ライフサイエンスコーパス: HDAC2

1 itors or knockdown of histone deacetylase 2 (HDAC2).

2 s mediated mostly via histone deacetylase 2 (HDAC2).

3 d decrease of ROS production and increase of HDAC2.

4 WRN co-precipitates with HDAC1 and HDAC2.

5 reased expression of the histone deacetylase HDAC2.

6 tivity of the histone deacetylases HDAC1 and HDAC2.

7 he CD8(+) lineage independently of HDAC1 and HDAC2.

8 ession of a single allele of either Hdac1 or Hdac2.

9 kinase C, delta, which is a direct target of HDAC2.

10 HDAC1 and 223-fold more active than against HDAC2.

11 K14 promoter-mediated reduction of Hdac1 or Hdac2.

12 ound conditional knockout mice for Hdac1 and Hdac2.

13 of the genes regulated by S-nitrosylation of HDAC2.

14 ctivated by selective depletion of HDAC1 and HDAC2.

15 ithout its LZ domain failed to interact with HDAC2.

16 on can be partially rescued by siRNA against HDAC2.

17 g decreased cortical synaptic plasticity via HDAC2.

18 ) promoter, resulting in the upregulation of HDAC2.

19 nates HDAC2, leading to the stabilization of HDAC2.

20 scues susceptibility to stress by modulating HDAC2/3 activity and suggests that HDAC2/3 play opposite

21 On the contrary, HDAC2/3 inhibition was antidepressant-like.

22 is paradigm, lactate regulated HDAC5 and not HDAC2/3 levels.

23 odulating HDAC2/3 activity and suggests that HDAC2/3 play opposite roles before and after establishme

24 ase (HDAC) levels and activity, specifically HDAC2/3.

25 ceptor (GR-alpha) and histone deacetylase 2 (HDAC2), a corepressor important for glucocorticoid actio

26 HDAC2, a deacetylase, interacts with and keeps MORF4L1 i

27 4) c-Abl induces tyrosine phosphorylation of HDAC2, a posttranslational modification, affecting both

28 Strikingly, complete ablation of Hdac1 and Hdac2 abrogated lymphomagenesis due to a block in early

29 uclear and retinal ganglion cell layers, and HDAC2 activity accounted for approximately 35% of the to

30 with severe asthma, and smokers with asthma, HDAC2 activity and expression are reduced by oxidative s

31 o investigate whether selective reduction in HDAC2 activity can protect the retina from ischemic inju

32 A reduction in histone deacetylase 2 (HDAC2) activity and expression has been reported to play

33 HDAC1/2 activity (Hdac1 deleted and a single Hdac2 allele) develop a lethal pathology by 3-months of

34 deleted different combinations of Hdac1 and Hdac2 alleles in neural cells.

35 Loss of either HDAC1 or HDAC2 alone has little effect, while dual inactivation r

36 Postsynaptic KD of HDAC2 also facilitated expression of long-term potentiat

37 Histone deacetylase-2 (HDAC2), an epigenetic regulator, is critical for stress-

38 was associated with an increase in levels of HDAC2 and a decrease in histone (H3-K9) acetylation and

39 induces p300 dissociation, allowing histone HDAC2 and cofactor Sin3A to deacetylate these histones a

40 ssay to analyze the distribution patterns of HDAC2 and detect its levels in the cochlea.

41 H knockout pachytene oocytes exhibit reduced HDAC2 and DNMT-1.

42 Together, these studies identify HDAC2 and downstream targets for the development of nove

43 uced alteration of key epigenetic regulators HDAC2 and Ehmt2, which determines the synaptic and behav

44 vity, interacts with the histone deacetylase HDAC2 and ensures that the poised ZRS remains transcript

45 s with class I histone deacetylases 2 and 3 (HDAC2 and HDAC3) to regulate chromatin dynamics by maint

46 Knock-down of HDAC2 and HDAC3, but not other HDACs, increased BDNF mRN

47 ts in the proteasome-mediated degradation of HDAC2 and HDAC3, compromised chromatin maturation, as in

48 of beta-hydroxybutyrate is specifically upon HDAC2 and HDAC3, which act upon selective Bdnf promoters

49 ncreased in IPAH-PAs and IPAH-PAAFs, whereas HDAC2 and HDAC8 showed predominant localization with ACT

50 ity mediated, in part, by S-nitrosylation of HDAC2 and histone acetylation, such plasticity is absent

51 (HDACs) activity, reduced protein levels of HDAC2 and increased acetylation in miR-466h-5p promoter

52 Cholate induced binding of SHP to HDAC2 and its recruitment to the Cyp7a1 promoter; these

53 ell as enhanced recruitment of co-repressors HDAC2 and LSD1 to the WNT/beta-CATENIN target gene promo

54 ablish the essential role of striatal Hdac1, Hdac2 and MeCP2 for suppression of repetitive behaviors.

55 that DeltaNp63 is a novel target of DEC1 and HDAC2 and modulates the efficacy of HDAC inhibitors in g

56 histone deacetylase core components (RbAp48, HDAC2 and MTA2) of NuRD through a critical contact regio

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

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

59 he CCNE1 promoter in a complex that included HDAC2 and negatively regulated CCNE1 expression.

60 ation and hydroxymethylation, Tet2 recruited Hdac2 and repressed transcription of Il6 via histone dea

61 y a protein complex, containing Wdr5, Hdac1, Hdac2 and Rere (named WHHERE), which regulates RA signal

62 PDH reduced cholate-induced nitrosylation of HDAC2 and SIRT1; this effect was accompanied by abrogati

63 diate the binding of the histone deacetylase HDAC2 and the enhancer-binding protein EP300.

64 , an effect that required expression of both HDAC2 and the serotonin 5-HT(2A) receptor.

65 r, these data establish a novel pathway that HDAC2 and TSP1 act downstream of CREB activation in beta

66 ght into the ubiquitination and stability of HDAC2 and uncovers a previously unknown function of USP4

67 In this study, we show that during mitosis, HDAC2 and, to a lesser extent, HDAC1 phosphorylation lev

68 ty, by recruiting the histone deacetylase 2 (HDAC2) and CCAAT/enhancer-binding protein alpha (c/EBPal

69 es S-nitrosylation of histone deacetylase 2 (HDAC2) and epigenetic changes in neurons.

70 by S-nitrosylation of histone deacetylase 2 (HDAC2) and Sirtuin 1 (SIRT1), deacetylases that particip

71 the histone deacetylases 1 and 2 (HDAC1 and HDAC2), and is defined by the presence of a CHD family r

72 s (ROS), which preceded the up-regulation of HDAC2, and consequent sensitization of cells to Dex.

73 hancer regions of RA-regulated genes; HDAC1, HDAC2, and HDAC3 bind at RAREs in the Hoxa1 and Cyp26a1

74 assays demonstrated the occupancy of KLF-4, HDAC2, and HDAC3 in the VEGF promoter in normal MCF-10A

75 Class I histone deacetylases (HDAC1, HDAC2, and HDAC3) are recruited by cognate corepressor p

76 in vitro assays for the inhibition of HDAC1, HDAC2, and HDAC3-NCoR2 by N-(2-aminophenyl)-benzamide 15

77 ated to histone modifications, such as HAT1, HDAC2, and KDM5B.

78 se histone remodeling complex subunits LSD1, HDAC2, and RBBP4, which are proximal regulators of the e

79 m regulating Edn1 transcription by Dot1a and HDAC2, and reinforces endothelin 1 as a therapeutic targ

80 ound nuclear fraction, interacts with HDAC1, HDAC2, and with the serine-threonine phosphatase PP1CC.

81 hibition of the class I HDAC isoforms HDAC1, HDAC2, and/or HDAC3 and promising antiproliferative effe

82 HDAC2 appears to mediate the action of steroids to switc

83 Our previous studies showed that Hdac1 and Hdac2 are bound to promoters of key renal developmental

84 Histone deacetylase 1 (HDAC1) and HDAC2 are components of corepressor complexes that are i

85 Together, these data indicate that Hdac1 and Hdac2 are crucial for kidney development.

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

87 ecipitation analysis revealed that HDAC1 and HDAC2 are present on the miR-133a enhancer regions.

88 We demonstrate that Wdr5, Hdac1, and Hdac2 are required for RA signaling in vitro and in vivo

89 Histone deacetylase 1 (HDAC1) and HDAC2 are responsible for reducing H4 acetylation as chr

90 ior, and that class I HDACs (e.g., HDAC1 and HDAC2) are most important in this response.

91 These observations support the view of HDAC2 as a promising new target for schizophrenia treatm

92 urthermore, knockdown experiments identified HDAC2 as being responsible for the regulation of RAD51.

93 f the compounds used implicates HDAC1 and/or HDAC2 as likely targets for the observed correction, alt

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

95 ng chromatin modifier histone deacetylase 2 (HDAC2) as revealed by chromatin immunoprecipitation, sma

96 he mouse kidney) with histone deacetylase 2 (HDAC2), as well as the function of the Dot1a-HDAC2 compl

97 ulation of histone deacetylase 1 (HDAC1) and HDAC2 at the Cd86 locus.

98 viously unrecognized role for an miR-21/PI3K/HDAC2 axis in SSIAAD.

99 e show that like AD, disruption of Tip60 HAT/HDAC2 balance with concomitant epigenetic repression of

100 ass-I histone deacetylases (HDACs) HDAC1 and HDAC2 belong to a family of 11 zinc-dependent human HDAC

101 Inhibition or knock-down of HDAC2 blocked the stress-induced impairment of synaptic

102 Strikingly, Hdac1(-/-)Hdac2(+/-) brains showed normal development and no obvio

103 ely display higher nuclear HDAC activity and HDAC2 but not HDAC 1, 3, 4, 5, and 6 protein levels and

104 y protecting this mark from removal and that HDAC2 but not HDAC1 can effectively compete with ATAD2 f

105 Using an RNAi approach, we find that HDAC2, but not HDAC1, inhibition in the ventral tegmenta

106 Therefore, blockade of upregulation of HDAC2 by HDACi normalizes GABA hyposensitivity of pDAerg

107 ts reveal a critical regulatory mechanism of HDAC2 by Mule and suggest this pathway determines the ce

108 Ablation of Hdac1 or Hdac2 by Nestin-Cre had no obvious consequences on brain

109 Consistently, knockdown of HDAC2 by siRNA or inhibition of HDAC with trichostatin A

110 ass I histone deacetylases (HDACs) HDAC1 and HDAC2 can act to suppress tumors in mouse thymocytes.

111 ass I histone deacetylases (HDACs) Hdac1 and Hdac2 can associate together in protein complexes with t

112 generated an ES cell line in which Hdac1 and Hdac2 can be inactivated simultaneously.

113 ATAD2 to nascent chromatin was increased in hdac2 cells over the wild type, and ATAD2 depletion redu

114 lication fork progression was noted only for hdac2 cells overexpressing the protein.

115 n-associated, acetylated H4 in wild-type and hdac2 cells.

116 dual transgenic mice (K14-Cre Hdac1(cKO/cKO) Hdac2(+/cKO)) have similar but more obvious abnormalitie

117 comparably suppressed angiotensin II-induced HDAC2 (class I) production, HDAC-activating phosphorylat

118 n between Dot1a and HDAC2 prevents the Dot1a-HDAC2 complex from association with DNA, providing a cou

119 HDAC2), as well as the function of the Dot1a-HDAC2 complex in regulating Edn1 transcription.

120 xpression is regulated by the Sp3/REST/HDAC1/HDAC2 complex in tMCAO and by the Sp1/HIF-1/p300 complex

121 tudy, we characterized the nonphosphorylated HDAC2 complexes recruited to the transcribed gene body a

122 t the class I histone deacetylases HDAC1 and HDAC2 contribute to maintain the expression of p53 mutan

123 3 and HDAC9 regulate BRM expression, whereas HDAC2 controls its acetylation.

124 ates eEF1A1, whereas the histone deacetylase HDAC2 deacetylates eEF1A1.

125 HDAC1 and HDAC2-deficient T helper type 0 (TH0) and TH1 cells furt

126 Mechanistically, Rg1 rescued UVB-induced HDAC2 degradation.

127 HDAC2-dependent deacetylation of MORF4L1 enhances MORF4L

128 , regulated by p300-mediated acetylation and HDAC2-dependent deacetylation of PD-L1.

129 ore, we found that, in stressed animals, the HDAC2-dependent downregulation of histone methyltransfer

130 Moreover, Hdac1- and Hdac2-dependent regulation of Sapap3 expression requires

131 increases them; (3) c-Abl inhibition reduces HDAC2-dependent repression activity and HDAC2 recruitmen

132 onal alteration occurred in association with HDAC2-dependent repressive histone modifications at the

133 eatment, ChIP showed, in fact, a significant HDAC2 detachment from the promoter region of insulin gro

134 ll fibroblasts, we determined that HDAC1 and HDAC2 do not fully compensate for each other in removing

135 Here, we show that knock-down of Hdac1 and Hdac2 dramatically accelerates leukemogenesis in transge

136 Hdac1 and Hdac2 dual transgenic mice (K14-Cre Hdac1(cKO/cKO) Hdac2

137 Loss of HDAC1 and HDAC2 during late T cell development led to the appearan

138 In the mouse brain, HDAC1 and HDAC2 exhibit different developmental stage- and lineage

139 d the protective effects of aminophylline on HDAC2 expression and glucocorticoid sensitivity in lipop

140 This study demonstrated that suppressing HDAC2 expression can effectively reduce ischemic retinal

141 inophylline and dexamethasone in maintaining HDAC2 expression levels, preventing hearing loss in LPS-

142 ation of glucocorticoid receptors, increased HDAC2 expression, and reduced expression of memory-relat

143 to reverse steroid resistance by increasing HDAC2 expression, which can be achieved with theophyllin

144 Mule specifically targets HDAC2 for ubiquitination and degradation.

145 Moreover, CHD4 depletion removes HDAC2 from the chromatin, leading to an increase and spr

146 D1 interacted with and sequestered HDAC1 and HDAC2 from the SOX11 locus, leading to SOX11 upregulatio

147 ribute to the beneficial effects of reducing HDAC2 function in wild-type mice or of inhibiting HDACs

148 To examine these aspects of HDAC2 function, we used sparse transfection of rat hippo

149 Peripheral blood histone acetylation and HDAC2 gene expression were associated with durable respo

150 that targeted deletion of both the Hdac1 and Hdac2 genes from the ureteric bud (UB) cell lineage of m

151 ndicating that a critical level of Hdac1 and Hdac2 governed HDAC-activity is required for tumor maint

152 nd tumors revealed a critical role for Hdac1/Hdac2-governed HDAC-activity in regulating a p53-depende

153 ng proper chromatin structures and show that HDAC2 has a unique role by controlling the fate of neura

154 Our data indicate that HDAC1 and HDAC2 have a common function in maintaining proper chrom

155 sion and regulation of class I HDACs (HDAC1, HDAC2, HDAC3 and HDAC8) was performed in cardiopulmonary

156 In vitro assays for the inhibition of HDAC1, HDAC2, HDAC3-NCoR1, and HDAC8 by the N-(2-aminophenyl)be

157 ors (HDACi), and also measured the levels of HDAC2, histone (H3-K9) acetylation, and GABA-Aalpha1 rec

158 at corepressor complexes, including HDAC1 or HDAC2 homodimers, might target different cellular protei

159 -7)), and rs7765004 at 6q21 (near MARCKS and HDAC2; HR, 1.38; 95% CI, 1.22 to 1.57; P = 7.09 x 10(-7)

160 Our results demonstrate that the loss of HDAC2 improves associative learning, with no effect in n

161 A) of P rats to determine the causal role of HDAC2 in anxiety-like and alcohol-drinking behaviors.

162 Deletion of HDAC2 in forebrain pyramidal neurons prevented the negat

163 Virally mediated overexpression of HDAC2 in frontal cortex decreased mGlu2 transcription an

164 Phosphorylation of HDAC1 and/or HDAC2 in interphase cells is required for the formation

165 precedented and essential role for HDAC1 and HDAC2 in maintenance of skeletal muscle structure and fu

166 orebrain-specific deletion of both Hdac1 and Hdac2 in mice impacts neuronal survival and results in a

167 Localization of HDAC2 in mice retinas was evaluated by immunohistochemic

168 Accumulation of HDAC2 in Mule-deficient cells leads to compromised p53 a

169 arning tasks, suggesting a specific role for HDAC2 in particular types of learning.

170 Together, these results highlight a role for HDAC2 in suppressing synaptic excitation and enhancing s

171 expressed single alleles of either Hdac1 or Hdac2 in the absence of the respective paralog in neural

172 ults also demonstrate that loss of Hdac1 and Hdac2 in the UB epithelium leads to marked hyperacetylat

173 rdiomyocyte-specific genetic inactivation of HDAC2 in transgenic mice attenuated the ultrastructural

174 Accumulation of HDAC2 in USP4-overexpression cells leads to compromised

175 losteric activators of recombinant HDAC1 and HDAC2 in vitro following a mixed activation kinetic.

176 cetylase 1 (Hdac1) or histone deacetylase 2 (Hdac2) in OPCs did not affect BMP4-dependent astroglioge

177 brin, and upstream transcriptional regulator HDAC2, in opiate-induced plasticity in the NAc.

178 ing mice lacking the class I HDACs, HDAC1 or HDAC2, in postmitotic forebrain neurons to investigate t

179 rease in neuronal gene expression induced by HDAC2 increase; however, the mechanisms involved are not

180 sk-dependent, with the predominant impact of HDAC2 inhibition being an enhancement in an animal's abi

181 rd, it has provided the epigenetic approach, HDAC2 inhibition or knock-down, to rescue synaptic and c

182 oviding the rationale for the development of HDAC2 inhibitors as a new epigenetic-based approach to i

183 t the idea that the development of selective HDAC2 inhibitors may provide an efficacious treatment fo

184 Arg starvation induces PHD2 and HDAC2 interaction which is sensitive to antioxidants.

185 We next uncovered that HDAC2 is a direct target of cAMP response element-bindin

186 Notably, HDAC2 is necessary for beta-adrenergic signaling to indu

187 Our results demonstrated that HDAC2 is primarily localized in nuclei in inner nuclear

188 Highly phosphorylated HDAC2 is recruited within corepressor complexes to regul

189 most cell types, deletion of both Hdac1 and Hdac2 is required to generate a discernible phenotype, s

190 One copy of either Hdac1 or Hdac2 is sufficient to sustain normal renal development.

191 ch it performs together with a close homolog HDAC2, is deacetylation of new histone H4 deposited at r

192 of this study was to investigate the role of HDAC2 isoform in a mouse model of ischemic retinal injur

193 ng for postsynaptic GABA(A)Rs confirmed that HDAC2 KD and OE can regulate the synaptic abundance of t

194 In contrast, HDAC2 KD reduced, whereas HDAC2 OE enhanced, inhibitory

195 synaptic but not tonic GABA(A)R currents by HDAC2 KD, suggesting that HDAC2 selectively affects syna

196 rface expression of the alpha2 subunit after HDAC2 KD.

197 Hdac2 knock-out had no impact on episodic memory or moto

198 HDAC2 knockdown (KD) in single postsynaptic pyramidal ne

199 The HDAC2 knockdown in the CeA attenuated anxiety-like behav

200 HDAC2 knockdown partially abolished the Rg1-induced up-r

201 ts moderately attenuated CAG expansion, with Hdac2 knockout decreasing nuclear huntingtin pathology.

202 LY379268, an effect that was not observed in HDAC2 knockout mice.

203 Hdac2 knockout resulted in a substantial transcriptional

204 sociated with histone deacetylases HDAC1 and HDAC2, known to interact with TIP60 and repress transcri

205 The pELK-1-KLF4 complex in turn recruits HDAC2, leading to reduced histone acetylation and epigen

206 interacts directly with and deubiquitinates HDAC2, leading to the stabilization of HDAC2.

207 We show that selective knock-out of Hdac2 led to a robust acceleration of the extinction rat

208 nary disease, in which reduced intracellular HDAC2 levels have been described.

209 y; and (5) treatment with Imatinib decreases HDAC2 levels in a transgenic mice model of AD.

210 pulmonary disease, which express negligible HDAC2 levels, are scarcely affected by IL-10 in terms of

211 ibed how the tyrosine kinase c-Abl increases HDAC2 levels, inducing transcriptional repression of syn

212 (2) c-Abl knockdown cells show a decrease in HDAC2 levels, while c-Abl overexpression increases them;

213 LY294002, reduced PI3K activity and restored HDAC2 levels.

214 inib prevents the AbetaO-induced increase in HDAC2 levels; (2) c-Abl knockdown cells show a decrease

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

216 HDAC2 may be an intriguing target for cognitive and psyc

217 CSF1 produced by tumor cells caused HDAC2-mediated downregulation of granulocyte-specific ch

218 These novel data demonstrate the role of HDAC2-mediated epigenetic mechanisms in anxiety and alco

219 s demonstrate that codepletion of Hdac1 with Hdac2 mediates a robust pro-apoptotic response.

220 Morphologic measurements demonstrated that Hdac2(+)/(-) mice exhibit significantly less retinal deg

221 can protect the retina from ischemic injury, Hdac2(+)/(-) mice were utilized.

222 In Hdac2(+)/(-) mice, ERG a- and b-waves from ischemic eyes

223 and no obvious phenotype, whereas Hdac1(+/-)Hdac2(-/-) mice displayed impaired brain development and

224 We previously determined that HDAC2 mRNA levels were lower in dorsolateral prefrontal

225 pids showed formation of a KLF4, pELK-1, and HDAC2 multiprotein complex dependent on the SM22alpha G/

226 Histone deacetylase 2 (HDAC2) negatively regulates excitatory synapse number an

227 Hdac1(+/-)Hdac2(-/-) neural precursor cells showed reduced prolife

228 Our study identifies NO and HDAC2 nitrosylation as part of a signaling pathway that

229 Here, we show that HDAC2 nitrosylation regulates neuronal radial migration

230 Using CRISPR-Cas9-generated hdac1- or hdac2-null fibroblasts, we determined that HDAC1 and HDA

231 In contrast, HDAC2 KD reduced, whereas HDAC2 OE enhanced, inhibitory synaptic transmission.

232 rs (GABA(A)Rs) likely underlie the impact of HDAC2 on inhibitory transmission.

233 e effect of conditionally deleting Hdac1 and Hdac2 on oocyte development.

234 e two histone-deacetylases (HDACs) HDAC1 and HDAC2 on the ncx1-Br, with a consequent hypoacetylation.

235 t of genetic knockout, in Htt(Q111) mice, of Hdac2 or Hdac3 in medium-spiny striatal neurons that exh

236 ion of HDAC activity and knockdown of HDAC1, HDAC2 or SRSF1 showed that these proteins were involved

237 ning PRMT5 and either histone deacetylase 2 (HDAC2) or HDAC3, enhanced binding of co-activator comple

238 shRNA knockdown of HDAC1, HDAC2, or HDAC3 differentially increases the deposition

239 ion of the responsible HDAC member to HDAC1, HDAC2, or HDAC3.

240 synaptic pyramidal neurons enhanced, whereas HDAC2 overexpression (OE) reduced, excitatory synaptic t

241 Furthermore, HDAC2 overexpression in the VTA prevents the actions of

242 A post mortem study confirmed that HDAC1 and HDAC2 paralogs are elevated in white matter tissue from

243 effects were partially mediated by the Nrf2/HDAC2 pathway.

244 complex (LSD1, RCOR1, HMG20A, HMG20B, HDAC1, HDAC2, PHF21A, GSE1, ZMYM2, and ZNF217) in an LSD1-depen

245 -gamma, possibly via suppression of PI3K/Akt/HDAC2 phosphorylation, and upregulation of the antioxida

246 nockdown studies demonstrated that HDAC1 and HDAC2 play a redundant role in regulation of Pax2/8 and

247 The interaction between Dot1a and HDAC2 prevents the Dot1a-HDAC2 complex from association

248 tors orchestrate the activation of HDAC1 and HDAC2 promoter activity in colon cancer cells.

249 p1 and Sp3 differentially regulate HDAC1 and HDAC2 promoter activity.

250 activity led to its increased binding at the Hdac2 promoter, thereby augmenting Hdac2 transcription.

251 d response element of histone deacetylase 2 (HDAC2) promoter, resulting in the upregulation of HDAC2.

252 In this study, we found that HDAC1 and HDAC2 promoters are regulated through collaborative bind

253 drographolide significantly restored nuclear HDAC2 protein levels and total HDAC activity, and it dim

254 osure decreased amygdaloid HDAC activity and HDAC2 protein levels, increased global and gene (Bdnf an

255 levels of histone deacetylase 1 (HDAC1) and HDAC2 proteins in HCC patient tissues.

256 uces HDAC2-dependent repression activity and HDAC2 recruitment to the promoter of several synaptic ge

257 he specific genetic elimination of HDAC1 and HDAC2, reduce the expression of mutant p53 mRNA and prot

258 Knockdown of HDAC2 reduces MORF4L1 self-assembly.

259 HDAC1 and HDAC2 regulate skeletal muscle autophagy by mediating th

260 curs in a cell-autonomous manner and whether HDAC2 regulates inhibitory synaptic functions are not we

261 However, whether HDAC2 regulation of excitatory synapses occurs in a cell

262 her demonstrated that, upon CREB activation, HDAC2 represses thrombospondin-1 (TSP1), a potent angiog

263 ned with certain genes showing inappropriate HDAC2 repressor enrichment.

264 HDAC inhibitors or knockdown of HDAC1 and/or HDAC2 restored FBP1 expression and inhibited HCC cell gr

265 tor 2 (NRF2), was also able to denitrosylate HDAC2, restoring dexamethasone sensitivity in alveolar m

266 By contrast, combined deletion of Hdac1 and Hdac2 resulted in impaired chromatin structure, DNA dama

267 fic demethylase Lsd1 and histone deacetylase Hdac2, resulting in the simultaneous removal of monometh

268 l muscle-specific deletion of both HDAC1 and HDAC2 results in perinatal lethality of a subset of mice

269 Moreover, the interaction of TLE3 with HDAC2 results in the maintenance of acetylation at a bas

270 BA(A)R currents by HDAC2 KD, suggesting that HDAC2 selectively affects synaptic abundance of function

271 sults support the participation of the c-Abl/HDAC2 signaling pathway in the epigenetic blockade of ge

272 Overexpression of HDAC1 and HDAC2 significantly attenuated Npr1 promoter activity, w

273 nt overexpression of HDAC3, but not HDAC1 or HDAC2, significantly reduced sGCbeta1 mRNA.

274 Here, we demonstrate that interplay of p300-HDAC2-Sin3A in the chromatin remodeling system is involv

275 We employed HDAC2 small interfering RNA infusion into the central nu

276 However, by using an HDAC2-targeting inhibitor (HDACi) during reconsolidation

277 o identify a protein complex of Wdr5, Hdac1, Hdac2 that act together with RA and coactivator Rere/Atr

278 n the cortex, expression of a mutant form of HDAC2 that cannot be nitrosylated dramatically inhibits

279 at chronic clozapine treatment decreased via HDAC2 the capabilities of the mGlu2/3 receptor agonist L

280 Moreover, USP4 targets HDAC2 to downregulate tumor necrosis factor TNFalpha-ind

281 polycomb proteins EZH2 and SUZ12 as well as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1)

282 p1, HMGA2 interferes with the recruitment of HDAC2 to the hTERT proximal promoter, enhancing localize

283 ruited the histone-modifying enzymes G9a and HDAC2 to the Il2ra and Cd27 loci, thereby repressing exp

284 endent upregulation and increased binding of HDAC2 to the mGlu2 promoter.

285 by DNA and recruiting histone deacetylase-2 (HDAC2) to reduce histone acetylation.

286 HRE before recruiting histone deacetylase 2 (HDAC2) to the promoter, leading to decreased histones H3

287 cellular factors (E2F6, E2F1, Rb, HDAC1, and HDAC2) together with EBV latent nuclear antigens using n

288 ng at the Hdac2 promoter, thereby augmenting Hdac2 transcription.

289 erved after histone deacetylase 1 (HDAC1) or HDAC2 was depleted by RNA interference or inhibited by t

290 HDAC2 was expressed in human gastric cancer cell lines a

291 In this condition, the class I member HDAC2 was found S-nitrosylated on cysteine, a post-trans

292 HDAC2 was induced by beta-adrenergic signaling in vitro

293 Genetic codepletion of Hdac1 with Hdac2 was pro-apoptotic in Emicro-Myc lymphoma in vitro

294 To dissect the individual roles of HDAC1 and HDAC2, we expressed single alleles of either Hdac1 or Hd

295 ence identity, we examined whether Hdac1 and Hdac2 were functionally redundant in mature mouse brain.

296 evels of nitrosylated GAPDH and nitrosylated HDAC2 were increased in cholestatic human and rat livers

297 ed by inactivation of histone deacetylase 2 (HDAC2), which is critical for the transrepressive activi

298 quent recruitment of histone de-acetylase 2 (HDAC2), which mediates epigenetic gene silencing.

299 iptionally repressed by the histone modifier HDAC2, which is relieved by pharmacological inhibition o

300 tionship between the expanded Htt allele and Hdac2 with implications for targeting transcriptional dy