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