PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
23819597-4	2013	In Lck-Bax38&1 mice, a 100 cGy dose of high-LET iron ions caused a significant dose dependent acceleration of lymphomagenesis in both males and females that was not seen with silicon ions.	Iron	52-56	BCL2-associated X protein	Mus musculus	3-18	
25301748-8	2015	Furthermore, our findings suggest that the increased nigral iron content exacerbates the oxidative stress levels, promoting apoptosis through the Bcl-2/Bax pathway and the activated caspase-3 pathway in the brain.	Iron	60-64	BCL2-associated X protein	Mus musculus	152-155	
27843711-11	2016	Iron contributed to the permeabilizatio of mitochondria, leading to the release of cytochrome C (cyto C), which, in turn, induced mitochondrial apoptosis in osteoblasts via activation of Caspase-3, up-regulation of Bax, and down-regulation of Bcl-2.	Iron	0-4	BCL2-associated X protein	Mus musculus	215-218	
27342530-12	2016	CD8+ T cell apoptosis in iron overload group was significantly higher than that in control groups (P<0.01); the expression of BCL-2 at mRNA level was lower than that in control group, but the expression of BAX at mRNA level was higher than that in control group (P<0.05).	Iron	25-29	BCL2-associated X protein	Mus musculus	209-212	
23605050-3	2013	The purpose of this study was to describe the effect of different iron and/or glucose concentrations over Mfn2, Bax, and Bcl2 expressions in a beta-pancreatic cell line (MIN6 cells).	Iron	66-70	BCL2-associated X protein	Mus musculus	112-115	
23605050-9	2013	Our study revealed that high glucose/Fe concentrations in MIN6 cells induced an increase of the Bcl2/Bax ratio, an indicator of increased cell apoptosis.	Iron	37-39	BCL2-associated X protein	Mus musculus	101-104	
16679553-3	2006	Iron-induced mitochondrial damage and apoptosis were characterized by reactive oxygen species production, increased metallothionein and glutathione synthesis, caspase- 3 activation, NF-kappaB induction, and decreased Bcl-2 expression, without any significant change in Bax expression.	Iron	0-4	BCL2-associated X protein	Mus musculus	269-272	
21346313-6	2011	Moreover, we demonstrated that both iron chelators were able to decrease TDP-43 protein aggregation and the proapoptotic molecule Bax, and to enhance antiapoptotic protein Bcl-2 expression, in the ALS mice.	Iron	36-40	BCL2-associated X protein	Mus musculus	130-133	
32373202-4	2020	Chronic exposure to excess iron induced epithelial-mesenchymal transition (EMT) in normal and cancer cell lines, loss of p53, and suppression of p53 transcriptional activity evidenced from decreased expression of p53 target genes (p21, cyclin D1, Bax, SLC7A11).	Iron	27-31	BCL2-associated X protein	Mus musculus	247-250	
34464637-7	2021	The protective effect of MAME against iron-overload-induced apoptosis was confirmed by upregulation of protein levels of Bax, Caspase-3, and PARP.	Iron	38-42	BCL2-associated X protein	Mus musculus	121-124	
28874056-9	2018	INNOVATION: CP alterations in iron contents were mediated through DMT1(-IRE) and changes in ROS levels, which in turn attenuated the progression of AD through the Erk/p38 and Bcl-2/Bax signaling pathways.	Iron	30-34	BCL2-associated X protein	Mus musculus	181-184