PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
27444655-5	2016	We found that STZ treatment causes apoptosis of INS-1 cells by enhancement of intracellular reactive oxygen species (ROS) accumulation, inducible nitric oxide synthase (iNOS) expression and nitric oxide release and activation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signalling pathways.	Streptozocin	14-17	mitogen-activated protein kinase 8	Rattus norvegicus	233-256	
30880178-0	2019	Paeoniflorin protects pancreatic beta cells from STZ-induced damage through inhibition of the p38 MAPK and JNK signaling pathways.	Streptozocin	49-52	mitogen-activated protein kinase 8	Rattus norvegicus	107-110	
30880178-9	2019	Furthermore, PF inhibited the phosphorylation of p38 and JNK, which is induced by STZ in INS-1 cells.	Streptozocin	82-85	mitogen-activated protein kinase 8	Rattus norvegicus	57-60	
30880178-11	2019	Meanwhile, PF suppressed the activation of p38 MAPK and JNK pathways in STZ-treated INS-1 cells.	Streptozocin	72-75	mitogen-activated protein kinase 8	Rattus norvegicus	56-59	
34565207-10	2022	Lastly, protein expression levels of p-p38, p-ERK, and p-JNK protein were up-regulated in streptozotocin-induced rats and high glucose-treated MPC5.	Streptozocin	90-104	mitogen-activated protein kinase 8	Rattus norvegicus	57-60	
32799731-5	2020	Moreover, FYGL markedly decreased the intracellular ROS accumulation and NO release, and deactivated NF-kappaB, JNK, and p38 MAPK signaling pathways in STZ-induced INS-1 cells.	Streptozocin	152-155	mitogen-activated protein kinase 8	Rattus norvegicus	112-115	
29475461-5	2018	STZ/nicotinamide-induced T2DM increased the expression of mitogen-activated protein kinases (MAPKs: p38, ERK, JNK) and inflammatory p65 protein.	Streptozocin	0-3	mitogen-activated protein kinase 8	Rattus norvegicus	110-113	
27444655-5	2016	We found that STZ treatment causes apoptosis of INS-1 cells by enhancement of intracellular reactive oxygen species (ROS) accumulation, inducible nitric oxide synthase (iNOS) expression and nitric oxide release and activation of the c-jun N-terminal kinase (JNK) and p38 mitogen-activated protein kinase (MAPK) signalling pathways.	Streptozocin	14-17	mitogen-activated protein kinase 8	Rattus norvegicus	258-261	
25683919-4	2015	STZ treatment causes apoptosis of INS-1 cells by activation of intracellular ROS, c-jun N-terminal kinase (JNK), caspase 3, and caspase 3-dependent activation of protein kinase C delta (PKCdelta).	Streptozocin	0-3	mitogen-activated protein kinase 8	Rattus norvegicus	82-105	
25683919-4	2015	STZ treatment causes apoptosis of INS-1 cells by activation of intracellular ROS, c-jun N-terminal kinase (JNK), caspase 3, and caspase 3-dependent activation of protein kinase C delta (PKCdelta).	Streptozocin	0-3	mitogen-activated protein kinase 8	Rattus norvegicus	107-110	
24422903-9	2014	JNK gene overexpression and JNK protein levels induced by STZ were significantly inhibited after NCD treatment of islets ( P = 0.0001).	Streptozocin	58-61	mitogen-activated protein kinase 8	Rattus norvegicus	28-31	
25359484-8	2015	The present study demonstrated that STZ-induced oxidative stress could reduce serum insulin levels and alter the JNK, PDX-1, and PKD1 expression.	Streptozocin	36-39	mitogen-activated protein kinase 8	Rattus norvegicus	113-116	
24422903-2	2014	This study aims to investigate the effects of a novel curcumin derivative (NCD) on JNK signaling pathway on insulin synthesis and secretion in streptozotocin (STZ)-treated rat pancreatic islets in vitro.	Streptozocin	143-157	mitogen-activated protein kinase 8	Rattus norvegicus	83-86	
24422903-11	2014	CONCLUSIONS: NCD improved insulin synthesis and secretion in vitro in isolated pancreatic islets treated with STZ through inhibition of the JNK pathway, up-regulation of the gene expressions of HO-1, TCF7L2, and GLP-1 and enhancing effects on calcium and zinc levels.	Streptozocin	110-113	mitogen-activated protein kinase 8	Rattus norvegicus	140-143	
24422903-2	2014	This study aims to investigate the effects of a novel curcumin derivative (NCD) on JNK signaling pathway on insulin synthesis and secretion in streptozotocin (STZ)-treated rat pancreatic islets in vitro.	Streptozocin	159-162	mitogen-activated protein kinase 8	Rattus norvegicus	83-86	
17917385-0	2007	Streptozotocin-induced diabetes increases apoptosis through JNK phosphorylation and Bax activation in rat testes.	Streptozocin	0-14	mitogen-activated protein kinase 8	Rattus norvegicus	60-63	
24422903-9	2014	JNK gene overexpression and JNK protein levels induced by STZ were significantly inhibited after NCD treatment of islets ( P = 0.0001).	Streptozocin	58-61	mitogen-activated protein kinase 8	Rattus norvegicus	0-3	
21939517-10	2011	CONCLUSIONS: Increased expression of SR in retina and higher levels of glutamate and D-serine in aqueous humor of STZ-treated rats may result from activation of the JNK pathway in diabetic sequelae.	Streptozocin	114-117	mitogen-activated protein kinase 8	Rattus norvegicus	165-168	
20600246-0	2010	SP600125, a competitive inhibitor of JNK attenuates streptozotocin induced neurocognitive deficit and oxidative stress in rats.	Streptozocin	52-66	mitogen-activated protein kinase 8	Rattus norvegicus	37-40	
20600246-2	2010	The present study was designed to investigate the role of JNK in intracerebroventricular streptozotocin (i.c.v.	Streptozocin	89-103	mitogen-activated protein kinase 8	Rattus norvegicus	58-61	
17917385-2	2007	The present study was designed to evaluate whether streptozotocin-induced diabetes increases apoptotic cell death in rat testes through activation of the JNK and Bax pathway.	Streptozocin	51-65	mitogen-activated protein kinase 8	Rattus norvegicus	154-157	
17917385-6	2007	Our findings suggest that streptozotocin-induced diabetes increases apoptotic cell death in rat testes through phosphorylation of JNK and activation of Bax.	Streptozocin	26-40	mitogen-activated protein kinase 8	Rattus norvegicus	130-133	
11689477-5	2001	In the dorsal root ganglia of streptozotocin-induced diabetic rats (a model of type I diabetes), ERK and p38 were activated at 8 wk duration, followed by activation of JNK at 12 wk duration.	Streptozocin	30-44	mitogen-activated protein kinase 8	Rattus norvegicus	168-171	
12805110-4	2003	In STZ-diabetic rats the relative levels of retrograde axonal transport of phosphorylated (activated) JNK and p38 were raised compared with age-matched controls (all data are in arbitrary units and expressed as fold increase over control: JNK 54-56 kDa isoforms, control 1.0 +/- 0.19, diabetic 2.5 +/- 0.26; p38, control 1.0 +/- 0.09, diabetic 2.9 +/- 0.52; both P < 0.05).	Streptozocin	3-6	mitogen-activated protein kinase 8	Rattus norvegicus	102-105	
12805110-6	2003	The transcription factor ATF-2, which is phosphorylated and activated by JNK and p38, also exhibited elevated retrograde axonal transport in STZ-diabetic animals (control 1.0 +/- 0.07, diabetic 3.0 +/- 0.41; P < 0.05).	Streptozocin	141-144	mitogen-activated protein kinase 8	Rattus norvegicus	73-76