PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
32519270-4	2020	We further demonstrated that KCNQ1OT1 directly bound to and suppressed the expression of miR-140-3p.	mir-140-3p	89-99	KCNQ1 opposite strand/antisense transcript 1	Homo sapiens	29-37	
32519270-5	2020	Overexpressing miR-140-3p significantly alleviated both the inflammation, oxidative stress, and cell apoptosis in OGD/R, while all those cytoprotective effects of miR-140-3p-overexpression were hindered by the co-overexpression of KCNQ1OT1.	mir-140-3p	15-25	KCNQ1 opposite strand/antisense transcript 1	Homo sapiens	231-239	
32519270-5	2020	Overexpressing miR-140-3p significantly alleviated both the inflammation, oxidative stress, and cell apoptosis in OGD/R, while all those cytoprotective effects of miR-140-3p-overexpression were hindered by the co-overexpression of KCNQ1OT1.	mir-140-3p	163-173	KCNQ1 opposite strand/antisense transcript 1	Homo sapiens	231-239	
32519270-6	2020	Furthermore, we found a direct interaction between miR-140-3p and the hypoxia-inducible factor-1alpha (HIF-1alpha), which was suppressed by the upregulation of KCNQ1OT1 in OGD/R.	mir-140-3p	51-61	KCNQ1 opposite strand/antisense transcript 1	Homo sapiens	160-168	
32519270-7	2020	Our results indicate that KCNQ1OT1 exacerbates cerebral ischemia-reperfusion injury by targeted binding to miR-140-3p, thus interfering its direct interaction with HIF-1alpha.	mir-140-3p	107-117	KCNQ1 opposite strand/antisense transcript 1	Homo sapiens	26-34