ライフサイエンスコーパス: histone deacetylase inhibitor

1 howcased by the formal synthesis of a potent histone deacetylase inhibitor.

2 tructurally unique, potent class 1 selective histone deacetylase inhibitor.

3 ght potentially benefit from the use of this histone deacetylase inhibitor.

4 rtezomib, lenalidomide dexamethasone, or pan-histone deacetylase inhibitor.

5 disruption of the human Sin3 network with a histone deacetylase inhibitor.

6 th suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor.

7 Panobinostat (pano) is an FDA-approved histone deacetylase inhibitor.

8 ated transcription factor regulators such as histone deacetylase inhibitors.

9 ensitivity to epigenetic modulators, such as histone deacetylase inhibitors.

10 ions had the highest level of sensitivity to histone deacetylase inhibitors.

11 fied these seleno-alpha-keto acids as potent histone deacetylase inhibitors.

12 hydroxamates (2) and 2-aminoanilides (3) as histone deacetylase inhibitors.

13 otypes can be partially rescued with certain histone deacetylase inhibitors.

14 agents, including ultraviolet radiation and histone deacetylase inhibitors.

15 d increased sensitivity of leukemia cells to histone deacetylase inhibitors.

16 sor effects are globally similar to those of histone deacetylase inhibitors.

17 gene expression alone or in combination with histone deacetylase inhibitors.

18 ndoles has been identified as a new class of histone deacetylase inhibitors.

19 ween the multikinase inhibitor sorafenib and histone deacetylase inhibitors.

20 -1beta in the absence or presence of various histone deacetylase inhibitors.

21 that RAE-1 is transcriptionally repressed by histone deacetylase inhibitor 3 (HDAC3) in healthy cells

22 These molecules include histone deacetylase inhibitors, 4-phenylbutyrate (4PBA)

23 Indeed, treatment with novel histone deacetylase inhibitors abolished hypoxia-induced

24 SAMHD1-dependent antiretroviral activity of histone deacetylase inhibitors acting via p53 activation

25 in A, and two small molecules without direct histone deacetylase inhibitor activity, hydroxyurea (HU)

26 ed to virus production by a combination of a histone deacetylase inhibitor and a protein kinase C act

27 rst US Food and Drug Administration-approved histone deacetylase inhibitor and is indicated for the t

28 nt epigenetic modulators and identified four histone deacetylase inhibitors and a bromodomain and ext

29 We further observed strong synergy between histone deacetylase inhibitors and EZH2 inhibitors.

30 menable to pharmacological intervention with histone deacetylase inhibitors and help to explain the b

31 , combinations of proteasome inhibitors with histone deacetylase inhibitors and ixabepilone and MK177

32 azole and its analogues are isoform-targeted histone deacetylase inhibitors and potent LRAs.

33 erferon alpha, extracorporeal photopheresis, histone deacetylase inhibitors, and antibody therapies s

34 poptotic triggers, including glucocorticoid, histone deacetylase inhibitors, and overexpression of th

35 at suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for cancer treatm

36 Romidepsin is a histone deacetylase inhibitor approved for the treatment

37 Histone deacetylase inhibitors are currently approved to

38 with Akt, mammalian target of rapamycin, or histone deacetylase inhibitors, are active even in borte

39 ted in humans, provides proof-of-concept for histone deacetylase inhibitors as a therapeutic class, a

40 (PARP) inhibitors, hedgehog inhibitors, and histone deacetylase inhibitors as examples of experiment

41 cacy and tolerability of belinostat, a novel histone deacetylase inhibitor, as a single agent in rela

42 HA), a Food and Drug Administration-approved histone deacetylase inhibitor, as an enhancer of GRN exp

43 cells could be induced into lytic phase with histone deacetylase inhibitors, as is known for latently

44 epigenome, such as DNA methyltransferase and histone deacetylase inhibitors, as well as classical che

45 ng histone acetylation via administration of histone deacetylase inhibitors before or after a learnin

46 beta receptor II (TGFbetaRII) induced by the histone deacetylase inhibitor belinostat, we observed re

47 her known P-TEFb-releasing agents, including histone deacetylase inhibitors, bromodomain and extrater

48 redict that combinations of standard agents, histone deacetylase inhibitors, bromodomain inhibitors,

49 sting primed hESC lines by preculture in the histone deacetylase inhibitors butyrate and suberoylanil

50 intact high-H3K27me3 levels; treatment with histone deacetylase inhibitors can relieve chromatin com

51 by a variety of anti-cancer drugs, including histone deacetylase inhibitors, confers chemoresistance

52 at the combination of an ACE inhibitor and a histone deacetylase inhibitor could have therapeutic pot

53 agents (IMiDs), proteasome inhibitors (PIs), histone deacetylase inhibitors (DACIs), and monoclonal a

54 Panobinostat, a histone deacetylase inhibitor, demonstrated potent activ

55 d 3' genetic elements and sublethal doses of histone deacetylase inhibitors demonstrates that while t

56 atin, a protein product of which is a direct histone deacetylase inhibitor-dependent repressor of Wnt

57 Histone deacetylase inhibitors (DIs) are promising drugs

58 been proposed for DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi), primar

59 relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respect

60 fic overexpression of Ascl1, together with a histone deacetylase inhibitor, enables adult mice to gen

61 Previously known functions include histone deacetylase inhibitor, endoplasmic reticulum str

62 Trichostatin A (TSA), a histone deacetylase inhibitor, enhanced ENaC acetylation

63 s reason, we investigated the ability of the histone deacetylase inhibitor entinostat (ENT) to trigge

64 eage of origin, which led us to identify the histone deacetylase inhibitor entinostat as a pharmacolo

65 rthermore, treatment with the clinical-grade histone deacetylase inhibitor entinostat enhances Lys(12

66 of the retinoic acid receptor (RAR)-beta The histone deacetylase inhibitor entinostat is emerging as

67 ved by combining EHMT1/2 inhibition with the histone deacetylase inhibitor entinostat or hypomethylat

68 Here we report that combining the histone deacetylase inhibitor entinostat with the demeth

69 PURPOSE Vorinostat, a histone deacetylase inhibitor, exerts anticancer effects

70 al organs, whereas a combination of PAD4 and histone deacetylase inhibitors further decreases tumor g

71 The development of clinically useful histone deacetylase inhibitors has expanded greatly.

72 Trichostatin A (TSA), a histone deacetylase inhibitor, has been shown to suppres

73 In some cases, the therapeutic effects of histone deacetylase inhibitors have been attributed to a

74 For more than a decade now, histone deacetylase inhibitors have been investigated fo

75 Histone deacetylase inhibitors have shown some activity

76 Treatment of mice with the histone deacetylase inhibitor (HDAC-I) vorinostat restor

77 molecular response to one such intervention, histone deacetylase inhibitor (HDACi) administration.

78 n agent that promotes chromatin opening, the histone deacetylase inhibitor (HDACi) AR-42, ameliorates

79 olated from ART-suppressed patients with the histone deacetylase inhibitor (HDACi) panobinostat toget

80 that treatment with the anticancer compounds histone deacetylase inhibitor (HDACi) results in a profo

81 The histone deacetylase inhibitor (HDACi) sodium butyrate pr

82 The therapeutic potential of histone deacetylase inhibitor (HDACi) treatment has attr

83 Our triazole-based histone deacetylase inhibitor (HDACI), octanedioic acid

84 g alone or in combination with vorinostat, a histone deacetylase inhibitor (HDACi), using MTS and Ann

85 Mechanisms underlying histone deacetylase inhibitor (HDACI)-mediated NF-kappaB

86 Treating differentiating osteoblasts with histone deacetylase inhibitors (HDACi) abrogated their a

87 Finally, we discovered how histone deacetylase inhibitors (HDACi) alone, when admin

88 Histone deacetylase inhibitors (HDACi) are a new group o

89 Histone deacetylase inhibitors (HDACi) are a novel class

90 Histone deacetylase inhibitors (HDACi) are being evaluat

91 Controversially, histone deacetylase inhibitors (HDACi) are in clinical t

92 Histone deacetylase inhibitors (HDACi) are potent anti-c

93 ing a chemical library screen, we identified histone deacetylase inhibitors (HDACi) as agents reducin

94 egulated upon treatment with pan- or class I histone deacetylase inhibitors (HDACi) as well as after

95 Histone deacetylase inhibitors (HDACi) developed as anti

96 We describe a set of novel histone deacetylase inhibitors (HDACi) equipped with eit

97 an TTNT of 8.7 months (95% CI 6.0-18.0), and histone deacetylase inhibitors (HDACi) gave a median TTN

98 Histone deacetylase inhibitors (HDACi) have been propose

99 Histone deacetylase inhibitors (HDACi) have been shown t

100 Histone deacetylase inhibitors (HDACi) have been suggest

101 s, we identified miR-31 as a novel target of histone deacetylase inhibitors (HDACi) in breast cancer

102 ines the interactive role of fenretinide and histone deacetylase inhibitors (HDACi) in inducing apopt

103 Histone deacetylase inhibitors (HDACi) induce growth arr

104 Clinical response to histone deacetylase inhibitors (HDACi) is strongly assoc

105 estigate this notion, we tested 24 different histone deacetylase inhibitors (HDACi) on colon cancer c

106 several structurally distinct small molecule histone deacetylase inhibitors (HDACi) reported, macrocy

107 Histone deacetylase inhibitors (HDACi) represent a new g

108 reactivation of dormant HIV-1 proviruses by histone deacetylase inhibitors (HDACi) represents a poss

109 Treatment with histone deacetylase inhibitors (HDACI) results in potent

110 Histone deacetylase inhibitors (HDACi) show promise as c

111 Histone deacetylase inhibitors (HDACi) target abnormal e

112 ing group (ZBG) have been the most effective histone deacetylase inhibitors (HDACi) to date.

113 n be restored by treatment of NMC cells with histone deacetylase inhibitors (HDACi), engaging a progr

114 By using a "drug repurposing" strategy, histone deacetylase inhibitors (HDACi), which are presen

115 that these were similar to those induced by histone deacetylase inhibitors (HDACi).

116 proposed as the major antitumor responses to histone deacetylase inhibitors (HDACi).

117 s inhibited by valproic acid (VPA) and other histone deacetylase inhibitors (HDACi).

118 Histone deacetylase inhibitors (HDACIs) activate the pro

119 ies include PKC and MAPK agonists as well as histone deacetylase inhibitors (HDACis) and bromodomain

120 Interactions between histone deacetylase inhibitors (HDACIs) and decitabine w

121 s on CD8+ T cell phenotype and function: the histone deacetylase inhibitors (HDACis) and protein kina

122 Interactions between histone deacetylase inhibitors (HDACIs) and the novel pr

123 Mechanisms of action and resistance of histone deacetylase inhibitors (HDACIs) are not well und

124 one methyltransferase inhibitors (HMTis) and histone deacetylase inhibitors (HDACis) are reported to

125 d progression that prompt the development of histone deacetylase inhibitors (HDACIs) as anticancer ag

126 Histone deacetylase inhibitors (HDACIs) can disrupt the

127 In this study, we show that histone deacetylase inhibitors (HDACIs) can inhibit apop

128 We presently demonstrate that histone deacetylase inhibitors (HDACIs) enhance toxicity

129 Modulating this pathway with histone deacetylase inhibitors (HDACis) has been shown t

130 Histone deacetylase inhibitors (HDACis) have been shown

131 methyltransferase inhibitors [DNMTis]) with histone deacetylase inhibitors (HDACis) holds promise fo

132 is review will focus on the emerging role of histone deacetylase inhibitors (HDACis) in patients with

133 rated that in malignant hematopoietic cells, histone deacetylase inhibitors (HDACIs) induced RelA hyp

134 n the present study, we investigated whether histone deacetylase inhibitors (HDACis) may induce a fav

135 It has been suggested that histone deacetylase inhibitors (HDACis) may purge HIV in

136 Recently, it has been suggested that histone deacetylase inhibitors (HDACIs) may reduce apopt

137 Recent evidence suggests histone deacetylase inhibitors (HDACis) may represent a

138 merous studies have looked at the effects of histone deacetylase inhibitors (HDACis) on HIV reactivat

139 We found that histone deacetylase inhibitors (HDACis) significantly in

140 In vivo studies have shown histone deacetylase inhibitors (HDACis) to be neuroprote

141 We showed previously that the histone deacetylase inhibitors (HDACIs) trichostatin A a

142 ced by AML1-ETO-targeting drugs, such as the histone deacetylase inhibitors (HDACis) valproic acid (V

143 laboratory previously demonstrated that the histone deacetylase inhibitors (HDACis) vorinostat and A

144 Several histone deacetylase inhibitors (HDACIs) were used in vit

145 scription reactivation (for example, through histone deacetylase inhibitors (HDACIs)) restores apopto

146 SDHB protein increased after treatment with histone deacetylase inhibitors (HDACis), implicating the

147 dividing CB CD34+ cells ex vivo with several histone deacetylase inhibitors (HDACIs).

148 0 antibodies and confirmed with nonselective histone deacetylase inhibitors (HDACis).

149 Among the most effective compounds were histone deacetylase inhibitors (HDACIs).

150 Addition of the histone deacetylase inhibitor (HDI) LBH589 (LBH) overcam

151 To identify molecular determinants of histone deacetylase inhibitor (HDI) resistance, we selec

152 Histone deacetylase inhibitors (HDI) have exhibited some

153 Histone deacetylase inhibitors (HDIs) promote terminal o

154 ndicating a potential therapeutic benefit of histone deacetylase inhibitors (HDIs), and preclinical d

155 In fact, two histone deacetylase inhibitors (HDIs), SAHA and Depsipep

156 rogression is suppressed by treatment with a histone deacetylase inhibitor; however, this treatment h

157 used for measurement of cellular potency of histone deacetylase inhibitors in intact cells.

158 y of mocetinostat, an oral isotype-selective histone deacetylase inhibitor, in patients with relapsed

159 identified the molecular mechanism by which histone deacetylase inhibitors increase the quantity and

160 Histone deacetylase inhibitors induce apoptosis and re-e

161 sing a high-throughput screen, we found that histone deacetylase inhibitors induce Id2 expression by

162 We also showed that AR-42, a pan-histone deacetylase inhibitor, inhibited proliferation o

163 We found that bilateral infusions of a histone deacetylase inhibitor into the CeA attenuated an

164 Panobinostat (a pan histone deacetylase inhibitor) is approved in combinatio

165 Valproic acid (VPA), an histone deacetylase inhibitor, is emerging as a promisin

166 Upon treatment with histone deacetylase inhibitors, KSHV-infected murine cel

167 atment of BALB/c murine macrophages with the histone deacetylase inhibitor LAQ824 induces chromatin c

168 The histone deacetylase inhibitor largazole 1 was synthesize

169 A number of analogues of the marine-derived histone deacetylase inhibitor largazole incorporating ma

170 We report that histone deacetylase inhibitor LBH589 (panobinostat) is a

171 A2, or suppressing HMGA2 expression with the histone deacetylase inhibitor LBH589, inhibits epithelia

172 oylanilide hydroxamic acid (SAHA), and other histone deacetylase inhibitors lead to a rapid release o

173 Nevertheless, derepression of frataxin by a histone deacetylase inhibitor leads to a decrease in miR

174 combination of a demethylating reagent and a histone deacetylase inhibitor led to rapid activation of

175 Notably, pan-histone deacetylase inhibitors lift promoter-specific re

176 We show that the small-molecule histone deacetylase inhibitor M344 reduces beta-amyloid

177 etic changes and that valproic acid (VPA), a histone deacetylase inhibitor, may reverse such changes.

178 The selectivity of histone deacetylase inhibitor-mediated silencing of AICD

179 compound identified from this screen was the histone deacetylase inhibitor methyl-4-(phenylthio)butan

180 Histone deacetylase inhibitors mimic the effects of IL-1

181 Treatment of Mof(F/F)/Pcp2-Cre(+) mice with histone deacetylase inhibitors modestly prolongs PC surv

182 ities incorporating antifolates, conjugates, histone deacetylase inhibitors, monoclonal antibodies, n

183 genes and prevented by administration of the histone deacetylase inhibitor MS-275.

184 A histone deacetylase inhibitor, MS-275, resulted in upreg

185 with extinction enhancements induced by the histone deacetylase inhibitor NaB.

186 One histone deacetylase inhibitor, NCH-51, was validated as

187 Preclinical studies have shown that the histone deacetylase inhibitor nicotinamide (vitamin B3)

188 NS and has several advantages over available histone deacetylase inhibitors now in clinical trials, o

189 egulation and demonstrate a direct effect of histone deacetylase inhibitors on the SS18-SSX complex c

190 d the in vitro effect of multiple compounds (histone deacetylase inhibitors) on this putative biomark

191 Romidepsin (depsipeptide or FK228) is a histone deacetylase inhibitor, one of a new class of age

192 Accordingly, histone deacetylase inhibitors or BET inhibitors, the la

193 Treatment with histone deacetylase inhibitors or depletion of the polyc

194 scent HSPCs are resistant to reactivation by histone deacetylase inhibitors or P-TEFb activation but

195 Cotreatment with BA and panobinostat (pan-histone deacetylase inhibitor) or palbociclib (CDK4/6 in

196 , we demonstrate that treatment with the pan-histone deacetylase inhibitor panobinostat (PS) depleted

197 nt alone, cotreatment with DZNep and the pan-histone deacetylase inhibitor panobinostat caused more d

198 The multi-histone deacetylase inhibitor panobinostat demonstrated

199 to determine the safety and activity of the histone deacetylase inhibitor panobinostat in patients w

200 We assessed the ability of the histone deacetylase inhibitor panobinostat to disrupt HI

201 organotypic cultures with trichostatin A, a histone deacetylase inhibitor, partially restored differ

202 Treatment with trichostatin A, but not other histone deacetylase inhibitors, partially restored reeli

203 r of small molecules, we have found that the histone deacetylase inhibitor phenylbutyrate increases D

204 in use or under development include statins, histone deacetylase inhibitors, PPAR agonists, and small

205 how the effector molecule HC-toxin (HCT), a histone deacetylase inhibitor produced by the fungal pat

206 with TEPP-46 and shikonin or treatment with histone deacetylase inhibitors produced similar results.

207 ibitors, and cell culture in the presence of histone deacetylase inhibitors, promote development to t

208 hput sequencing (ATAC-seq), we show that the histone deacetylase inhibitor promotes accessibility at

209 Treating ECs with histone deacetylase inhibitors rapidly reverses this sil

210 PSC clone that had silenced Dlk1-Dio3 with a histone deacetylase inhibitor reactivated the locus and

211 f REST was blocked by cycloheximide; and (c) histone deacetylase inhibitors reactivated the WT parent

212 lly, growth of Salmonella in the presence of histone deacetylases inhibitors reduced expression of SP

213 Treatment with histone deacetylase inhibitors rescued IR-induced ATM si

214 Histone deacetylase inhibitors reversed the effects of c

215 ombination with bromodomain inhibitor JQ1 or histone deacetylase inhibitors robustly induce HIV-1 tra

216 The histone deacetylase inhibitor romidepsin has single agen

217 CONCLUSION The histone deacetylase inhibitor romidepsin has single-agen

218 Administration of the histone deacetylase inhibitor SAHA (suberoylanilide hydr

219 and Drug Administration-approved anticancer histone deacetylase inhibitor, SAHA, reduces myocardial

220 ion in aging and AD models and suggests that histone deacetylase inhibitors should be further explore

221 rowth inhibition of ATC, as treatment with a histone deacetylase inhibitor shown to increase RhoB exp

222 hat butyrate, a natural small fatty acid and histone deacetylase inhibitor, significantly increases t

223 DNA methyltransferase and histone deacetylase inhibitors similarly reset the trans

224 dial prefrontal cortex administration of the histone deacetylase inhibitor sodium butyrate (NaB) afte

225 In particular, the histone deacetylase inhibitor sodium butyrate (SB) may i

226 inhibitor N-omega-hydroxy-l-norarginine and histone deacetylase inhibitor sodium valproate.

227 ting pair-bond regulation and found that the histone deacetylase inhibitors sodium butyrate and trich

228 Systemic administration of a histone deacetylase inhibitor, sodium butyrate (NaB; 0.3

229 e and resveratrol) and were increased by the histone deacetylase inhibitor, suberolylanilide hydroxam

230 cal studies of in vivo administration of the histone deacetylase inhibitor suberoylanilide hydroxamic

231 ow that the chromatin opening induced by the histone deacetylase inhibitor suberoylanilide hydroxamic

232 that treatment with epigenetic therapy, the histone deacetylase inhibitor suberoylanilide hydroxamic

233 ant hypermethylation and synergized with the histone deacetylase inhibitor suberoylanilide hydroxamic

234 Treating Gialpha2-/- mice with the histone deacetylase inhibitor suberoylanilide hydroxamic

235 (Dznep) either alone or in combination with histone deacetylase inhibitor suberoylanilide hydroxamic

236 olecules, both of which were reversed by the histone deacetylase inhibitor suberoylanilide hydroxanic

237 orated in mice treated with the FDA-approved histone deacetylase inhibitor, suberoylanilide hydroxami

238 Although histone deacetylase inhibitors such as suberoylanilide h

239 ression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic c

240 Combined treatment with MAPK-pathway and histone-deacetylase inhibitors suppressed MITF expressio

241 Vorinostat is a histone deacetylase inhibitor that changes gene expressi

242 Entinostat is a histone deacetylase inhibitor that has been combined wit

243 in Cpt2M(-/-) hearts, but trichostatin A, a histone deacetylase inhibitor that improves cardiac remo

244 Modulation of chromatin conformation using a histone deacetylase inhibitor that increases transcripti

245 A histone deacetylase inhibitor that suppresses neurodegen

246 Entinostat is an oral isoform selective histone deacetylase inhibitor that targets resistance to

247 Moreover, valproic acid, a histone deacetylase inhibitor that we previously showed

248 Histone deacetylase inhibitors that increased the acetyl

249 ignature-relevant drug candidates, including histone deacetylase inhibitors that specifically reduced

250 nical and clinical data with cdk inhibitors, histone deacetylase inhibitors, the proteasome inhibitor

251 ic assessments of response and resistance to histone deacetylase inhibitor therapy.

252 Treatment of mammalian cells with histone deacetylase inhibitors to increase euchromatin o

253 that all functional NKG2D ligands induced by histone deacetylase inhibitor treatment were abolished b

254 ivation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment.

255 inhibited surface expression of MICA/B after histone deacetylase inhibitor treatment; the inhibition

256 nsferase inhibitor 5-Aza 2-deoxycytidine and histone deacetylase inhibitor trichostatin A (herein ref

257 The histone deacetylase inhibitor trichostatin A (TSA) inhib

258 ces of acute intra-CA1 administration of the histone deacetylase inhibitor Trichostatin A (TSA) on cu

259 Combining bortezomib with the histone deacetylase inhibitor trichostatin A (TSA) resul

260 a combination regimen of bortezomib and the histone deacetylase inhibitor trichostatin A abolished H

261 of skin repair we found that the class I-IIa histone deacetylase inhibitor trichostatin A accelerated

262 ngly enhanced MOR promoter activity, and the histone deacetylase inhibitor trichostatin A also increa

263 Finally, treatment with the histone deacetylase inhibitor trichostatin A, a drug kno

264 t did inhibit the relaxation produced by the histone deacetylase inhibitor trichostatin A, an effect

265 n agent 5'-aza-2'-deoxycytidine, but not the histone deacetylase inhibitor trichostatin A, drasticall

266 trodifferentiation process is blocked by the histone deacetylase inhibitor trichostatin A, opening ne

267 versal of endotoxin tolerance exerted by the histone deacetylase inhibitor trichostatin A.

268 (THLE-2 and THLE-3) were incubated with the histone deacetylase inhibitor trichostatin A.

269 ration and angiogenesis were reversed by the histone deacetylase inhibitor trichostatin A.

270 D promoter, an effect that is blocked by the histone deacetylase inhibitor trichostatin A.

271 IGF-1(NEG) and mIGF-1(POS) SMA mice with the histone deacetylase inhibitor, trichostatin A (TSA), res

272 When treated with the histone deacetylase inhibitor, Trichostatin A, genes nea

273 eased the sensitivity of cancer cells to the histone deacetylase inhibitor, trichostatin A, in C42B,

274 Together with our observation that histone deacetylase inhibitor, trichostatin A, increased

275 Administration of a histone deacetylase inhibitor, trichostatin A, rescued t

276 anti-microtubule drug thiabendazole and the histone deacetylase inhibitor tricostatin A when a histo

277 Treatment of cells with phorbol ester or histone deacetylase inhibitors triggered the expression

278 ormal cells, by DNA-demethylating agents and histone deacetylase inhibitors using clinically achievab

279 uciferase activity assay, we found that both histone deacetylase inhibitor valproic acid (VPA) and DN

280 Addition of the histone deacetylase inhibitor valproic acid partially re

281 vated levels of hTdp1 were more sensitive to histone deacetylase inhibitors valproic acid (VPA) and t

282 We show that histone deacetylase inhibitors valproic acid and butyrat

283 th all-trans retinoic acid combined with the histone-deacetylase inhibitor valproic acid.

284 tion is further promoted by treatment with a histone deacetylase inhibitor, valproic acid (VPA).

285 Importantly, the histone deacetylase inhibitor, valproic acid, blocked ME

286 d) obtained by conjugation to valproic acid (histone deacetylase inhibitor) via an ester bond, exhibi

287 gated the mechanism of MMP-13 suppression by histone deacetylase inhibitor vorinostat (SAHA).

288 A single dose of the histone deacetylase inhibitor vorinostat (VOR) up-regula

289 n the present study, we demonstrate that the histone deacetylase inhibitor vorinostat not only reprog

290 al administration of the clinically approved histone deacetylase inhibitor vorinostat not only restor

291 lowed to devise an inactive precursor of the histone deacetylase inhibitor vorinostat that was effici

292 Notably, combining the histone deacetylase inhibitor vorinostat with a PI3K inh

293 Epigenetic modifiers, including the histone deacetylase inhibitor vorinostat, may sensitize

294 hone enhanced the anticancer activity of the histone deacetylase inhibitor vorinostat.

295 nergistically increased upon exposure to the histone deacetylase inhibitor vorinostat.

296 Combining a demethylation agent and a histone deacetylase inhibitor was sufficient to reexpres

297 As a class, histone deacetylase inhibitors were greatly overrepresen

298 Histone deacetylase inhibitors were used to treat cells.

299 vity relationship for designing novel potent histone deacetylase inhibitors, which can be applied tow

300 nsin-converting enzyme (ACE) inhibitor and a histone deacetylase inhibitor would maximally reverse th