PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26645248-7	2016	RESULTS: TNBS injection significantly upregulated expression of TGF-beta1 in the pancreas and DRGs, and TGF-beta1 receptors in DRGs (T9-T13)in CP rats.	Trinitrobenzenesulfonic Acid	9-13	transforming growth factor, beta 1	Rattus norvegicus	64-73	
26645248-7	2016	RESULTS: TNBS injection significantly upregulated expression of TGF-beta1 in the pancreas and DRGs, and TGF-beta1 receptors in DRGs (T9-T13)in CP rats.	Trinitrobenzenesulfonic Acid	9-13	transforming growth factor, beta 1	Rattus norvegicus	104-113	
26273312-4	2015	Meanwhile, assessments by ELISA revealed an increment in concentrations of IL-2, IL-6, and IL-17 and a reduction in level of TGF-beta after TNBS challenge.	Trinitrobenzenesulfonic Acid	140-144	transforming growth factor, beta 1	Rattus norvegicus	125-133	
25561788-0	2014	2,4,6-trinitrobenzene sulfonic acid-induced chronic colitis with fibrosis and modulation of TGF-beta1 signaling.	Trinitrobenzenesulfonic Acid	0-35	transforming growth factor, beta 1	Rattus norvegicus	92-101	
25561788-11	2014	Colonic production of TGF-beta production tended to be higher in TNBS-treated rats (P < 0.06).	Trinitrobenzenesulfonic Acid	65-69	transforming growth factor, beta 1	Rattus norvegicus	22-30	
22040876-13	2011	The expression levels of mRNA and proteins for TGF-beta1, HSP47, and collagen I were elevated in colonic mucosa treated with TNBS.	Trinitrobenzenesulfonic Acid	125-129	transforming growth factor, beta 1	Rattus norvegicus	47-56	
20363741-9	2010	Transforming growth factor (TGF)-beta1, a known inducer of EMT in epithelial cells, induces EMT in rat intestinal epithelial cells in vitro, and bone morphogenic protein-7, an antagonist of TGF-beta1, inhibits EMT and fibrosis both in vitro and in the TNBS-treated mice.	Trinitrobenzenesulfonic Acid	252-256	transforming growth factor, beta 1	Rattus norvegicus	0-38	
7600140-10	1995	CONCLUSIONS: Direct intramuscular transforming growth factor-beta 1 gene delivery effectively ameliorates trinitrobenzene sulfonic acid-induced colitis, suggesting that gene therapy with immunosuppressive cytokines may be a novel approach for the treatment of inflammatory bowel disease.	Trinitrobenzenesulfonic Acid	106-135	transforming growth factor, beta 1	Rattus norvegicus	34-67