ライフサイエンスコーパス: trichostatin A

1 deacetylase activity based on sensitivity to trichostatin A.

2 by the histone deacetylase (HDAC) inhibitor trichostatin A.

3 enes by E1B is insensitive to HDAC inhibitor trichostatin A.

4 er treatments with 5-aza-2-deoxycytidine and trichostatin A.

5 is affected by histone deacetylase inhibitor trichostatin A.

6 ation with the histone deacetylase inhibitor trichostatin A.

7 h the specific histone deacetylase inhibitor trichostatin A.

8 ne and histone deacetylation inhibiting drug trichostatin A.

9 siRNA and the histone deacetylase inhibitor trichostatin A.

10 TPE in mouse ES cells was not reversed with trichostatin A.

11 ng treatment with 5-aza-2'-deoxycytidine and trichostatin A.

12 romoter by the histone deacetylase inhibitor trichostatin A.

13 ype-specific responses to the HDAC inhibitor trichostatin A.

14 inhibiting histone deacetylase activity with Trichostatin A.

15 Rb-defective cells with the HDAC inhibitor, trichostatin A.

16 exerted by the histone deacetylase inhibitor trichostatin A.

17 with effects elicited by an HDAC inhibitor, trichostatin A.

18 but not by the histone deacetylase inhibitor trichostatin A.

19 bated with the histone deacetylase inhibitor trichostatin A.

20 eversed by the histone deacetylase inhibitor trichostatin A.

21 nsitive to treatment with the HDAC inhibitor trichostatin A.

22 blocked by the histone deacetylase inhibitor trichostatin A.

23 hydroxamate-containing HDACi vorinostat and trichostatin-A.

24 tors and were designed from the structure of trichostatin A (1).

25 Trichostatin A, 3-deaza-adenosine, cycloleucine, and oka

26 ilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulted in a higher degree o

27 cells with Decitabine (a DNMT inhibitor) or trichostatin A (a histone deacetylase inhibitor) up-regu

28 In the presence of trichostatin A, a deacetylase inhibitor, DEX-mediated in

29 tment with the histone deacetylase inhibitor trichostatin A, a drug known to benefit phenotypes of SM

30 In Tribolium castaneum TcA cells, Trichostatin A, a histone deacetylase (HDAC) inhibitor,

31 approximately 50% in Cpt2M(-/-) hearts, but trichostatin A, a histone deacetylase inhibitor that imp

32 discovered that MCF7/AdrR cells treated with trichostatin A, a histone deacetylase inhibitor, exhibit

33 AZA), a DNA methyltransferase inhibitor, and trichostatin A, a histone deacetylase inhibitor, led to

34 posed monolayer or organotypic cultures with trichostatin A, a histone deacetylase inhibitor, partial

35 Trichostatin A, a pan inhibitor, and mocetinostat (MGCD0

36 sm of S6 kinase deacetylation, we found that trichostatin A, a pan-histone deacetylase (HDAC) inhibit

37 Pretreatment with trichostatin A, a pan-histone deacetylase inhibitor that

38 anied by histone acetylation and mimicked by trichostatin A, a pan-histone deacetylase inhibitor.

39 rug that reduces p53 sumoylation, as well as trichostatin A, a potential inducer of p53 sumoylation b

40 We also show that trichostatin-A, a class I and II HDAC inhibitor, increas

41 ezomib and the histone deacetylase inhibitor trichostatin A abolished HDAC6 activity and decreased au

42 he class I-IIa histone deacetylase inhibitor trichostatin A accelerated tissue regeneration.

43 eacetylase inhibitors (HDA-CIs) butyrate and trichostatin A activate gamma-globin expression via a p3

44 Maintenance of MT acetylation through trichostatin A administration or MAP1B overexpression mi

45 ivity, and the histone deacetylase inhibitor trichostatin A also increased promoter activity.

46 hibitors (phenylbutyrate, sodium butyrate or trichostatin A) also caused synergistic neuroprotection

47 5,5-tetramethylimidazoline-1-oxyl-3-oxide or trichostatin A (an HDAC inhibitor) were quantified, ther

48 roduced by the histone deacetylase inhibitor trichostatin A, an effect that in turn was abolished by

49 Furthermore, trichostatin A, an HDAC inhibitor, can reduce inflammati

50 First we show that trichostatin A, an HDAC inhibitor, enhances Tax expressi

51 Finally, trichostatin A, an HDAC inhibitor, prevents IFNgamma inh

52 Treatment of mitotic cells with Trichostatin A, an HDAC inhibitor, resulted in similar s

53 onsive to induction of NF-kappaB activity by trichostatin A, an HDAC inhibitor, suggesting that c-Abl

54 ss TrkA expression, which can be relieved by trichostatin A, an HDAC inhibitor.

55 Moreover, trichostatin A, an inhibitor of histone deacetylase acti

56 histone H3 tails, and are readily killed by trichostatin A, an inhibitor of histone deacetylases.

57 rthermore, the histone deacetylase inhibitor trichostatin A, an inhibitor of NRSF silencing activity,

58 eport the structures of HDAC8 complexes with trichostatin A and 3-(1-methyl-4-phenylacetyl-1H-2-pyrro

59 Following treatment with trichostatin A and 5-aza-dC, the formerly unresponsive E

60 sensitive to histone deacetylase inhibition/trichostatin A and associated with a decrease in H3/H4 h

61 s treated with histone deacetylase inhibitor trichostatin A and BMP2+IBMX display increased endogenou

62 0 mM) compared to the established inhibitors trichostatin A and butyrate, but the genes deregulated o

63 Our results demonstrate that trichostatin A and MGCD0103 enhanced Npr1 gene expressio

64 Trichostatin A and scriptaid can either enhance fenretin

65 the histone deacetylase inhibitors (HDACIs) trichostatin A and sodium butyrate (SB) ameliorate mitoc

66 en previously reported that HDAC inhibitors, trichostatin A and sodium butyrate, suppress osteoclast

67 Trichostatin A and suberoylanilide hydroxamic acid, two

68 Trichostatin A and suberoylanilide hydroxamic acid, two

69 dings that the histone deacetylase inhibitor trichostatin A and the methyltransferase inhibitor 5'-de

70 BCL-3-mediated repression was reversed by trichostatin A and was enhanced by overexpression of HDA

71 Trichostatin A and/or 5-azadeoxycytidine treatment reduc

72 deacetylase inhibitors (HDACi) (butyrate or trichostatin A) and 1,25D3 increased cathelicidin and CD

73 reliminary studies using ChIP-chip analysis, Trichostatin A, and 5-aza-2'-deoxycytidine further suppo

74 tumor drugs, including geldanamycin, PS-341, Trichostatin A, and doxorubicine.

75 a cells treated with the HbF inducers hemin, trichostatin A, and sodium butyrate had significantly re

76 stone deacetylase (HDAC) activity, butyrate, trichostatin A, and suberoylanilide hydroxamic acid, pre

77 lase inhibitors, 4-phenylbutyrate (4PBA) and trichostatin A, and two small molecules without direct h

78 Inhibition of HDAC activity with trichostatin A blocked deacetylation and methylation of

79 Trichostatin-A blocked the effects of Gfi1, suggesting t

80 Treatment with the HDAC inhibitor trichostatin A blocks attenuation of IL-8 transcription.

81 histone deacetylase (HDAC) enzyme inhibitor trichostatin A blocks the ability of lipopolysaccharide

82 mide or histone deacetylase (HDAC) inhibitor trichostatin A but inhibited by expressing exogenous dea

83 Treatment with trichostatin A, but not other histone deacetylase inhibi

84 The histone deacetylase inhibitor trichostatin A, but not the DNA methylation inhibitor 5'

85 ment with the histone deacetylase inhibitor, trichostatin A, but not with the DNA demethylation agent

86 the histone/protein deacetylation inhibitor trichostatin A can block this conversion suggest that an

87 sfected cells with the deacetylase inhibitor trichostatin A caused a partial relief of repression.

88 hat the histone deacetylase (HDAC) inhibitor trichostatin A caused a reduction in DNA methylation, su

89 with 5-azadeoxycytidine in combination with Trichostatin A caused chromatin remodeling of both promo

90 ibitors, including sodium butyrate (NaB) and trichostatin A, caused the rapid dissociation of LANA fr

91 deacetylase inhibitors such as FR901228 and trichostatin A completely depleted mutant p53 in cancer

92 When administered together, wortmannin and trichostatin A completely negated the inhibitory effect

93 ultrahigh-resolution structure of the HDAC6-trichostatin A complex, which reveals two Zn(2+)-binding

94 histone deacetylase inhibitors butyrate and trichostatin A could block Cox-2 activation in a gene-sp

95 Vorinostat or trichostatin A decreased MYC mRNA and protein as well as

96 at CG-1521 induces p21 transcription whereas trichostatin A does not alter the steady state level of

97 Furthermore, we show that the HDAC inhibitor trichostatin A does not globally alter gene expression b

98 inhibition of histone deacetylases (HDAC) by trichostatin A dramatically enhanced induction of HBD2 e

99 e, but not the histone deacetylase inhibitor trichostatin A, drastically stimulated the expression of

100 tment with the histone deacetylase inhibitor trichostatin A elevated G1 and G2/M activity to that of

101 oxycinnamic acid bis-hydroxamide, MS-275 and trichostatin A) enhance the apoptosis-inducing potential

102 omeres, and a class I and II HDAC inhibitor, trichostatin A, enhances contractile activity of myofila

103 es and that a class I and II HDAC inhibitor, trichostatin A, enhances contractile activity of myofila

104 ith the histone deacetylase (HDAC) inhibitor trichostatin A fails to induce Rac2 gene expression.

105 ated with the histone deacetylase inhibitor, Trichostatin A, genes nearby this latter class of enhanc

106 Notably, the HDAC inhibitor trichostatin A had no effect on MeCP2-mediated repressio

107 xycytidine and histone deacetylase inhibitor trichostatin A (herein referred to as Aza+TSA) after end

108 eoxycytosine, a DNA demethylation agent, and trichostatin, a histone deacetylation inhibitor.

109 A methyltransferase inhibitor) compared with trichostatin A (histone deacetylase inhibitor) and retin

110 promoter region and can be re-activated with Trichostatin A (histone deacetylase inhibitor) and/or 5-

111 9 cells are treated with both calcitriol and trichostatin A (histone deacetylase inhibitor), the leve

112 acytidine (DNA hypomethylating agent) and/or trichostatin A (histone deacetylase inhibitor).

113 m of IkappaBalpha, as well as treatment with trichostatin A, implicating a role for the NF-kappaB pat

114 tment with the histone deacetylase inhibitor trichostatin A in a dose-dependent manner, and deletion

115 Treatment with Trichostatin A in cell lines having low LINC00152 expres

116 t iTreg induction by a deacetylase inhibitor trichostatin A in vivo, although the loss of the Smad2 o

117 -2 after a combined treatment with 5-aza and trichostatin-A in metastatic prostate cells resulted in

118 cells to the histone deacetylase inhibitor, trichostatin A, in C42B, HCT116 and HL-60 cells.

119 by the HDAC inhibitors, sodium butyrate and trichostatin A, in HH-B2 primary effusion lymphoma cells

120 After treatment with trichostatin A, in1814 and 17+ reactivated efficiently,

121 The histone deacetylase inhibitor trichostatin A increased global histone acetylation and

122 sing 5-aza-2'-deoxycytidine (decitabine) and trichostatin A increased H3K4me3 and maintained H3K27me3

123 f histone deacetylase (HDAC) signalling with trichostatin A increased nuclear MLP following passive s

124 Treatment with trichostatin A increased PRR5 mRNA levels in BT549 and M

125 HDACi using trichostatin A increased the number of Tregs and boosted

126 ervation that histone deacetylase inhibitor, trichostatin A, increased the level of caspase-3 mRNA in

127 as the histone deacetylase (HDAC) inhibitor trichostatin A increases both CREB binding to the promot

128 tored by the protein deacetylation inhibitor trichostatin A, indicating a complex dynamic aspect of T

129 by the histone deacetylase (HDAC) inhibitor trichostatin A, indicating that ceramide promotes tubuli

130 at the repression of HDAC7 is insensitive to trichostatin A, indicating that HDAC7 represses Mitf at

131 diminished in the presence of the inhibitor trichostatin A, indicating the requirement of histone de

132 idine and/or histone deacetylation inhibitor trichostatin A induced gene reexpression in thyroid cell

133 tion and DNA methylation following transient trichostatin A-induced histone hyperacetylation in Stat4

134 Here we report that treatment with trichostatin A induces histone acetylation and is suffic

135 The general HDAC inhibitor, trichostatin A, inhibited the SLUG-mediated regulation o

136 te that gamma-gene induction by butyrate and trichostatin A involves ATF-2 and CREB1 activation via p

137 ] and histone deacetylase (HDAC) inhibitors (trichostatin A) leads to expression of ER mRNA and funct

138 ibition, especially with sodium butyrate and trichostatin A, led to increased TRAIL-R2 gene transcrip

139 creatine, beta-hydroxy-beta-methylbutyrate, trichostatin A, lisinopril, and 6 from the glucocorticoi

140 d in the tissue specificity of SCA7 and that trichostatin A may ameliorate deleterious effects of the

141 tates with the histone deacetylase inhibitor Trichostatin A, Nkx3.1 can bind to and reactivate the ex

142 reated with a histone deacetylase inhibitor, Trichostatin A, no significant changes in APC expression

143 y to determine the influence of butyrate and trichostatin A on polymerase distribution on the Cox-2 g

144 blocked by the histone deacetylase inhibitor trichostatin A, opening new therapeutic opportunities.

145 Furthermore, chromatin modulation with trichostatin A or 5-aza-2'-deoxycytidine elevates USP9X

146 The suppression of NRSF activity with either trichostatin A or a dominant-negative NRSF induced MOR p

147 On treatment with trichostatin A or SAHA, H1299 cells carrying p21-3H show

148 he use of the histone deacetylase inhibitors trichostatin A or sodium butyrate enhanced induction of

149 in apoptotic resistance to HDAC inhibitors (trichostatin A or suberoylanilide hydroxamic acid), desp

150 mented by the histone deacetylase inhibitors trichostatin A or suberoylanilide hydroxamic acid.

151 Incubation of HCC cells with trichostatin A or transfection with miR-449 reduced expr

152 These cells were treated with trichostatin A or vorinostat (suberoylanilide hydroxamic

153 tylase (HDAC) inhibitors, sodium butyrate or trichostatin A, or a DNA methyltransferase inhibitor, 5-

154 tion because both 5-aza-2'-deoxycytidine and trichostatin A partially rescued transgene silencing in

155 ment with the histone deacetylase inhibitor, trichostatin A, plus nutritional support extended median

156 of HDAC2 by siRNA or inhibition of HDAC with trichostatin A prevented a H2O2-induced decrease in TRPC

157 of histone deacetylase (HDAC) activity with trichostatin A promotes binding of RNA polymerase II to

158 demethylation by 5-aza-2'-deoxycytidine and trichostatin A reactivated TIMP-2 and restored its expre

159 A specific histone deacetylase inhibitor, trichostatin A, relieved Tal1/SCL-mediated repression by

160 The histone deacetylase inhibitor, trichostatin A, repressed bcl-2 transcription and decrea

161 e deacetylase inhibitors sodium butyrate and trichostatin A require a relatively long period of expos

162 ent with epigenetic compounds decitabine and trichostatin A rescued the BPA effects as did knockdown

163 alcohol withdrawal with the HDAC inhibitor, trichostatin A, rescued the deficits in H3 and H4 acetyl

164 stration of a histone deacetylase inhibitor, trichostatin A, rescued the reduction of acetylated hist

165 a subset of AR phosphorylation sites reduced trichostatin A responsiveness and trans-activation by hi

166 mbryos with a histone deacetylase inhibitor, Trichostatin A, restores scl and gata1 expression, and a

167 lines with the histone deacetylase inhibitor trichostatin A resulted in significant induction of CST6

168 tidine and the histone deacetylase inhibitor trichostatin A resulted in significant synergistic induc

169 ned treatment with 5-aza-2'-deoxycytidie and trichostatin A resulted in synergistic induction of masp

170 hosphate) or decrease chromosome compaction (trichostatin A) results in a parallel increase or decrea

171 and experiments utilizing the HDAC inhibitor trichostatin A revealed that LRF-mediated repression req

172 Transcriptional repression by RFP was trichostatin A sensitive and did not involve an Id-like

173 In this study, we identified a trichostatin A-sensitive autonomous repression domain in

174 The repressive activity requires a trichostatin A-sensitive histone deacetylase (HDAC) acti

175 BCL11B complexes from T lymphocytes possess trichostatin A-sensitive histone deacetylase activity, c

176 ng of c-kit(+) CSCs via HDAC inhibition with trichostatin A significantly increased c-kit(+) CSC-deri

177 e results, the histone deacetylase inhibitor trichostatin A stimulated the expression of Sox9-regulat

178 Trichostatin A stimulates the acetylation of RFX protein

179 uction of alpha-tubulin K40 acetylation upon Trichostatin A stimulation of ONS cells.

180 Trichostatin A stimulation of RGS4 promoter activity, ac

181 rally unrelated inhibitors of HDAC activity, trichostatin A, suberoylanilide hydroxamic acid, and api

182 prostate cancer cells with HDAC inhibitors (trichostatin A, suberoylanilide hydroxamic acid, MS-275,

183 s represses transcription in the presence of trichostatin A, suggesting that it functions by a histon

184 nhibition of histone deacetylase activity by trichostatin A suppressed AFP effects on a small fractio

185 Trichostatin A (TA), an inhibitor of histone deacetylase

186 Unexpectedly, we found trichostatin A to be a mutagen that caused DNA damage an

187 expression analysis of Hdac1 knockout ES and trichostatin A-treated ES and TS cells, we found that HD

188 Trichostatin A treatment also resulted in cell stiffenin

189 ation induced by 5-aza-2'-deoxycytidine plus trichostatin A treatment and the DNA methylation levels

190 ed repression of MOR promoter activity after trichostatin A treatment in neuroblastoma NMB cells.

191 nd delocalization of replication initiation, trichostatin A treatment of cells led to a parallel qual

192 Trichostatin A treatment of quiescently infected neurons

193 s up-regulated by 5-aza-2'-deoxycytidine and trichostatin A treatment.

194 n of BNIP3 was restored in 4/6 cell lines by trichostatin-A treatment alone.

195 Histone deacetylation inhibition by Trichostatin-A treatment restored E-cadherin expression.

196 (HDAC) inhibitors 4-phenylbutanoic acid and trichostatin A; treatment with these HDAC inhibitors als

197 Interestingly, trichostatin A triggered upregulation of CYGB expression

198 nsitive to the histone deacetylase inhibitor trichostatin A (TSA(S)) accounts for approximately 70%.

199 The HDAC inhibitor trichostatin A (TSA) acts on the gene 50 promoter to ind

200 hat the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) acts synergistically with the DNA m

201 nt evidence that deacetylase inhibition with trichostatin A (TSA) affects the normal epidermal tissue

202 HDAC inhibitor trichostatin A (TSA) also significantly increased P-Rex1

203 ssion on melanoma cells after treatment with trichostatin A (TSA) and 5-Aza-2-deoxycytidine (5-Aza).

204 Activity of HDAC6 was suppressed by trichostatin A (TSA) and by siRNA specific to HDAC6.

205 Of four HDAC inhibitors examined, trichostatin A (TSA) and HDAC42 exhibit the highest acti

206 Deacetylase inhibitors trichostatin A (TSA) and nicotinamide (NIA) increase Dro

207 two structurally different HDAC inhibitors, trichostatin A (TSA) and sodium butyrate (NaB), on the c

208 ion by histone deacetylase (HDAC) inhibitors trichostatin A (TSA) and sodium butyrate was observed in

209 Transcriptional activators such as trichostatin A (TSA) and tumor necrosis factor alpha (TN

210 ith the nonisoform selective HDAC inhibitors trichostatin A (TSA) and vorinostat (suberoylanilide hyd

211 e of histone deacetylase-like protein (HDLP)-trichostatin A (TSA) complexes.

212 rmore, inhibition of histone deacetylases by trichostatin A (TSA) enhances the expression of CYP24A1

213 The HDAC inhibitor trichostatin A (TSA) evoked robust but significantly low

214 e deacetylase inhibitors sodium butyrate and trichostatin A (TSA) facilitated partner preference form

215 ncubated with the HDACi SAHA (vorinostat) or trichostatin A (TSA) for 2 h, the hyposensitivity of pDA

216 of the histone deacetylase (HDAC) inhibitor trichostatin A (TSA) in a retinal ischemic model.

217 Blocking HDAC activity with trichostatin A (TSA) in cultured male gametophytes of Br

218 Single intraperitoneal doses of 10 mg/kg trichostatin A (TSA) in nontransgenic and SMA model mice

219 Trichostatin A (TSA) induced histone acetylation and gen

220 cycle gene expression in 75% of cells, while trichostatin A (TSA) induced less widespread lytic gene

221 tment with the histone deacetylase inhibitor trichostatin A (TSA) induces GFP activation in GFP(-) ce

222 The histone deacetylase inhibitor trichostatin A (TSA) inhibited EMT; this was reflected b

223 bitors sodium butyrate (NaB) systemically or trichostatin A (TSA) intrahippocampally prior to a brief

224 tration of the histone deacetylase inhibitor Trichostatin A (TSA) on cue versus place learning strate

225 of microRNA-1296 (miR-1296), genistein, and trichostatin A (TSA) on the MCM complex.

226 Blocking histone deacetylation with trichostatin A (TSA) or blocking cytosine methylation us

227 of histone deacetylase (HDAC) activity with trichostatin A (TSA) or valproic acid (VPA) at concentra

228 Treatment with the HDAC inhibitor trichostatin A (TSA) prevented the pressure-overload-sti

229 residues at the AR acetylation site reduced trichostatin A (TSA) responsiveness and ligand-induced p

230 microtubules, and the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.

231 zomib with the histone deacetylase inhibitor trichostatin A (TSA) resulted in a synergistic increase

232 ibition of histone deacetylases (HDACs) with trichostatin A (TSA) revealed that HDACs are essential f

233 Treatment of HeLa cells with trichostatin A (TSA) reversibly increased the acetylatio

234 tudy that the histone deacetylase inhibitor, trichostatin A (TSA) stimulated 3' enhancer activity thr

235 , we found that denervation was amendable by trichostatin A (TSA) treatment, which increased innervat

236 with either 5-Aza-2-deoxycytidine (5-Aza) or trichostatin A (TSA) was used to induce demethylation or

237 We investigated whether trichostatin A (TSA) would alter the expression of NAG-1

238 namide (NAM), a Sir2 inhibitor, or 50 nmol/L Trichostatin A (TSA), a class I and II HDAC inhibitor.

239 e same coat components in cells treated with trichostatin A (TSA), a deacetylase inhibitor that leads

240 e, isobutylmethylxanthine (IDX), or IDX plus trichostatin A (TsA), a histone deacetylase inhibitor an

241 or Bloom's syndrome, Blm) for sensitivity to trichostatin A (TSA), a histone deacetylase inhibitor th

242 Trichostatin A (TSA), a histone deacetylase inhibitor, e

243 Trichostatin A (TSA), a histone deacetylase inhibitor, h

244 Treatment of the cells with trichostatin A (TSA), a histone deacetylase inhibitor, i

245 tient-derived primary glioma cell lines with trichostatin A (TSA), a histone deacetylase inhibitor, o

246 n D1 promoter was reversed by treatment with trichostatin A (TSA), a histone deacetylase inhibitor, o

247 We identified trichostatin A (TSA), a pan-HDAC (histone deacetylase) i

248 sion in HepG2 and F9 cell lines treated with Trichostatin A (TSA), a potent histone deacetylase inhib

249 nalysis revealed that the effects of VPA and trichostatin A (TSA), a structurally unrelated HDAC inhi

250 Addition of trichostatin A (TSA), an HDAC6 inhibitor, induced microt

251 port, we demonstrated the mechanism by which trichostatin A (TSA), an inhibitor of HDAC, induces the

252 nt p53-mediated repression was attenuated by trichostatin A (TSA), an inhibitor of histone deacetylas

253 (HDAC) inhibitors, sodium butyrate (NaB) and trichostatin A (TSA), and the DNA methyltransferase inhi

254 fects of three HDACi, sodium butyrate (NaB), trichostatin A (TSA), and valproic acid (VPA).

255 The prototypical HDAC inhibitor (HDACi), trichostatin A (TSA), attenuated both load- and agonist-

256 ng agents 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA), but not treatment with small molec

257 tone deacetylase inhibitors (HDACi), such as trichostatin A (TSA), can regulate gene expression by pr

258 Evaluation of the top scoring hit, Trichostatin A (TSA), demonstrated utrophin upregulation

259 sted a histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), for efficacy in reducing endotheli

260 e inhibitor of histone deacetylases (HDACs), trichostatin A (TSA), in that the three agents enhanced

261 a), tetradecanoyl phorbol acetate (TPA), and trichostatin A (TSA), in U1 monocytic and J-Lat 10.6 lym

262 ated that the histone deacetylase inhibitor, trichostatin A (TSA), induces derepression of the human

263 s of a histone deacetylase (HDAC) inhibitor, trichostatin A (TSA), on neuronal mu-opioid receptor (MO

264 llowed by the histone deacetylase inhibitor, trichostatin A (TSA), on the behavior of IM CD34(+) cell

265 al ganglion cell line RGC-5 was treated with trichostatin A (TSA), other HDAC inhibitors, and stauros

266 acetylase inhibitors valproic acid (VPA) and trichostatin A (TSA), recapitulating the SDL interaction

267 mice with the histone deacetylase inhibitor, trichostatin A (TSA), resulted in a further extension of

268 ion by histone deacetylase (HDAC) inhibitors trichostatin A (TSA), sodium butyrate, and scriptaid was

269 For the binding of trichostatin A (TSA), suberoylanilide hydroxamic acid (S

270 CP0 and an inhibitor of histone deacetylase, trichostatin A (TSA), to activate GFP expression from no

271 this study, we show that sodium butyrate and Trichostatin A (TSA), two structurally different and wid

272 at the histone deacetylase (HDAC) inhibitors trichostatin A (TSA), valproic acid (VPA), and FK228 pot

273 egy using 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA), which expands transplantable HSC 7

274 In this paper, we describe that trichostatin A (TSA), which inhibits deacetylase activit

275 nhibited the LHR basal promoter activity and trichostatin A (TSA)-induced gene transcriptional activa

276 or with the histone deacetylase 6 inhibitor trichostatin A (TSA).

277 modifiers 5-aza-2'-deoxycytidine (5-aza) and trichostatin A (TSA).

278 g agents, 5-aza-2'-deoxycytidine (5azaD) and trichostatin A (TSA).

279 HDAC inhibitors sodium 4-phenylbutyrate and trichostatin A (TSA).

280 versed by the addition of the HDAC inhibitor trichostatin A (TSA).

281 tone deacetylase (HDAC) class I/II inhibitor trichostatin A (TSA).

282 th the histone deacetylase (HDAC) inhibitor--trichostatin A (TSA).

283 to the histone deacetylase (HDAC) inhibitor, trichostatin A (TSA).

284 rofile of 19i in comparison to vorinostat or trichostatin A (TSA).

285 s the in vivo activity of the HDAC inhibitor trichostatin A (TSA).

286 by inhibition of histone deacetylation with trichostatin A (TSA).

287 interrogated using the global HDAC inhibitor trichostatin A (TSA).

288 The HDAC inhibitor, trichostatin A (TSA, 0.1 mg/kg), was intraperitoneally i

289 ith RA and the histone deacetylase inhibitor trichostatin-A (TSA) completely relieved p53-NRD-mediate

290 Trichostatin-A (TSA; 3.31 muM) was used to induce cell d

291 We found that HDAC inhibition with trichostatin A was associated with a decreased presentat

292 ed intact neuromuscular junctions long after trichostatin A was discontinued.

293 ibition of histone deacetylase activity with trichostatin A was unable to complement the defect of IC

294 Using the HDAC inhibitor trichostatin A, we demonstrate that ISRE, IFNA, and IL6

295 and a histone deacetylase (HDAC) inhibitor, trichostatin A, we found that in the context of specific

296 Values of K(i) for the inhibitor trichostatin A were determined for each isozyme.

297 suberoylanilide hydroxamic acid, MS-275, and trichostatin A) were studied in two PEL B cell lines (BC

298 Trichostatin A, which improves motor behavior and surviv

299 Treatment of KFs with trichostatin A, which increased the acetylation level of

300 e action of two HDAC inhibitors, CG-1521 and trichostatin A, which stabilize Ac-Lys-373 p53 and Ac-Ly