PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31880296-0	2019	miR-206 Inhibits Cell Proliferation and Extracellular Matrix Accumulation by Targeting Hypoxia-Inducible Factor 1-alpha (HIF-1alpha) in Mesangial Cells Treated with High Glucose.	Glucose	170-177	microRNA 206	Homo sapiens	0-7	
20655308-0	2010	miR-1/miR-206 regulate Hsp60 expression contributing to glucose-mediated apoptosis in cardiomyocytes.	Glucose	56-63	microRNA 206	Homo sapiens	6-13	
20655308-2	2010	After stimulation of cardiomyocytes with high glucose in vivo and in vitro, significant up-regulation of miR-1/miR-206 and post-transcriptional modulation of Hsp 60 were observed.	Glucose	46-53	microRNA 206	Homo sapiens	111-118	
20655308-5	2010	These results revealed that miR-1 and miR-206 regulate Hsp60 expression, contributing to high glucose-mediated apoptosis in cardiomyocytes.	Glucose	94-101	microRNA 206	Homo sapiens	38-45	
31742336-12	2020	Furthermore, miR-206 reduced glucose uptake, lactate production and ATP generation in NSCLC cells via HK2 repression.	Glucose	29-36	microRNA 206	Homo sapiens	13-20	
31880296-1	2019	BACKGROUND The goal of this study was to investigate the expression of miR-206 in human glomerular mesangial cells (hMCs) treated by exposure to high glucose (HG) levels, to assess the influence of miR-206 on the proliferation and extracellular matrix (ECM) deposition of hMCs, and to investigate the potential mechanisms of action.	Glucose	150-157	microRNA 206	Homo sapiens	71-78