ライフサイエンスコーパス: HDAC

1 HDAC inhibition caused a drop in intracellular Ca(2+) an

2 HDAC-inhibition may underlie greater efficacy of statins

3 HDAC-mediated suppression of FBP1 expression correlated

4 HDACs 1 and 2 are recruited by the MTA1 corepressor to f

5 HDACs are known to be powerful negative regulators of me

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

7 minished the total histone acetyltransferase/HDAC activity ratio in mouse lungs exposed to LPS/IFN-ga

8 ncreased the total histone acetyltransferase/HDAC activity ratio in mouse lungs.

9 In addition, HDAC inhibition induces acetylation of p65 and histone H

10 nally truncated MRE11, which is formed after HDAC inhibition as full-length MRE11 is downregulated.

11 HDACs 2 and 10, submicromolar potent against HDACs 1, 8, and 11, and >50-fold selective for JAK2 in a

12 nanomolar potency, is <100 nM potent against HDACs 2 and 10, submicromolar potent against HDACs 1, 8,

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

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

15 etylation, demonstrating that acetate was an HDAC inhibitor.

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

17 marily by myocyte contractility via HO-1 and HDAC signalling.

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

19 ta strongly suggest that concurrent BCL2 and HDAC inhibition may offer synergy in the treatment of pa

20 g further investigation of combined DNMT and HDAC inhibition in refractory or drug-resistant breast c

21 evaluation of antiproliferative effects and HDAC inhibitory activity in the human ovarian cancer cel

22 provides new leads for assessment of JAK and HDAC pathway dual inhibiton achieved with a single molec

23 ispecific single molecules with both JAK and HDAC targeted inhibition.

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

25 creatinine ratio (ACR), kidney pathology and HDAC activity, and reduced renal E-cadherin levels.

26 ve than EZT at reducing kidney pathology and HDAC activity.

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

28 s supported by demonstration of JAK-STAT and HDAC pathway blockade in several hematological cell line

29 transactivation through activated Stat3 and HDAC inhibition.

30 ted pyrrolopyrimidine, 24, inhibits JAK1 and HDACs 1, 2, 3, 6, and 10 with IC50 values of less than 2

31 recruitment of corepressors such as NCoR and HDACs, indicating that this class of coregulators may pl

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

33 As HDACs are promising targets of cancer therapy, it is imp

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

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

36 Sustained PEITC exposure not only blocked HDAC binding to euchromatin but was also associated with

37 Inhibiting both HDACs has been suggested as a potential therapy in HD.

38 pithelial barrier leakiness was confirmed by HDAC inhibition, which improved barrier integrity throug

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

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

41 nt regulators of Golgi breakdown mediated by HDAC inhibition.

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

43 findings suggest that repression of FBP1 by HDACs has important implications for HCC prognosis and t

44 fferences are mediated, at least in part, by HDACs.

45 nding recognition of full-length proteins by HDACs.

46 thesized compounds were tested in a cellular HDAC inhibition assay and an MTT assay for cytotoxicity.

47 e most potent HDAC inhibitor in the cellular HDAC assay, revealed remarkable chemosensitizing propert

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

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

50 ffect was markedly potentiated by concurrent HDAC inhibition with 93% of samples treated with venetoc

51 or MS-275 (entinostat) appear to counteract HDAC- and RAD51/FANCD2-mediated melanoma cell resistance

52 A) versus conventional high-dose cytarabine (HDAC) as postremission chemotherapy in younger patients

53 To date, HDAC substrate specificity and selectivity have been lar

54 is study, we found that histone deacetylase (HDAC) 3 is required for T cell development.

55 Histone deacetylase (HDAC) 6 exists exclusively in cytoplasm and deacetylates

56 derivatives that act as histone deacetylase (HDAC) 6/8 dual inhibitors and were designed from the str

57 fluorescence assay for histone deacetylase (HDAC) activity and for inhibitor screening and IC50 dete

58 e ascribed to intrinsic histone deacetylase (HDAC) activity in Tcf1 and Lef1.

59 esigned to inhibit both histone deacetylase (HDAC) and PI3K enzymes, which are members of common onco

60 In mammalian cells, histone deacetylase (HDAC) and Sirtuin (SIRT) are two families responsible fo

61 e describe a Cas9-based histone deacetylase (HDAC) and the design principles required to achieve locu

62 cts as a scaffold for a histone deacetylase (HDAC) complex.

63 How remodeler and histone deacetylase (HDAC) cooperate within NuRD complexes remains unresolved

64 We show that the histone deacetylase (HDAC) enzyme inhibitor trichostatin A blocks the ability

65 Even though histone deacetylase (HDAC) inhibition has shown remarkable antitumor activity

66 both effects are due to histone deacetylase (HDAC) inhibition possibly linked to autophagy regulation

67 on balance, in part via histone deacetylase (HDAC) inhibition.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

92 ased stability, reduced histone deacetylase (HDAC) interaction, and increased DNA binding.

93 cells and show that the histone deacetylase (HDAC) repressor complex is recruited to these miR promot

94 Inhibition of histone deacetylase (HDAC) signalling with trichostatin A increased nuclear M

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

96 1 (SIRT1), a class-III histone deacetylase (HDAC), resulting in epigenetic transactivation of KSHV l

97 gative human cells in a histone deacetylase (HDAC)-dependent manner, replicating the expression of th

98 ncer agents that target histone deacetylase (HDAC).

99 , and decreased nuclear histone deacetylase (HDAC)2 levels.

100 ed the nuclear level of histone deacetylase (HDAC)2, an essential epigenetic enzyme that mediates ste

101 entiation by recruiting histone deacetylases HDAC 1 and 2 (HDAC1/2) and nucleosome remodeling and dea

102 wed that inhibition of histone deacetylases (HDAC) by trichostatin A dramatically enhanced induction

103 Histone deacetylases (HDAC) contain eighteen isoforms that can be divided into

104 ry proteins, including histone deacetylases (HDAC), histone methyltransferases, bromodomain-containin

105 ved that expression of histone deacetylases (HDACs) 1 and 9, and Silent information regulator genes (

106 Histone deacetylases (HDACs) 1, 2 and 3 form the catalytic subunit of several

107 d chromatin-binding of histone deacetylases (HDACs) and Polycomb-group (PcG) proteins.

108 we review the role of histone deacetylases (HDACs) and the NAD(+) dependent sirtuins (SIRTs) in the

109 acetyltransferases and histone deacetylases (HDACs) are important epigenetic coregulators.

110 Histone deacetylases (HDACs) are important modulators of epigenetic gene regul

111 Class I histone deacetylases (HDACs) are known to remove acetyl groups from histone ta

112 Class IIa histone deacetylases (HDACs) are very important for tissue specific gene regul

113 Histone deacetylases (HDACs) catalyze deacetylation of acetyl-lysine residues

114 ransferases (HATs) and histone deacetylases (HDACs) compete to modulate histone acetylation, allowing

115 methylase 1 (LSD1) and histone deacetylases (HDACs) facilitates breast cancer proliferation.

116 Class I histone deacetylases (HDACs) Hdac1 and Hdac2 can associate together in protein

117 the specific roles of histone deacetylases (HDACs) in rod differentiation in neonatal mouse retinas,

118 Inhibiting class I histone deacetylases (HDACs) increases energy expenditure, reduces adiposity,

119 Histone deacetylases (HDACs) modulate acetylation of lysine residues, a protei

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

121 evidence that specific histone deacetylases (HDACs) play essential roles in the CSC phenotype.

122 isms by which specific histone deacetylases (HDACs) regulate differentiation in solid tumors remains

123 Histone deacetylases (HDACs) regulate myriad cellular processes by catalyzing

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

125 inhibitors of CBP and histone deacetylases (HDACs) revealed hundreds of genes linked to hyperacetyla

126 ach, the inhibition of histone deacetylases (HDACs), has been reported to suppress pancreatic islet i

127 ransferases (HATs) and histone deacetylases (HDACs), is a major epigenetic regulatory mechanism of ge

128 acetyltransferases and histone deacetylases (HDACs).

129 cause parasitic Zn(2+)- and NAD(+)-dependent HDACs play crucial roles in the modulation of parasite g

130 ino acids in the Tcf1 HDAC domain diminishes HDAC activity and the ability to suppress CD4(+) lineage

131 The inhibition of endogenous HDAC activity reconstitutes defective barrier by increas

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

133 r Geneome Atlas (TCGA) data was analyzed for HDAC, PI3K, HER2, and MAPK/RAS/RAF gene alterations from

134 Knockout mouse models for HDACs 1-9 have been important for guiding the developmen

135 While for HDACs 1-3 and 6 many potent selective inhibitors have be

136 A complex lacking CHD4 that has HDAC activity can exist as a stable species.

137 However, HDAC inhibition causes diverse cellular outcomes, and id

138 itory activity against schistosome and human HDACs.

139 monomeric actin is able to bind the class I HDAC complex.

140 to recruit the catalytically active class I HDAC complexes to their substrate.

141 taining a low and tolerable level of class I HDAC inhibition.

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

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

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

145 4a showed more specificity toward class I HDAC isoforms.

146 th at least 464-fold selectivity for class I HDAC proteins over class II HDAC6 compared to a 22-fold

147 enzymatic activity of an individual Class I HDAC, HDAC3, has a role in fear memory formation in subr

148 illustrate a previously unrecognized class I HDAC-dependent control of the TP53 gene and provide evid

149 ism, with HDAC3 as the most affected class I HDAC.

150 This repression depended on class I HDACs and involved multiple corepressor complexes, inclu

151 Moreover, the interaction between class I HDACs and nuclear actin was found to be activity depende

152 eversible, and the results implicate class I HDACs in repeat-mediated promoter silencing.

153 llectively, HIV-1 Vpr down-regulates class I HDACs on chromatin to counteract latent infections of ma

154 The influence of class I HDACs on DSB repair by homologous recombination and the

155 Here, we report on the impact of class I HDACs on the response of malignant melanoma cells treate

156 hermore, pharmacologic inhibition of class I HDACs sensitizes malignant melanoma cells to apoptosis f

157 ns of HDAC6-inhibitor complexes with class I HDACs suggest active site features that contribute to th

158 ds and depletes chromatin-associated class I HDACs through a VprBP-dependent mechanism, with HDAC3 as

159 ory protein Vpr induces depletion of class I HDACs, including HDAC1, 2, 3, and 8, to overcome latency

160 ent animal models of AUD may involve class I HDACs, we herein report the development of class I HDACI

161 but weak inhibitory activity against class I HDACs.

162 R)-based phenotypic screen of class I and II HDAC genes.

163 Because class IIa HDAC catalytic activity is low, their exact molecular ro

164 These data introduce class IIa HDAC inhibition as a means to harness the anti-tumour po

165 A prominent example is HDAC7, a class IIa HDAC that shows a lymphoid-specific expression pattern w

166 re we directly address whether the class IIa HDAC, HDAC5 may function as a scaffold to recruit co-rep

167 gulation is mediated by both class I and IIa HDACs.

168 Class IIa HDACs are reportedly associated with some neuronal disor

169 that inhibition of class I but not class IIa HDACs caused the same phenotypic changes seen with broad

170 gs support a non-canonical role of class IIa HDACs in the scaffolding of transcriptional regulatory c

171 Studies have suggested that class IIa HDACs may serve as a scaffold to recruit the catalytical

172 strong inhibitory activity against class IIa HDACs, but weak inhibitory activity against class I HDAC

173 he cavity size between class I and class IIa HDACs, thus contributing to the selectivity of HDAC inhi

174 Histone deacetylase 6 (HDAC6), a class IIb HDAC, plays an important role in many biological and pat

175 d levels of CIDEC and its acetylated form in HDAC-deficient adipocytes as well as the adipose tissue

176 ersely, polymerizing nuclear actin increased HDAC activity and decreased histone acetylation.

177 residues to phenylalanine modestly increased HDAC interaction, modestly reduced stability, and marked

178 hatic chain as a linker was found to inhibit HDACs.

179 mone against biotrophic pathogens, inhibited HDAC activity and increased histone acetylation by induc

180 tone acetylation by targeting and inhibiting HDAC complexes, resulting in the hyperacetylation of spe

181 microglial signaling mediator that inhibits HDAC activity, enhances basal Rgs10 expression in BV-2 m

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

183 transcription factors can utilize intrinsic HDAC activity to guard cell identity by repressing linea

184 to treat skin diseases led us to investigate HDAC's role in the regulation of AQP3.

185 ompounds for further exploration of dual JAK-HDAC pathway inhibiton achieved with a single molecule.

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

187 ociated with some neuronal disorders, making HDACs therapeutic targets for treating neurodegenerative

188 To date, 18 different mammalian HDAC isoforms have been identified, and these have been

189 Mechanistically, HDAC inhibitor treatment suppressed HDAC6 activity and l

190 our findings indicate that virally mediated HDAC inhibition can act as a signal for the host to acti

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

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

193 Nevertheless, HDAC activity contributed to stable gene silencing.

194 ates with zinc ion to become the cofactor of HDAC enzymes.

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

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

197 egulator of the antiproliferative effects of HDAC inhibition.

198 influences the antiproliferative effects of HDAC inhibitors.

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

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

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

202 Although the functions of HDAC proteins are becoming apparent both biochemically a

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

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

205 ciated Mi2beta/CHD4, but were independent of HDAC activity.

206 annoma cells in vitro, via the inhibition of HDAC activity and the activation of ERK.

207 Inhibition of HDAC activity by sodium butyrate enhances recruitment of

208 kely triggered by NO-dependent inhibition of HDAC activity, since GSNO and S-nitroso-N-acetyl-dl-peni

209 Pharmacologic inhibition of HDAC elevated a SOX9-positive cell population from SOX2-

210 ically relevant discovery that inhibition of HDAC induces the BTK-targeting miRs in ibrutinib-sensiti

211 is important to understand the mechanisms of HDAC regulation.

212 nzyme inhibitory activity against a panel of HDAC isoforms revealed these compounds had strong inhibi

213 ring pneumonia and indicate the potential of HDAC inhibition as a therapy.

214 The role of HDAC activation on epithelial barrier leakiness was conf

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

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

217 Use of HDAC inhibitors with different specificities limited our

218 Unexpectedly, the enzymatic activity of HDACs in these complexes has been shown to be regulated

219 13 significantly increased the expression of HDACs and SIRTs.

220 ression, phosphorylation, and interaction of HDACs and STAT3.

221 s not clear whether this function depends on HDAC enzymatic activity per se.

222 rated a direct effect of AT, but not EZT, on HDAC-inhibition and, H3 and H4- acetylation in primary g

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

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

225 ment x SCT interaction, the HR of CLARA over HDAC before or in absence of SCT was 0.65 (95% CI, 0.43

226 uclear extracts was able to suppress overall HDAC function.

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

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

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

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

231 se effects, the identification of particular HDAC isoforms involved in CD20 regulation seems to be of

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

233 investigating the inhibition of recombinant HDAC enzymes and the protein acetylation in cells by Wes

234 short isoform lacking the ability to recruit HDACs.

235 ta suggest nuclear actin is able to regulate HDAC 1 and 2 activity.

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

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

238 f-renewal and lineage specification-requires HDAC activity for gene activation.

239 s limited our exploration of the responsible HDAC member to HDAC1, HDAC2, or HDAC3.

240 Analysis of TCGA data revealed HDAC, PI3K, HER2, and MAPK/RAS/RAF gene alterations in 1

241 isoforms, with all isoforms sharing the same HDAC and DNA-binding domains and the long isoforms conta

242 In animals, several HDACs are subjected to regulation by nitric oxide (NO);

243 nd us revealed interactions between the Sin3/HDAC complex, the H3K4me3 demethylase KDM5A, GATAD1, and

244 luding JUN/JUN homodimers and P54(nrb)/Sin3A/HDAC to repress transcription of the key labour gene, Cx

245 ion between class I, II, or IV (non-sirtuin) HDACs and linker histones has been reported.

246 s the local balance between the underln]Snf2/HDAC-containing repressor complex (SHREC) histone deacet

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

248 review, we endeavor to identify the specific HDAC targeted by HDACi leading to therapy sensitization.

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

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

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

252 ylates HDAC3 at Ser-424, thereby stimulating HDAC activity.

253 nt to consider when utilizing this synthetic HDAC.

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

255 on of five conserved amino acids in the Tcf1 HDAC domain diminishes HDAC activity and the ability to

256 hematologic and nonhematologic toxicity than HDAC cycles.

257 Together, our results demonstrate that HDAC inhibition specifically induces IL-8/CXCL8 expressi

258 -2 and primary microglia, demonstrating that HDAC enzymes are required for LPS silencing of Rgs10 Fur

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

260 Accordingly, we found that HDAC inhibiting proteins from human herpesviruses induce

261 ects of broadly acting HDACi vary, such that HDAC isoform-selective targeting is likely required.

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

263 P following passive stretch, suggesting that HDACs block MLP nuclear accumulation.

264 It has been thought that HDACs associate with corepressor complexes and repress g

265 ibitor or small interfering RNAs against the HDAC Rpd3 into young major brains induced and sustained

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

267 hich bind in a pocket sandwiched between the HDAC and co-repressor proteins.

268 RA arm and 31.0% (95% CI, 19% to 43%) in the HDAC arm (HR, 0.63; 95% CI, 0.41 to 0.98; P = .043).

269 be modulated by the expression level of the HDAC-associated Clr1 domain alone.

270 relapse observed in the CLARA arm versus the HDAC arm (33.9% v 46.4% at 2 years, respectively; cause-

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

272 Targeting the HDACs by using either RNA interference against HDAC1 in

273 ng a novel CSC model, we discovered that the HDACs, HDAC1 and HDAC7, are specifically over-expressed

274 Our data reveal that the inhibition of these HDACs with small molecule HDAC inhibitors (HDACi), as we

275 mly assigned to receive three CLARA or three HDAC consolidation cycles.

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

277 in cell proliferation and sensitize cells to HDAC inhibition.

278 er whose upregulation had similar effects to HDAC inhibition.

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

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

281 ein 2 (cIAP2) was upregulated in response to HDAC inhibition and was validated as a new MRE11 binding

282 d mediated radiosensitization in response to HDAC inhibition.

283 rmediate induced and degraded in response to HDAC inhibition.

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

285 65P, conferred increased cell sensitivity to HDAC inhibitors.

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

287 ne deacetylation by an inhibitor specific to HDACs 1-3, CI-994, correlates with increased processing

288 tored nuclear HDAC2 protein levels and total HDAC activity, and it diminished the total histone acety

289 LPS/IFN-gamma also decreased total HDAC activity but increased the total histone acetyltran

290 e significantly and reversibly reduced total HDAC activity in vitro (in nuclear extracts) and in vivo

291 t NF-kappaB was modified by acetylation upon HDAC inhibition, partly by the histone acetyltransferase

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

293 Acetylated STAT3 emerged upon HDAC inhibition was protected from the proteasome-mediat

294 However, the molecular mechanisms by which HDAC inhibition (HDACi) induces tumor cell death remain

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

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

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

298 ough either of these methods synergizes with HDAC inhibition, and DIPG cells resistant to HDAC inhibi

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

300 ur findings indicate that WRN interacts with HDACs 1 and 2 to facilitate activity of stalled replicat