PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32836151-6	2020	Moreover, co-treatment with Cd and 3-MA could notably elevate Caspase-3, Cyt C, Bax, and Bak-1 mRNA levels, Caspase-3 and cleaved Caspase-3 protein levels, and cell apoptotic rate as well as cell damage, decreased mitochondrial membrane potential (MMP), Bcl-2 mRNA level and the ratio of Bcl-2 to Bax compared to treatment with Cd alone.	3-methyladenine	35-39	BCL2 associated X, apoptosis regulator	Homo sapiens	80-83	
33880372-7	2021	The autophagy inhibitor 3-methyladenine and chloroquine decreased apoptosis and cleaved-caspase-3 protein level and increased the Bcl-2/Bax ratio.	3-methyladenine	24-39	BCL2 associated X, apoptosis regulator	Homo sapiens	136-139	
32836151-6	2020	Moreover, co-treatment with Cd and 3-MA could notably elevate Caspase-3, Cyt C, Bax, and Bak-1 mRNA levels, Caspase-3 and cleaved Caspase-3 protein levels, and cell apoptotic rate as well as cell damage, decreased mitochondrial membrane potential (MMP), Bcl-2 mRNA level and the ratio of Bcl-2 to Bax compared to treatment with Cd alone.	3-methyladenine	35-39	BCL2 associated X, apoptosis regulator	Homo sapiens	297-300	
33010382-9	2020	Furthermore, 3MA reversed both the nicotine-induced decrease in Bcl-2 and the increase in Bax in both groups.	3-methyladenine	13-16	BCL2 associated X, apoptosis regulator	Homo sapiens	90-93	
33243748-13	2020	Blocking autophagy with 3-MA significantly increased DDP- induced apoptosis of SKOV3 cells with IL-17RA silencing, lowered the expression of Bcl-2 and enhanced Bax expression in the cells (P < 0.05).	3-methyladenine	24-28	BCL2 associated X, apoptosis regulator	Homo sapiens	160-163	
33260158-5	2020	Autophagy inhibition using 3-methyladenine (3-MA) or Atg5-targeted siRNA decreased the Bax/Bcl-2 ratio, caspase-3 activation, and PARP cleavage and protected cells against ISO-induced apoptosis.	3-methyladenine	44-48	BCL2 associated X, apoptosis regulator	Homo sapiens	87-90	
27604425-11	2016	Furthermore, the inhibition of autophagy by 3-MA further increased the expression of activated caspase 3, Bax, BNIP3, and BNIP3L, all are critical apoptotic mediators.	3-methyladenine	44-48	BCL2 associated X, apoptosis regulator	Homo sapiens	106-109	
30116320-9	2018	Inhibiting autophagy using 3-MA, resulted in a significant decrease in LC3-II, beclin-1 and LDH, as well as increase in the expression of BIP, CHOP, caspase 3, cleaved caspase 3 and Bax.	3-methyladenine	27-31	BCL2 associated X, apoptosis regulator	Homo sapiens	182-185	
28046018-8	2017	Joint application of 3-MA or Atg7 siRNA enhanced the cell growth inhibition and apoptosis effects of NVP-AEW541 by arresting cells at G1/G0 phase and increasing Bax expression and decreasing that of Bcl-2.	3-methyladenine	21-25	BCL2 associated X, apoptosis regulator	Homo sapiens	161-164	
33178023-8	2020	Among them, 3-methyladenine, SBI-0206965, Chloroquine, and Bafilomycin A1 triggered BAX- and/or BAK-dependent cytotoxicity and caspase activation.	3-methyladenine	12-27	BCL2 associated X, apoptosis regulator	Homo sapiens	84-87	
32424110-13	2020	After inhibiting autophagy with 3-MA or CQ, compared with OA alone, cell mitochondrial membrane potential and ATP concentration were significantly reduced, cell p62 expression was reduced, and LC3-II expression was increased, apoptosis-related protein Bax protein was increased, and Bcl-2 protein was decreased, which suggested that 3-MA or CQ treatment increased OA-induced apoptosis of SMMC-7721 cells.	3-methyladenine	32-36	BCL2 associated X, apoptosis regulator	Homo sapiens	252-255	
30194633-8	2018	Inhibiting autophagy with 3-MA attenuated the PA and ER stress-induced cell apoptosis and the apoptosis-related gene expression (Caspase 3 and BAX), but seemed to have no obvious effects on ER stress, although the CHOP expression was downregulated.	3-methyladenine	26-30	BCL2 associated X, apoptosis regulator	Homo sapiens	143-146	
29344024-8	2017	3-Methyladenine, an autophagy inhibitor, inhibited apoptosis significantly in FITC-annexin V staining, and the inhibition of Bax, cytochrome c, and c-caspase-3 was shown by Western blotting.	3-methyladenine	0-15	BCL2 associated X, apoptosis regulator	Homo sapiens	125-128	
25042557-6	2015	The autophagy inhibitor 3-methyladenine significantly increased the apoptotic rate induced by olaquindox, which was correlated with increased ratio of Bax/Bcl-2.	3-methyladenine	24-39	BCL2 associated X, apoptosis regulator	Homo sapiens	151-154	
26676298-9	2016	Moreover, the inhibition of autophagy by 3-methyladenine or Atg5 siRNA significantly enhanced ramalin-induced apoptosis, which was accompanied by a decrease in Bcl-2 levels and an increase in Bax levels.	3-methyladenine	41-56	BCL2 associated X, apoptosis regulator	Homo sapiens	192-195	
24675684-7	2014	Specific inhibition of autophagy by 3-methyladenine and chloroquine had little effect on cell apoptosis but could enhance the pro-apoptotic effects of meloxicam by further upregulating the expression of Bax.	3-methyladenine	36-51	BCL2 associated X, apoptosis regulator	Homo sapiens	203-206	
25088259-0	2014	Inhibition of autophagy by 3-MA potentiates purvalanol-induced apoptosis in Bax deficient HCT 116 colon cancer cells.	3-methyladenine	27-31	BCL2 associated X, apoptosis regulator	Homo sapiens	76-79	
25088259-8	2014	Inhibition of autophagy by 3-MA treatment enhanced the purvalanol induced apoptotic cell death in HCT 116 Bax(-/-) cells.	3-methyladenine	27-31	BCL2 associated X, apoptosis regulator	Homo sapiens	106-109	
26394653-8	2015	3-MA pretreatment enhanced the TDT-induced up-regulation of Bax and cleaved-PARP.	3-methyladenine	0-4	BCL2 associated X, apoptosis regulator	Homo sapiens	60-63	
35365454-8	2022	Compared with melatonin treatment alone, melatonin treatment combined with 3-MA significantly decreased the expressions of Beclin1 (P < 0.001), LC3-II/LC3-I (P < 0.05), Bax (P < 0.01), and E-cadherin (P < 0.001) and increased the expressions of Bcl2 (P < 0.05), Snail, and Bcl2/Bax ratio (P < 0.01).	3-methyladenine	75-79	BCL2 associated X, apoptosis regulator	Homo sapiens	169-172	
23849780-9	2014	Quantification of Bax, mitochondrial integrity, caspase-3 cleavage, and caspase-3 immunolocalization and activity showed that 3-MA induced a significant decrease of Gad67-GFP precursor apoptosis.	3-methyladenine	126-130	BCL2 associated X, apoptosis regulator	Homo sapiens	18-21	
23352508-10	2013	However, pretreatment of cells with the autophagy inhibitor, 3-methyladenine (3MA), remarkably increased CPF toxicity in these cells; this with correlated with increased expression of Bax and decreased expression of Bcl-2 in mitochondria.	3-methyladenine	61-76	BCL2 associated X, apoptosis regulator	Homo sapiens	184-187	
23352508-10	2013	However, pretreatment of cells with the autophagy inhibitor, 3-methyladenine (3MA), remarkably increased CPF toxicity in these cells; this with correlated with increased expression of Bax and decreased expression of Bcl-2 in mitochondria.	3-methyladenine	78-81	BCL2 associated X, apoptosis regulator	Homo sapiens	184-187	
17473426-9	2007	In addition, 3-MA application downregulated DNA ladder and Bax expression but upregulated Bcl-2 expression, compared with oridonin alone treatment.	3-methyladenine	13-17	BCL2 associated X, apoptosis regulator	Homo sapiens	59-62	
35365454-5	2022	The effects of melatonin treatment alone or in combination with 3-methyladenine (3-MA) on the expressions of the proteins associated with autophagy (LC3, P62 and Beclin1), apoptosis (Bcl2 and Bax) and epithelial-mesenchymal transition (E-cadherin and Snail) were examined with Western blotting.	3-methyladenine	64-79	BCL2 associated X, apoptosis regulator	Homo sapiens	192-195	
35365454-5	2022	The effects of melatonin treatment alone or in combination with 3-methyladenine (3-MA) on the expressions of the proteins associated with autophagy (LC3, P62 and Beclin1), apoptosis (Bcl2 and Bax) and epithelial-mesenchymal transition (E-cadherin and Snail) were examined with Western blotting.	3-methyladenine	81-85	BCL2 associated X, apoptosis regulator	Homo sapiens	192-195	
35365454-8	2022	Compared with melatonin treatment alone, melatonin treatment combined with 3-MA significantly decreased the expressions of Beclin1 (P < 0.001), LC3-II/LC3-I (P < 0.05), Bax (P < 0.01), and E-cadherin (P < 0.001) and increased the expressions of Bcl2 (P < 0.05), Snail, and Bcl2/Bax ratio (P < 0.01).	3-methyladenine	75-79	BCL2 associated X, apoptosis regulator	Homo sapiens	278-281