PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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	
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	
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	
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	
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	
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	
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	
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	455-459	BCL2 apoptosis regulator	Homo sapiens	285-290	
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	
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	
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	
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	
15184882-9	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	
15184882-11	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