PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
12807754-8	2003	Androgen stimulation with dihydrotestosterone, a major endogenous metabolite of testosterone, also significantly inhibited p38/NFkappaB and JNK/AP-1 activation and apoptosis.	Testosterone	33-45	mitogen-activated protein kinase 8	Homo sapiens	140-143	
12619033-5	2003	In addition, testosterone significantly enhanced in vivo phosphorylation of c-jun by 4-HPR as well as JNK activation.	Testosterone	13-25	mitogen-activated protein kinase 8	Homo sapiens	102-105	
12619033-6	2003	Transfection with an antisense oligonucleotide of c-jun blocked 4-HPR-induced apoptosis and the testosterone-induced sensitization, suggesting a major contribution of the JNK/c-jun mediated pathway in androgen-dependent sensitization.	Testosterone	96-108	mitogen-activated protein kinase 8	Homo sapiens	171-174	
20189893-4	2010	We provide evidence that p38 MAPK and PI3K/Akt/NFkappaB and/or Rho/Actin pathways are directly involved in testosterone-induced apoptosis, while the JNK/c-JUN pathway is involved in membrane site-initiated transcription.	Testosterone	107-119	mitogen-activated protein kinase 8	Homo sapiens	149-152	
28633436-6	2017	Transfection with small interfering RNA targeting croaker ZIP9 blocked testosterone-induced increase in bax, p53, and jnk expression.	Testosterone	71-83	mitogen-activated protein kinase 8	Homo sapiens	118-121	
25014355-6	2014	Testosterone treatment caused up-regulation of proapoptotic genes Bax (Bcl-2-associated X protein), p53 (tumor protein p53), and JNK (c-Jun N-terminal kinases) in both cell lines and increased expression of Bax, Caspase 3, and cytochrome C proteins.	Testosterone	0-12	mitogen-activated protein kinase 8	Homo sapiens	129-132	
25014355-6	2014	Testosterone treatment caused up-regulation of proapoptotic genes Bax (Bcl-2-associated X protein), p53 (tumor protein p53), and JNK (c-Jun N-terminal kinases) in both cell lines and increased expression of Bax, Caspase 3, and cytochrome C proteins.	Testosterone	0-12	mitogen-activated protein kinase 8	Homo sapiens	134-158	
25014355-7	2014	Treatment with a zinc chelator or a MAPK inhibitor blocked testosterone-induced increases in Bax, p53, and JNK mRNA expression.	Testosterone	59-71	mitogen-activated protein kinase 8	Homo sapiens	107-110	
20442653-3	2010	The level of testosterone regulating several signaling pathways, including extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun-N-terminal kinase (JNK), and p38 MAPK, was measured by western blot in HUVECs.	Testosterone	13-25	mitogen-activated protein kinase 8	Homo sapiens	128-151	
20442653-3	2010	The level of testosterone regulating several signaling pathways, including extracellular signal-regulated kinases 1/2 (ERK1/2), c-Jun-N-terminal kinase (JNK), and p38 MAPK, was measured by western blot in HUVECs.	Testosterone	13-25	mitogen-activated protein kinase 8	Homo sapiens	153-156	
20442653-5	2010	Testosterone-induced a rapid phosphorylation of ERK1/2, JNK and p38 MAPK in HUVECs, which could not be inhibited by androgen receptor antagonist flutamide.	Testosterone	0-12	mitogen-activated protein kinase 8	Homo sapiens	56-59	
20442653-6	2010	Blocking ERK1/2 or JNK pathway could significantly impair testosterone-induced TFPI at both translational and transcriptional levels in HUVECs.	Testosterone	58-70	mitogen-activated protein kinase 8	Homo sapiens	19-22	
20442653-7	2010	Testosterone at a physiological concentration may help to prevent thrombosis development by stimulating TFPI expression in HUVECs, partly through the ERK1/2 and JNK MAPK pathway.	Testosterone	0-12	mitogen-activated protein kinase 8	Homo sapiens	161-164	
21475848-3	2009	Here, we report that progesterone and testosterone induce apoptosis in HUVECs in a p38- and JNK-dependent manner, and that estradiol promotes proliferation via the activation of ERK2.	Testosterone	38-50	mitogen-activated protein kinase 8	Homo sapiens	92-95	
21475848-4	2009	We showed that, at physiological doses, progesterone and testosterone promoted p38, but not JNK, phosphorylation.	Testosterone	57-69	mitogen-activated protein kinase 8	Homo sapiens	92-95	
21475848-10	2009	In conclusion, these findings suggest that JNK has an important pro-apoptotic function following progesterone and testosterone treatment in human endothelial cells, and that ERK2 has a proliferative effect following estradiol treatment.	Testosterone	114-126	mitogen-activated protein kinase 8	Homo sapiens	43-46