PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
14724828-8	2003	RESULTS: Colons of TNBS-treated mice contained acute and chronic inflammatory infiltrates, increased collagen, fibrogenic tissue architecture, and increased expression of TNF-alpha, TGF-beta 1, IGF-1, Col1a2, MMP-1, and TIMP-1.	Trinitrobenzenesulfonic Acid	19-23	insulin-like growth factor 1	Mus musculus	194-199	
20889569-3	2010	We found increased mRNA expression levels of collagen, vimentin, and the fibrogenic factors transforming growth factor beta1 and insulin-like growth factor 1 in the chronically inflamed colons of WT mice treated with repeated intracolonic TNBS administrations.	Trinitrobenzenesulfonic Acid	239-243	insulin-like growth factor 1	Mus musculus	73-157	
20722057-2	2011	Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis.	Trinitrobenzenesulfonic Acid	154-183	insulin-like growth factor 1	Mus musculus	0-28	
20722057-2	2011	Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis.	Trinitrobenzenesulfonic Acid	154-183	insulin-like growth factor 1	Mus musculus	30-35	
20722057-2	2011	Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis.	Trinitrobenzenesulfonic Acid	185-189	insulin-like growth factor 1	Mus musculus	0-28	
20722057-2	2011	Insulin-like growth factor-I (IGF-I) expression is increased in smooth muscle cells of the muscularis propria in CD and in animal models of CD, including trinitrobenzene sulfonic acid (TNBS)-induced colitis.	Trinitrobenzenesulfonic Acid	185-189	insulin-like growth factor 1	Mus musculus	30-35	
20546811-9	2010	These data suggest that TNBS-induced colitis is independent of a change in muscle protein synthesis but dependent on stimulation of protein degradation via increased expression of muscle-specific atrogenes, which may be mediated in part by the reduction in circulating concentration of IGF-I and the concomitant increase in inflammatory mediators observed in the blood and muscle per se.	Trinitrobenzenesulfonic Acid	24-28	insulin-like growth factor 1	Mus musculus	286-291