PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
10913135-0	2000	Vinblastine-induced phosphorylation of Bcl-2 and Bcl-XL is mediated by JNK and occurs in parallel with inactivation of the Raf-1/MEK/ERK cascade.	Vinblastine	0-11	BCL2 like 1	Homo sapiens	49-55	
31367011-4	2020	In vinblastine-treated cells, PGAM5 dephosphorylates BCL-xL at Ser62 to restore BCL-xL sequestration of BAX and BAK and thereby resistance to apoptosis.	Vinblastine	3-14	BCL2 like 1	Homo sapiens	53-59	
31367011-4	2020	In vinblastine-treated cells, PGAM5 dephosphorylates BCL-xL at Ser62 to restore BCL-xL sequestration of BAX and BAK and thereby resistance to apoptosis.	Vinblastine	3-14	BCL2 like 1	Homo sapiens	80-86	
18974096-1	2008	Vinblastine and other microtubule inhibitors used as antimitotic cancer drugs characteristically promote the phosphorylation of the key anti-apoptotic protein, Bcl-xL.	Vinblastine	0-11	BCL2 like 1	Homo sapiens	160-166	
18974096-5	2008	Vinblastine-treated cells overexpressing a Ser-62 --> Ala mutant showed highly significantly reduced apoptosis compared with cells expressing wild-type Bcl-xL.	Vinblastine	0-11	BCL2 like 1	Homo sapiens	155-161	
11592339-4	2001	Western blot and flow cytometry were performed to determine the effects of Taxol and vinblastine on topoisomerase I and Bcl-xL protein levels and cell cycle distribution.	Vinblastine	85-96	BCL2 like 1	Homo sapiens	120-126	
11592339-8	2001	Under these conditions, both Taxol and vinblastine caused an increase in topoisomerase I protein levels, fraction of S phase cells, and extent of Bcl-xL phosphorylation immediately prior to the addition of topotecan.	Vinblastine	39-50	BCL2 like 1	Homo sapiens	146-152	
22024133-5	2012	Vinblastine treatment caused degradation of Mcl-1 in cells in which apoptosis was blocked by Bcl-xL overexpression, indicating that Mcl-1 degradation was not a consequence of apoptosis.	Vinblastine	0-11	BCL2 like 1	Homo sapiens	93-99	
19427996-0	2009	Regulation of Bax by c-Jun NH2-terminal kinase and Bcl-xL in vinblastine-induced apoptosis.	Vinblastine	61-72	BCL2 like 1	Homo sapiens	51-57	
16574665-1	2006	To gain a broader insight into the role of Bcl-2 proteins in apoptosis induced after mitotic arrest, we investigated the subcellular location, oligomeric structure, and protein interactions of Bax, Bcl-2, and Bcl-xL in vinblastine-treated KB-3 cells.	Vinblastine	219-230	BCL2 like 1	Homo sapiens	209-215	
16574665-7	2006	Both wild-type and Bax-deficient HCT116 cells expressed the 150-kDa form of Bcl-xL, which was depleted similarly in both cell lines upon vinblastine treatment.	Vinblastine	137-148	BCL2 like 1	Homo sapiens	76-82	
16574665-10	2006	Overexpression of Bcl-xL inhibited vinblastine-induced Bax activation and Bax dimerization and in parallel inhibited apoptosis.	Vinblastine	35-46	BCL2 like 1	Homo sapiens	18-24	
16574665-11	2006	The results indicate that vinblastine-induced apoptosis requires translocation, activation, and oligomerization of Bax and is associated with specific changes in the oligomeric properties of Bcl-xL, which occur independently of Bax.	Vinblastine	26-37	BCL2 like 1	Homo sapiens	191-197	
15531923-0	2005	Characterization of vinblastine-induced Bcl-xL and Bcl-2 phosphorylation: evidence for a novel protein kinase and a coordinated phosphorylation/dephosphorylation cycle associated with apoptosis induction.	Vinblastine	20-31	BCL2 like 1	Homo sapiens	40-46	
15531923-2	2005	In this study, we investigated the characteristics of Bcl-xL and Bcl-2 phosphorylation in KB-3 carcinoma cells treated with vinblastine.	Vinblastine	124-135	BCL2 like 1	Homo sapiens	54-60	
15531923-7	2005	Bcl-xL kinase activity was demonstrated in mitochondrial extracts from vinblastine-treated, but not control, cells.	Vinblastine	71-82	BCL2 like 1	Homo sapiens	0-6	
11929841-8	2002	The down-regulation of bcl-xL in both DU145 (and to a much lesser extent in LNCaP) cells led to their resistance to cytotoxic agents, including docetaxel, mitoxantrone, etoposide, vinblastine, and carboplatin.	Vinblastine	180-191	BCL2 like 1	Homo sapiens	23-29	
10913135-2	2000	Because microtubule inhibitors activate JNK, we sought to determine whether JNK was responsible for Bcl-2/Bcl-X(L) phosphorylation in KB-3 cells treated with vinblastine.	Vinblastine	158-169	BCL2 like 1	Homo sapiens	106-114	
9699663-9	1998	Herein, we report that Bcl-xL is phosphorylated in malignant cells after incubation with agents that target tubulin, including paclitaxel, vincristine, vinblastine, colchicine, and nocodazole.	Vinblastine	152-163	BCL2 like 1	Homo sapiens	23-29	
9570926-5	1998	Modulation of cell death by Bcl-xL was also observed in cells treated with etoposide, vinblastine, paclitaxel, and cisplatinum (II) diammine dichloride.	Vinblastine	86-97	BCL2 like 1	Homo sapiens	28-34