ライフサイエンスコーパス: HDAC1

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

2 HDAC1 and HDAC3 then mediated histone deacetylation at c

3 HDAC1 decreased the acetylation of S6 kinase and mimicke

4 HDAC1 deficiency causes impaired OGG1 activity, 8-oxoG a

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 may be an essential epigenetic regulator of the tr

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

10 HDAC1 stimulates OGG1, a DNA glycosylase known to remove

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

12 HDAC1-deficient mice display age-associated DNA damage a

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 responsible for reducing H4 acetyla

16 eased accumulation of histone deacetylase 1 (HDAC1) and HDAC2 at the Cd86 locus.

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

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

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

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

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

22 s also observed after histone deacetylase 1 (HDAC1) or HDAC2 was depleted by RNA interference or inhi

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 -transferase P300 and histone deacetylase 1 (HDAC1) to circularized HBV DNA (which resembles covalent

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

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

29 2 gene and recruiting histone deacetylase 1 (HDAC1) to this region.

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

31 irectly phosphorylate histone deacetylase 1 (HDAC1), as well as T cell factor/lymphoid enhancer-bindi

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

33 protein 2 (ASPP2) and histone deacetylase 1 (HDAC1), were also identified.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

48 i were the most potent and selective against HDAC1.

49 In contrast, siRNA against HDAC1 inhibited these effects by high glucose.

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

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

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

53 pical protein kinase Ciota/lambda (aPKC) and HDAC1.

54 omplex, which includes MTA1, MBD3, CHD4, and HDAC1 among other components, is of importance for devel

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

56 recruits the epigenetic modifiers KDM1A and HDAC1 to the promoter regions of LAMB3 and CTNNAL1, infl

57 otent inhibition activities against mTOR and HDAC1 with half-maximal inhibitory concentration of 1.2

58 ivities against BRD4 BD1 (IC(50) =11 nm) and HDAC1 (IC(50) =21 nm).

59 trate normal localization to the nucleus and HDAC1 interaction.

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

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

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

63 in SK-RC-45 cells was accompanied by Sp1 and HDAC1 loss from the +38/+187 region.

64 d reduced phosphorylation of LEF1 as well as HDAC1 among NLK-deleted SP CD8(+) cells.

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

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

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

68 Both HDAC1 and HDAC3 are stably associated with PPARgamma in

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

70 D to counteract their upregulation driven by HDAC1/-2 inhibition.

71 hese phenotypic alterations are initiated by HDAC1 in GBM core cells which subsequently affect edge c

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

73 nce and that deacetylation of these sites by HDAC1 decreases protein levels.

74 ners: (a) Plectin1/STAT1, (b) ASPP2, and (c) HDAC1/GADD45alpha signaling pathways.

75 wnregulating MUC1-C decreased MTA1/MBD3/CHD4/HDAC1 occupancy and increased H3K27 acetylation on the E

76 Loss of CHD7-HDAC1/2-dependent cNHEJ reinforces 53BP1 assembly at the

77 Importantly, complementing HDAC1 and HDAC3 in Twist1/Twist2-deficient monocyte-deri

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

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

80 the transcription factor Sp1 and corepressor HDAC1 associated with the +38/+187 region when the GM2-s

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

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

83 OCKI-APEX1 recruited the histone deacetylase HDAC1, which removed the H3K27ac modification from the p

84 , acting by association with the deacetylase HDAC1.

85 oter and recruiting the histone deacetylase, HDAC1.

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

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

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

89 to the promoters of the histone deacetylases HDAC1 and HDAC3 and induced HDAC1 and HDAC3 expression.

90 tly, we identified that histone deacetylases HDAC1 and HDAC7 are necessary to maintain cancer stem ce

91 n to associate with the histone deacetylases HDAC1/2 and the histone demethylase LSD1, enzymes that a

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

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

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

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

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

97 21b triggered the depletion of EGFR, HDAC1, and p70S6 kinase from the cancer cells, with pote

98 reduced, which was associated with elevated HDAC1, HDAC4, and SIRT1 in colon adenocarcinomas.

99 ment of chromatin to the deacetylase enzyme, HDAC1/2.

100 way, we found that histone modifying enzymes HDAC1 and KDM5A play critical, regulatory roles in this

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

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

103 Our work uncovers important roles for HDAC1 in 8-oxoG repair and highlights the therapeutic po

104 like behavior, and that class I HDACs (e.g., HDAC1 and HDAC2) are most important in this response.

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

106 expression and regulation of class I HDACs (HDAC1, HDAC2, HDAC3 and HDAC8) was performed in cardiopu

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

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

109 deling complex (LSD1, RCOR1, HMG20A, HMG20B, HDAC1, HDAC2, PHF21A, GSE1, ZMYM2, and ZNF217) in an LSD

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

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

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

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

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

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

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

117 axation around DNA break sites and brings in HDAC1/2 for localized chromatin de-acetylation.

118 Importantly, we confirmed changes in HDAC1 expression in the NAc of depressed patients withou

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

120 proteins recruit K7 deacetylases, including HDAC1.

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

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

123 ificantly reduced concomitant with increased HDAC1 and S6 kinase activity.

124 one deacetylases HDAC1 and HDAC3 and induced HDAC1 and HDAC3 expression.

125 of MageB2 to interact with the E2F inhibitor HDAC1.

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

127 tent inhibition of the class I HDAC isoforms HDAC1, HDAC2, and/or HDAC3 and promising antiproliferati

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

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

130 ciferase activity of this region by limiting HDAC1 recruitment.

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

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

133 repressed targets of the epigenetic markers HDAC1, HDAC3 and EZH2 were further suppressed by LPS tre

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

135 nced the recruitment of the histone modifier HDAC1 at the Il9 gene promoter.

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

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

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

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

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

141 d, 3d (IC(50), 4 nM, HDAC6; IC(50) > 10 muM, HDAC1), substantially increased acetylation of alpha-tub

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

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

144 an class I HDACs (e.g., JT86, IC(50) 0.7 nM, HDAC1), 25-fold increased cytotoxicity against five huma

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

146 his mark from removal and that HDAC2 but not HDAC1 can effectively compete with ATAD2 for the target

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

148 AC4 or catalytically inactive HDAC4, but not HDAC1 or HDAC5.

149 n RNAi approach, we find that HDAC2, but not HDAC1, inhibition in the ventral tegmental area (VTA) is

150 Notably, pharmacological activation of HDAC1 alleviates the deleterious effects of 8-oxoG in ag

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

152 increased the expression and association of HDAC1 with S6 kinase.

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

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

155 Four copies of HDAC1 are positioned at the periphery with outward-facin

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

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

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

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

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

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

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

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

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

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

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

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

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

169 to investigate the CSC-specific function of HDAC1 and HDAC7 mechanistically by using a stem-like bre

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

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

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

173 ctivation, directly or through inhibition of HDAC1 and HDAC3, can result in the inhibition of the CSC

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

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

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

177 ld selectivity relative to the inhibition of HDAC1, HDAC4, and HDAC8), as rationalized by molecular m

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

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

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

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

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

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

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

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

186 Overexpression or knockdown of HDAC1, SIN3, or both resulted in a decrease or increase

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

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

189 Loss of HDAC1 activity via either chemical inhibitor or genetic

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

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

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

193 potential posttranslational modifications of HDAC1 remained elusive.

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

195 Overexpression of HDAC1 and HDAC2 significantly attenuated Npr1 promoter a

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

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

198 and highlights the therapeutic potential of HDAC1 activation to counter functional decline in brain

199 as unable to induce Kr-h1 in the presence of HDAC1 or SIN3.

200 odifications at this site via recruitment of HDAC1.

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

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

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

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

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

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

207 plausible site-specific repressive roles of HDAC1 and Sp1 in GM2-synthase mRNA expression.

208 n of histone acetylation and upregulation of HDAC1 expression were associated with the increased infl

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

210 Moreover, Sp1 or HDAC1 knock down increased GM2-synthase transcription, a

211 complex was a potent inhibitor of HDAC6 over HDAC1 and HDAC8.

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

213 1/2 and malignant melanoma cells overexpress HDAC1/2/3 compared with noncancer cells.

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

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

216 Particularly, HDAC1 and HDAC8 were consistently increased in IPAH-PAs

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

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

219 of several cellular factors (E2F6, E2F1, Rb, HDAC1, and HDAC2) together with EBV latent nuclear antig

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

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

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

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

224 ndent manner, HDAC inhibitors and RA reduced HDAC1, HDAC4, and sirtuin 1 (SIRT1), which were involved

225 e observe elevated 8-oxoG along with reduced HDAC1 activity and downregulation of a similar gene set

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

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

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

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

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

231 unrelated SANT domain in promoting the SAP30-HDAC1 interaction and enhancing HDAC activity.

232 tes with LAP2beta for GLI1 while scaffolding HDAC1 to deacetylate the secondary binding site.

233 d that CCND1 interacted with and sequestered HDAC1 and HDAC2 from the SOX11 locus, leading to SOX11 u

234 We show HDAC1/2/3 are the co-essential isoforms that when co-inh

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

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

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

238 tive inhibition of HDAC3/6, but not specific HDAC1, HDAC6, or HDAC8 inhibition, reproduced the suppre

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

240 um larvae and JH III to TcA cells suppressed HDAC1 expression.

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

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

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

244 injected with double-stranded RNA targeting HDAC1 (dsHDAC1).

245 A post mortem study confirmed that HDAC1 and HDAC2 paralogs are elevated in white matter ti

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

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

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

249 r hdac2-null fibroblasts, we determined that HDAC1 and HDAC2 do not fully compensate for each other i

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

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

252 We found that HDAC1 and HDAC3 inhibition or knockdown results in HDAC7

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

254 We found that HDAC1 knockdown or inactivation leads to increased RBPJ

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

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

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

258 We show that HDAC1 depletion exacerbates defects in fork reactivation

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

260 We show that HDAC1 modulates OGG1-initated 8-oxoguanine (8-oxoG) repa

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

262 d pulldown and NMR experiments, we show that HDAC1/2 deacetylase activity in one of the most ancient

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

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

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

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

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

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

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

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

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

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

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

274 ly we reported the results of studies on the HDAC1 containing CoREST complex and acetylated nucleosom

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

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

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

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

279 Thus, HDAC1 negatively regulates the brown adipocyte thermogen

280 re-activity relationships support binding to HDAC1 with tetrahydropyran acting as a hydrophobic shiel

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

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

283 the intestinal environment, TWIST1, TWIST2, HDAC1, and HDAC3 were upregulated in human intestinal re

284 In addition, we uncovered HDAC1 as a novel miR-22 target.

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 ults uncover a regulatory mechanism in which HDAC1 negatively regulates RBPJ binding on mitotic chrom

288 wild type) and an augmented association with HDAC1 (mean % input: 4.01-14.0% vs. 1.53% in wild type)

289 Rather, TET1 coordinates with HDAC1 to mediate the epigenetic changes to suppress ther

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

291 ulator of DeltaNp63alpha by interacting with HDAC1.

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

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

294 matin-bound nuclear fraction, interacts with HDAC1, HDAC2, and with the serine-threonine phosphatase

295 Mechanistically, interference with HDAC1/-2 elicited a suppression of c-Myc protein levels

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.