PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29936187-10	2018	mRNA and protein ratios of apoptotic modulators (Bax/Bcl2) are higher in 158JP oligodendrocytes which are also more vulnerable than 158N cells to tunicamycin-induced ER-stress.	Tunicamycin	146-157	BCL2 associated X, apoptosis regulator	Homo sapiens	49-52	
34604209-4	2021	In the current study, we demonstrated that tunicamycin (a novel ERS inducer) can induce the apoptosis of HSCs and increase the concentration of intracellular Ca2+ and the expression of ERS protein GRP78, apoptosis protein caspase-12, and Bax, while it can decrease the antiapoptosis protein expression of Bcl-2.	Tunicamycin	43-54	BCL2 associated X, apoptosis regulator	Homo sapiens	238-241	
32266019-9	2020	Western blot analysis demonstrated that the expression of Bax and caspase-3 was upregulated and the expression of Bcl-2 was downregulated in TM-treated human melanocytes.	Tunicamycin	141-143	BCL2 associated X, apoptosis regulator	Homo sapiens	58-61	
22225575-7	2012	Interestingly, co-treatment with tunicamycin and melatonin also decreased the expression of COX-2 and significantly increased the rate of apoptosis by elevating the levels of CHOP and reducing the Bcl-2/Bax ratio.	Tunicamycin	33-44	BCL2 associated X, apoptosis regulator	Homo sapiens	203-206	
22699051-4	2012	The expressions of Bax, Bcl-2, and GRP78 in cells treated with 3 micromol/L tunicamycin with or without 6.00 micromol/L cisplatin were measured with Western blotting.	Tunicamycin	76-87	BCL2 associated X, apoptosis regulator	Homo sapiens	19-22	
28631572-10	2017	With the increased tunicamycin concentration, there were increased expressions of Bax and cleaved caspase-3, decreased expression of Bcl-2, and lower phosphorylation of PI3K/Akt/mTOR signaling pathway-related proteins.	Tunicamycin	19-30	BCL2 associated X, apoptosis regulator	Homo sapiens	82-85	
17655822-1	2007	Experimental sarcoplasmic reticulum damage induced by 3 microM thapsigargin or 1 microg/ml tunicamycin provoked viability loss of the cell population in approximately 72 h. Release of cytochrome c from mitochondria was an early event and Bax translocation to the mitochondria preceded or was simultaneous with cytochrome c release.	Tunicamycin	91-102	BCL2 associated X, apoptosis regulator	Homo sapiens	238-241	
21241252-5	2011	Tunicamycin-treated Bak-/-Bax-/- cells remain viable, but cease growth, arresting in G1-phase and undergoing autophagy in the absence of apoptosis.	Tunicamycin	0-11	BCL2 associated X, apoptosis regulator	Homo sapiens	26-29