PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22134971-2	2012	Exposure of cells to taxol induced time-dependent cytotoxicity and cytoplasmic vacuolization without the involvement of Bax, Bak, Mcl-1, Bcl-XL, and caspase-3.	Paclitaxel	21-26	BCL2-associated X protein	Mus musculus	120-123	
22820595-7	2012	CG combined with Taxol increased the expression of Bax and reduced the expression of p53 and VEGF in the tumor xenografts.	Paclitaxel	17-22	BCL2-associated X protein	Mus musculus	51-54	
22848173-6	2012	METHODS AND RESULTS: Intravenous administration of folate-targeted, paclitaxel-loaded micelles was demonstrated to be more efficient in inhibiting subcutaneous xenograft tumors and extending the survival rate of tumor-bearing nude mice than free paclitaxel and plain paclitaxel micelles at an equivalent paclitaxel dose of 20 mg/kg, which was further backed up by flow cytometry, TUNEL, and expression of apoptosis-related proteins, including Bax, Bcl2, and caspase 3 in this study.	Paclitaxel	68-78	BCL2-associated X protein	Mus musculus	443-446	
21642840-5	2011	A combined treatment with taxol and pristimerin induced cervical cancer cell death by increasing intracellular reactive oxygen species levels, upregulation of death receptor death receptor 5 (DR5), activation of Bax, and dissipation of mitochondrial membrane potential.	Paclitaxel	26-31	BCL2-associated X protein	Mus musculus	212-215	
17449502-10	2007	Moreover, transcriptional analysis by real-time RT-PCR showed an increased level of pro-apoptotic mRNA transcripts (FAS, BAX, caspase 3) in paclitaxel-treated arteries.	Paclitaxel	140-150	BCL2-associated X protein	Mus musculus	121-124	
20353770-4	2010	Results showed a massive impairment of erythropoiesis early post paclitaxel administration (1-2 days), which involved induction of high Bax/Bcl-x(L) ratio, caspase-3 activation, disruptions of the medullar niche and cell death by both apoptosis and necrosis.	Paclitaxel	65-75	BCL2-associated X protein	Mus musculus	136-139	
20708296-7	2010	Furthermore, overexpression of TIP47 facilitated Bcl-2 expression and suppressed Bax expression in taxol-treated cells.	Paclitaxel	99-104	BCL2-associated X protein	Mus musculus	81-84	
20731895-7	2008	RESULTS: The tumor-inhibiting rate of paclitaxel plus LY294002 (92.47%) was significantly higher than the paclitaxel alone (65.59%)(P <0.05).The protein expression of bcl-2 in paclitaxel plus LY294002 group were significantly higher, while bax was significantly lower than that in the other two groups (P <0.05).	Paclitaxel	38-48	BCL2-associated X protein	Mus musculus	243-246	
32005098-5	2020	Tumors from mice treated with stampidine or stampidine plus paclitaxel displayed unique changes of a signature protein cassette comprised of BRCA1, p21, Bax, and Bcl-2.Conclusion: Stampidine has potent chemopreventive activity and is as effective as the standard chemotherapy drug paclitaxel in the chemical carcinogenesis model of DMBA-induced murine breast cancer.	Paclitaxel	60-70	BCL2-associated X protein	Mus musculus	153-156	
15389801-10	2005	Chemotherapeutic drugs (paclitaxel, vincristine, vinblastine, etoposide, doxorubicin, and camptothecin) significantly augmented TRAIL-induced apoptosis in cancer cells through up-regulation of DR4, DR5, Bax, and Bak, and induction of caspase activation.	Paclitaxel	24-34	BCL2-associated X protein	Mus musculus	203-206	
34907739-9	2021	Furthermore, in Ehrlich solid tumor mice, rosmarinic acid, and/or Paclitaxel significantly suppressed tumor growth with an increase in apoptotic markers P53 and Caspase-3 levels, and suppressed the Bcl2/Bax ratio.	Paclitaxel	66-76	BCL2-associated X protein	Mus musculus	203-206	
33323915-17	2020	The paclitaxel effects were accompanied by inhibition of the inflammatory cytokines, MCP-1, TNF-alpha, TNF-R2, and TLR4, as well as attenuation of the apoptosis markers, Bax, Bcl-2, and Caspase-3.	Paclitaxel	4-14	BCL2-associated X protein	Mus musculus	170-173	
29179722-10	2017	The caspase-9 and caspase-3 cascade was activated by the AG-PEG-SS-PLA/PTX nanomicelles through upregulation of the pro-apoptotic proteins Bax and Bid and suppression of the anti-apoptotic protein Bcl-2, thereby increasing apoptosis.	Paclitaxel	71-74	BCL2-associated X protein	Mus musculus	139-142	
24469707-3	2014	Results showed that treatment of Taxol could increase the inhibition rate of tumour growth, positive expression levels of Caspase-3, Bax and decrease positive expression levels of Bcl-2 and Bcl-2/Bax, expression levels of HGF, MACC1 and C-met proteins and MACC1 mRNA in tumour tissue of CC mice.	Paclitaxel	33-38	BCL2-associated X protein	Mus musculus	133-136	
24469707-3	2014	Results showed that treatment of Taxol could increase the inhibition rate of tumour growth, positive expression levels of Caspase-3, Bax and decrease positive expression levels of Bcl-2 and Bcl-2/Bax, expression levels of HGF, MACC1 and C-met proteins and MACC1 mRNA in tumour tissue of CC mice.	Paclitaxel	33-38	BCL2-associated X protein	Mus musculus	196-199	
24469707-4	2014	It can be concluded that inhibitory activity of Taxol against tumour growth in CC mice is closely associated with its modulating positive expression of Bcl-2, Bax, Caspase-3, expression of HGF, MACC1, Caspase-3 and C-met proteins and MACC1 mRNA in tumour of CC mice.	Paclitaxel	48-53	BCL2-associated X protein	Mus musculus	159-162	
28856937-6	2017	In vivo, AP/PTX-SLNs were revealed to be much more effective in suppressing tumor growth in B16F10-bearing mice and in eliminating cancer cells in the lungs than single drug (AP or PTX)-loaded SLNs via a synergistic effect through reducing the Bcl-2/Bax ratio.	Paclitaxel	12-15	BCL2-associated X protein	Mus musculus	250-253