PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
30873870-0	2019	Shikonin induces apoptosis and prosurvival autophagy in human melanoma A375 cells via ROS-mediated ER stress and p38 pathways.	shikonin	0-8	mitogen-activated protein kinase 14	Homo sapiens	113-116	
34829701-12	2021	Shikonin treatment elevated p38 activity in a dose-dependent manner.	shikonin	0-8	mitogen-activated protein kinase 14	Homo sapiens	28-31	
34829701-13	2021	In conclusion, our results revealed that shikonin triggered programmed cell death via the elevation of ROS level and p38 activity in different types of RCC cells.	shikonin	41-49	mitogen-activated protein kinase 14	Homo sapiens	117-120	
33164437-7	2020	Shikonin also significantly reduced the TNF-alpha-induced migration, adhesion, invasion and phosphorylation levels of Akt, JNK, p38, ERK in MH7 A cells within 24 h. These results suggested that shikonin could reduce the proliferation, migration, adhesion and invasion ability of MH7 A cells induced by TNF-alpha, and its mechanism may be related to the down-regulation of Akt and MAPK signaling pathway activation.	shikonin	0-8	mitogen-activated protein kinase 14	Homo sapiens	128-131	
33164437-7	2020	Shikonin also significantly reduced the TNF-alpha-induced migration, adhesion, invasion and phosphorylation levels of Akt, JNK, p38, ERK in MH7 A cells within 24 h. These results suggested that shikonin could reduce the proliferation, migration, adhesion and invasion ability of MH7 A cells induced by TNF-alpha, and its mechanism may be related to the down-regulation of Akt and MAPK signaling pathway activation.	shikonin	194-202	mitogen-activated protein kinase 14	Homo sapiens	128-131	
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	shikonin	53-61	mitogen-activated protein kinase 14	Homo sapiens	179-182	
30873870-8	2019	Moreover, after pretreatment with N-acetyl-cysteine, Shikonin increased the production of reactive oxygen species that are involved in regulating ER stress-mediated apoptosis and p38-activated autophagy, as evidenced by the reversion of cell viability and apoptosis and a decrease in p-eIF2alpha, CHOP, p-p38, LC3B-II, and Beclin 1 levels.	shikonin	53-61	mitogen-activated protein kinase 14	Homo sapiens	305-308	
30873870-9	2019	Thus, we demonstrated that Shikonin induced apoptosis and autophagy in A375 cells via the activation of ROS-mediated ER stress and p38 pathways, indicating that Shikonin can serve as a potential agent for human melanoma therapy.	shikonin	27-35	mitogen-activated protein kinase 14	Homo sapiens	131-134	
30873870-9	2019	Thus, we demonstrated that Shikonin induced apoptosis and autophagy in A375 cells via the activation of ROS-mediated ER stress and p38 pathways, indicating that Shikonin can serve as a potential agent for human melanoma therapy.	shikonin	161-169	mitogen-activated protein kinase 14	Homo sapiens	131-134	
29422643-9	2018	Therefore, our results suggest that shikonin induces the expression of DUSP1 and DUSP2 which consequently switches off JNK and p38 MAPK pathways and causes cell cycle arrest and apoptosis in breast cancer cells.	shikonin	36-44	mitogen-activated protein kinase 14	Homo sapiens	127-130	
23546866-3	2013	Here, we demonstrated that shikonin-induced apoptosis is caused by reactive oxygen species (ROS)-mediated activation of Akt/ASK1/p38 mitogen-activated protein kinase (MAPK) and downregulation of p21(Cip1).	shikonin	27-35	mitogen-activated protein kinase 14	Homo sapiens	129-132	
28922731-0	2017	Shikonin suppresses pulmonary fibroblasts proliferation and activation by regulating Akt and p38 MAPK signaling pathways.	shikonin	0-8	mitogen-activated protein kinase 14	Homo sapiens	93-96	
24905636-7	2014	In addition, shikonin significantly decreased the phosphorylation of AKT and mTOR in a dose-dependent manner while it induced extracellular signal-regulated kinase (ERK), p38 mitogen activated protein kinase (MAPK) and c-Jun N terminal kinase (JNK) phosphorylation.	shikonin	13-21	mitogen-activated protein kinase 14	Homo sapiens	171-207	
24962386-11	2014	Shikonin effectively inhibited the phosphorylation of ERK, while it activated the phosphorylation of JNK and p38.	shikonin	0-8	mitogen-activated protein kinase 14	Homo sapiens	109-112	
23546866-13	2013	These findings suggest that shikonin-induced ROS activated ASK1 by decreasing Ser83 phosphorylation and by dissociation of the negative regulator p21(Cip1), leading to p38 MAPK activation, and finally, promoting apoptosis.	shikonin	28-36	mitogen-activated protein kinase 14	Homo sapiens	168-171	
18663379-2	2008	Treatment of K562 cells with shikonin (e.g., 0.5 muM) resulted in profound induction of apoptosis accompanied by rapid generation of reactive oxygen species (ROS), striking activation of c-Jun-N-terminal kinase (JNK) and p38, marked release of the mitochondrial proteins cytochrome c and Smac/DIABLO, activation of caspase-9 and -3, and cleavage of PARP.	shikonin	29-37	mitogen-activated protein kinase 14	Homo sapiens	221-224