PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
31652494-4	2019	Copper sulfate also increased the levels of apoptosis, senescence, mitochondrial dysfunction, autophagy, ROS, and the expression of several stress proteins, including ATF3, c-Fos, DEC1 (differentiated embryonic chondrocyte gene 1), p21, p53, and HIF-1alpha (hypoxia-inducible factor 1 alpha).	Copper Sulfate	0-14	hypoxia inducible factor 1 subunit alpha	Homo sapiens	246-256	
31652494-4	2019	Copper sulfate also increased the levels of apoptosis, senescence, mitochondrial dysfunction, autophagy, ROS, and the expression of several stress proteins, including ATF3, c-Fos, DEC1 (differentiated embryonic chondrocyte gene 1), p21, p53, and HIF-1alpha (hypoxia-inducible factor 1 alpha).	Copper Sulfate	0-14	hypoxia inducible factor 1 subunit alpha	Homo sapiens	258-290	
26415222-3	2015	Here, we show that copper sulfate (CuSO4) induces the expression of HIF-1alpha as well as GPER and VEGF in breast and hepatic cancer cells through the activation of the EGFR/ERK/c-fos transduction pathway.	Copper Sulfate	19-33	hypoxia inducible factor 1 subunit alpha	Homo sapiens	68-78	
26415222-3	2015	Here, we show that copper sulfate (CuSO4) induces the expression of HIF-1alpha as well as GPER and VEGF in breast and hepatic cancer cells through the activation of the EGFR/ERK/c-fos transduction pathway.	Copper Sulfate	35-40	hypoxia inducible factor 1 subunit alpha	Homo sapiens	68-78	
26415222-5	2015	We also ascertained that HIF-1alpha and GPER are required for the transcriptional activation of VEGF induced by CuSO4.	Copper Sulfate	112-117	hypoxia inducible factor 1 subunit alpha	Homo sapiens	25-35	
26415222-6	2015	In addition, in human endothelial cells, the conditioned medium from breast cancer cells treated with CuSO4 promoted cell migration and tube formation through HIF-1alpha and GPER.	Copper Sulfate	102-107	hypoxia inducible factor 1 subunit alpha	Homo sapiens	159-169