PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
35396529-4	2022	Both soluble factors and direct-cell contact interactions, such as JAG/NOTCH and COX-2/PGE2 pathways, are critically involved in the HSC-monocyte crosstalk.	Dinoprostone	87-91	fucosyltransferase 1 (H blood group)	Homo sapiens	133-136	
26758420-7	2016	Furthermore, in vivo animal studies confirmed that inhibition of HSC-derived PGE2 could inhibit HSC-induced MDSC accumulation and HCC growth.	Dinoprostone	77-81	fucosyltransferase 1 (H blood group)	Homo sapiens	65-68	
26758420-7	2016	Furthermore, in vivo animal studies confirmed that inhibition of HSC-derived PGE2 could inhibit HSC-induced MDSC accumulation and HCC growth.	Dinoprostone	77-81	fucosyltransferase 1 (H blood group)	Homo sapiens	96-99	
26758420-8	2016	Thus, our data show that HSCs are required for MDSC accumulation mediated by the COX2-PGE2-EP4 pathway, and these data are the first to link HSC and MDSC subsets in HCC immune microenvironment and provide a rationale for targeting PGE2 signaling for HCC therapy.	Dinoprostone	86-90	fucosyltransferase 1 (H blood group)	Homo sapiens	25-28	
26758420-8	2016	Thus, our data show that HSCs are required for MDSC accumulation mediated by the COX2-PGE2-EP4 pathway, and these data are the first to link HSC and MDSC subsets in HCC immune microenvironment and provide a rationale for targeting PGE2 signaling for HCC therapy.	Dinoprostone	231-235	fucosyltransferase 1 (H blood group)	Homo sapiens	25-28	
23485965-4	2013	Recently, we and others described a positive regulatory role for prostaglandin E2 (PGE2) on HSC function ex vivo.	Dinoprostone	65-81	fucosyltransferase 1 (H blood group)	Homo sapiens	92-95	
23485965-4	2013	Recently, we and others described a positive regulatory role for prostaglandin E2 (PGE2) on HSC function ex vivo.	Dinoprostone	83-87	fucosyltransferase 1 (H blood group)	Homo sapiens	92-95	
23485965-5	2013	Here we show that inhibition of endogenous PGE2 by non-steroidal anti-inflammatory drug (NSAID) treatment in mice results in modest HSC egress from the bone marrow.	Dinoprostone	43-47	fucosyltransferase 1 (H blood group)	Homo sapiens	132-135