PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
22262759-6	2012	We show that carbon monoxide (CO) suppresses hepcidin expression elicited by IL-6- and ER-stress agents by inhibiting STAT-3 phosphorylation and CREBH maturation, respectively.	Carbon Monoxide	13-28	hepcidin antimicrobial peptide	Mus musculus	45-53	
22262759-6	2012	We show that carbon monoxide (CO) suppresses hepcidin expression elicited by IL-6- and ER-stress agents by inhibiting STAT-3 phosphorylation and CREBH maturation, respectively.	Carbon Monoxide	30-32	hepcidin antimicrobial peptide	Mus musculus	45-53	
31295319-5	2019	Because CO is physiologically generated during heme degradation by heme oxygenase 1 (HO-1), an IL-6-inducible enzyme with anti-inflammatory properties, we hypothesized that hepatocellular HO-1 may operate as a physiological feedback regulator of hepcidin that resolves inflammatory signaling.	Carbon Monoxide	8-10	hepcidin antimicrobial peptide	Mus musculus	246-254	
19924283-10	2009	In mice exposed to carbon monoxide, hypoxia or the chemical HIF inducer N-oxalylglycine, liver hepcidin 1 mRNA was elevated rather than decreased.	Carbon Monoxide	19-34	hepcidin antimicrobial peptide	Mus musculus	95-103	
31295319-4	2019	Previous work showed that carbon monoxide (CO) releasing drugs (CORMs) can attenuate inflammatory induction of hepcidin.	Carbon Monoxide	26-41	hepcidin antimicrobial peptide	Mus musculus	111-119