PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22211240-3	2012	Previous studies in our lab revealed that imatinib-induced apoptosis in K562 cells involves a shift in production of Bcl-x splice isoforms towards the pro-apoptotic Bcl-xs splice variant.	Imatinib Mesylate	42-50	BCL2 like 1	Homo sapiens	117-122	
28319085-4	2017	These included the BCL2L1 and MCL1 combination, which was also effective in imatinib-resistant cells.	Imatinib Mesylate	76-84	BCL2 like 1	Homo sapiens	19-25	
26987906-5	2016	Disrupting this antiapoptotic phenotype by inhibition of BCL-XL via RNA interference or A-1331852, a novel, potent and BCL-XL-selective inhibitor, resulted in extensive apoptosis either alone or in combination with imatinib, dasatinib or nilotinib, both in cell lines and in primary CD34(+) cells from patients with high levels of CIP2A.	Imatinib Mesylate	215-223	BCL2 like 1	Homo sapiens	57-63	
24504921-8	2014	Mechanistically, depletion of the transcription factor GATA4 resulting in decreased levels of its prosurvival targets Bcl-2 and Bcl-XL was an underlying cause of imatinib toxicity.	Imatinib Mesylate	162-170	BCL2 like 1	Homo sapiens	128-134	
24088895-9	2014	Sequential treatment with activin A and imatinib decreased Bcr-Abl, procaspase-3, Mcl-1, and Bcl-xL and also induced cleavage of procaspase-3/poly(ADP-ribose)polymerase.	Imatinib Mesylate	40-48	BCL2 like 1	Homo sapiens	93-99	
23613979-8	2013	Sequential treatment with ACM and imatinib induced Bcr-Abl down-regulation, cytochrome c release into the cytosol, and caspase-3 activation, as well as decreased Mcl-1 and Bcl-xL expressions, but did not affect Fas ligand/Fas death receptor and procaspase-8 expressions.	Imatinib Mesylate	34-42	BCL2 like 1	Homo sapiens	172-178	
26473951-6	2015	In KOSR-protected CML cells, imatinib still inhibited the BCR-ABL tyrosine kinase, reduced the phosphorylation of STAT, ERK and AKT, down-regulated BCL2, BCLxL, MCL1 and up-regulated BIM.	Imatinib Mesylate	29-37	BCL2 like 1	Homo sapiens	154-159	
21115411-10	2011	CONCLUSION: We provide the first preclinical evidence that Bcl-2/Bcl-x(L) inhibition with ABT-737 synergistically enhances imatinib-induced cytotoxicity via apoptosis, and that direct engagement of apoptotic cell death may be an effective approach to circumvent imatinib-resistance in GIST.	Imatinib Mesylate	123-131	BCL2 like 1	Homo sapiens	65-70	
21115411-10	2011	CONCLUSION: We provide the first preclinical evidence that Bcl-2/Bcl-x(L) inhibition with ABT-737 synergistically enhances imatinib-induced cytotoxicity via apoptosis, and that direct engagement of apoptotic cell death may be an effective approach to circumvent imatinib-resistance in GIST.	Imatinib Mesylate	262-270	BCL2 like 1	Homo sapiens	65-70	
17926190-7	2007	Enhanced apoptosis, cytochrome C release, and caspase 3 cleavage as well as noticeable decrease of Mcl-1 and Bcl-XL were observed in K562 cells treated with both (-)gossypol and imatinib.	Imatinib Mesylate	178-186	BCL2 like 1	Homo sapiens	109-115	
20094798-5	2010	Nutlin-3 and imatinib synergistically induced Bax activation, mitochondrial membrane depolarization, and caspase-3 cleavage leading to caspase-dependent apoptosis, which was inhibited by overexpression of Bcl-XL.	Imatinib Mesylate	13-21	BCL2 like 1	Homo sapiens	205-211	
19934315-12	2009	We conclude that imatinib sensitizes Bcr-Abl(+) cells to cisplatin by simultaneous inhibition of p53 transactivation, induction of p53 accumulation predominantly in the cytoplasm, and reduction of Bcl-x(L).	Imatinib Mesylate	17-25	BCL2 like 1	Homo sapiens	197-205	
20723293-0	2010	[Effects of STI571 combined with As2O3 on proliferation, apoptosis and caspase 3, Bcl-xL expression of K562 cells].	Imatinib Mesylate	12-18	BCL2 like 1	Homo sapiens	82-88	
20723293-8	2010	The STI571 combined with As2O3 can enhance these two effects, increase the expression of caspase-3 mRNA and decrease the expression of bcl-xL mRNA.	Imatinib Mesylate	4-10	BCL2 like 1	Homo sapiens	135-141	
20723293-9	2010	Therefore, the effect of STI571 combined with As2O3 on expression of caspase 3 and bcl-xL mRNA may be one of molecular mechanisms underlying their synergic antileukemia efficacy.	Imatinib Mesylate	25-31	BCL2 like 1	Homo sapiens	83-89	
18088462-0	2007	[STI571 induces apoptosis of K562 cells through down-regulation of anti-apoptotic protein Mcl-1 and Bcl-xl expression].	Imatinib Mesylate	1-7	BCL2 like 1	Homo sapiens	100-106	
18088462-8	2007	It is concluded that STI571 induces the apoptosis of CML cells by down-regulating the expressions of Mcl-1 and Bcl-xl, which suggests that Mcl-1 and Bcl-xl may play an important role in anti-apoptotic process of CML cells.	Imatinib Mesylate	21-27	BCL2 like 1	Homo sapiens	111-117	
18088462-8	2007	It is concluded that STI571 induces the apoptosis of CML cells by down-regulating the expressions of Mcl-1 and Bcl-xl, which suggests that Mcl-1 and Bcl-xl may play an important role in anti-apoptotic process of CML cells.	Imatinib Mesylate	21-27	BCL2 like 1	Homo sapiens	149-155	
17545631-5	2007	By treating CML cells with imatinib, we could show that the resulting inhibition of BCR-ABL leads to a decreased expression of tumor antigens, including survivin, adipophilin, hTERT, WT-1, Bcl-x(L), and Bcl-2 in correlation to a decreased development of CML-specific CTLs.	Imatinib Mesylate	27-35	BCL2 like 1	Homo sapiens	189-194	
17420275-9	2007	Furthermore, we show that the inhibition of Bcr-Abl kinase by treatment with imatinib caused the up-regulation of Gfi-1B in K562 cells, where Gfi-1B also cooperated with GATA-1 to repress Bcl-x(L) transcription.	Imatinib Mesylate	77-85	BCL2 like 1	Homo sapiens	188-193	
15039284-4	2004	In imatinib mesylate-resistant K562 cells displaying increased Bcr/Abl expression, bortezomib/flavopiridol treatment markedly increased apoptosis in association with down-regulation of Bcr/Abl and BclxL, and diminished phosphorylation of Lyn, Hck, CrkL, and Akt.	Imatinib Mesylate	3-20	BCL2 like 1	Homo sapiens	197-202	
11782377-7	2002	Synergistic potentiation of STI571-mediated lethality by PD184352 was associated with multiple perturbations in signaling and apoptotic regulatory pathways, including caspase-dependent down-regulation of Bcr-Abl and Bcl-2; caspase-independent down-regulation of Bcl-x(L) and Mcl-1; activation of JNK, p38 MAPK, and p34(cdc2); and diminished phosphorylation of Stat5 and CREB.	Imatinib Mesylate	28-34	BCL2 like 1	Homo sapiens	262-270	
12231544-5	2002	STI571/flavopiridol-mediated apoptosis was associated with the caspase-independent down-regulation of Bcl-x(L) and Mcl-1, activation of extracellular signal-regulated kinase and c-Jun NH(2)-terminal kinase, and the caspase-dependent release of Smac/DIABLO and loss of deltapsi(m).	Imatinib Mesylate	0-6	BCL2 like 1	Homo sapiens	102-110	
11313280-6	2001	STI-571-mediated apoptosis correlated with the inhibition of Stat-5 and MAP kinase activation and a reduction in overexpressed bcl-x(L) but not in PTP1B.	Imatinib Mesylate	0-7	BCL2 like 1	Homo sapiens	127-135	
10815921-0	2000	The tyrosine kinase inhibitor CGP 57148 (ST1 571) induces apoptosis in BCR-ABL-positive cells by down-regulating BCL-X.	Imatinib Mesylate	30-39	BCL2 like 1	Homo sapiens	113-118	
11368438-4	2001	Combined treatment with As2O3 and STI-571 also resulted in greater reductions in the levels of Bcl-x(L), XIAP and Akt, and inhibition of Akt kinase activity.	Imatinib Mesylate	34-41	BCL2 like 1	Homo sapiens	95-103	
11179439-6	2001	Use of the Bcr-Abl tyrosine kinase inhibitor STI-571 resulted in a reduction in Bcl-xL levels and potentiation of dexrazoxane-induced apoptosis related to an earlier onset and more extensive cleavage of caspase-3.	Imatinib Mesylate	45-52	BCL2 like 1	Homo sapiens	80-86