PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
29777777-7	2018	Contrary to VEGFC, miR-128 overexpression remarkably suppressed LEC proliferation, Ca2+ release and ERK1/2-Akt signaling; moreover, the effect of VEGFC could be partially attenuated by miR-128.	mir-128	19-26	AKT serine/threonine kinase 1	Homo sapiens	107-110	
22614013-7	2013	In addition, we found that miR-128 through BMI1 direct binding on the PTEN promoter affected PTEN expression levels and AKT activity in the pituitary tumor cells.	mir-128	27-34	AKT serine/threonine kinase 1	Homo sapiens	120-123	
30546426-11	2018	Markedly decreased Akt phosphorylation and cyclin D1 levels and increased p53 levels were detected when cells were transfected with miR-128 mimics.	mir-128	132-139	AKT serine/threonine kinase 1	Homo sapiens	19-22	
30546426-14	2018	In conclusion, the results suggested that miR-128 was a specific negative regulator of RPN2, which regulated colorectal cancer cell proliferation and migration by affecting the Akt-p53-cyclin pathway.	mir-128	42-49	AKT serine/threonine kinase 1	Homo sapiens	177-180	
29777777-8	2018	In summary, miR-128 interacts with the 3"-UTR of VEGFC and VEGFR3 to inhibit their expression, thus suppressing LEC proliferation through Ca2+ and ERK1/2-Akt signaling.	mir-128	12-19	AKT serine/threonine kinase 1	Homo sapiens	154-157	
28424413-8	2017	In fact, we found that miR-128 could reverse epithelial-to-mesenchymal transition induced by Bmi-1 via the PI3K/AKT pathway.	mir-128	23-30	AKT serine/threonine kinase 1	Homo sapiens	112-115	
30223934-6	2018	Besides, the association between miR-128-3p and ERK and PI3K/AKT pathways was further explored.	mir-128	33-40	AKT serine/threonine kinase 1	Homo sapiens	61-64	
27186417-7	2016	Mechanistically, we showed that miR-128 regulates PFKL via a feedback loop that involves inhibition of the AKT signaling pathway.	mir-128	32-39	AKT serine/threonine kinase 1	Homo sapiens	107-110	
27690301-0	2016	MiR-128 reverses the gefitinib resistance of the lung cancer stem cells by inhibiting the c-met/PI3K/AKT pathway.	mir-128	0-7	AKT serine/threonine kinase 1	Homo sapiens	101-104	
27150726-9	2016	Activation of Akt (p-Akt), Mcl-1 and PPARG expression in the myocardium were increased by miR-128 inhibition.	mir-128	90-97	AKT serine/threonine kinase 1	Homo sapiens	14-17	
27150726-9	2016	Activation of Akt (p-Akt), Mcl-1 and PPARG expression in the myocardium were increased by miR-128 inhibition.	mir-128	90-97	AKT serine/threonine kinase 1	Homo sapiens	19-24	
25001183-6	2014	In addition, overexpression of miR-128 in NSCLC cells and human umbilical vein endothelial cells (HUVECs) cells led to decreased expression of VEGF-A, vascular endothelial growth factor receptor (VEGFR)-2 and VEGFR-3, critical factors responsible for cancer angiogenesis and lymphangiogenesis, and subsequently decreased phosphorylation of extracellular signal-regulated kinase (ERK), phosphatidylinositol 3-kinase (AKT) and p38 signalling pathways.	mir-128	31-38	AKT serine/threonine kinase 1	Homo sapiens	416-419	
25001183-8	2014	These findings suggest that miR-128 could play a role in NSCLC tumourigenesis at least in part by modulation of angiogenesis and lymphangiogenesis through targeting VEGF-C, and could simultaneously block ERK, AKT and p38 signalling pathways.	mir-128	28-35	AKT serine/threonine kinase 1	Homo sapiens	209-212