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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

23 ibition of histone deacetylases (HDACs) with trichostatin A (TSA) disrupted ATRX binding to the centr

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

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

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

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

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

29 tration of the histone deacetylase inhibitor Trichostatin A (TSA) in adult animals.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

85 identify gene targets of the HDAC inhibitor trichostatin A (TSA), we compared the gene expression pr

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

101 nt with low doses of HDAC inhibitors such as trichostatin A (TSA, 15 nM) to induce apoptosis in prost

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

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

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

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

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

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

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

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

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

111 0 mM) compared to the established inhibitors trichostatin A and butyrate, but the genes deregulated o

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

113 Trichostatin A and scriptaid can either enhance fenretin

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

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

116 Trichostatin A and suberoylanilide hydroxamic acid, two

117 Trichostatin A and suberoylanilide hydroxamic acid, two

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

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

120 Trichostatin A and/or 5-azadeoxycytidine treatment reduc

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

176 Trichostatin A stimulates the acetylation of RFX protein

177 Trichostatin A stimulation of RGS4 promoter activity, ac

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

179 Trichostatin A treatment also resulted in cell stiffenin

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

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

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

183 Trichostatin A treatment of quiescently infected neurons

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

185 Interestingly, trichostatin A triggered upregulation of CYGB expression

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

251 AT1 signaling and was abrogated by butyrate, trichostatin A, suberoylanilide hydroxamic acid, and STA

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

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

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

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

256 Trichostatin A, which improves motor behavior and surviv

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

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

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

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

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

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

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

264 deacetylase activity based on sensitivity to trichostatin A.

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

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

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

268 is affected by histone deacetylase inhibitor trichostatin A.

269 ation with the histone deacetylase inhibitor trichostatin A.

270 h the specific histone deacetylase inhibitor trichostatin A.

271 ne and histone deacetylation inhibiting drug trichostatin A.

272 siRNA and the histone deacetylase inhibitor trichostatin A.

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

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

275 romoter by the histone deacetylase inhibitor trichostatin A.

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

277 inhibiting histone deacetylase activity with Trichostatin A.

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

279 transactivating factors VP16 and ICP4 and to trichostatin A.

280 ffect that was blocked by the HDAC inhibitor trichostatin A.

281 exerted by the histone deacetylase inhibitor trichostatin A.

282 with effects elicited by an HDAC 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