ライフサイエンスコーパス: HDAC inhibitor

1 preclinical validation of a novel selective HDAC inhibitor.

2 e beneficial effect of the class I-selective HDAC inhibitor.

3 so butyrate accumulated and functioned as an HDAC inhibitor.

4 etylation, demonstrating that acetate was an HDAC inhibitor.

5 lly attenuated with either AR antagonists or HDAC inhibitors.

6 TAT3/IL-17 pathway as an important target of HDAC inhibitors.

7 ot require catalytic activity using specific HDAC inhibitors.

8 tivity and increased sensitivity to selected HDAC inhibitors.

9 3 proteins are decreased upon treatment with HDAC inhibitors.

10 artially rescued cellular sensitivity to the HDAC inhibitors.

11 econsideration of the mechanism of action of HDAC inhibitors.

12 rrogate indicator of cellular sensitivity to HDAC inhibitors.

13 r mechanism of action and therapeutic use of HDAC inhibitors.

14 ocytes as well as in chondrocytes exposed to HDAC inhibitors.

15 of UPR regulation and mechanism of action of HDAC inhibitors.

16 aging biomarker for monitoring the action of HDAC inhibitors.

17 the development of more specific and potent HDAC inhibitors.

18 m cells that can be selectively modulated by HDAC inhibitors.

19 eliorated, but not completely blocked, using HDAC inhibitors.

20 the potent antiinflammatory activity of pan-HDAC inhibitors.

21 65P, conferred increased cell sensitivity to HDAC inhibitors.

22 w molecules that are bispecific targeted JAK/HDAC inhibitors.

23 influences the antiproliferative effects of HDAC inhibitors.

24 vide implications for the therapeutic use of HDAC inhibitors.

25 chain fatty acid (SCFA) histone deacetylase (HDAC) inhibitor.

26 on for design of potent histone deacetylase (HDAC) inhibitors.

27 odifying drugs, such as histone deacetylase (HDAC) inhibitors.

28 ir potent activities as histone deacetylase (HDAC) inhibitors.

29 d-acting drugs known as histone deacetylase (HDAC) inhibitors.

30 kinetics for a panel of histone deacetylase (HDAC) inhibitors.

31 he first small molecule histone deacetylase (HDAC) inhibitor (3, BRD73954) capable of potently and se

32 ation, and unlike many natural product based HDAC inhibitors, 4a was found to be nontoxic under in vi

33 y demonstrated that the histone deacetylase (HDAC) inhibitor, 4b, which preferentially targets HDAC1

34 t-term treatment of preleukemic mice with an HDAC inhibitor accelerated leukemogenesis.

35 HDAC inhibitor activity was detected by Western blotting

36 three oxazolinyl inhibitors evaluated; those HDAC inhibitors also lowered cyclin E expression in U937

37 Several other HDAC inhibitors also mimicked NaBu.

38 The study reveals that a class I HDAC inhibitor alters the formation of auditory memory b

39 n levels increased upon treatment with a pan-HDAC inhibitor, an HDAC6-specific inhibitor, or depletio

40 ink between the global acetylation caused by HDAC inhibitor and gene promoter recruitment of CDK8 was

41 Pre-incubation of cells with an HDAC inhibitor and overexpression of CITED2-sensitized g

42 The effects of combination chemotherapy of HDAC inhibitors and anthracyclines were studied in CEA42

43 p53 transcription via HDAC8 and suggest that HDAC inhibitors and especially HDAC8-targeting agents mi

44 tudies that go beyond the traditional use of HDAC inhibitors and have begun to dissect the roles of i

45 of IFN-lambda, revealing the combination of HDAC inhibitors and IFN-lambda to be a potential antitum

46 cation, we tested known histone deacetylase (HDAC) inhibitors and a focused library of structurally s

47 Histone deacetylase (HDAC) inhibitors and DNA-damaging agents were identified

48 Experiments using histone deacetylase (HDAC) inhibitors and HDAC3 short hairpin RNA indicate th

49 agents (LRAs), such as histone deacetylase (HDAC) inhibitors and protein kinase C (PKC) modulators,

50 ampal sphingosine-1-phosphate, an endogenous HDAC inhibitor, and reduced histone acetylation, and dis

51 ver, many of these classical agents are "pan-HDAC" inhibitors, and their use makes it difficult to de

52 cells were treated with histone-deacetylase (HDAC) inhibitors, and expression of Fam65b and interacti

53 he first time, the present studies show that HDAC inhibitors are clearly beneficial for hypothyroidis

54 zophrenia, clinical studies demonstrate that HDAC inhibitors are efficacious when given in combinatio

55 roles in fundamental cellular processes, and HDAC inhibitors are emerging as promising cancer therape

56 Histone deacetylase (HDAC) inhibitors are an important new class of therapeut

57 Histone deacetylase (HDAC) inhibitors are currently approved for cutaneous T-

58 In addition, histone deacetylase complex (HDAC) inhibitors are known to reverse BRM silencing, but

59 Broad-spectrum histone deacetylase (HDAC) inhibitors are useful in the treatment of allergic

60 ene expression, such as histone deacetylase (HDAC) inhibitors, are among the new agents being used in

61 igenetic drugs, such as histone deacetylase (HDAC) inhibitors, are finding their way into clinical pr

62 trial with the pan-histone deacetylase (pan-HDAC) inhibitor arginine butyrate and the antiherpes vir

63 may have relevance for the use of selective Hdac inhibitors as antiinflammatory agents.

64 guiding the development of isoform specific HDAC inhibitors as effective therapeutics.

65 ation in irinotecan resistance and establish HDAC inhibitors as potential therapeutic means to overco

66 munoprecipitation, small interfering RNA and HDAC inhibitor assays.

67 t such epigenetic silencing may benefit from HDAC inhibitor-based therapy.

68 ity of malignancies of hematologic origin to HDAC inhibitor-based therapy.

69 Histone deacetylase (HDAC) inhibitors blocked GRP78 release by inducing its a

70 results demonstrate that glucocorticoids and HDAC inhibitors, both of which are currently in clinical

71 t with three additional histone deacetylase (HDAC) inhibitors, but not other antipsychotics, chemical

72 of the DNMT inhibitor 5-azacytidine and the HDAC inhibitor butyrate markedly reduced CSC abundance a

73 These findings indicate that HDAC inhibitors can elicit transgenerational effects, vi

74 However, it is not yet known whether HDAC inhibitors can modulate age-related epigenetic chan

75 arental, CRC cells with histone deacetylase (HDAC) inhibitors can effectively overcome resistance.

76 shown that nonselective histone deacetylase (HDAC) inhibitors can protect the retina from ischemic in

77 s of anticancer agents, histone deacetylase (HDAC) inhibitors, can induce autophagy.

78 a strong rationale for using the proteasome/HDAC inhibitor combination therapy in PEL.

79 Additionally, some reported HDAC inhibitors contain hydroxamate moiety that chelates

80 of MYD88 exhibited increased sensitivity to HDAC inhibitors; conversely, low expression coincided wi

81 treatment of patients with class I-specific HDAC inhibitors could induce latent viruses without incr

82 ity, highly competitive with the most potent HDAC inhibitors, currently under clinical trials.

83 f CASZ1, treatment with histone deacetylase (HDAC) inhibitor decreased expression of EZH2 and the Pol

84 aerobic metabolic capacity, is an endogenous HDAC inhibitor, deregulating transcription in an HDAC-de

85 re-induction of HLA class-I by interferons, HDAC inhibitors did not interfere with the expression of

86 ACs, thus contributing to the selectivity of HDAC inhibitors discovered in this study.

87 ort that treatment with histone deacetylase (HDAC) inhibitors downregulates renal CLDN14 mRNA and dra

88 n (e.g., Dacogen, Vidaza) and broad-spectrum HDAC inhibitors (e.g., Vorinostat, Romidepsin).

89 hydroxamic acid and PXD101, all of the other HDAC inhibitors effectively sensitized EBV(+) lymphoma c

90 Importantly, HDAC inhibitors elevate receptor expression and restore

91 with a class I- but not a class II-selective HDAC inhibitor enhanced oxidative metabolism in skeletal

92 Both HDAC4 knockdown and HDAC inhibitor enhanced radiation-induced cell death and

93 id (VPA) and enhanced by the narrow-spectrum HDAC inhibitor entinostat.

94 Histone deacetylase (HDAC) inhibitors, especially vorinostat, are currently u

95 While pharmacological doses of HDAC inhibitors exert positive effects on Bdnf gene tran

96 r treatment, as shown by the approval of two HDAC inhibitors for the treatment of cutaneous T-cell ly

97 Off-label use of VPA and other HDAC inhibitors for the treatment of RP should be limite

98 Combining Plk1 inhibitors with HDAC inhibitors had synergistic antitumor effects in vit

99 However, MC1568 (class II HDAC inhibitor) had no discernible effect.

100 ently, the development and implementation of HDAC inhibitors has proven to be therapeutically benefic

101 HDAC inhibitors have been reported to produce antidepres

102 HDAC inhibitors have been shown to counteract key steps

103 nct pathogenic mechanisms, isoform-selective HDAC inhibitors have potential as novel therapeutics for

104 However, while studies of VOR or other HDAC inhibitors have reported reversal of latency, none

105 Because current pan-HDAC inhibitors have shown disappointing results in clin

106 Histone deacetylase (HDAC) inhibitors have been associated primarily with an

107 Small molecule histone deacetylase (HDAC) inhibitors have been shown to suppress cardiac hyp

108 Histone deacetylase (HDAC) inhibitors have been used to promote neuronal surv

109 Histone deacetylase (HDAC) inhibitors have proven useful therapeutic agents f

110 Neither a VDR agonist (VDA) nor an HDAC inhibitor (HDACI) nor a demethylating agent (DAC) i

111 ed autophagosomes in rod inner segments with HDAC inhibitor (HDACi) treatment, potentially linking th

112 Mice were treated with class I and IIb HDAC inhibitor (HDACi) via drinking water for 2 and 4 we

113 therefore support the further assessment of HDAC inhibitors (HDACi's) in FRDA and diseases caused by

114 HDAC inhibitors (HDACi) are widely used in the clinic to

115 reasing data from nononcologic settings that HDAC inhibitors (HDACi) can exhibit useful anti-inflamma

116 HDAC inhibitors (HDACi) employing different zinc chelati

117 this report, we demonstrate the efficacy of HDAC inhibitors (HDACi) in vivo We show that daily admin

118 HDAC inhibitors (HDACi) increase transcription of some g

119 NAD(+), and the influence of small molecule HDAC inhibitors (HDACi) on cancer cell resistance to gen

120 CD48 messenger RNA, and that treatment with HDAC inhibitors (HDACi) restores the expression of CD48.

121 e also demonstrate that clinically available HDAC inhibitors (HDACi) targeting HDAC1 and HDAC7 can be

122 GABA sensitivity of pDAergic VTA neurons by HDAC inhibitors (HDACi), and also measured the levels of

123 nhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as well as the specific genetic

124 further the depth of the SAR of 3HPT-derived HDAC inhibitors (HDACi), we have extended the SAR studie

125 mesangial cells treated with class-specific HDAC inhibitors (HDACi).

126 Histone deacetylase (HDAC) inhibitors (HDACi) are clinically approved antican

127 HDAC inhibitors (HDACIs) are currently being explored as

128 echanisms underlying AUD and the efficacy of HDAC inhibitors (HDACIs) in different animal models of A

129 cal assessment indicated that treatment with HDAC inhibitors (HDACis) may be effective in t(8;21) AML

130 We examine HDAC inhibitors (HDACis) targeting class I, II, and IV H

131 Histone deacetylase (HDAC) inhibitors (HDACis) have demonstrated activity in

132 et al demonstrate that histone deacetylase (HDAC) inhibitors (HDACis) in glucose-6-phosphate dehydro

133 Histone deacetylase (HDAC) inhibitors (HDACis) reactivate latent KSHV and dra

134 duced histone acetylation and sensitivity to HDAC inhibitors (HDIs) (Figure 4A-B).

135 Histone deacetylase (HDAC) inhibitors (HDIs) are promising anticancer therapi

136 Compound 4j, the most potent HDAC inhibitor in the cellular HDAC assay, revealed rema

137 69 genome was not induced in the presence of HDAC inhibitors in either KG-1 or Kasumi-3 cells.

138 evidence for an anti-inflammatory potency of HDAC inhibitors in models of experimental colitis.

139 , with important implications for the use of HDAC inhibitors in the treatment of cancer.

140 sts there may be a therapeutic potential for HDAC inhibitors in this disease.

141 We examined the role of histone deacetylase (HDAC) inhibitors in regulating sGCalpha1 and -beta1 expr

142 KSHV was reactivated by all SCFAs that are HDAC inhibitors, including phenylbutyrate.

143 d us to investigate the potential of several HDAC inhibitors, including some new, highly potent compo

144 ed as corepressors of YY1, and, accordingly, HDAC inhibitors increased EAAT2 promoter activity and re

145 The class I HDAC inhibitors increased the expression of sGCbeta1 mor

146 transcription factor involved in regulating HDAC inhibitor-induced AQP3 expression.

147 reased transcriptional activity, as shown by HDAC inhibitor-induced chromatin relaxation and observed

148 the use of a loop diuretic in mice abrogated HDAC inhibitor-induced hypocalciuria.

149 Valproic acid (VPA), another SCFA and an HDAC inhibitor, induces the lytic cycle of KSHV but bloc

150 ontinued improvement of histone deacetylase (HDAC) inhibitors is finding alternative motifs equipoten

151 nt of isoform-selective histone deacetylase (HDAC) inhibitors is important in elucidating the functio

152 a unique and unexplored histone deacetylase (HDAC) inhibitor, is reported.

153 of two hits revealed that the small molecule HDAC inhibitors, ISOX and vorinostat, increased MBNL1 ex

154 des have provided potent and class-selective HDAC inhibitors, it will be challenging to distinguish b

155 he goal of developing a second generation of HDAC inhibitors lacking this hydroxamate, we designed a

156 The HDAC inhibitors LAQ824 and SAHA increase phosphocholine

157 eptide apicidin; and the recently discovered HDAC inhibitor largazole.

158 e highly potent class I histone deacetylase (HDAC) inhibitor largazole cooperated to induce E-cadheri

159 eacetylases (HDAC) and were increased by the HDAC inhibitor LBH589 (panobinostat).

160 synthesis of a focused histone deacetylase (HDAC) inhibitor library with peptoid-based cap groups an

161 The effectiveness and potency of these HDAC inhibitors make them potentially applicable as sens

162 cific memory promoting properties of class I HDAC inhibitors may depend on isoform selectivity and th

163 l cell transdifferentiation, suggesting that HDAC inhibitors may enhance repair by promoting acquisit

164 r results suggest that hydroxamic acid-based HDAC inhibitors may mediate neuroprotection via HDAC-ind

165 These results suggest that class I HDAC inhibitors may provide a pharmacologic approach to

166 uncover an alternate mechanism by which pan-HDAC inhibitors may regulate stress-related behaviors in

167 the class IIa selective histone deacetylase (HDAC) inhibitor MC1568 are described.

168 However, use of more specific HDAC inhibitors might limit the toxicities caused by HDA

169 Histone deacetylase (HDAC) inhibitors modify chromatin and can block cancer c

170 phenotypic changes seen with broad spectrum HDAC inhibitors, most notably a block in the differentia

171 (RX) (24 h), the neuroprotection of Class I HDAC inhibitor MS-275 was counteracted, whereas in neuro

172 le of ATRA with a 2-aminoanilide tail of the HDAC inhibitor MS-275, yielding MC2392.

173 rate group of rats, the histone deacetylase (HDAC) inhibitor, MS275, was delivered to the renal medul

174 ocytes treated with highly selective class I HDAC inhibitors, nuclear ERK1/2 signaling is suppressed

175 Neither physiological oxygen levels nor HDAC inhibitors offer advantages to culturing female hiP

176 ope, which suggests a positive impact of the HDAC inhibitor on pulmonary vascular remodeling and stif

177 previously unknown cytoplasmic mechanism of HDAC inhibitors on HIV replication that is distinct from

178 his study explores the regulatory potency of HDAC inhibitors on T cell polarization as a mechanistic

179 rrogate indicator of cellular sensitivity to HDAC inhibitors.Oncogene advance online publication, 3 S

180 Although the class I HDAC inhibitor only modestly reduced right ventricular h

181 nd an ectopic xenograft were pretreated with HDAC inhibitor or short hairpin RNA to knock down expres

182 Majors rarely forage, but injection of a HDAC inhibitor or small interfering RNAs against the HDA

183 ifically, we showed that HDAC1 inhibition by HDAC inhibitors or by siRNA shortened the half-life of T

184 Treatment of HCC cells with HDAC inhibitors or knockdown of HDAC1 and/or HDAC2 resto

185 dies showed that either histone deacetylase (HDAC) inhibitors or tumor necrosis factor-related apopto

186 d the selection of a new class of potent pan-HDAC inhibitors (pan-HDACis).

187 found that the CDK inhibitor dinaciclib and HDAC inhibitor panobinostat were the most potent inducer

188 ate GAS5-AS1 in NSCLC cells, whereas the pan-HDAC inhibitors panobinostat and SAHA significantly indu

189 ydroxyamic acid-derived histone deacetylase (HDAC) inhibitors Panobinostat and Vorinostat also enhanc

190 DAC4 silencing and the administration of the HDAC inhibitor parthenolide during obstructive cholestas

191 HDAC inhibitors, particularly vorinostat, are currently

192 rates in part like NaB and potentially other HDAC inhibitors, placing the brain into a state of readi

193 The precise molecular mechanisms whereby HDAC inhibitors prevent neuronal death are currently the

194 We further show that HDAC inhibitors prevent the formation of nuclear Htt agg

195 All of the HDAC inhibitors prevented degradation of BNC, in which T

196 Conversely, HDAC inhibitors prevented the repressive histone modific

197 usion criteria included previous exposure to HDAC inhibitors; previous allogeneic stem-cell transplan

198 odium butyrate (NaB), a histone deacetylase (HDAC) inhibitor previously shown to enable subthreshold

199 monstrated administration of pharmacological HDAC inhibitors, primarily those targeted to class I HDA

200 Importantly, fibroblasts treated with HDAC inhibitors promoted tumor growth in vivo.

201 l a previously unknown cytoplasmic effect of HDAC inhibitors promoting productive infection of CD4(+)

202 A novel class IIa-selective HDAC inhibitor reduced recombinant human HDAC7 enzyme ac

203 HDAC inhibitors regulate several hundred transcripts irr

204 -induced plasticity, and previous studies of HDAC inhibitors report conflicting effects on cocaine-el

205 modifications, because histone deacetylase (HDAC) inhibitors reproduced starvation-induced transgene

206 As memory enhancement by HDAC inhibitors requires CREB-CBP interaction and Nr4a g

207 R-9 and miR-374 genes, and treatment with an HDAC inhibitor rescued the phenotypes of cell and animal

208 Systemic administration of an HDAC inhibitor rescues the detrimental effects of ELS wh

209 In line with these results, HDAC inhibitors restore in part C/EBPalpha target gene e

210 ent with 109, a class I histone deacetylase (HDAC) inhibitor, resulted in increased level of FXN tran

211 Treatment with HDAC inhibitor results in an increase in TAF9 acetylatio

212 We used a class I HDAC inhibitor, RGFP966 (C21H19FN4O), to test the role o

213 servations provide a proof-of principle that HDAC inhibitor SAHA may have a therapeutic potential for

214 Importantly, we show that treatment with the HDAC inhibitor SAHA restores sensitivity to prednisolone

215 Combining P5091 with lenalidomide, HDAC inhibitor SAHA, or dexamethasone triggers synergist

216 treating cells with the histone deacetylase (HDAC) inhibitor SAHA led to detectable clusters of DNA-P

217 The histone deacetylase (HDAC) inhibitor SAHA synergizes with JQ1 to augment cell

218 n adipocytes treated with a class I-specific HDAC inhibitor showed higher expression of Pgc-1alpha, i

219 Many of the new HDAC inhibitors showed higher solubilities and lower bin

220 HDAC4 knockdown with or without an HDAC inhibitor significantly delayed tumor growth in a r

221 itor, and mocetinostat (MGCD0103), a class I HDAC inhibitor, significantly enhanced Npr1 promoter act

222 Strikingly, coadministration of the HDAC inhibitor sodium butyrate with PNFlx prevented the

223 Treatment with histone deacetylase (HDAC) inhibitor sodium butyrate (NaBu) induced PKCdelta

224 y administration of the histone deacetylase (HDAC) inhibitor sodium butyrate for 1 wk after stress.

225 etinoic acid (ATRA) and histone deacetylase (HDAC) inhibitor, sodium butyrate (NaBu) to examine the e

226 Furthermore, treatment of mice with HDAC inhibitors stimulated the transcription of renal mi

227 The broad-spectrum HDAC inhibitor suberoylanilide hydroxamic acid induced A

228 Treatment with histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) c

229 is study, we found that histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) i

230 e to treatment with the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA),

231 One of the HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA),

232 Histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA),

233 ID/DeltaID) mice with a histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxyamic acid (SAHA)

234 ination of Btz with the histone deacetylase (HDAC) inhibitor suberoylanilidehydroxamic acid (SAHA, al

235 uggests a combination approach where class I HDAC inhibitors such as valproic acid or MS-275 (entinos

236 However, several fatty acid HDAC inhibitors, such as isobutyrate and phenylbutyrate,

237 the antidepressant-like properties of other HDAC inhibitors, such as SAHA and MS-275, in the tail su

238 Histone deacetylase (HDAC) inhibitors, such as vorinostat (SAHA), have shown

239 Here we found that histone deacetylase (HDAC) inhibitors suppress both wild-type and mutant p53

240 nosis of HCC and restored FBP1 expression by HDAC inhibitors suppresses HCC growth.

241 Significantly, these isoform-targeted HDAC inhibitors synergize with PKC modulators, namely br

242 Hdac3 is a key target for Hdac inhibitors that are efficacious in cutaneous T cell

243 Selective HDAC inhibitors that bind to the 14 A cavity have also b

244 ogical brain states may be more receptive to HDAC inhibitors that improve network function by enhanci

245 uring vorinostat treatment and indicate that HDAC inhibitors that selectively target nuclear class I

246 syntheses of a class of cyclic tetrapeptide HDAC inhibitors, the azumamides, by a concise route in w

247 nt stimuli, including a histone deacetylase (HDAC) inhibitor, the transforming growth factor beta (TG

248 HDAC inhibition, and DIPG cells resistant to HDAC inhibitor therapy retain sensitivity to CDK7 blocka

249 try aimed at identifying a new generation of HDAC inhibitors, through the introduction of a thiol zin

250 ass selective class IIa histone deacetylase (HDAC) inhibitor, TMP195, influenced human monocyte respo

251 R4A signaling interfered with the ability of HDAC inhibitors to enhance memory.

252 Cs in HIV latency, and recent efforts to use HDAC inhibitors to reactivate latent HIV in vitro and in

253 lation about the use of histone deacetylase (HDAC) inhibitors to treat skin diseases led us to invest

254 tubule perfusion techniques, we showed that HDAC inhibitors transiently increase the paracellular ca

255 Akt and its substrates in Hdac3-deficient or HDAC inhibitors treated chondrocytes correlated with inc

256 ged to the genes most strongly responding to HDAC inhibitor treatment of neuroblastoma cells in a gen

257 Mechanistically, HDAC inhibitor treatment suppressed HDAC6 activity and l

258 P53 gene and that MYC recruitment drops upon HDAC inhibitor treatment.

259 s used to assess the in vivo activity of the HDAC inhibitor trichostatin A (TSA).

260 g glaucoma was interrogated using the global HDAC inhibitor trichostatin A (TSA).

261 Notably, the HDAC inhibitor trichostatin A had no effect on MeCP2-med

262 xes was shared with the nonisoform selective HDAC inhibitors trichostatin A (TSA) and vorinostat (sub

263 nesis is rescued by the histone deacetylase (HDAC) inhibitor trichostatin A, indicating that ceramide

264 The HDAC inhibitor, trichostatin A (TSA, 0.1 mg/kg), was int

265 cardiac sarcomeres and that a class I and II HDAC inhibitor, trichostatin A, enhances contractile act

266 ells, consistent with effects elicited by an HDAC inhibitor, trichostatin A.

267 nd panobinostat (LBH589), two broad-spectrum HDAC inhibitors up-regulate hsa-miR-31 (miR-31).

268 ned a series of potent and selective class I HDAC inhibitors using a hydrazide motif.

269 oneal administration of the class I-specific HDAC inhibitor valproic acid into bromodeoxyuridine (Brd

270 lls is inhibited by the histone deacetylase (HDAC) inhibitor valproic acid (VPA) and enhanced by the

271 and in combination with histone deacetylase (HDAC) inhibitors valproic acid and vorinostat.

272 demethylating agent, 5-azacytidine, and the HDAC inhibitor, valproic acid.

273 The effectiveness of HDAC inhibitors, valproic acid, and suberoylanilide hydr

274 nized with the class III histone deactylase (HDAC) inhibitor vitamin B3 (nicotinamide) which activate

275 JAK1/2 inhibitor, have been merged with the HDAC inhibitor vorinostat (2), leading to new molecules

276 The clinically approved HDAC inhibitor Vorinostat specifically increases HIF-2al

277 The histone deacetylase (HDAC) inhibitor vorinostat (VOR) can increase HIV RNA ex

278 Recently, the histone deacetylase (HDAC) inhibitor vorinostat has been demonstrated to indu

279 is now marketed as the histone deacetylase (HDAC) inhibitor vorinostat, also has been reported to tr

280 The oral histone deacetylase (HDAC) inhibitor (vorinostat) is safe and results in low

281 e JAK2/FLT3 inhibitor pacritnib with the pan-HDAC inhibitor, vorinostat, to create bispecific single

282 d in combination with a histone deacetylase (HDAC) inhibitor, vorinostat or romidepsin.

283 pression patterns to elucidate the effect of HDAC inhibitors VPA and entinostat (MS-275) on behaviora

284 targeting histone deacetylases (HDACs) using HDAC inhibitors was shown to be neuroprotective and to i

285 sly or as a consequence of treatment with an HDAC inhibitor, was accompanied by decreased APP protein

286 azoline-1-oxyl-3-oxide or trichostatin A (an HDAC inhibitor) were quantified, thereby identifying gen

287 inhibitors may increase the effectiveness of HDAC inhibitors when treating ovarian cancer and other s

288 mor activity of class I histone deacetylase (HDAC) inhibitors, which primarily target class I HDACs.

289 In this study, we show that belinostat, an HDAC inhibitor with an alternative chemical scaffold, al

290 dies indicated that 12 functions as a potent HDAC inhibitor with an IC50 value of 0.1 muM.

291 l evaluation of new potent hydroxamate-based HDAC inhibitors with a novel alkoxyamide connecting unit

292 Combining HDAC inhibitors with BI 2536 or BI 6727 may be an effect

293 Use of HDAC inhibitors with different specificities limited our

294 -hydroxypyrrolidine cap for the synthesis of HDAC inhibitors with good potency.

295 A goal shared by many is to develop HDAC inhibitors with increased isoform selectivity in or

296 wever, the underling mechanisms of combining HDAC inhibitors with TRAIL in the treatment of breast ca

297 While known HDAC inhibitors with varied inhibitory profiles proved t

298 terrogated the biological effects of class I HDAC inhibitors with varying selectivity and assessed a

299 , hydroxamic-containing histone deacetylase (HDAC) inhibitor with broad anti-inflammatory properties,

300 inhibitors with VPA or histone deacetylase (HDAC) inhibitors with lithium synergistically increased