PMID-sentid	Pub_year	Sent_text		comp_official_name	comp_offsetprotein_name	organism	prot_offset
26108328-6	2015	RESULTS: The serum levels of IL-4 and IL-8 in the untreated asthma group were higher than in the control, hormone treatment and TSA treatment groups (P<0.05).	trichostatin A	128-131	interleukin 4	Mus musculus	29-33	
26330919-9	2015	TSA suppressed OVA-specific IgE levels and reduced expression of the IL-4 and IL-5.	trichostatin A	0-3	interleukin 4	Mus musculus	69-73	
20728595-8	2010	Furthermore, IL-4 production by CD4+ T cells from the lymph nodes of DNFB-treated NC/Nga mice was significantly inhibited by TSA, although levels of IFN-gamma were not.	trichostatin A	125-128	interleukin 4	Mus musculus	13-17	
25896783-11	2015	IL-4-mediated inhibition of RANKL in macrophages was abolished by TSA.	trichostatin A	66-69	interleukin 4	Mus musculus	0-4	
22865229-3	2012	Trichostatin A (TSA), a pan-inhibitor of histone deacetylases (HDACs), inhibited IL-4-induced arginase-1 expression.	trichostatin A	0-14	interleukin 4	Mus musculus	81-85	
22865229-3	2012	Trichostatin A (TSA), a pan-inhibitor of histone deacetylases (HDACs), inhibited IL-4-induced arginase-1 expression.	trichostatin A	16-19	interleukin 4	Mus musculus	81-85	
21305388-14	2011	T cells from TSA-treated mice produced higher levels of IL-4 than cells from the control group.	trichostatin A	13-16	interleukin 4	Mus musculus	56-60	
21305388-16	2011	In addition, TSA enhanced IL-4 gene expression of in vitro differentiated Th2 cells, and the mechanism is associated with an increased level of histone acetylation in the IL-4 gene promoter.	trichostatin A	13-16	interleukin 4	Mus musculus	26-30	
21305388-16	2011	In addition, TSA enhanced IL-4 gene expression of in vitro differentiated Th2 cells, and the mechanism is associated with an increased level of histone acetylation in the IL-4 gene promoter.	trichostatin A	13-16	interleukin 4	Mus musculus	171-175	
21305388-17	2011	CONCLUSIONS: While TSA selectively suppresses a Th1 response by inducing apoptosis, it upregulates IL-4 expression probably by increasing histone H3 and H4 acetylation of the IL-4 gene promoter.	trichostatin A	19-22	interleukin 4	Mus musculus	99-103	
21305388-17	2011	CONCLUSIONS: While TSA selectively suppresses a Th1 response by inducing apoptosis, it upregulates IL-4 expression probably by increasing histone H3 and H4 acetylation of the IL-4 gene promoter.	trichostatin A	19-22	interleukin 4	Mus musculus	175-179	
20728595-10	2010	These findings suggest that TSA suppresses the development of AD-like dermatitis in DNFB-treated NC/Nga mice by reducing IL-4 production and increasing the T reg cell population.	trichostatin A	28-31	interleukin 4	Mus musculus	121-125	
15649272-11	2005	TSA also reduced infiltration of CD4+ and inflammatory cells and mucus occlusions in lung tissue, and decreased the concentrations of IL-4, IL-5, and IgE in BALF.	trichostatin A	0-3	interleukin 4	Mus musculus	134-138	
15649272-12	2005	CONCLUSION: TSA attenuated the development of allergic airway inflammation by decreasing expression of the Th2 cytokines, IL-4 and IL-5, and IgE, which resulted from reduced T cell infiltration.	trichostatin A	12-15	interleukin 4	Mus musculus	122-126	
8827437-3	1996	Thus, this study was accomplished to examine the involvement of histone hyperacetylation in IL-4-induced class switching promotion by NaBu with a specific histone deacetylase inhibitor, trichostatin A (TSA).	trichostatin A	186-200	interleukin 4	Mus musculus	92-96	
8827437-3	1996	Thus, this study was accomplished to examine the involvement of histone hyperacetylation in IL-4-induced class switching promotion by NaBu with a specific histone deacetylase inhibitor, trichostatin A (TSA).	trichostatin A	202-205	interleukin 4	Mus musculus	92-96	
8827437-4	1996	TSA was found to enhance IL-4-dependent IgE production in a concentration-dependent manner (0.3-30 nM) as did NaBu, although neither compound affected the IgE production in the absence of IL-4.	trichostatin A	0-3	interleukin 4	Mus musculus	25-29	
8827437-7	1996	Furthermore, enhancement of IgE production by TSA or NaBu was confirmed to be absolutely IL-4 dependent and was not due to the shift of kinetics.	trichostatin A	46-49	interleukin 4	Mus musculus	89-93	
7954438-6	1994	Complete tumor regression, however, was obtained in 10-20% of mice treated with TSA cells transduced with IL-2, IL-4, IL-7, or IL-10 and in 30% of those treated with TSA cells transduced with gamma-interferon gene.	trichostatin A	80-83	interleukin 4	Mus musculus	112-116