PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31368586-10	2019	NAC-pretreated cells showed increased anti-apoptotic protein Bcl-2 and decreased pro-apoptotic protein Bax expression.	Acetylcysteine	0-3	BCL2-associated X protein	Mus musculus	103-106	
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	45-61	BCL2-associated X protein	Mus musculus	214-217	
33825597-8	2021	However, Pifithrin-alpha (p53 inhibitor) and N-Acetylcysteine (NAC) could reduce cell apoptosis, lung structural damage and oxidative stress, accelerate the expression of Bcl-2, while suppressing the expression of Bax, total caspase-3 and cleaved caspase-3.	Acetylcysteine	63-66	BCL2-associated X protein	Mus musculus	214-217	
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	27-44	BCL2-associated X protein	Mus musculus	210-213	
30315841-8	2019	Interestingly, NAC supplementation not only attenuated elevated 8-OHdG, PARP-1, caspase-3, cleaved caspase-9, and Bax, but also the TCE-mediated autoimmune response supported by significantly reduced serum anti-ssDNA antibodies.	Acetylcysteine	15-18	BCL2-associated X protein	Mus musculus	114-117	
25264893-13	2014	In addition, JNK, p-JNK, Bax, TNF-alpha, NF-kappaB, IL2, IL6 and levels were also decreased in NAC-treated mice.	Acetylcysteine	95-98	BCL2-associated X protein	Mus musculus	25-28	
23103613-9	2013	Pretreatment with NAC and specific p38-MAPK inhibitor (SB203580), but not JNK inhibitor (SP600125) effectively abrogated the phosphorylation of p38-MAPK and attenuated the apoptotic signals (including: decrease in cytotoxicity, caspase-3/-7 activation, the cytosolic cytochrome c release, and the reversed alteration of Bcl-2 and Bax mRNA) in CA-treated Neuro-2a cells.	Acetylcysteine	18-21	BCL2-associated X protein	Mus musculus	330-333	
22701695-9	2012	The free radical scavenger N-acetyl-cysteine (NAC) was able to completely suppress cell death induced by jacaranone as it blocked Akt downregulation, p38 MAPK activation as well as upregulation of proapoptotic Bax.	Acetylcysteine	46-49	BCL2-associated X protein	Mus musculus	210-213	
18034189-8	2008	The antioxidant N-acetyl-L-cysteine substantially inhibited conformational changes of Bax, loss of mitochondrial membrane potential, nuclear relocation of mitochondrial factors, and apoptosis induction in 4-OOH-CY-treated T cells.	Acetylcysteine	16-35	BCL2-associated X protein	Mus musculus	86-89	
21642840-6	2011	Treatment with N-acetyl-L-cysteine, a thiol-containing antioxidant completely blocked combined treatment-induced Bax translocation as well as DR5 upregulation.	Acetylcysteine	15-34	BCL2-associated X protein	Mus musculus	113-116	
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	137-140	BCL2-associated X protein	Mus musculus	42-45	
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	46-66	BCL2-associated X protein	Mus musculus	93-96	
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	46-66	BCL2-associated X protein	Mus musculus	128-131	
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	68-71	BCL2-associated X protein	Mus musculus	93-96	
15604726-7	2004	Treatment of protoplasts with the antioxidant N -acetyl- -cysteine (NAC) during induction of Bax expression strongly suppressed Bax-mediated ROS production and the cell death phenotype.	Acetylcysteine	68-71	BCL2-associated X protein	Mus musculus	128-131	
35507947-8	2022	In addition, the expression of Gdf9, Lif, Bax, and Bcl2 genes were increased and Amh was decreased in groups cultured in the presence of NAC compared to groups cultured without NAC.	Acetylcysteine	177-180	BCL2-associated X protein	Mus musculus	42-45