PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
16015388-6	2005	Using pharmacologic and genetic approaches, generation of ROS, p21CIP1 downregulation, and inactivation of Akt and MEK were found to play significant functional roles in SAHA/PD184352-mediated lethality, whereas JNK activation and Raf-1 downregulation were determined to represent secondary events.	Vorinostat	170-174	mitogen-activated protein kinase 8	Homo sapiens	212-215	
20233973-4	2010	Genetic or pharmacologic JNK inhibition significantly diminished CFZ/vorinostat lethality.	Vorinostat	69-79	mitogen-activated protein kinase 8	Homo sapiens	25-28	
20233973-7	2010	However, CFZ/vorinostat dramatically induced resistant cell apoptosis, accompanied by increased JNK activation and gammaH2A.X expression.	Vorinostat	13-23	mitogen-activated protein kinase 8	Homo sapiens	96-99	
18636153-4	2008	Moreover, SAHA increased the levels of phosphorylated active forms of p38 and JNK.	Vorinostat	10-14	mitogen-activated protein kinase 8	Homo sapiens	78-81	
21750224-8	2011	Finally, carfilzomib/vorinostat coadministration resulted in a pronounced reduction in tumor growth compared with single agent treatment in an MCL xenograft model associated with enhanced apoptosis, lambdaH2A.X formation, and JNK activation.	Vorinostat	21-31	mitogen-activated protein kinase 8	Homo sapiens	226-229	
14614324-2	2003	Exposure of K562 cells to greater or less than 3.0 mM SB or 3.0 mM SAHA for 24-48 hr resulted in a marked induction of mitchondrial damage (e.g., cytochrome c release) and apoptosis, events associated with downregulation of Bcr/Abl and Raf-1, induction of p21CIP1, inactivation of MEK1/2, ERK1/2, and p70S6K, and a dramatic increase in JNK activation.	Vorinostat	67-71	mitogen-activated protein kinase 8	Homo sapiens	336-339	
26623653-0	2015	The Bone Marrow-Mediated Protection of Myeloproliferative Neoplastic Cells to Vorinostat and Ruxolitinib Relies on the Activation of JNK and PI3K Signalling Pathways.	Vorinostat	78-88	mitogen-activated protein kinase 8	Homo sapiens	133-136	
27074555-2	2016	Here we report that combination treatment of carfilzomib and vorinostat enhanced cell apoptosis and induced a marked increase in G2-M arrest, reactive oxygen species (ROS) generation, and activated the members of mitogen-activated protein kinases (MAPK) family, including the stress-activated kinases JNK, p38MAPK, and ERK1/2.	Vorinostat	61-71	mitogen-activated protein kinase 8	Homo sapiens	301-304	
27074555-4	2016	The JNK inhibitor SP600125 and the p38MAPK inhibitor SB203580 but not the MEK1/2 inhibitor U0126 significantly attenuated carfilzomib/vorinostat-induced apoptosis, suggesting that p38MAPK and JNK activation contribute to carfilzomib and vorinostat-induced apoptosis.	Vorinostat	134-144	mitogen-activated protein kinase 8	Homo sapiens	4-7	
27074555-4	2016	The JNK inhibitor SP600125 and the p38MAPK inhibitor SB203580 but not the MEK1/2 inhibitor U0126 significantly attenuated carfilzomib/vorinostat-induced apoptosis, suggesting that p38MAPK and JNK activation contribute to carfilzomib and vorinostat-induced apoptosis.	Vorinostat	134-144	mitogen-activated protein kinase 8	Homo sapiens	192-195	
27074555-6	2016	Interestingly, the ROS scavenger NAC attenuated carfilzomib/vorinostat-mediated activation of p38MAPK and JNK.	Vorinostat	60-70	mitogen-activated protein kinase 8	Homo sapiens	106-109	
26438393-6	2015	Results indicate that signaling pathways involving JNK and related factors as predicted by SDREM are essential for virus reactivation by suberoylanilide hydroxamic acid.	Vorinostat	137-168	mitogen-activated protein kinase 8	Homo sapiens	51-54	
25667457-7	2015	However, a decrease in phosphorylation of JNK occurred in non-tumorigenic WBras1 cells following vorinostat treatment but not PBA treatment.	Vorinostat	97-107	mitogen-activated protein kinase 8	Homo sapiens	42-45	
24980831-9	2014	By showing that down-regulation of CCL2-driven signals by SAHA and temozolomide via JNK contributes to reduce melanoma growth, we provide a rationale for the therapeutic advantage of the drug combination.	Vorinostat	58-62	mitogen-activated protein kinase 8	Homo sapiens	84-87