ライフサイエンスコーパス: trichostatin

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

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

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

4 5,5-tetramethylimidazoline-1-oxyl-3-oxide or trichostatin A (an HDAC inhibitor) were quantified, ther

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

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

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

8 9 cells are treated with both calcitriol and trichostatin A (histone deacetylase inhibitor), the leve

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

32 Trichostatin A (TSA) induced histone acetylation and gen

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

109 0 mM) compared to the established inhibitors trichostatin A and butyrate, but the genes deregulated o

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

111 Trichostatin A and scriptaid can either enhance fenretin

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

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

114 Trichostatin A and suberoylanilide hydroxamic acid, two

115 Trichostatin A and suberoylanilide hydroxamic acid, two

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

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

118 Trichostatin A and/or 5-azadeoxycytidine treatment reduc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

173 Trichostatin A stimulates the acetylation of RFX protein

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

175 Trichostatin A stimulation of RGS4 promoter activity, ac

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

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

178 Trichostatin A treatment also resulted in cell stiffenin

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

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

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

182 Trichostatin A treatment of quiescently infected neurons

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

184 Interestingly, trichostatin A triggered upregulation of CYGB expression

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

258 Trichostatin A, which improves motor behavior and surviv

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

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

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

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

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

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

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

266 deacetylase activity based on sensitivity to trichostatin A.

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

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

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

270 is affected by histone deacetylase inhibitor trichostatin A.

271 ation with the histone deacetylase inhibitor trichostatin A.

272 h the specific histone deacetylase inhibitor trichostatin A.

273 ne and histone deacetylation inhibiting drug trichostatin A.

274 siRNA and the histone deacetylase inhibitor trichostatin A.

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

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

277 romoter by the histone deacetylase inhibitor trichostatin A.

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

279 inhibiting histone deacetylase activity with Trichostatin A.

280 exerted by the histone deacetylase inhibitor trichostatin A.

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

282 but not by the histone deacetylase inhibitor trichostatin A.

283 bated with the histone deacetylase inhibitor trichostatin A.

284 eversed by the histone deacetylase inhibitor trichostatin A.

285 nsitive to treatment with the HDAC inhibitor trichostatin A.

286 blocked by the histone deacetylase inhibitor trichostatin A.

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

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

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 Trichostatin-A blocked the effects of Gfi1, suggesting t

292 -2 after a combined treatment with 5-aza and trichostatin-A in metastatic prostate cells resulted in

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

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

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

296 hydroxamate-containing HDACi vorinostat and trichostatin-A.

297 Inhibition of HDAC by trichostatin blocked the deacetylation of p53 and its tr

298 In 5-aza-2'-deoxycytosine/trichostatin-treated NCI-H441 cells, overexpression of C

299 The histone deacetylase inhibitors trichostatin (TSA, 1), MS-275 (2) and suberoylanilide hy

300 , suberoylanilide hydroxamic acid (SAHA), or trichostatin with perifosine synergistically induced mit