PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
24141792-6	2014	Vit significantly inhibited the neuronal apoptosis induced by NMDA exposure by regulating balance of Bcl-2 and Bax expression and the cleavages of poly (ADP-ribose) polymerase and pro-caspase 3.	N-Methylaspartate	62-66	BCL2-associated X protein	Mus musculus	111-114	
22828802-11	2012	With longer NMDA exposure (72 h), we observed loss of cells associated with nuclear fragmentation and increased expression of caspase-3, caspase-6, and Bax, suggesting an apoptotic process.	N-Methylaspartate	12-16	BCL2-associated X protein	Mus musculus	152-155	
32907306-6	2020	The results found that NMDA can increase the oxidative stress of HT22 cells in a dose-dependent manner, downregulate the expression of miR-382-3p, upregulate the expression of mRNA and protein abundance of ROCK1 and RhoC, increase the expression levels of proapoptotic proteins Bax, Caspase-3, and Caspase-9, increase the apoptosis of HT22 cells, and reduce the activity and survival rate of HT22 cells.	N-Methylaspartate	23-27	BCL2-associated X protein	Mus musculus	278-281	
11006977-0	2000	p53 and Bax implication in NMDA induced-apoptosis in mouse hippocampus.	N-Methylaspartate	27-31	BCL2-associated X protein	Mus musculus	8-11	
21850191-8	2011	RESULTS: WB experiments and luciferase reporter assays showed that NF-kappaB-inducible BCL2-associated X protein (Bax) and a pro-apoptotic factor, activated caspase 3 were expressed in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells.	N-Methylaspartate	229-233	BCL2-associated X protein	Mus musculus	87-112	
21850191-8	2011	RESULTS: WB experiments and luciferase reporter assays showed that NF-kappaB-inducible BCL2-associated X protein (Bax) and a pro-apoptotic factor, activated caspase 3 were expressed in the retina of p50-deficient mice as well as NMDA-treated RGC-5 cells.	N-Methylaspartate	229-233	BCL2-associated X protein	Mus musculus	114-117	
32907306-7	2020	Compared with the NMDA-induced group, the miR-382-3p mimic-transfected HT22 cells increased the expression of miR- 382-3p, reduced the expression of the mRNA and protein abundance of ROCK1 and RhoC, inhibited the expression of proapoptotic proteins Bax, Caspase-3, and Caspase-9, reduced the apoptosis of HT22 cells, and increased the activity and survival rate of HT22 cells.	N-Methylaspartate	18-22	BCL2-associated X protein	Mus musculus	249-252	
25632145-7	2015	However, when Ca(2+) uptake into the sarco/endoplasmic reticulum was blocked with the Ca(2+)-ATPase inhibitor thapsigargin, bax-deficient neurons showed strongly elevated cytosolic Ca(2+) levels during NMDA excitation, suggesting that the ability of Bax to support dynamic ER Ca(2+) handling is critical for cell death signaling during periods of neuronal overexcitation.	N-Methylaspartate	202-206	BCL2-associated X protein	Mus musculus	124-127	
29029408-7	2017	Western blotting showed that levels of activated Bax and cleaved caspase 3 were decreased, while Bcl-2 and pro-caspase 3 were increased in NMDA-treated mRGCs and murine retinal tissues, which corroborated the decreased apoptosis.	N-Methylaspartate	139-143	BCL2-associated X protein	Mus musculus	49-52	
25632145-3	2015	Neuronal Ca(2+) and mitochondrial membrane potential (Deltapsim) analysis during excitotoxic injury revealed that bax-deficient neurons showed significantly reduced Ca(2+) transients during the NMDA excitation period and did not exhibit the deregulation of Deltapsim that was observed in their wild-type (WT) counterparts.	N-Methylaspartate	194-198	BCL2-associated X protein	Mus musculus	114-117	
25613943-12	2015	Meanwhile, TO90 suppressed the elevation of apoptosis factors caspase-3 and bax induced by NMDA and upregulated the level of an antiapoptotic factor bcl-2.	N-Methylaspartate	91-95	BCL2-associated X protein	Mus musculus	76-79