PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
20803121-10	2010	Moreover, quercetin increased the AIF protein released from mitochondria to nuclei and the GADD153 protein translocation from endoplasmic reticulum to the nuclei.	Quercetin	10-19	DNA damage inducible transcript 3	Homo sapiens	91-98	
19017364-6	2009	Moreover, our studies reveal that HSP70 knockdown or quercetin induces other typical components of the UPR, including CHOP expression, eIF2alpha and JNK phosphorylation, caspases activation and XBP-1 splicing.	Quercetin	53-62	DNA damage inducible transcript 3	Homo sapiens	118-122	
34150114-8	2021	The of Caspase-3, GRP78, and CHOP expression levels in the quercetin intervention group rose significantly in comparison with the blank control group (P<0.05).	Quercetin	59-68	DNA damage inducible transcript 3	Homo sapiens	29-33	
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	174-223	
24612139-0	2014	Quercetin enhances apoptotic effect of tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) in ovarian cancer cells through reactive oxygen species (ROS) mediated CCAAT enhancer-binding protein homologous protein (CHOP)-death receptor 5 pathway.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	225-229	
24612139-5	2014	The induction of DR5 was mediated through activation of JNK and through upregulation of a transcription factor CCAAT enhancer-binding protein homologous protein (CHOP); as silencing of these signaling molecules abrogated the effect of quercetin.	Quercetin	235-244	DNA damage inducible transcript 3	Homo sapiens	111-160	
24612139-5	2014	The induction of DR5 was mediated through activation of JNK and through upregulation of a transcription factor CCAAT enhancer-binding protein homologous protein (CHOP); as silencing of these signaling molecules abrogated the effect of quercetin.	Quercetin	235-244	DNA damage inducible transcript 3	Homo sapiens	162-166	
24612139-6	2014	Upregulation of DR5 was mediated through the generation of reactive oxygen species (ROS), as ROS scavengers reduced the effect of quercetin on JNK activation, CHOP upregulation, DR induction, TRAIL sensitization, downregulated the expression of cell survival proteins and upregulated the proapoptotic proteins.	Quercetin	130-139	DNA damage inducible transcript 3	Homo sapiens	159-163	
24612139-7	2014	Furthermore, quercetin enhances TRAIL mediated inhibition of tumor growth of human SKOV-3 xenograft was associated with induction of apoptosis, activation of caspase-3, CHOP and DR5.	Quercetin	13-22	DNA damage inducible transcript 3	Homo sapiens	169-173	
24612139-8	2014	Overall, our data suggest that quercetin enhances apoptotic death of ovarian cancer cells to TRAIL through upregulation of CHOP-induced DR5 expression following ROS mediated endoplasmic reticulum-stress.	Quercetin	31-40	DNA damage inducible transcript 3	Homo sapiens	123-127	
22431435-9	2014	Quercetin also stimulated the protein expression of ATF, GRP78, and GADD153 which is a hall marker of ER stress.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	68-75	
35149956-9	2022	PERK, CHOP, and the concomitant responses of quercetin in restoring the ER homeostasis in cellular organelles like mitochondria and ER, against Cu-induced toxic insults by modulating autophagic pathways.	Quercetin	45-54	DNA damage inducible transcript 3	Homo sapiens	6-10	
24666891-6	2014	Quercetin administration modulated expression level of ER stress genes coding for glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP), and antioxidant enzymes such as superoxide dismutase and catalase, along with free radical generation assessed by malondialdehyde assay.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	123-147	
24666891-6	2014	Quercetin administration modulated expression level of ER stress genes coding for glucose-regulated protein 78 (GRP78) and C/EBP-homologous protein (CHOP), and antioxidant enzymes such as superoxide dismutase and catalase, along with free radical generation assessed by malondialdehyde assay.	Quercetin	0-9	DNA damage inducible transcript 3	Homo sapiens	149-153	
24666891-8	2014	CONCLUSION: The current study indicates that quercetin modulated stress responsive genes GRP78 and CHOP, helping endothelial cells prevent TUN-induced ER stress.	Quercetin	45-54	DNA damage inducible transcript 3	Homo sapiens	99-103	
24368982-11	2013	Treatment with quercetin also increased the expression of Grp78/Bip and GADD153/CHOP protein and induced mitochondrial dysfunction.	Quercetin	15-24	DNA damage inducible transcript 3	Homo sapiens	72-79	
24368982-11	2013	Treatment with quercetin also increased the expression of Grp78/Bip and GADD153/CHOP protein and induced mitochondrial dysfunction.	Quercetin	15-24	DNA damage inducible transcript 3	Homo sapiens	80-84