PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
34281166-7	2021	Carfilzomib displayed potent antiproliferative effects, induced the unfolded protein response as determined by enhanced CHOP expression and ATF6 activity, and enhanced apoptosis as determined by enhanced caspase-3/7 activity.	carfilzomib	0-11	DNA damage inducible transcript 3	Homo sapiens	120-124	
29948946-7	2019	Our data suggest that treatment with CFZ produces ER stress in NB without activation of CHOP-mediated apoptosis, whereas co-treatment with CFZ and LS1/71 led to apoptosis activation and CHOP expression induction.	carfilzomib	139-142	DNA damage inducible transcript 3	Homo sapiens	186-190	
33713737-6	2021	Combination of ASCT2 inhibitor V9302 and proteasome inhibitor carfilzomib upregulates the intracellular levels of ROS and oxidative stress markers and triggers catastrophic UPR as shown by upregulated spliced Xbp1 mRNA, ATF3 and CHOP levels.	carfilzomib	62-73	DNA damage inducible transcript 3	Homo sapiens	229-233	
32669378-9	2020	Interestingly, Carfilzomib sensitive transcriptomic profile did not show any association with the proteasome activity but strongly correlates with ATF4 and CHOP expression which are key markers of the unfolded protein response and critical to trigger the cell death program.	carfilzomib	15-26	DNA damage inducible transcript 3	Homo sapiens	156-160	
27026200-7	2016	Consequently, the transcription factor CCAAT/enhancer-binding protein homology protein (CHOP) accumulated in response to carfilzomib, and CHOP depletion conferred protection against cytotoxicity.	carfilzomib	121-132	DNA damage inducible transcript 3	Homo sapiens	39-86	
28415782-8	2017	Mechanistically, CB-839 enhanced Crflz-induced ER stress and apoptosis, characterized by a robust induction of ATF4 and CHOP and the activation of caspases.	carfilzomib	33-38	DNA damage inducible transcript 3	Homo sapiens	120-124	
29483217-8	2018	Mechanistically, we found that the apoptosis following combined Carfilzomib/ACY-1215 treatment is mediated through increased CHOP expression.	carfilzomib	64-75	DNA damage inducible transcript 3	Homo sapiens	125-129	
27026200-7	2016	Consequently, the transcription factor CCAAT/enhancer-binding protein homology protein (CHOP) accumulated in response to carfilzomib, and CHOP depletion conferred protection against cytotoxicity.	carfilzomib	121-132	DNA damage inducible transcript 3	Homo sapiens	88-92	
27026200-10	2016	CONCLUSIONS: Collectively, carfilzomib induced ER stress culminating in activation of intrinsic and extrinsic caspase pathways, and we identified the CHOP protein level as a biomarker that could predict sensitivity to carfilzomib in CLL.	carfilzomib	218-229	DNA damage inducible transcript 3	Homo sapiens	150-154