PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
17715378-7	2007	Inhibition of isochaihulactone-induced NAG-1 expression by EGR-1 small interfering RNA blocked isochaihulactone-induced apoptosis in A549 cells, suggesting that induction of EGR-1 expression decreases survival of A549 cells.	isochaihulactone	14-30	growth differentiation factor 15	Homo sapiens	39-44	
17715378-7	2007	Inhibition of isochaihulactone-induced NAG-1 expression by EGR-1 small interfering RNA blocked isochaihulactone-induced apoptosis in A549 cells, suggesting that induction of EGR-1 expression decreases survival of A549 cells.	isochaihulactone	95-111	growth differentiation factor 15	Homo sapiens	39-44	
17715378-8	2007	RNA interference using double-stranded RNA specific for NAG-1 also inhibited isochaihulactone-induced apoptosis, and cells transfected to increased NAG-1 expression had a greater apoptotic response to isochaihulactone and reduced colony formation efficiency.	isochaihulactone	77-93	growth differentiation factor 15	Homo sapiens	56-61	
17715378-8	2007	RNA interference using double-stranded RNA specific for NAG-1 also inhibited isochaihulactone-induced apoptosis, and cells transfected to increased NAG-1 expression had a greater apoptotic response to isochaihulactone and reduced colony formation efficiency.	isochaihulactone	201-217	growth differentiation factor 15	Homo sapiens	148-153	
17715378-10	2007	Isochaihulactone treatment increased the luciferase activity of NAG-1 in A549 cells transfected with the NAG-1 promoter construct.	isochaihulactone	0-16	growth differentiation factor 15	Homo sapiens	64-69	
17715378-10	2007	Isochaihulactone treatment increased the luciferase activity of NAG-1 in A549 cells transfected with the NAG-1 promoter construct.	isochaihulactone	0-16	growth differentiation factor 15	Homo sapiens	105-110	
17715378-12	2007	Our findings suggest that NAG-1 expression is up-regulated by isochaihulactone through an ERK-dependent pathway involving the activation of EGR-1.	isochaihulactone	62-78	growth differentiation factor 15	Homo sapiens	26-31	
27852055-6	2017	Isochaihulactone induced DDIT3 led to the expression of NAG-1.	isochaihulactone	0-16	growth differentiation factor 15	Homo sapiens	56-61	
27852055-8	2017	Overall, the data revealed that isochaihulactone disrupted ER homeostasis in cancer cells by increasing DDIT3 and NAG-1 expression.	isochaihulactone	32-48	growth differentiation factor 15	Homo sapiens	114-119	
21391217-3	2012	Here, we show that isochaihulactone (K8) enhanced paclitaxel-induced apoptotic death in human lung cancer cells, and the enhancing effect was related to increased NSAID-activated gene-1 (NAG-1) expression.	isochaihulactone	19-35	growth differentiation factor 15	Homo sapiens	163-185	
21391217-3	2012	Here, we show that isochaihulactone (K8) enhanced paclitaxel-induced apoptotic death in human lung cancer cells, and the enhancing effect was related to increased NSAID-activated gene-1 (NAG-1) expression.	isochaihulactone	19-35	growth differentiation factor 15	Homo sapiens	187-192	
21504622-0	2011	Activation of NAG-1 via JNK signaling revealed an isochaihulactone-triggered cell death in human LNCaP prostate cancer cells.	isochaihulactone	50-66	growth differentiation factor 15	Homo sapiens	14-19	
21504622-12	2011	Isochaihulactone also induced the expressions of EGR-1 and NAG-1.	isochaihulactone	0-16	growth differentiation factor 15	Homo sapiens	59-64	
21504622-13	2011	Expression of NAG-1 was reduced by JNK inhibitor, and knocking down of NAG-1 inhibited isochaihulactone-induced cell death.	isochaihulactone	87-103	growth differentiation factor 15	Homo sapiens	14-19	
21504622-13	2011	Expression of NAG-1 was reduced by JNK inhibitor, and knocking down of NAG-1 inhibited isochaihulactone-induced cell death.	isochaihulactone	87-103	growth differentiation factor 15	Homo sapiens	71-76	
21504622-14	2011	CONCLUSIONS: Isochaihulactone apparently induces G2/M cell cycle arrest via downregulation of cyclin B1 and cdc2, and induces cellular death by upregulation of NAG-1 via JNK activation in LNCaP cells.	isochaihulactone	13-29	growth differentiation factor 15	Homo sapiens	160-165	
17715378-3	2007	Isochaihulactone-inducible genes included the early growth response gene-1 (EGR-1) and nonsteroidal anti-inflammatory drug-activated gene (NAG-1).	isochaihulactone	0-16	growth differentiation factor 15	Homo sapiens	139-144	
17715378-4	2007	Isochaihulactone increased EGR-1 and then NAG-1 mRNA and protein expression.	isochaihulactone	0-16	growth differentiation factor 15	Homo sapiens	42-47	
17715378-6	2007	Isochaihulactone-induced increases in EGR-1 and NAG-1 expression were reduced by the mitogen-activated protein kinase kinase 1/2 inhibitor 2"-amino-3"-methoxyflavone (PD98059), and this effect was not blocked by the phosphatidylinositol 3-kinase/protein kinase B pathway inhibitor 2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one hydrochloride (LY294002).	isochaihulactone	0-16	growth differentiation factor 15	Homo sapiens	48-53