ライフサイエンスコーパス: HDAC2

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

2 perphosphorylation of histone deacetylase 2 (HDAC2).

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

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

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

6 K14 promoter-mediated reduction of Hdac1 or Hdac2.

7 ound conditional knockout mice for Hdac1 and Hdac2.

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

9 ctivated by selective depletion of HDAC1 and HDAC2.

10 ithout its LZ domain failed to interact with HDAC2.

11 on can be partially rescued by siRNA against HDAC2.

12 ase (HDAC) homologous to mammalian HDAC1 and HDAC2.

13 d mice with conditional alleles to HDAC1 and HDAC2.

14 ) promoter, resulting in the upregulation of HDAC2.

15 nates HDAC2, leading to the stabilization of HDAC2.

16 d decrease of ROS production and increase of HDAC2.

17 g decreased cortical synaptic plasticity via HDAC2.

18 WRN co-precipitates with HDAC1 and HDAC2.

19 reased expression of the histone deacetylase HDAC2.

20 tivity of the histone deacetylases HDAC1 and HDAC2.

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

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

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

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

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

26 Importantly, we show in vivo that Foxp1 and HDAC2 act cooperatively to regulate expression of the cy

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

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

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

30 rophages from individuals with COPD restored HDAC2 activity.

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

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

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

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

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

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

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

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

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

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

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

42 s by small interfering RNA demonstrated that HDAC2 and HDAC3 contribute to repression of HIV-1 long t

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 es S-nitrosylation of histone deacetylase 2 (HDAC2) and interferes with its binding to MTA1, which, i

63 Here, we show that histone deacetylase (HDAC2) and PAD4 interact with p53 through distinct domai

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

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

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

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

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

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

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

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

72 HDAC2 appears to mediate the action of steroids to switc

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

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

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

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

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

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

79 We show that PRDM1 co-repressors, G9a and HDAC2, are recruited to CIITApI, leading to a loss of hi

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

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

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

83 A interference, we have identified HDAC1 and HDAC2 as molecular targets mediating fetal hemoglobin in

84 nts uncovered the class I isoforms HDAC1 and HDAC2 as required for the autophagic response.

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

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

87 revealed that each US3 kinase phosphorylates HDAC2 at the same unique conserved Ser residue in its C

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

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

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

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

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

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

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

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

96 ase, indicating that hyperphosphorylation of HDAC2 by PRV occurs in a US3-independent manner.

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

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

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

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

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

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

103 sed endogenous corepressor (Eto2, Sin3A, and Hdac2) coimmunoprecipitation with Pu.1.

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

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

106 s recruitment of MTA1-histone deacetylase 2 (HDAC2) complexes onto two selective regions of the p21(W

107 resistance to hyperoxic lung injury in Foxp1/HDAC2 compound mutant animals.

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

109 3 and HDAC9 regulate BRM expression, whereas HDAC2 controls its acetylation.

110 e body, HSV uses components of the HDAC1- or HDAC2/CoREST/LSD1/REST repressor complex to activate alp

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

112 Mechanistically, Rg1 rescued UVB-induced HDAC2 degradation.

113 HDAC2-dependent deacetylation of MORF4L1 enhances MORF4L

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

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

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

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

118 After DNA damage, PAD4 and HDAC2 dissociate from several p53-target gene promoters

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

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

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

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

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

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

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

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

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

128 of isoform-selective inhibitors of HDAC1 and HDAC2 for the treatment of sickle cell disease.

129 Mule specifically targets HDAC2 for ubiquitination and degradation.

130 Therefore, we propose that HDAC1 and HDAC2 form a developmental switch that controls synapse

131 the dissociation of the repressive HDAC1 and HDAC2 from the Sp1 binding region.

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

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

134 atin-modifying enzyme histone deacetylase 2 (Hdac2) functions with a small homeodomain factor, Hopx,

135 ion, and this effect is abrogated by loss of Hdac2-Gata4 interaction.

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

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

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

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

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

141 These data demonstrate that HDAC2 has an unexpected sumoylation-promoting activity a

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

143 ional repressors histone deacetylase type 2 (HDAC2), HDAC3, YY1, CBF-1/RBP-Jk, Daxx, and CIR to the M

144 tion of class I histone deacetylases (HDAC1, HDAC2, HDAC3, and HDAC8) without affecting the class II

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

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

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

148 get of Hdac2-mediated deacetylation and that Hdac2, Hopx, and Gata4 coordinately regulate cardiac myo

149 -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)

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

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

152 enotypes, whereas deletion of both HDAC1 and HDAC2 in developing neurons results in severe hippocampa

153 Deletion of HDAC2 in forebrain pyramidal neurons prevented the negat

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

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

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

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

158 Localization of HDAC2 in mice retinas was evaluated by immunohistochemic

159 In the absence of Hopx and Hdac2 in mouse embryos, Gata4 hyperacetylation is associ

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

161 s and fully rescued by lowering the elevated HDAC2 in Mule-null cells to the normal levels as in wild

162 Mice lacking HDAC1 or HDAC2 in neuronal precursors show no overt histoarchitec

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

164 SphK2 associated with HDAC1 and HDAC2 in repressor complexes and was selectively enriche

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

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

167 To delineate the contribution of HDAC1 and HDAC2 in the brain, we have used pharmacological inhibit

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

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

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

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

172 le of histone deacetylase 1 and 2 (HDAC1 and HDAC2) in regulating cartilage-specific gene expression

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

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

175 By stimulating eIF4E sumoylation, HDAC2 induces the formation of the active eukaryotic ini

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

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

178 n, suggesting that a combination of PAD4 and HDAC2 inhibitors as a potential strategy for cancer trea

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

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

181 Thus, we have demonstrated that while HDAC2 is a conserved target of alphaherpesvirus US3 kina

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

183 Here we show that HDAC2 is also involved in cap-dependent mRNA translation

184 from patients with COPD, S-nitrosylation of HDAC2 is increased and that this abolishes its GR-transr

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

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

187 Highly phosphorylated HDAC2 is recruited within corepressor complexes to regul

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

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

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

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

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

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

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

195 rface expression of the alpha2 subunit after HDAC2 KD.

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

197 HDAC2 knockdown (KD) in single postsynaptic pyramidal ne

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

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

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

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

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

203 d HDAC2 physically interact and knockdown of HDAC2 leads to increased binding of DEC1 to the DeltaNp6

204 or cells, we show that deletion of HDAC1 and HDAC2 leads to reduced lipid accumulation, revealing red

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

206 ther, exchange of the CTDs between HDAC1 and HDAC2 led to proteins that were enzymatically active but

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

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

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

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

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

212 LY294002, reduced PI3K activity and restored HDAC2 levels.

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

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

215 nhibitors or silence of endogenous HDAC1 and HDAC2 markedly elevated P-Rex1 transcription in non-meta

216 HDAC2 may be an intriguing target for cognitive and psyc

217 suggest that Gata4 is a nonhistone target of Hdac2-mediated deacetylation and that Hdac2, Hopx, and G

218 ctivate cell cycle genes is impaired by Hopx/Hdac2-mediated deacetylation, and this effect is abrogat

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

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

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

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

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

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

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

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

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

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

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

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

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 on PS2 transcription, probably by recruiting HDAC2 onto the PS2 promoter.

236 Short hairpin RNA silencing of either HDAC2 or HDAC4 is sufficient to induce p21 expression.

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

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 effects were partially mediated by the Nrf2/HDAC2 pathway.

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

243 Consistent with this, we found that DEC1 and HDAC2 physically interact and knockdown of HDAC2 leads t

244 Hdac2 physically interacts with Gata4, and this interact

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

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

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

248 In contrast, HDAC2 promoter association and histone Lys acetylation a

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

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

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

252 with these effects, E(2) decreased levels of HDAC2 protein and increased DNMT expression in the dorsa

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 We show that HDAC1 and HDAC2 redundantly control neuronal development and are r

260 HDAC1 and HDAC2 regulate skeletal muscle autophagy by mediating th

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

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

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

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 e find that deletion of ectodermal Hdac1 and Hdac2 results in dramatic failure of hair follicle speci

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

280 iates with histone deacetylase 1 (HDAC1) and HDAC2 to form an active transcriptional repressor comple

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 ng at the Hdac2 promoter, thereby augmenting Hdac2 transcription.

288 HDAC2 was also hyperphosphorylated in cells infected wit

289 HDAC2 was expressed in human gastric cancer cell lines a

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

291 HDAC2 was induced by beta-adrenergic signaling in vitro

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

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

294 Cys-262 and Cys-274 of HDAC2 were found to be the targets of S-nitrosylation, a

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 miR-155 expression via its association with HDAC2, which deacetylates histones H2A and H3 on the miR

300 positioning is caused by the dissociation of HDAC2 with the ITGB8 core promoter, leading to increased