PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
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 apoptosis regulator	Homo sapiens	199-204	
26721623-8	2016	This was also observed with the organelle-specific variants Bcl-xL-ActA and Bcl-2-ActA (mitochondrial) as well as Bcl-xL-cb5 and Bcl-2-cb5 (ER) which all reduced AT-101-induced cell death, but did not affect the death-enhancing effects of 3-MA.	3-methyladenine	239-243	BCL2 apoptosis regulator	Homo sapiens	76-81	
27261572-11	2016	CSPCs also induced the expression of Bad, Bax and Beclin-1 proteins and decreased the expression of Bcl-2, which was inhibited by 3-MA and Z-VAD.	3-methyladenine	130-134	BCL2 apoptosis regulator	Homo sapiens	100-105	
26721623-8	2016	This was also observed with the organelle-specific variants Bcl-xL-ActA and Bcl-2-ActA (mitochondrial) as well as Bcl-xL-cb5 and Bcl-2-cb5 (ER) which all reduced AT-101-induced cell death, but did not affect the death-enhancing effects of 3-MA.	3-methyladenine	239-243	BCL2 apoptosis regulator	Homo sapiens	129-134	
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 apoptosis regulator	Homo sapiens	130-135	
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 apoptosis regulator	Homo sapiens	160-165	
26398820-5	2015	The negative correlation with Bcl2 and survivin, and the chemotherapy drug 5-FU increased the level of autophagy and the autophagy inhibitor 3-MA inhibited this effect in SSCC cells, time- and dose-dependently.	3-methyladenine	141-145	BCL2 apoptosis regulator	Homo sapiens	30-34	
25110043-5	2014	3-Methyladenine, an autophagy inhibitor, not only increased cell viability through inhibiting autophagic cell death and apoptosis, but also reversed the upregulation of Beclin-1 gene and the downregulation of Bcl-2 gene in the Raji cells induced by As2O3.	3-methyladenine	0-15	BCL2 apoptosis regulator	Homo sapiens	209-214	
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 apoptosis regulator	Homo sapiens	216-221	
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 apoptosis regulator	Homo sapiens	216-221	
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 apoptosis regulator	Homo sapiens	245-249	
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 apoptosis regulator	Homo sapiens	273-277	
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 apoptosis regulator	Homo sapiens	155-160	
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 apoptosis regulator	Homo sapiens	90-95	
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 apoptosis regulator	Homo sapiens	183-187	
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 apoptosis regulator	Homo sapiens	183-187	
33613969-10	2021	CSC-induced apoptosis was further increased, Bax expressions and cleaved-caspase 3/pro-caspase 3 ratio were improved, but Bcl-2 expressions were decreased after 3-MA or 4-PBA treatment.	3-methyladenine	161-165	BCL2 apoptosis regulator	Homo sapiens	122-127	
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 apoptosis regulator	Homo sapiens	141-146	
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 apoptosis regulator	Homo sapiens	254-259	
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 apoptosis regulator	Homo sapiens	288-293	
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 apoptosis regulator	Homo sapiens	64-69	
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 apoptosis regulator	Homo sapiens	91-96	
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 apoptosis regulator	Homo sapiens	283-288	
28408883-8	2017	An autophagy inhibitor, 3-methyladenine, could partially reverse cell viability and conversely change the ratio of LC3II/LC3I and the protein expression of Bcl-2 and Kim-1.	3-methyladenine	24-39	BCL2 apoptosis regulator	Homo sapiens	156-161