PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
25689303-2	2015	The celecoxib derivative OSU-03012 (also called AR-12) interacts with Viagra or Cialis in eukaryotic cells to rapidly reduce HSPA5 levels as well as blunt the functions of many other chaperone proteins.	Celecoxib	4-13	heat shock protein family A (Hsp70) member 5	Homo sapiens	125-130	
24692703-4	2014	RESULTS: Celecoxib triggered an ER stress response in this HNSCC cell line as shown by activation of CHOP, GRP78 and XBP1.	Celecoxib	9-18	heat shock protein family A (Hsp70) member 5	Homo sapiens	107-112	
21567098-8	2011	In HCT116 cells, celecoxib increased VEGF production with time-course and dose-response curves similar to those observed for the increase of the ER chaperone, GRP78.	Celecoxib	17-26	heat shock protein family A (Hsp70) member 5	Homo sapiens	159-164	
16205636-4	2006	Celecoxib, an NSAID, upregulated ER chaperones (GRP78 and its cochaperones ERdj3 and ERdj4) but also C/EBP homologous transcription factor (CHOP), a transcription factor involved in apoptosis.	Celecoxib	0-9	heat shock protein family A (Hsp70) member 5	Homo sapiens	48-53	
16205636-7	2006	Suppression of ATF4 expression by small interfering RNA (siRNA) partially inhibited the celecoxib-dependent upregulation of GRP78.	Celecoxib	88-97	heat shock protein family A (Hsp70) member 5	Homo sapiens	124-129	
16205636-10	2006	Overexpression of GRP78 partially suppressed the apoptosis and induction of CHOP in the presence of celecoxib and this suppression was stimulated by coexpression of either ERdj3 or ERdj4.	Celecoxib	100-109	heat shock protein family A (Hsp70) member 5	Homo sapiens	18-23	
16205636-11	2006	On the other hand, suppression of GRP78 expression by siRNA drastically stimulated cellular apoptosis and production of CHOP in the presence of celecoxib.	Celecoxib	144-153	heat shock protein family A (Hsp70) member 5	Homo sapiens	34-39	
32966814-1	2020	AR12 is a derivative of celecoxib which no-longer acts against COX2 but instead inhibits the ATPase activity of multiple chaperone proteins, in particular GRP78.	Celecoxib	24-33	heat shock protein family A (Hsp70) member 5	Homo sapiens	155-160	
29354301-11	2017	Taken together, celecoxib triggered ER stress on lung cancer cells and celecoxib-induced apoptosis might be involved in both non-classical caspase-4 and GRP78.	Celecoxib	71-80	heat shock protein family A (Hsp70) member 5	Homo sapiens	153-158	
22438966-0	2012	Down-regulation of glucose-regulated protein (GRP) 78 potentiates cytotoxic effect of celecoxib in human urothelial carcinoma cells.	Celecoxib	86-95	heat shock protein family A (Hsp70) member 5	Homo sapiens	19-53	
22438966-7	2012	Celecoxib possessed the ability to activate ER stress-related chaperones (IRE-1alpha and GRP78), caspase-4, and CCAAT/enhancer binding protein homologous protein (CHOP), which were involved in UC cell apoptosis.	Celecoxib	0-9	heat shock protein family A (Hsp70) member 5	Homo sapiens	89-94	
22438966-8	2012	Down-regulation of GRP78 by siRNA, co-treatment with EGCG (a GRP78 inhibitor) or with MG132 (a proteasome inhibitor) could enhance celecoxib-induced apoptosis.	Celecoxib	131-140	heat shock protein family A (Hsp70) member 5	Homo sapiens	19-24	
22438966-8	2012	Down-regulation of GRP78 by siRNA, co-treatment with EGCG (a GRP78 inhibitor) or with MG132 (a proteasome inhibitor) could enhance celecoxib-induced apoptosis.	Celecoxib	131-140	heat shock protein family A (Hsp70) member 5	Homo sapiens	61-66	
22438966-10	2012	The down-regulation of ER chaperone GRP78 by siRNA, EGCG, or proteosome inhibitor potentiated the cytotoxicity of celecoxib in UC cells.	Celecoxib	114-123	heat shock protein family A (Hsp70) member 5	Homo sapiens	36-41	
18245486-6	2008	When combined, bortezomib and celecoxib triggered elevated expression of the ER stress markers GRP78/BiP and CHOP/GADD153, caused activation of c-Jun NH(2)-terminal kinase and ER stress-associated caspase-4, and greatly increased apoptotic cell death.	Celecoxib	30-39	heat shock protein family A (Hsp70) member 5	Homo sapiens	95-100	
18245486-6	2008	When combined, bortezomib and celecoxib triggered elevated expression of the ER stress markers GRP78/BiP and CHOP/GADD153, caused activation of c-Jun NH(2)-terminal kinase and ER stress-associated caspase-4, and greatly increased apoptotic cell death.	Celecoxib	30-39	heat shock protein family A (Hsp70) member 5	Homo sapiens	101-104	
32994805-0	2020	Aspirin potentiates celecoxib-induced growth inhibition and apoptosis in human non-small cell lung cancer by targeting GRP78 activity.	Celecoxib	20-29	heat shock protein family A (Hsp70) member 5	Homo sapiens	119-124	
29354301-8	2017	As checking ER stress associated molecules, celecoxib did not increase expressions of growth arrest and DNA damage inducible protein 34, activating transcription factor 4, and spliced X-box binding protiens-1, but increase of both glucose-regulated protein 78 (GRP78) and C/EBP homologous transcription factor were detected.	Celecoxib	44-53	heat shock protein family A (Hsp70) member 5	Homo sapiens	231-259	
29354301-8	2017	As checking ER stress associated molecules, celecoxib did not increase expressions of growth arrest and DNA damage inducible protein 34, activating transcription factor 4, and spliced X-box binding protiens-1, but increase of both glucose-regulated protein 78 (GRP78) and C/EBP homologous transcription factor were detected.	Celecoxib	44-53	heat shock protein family A (Hsp70) member 5	Homo sapiens	261-266	
29354301-10	2017	Instead, celecoxib-induced apoptosis might be deeply associated with ER stress depending on GRP78 because siRNA for GRP78 enhanced apoptosis.	Celecoxib	9-18	heat shock protein family A (Hsp70) member 5	Homo sapiens	92-97	
29354301-10	2017	Instead, celecoxib-induced apoptosis might be deeply associated with ER stress depending on GRP78 because siRNA for GRP78 enhanced apoptosis.	Celecoxib	9-18	heat shock protein family A (Hsp70) member 5	Homo sapiens	116-121	
26931344-5	2016	RESULTS: Celecoxib (>=60 microM) up-regulated the expression of ER stress markers (GRP78 and CHOP) and induced cell apoptosis accompanying with a correlated increased expression of VEGF in HT29 cells.	Celecoxib	9-18	heat shock protein family A (Hsp70) member 5	Homo sapiens	86-91	
26931344-7	2016	In xenograft models, celecoxib treatment inhibited tumor growth with increased GRP78 and VEGF, which was consistent with the results in vitro.	Celecoxib	21-30	heat shock protein family A (Hsp70) member 5	Homo sapiens	79-84	
26225471-0	2015	The interplay between GRP78 expression and Akt activation in human colon cancer cells under celecoxib treatment.	Celecoxib	92-101	heat shock protein family A (Hsp70) member 5	Homo sapiens	22-27	
26225471-7	2015	Besides, silencing the GRP78 expression regulated Akt activation in a time-dependent manner and increased the induction of the C/EBP homologous protein (CHOP) as well as considerably promoted celecoxib-induced apoptosis.	Celecoxib	192-201	heat shock protein family A (Hsp70) member 5	Homo sapiens	23-28	
26225471-8	2015	In conclusion, these findings provide evidence that under the celecoxib treatment, GRP78 plays a protective role by modulating Akt activation and abrogating CHOP expression.	Celecoxib	62-71	heat shock protein family A (Hsp70) member 5	Homo sapiens	83-88