ライフサイエンスコーパス: HDAC

1 HDAC class IIa enzymes (HDAC4, 5, 7, 9) are important fo

2 HDAC inhibitors (HDACi) suppress inflammatory activation

3 HDAC inhibitors synergize with BPTF knockdown against HG

4 HDACs are commonly found in various protein complexes to

5 d histone H3 (AC-H3), histone deacetylase 1 (HDAC)1, tumor necrosis factor-alpha (TNFalpha), and Toll

6 PAH1 domain and recruits SIN-3 and the HDA-1/HDAC subunit to H3K4me3 enriched promoters.

7 Knockdown of 12 HDAC genes showed variable phenotypes; the most severe p

8 I-3K pathways and modulated by CREB, HSF-4a, HDACs, and modified histones.

9 s share common underlying causes of aberrant HDACs and dysregulated RNA splicing and, thus, further s

10 wi3, Ada2, N-Cor, and TFIIIB) domains in all HDAC complexes except those that contain the Sin3 transc

11 ve the way for the development of allosteric HDAC inhibitors and regulators to improve the therapy fo

12 n patients with SCZ and suggest that altered HDAC expression may impact cognitive function in humans.

13 Although HDACs function at the histone level, they also regulate

14 Analogously, an HDAC-RNA splicing connection suggests that splicing is r

15 ual PI3K/HDAC inhibitors by incorporating an HDAC pharmacophore into a PI3K inhibitor (Idelalisib) vi

16 issue-specific enhancer activity in which an HDAC-associated GLI repression complex regulates target

17 no HDAC drug or combination therapy with an HDAC drug has been approved for the treatment of PDAC.

18 is induced by TH2 cells, IL-4, and IL-13 and HDAC activity.

19 ndings reveal that sialic acid analogues and HDAC inhibitors enhance GD2 expression and could potenti

20 ombinant proteins, coimmunoprecipitation and HDAC assays, and pulldown and NMR experiments, we show t

21 nts with SCZ/SAD compared with controls, and HDAC expression positively correlated with cognitive per

22 o monitor cellular responses to the DNMT and HDAC inhibitors 5-Aza-2'-deoxycytidine and suberoylanili

23 licited the antitumor response after PDI and HDAC inhibition.

24 synergistic antitumor combination of PDI and HDAC inhibitors and demonstrates a mechanistic and tumor

25 e have discovered a series of novel PI3K and HDAC dual inhibitors in which the hydroxamic acid moiety

26 CUDC-907 inhibits both PI3K and HDAC functionality to exert synergistic or additive effe

27 pproach of simultaneously targeting PI3K and HDAC pathways with a single molecule.

28 nd 36 that simultaneously inhibited PI3K and HDAC with nanomolar potencies and demonstrated favorable

29 that despite having different potencies and HDAC specificities, SAHA and RMD modulate an overlapping

30 IPAH-PAAFs was augmented by HDAC8 siRNA and HDAC inhibitors, which also attenuated IPAH-associated h

31 s supported by demonstration of JAK-STAT and HDAC pathway blockade in hematological cell lines.

32 g DIPG by simultaneously inhibiting LSD1 and HDACs.

33 he role of histone/protein modifications and HDACs in RNA splicing and discuss the convergence of two

34 HC toxin, another HDAC inhibitor, enhances beta-cell function in primary m

35 pyrimidine-pyrazolyl pharmacophore to append HDAC recognition cap and hydroxamic acid as a zinc-bindi

36 se 3 (Hdac3) is a target of the FDA approved HDAC inhibitors, which are used for the treatment of lym

37 Currently, all four FDA-approved HDAC-targeting drugs are nonselective, pan-HDAC inhibito

38 By acting as HDAC inhibitors, not as energy substrates or through GPR

39 bination, highlighting the advantages of BET/HDAC dual inhibitors for more effective treatment of pan

40 , further support the potential link between HDACs and RNA splicing.

41 Blocking HDAC activity is a promising novel target for therapeuti

42 Surprisingly, hypoxia preferentially blocks HDAC inhibitor-induced differentiation of the BRCA1-reco

43 ntrols hMSC osteogenic potential mediated by HDAC epigenetic remodeling and that this cellular mechan

44 nding recognition of full-length proteins by HDACs.

45 of their noteworthy activity in the cellular HDAC assays, four compounds were further screened for th

46 Several of the 11 classical HDAC enzymes are necessary for optimal Treg function whi

47 rol of the Set3 histone deacetylase complex (HDAC) by H3K4 di-methylation, histone sumoylation direct

48 e activity of histone deacetylase complexes (HDACs).

49 ve elements of the BRAF-histone deacetylase (HDAC) (BHC) chromatin-remodeling complex (LSD1, RCOR1, H

50 isms: the inhibition of histone deacetylase (HDAC) activity and the activation of fatty acid receptor

51 Histone deacetylase (HDAC) activity has been identified as a crucial driver o

52 cological inhibition of Histone Deacetylase (HDAC) activity restores histone H3 acetylation levels an

53 iated inhibition of the histone deacetylase (HDAC) and glycogen synthase kinase-3 (GSK-3) pathways, w

54 es of novel dual-target histone deacetylase (HDAC) and mammalian target of rapamycin (mTOR) inhibitor

55 s a recently identified histone deacetylase (HDAC) complex.

56 Histone deacetylase (HDAC) enzymes play a crucial role either as biomarkers o

57 yltransferase (HAT) and histone deacetylase (HDAC) enzymes that were first characterized as regulator

58 ranscription factor and histone deacetylase (HDAC) essential for commitment to both the T cell and th

59 eriod of plasticity via histone deacetylase (HDAC) inhibition, caused adult stress to produce changes

60 tly modulated following histone deacetylase (HDAC) inhibition; three (H1F0, IRGM, and WIPI49) were up

61 a potent zinc-dependent histone deacetylase (HDAC) inhibitor appeared.

62 small-molecule Class 1 histone deacetylase (HDAC) inhibitor Entinostat (MS-275) enhances GLP-1R agon

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

64 ases sensitivity to the histone deacetylase (HDAC) inhibitor panobinostat.

65 tralized effects of the histone deacetylase (HDAC) inhibitor romidepsin.

66 ous betaOHB and class I histone deacetylase (HDAC) inhibitor treatment.

67 hibitor hydralazine and histone deacetylase (HDAC) inhibitor valproic acid (VPA) will reverse this in

68 The histone deacetylase (HDAC) inhibitor vorinostat disrupts EBV/HHV-8 latency, e

69 in cells treated with a histone deacetylase (HDAC) inhibitor was accompanied by increased histone ace

70 t trichostatin A, a pan-histone deacetylase (HDAC) inhibitor, blocked all high glucose-induced effect

71 ells, Trichostatin A, a histone deacetylase (HDAC) inhibitor, mimics juvenile hormone (JH) in inducin

72 , a selective class IIa histone deacetylase (HDAC) inhibitor, on the development and progression of r

73 e more sensitive to the histone deacetylase (HDAC) inhibitor-induced loss of stemness than the BRCA1-

74 gain by elimination of histone deacetylase (HDAC) inhibitor-producing microbes, which are anti-infla

75 evidence has shown that histone deacetylase (HDAC) inhibitors (HDACi) can have significant benefit in

76 Histone deacetylase (HDAC) inhibitors (HDACis) have been widely tested in cli

77 ltransferase (DNMT) and histone deacetylase (HDAC) inhibitors are currently in use and under developm

78 Histone deacetylase (HDAC) inhibitors are effective in killing pancreatic can

79 IFICANCE STATEMENT Some histone deacetylase (HDAC) inhibitors are known to have neuroprotective and c

80 ncreasing evidence that histone deacetylase (HDAC) inhibitors can (re)sensitize cancer cells for chem

81 selective (romidepsin) histone deacetylase (HDAC) inhibitors elicited metabolic reprogramming in con

82 ry of isozyme-selective histone deacetylase (HDAC) inhibitors is critical for understanding the biolo

83 Histone deacetylase (HDAC) inhibitors may have therapeutic utility in multipl

84 retinoic acid (RA) and histone deacetylase (HDAC) inhibitors, including short-chain fatty acids and

85 c combined with various histone deacetylase (HDAC) inhibitors, including vorinostat, enhanced GD2 exp

86 A methyltransferase and histone deacetylase (HDAC) inhibitors.

87 ensitizes DIPG cells to histone deacetylase (HDAC) inhibitors.

88 ing hippocampal class I histone deacetylase (HDAC) levels and activity, specifically HDAC2/3.

89 activation of the mTOR, histone deacetylase (HDAC), MAPK, and ERBB4 pathways.

90 xtra-terminal (BET) and histone deacetylase (HDAC), potentially serving as promising therapeutic agen

91 (GPR41) and inhibiting histone deacetylase (HDAC).

92 were more sensitive to histone deacetylase (HDAC)6 inhibition than JAK3 mutant leukemia cells.

93 modulation of class I histone deacetylases (HDAC) has been evaluated as a therapeutic strategy for p

94 les of various histone/protein deacetylases (HDAC) are key to promoting Treg-based immunotherapy.

95 activities of Class I histone deacetylases (HDACs 1/2), thereby decreased histone acetylation of H3K

96 constitutively nuclear histone deacetylases (HDACs) 1, 2, and 3 erase acetyl marks on acetyllysine re

97 ically associated with histone deacetylases (HDACs) and many known players in ASD etiology such as tr

98 we found that several histone deacetylases (HDACs) and sirtuins (SIRTs), including HDACs 2, 7, 8, an

99 The histone deacetylases (HDACs) are a superfamily of chromatin-modifying enzymes

100 Histone deacetylases (HDACs) are an attractive therapeutic target for a variet

101 Histone deacetylases (HDACs) are enzymes that regulate cognitive circuitry; ho

102 tionally, we find that histone deacetylases (HDACs) are essential for CR TF transcription.

103 Histone deacetylases (HDACs) are important regulators of gene expression that

104 Histone deacetylases (HDACs) are involved in diverse cellular regulatory mecha

105 Histone deacetylases (HDACs) are key enzymes in epigenetics and important drug

106 anomolar range against histone deacetylases (HDACs) as the key target for SAHA.

107 Histone deacetylases (HDACs) have been shown to alleviate renal fibrosis, howe

108 ly active inhibitor of histone deacetylases (HDACs) in clinical trials for multiple myeloma, leukemia

109 ation as inhibition of histone deacetylases (HDACs) not only induced acetylation of histones in the r

110 Histone deacetylases (HDACs) perform multiple functions in regulating gene exp

111 one modifying enzymes, histone deacetylases (HDACs) play critical roles in governing cellular behavio

112 Histone deacetylases (HDACs) remove acetyl groups from lysine residues on hist

113 Class IIa histone deacetylases (HDACs) repress cardiomyocyte hypertrophy through associa

114 Mammalian histone deacetylases (HDACs) undergo phosphorylation to regulate their localiz

115 The histone deacetylases (HDACs), a family of 18 host enzymes classified into four

116 he epigenetic enzymes, histone deacetylases (HDACs), across healthy human aging and between sexes usi

117 and the activities of histone deacetylases (HDACs), and Tet2 hydroxylase play a critical role in kee

118 ncluding inhibitors of histone deacetylases (HDACs), DNA methyltransferases (DNMTs), enhancer of zest

119 While in mammals, histone deacetylases (HDACs), histone H3 lysine 9 methyltransferase (KMT1/SUV3

120 ransferases (HATs) and histone deacetylases (HDACs), is necessary for appropriate gene expression and

121 (1) altering class IIa histone deacetylases (HDACs), which integrate effects of stress on gene expres

122 sion and is removed by histone deacetylases (HDACs).

123 transcription through histone deacetylases (HDACs).

124 of STAT3, particularly histone deacetylases (HDACs).

125 through the class IIa histone deacetylases (HDACs).

126 on via deactivation of histone deacetylases (HDACs).

127 ession, is mediated by histone deacetylases (HDACs).

128 through inhibition of histone deacetylation (HDAC) of those miRNA host genes.

129 he function of histone deacetyltransferases (HDACs).

130 Importantly, we show that low-dose HDAC inhibitors restore expression of most nuclear-encod

131 vulnerability may stem in part from dynamic HDAC changes following trauma that are shaped by adolesc

132 ng the SAP30-HDAC1 interaction and enhancing HDAC activity.

133 Since then, five HDAC inhibitors have received regulatory approval for ca

134 ficient mouse embryonic stem cells following HDAC inhibition.

135 NF) expression and improved memory following HDAC inhibition.

136 rotrophic factor (BDNF) and memory following HDAC inhibition.

137 s hypothesis, we identified genes coding for HDACs in T. castaneum and studied their function.

138 Furthermore, HDAC inhibitor treatment increased mRNA expression of th

139 General HDAC activity was greater in nasal epithelial cells of p

140 In the heart, HDACs (histone deacetylases) control remodeling associat

141 itors that discriminate between the 11 human HDAC isoforms.

142 yze the enzymatic properties of five class I HDAC complexes: CoREST, NuRD, Sin3B, MiDAC and SMRT with

143 tment with CI-994, a brain-permeable class I HDAC inhibitor.

144 Class I HDAC isoforms are significantly dysregulated in human PA

145 ds revealed potent inhibition of the class I HDAC isoforms HDAC1, HDAC2, and/or HDAC3 and promising a

146 creening identifies dysregulation of class I HDAC isoforms in IPAH.

147 ly associated with the inhibition of Class I HDAC isoforms.

148 The class I HDAC, HDAC3, is of particular interest because it plays

149 or entinostat (a clinically relevant class-I HDAC inhibitor) efficiently promoted apoptosis in colore

150 lizing manic-like behavior, and that class I HDACs (e.g., HDAC1 and HDAC2) are most important in this

151 fold increased potency against human class I HDACs (e.g., JT86, IC(50) 0.7 nM, HDAC1), 25-fold increa

152 ysis of expression and regulation of class I HDACs (HDAC1, HDAC2, HDAC3 and HDAC8) was performed in c

153 regulating gene expression and some class I HDACs and the class IV HDAC, HDAC11, influence type I IF

154 s higher potency and specificity for class I HDACs implicated in maintaining HIV provirus in the late

155 DAC8 corresponds to regions in other class I HDACs known to bind regulators, thus suggesting a genera

156 Such potent inhibitors of class I HDACs may show benefits in diseases (cancers, parasitic

157 tly, co-administration of the class I and II HDAC inhibitor SAHA (vorinostat) preserved the antipsych

158 Pharmacological inhibition of class II HDAC activity, or knockout of HDAC4 from HEK-293T and He

159 Here, HDAC4, a class II HDAC, is shown to promote type I IFN signaling and copre

160 alloenzyme inhibitors of Zn(II)-ACE1, Zn(II)-HDAC, Fe(II)/(III)-5-LO or Cu(II)-tyrosinase from a cura

161 Thus, the biological function of class IIa HDAC catalytic activity in the heart remains unknown.

162 gical inhibition of HDAC9 with the class IIa HDAC inhibitor TMP195 attenuates lesion formation by red

163 195 or TMP269, which are selective class IIa HDAC inhibitors, or shRNA-mediated knockdown of HDAC5 bu

164 suggest that selectively targeting class IIa HDAC isoforms (in particular HDAC4) may inhibit developm

165 All 4 class IIa HDAC isoforms, in particular HDAC4, were up-regulated in

166 FFSS signaling drives class IIa HDAC nuclear translocation through a signaling pathway i

167 The four class IIa HDACs - HDAC4, -5, -7, and -9 - are subject to signal-de

168 onse genes (ERGs) are regulated by class IIa HDACs 4 and 5, transcriptional repressors that transient

169 nipulating the nuclear activity of class IIa HDACs in behaving animals using a chemical-genetic techn

170 eacetylase 5 (HDAC5) and HDAC9 are class IIa HDACs that function as signal-responsive repressors of t

171 at, in sharp contrast to the other class IIa HDACs, HDAC7 is constitutively localized to the cardiomy

172 nical MEF2 corepressor function of class IIa HDACs.

173 ease in BDNF mRNA induced by the class I/IIb HDAC inhibitor suberoylanilide hydroxamic acid (SAHA).

174 ensitive to many ASD risk factors, including HDAC inhibitor valproic acid and a variety of endocrine

175 investigating combination therapy including HDAC inhibitors, no HDAC drug or combination therapy wit

176 ases (HDACs) and sirtuins (SIRTs), including HDACs 2, 7, 8, and 11 and SIRTs 4 and 6, repress KSHV or

177 Our findings identify increased HDAC activity as a potential tissue-injury mechanism res

178 3K27M histones, and simultaneously increases HDAC-targeted H3K27ac and LSD1-targeted H3K4me1 at diffe

179 al fibrosis, however, the role of individual HDAC isoforms in this process is poorly understood.

180 nding the biological functions of individual HDACs and for validating HDACs as drug targets.

181 Mechanistically, betaOHB acts by inhibiting HDACs to reinforce Notch signaling, instructing ISC self

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

183 reasing numbers of clinical trials involving HDAC inhibitors in human cancers, our observations stron

184 new promising target associations involving HDACs (histone deacetylases) and sigma receptors by empl

185 sion and some class I HDACs and the class IV HDAC, HDAC11, influence type I IFN signaling.

186 nd its partner LSD1, and ZMYM2 recruits LSD1/HDAC corepressor complex to MERVL LTR for transcriptiona

187 In an miR-22-dependent manner, HDAC inhibitors and RA reduced HDAC1, HDAC4, and sirtuin

188 Hippocampus and white matter HDAC expression negatively correlates with emotion regul

189 In mouse models, HDAC inhibitors also suppress oxidative stress, CCF, inf

190 ell-characterized role as histone modifiers, HDACs also interact with several nonhistone substrates a

191 Nevertheless, HDAC activity contributed to stable gene silencing.

192 nation therapy including HDAC inhibitors, no HDAC drug or combination therapy with an HDAC drug has b

193 n and to optimize therapeutic doses of novel HDACs class IIa inhibitors in gliomas.

194 Nuclear HDACs exist as at least six giant multiprotein complexes

195 damage that may be mediated by the action of HDAC and PP1CC, respectively.

196 r monitoring the pharmacodynamic activity of HDAC inhibitors.

197 s of Xyzidepsin, a depsipeptidic analogue of HDAC inhibitor Romidepsin (FK228), using a solid-phase s

198 This Perspective outlines the application of HDAC(6) inhibitors in rare diseases, such as Rett syndro

199 We further dissect the contribution of HDAC isoforms using selective inhibitors, including the

200 The pronounced additive effect of HDAC inhibition in DNA methylation-deficient cells demon

201 rent study, we sought to study the effect of HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) on

202 that may affect the therapeutic efficacy of HDAC inhibitors.

203 that may explain the decreased efficiency of HDAC inhibition in EOC, based on our data demonstrating

204 These findings provide in vivo evidence of HDAC dysregulation in patients with SCZ and suggest that

205 for non-invasive and quantitative imaging of HDAC class IIa expression-activity in intracerebral 9L a

206 as TNFalpha and IL-1beta; the inhibition of HDAC may be a potential therapeutic approach for the tre

207 Despite the abundant presence of HDAC inhibitors such as butyrate in the intestine, we fo

208 Regulation of HDAC levels was consistent with the pattern of cognitive

209 studies have identified a prominent role of HDAC (histone deacetylase)-9 in atherosclerosis and its

210 facilitate studies to elucidate the roles of HDAC class IIa enzymes in gliomagenesis and progression

211 Fs and suggest that therapeutic targeting of HDAC activity, in particular HDAC3, may be clinically be

212 lar functions and transcriptional targets of HDAC enzymes were investigated.

213 from LNs and suggest caution with the use of HDAC inhibitors.

214 The deacetylase activity of HDACs has been shown previously to be enhanced by inosit

215 tumors was observed after administration of HDACs class IIa specific inhibitor MC1568, but not the S

216 Both catalytic and noncatalytic functions of HDACs are being actively studied in the field of specifi

217 urther our understanding of the influence of HDACs on microbiome composition and are important for th

218 tion of TNF or pharmacological inhibition of HDACs protected mice from LPS-induced smooth muscle CPI-

219 istently, Corin, a bifunctional inhibitor of HDACs and LSD1, potently inhibits DIPG growth in vitro a

220 We developed an inhibitor of HDACs, AES-135, that exhibits nanomolar inhibitory activ

221 notypic studies on Arabidopsis, HDA6 (one of HDACs) was found to be a critical part of many biologica

222 te cognitive circuitry; however, the role of HDACs in cognitive disorders, including SCZ, remains unk

223 Here, we analyzed the role of HDACs in inflammatory responses of GFs.

224 mRNA polyadenylation in humans, the role of HDACs in regulating polyadenylation has not been uncover

225 ck of knowledge exists regarding the role of HDACs in splicing.

226 -26481585 to demonstrate the in vivo role of HDACs.

227 issue sections revealing the upregulation of HDACs 4, 5, and 9, and HIF-1alpha, hypoacetylation of H2

228 function that cannot be compensated by other HDAC complexes.

229 ousand-fold HDAC6 selectivity over the other HDAC isoforms.

230 While other HDAC complexes have been implicated in neurogenesis, the

231 Knock-down of HDAC2 and HDAC3, but not other HDACs, increased BDNF mRNA expression, whereas knock-dow

232 normal brain structures known to overexpress HDACs class IIa: hippocampus, n.accumbens, PAG, and cere

233 the first HDAC6 degrader by tethering a pan-HDAC inhibitor with cereblon (CRBN) E3 ubiquitin ligase

234 identified Panobinostat, an FDA approved pan-HDAC inhibitor, could elevate and restore SOX7 expressio

235 d HDAC-targeting drugs are nonselective, pan-HDAC inhibitors, exhibiting adverse side effects at ther

236 Therapeutic effects of pan-HDAC (Vorinostat), class-selective (VPA) and isoform-sel

237 Thus, this work demonstrates that pan-HDAC inhibition or dual class I/class IIb inhibition is

238 m-selective (CAY10398, Romidepsin, PCI34051) HDAC inhibitors were evaluated ex vivo (IPAH-PAAF, IPAH-

239 Histone deacetylase 6 (HDAC6) is a peculiar HDAC isoform whose expression and functional alterations

240 designed and synthesized as novel dual PI3K/HDAC inhibitors by incorporating an HDAC pharmacophore i

241 ittle is known about the regulation of plant HDAC function and activity by phosphorylation.

242 s that inhibit histone deacetylase proteins (HDACs) are effective in normalizing manic-like behavior,

243 Our results show that the E2F-Rb-HDAC complex exhibits similar distributions in genomic r

244 scribe the regulatory profiles of the E2F-Rb-HDAC complex together with EBV latent antigens, and we f

245 this multisubunit repressor complex (E2F-Rb-HDAC) to reverse its suppressive activities and facilita

246 o selectively inhibit HDAC6 by a recombinant HDAC enzyme assay, by determining the protein acetylatio

247 investigating the inhibition of recombinant HDAC enzymes and protein acetylation.

248 ed miR-22, NUR77, and RARbeta and by reduced HDACs.

249 e nucleus from the cytoskeleton up-regulates HDACs and prevents osteogenesis.

250 ined whether lactate functions by regulating HDACs using co-treatment with CI-994, a brain-permeable

251 Relative HDAC expression increases with age in cerebral white mat

252 Relative HDAC expression was lower in the DLPFC of patients with

253 and orbitofrontal gyrus, and higher relative HDAC expression in the cerebral white matter, pons, and

254 ents with SCZ/SAD also showed lower relative HDAC expression in the dorsomedial prefrontal cortex and

255 Resetting HDAC activity back to healthy levels rescues the epigene

256 te viral reactivation in vivo despite robust HDAC activity.

257 ilencing by physiological Tel1(ATM) and Rpd3(HDAC) activities coveys tolerance to glucose restriction

258 tutive regulatory mechanisms within the same HDAC complex.

259 Although selective HDAC inhibition has been proposed to mitigate toxicity,

260 e synthesis of a series of class I-selective HDAC inhibitors with 2-aminoanilides as zinc-binding gro

261 Isoform-selective HDAC inhibition is a viable approach to circumvent off-t

262 ublications have demonstrated that selective HDAC inhibitors (HDACi) can influence tumor immunogenici

263 Histone H2B sumoylation and the Set3 HDAC coordinately suppress cryptic ncRNA transcription i

264 interaction between SET1/COMPASS and a Sin3S HDAC complex at promoters.

265 zymatic and biological functions of specific HDAC complexes.

266 entrations of JNJ-26481585, a broad-spectrum HDAC inhibitor.

267 indicate that inositol phosphates stimulate HDAC activity and that the SAP30 zinc finger motif perfo

268 eria, including Escherichia coli, stimulated HDAC activity through metabolism of phytate and producti

269 selectivity for HDAC8 over the next targeted HDAC.

270 hematologic and nonhematologic toxicity than HDAC cycles.

271 in EOC, based on our data demonstrating that HDAC inhibition specifically induces expression of IL-8/

272 ux and carbon-tracing analyses revealed that HDAC inhibitors blunted glycolysis in a c-Myc-dependent

273 form-specific RNA-interference revealed that HDAC isoforms regulate distinct subset of transcriptome

274 Our results show that HDAC activity is required at the time of tail amputation

275 These data suggest that HDAC activity may oppose Kismet to promote synaptic vesi

276 lel fields, which supports the argument that HDACs, and perhaps most histone modifying enzymes, are m

277 Whilst it has been established that HDACs regulate many cellular processes, far less is know

278 Recent studies however, reveal that HDACs interact with spliceosomal and ribonucleoprotein c

279 esponse genes (e.g., Kr-h1), suggesting that HDACs may be involved in JH action.

280 tency than the BET inhibitor (+)-JQ1 and the HDAC inhibitor vorinostat, either alone or and in combin

281 eted by RNA interference or inhibited by the HDAC inhibitor vorinostat.

282 A) genes via a SUMO-interacting motif in the HDAC Cpr1 subunit.

283 Here, we analyzed, whether the HDAC class I/IIa inhibitor valproic acid (VPA) is able t

284 folds to mimic the niche for 5-days with the HDAC inhibitor Scriptaid and cytokines.

285 regulating the acetylation level, hence the HDACs would not be favorable to IAV.

286 Our results demonstrate that these HDAC complexes show a wide variety of deacetylase rates

287 Thus, HDAC inhibition restored HLA class-I surface expression

288 Thus, HDAC inhibitors and RA-induced miR-22 resulted in simult

289 Thus, HDAC regulation caused by severe stress in adulthood int

290 reviously cytotoxic properties attributed to HDAC inhibitors.

291 tions of individual HDACs and for validating HDACs as drug targets.

292 nvestigated the relationship between in vivo HDAC expression and cognitive impairment in patients wit

293 There are also sex-specific in vivo HDAC expression differences in brain regions associated

294 d transgenic mice verified effective in vivo HDAC inhibition.

295 matin accessibility at retrotransposons when HDACs are inhibited, and this is magnified when cells al

296 We investigated whether HDAC activity has been altered in patients with AR and i

297 Age and sex are associated with HDAC expression in vivo, which could drive age- and sex-

298 TSC2(+/-) mice that is also normalized with HDAC inhibitors (HDACis).

299 hat breast cancer prevention strategies with HDAC/DNMT inhibitors need to be individually tailored.

300 demonstrated that combination treatment with HDAC and FAO inhibitors extended animal survival in pati