PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
21424108-8	2011	After administrations of TNBS, vaccinated mice had significantly less body weight loss and a significant decrease of inflammatory scores, collagen deposition and expression of p40, IL-12, IL-23, IL-17, TNF, iNOS and Bcl-2 in colon tissues, compared with carrier and saline groups.	Trinitrobenzenesulfonic Acid	25-29	nitric oxide synthase 2, inducible	Mus musculus	207-211	
27754929-5	2017	TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively).	Trinitrobenzenesulfonic Acid	0-4	nitric oxide synthase 2, inducible	Mus musculus	150-181	
27754929-5	2017	TNBS-induced upregulation of inflammatory cytokines (tumor necrosis factor (TNF)-alpha and interleukin (IL)-1beta), chemokines (CXCL1 and CXLC2), and inducible nitric oxide synthase (iNOS) was also significantly less in NOX1KO than in WT mice (the inhibitions were 100.8%, 89.0%, 63.5%, 96.7%, and 97.1%, respectively).	Trinitrobenzenesulfonic Acid	0-4	nitric oxide synthase 2, inducible	Mus musculus	183-187	
25213465-8	2014	Ursolic acid also suppressed TNBS-induced COX-2 and iNOS expression as well as NF-kappaB activation in colon tissues.	Trinitrobenzenesulfonic Acid	29-33	nitric oxide synthase 2, inducible	Mus musculus	52-56	
24944202-5	2014	TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity.	Trinitrobenzenesulfonic Acid	0-4	nitric oxide synthase 2, inducible	Mus musculus	67-98	
24944202-5	2014	TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity.	Trinitrobenzenesulfonic Acid	0-4	nitric oxide synthase 2, inducible	Mus musculus	100-104	
24944202-5	2014	TNBS treatment in vivo and IL-1beta and TNF-alpha in vitro induced inducible nitric oxide synthase (iNOS) expression, stimulated ERK1/2 activity, caused iNOS-mediated S-nitrosylation and inhibition of AC5/6, and induced phosphorylation of PDE4D5 and stimulated its activity.	Trinitrobenzenesulfonic Acid	0-4	nitric oxide synthase 2, inducible	Mus musculus	153-157	
21600888-4	2011	Both ginsenoside Rb1 and compound K blocked the TNBS-induced expressions of COX-2 and iNOS and the activation of NF-kappaB in mice.	Trinitrobenzenesulfonic Acid	48-52	nitric oxide synthase 2, inducible	Mus musculus	86-90	
25562655-8	2015	In a mouse model, the stereotypic loss of myenteric neurons by Day 4 post-TNBS was abrogated by the selective iNOS inhibitors L-NIL or 1400W without effect on other parameters of intestinal inflammation.	Trinitrobenzenesulfonic Acid	74-78	nitric oxide synthase 2, inducible	Mus musculus	110-114	
24972244-11	2014	Mangiferin suppressed TNBS-induced up-regulation of cyclooxygenase-2 and inducible NO synthase.	Trinitrobenzenesulfonic Acid	22-26	nitric oxide synthase 2, inducible	Mus musculus	73-94	
15857607-6	2005	Colonic nitrite and nitrate levels and protein expression of inducible nitric oxide synthase (iNOS) were also lower in the treated groups in comparison to the TNBS control.	Trinitrobenzenesulfonic Acid	159-163	nitric oxide synthase 2, inducible	Mus musculus	61-92	
19238344-5	2009	The upregulation of WISP-1 was positively correlated with iNOS expression in two models of colitis, induced by intrarectal trinitrobenzenesulfonic acid (TNBS) or occurring spontaneously in IL-10 deficient mice.	Trinitrobenzenesulfonic Acid	123-151	nitric oxide synthase 2, inducible	Mus musculus	58-62	
19238344-5	2009	The upregulation of WISP-1 was positively correlated with iNOS expression in two models of colitis, induced by intrarectal trinitrobenzenesulfonic acid (TNBS) or occurring spontaneously in IL-10 deficient mice.	Trinitrobenzenesulfonic Acid	153-157	nitric oxide synthase 2, inducible	Mus musculus	58-62	
19238344-6	2009	Loss of iNOS, studied using iNOS(-/-) mice in both TNBS-induced and IL-10(-/-) colitis models, significantly attenuated the colitis-related WISP-1 increase.	Trinitrobenzenesulfonic Acid	51-55	nitric oxide synthase 2, inducible	Mus musculus	8-12	
10403731-3	1999	METHODS: Trinitrobenzene sulphonic acid (TNBS) was instilled per rectum to induce a lethal colitis in iNOS deficient mice and in wild type controls.	Trinitrobenzenesulfonic Acid	41-45	nitric oxide synthase 2, inducible	Mus musculus	102-106	
10562585-9	1999	A four- to fivefold increase in iNOS mRNA was observed in wild type mice at 72 hours and seven days post-TNBS and was absent in iNOS deficient mice.	Trinitrobenzenesulfonic Acid	105-109	nitric oxide synthase 2, inducible	Mus musculus	32-36	
10403731-6	1999	Genetic ablation of iNOS gene conferred to mice a significant resistance to TNBS induced lethality and colonic damage, and notably reduced nitrotyrosine formation and concentrations of malondialdehyde; it did not, however, affect neutrophil infiltration and intestinal ICAM-1 expression in the injured tissue.	Trinitrobenzenesulfonic Acid	76-80	nitric oxide synthase 2, inducible	Mus musculus	20-24