PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32808351-8	2020	Inhibition of mTOR/FOXO1 by rapamycin/AS1842856 decreased the ratio of Bcl-2/Bax and exacerbated TJ protein loss.	Sirolimus	28-37	BCL2-associated X protein	Mus musculus	77-80	
28086065-11	2017	In addition, rapamycin suppressed cell apoptosis, and decreased Bax/Bcl-2 ratio and cleaved caspase-3 expression.	Sirolimus	13-22	BCL2-associated X protein	Mus musculus	64-67	
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	97-106	BCL2-associated X protein	Mus musculus	0-3	
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3	
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3	
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3	
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	326-335	BCL2-associated X protein	Mus musculus	0-3	
30905858-5	2019	Bax expression was significantly high compared to Bcl-2 expression in a dose-dependent manner of rapamycin for 12 h. For further study of rapamycin-induced autophagy in C2C12 myoblast cells, we investigated rapamycin treatment for 24, 36, and 48 h. Cell viability did not change with rapamycin treatment for 24, 36, and 48 h. Rapamycin-induced LC3-II, Beclin-1, Bax, and Bcl-2 proteins were significantly increased compared to without rapamycin.	Sirolimus	138-147	BCL2-associated X protein	Mus musculus	0-3	
30594149-9	2018	Pro-apoptotic protein, Bcl-2 associated x (Bax), exhibited a slight, but significant decrease with rapamycin treatment, while its anti-apoptotic counterpart, B cell lymphoma-2 (Bcl-2), was to a similar degree upregulated.	Sirolimus	99-108	BCL2-associated X protein	Mus musculus	23-41	
30594149-9	2018	Pro-apoptotic protein, Bcl-2 associated x (Bax), exhibited a slight, but significant decrease with rapamycin treatment, while its anti-apoptotic counterpart, B cell lymphoma-2 (Bcl-2), was to a similar degree upregulated.	Sirolimus	99-108	BCL2-associated X protein	Mus musculus	43-46	
28373901-11	2017	Rapamycin also attenuated Bax and increased Bcl-2/Bax ratio.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	26-29	
28373901-11	2017	Rapamycin also attenuated Bax and increased Bcl-2/Bax ratio.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	50-53	
22999860-13	2012	Rapamycin triggered unique cardioprotective signaling including phosphorylation of ERK, STAT3, eNOS and glycogen synthase kinase-3ss in concert with increased prosurvival Bcl-2 to Bax ratio.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	180-183	
25438952-0	2015	Rapamycin protects against apoptotic neuronal death and improves neurologic function after traumatic brain injury in mice via modulation of the mTOR-p53-Bax axis.	Sirolimus	0-9	BCL2-associated X protein	Mus musculus	153-156	
25438952-9	2015	RESULTS: Rapamycin administration after TBI was associated with an increased number of neurons, decreased apoptosis index, and improved neurobehavioral function, which was potentially mediated by inactivation of the mTOR-p53-Bax axis.	Sirolimus	9-18	BCL2-associated X protein	Mus musculus	225-228	
24850187-9	2014	Down-regulation of bax and caspase-3 protein, and up-regulation of nephrin and podocin protein were observed in the glomeruli of diabetic mice after administration of rapamycin.	Sirolimus	167-176	BCL2-associated X protein	Mus musculus	19-22	
22901235-6	2012	In addition, rapamycin preconditioning decreased the production of NF-kappaB, TNF-alpha, and Bax, but not Bcl-2, an antiapoptotic protein in the ischemic area.	Sirolimus	13-22	BCL2-associated X protein	Mus musculus	93-96	
22559167-12	2012	The alteration of the mRNA expression of cell cycle inhibitors p53, p27, p21 and apoptosis associated genes Bcl-2, Bax were also involved in the synergistic antitumor effects of rapamycin and bortezomib.	Sirolimus	178-187	BCL2-associated X protein	Mus musculus	115-118	
21193837-9	2011	In addition, we have demonstrated that rapamycin treatment in the ALS mice causes more severe mitochondrial impairment, higher Bax levels and greater caspase-3 activation.	Sirolimus	39-48	BCL2-associated X protein	Mus musculus	127-130