of caspase-3 activity in diallyl trisulfide (DATS)-induced apoptosis of human gastric cancer cell line MGC803.	diallyl trisulfide	84-102	caspase 3	Homo sapiens	62-71
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	435-453	programmed cell death 5	Homo sapiens	44-49
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	435-453	programmed cell death 5	Homo sapiens	215-220
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	435-453	BCL2 apoptosis regulator	Homo sapiens	285-290
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	435-453	programmed cell death 5	Homo sapiens	215-220
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	455-459	programmed cell death 5	Homo sapiens	44-49
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	455-459	programmed cell death 5	Homo sapiens	215-220
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	455-459	BCL2 apoptosis regulator	Homo sapiens	285-290
16547588-4	2006	Our data revealed that the positive rate of PDCD5 expression in the gastric tumor tissues was significantly less than that of the normal tissues (14 out of 102 vs 36 out of 51), whereas, the decreased expression of PDCD5 protein was well correlated with the up-regulated expression of Bcl-2 in these tissues, and the up-regulated expression and nuclear translocation of PDCD5 protein were verified in the apoptotic GC cells induced by Diallyl trisulfide (DATS).	diallyl trisulfide	455-459	programmed cell death 5	Homo sapiens	215-220
16707465-6	2006	Interestingly, DATS-mediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arrest were significantly attenuated by ectopic expression of a catalytically inactive mutant of JNK kinase 2 and RNA interference of stress-activated protein kinase/extracellular signal-regulated kinase 1 (SEK1), upstream kinases in JNK signal transduction pathway.	diallyl trisulfide	15-19	mitogen-activated protein kinase 8	Homo sapiens	215-218
16707465-6	2006	Interestingly, DATS-mediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arrest were significantly attenuated by ectopic expression of a catalytically inactive mutant of JNK kinase 2 and RNA interference of stress-activated protein kinase/extracellular signal-regulated kinase 1 (SEK1), upstream kinases in JNK signal transduction pathway.	diallyl trisulfide	15-19	mitogen-activated protein kinase 3	Homo sapiens	284-323
16707465-6	2006	Interestingly, DATS-mediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arrest were significantly attenuated by ectopic expression of a catalytically inactive mutant of JNK kinase 2 and RNA interference of stress-activated protein kinase/extracellular signal-regulated kinase 1 (SEK1), upstream kinases in JNK signal transduction pathway.	diallyl trisulfide	15-19	mitogen-activated protein kinase kinase 4	Homo sapiens	325-329
16707465-6	2006	Interestingly, DATS-mediated degradation of ferritin, increase in labile iron pool, ROS generation, and/or cell cycle arrest were significantly attenuated by ectopic expression of a catalytically inactive mutant of JNK kinase 2 and RNA interference of stress-activated protein kinase/extracellular signal-regulated kinase 1 (SEK1), upstream kinases in JNK signal transduction pathway.	diallyl trisulfide	15-19	mitogen-activated protein kinase 8	Homo sapiens	352-355
16796841-11	2006	CONCLUSION: Stent coated with diallyl trisulfide promotes the endothelialization and expression of eNOS, and raises the NO level.	diallyl trisulfide	30-48	nitric oxide synthase 3	Canis lupus familiaris	99-103
16169930-0	2006	Diallyl trisulfide, a constituent of processed garlic, inactivates Akt to trigger mitochondrial translocation of BAD and caspase-mediated apoptosis in human prostate cancer cells.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	67-70
16169930-1	2006	We have shown previously that apoptosis induction by diallyl trisulfide (DATS), a constituent of processed garlic, in PC-3 and DU145 human prostate cancer cells is associated with c-Jun N-terminal kinase and extracellular signal-regulated kinase-mediated phosphorylation of Bcl-2.	diallyl trisulfide	53-71	BCL2 apoptosis regulator	Homo sapiens	274-279
16169930-1	2006	We have shown previously that apoptosis induction by diallyl trisulfide (DATS), a constituent of processed garlic, in PC-3 and DU145 human prostate cancer cells is associated with c-Jun N-terminal kinase and extracellular signal-regulated kinase-mediated phosphorylation of Bcl-2.	diallyl trisulfide	73-77	BCL2 apoptosis regulator	Homo sapiens	274-279
16169930-3	2006	Here, we demonstrate that DATS inactivates Akt to trigger apoptosis in prostate cancer cells.	diallyl trisulfide	26-30	AKT serine/threonine kinase 1	Homo sapiens	43-46
16169930-4	2006	Treatment of PC-3/DU145 cells with apoptosis inducing concentration of DATS (40 microM) resulted in a rapid decrease in Ser(473) and Thr(308) phosphorylation of Akt leading to inhibition of its kinase activity.	diallyl trisulfide	71-75	AKT serine/threonine kinase 1	Homo sapiens	161-164
16169930-6	2006	DATS treatment (40 microM) also caused a decrease in Ser(155) and Ser(136) phosphorylation of BAD (a proapoptotic protein), which is a downstream target of Akt.	diallyl trisulfide	0-4	AKT serine/threonine kinase 1	Homo sapiens	156-159
16169930-10	2006	Ectopic expression of constitutively active Akt conferred statistically significant protection against DATS-induced apoptosis.	diallyl trisulfide	103-107	AKT serine/threonine kinase 1	Homo sapiens	44-47
16169930-12	2006	In conclusion, the present study demonstrates that DATS-induced apoptosis in human prostate cancer cells is mediated, at least in part, by inactivation of Akt signaling axis.	diallyl trisulfide	51-55	AKT serine/threonine kinase 1	Homo sapiens	155-158
16965246-7	2006	DATS treatment inhibited the formation of capillary-like tube structure and migration by HUVECs in association with suppression of vascular endothelial growth factor (VEGF) secretion and VEGF receptor-2 protein level and inactivation of Akt kinase.	diallyl trisulfide	0-4	vascular endothelial growth factor A	Homo sapiens	131-165
16707465-7	2006	In conclusion, the present study provides experimental evidence to indicate existence of a novel pathway involving JNK signaling axis in regulation of DATS-induced ROS generation.	diallyl trisulfide	151-155	mitogen-activated protein kinase 8	Homo sapiens	115-118
16965246-7	2006	DATS treatment inhibited the formation of capillary-like tube structure and migration by HUVECs in association with suppression of vascular endothelial growth factor (VEGF) secretion and VEGF receptor-2 protein level and inactivation of Akt kinase.	diallyl trisulfide	0-4	vascular endothelial growth factor A	Homo sapiens	167-171
16965246-7	2006	DATS treatment inhibited the formation of capillary-like tube structure and migration by HUVECs in association with suppression of vascular endothelial growth factor (VEGF) secretion and VEGF receptor-2 protein level and inactivation of Akt kinase.	diallyl trisulfide	0-4	vascular endothelial growth factor A	Homo sapiens	187-191
16965246-7	2006	DATS treatment inhibited the formation of capillary-like tube structure and migration by HUVECs in association with suppression of vascular endothelial growth factor (VEGF) secretion and VEGF receptor-2 protein level and inactivation of Akt kinase.	diallyl trisulfide	0-4	AKT serine/threonine kinase 1	Homo sapiens	237-240
16965246-0	2006	Diallyl trisulfide inhibits angiogenic features of human umbilical vein endothelial cells by causing Akt inactivation and down-regulation of VEGF and VEGF-R2.	diallyl trisulfide	0-18	AKT serine/threonine kinase 1	Homo sapiens	101-104
16965246-0	2006	Diallyl trisulfide inhibits angiogenic features of human umbilical vein endothelial cells by causing Akt inactivation and down-regulation of VEGF and VEGF-R2.	diallyl trisulfide	0-18	vascular endothelial growth factor A	Homo sapiens	141-145
16965246-0	2006	Diallyl trisulfide inhibits angiogenic features of human umbilical vein endothelial cells by causing Akt inactivation and down-regulation of VEGF and VEGF-R2.	diallyl trisulfide	0-18	kinase insert domain receptor	Homo sapiens	150-157
16965246-1	2006	We have shown recently that diallyl trisulfide (DATS), a cancer-chemopreventive constituent of garlic, inactivates Akt to trigger mitochondrial translocation of proapoptotic protein BAD in human prostate cancer cells.	diallyl trisulfide	28-46	AKT serine/threonine kinase 1	Homo sapiens	115-118
16965246-1	2006	We have shown recently that diallyl trisulfide (DATS), a cancer-chemopreventive constituent of garlic, inactivates Akt to trigger mitochondrial translocation of proapoptotic protein BAD in human prostate cancer cells.	diallyl trisulfide	48-52	AKT serine/threonine kinase 1	Homo sapiens	115-118
15940258-0	2005	Diallyl trisulfide-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by reactive oxygen species-dependent destruction and hyperphosphorylation of Cdc 25 C.	diallyl trisulfide	0-18	cell division cycle 25C	Homo sapiens	176-184
15940258-7	2005	DATS treatment also caused an increase in the protein level of Cdk inhibitor p21, but DATS-induced G(2)-M phase arrest was not affected by antisense-mediated suppression of p21 protein level.	diallyl trisulfide	0-4	cyclin dependent kinase inhibitor 1A	Homo sapiens	77-80
15940258-8	2005	In conclusion, the results of the present study indicate that DATS-induced G(2)-M phase cell cycle arrest in human prostate cancer cells is caused by ROS-mediated destruction and hyperphosphorylation of Cdc 25 C.	diallyl trisulfide	62-66	cell division cycle 25C	Homo sapiens	203-211
16382202-6	2005	The results showed that peroxisome proliferator activated receptor alpha (PPAR-alpha) and hepatocyte nuclear factor 4alpha (HNF-4alpha) mRNA were up-regulated, and CYP7A1 mRNA was down-regulated following DT treatment, suggesting that the lipid-lowering effects of DT may be at least in part mediated through the regulation of PPAR-alpha dependent pathways.	diallyl trisulfide	205-207	peroxisome proliferator activated receptor alpha	Homo sapiens	24-72
16382202-6	2005	The results showed that peroxisome proliferator activated receptor alpha (PPAR-alpha) and hepatocyte nuclear factor 4alpha (HNF-4alpha) mRNA were up-regulated, and CYP7A1 mRNA was down-regulated following DT treatment, suggesting that the lipid-lowering effects of DT may be at least in part mediated through the regulation of PPAR-alpha dependent pathways.	diallyl trisulfide	205-207	peroxisome proliferator activated receptor alpha	Homo sapiens	74-84
16382202-6	2005	The results showed that peroxisome proliferator activated receptor alpha (PPAR-alpha) and hepatocyte nuclear factor 4alpha (HNF-4alpha) mRNA were up-regulated, and CYP7A1 mRNA was down-regulated following DT treatment, suggesting that the lipid-lowering effects of DT may be at least in part mediated through the regulation of PPAR-alpha dependent pathways.	diallyl trisulfide	205-207	hepatocyte nuclear factor 4 alpha	Homo sapiens	124-134
16382202-6	2005	The results showed that peroxisome proliferator activated receptor alpha (PPAR-alpha) and hepatocyte nuclear factor 4alpha (HNF-4alpha) mRNA were up-regulated, and CYP7A1 mRNA was down-regulated following DT treatment, suggesting that the lipid-lowering effects of DT may be at least in part mediated through the regulation of PPAR-alpha dependent pathways.	diallyl trisulfide	205-207	cytochrome P450 family 7 subfamily A member 1	Homo sapiens	164-170
16382202-6	2005	The results showed that peroxisome proliferator activated receptor alpha (PPAR-alpha) and hepatocyte nuclear factor 4alpha (HNF-4alpha) mRNA were up-regulated, and CYP7A1 mRNA was down-regulated following DT treatment, suggesting that the lipid-lowering effects of DT may be at least in part mediated through the regulation of PPAR-alpha dependent pathways.	diallyl trisulfide	265-267	peroxisome proliferator activated receptor alpha	Homo sapiens	74-84