ライフサイエンスコーパス: HDAC1

1 HDAC1 and -2 form homo- and heterodimers, and their acti

2 HDAC1 and 2 were coimmunoprecipitated with several splic

3 HDAC1 and HDAC2-deficient T helper type 0 (TH0) and TH1

4 HDAC1 associates with chromatin by protein-protein inter

5 HDAC1 expression in RASFs was inhibited using small inte

6 HDAC1 in particular has been linked to cell growth and c

7 HDAC1 inhibition triggered an increase in H3K9/14 acetyl

8 HDAC1 is a transcriptional corepressor that acts to sile

9 HDAC1 may be an essential epigenetic regulator of the tr

10 HDAC1 mutations that mimic a constitutively acetylated s

11 HDAC1 protein, but not mRNA, is reduced in cell and anim

12 HDAC1(KD) resulted in reduced proliferation, invasion an

13 HDAC1/2 activity is regulated through binding of an inos

14 HDAC1/2 and KAT2B were associated with nascent pre-mRNA

15 Histone deacetylase 1 (HDAC1) and HDAC2 are components of corepressor complexes

16 d with high levels of histone deacetylase 1 (HDAC1) and HDAC2 proteins in HCC patient tissues.

17 urotoxic potential of histone deacetylase 1 (HDAC1) and its subcellular localization are not fully un

18 methyltransferase and histone deacetylase 1 (HDAC1) and the disruption of their occupancy at p53 targ

19 sm analyses show that histone deacetylase 1 (HDAC1) interacts with Daxx and binds to the promoter of

20 HDACs and found that histone deacetylase 1 (HDAC1) is a key regulator of TAp73 protein stability.

21 ced ubiquitination of histone deacetylase 1 (HDAC1) mediates VC.

22 protein 4 (CHD4) and histone deacetylase 1 (HDAC1) occupy the promoters of several of these hypermet

23 ain of Slug, impeding histone deacetylase 1 (HDAC1) recruitment and antagonizing Slug E-box binding.

24 omoters and increased histone deacetylase 1 (HDAC1) recruitment, thereby decreasing transcription at

25 of MRG15, Sin3B, and histone deacetylase 1 (HDAC1) that functions as a transcriptional modulator.

26 ne 1) cooperates with histone deacetylase 1 (HDAC1) to regulate Nanog expression.

27 ctivity by recruiting histone deacetylase 1 (HDAC1) to the protein complexes.

28 2 gene and recruiting histone deacetylase 1 (HDAC1) to this region.

29 ent nuclear export of histone deacetylase 1 (HDAC1) was shown previously to precede axonal damage in

30 rect interaction with histone deacetylase 1 (HDAC1), and the recruitment of FUS to double-stranded br

31 modifiers, including histone deacetylase 1 (HDAC1), SET domain, bifurcated 1 (SETDB1), DNA methyltra

32 tions between FUS and histone deacetylase 1 (HDAC1).

33 pUL97 associates with histone deacetylase 1 (HDAC1).

34 ding protein beta and histone deacetylase 1 (HDAC1).

35 ial morphogenesis is histone deacetylase-1- (HDAC1) dependent and that interstitial flow increases th

36 on and invasion by inhibiting the HIF-1alpha/HDAC1/Slug pathway.

37 act as a repressor in controlling HIF-1alpha/HDAC1/Slug-mediated cancer cell invasion and is a potent

38 Here we show histone deacetylases 1 and 2 (HDAC1 and HDAC2) as crucial regulators of this process.

39 including the histone deacetylases 1 and 2 (HDAC1 and HDAC2), and is defined by the presence of a CH

40 ecruiting histone deacetylases HDAC 1 and 2 (HDAC1/2) and nucleosome remodeling and deacetylase compl

41 show here that histone deacetylases 1 and 2 (HDAC1/2) are essential for the specification of neural c

42 Histone deacetylases 1 and 2 (HDAC1/2) form the core catalytic components of corepress

43 Histone deacetylase 1 and 2 (HDAC1/2) regulate chromatin structure as the catalytic c

44 o and inhibits histone deacetylases 1 and 2 (HDAC1/2).

45 se1/3 (DNMT1/3)-, histone deacetylase 1/2/4 (HDAC1/2/4)-, Setdb1/Suv39h1-, and Ezh1/2-containing comp

46 oter in progenitor cells, whereas acetylated HDAC1, which is inactive, is on the silenced PU.1 promot

47 We found that active HDAC1 is directly recruited to active PU.1 promoter in p

48 In addition, HDAC1/2 were bound to the P0 promoter and activated P0 t

49 and has a selectivity index of >200 against HDAC1 and HDAC8.

50 d HDAC8 activities that are inactive against HDAC1.

51 ACs by using either RNA interference against HDAC1 in CLL or a small molecule inhibitor (HDACi) in CL

52 i were the most potent and selective against HDAC1.

53 AC6) and is 60-fold more active than against HDAC1 and 223-fold more active than against HDAC2.

54 .005), FKBP12 (p < 0.03), ID (p < 0.03), and HDAC1 (p < 0.002).

55 BV-2 microglia following LPS activation, and HDAC1 association at the Rgs10 promoter is enhanced foll

56 mplex increases translation of C/EBPbeta and HDAC1, resulting in an increase of C/EBPbeta-HDAC1 compl

57 hrough the interaction with NF-kappaBp50 and HDAC1 in HSCs.

58 trate normal localization to the nucleus and HDAC1 interaction.

59 Lnc34a recruits Dnmt3a via PHB2 and HDAC1 to methylate and deacetylate the miR-34a promoter

60 demonstrate that the recruitment of PIP2 and HDAC1 to WT1 target genes is also dependent on the conce

61 e in leukaemia, which also recruits PRCs and HDAC1 to regulate p16(INK4a).

62 (INK4a) transcription by recruiting PRCs and HDAC1.

63 ssive complex composed of LSD1, Co-REST, and HDAC1.

64 he binding among TRIM28, DNMT3A, SETDB1, and HDAC1.

65 ANT domains from MTA1 wrap completely around HDAC1 occupying both sides of the active site such that

66 ific epigenetic repressor and its associated HDAC1 from deacetylating and suppressing E2F1.

67 g intracellular residence times for FK228 at HDAC1, explaining the protracted intracellular behaviour

68 Furthermore, because HDAC1 and -2 are overexpressed in several types of cance

69 ation of CCAAT/enhancer binding protein beta-HDAC1 complexes in the development of liver cancer media

70 Both HDAC1 and HDAC3 are stably associated with PPARgamma in

71 In the mouse brain, HDAC1 and HDAC2 exhibit different developmental stage- a

72 as present in BRG1-BAF155 complexes and BRG1-HDAC1 interactions were enriched in the trophoblast line

73 for the enhanced cell migration mediated by HDAC1 knockdown.

74 mice, the inhibition of TERT is mediated by HDAC1-C/EBPalpha complexes.

75 ter understand the key pathways regulated by HDAC1/2 in the adaptive immune system and inform their e

76 vel regulation of TAp73 protein stability by HDAC1-heat shock protein 90 chaperone complex, and our d

77 In neural crest cells, HDAC1/2 induced expression of the transcription factor P

78 In contrast, HDAC1 inhibits HSF1 in a deacetylase-independent manner.

79 In contrast, HDAC1/2 regulated gene expression during the transition

80 olymerase II and transcriptional corepressor HDAC1 on endogenous ER target gene promoter in the prese

81 hances expression of the histone deacetylase HDAC1 and DNA methyl transferases DNMT3b and DNMT1.

82 d for recruitment of the histone deacetylase HDAC1 to repress transcription of the gene encoding C/EB

83 n the recruitment of the histone deacetylase HDAC1 to this intronic site.

84 neuroprotective class I histone deacetylase HDAC1.

85 demethylase JARID1B and histone deacetylase HDAC1.

86 , acting by association with the deacetylase HDAC1.

87 oter and recruiting the histone deacetylase, HDAC1.

88 The histone deacetylases HDAC1 and HDAC2 are crucial regulators of chromatin stru

89 e show that the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of

90 by the activity of the histone deacetylases HDAC1 and HDAC2.

91 ependent recruitment of histone deacetylases HDAC1/5, inhibiting Nkx2.5 expression.

92 Class I histone deacetylases (HDAC1, HDAC2, and HDAC3) are recruited by cognate corepr

93 We found that SIRT1 deacetylated HDAC1 and stimulated its enzymatic activity, which was n

94 tive but not inactive pUL97 kinase decreased HDAC1 interaction with the transcriptional repressor pro

95 is a key transcription factor that delivers HDAC1 to gankyrin promoter and causes epigenetic silenci

96 ing, reveals the architecture of the dimeric HDAC1:MTA1:RBBP4 assembly which forms the core of the Nu

97 evaluation of potent hydroxamate-based dual HDAC1/6 inhibitors with modest HDAC6 preference and a no

98 The C/EBPbeta-HDAC1 complexes also repress promoters of enzymes of glu

99 cells and in mouse livers reduces C/EBPbeta-HDAC1 complexes and activates the gankyrin promoter.

100 HDAC1, resulting in an increase of C/EBPbeta-HDAC1 complexes at later stages of liver cancer.

101 ound that the proper regulation of C/EBPbeta-HDAC1 complexes is required for the maintenance of biolo

102 es a tight regulation of levels of C/EBPbeta-HDAC1 complexes on the levels of transcription, translat

103 We found that C/EBPbeta-HDAC1 complexes repress promoters of three key regulator

104 hibiting the gankyrin promoter via C/EBPbeta-HDAC1 complexes, leading to subsequent protection of tum

105 FXR, SIRT1, PGC1alpha, and TERT by C/EBPbeta-HDAC1 complexes.

106 21b triggered the depletion of EGFR, HDAC1, and p70S6 kinase from the cancer cells, with pote

107 Loss of either HDAC1 or HDAC2 alone has little effect, while dual inact

108 Excessive HDAC1 activity, due to developmental defects or other fa

109 ring mitosis, HDAC2 and, to a lesser extent, HDAC1 phosphorylation levels dramatically increase.

110 e first demonstration of a specific role for HDAC1 and -2 in the induction of type I interferon respo

111 us, these results demonstrate a key role for HDAC1 in PU.1 gene transcription and, more importantly,

112 These data demonstrate a crucial role for HDAC1/2 in T-cell development and the maintenance of gen

113 nstrate that transcription of one such gene, HDAC1, is dependent on FGF signalling, making a novel li

114 ion of Pax3 and Sox10 on their target genes, HDAC1/2 direct the specification of neural crest cells i

115 s or enhancer regions of RA-regulated genes; HDAC1, HDAC2, and HDAC3 bind at RAREs in the Hoxa1 and C

116 e major class I histone deacetylases (HDACs) HDAC1 and HDAC2 can act to suppress tumors in mouse thym

117 ed with the two histone-deacetylases (HDACs) HDAC1 and HDAC2 on the ncx1-Br, with a consequent hypoac

118 proach using mice lacking the class I HDACs, HDAC1 or HDAC2, in postmitotic forebrain neurons to inve

119 vel CSC model, we discovered that the HDACs, HDAC1 and HDAC7, are specifically over-expressed in CSCs

120 e Schizosaccharomyces pombe HDAC Clr6 (human HDAC1) binds to different sets of proteins that define f

121 ntrast to HDAH, all compounds bound to human HDAC1, HDAC6, and HDAC8 through a two-step mechanism.

122 roliferation-associated genes and of class I HDAC1 and 2, highlighting a hierarchical control between

123 Further analysis identified HDAC1/HDAC9 as well as BRD8 and DNA-PK as important regu

124 after hydroxyurea treatment, and identified HDAC1, a member of the class I histone deacetylase famil

125 Together, our data identify HDAC1 and the phosphorylation of specific serine residue

126 These results implicate HDAC1 as an important mediator of tissue damage in RA an

127 ition, these mutagenesis studies will aid in HDAC1-inhibitor design that exploits the 14 A cavity.

128 uggest that corepressor complexes, including HDAC1 or HDAC2 homodimers, might target different cellul

129 ed multiple corepressor complexes, including HDAC1/2-containing Sin3B, nucleosome remodeling and hist

130 bit class II and/or class I HDACs, including HDAC1, 2, 3, and 6.

131 nduces depletion of class I HDACs, including HDAC1, 2, 3, and 8, to overcome latency in macrophages.

132 letion of pUL97 kinase resulted in increased HDAC1 and decreased histone H3 lysine 9 acetylation asso

133 of MageB2 to interact with the E2F inhibitor HDAC1.

134 d by MDM2 E3 ubiquitin ligase that initiates HDAC1 K74 ubiquitination.

135 Interestingly, HDAC1 and -2 are deregulated in cancer and are attractiv

136 chromatin structure, and a DAXX-SETDB1-KAP1-HDAC1 complex that represses endogenous retroviruses ind

137 d to this region as part of the NF-kappaBp50-HDAC1 complex, repressing transcriptional activity of th

138 that LPS- and TNF-alpha-induced NF-kappaBp50-HDAC1 interaction represses BAMBI transcriptional activi

139 s (MEFs) recruited cytoplasmically localized HDAC1 to the nucleus.

140 , together, our data suggest that an ATX-LPA-HDAC1/2 axis regulates OLG differentiation specifically

141 uitination pathway and suggest MDM2-mediated HDAC1 ubiquitination as a new therapeutic target in VC.

142 ysoPLD activity of ATX was found to modulate HDAC1/2 regulated gene expression during a time window c

143 The amino acid residues modulating HDAC1 subcellular localization were identified by site-d

144 (ATX) as a novel upstream signal modulating HDAC1/2 activity and gene expression in cells of the OLG

145 ing transcriptional repressor complex mSin3A-HDAC1 at the proximal promoter region of OGA and corresp

146 genomic context and is mediated by multiple HDAC1-containing corepressor complexes.

147 opment-related genes, including CDK6, c-MYC, HDAC1 and BCL-2, are targets of miR-449b.

148 gulate the expression levels of CDK6, c-MYC, HDAC1 and BCL-2.

149 Thus, nonphosphorylated HDAC1/2 is recruited to pre-mRNA by splicing factors to

150 Transient overexpression of HDAC3, but not HDAC1 or HDAC2, significantly reduced sGCbeta1 mRNA.

151 tic modulators orchestrate the activation of HDAC1 and HDAC2 promoter activity in colon cancer cells.

152 approximately 35% of the total activities of HDAC1, 2, 3, and 6 in the retina.

153 t abolish IP4 binding reduce the activity of HDAC1/2 in vivo.

154 Daxx silencing decreases the association of HDAC1 to IL-6 promoter.

155 pitation studies revealed the association of HDAC1, DNMT3b, DNMT1, and mSin3A with SNAIL.

156 vivo showed significantly reduced binding of HDAC1 and -2 and increased accumulation of acetylated H3

157 rate that specific and prolonged blockade of HDAC1 in NAc of mice increased global levels of histone

158 Combined deficiency of HDAC1 and 2 rescued attenuated replication and viral DNA

159 ucing conditions, proteasomal degradation of HDAC1 precedes VC and it is mediated by MDM2 E3 ubiquiti

160 Consistently, in vivo genetic deletion of HDAC1/2 in mouse neural crest cells led to strongly decr

161 in infected macrophages induced depletion of HDAC1 and 3 on the HIV-1 LTR that was associated with hy

162 nes were activated by selective depletion of HDAC1 and HDAC2.

163 onsidered during the clinical development of HDAC1- and -2-specific inhibitors.

164 ctivity against HDAC6 or HDAC8 but devoid of HDAC1 inhibition.

165 on by phosphorylation-mediated disruption of HDAC1 binding to the MIE promoter.

166 rown adipocytes results in a dissociation of HDAC1 from promoters of BAT-specific genes, including un

167 Additionally, downregulation of HDAC1, an increase in the level of histone H3 acetylatio

168 d bone destruction and determined effects of HDAC1 inhibition on both RASF phenotype in vitro, and jo

169 Effects of HDAC1 knockdown (KD) on the transcriptome were assessed

170 indings illuminate potential side effects of HDAC1- and -2-specific inhibitors that are currently und

171 well as the specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRN

172 In this study, we show that expression of HDAC1 and -2 by macrophages is required to mount a type

173 enetic approaches to show that expression of HDAC1 and -2 is critical for induction of a type I inter

174 Specifically, expression of HDAC1 and -2 was required for phosphorylation of interfe

175 n inverse relationship between expression of HDAC1 and 2 and these TSGs in a large panel of primary c

176 Expression of HDAC1 was significantly higher in RASFs than OASFs.

177 One of the functions of HDAC1, which it performs together with a close homolog H

178 The co-chromatin immunoprecipitation of HDAC1/2 and SRSF1 to the gene body was RNA-dependent.

179 tures of the CD8(+) lineage independently of HDAC1 and HDAC2.

180 Furthermore, inhibition of HDAC1 in CIA resulted in reduced joint swelling, cartila

181 Inhibition of HDAC1 resulted in increase of acetylation of lysine 9 of

182 NCoR2, in vitro assays for the inhibition of HDAC1, HDAC2, and HDAC3-NCoR2 by N-(2-aminophenyl)-benza

183 In vitro assays for the inhibition of HDAC1, HDAC2, HDAC3-NCoR1, and HDAC8 by the N-(2-aminoph

184 l four compounds showed potent inhibition of HDAC1-3 as well as significant inhibition of HDAC6 with

185 d Npr1 gene expression through inhibition of HDAC1/2 and increased both acetylation of histones (H3-K

186 Inhibition of HDAC1/2/3 caused sensitization of melanoma cells to temo

187 IFN-gamma-induced interaction of HDAC1 and p53 resulted in the deacetylation of p53 and s

188 The involvement of HDAC1 and -2 in the type I interferon response highlight

189 C cells with HDAC inhibitors or knockdown of HDAC1 and/or HDAC2 restored FBP1 expression and inhibite

190 can be upregulated by specific knockdown of HDAC1 or HDAC3.

191 Knockdown of HDAC1 or inhibition of HDAC activity at least partially

192 Inhibition of HDAC activity and knockdown of HDAC1, HDAC2 or SRSF1 showed that these proteins were in

193 shRNA knockdown of HDAC1, HDAC2, or HDAC3 differentially increases the depo

194 nt melanomas in situ contain a high level of HDAC1/2 and malignant melanoma cells overexpress HDAC1/2

195 In aging cells, the levels of HDAC1 are elevated and the HSR is impaired, yet reductio

196 Loss of HDAC1 activity via either chemical inhibitor or genetic

197 Loss of HDAC1 and HDAC2 during late T cell development led to th

198 Loss of HDAC1/2 resulted in a 60% reduction in total HDAC activi

199 We then studied the mechanism of HDAC1-mediated activation.

200 t TAp73 is a critical downstream mediator of HDAC1-regulated cell migration.

201 potential posttranslational modifications of HDAC1 remained elusive.

202 is also observed with a catalytic mutant of HDAC1; however, it does not correlate with changes in hi

203 Overexpression of HDAC1 and HDAC2 significantly attenuated Npr1 promoter a

204 tein kinase CK2-catalyzed phosphorylation of HDAC1 and -2 is crucial for the dissociation of these tw

205 Phosphorylation of HDAC1 and/or HDAC2 in interphase cells is required for t

206 The physiological phosphorylation of HDAC1 was decreased by neurotoxic stimuli, which stimula

207 titial flow increases the phosphorylation of HDAC1, its activity, and its export from the nucleus.

208 odifications at this site via recruitment of HDAC1.

209 ed and the HSR is impaired, yet reduction of HDAC1 in aged cells restores the HSR.

210 68 mutant, indicating that the regulation of HDAC1 and 2 by orf36 was relevant for viral replication.

211 nic lines to define the in vivo relevance of HDAC1 and identify calcineurin-dependent serine dephosph

212 e of gammaherpesvirus infection, the role of HDAC1 and -2 in the induction of type I interferon respo

213 the signal modulating the neurotoxic role of HDAC1 in response to neurotoxic stimuli.

214 aling axis, pointing to the critical role of HDAC1/2-NuRD activity in peripheral neuropathies caused

215 To dissect the individual roles of HDAC1 and HDAC2, we expressed single alleles of either H

216 The skin of HDAC1 null (K14-Cre Hdac1(cKO/cKO)) mice exhibited a spe

217 Here we report the structure of HDAC1 in complex with MTA1 from the NuRD complex.

218 Importantly, targeting of HDAC1 and 2 by orf36 was independent of the kinase's enz

219 Once HDAC1 is tethered, histone acetyltransferase p300 is no

220 yp26a1 gene regulatory regions, whereas only HDAC1 binds at the RARbeta2 RARE.

221 for HDAC6 with up to 15-fold preference over HDAC1, >3500-fold selectivity over HDAC4, and >100-fold

222 1/2 and malignant melanoma cells overexpress HDAC1/2/3 compared with noncancer cells.

223 its associated transcription cofactors p300/HDAC1 to these co-regulated genes, thereby altering the

224 tion designed to selectively disrupt p50:p50:HDAC1 complexes are more susceptible to HCC; by contrast

225 on and enhanced recruitment of NF-kappaB p52-HDAC1 repressor complexes to the cyclin D1 promoter.

226 resulted in nuclear accumulation of phospho-HDAC1 and was neuroprotective.

227 s in 112/243 (46%) of patients predominantly HDAC1-11 (41%) alterations.

228 armacological SIRT1 activators that promoted HDAC1 deacetylation also reduced DNA damage in two mouse

229 heir inhibitory activity against recombinant HDAC1-3, HDAC6, and HDAC8.

230 , repressing its transcription by recruiting HDAC1 and licensing the removal of activating histone ac

231 e, Zeb2 controls SC maturation by recruiting HDAC1/2-NuRD complexes and inhibiting a Notch-Hey2 signa

232 n3A rather than Sds3 functions in recruiting HDAC1 into the complex by engaging the latter through a

233 Furthermore, RARalpha-PLZF recruits HDAC1 and causes histone H3 deacetylation at C/EBPalpha

234 Furthermore, mice with reduced HDAC1/2 activity (Hdac1 deleted and a single Hdac2 allel

235 stingly, Sp1 and Sp3 differentially regulate HDAC1 and HDAC2 promoter activity.

236 anistic study, CQ was found to down-regulate HDAC1, -3, -4, and -5 in both myeloma and leukemia cells

237 ting via p50:p50 dimers and the co-repressor HDAC1.

238 ive complex 2 (PRC2) and ZNF198/LSD1/Co-REST/HDAC1 chromatin-modifying complexes.

239 promoter, a target of PRC2 and LSD1/Co-REST/HDAC1 complexes.

240 NCX1 expression is regulated by the Sp3/REST/HDAC1/HDAC2 complex in tMCAO and by the Sp1/HIF-1/p300 c

241 lation of SMAR1 ensures recruitment of SMAR1-HDAC1 repressor complex at the LCR and E6 MAR sequences,

242 ssion of Slug by direct recruitment of SMAR1/HDAC1 complex to the matrix attachment region site prese

243 Decoy peptide spanning HDAC1 K74 and RG 7112, an MDM2 inhibitor, prevent VC in

244 romatin bridges, and micronuclei, suggesting HDAC1/2 are necessary for accurate chromosome segregatio

245 Targeting HDAC1 may be beneficial in prevention and treatment of o

246 A combined approach targeting HDAC1/HDAC2 and MYC may present a novel and molecularly

247 available HDAC inhibitors (HDACi) targeting HDAC1 and HDAC7 can be used to preferentially target CSC

248 These results demonstrate that HDAC1 and HDAC2 maintain integrity of the CD4 lineage by

249 Here, we demonstrate that HDAC1 is a negative regulator of the brown adipocyte the

250 Biochemical studies demonstrated that HDAC1 was present in BRG1-BAF155 complexes and BRG1-HDAC

251 Furthermore, we determine that HDAC1 and HDAC7 are necessary to maintain CSCs, and that

252 We discovered that HDAC1 activates PU.1 gene transcription via deacetylatio

253 In this study, we found that HDAC1 and HDAC2 promoters are regulated through collabor

254 We also found that HDAC1 is bound to this region as part of the NF-kappaBp5

255 ally, using mass spectrometry, we found that HDAC1 is uniquely phosphorylated upon expression of pUL9

256 Mechanistically, we found that HDAC1 knockdown resulted in hyperacetylation and inactiv

257 Our data indicate that HDAC1 and HDAC2 have a common function in maintaining pr

258 Our data indicate that HDAC1/2 have essential and pleiotropic roles in cellular

259 n immunoprecipitation analysis revealed that HDAC1 and HDAC2 are present on the miR-133a enhancer reg

260 We show that HDAC1 depletion exacerbates defects in fork reactivation

261 Furthermore, we show that HDAC1 inhibition decreases endothelial morphogenesis and

262 We further show that HDAC1, HDAC2 and MYC directly bind to the TP53 gene and

263 Specifically, we showed that HDAC1 inhibition by HDAC inhibitors or by siRNA shortene

264 Postmortem brain studies have shown that HDAC1-a lysine deacetylase with broad activity against h

265 Our data suggest that HDAC1 inhibition should be considered as a therapeutic a

266 Our results suggest that HDAC1 modulates angiogenesis in response to flow, provid

267 Based on our results, we suggest that HDAC1-specific inhibition prevents progenitor cells of t

268 The HDAC1 active site contains a hydrophobic 11 A active-sit

269 Functional assays of both the HDAC1 and HDAC3 complexes reveal that Ins(1,4,5,6)P4 is

270 vitro and in vivo and was phenocopied by the HDAC1/2-specific agent RGFP233.

271 as a dimeric chromatin binding module in the HDAC1:MIDEAS corepressor complex.

272 tand the influence of amino acids lining the HDAC1 14 A cavity in acetate escape and inhibitor bindin

273 HDAC5 is required for the interaction of the HDAC1/2/Sin3a co-repressor complexes with the Nkx2.5 and

274 factors and critical for recruitment of the HDAC1/Sin3a co-repressor complex to either the Ncx1 or B

275 interacts with and mediates assembly of the HDAC1:MIDEAS complex.

276 The crystal structure of the HDAC1:MTA1 complex bound to a novel peptide-based inhibi

277 n by IFRD1 shRNA, cetuximab treatment or the HDAC1/3 inhibitor entinostat increases basal and induced

278 Further, SET1 KD reduces Sp1 binding to the HDAC1 promoter through the increase of Sp1 acetylation.

279 on brain and muscle samples treated with the HDAC1/3-targeting inhibitor, HDACi 4b.

280 s by silencing the gankyrin promoter through HDAC1-C/EBPbeta complexes.

281 ctively represses IL-6 transcription through HDAC1-mediated histone deacetylation in LPS-induced macr

282 Thus, HDAC1 negatively regulates the brown adipocyte thermogen

283 xploration of the responsible HDAC member to HDAC1, HDAC2, or HDAC3.

284 encing activity by recruitment of the TRIM28/HDAC1/SETDB1/DNMT3A/DNMT3L complex to newly integrated M

285 ed that MTA1 represses DNMT3a expression via HDAC1/YY1 transcription factor complex.

286 in vitro and in melanoma xenografts in vivo HDAC1/2/3 inhibition resulted in suppression of DNA doub

287 When HDAC1 and -2 are displaced from the chromosome during me

288 ion of these genes suggests a model in which HDAC1/2 deficiency results in defective propagation of T

289 markedly reduced co-immunoprecipitation with HDAC1 and HDAC3, markedly increased stability in cyclohe

290 Furthermore, the ability to interact with HDAC1 and 2 was not limited to the MHV68 orf36, as BGLF4

291 encoded protein kinase orf36 interacted with HDAC1 and 2 and prevented association of these HDACs wit

292 coded by Epstein-Barr virus, interacted with HDAC1 in vitro.

293 air and showed a diminished interaction with HDAC1.

294 ilson syndrome disrupts the interaction with HDAC1/2-NuRD and abolishes Zeb2 activity for SC differen

295 mmaherpesvirus protein kinase interacts with HDAC1 and -2 to promote gammaherpesvirus replication in

296 ith histone deacetylases, in particular with HDAC1.

297 WRN co-precipitates with HDAC1 and HDAC2.

298 HDACi attenuated the interaction of Sp1 with HDAC1/2 and promoted Sp1 association with p300 and p300/

299 The additive WRN, HDAC1 loss-of-function phenotype is also observed with a

300 rs of E-cadherin expression, including ZEB1, HDAC1, and MMP14.