ライフサイエンスコーパス: hyperacetylation

1 d loss of the domain-wide pattern of histone hyperacetylation.

2 ene promoters, flanked by regions of histone hyperacetylation.

3 nd drastically altered pattern of histone H3 hyperacetylation.

4 that have genomewide and constitutive H3 K56 hyperacetylation.

5 rest, apoptosis, and histone (H3K9 and H4K8) hyperacetylation.

6 st in part from p53 hyperphosphorylation and hyperacetylation.

7 n inhibit HDAC activity resulting in histone hyperacetylation.

8 ibition of HDAC6 activity leads to cortactin hyperacetylation.

9 biochemical link between K4 methylation and hyperacetylation.

10 ar concentrations also induced alpha-tubulin hyperacetylation.

11 n K562 cells, in conjunction with histone H4 hyperacetylation.

12 HIV-1 expression but does not induce histone hyperacetylation.

13 eracetylation but not always like that of H4 hyperacetylation.

14 oter TATA box, and is independent of histone hyperacetylation.

15 ckdown of SIRT2 via siRNA results in tubulin hyperacetylation.

16 ransferase p300 on ncx1-Br with a consequent hyperacetylation.

17 d that mutation of H3K36 also resulted in H4 hyperacetylation.

18 s were associated with NF-kappaB subunit p65 hyperacetylation.

19 transcription of some genes through histone hyperacetylation.

20 super enhancers, despite persistent histone hyperacetylation.

21 iption factor--rather than global chromatin--hyperacetylation.

22 rate that Akita type 1 diabetic mice exhibit hyperacetylation.

23 tone acetyl-transferases and local chromatin hyperacetylation.

24 me, superoxide dismutase 2 (SOD2) because of hyperacetylation.

25 appaB and acetyltransferase p300 and histone hyperacetylation.

26 y interrupted, with corresponding hMOF/TIP60 hyperacetylation.

27 of the natural repertoire, including lysine hyperacetylation.

28 Enhancer blocking by cHS4 reduced histone hyperacetylation across a zone extending from the enhanc

29 oreover, SIRT1-deficient cells exhibited p53 hyperacetylation after DNA damage and increased ionizing

30 eficient embryonic fibroblasts, however, p53 hyperacetylation after DNA damage was not accompanied by

31 intracellular calcium levels lead to histone hyperacetylation along the body of the genes containing

32 Furthermore, hyperacetylation and accessibility of unrearranged V(H)

33 H3-K36Me2, and H3-K79Me2 are associated with hyperacetylation and active genes, whereas H3-K9Me2, H3-

34 lysine residues in hsp90, induces reversible hyperacetylation and attenuates ATP binding and chaperon

35 a suggest a mechanistic link between tubulin hyperacetylation and autophagy induction and points to H

36 tone H3 Lys-4 dimethylation (H3K4me2) and H3 hyperacetylation and by a global reduction of H3K27me3.

37 age pathway suppressed mitochondrial protein hyperacetylation and cardiac hypertrophy, and improved c

38 in transcribing SV40 minichromosomes histone hyperacetylation and deacetylation is dependent upon the

39 Previously shown to cause histone hyperacetylation and delocalization of replication initi

40 used as experimental tools to induce histone hyperacetylation and deregulate gene transcription, but

41 In addition, histone hyperacetylation and dimethylation of histone H3 K4 are

42 mponents, resulting from coordinated histone hyperacetylation and DNA demethylation, lead to derepres

43 might activate ATM through histone H3 and H4 hyperacetylation and DNA promoter hypomethylation.

44 lines, tolerated exposure alone led to H3K9 hyperacetylation and E2F1 binding at the FOS promoter, w

45 sue SirT1 expression, which leads to histone hyperacetylation and ectopic inflammatory gene expressio

46 ed cell proliferation accompanied by histone hyperacetylation and elevated p21(WAF/CIP1) expression,

47 the SOCS3 promoter, concomitant with histone hyperacetylation and enhanced STAT3-dependent transcript

48 in erythroleukemia cells, induces histone H3 hyperacetylation and H3-meK4 at the adult beta-globin ge

49 ors (HDACi) induced global histone H3 and H4 hyperacetylation and H3K4 hypermethylation.

50 lobin gene expression accompanied by histone hyperacetylation and hypomethylation in chromatin from t

51 y, we found that HDAC1 knockdown resulted in hyperacetylation and inactivation of heat shock protein

52 were further supported by the fact that p53 hyperacetylation and increased radiation-induced apoptos

53 ce fed CA diet also demonstrated hepatic FXR hyperacetylation and induction of the Janus kinase/p53 p

54 itors or depletion of HDAC6 by siRNA induces hyperacetylation and inhibits ATP binding and chaperone

55 deacetylase inhibitors (HDACIs) induced RelA hyperacetylation and NF-kappaB activation, attenuating l

56 nstrate that TSA treatment induces H3 and H4 hyperacetylation and nuc-1 remodeling.

57 Consequently, SIRT1 deficiency induces hyperacetylation and nuclear accumulation of CRABPII, en

58 This, in turn, led to hyperacetylation and nuclear localization of the forkhea

59 lanilide hydroxamic acid was associated with hyperacetylation and nuclear translocation of RelA/p65.

60 cells, IL-7/IL-7R signaling induces histone hyperacetylation and nuclease accessibility of the large

61 0.1 microM was effective in causing histone hyperacetylation and p21(WAF/CIP1) overexpression and su

62 es vascular oxidative stress because of SOD2 hyperacetylation and promotes endothelial dysfunction an

63 dramatic chromatin reorganization involving hyperacetylation and replacement of most histones with p

64 interaction and decreased both histone H3/H4 hyperacetylation and RNA polymerase II occupancy at the

65 in mast cells showed that H3 and H4 histone hyperacetylation and RNA polymerase II recruitment withi

66 mplex can create a sizable region of histone hyperacetylation and serve as a barrier to encroaching r

67 g liver I/R is a mechanism that promotes the hyperacetylation and subsequent release of HMGB1.

68 We demonstrate that histone hyperacetylation and the binding of C/EBP activators, po

69 ies establish that HOXA10 mediates chromatin hyperacetylation and trimethyl histone K4 (H3K4) methyla

70 n with DNA cytosine hypomethylation, histone hyperacetylation and upregulated expression.

71 Changes in promoter structure, histone hyperacetylation, and binding of C/EBP activators, Pol I

72 /CREB-binding protein (CBP), induces histone hyperacetylation, and enriches BRD4 to the transgene arr

73 of a given S region, and that transcription, hyperacetylation, and mutation are not sufficient to gua

74 2, more effective as an initiator of histone hyperacetylation, and significantly more effective than

75 privation, but the mechanisms of microtubule hyperacetylation are still unknown.

76 howed that zinc deprivation caused histone 3 hyperacetylation as well as increased NF-kappaB binding

77 C6 inhibition is related to cortactin (CTTN) hyperacetylation associated with actin disorganization i

78 Extended histone hyperacetylation at great distances from coding regions

79 lly, Tax favors p300 recruitment and histone hyperacetylation at late replication domains, advancing

80 Zinc deprivation induced histone 3 hyperacetylation at lysine 9 through suppression of HDAC

81 Small T but not middle T was important in hyperacetylation at major sites in H3 and H4.

82 Myc induces TRRAP recruitment and histone hyperacetylation at specific Myc-activated genes in vivo

83 us Smad-binding DNA sequences and histone H4 hyperacetylation at the COL1A2 locus, were all prevented

84 r recruitment of coregulator CBP and histone hyperacetylation at the ER target chromatin.

85 1 expression established a domain of histone hyperacetylation at the LCR and hGH-N promoter in these

86 SIRT6 loss results in histone hyperacetylation at the Lin28b promoter, Myc recruitment

87 one acetyltransferase binding and histone H4 hyperacetylation at the VEGF promoter in NSCLC cells.

88 and Brdt increases dramatically upon histone hyperacetylation both in vitro and in vivo.

89 bition in primary hepatocytes causes histone hyperacetylation but does not upregulate expression of H

90 e II with S regions was much like that of H3 hyperacetylation but not always like that of H4 hyperace

91 ing both nucleosome mobilization and histone hyperacetylation, but lacked differences in restriction

92 hondrial origin are required for microtubule hyperacetylation by activating the AMP kinase, which in

93 gulator Hu proteins can induce local histone hyperacetylation by association with their target sequen

94 This hyperacetylation by chronic imipramine was associated wi

95 ow H3K4me3 binding by Sgf29 leads to histone hyperacetylation by Gcn5, we used differential fluoresce

96 Finally, we show that preventing microtubule hyperacetylation by knocking down MEC-17 affects cell su

97 Hyperacetylation by NPI-0052 occurred to a lesser extent

98 Our rationale was that hyperacetylation caused by HDAC inhibitor treatment woul

99 loric intake on insulin levels, GH1 promoter hyperacetylation, chromosomal architecture, and expressi

100 data suggest that heroin-related histone H3 hyperacetylation contributes to glutamatergic transcript

101 Other recent studies suggest that lysine hyperacetylation contributes to the accumulation of amyl

102 Likewise, histone hyperacetylation correlates with the active state of tra

103 The hyperacetylation defect of hr-t mutant NG59 was partiall

104 d H3 during transcription alternates between hyperacetylation directed by an RNAPII associated histon

105 as the LAT promoter, and (ii) the region of hyperacetylation does not extend to the ICP0 promoter.

106 We show that mitochondrial protein hyperacetylation due to NAD(+) redox imbalance contribut

107 To investigate histone hyperacetylation dynamics we used sodium butyrate, a his

108 CREB to DCR3, a broad domain of histone H3K9-hyperacetylation extending from DCR1 to DCR3, and increa

109 cus and several other loci, however, histone hyperacetylation extends beyond the promoter, over tens

110 l H3K9 hypoacetylation and promoter-specific hyperacetylation facilitate E2F1-mediated FOS induction

111 deacetylase (HDAC) Rpd3 induced genome-wide hyperacetylation, genomic replication and a redistributi

112 y PXY-1 were impaired in inducing histone H3 hyperacetylation, H3-meK4, and RNA polymerase II recruit

113 ation appears related to ATM activation, its hyperacetylation has been attributed to the increased ex

114 expectedly, HDAC6 inhibition-induced tubulin hyperacetylation has no effect on PPF.

115 al and replacement, including histone 4 (H4) hyperacetylation, histone variant expression, nucleosome

116 sequences within beta-globin domains exhibit hyperacetylation in a context-dependent manner, and doma

117 were cross-analyzed for induction of histone hyperacetylation in a human myeloma cell line to identif

118 ummary, all four HDAI tested induced histone hyperacetylation in all cells, KSHV reactivation in a mi

119 CREB)-binding protein (CBP)-mediated H3K9/14 hyperacetylation in approximately 5000 gene promoters in

120 ty despite the fact that they induce histone hyperacetylation in both normal and tumor cells.

121 cetylase 6-selective inhibitor, led to Hsp90 hyperacetylation in brain and in neuronal culture.

122 HDAC inhibition in vivo induced tubulin hyperacetylation in CryAB(R120G) TG hearts, which preven

123 ely, our data suggest that H3 and H4 histone hyperacetylation in different S regions is regulated dif

124 ng ligand, termed SirReal2, leads to tubulin hyperacetylation in HeLa cells and induces destabilizati

125 The potential role of hyperacetylation in mediating this impaired pyruvate upt

126 eeding induces hepatic mitochondrial protein hyperacetylation in mice and downregulation of the major

127 ta cells, and is consistent with the role of hyperacetylation in promoting euchromatin formation.

128 Although histone H3 hyperacetylation in recipient S regions was recently rep

129 ween the generation of mutations and histone hyperacetylation in S regions have not been addressed.

130 ing transient trichostatin A-induced histone hyperacetylation in Stat4-/-Th1 cultures.

131 deacetylase inhibitor that leads to protein hyperacetylation in the absence of ethanol.

132 Protein lysine hyperacetylation in the EE biomarker subset was associat

133 in A and associated with a decrease in H3/H4 hyperacetylation in the proximal hGH1 promoter region.

134 of dieldrin in mouse models induced histone hyperacetylation in the striatum and substantia nigra.

135 histone acetyltransferases to induce histone hyperacetylation in these chromatin foci, which provide

136 taining peptides and is required for histone hyperacetylation in vivo.

137 matin structure (H3K27 hypomethylation/H3K18 hyperacetylation) in activated naive CD4(+) T cells and

138 udy and computer simulation demonstrate that hyperacetylation increases the content of ordered second

139 ta support a mechanism wherein the transient hyperacetylation induced by Stat4 prevents the recruitme

140 region revealed that four GC boxes conferred hyperacetylation-induced PKCdelta promoter activation.

141 on, the capacity of HDAC6 to prevent tubulin hyperacetylation influences the speed of platelet spread

142 In this study, we show that this hyperacetylation is a common response to several cellula

143 ce of Hopx and Hdac2 in mouse embryos, Gata4 hyperacetylation is associated with a marked increase in

144 Protein hyperacetylation is associated with glucose intolerance

145 This hyperacetylation is highly correlated to recruitment of

146 At the cFos promoter, H4 hyperacetylation is seen within 30 min of a single cocai

147 by which H3K4me3 recognition leads to lysine hyperacetylation is unknown, as in vitro studies show no

148 tabolic consequence of mitochondrial protein hyperacetylation is unknown.

149 indings suggest that remodeling, not histone hyperacetylation, is the limiting step in transcriptiona

150 Inactivation of HDAC6 leads to Hsp90 hyperacetylation, its dissociation from an essential coc

151 embryonic stem cell-derived neurons, histone hyperacetylation leads to an increased local transcripti

152 control and FSHD cells displayed similar H4 hyperacetylation (like that of expressed genes) at the 5

153 We further demonstrate that protein hyperacetylation may be a common feature of mitochondria

154 on mediated at least in part by histone H3K9 hyperacetylation may be responsible for the rapid and ro

155 Thus, reversible hyperacetylation modulates the intracellular and extrace

156 In hst3 hst4 mutants, K56 hyperacetylation nears 100%.

157 6Ac) histone H4 isoforms, suggesting that H4 hyperacetylation occurs in a processive fashion, beginni

158 mbryonic stem cells (ES cells) are marked by hyperacetylation of all core histones, hyper(di)methylat

159 ventricular protein is hypoacetylated while hyperacetylation of alpha-tubulin, a substrate of histon

160 induced apoptosis, which was accompanied by hyperacetylation of BCL6 and p53.

161 Moreover, AngII induced hyperacetylation of BdkrB2 promoter-associated H4 histon

162 tylase inhibitors (HDACi) is ascribed to the hyperacetylation of both core nucleosomal histones and n

163 These analogs also induce hyperacetylation of core histones H3 and H4 in intact ce

164 caused induction of TGF-beta1 expression and hyperacetylation of glycogen synthase kinase 3beta (GSK3

165 erase-positive cell lines is associated with hyperacetylation of H3 and H4 and methylation of Lys4 H3

166 Infection with R8507 did not result in the hyperacetylation of H3 and H4.

167 ted lytic induction by TPA, yet NaB promoted hyperacetylation of H3 and H4.

168 most cases, synthetic lethality depends upon hyperacetylation of H3 K56 because it can be suppressed

169 contrast, loss of HST3 and HST4 resulted in hyperacetylation of H3 K56 within silent loci and telome

170 AR-42 promoted hyperacetylation of H3, H4, and alpha-tubulin, and up-re

171 Sirt6-deficient macrophages displayed hyperacetylation of H3K9 and increased occupancy of c-JU

172 In SIRT6-deficient cells, hyperacetylation of H3K9 at these target promoters is as

173 These results suggest that the extent of hyperacetylation of H4 and H3 during transcription alter

174 ed expression of SirT1 in human cells causes hyperacetylation of H4-K16 and H3-K9 in vivo.

175 as their knockdown specifically induces the hyperacetylation of H4K16 in oocytes, which may be assoc

176 Specifically, MOF-mediated hyperacetylation of H4K16 on the X chromosome promotes b

177 but lack HDAC6 expression, with concomitant hyperacetylation of heat shock protein 90 (hsp90).

178 pendent decrease in SpHst4 protein level and hyperacetylation of histone 3 Lys56.

179 HU treatment correlated with hyperacetylation of histone H3 and loss of telomere repe

180 Hyperacetylation of histone H3 and recruitment of the ge

181 th inhibition of HDAC activity, resulting in hyperacetylation of histone H3 in the alpha-syn promoter

182 ecularly, Sirt6 deletion results in striking hyperacetylation of histone H3 lysine 9 (H3K9) and lysin

183 gly activated the EBV lytic cycle and caused hyperacetylation of histone H3 on Zp and Rp.

184 VPA behaves as an HDAC inhibitor; it causes hyperacetylation of histone H3.

185 ations responded to the inducing stimulus by hyperacetylation of histone H3.

186 ressed following activation, indicating that hyperacetylation of histone H3K9 may play a role in sele

187 RNAi-mediated reduction of HDAC1 leads to hyperacetylation of histone H4 and a developmental delay

188 ant, including the validating observation of hyperacetylation of histone H4 and both H2B isoforms.

189 fic chromatin machinery that leads to global hyperacetylation of histone H4 at lysine 16 specifically

190 stimulate insulin gene expression by causing hyperacetylation of histone H4 at the insulin gene promo

191 to high concentrations of glucose results in hyperacetylation of histone H4 at the insulin gene promo

192 stimulate insulin gene expression by causing hyperacetylation of histone H4 at the insulin gene promo

193 n immunoprecipitation analysis revealed that hyperacetylation of histone H4 by NaBu is associated wit

194 ore, we have shown that the glucose-mediated hyperacetylation of histone H4 depends on the recruitmen

195 In addition, hyperacetylation of histone H4 was caused by drug treatm

196 of lysine 9 and lysine 27 of histone H3 and hyperacetylation of histone H4 within the FLC locus, in

197 s; this increased expression correlates with hyperacetylation of histone H4.

198 ation at lysine 27 of histone H3, as well as hyperacetylation of histone H4.

199 d BRLF1, are repressed by chromatin and that hyperacetylation of histone tails, by allowing the acces

200 have correlated the function of TSA with the hyperacetylation of histone.

201 Furthermore, hyperacetylation of histones 3 and 4 was detected.

202 induced CpG demethylation of Oct4 promoter, hyperacetylation of histones 3 and 4, and decreased lysi

203 This is accompanied by hyperacetylation of histones and a reduction in histone

204 ion in the presence of Trichostatin A causes hyperacetylation of histones associated with the constan

205 A null mutation in SWP1 results in hyperacetylation of histones H3 and H4 in LRP1 chromatin

206 ho- and beta(H)-globin genes correlated with hyperacetylation of histones H3 and H4, loss of histone

207 C8 activity by hyperphosphorylation leads to hyperacetylation of histones H3 and H4, suggesting that

208 , neither hybrid molecule caused substantial hyperacetylation of histones H3 and H4.

209 -binding protein (TBP) and TFIIB, as well as hyperacetylation of histones H3 and H4.

210 of male gametophytes is associated with the hyperacetylation of histones H3 and H4.

211 enhanced promoter activity, suggesting that hyperacetylation of histones is an important component o

212 As a result of hyperacetylation of histones on HIV-1 promotor, the viru

213 3 on the HIV-1 LTR that was associated with hyperacetylation of histones on the HIV-1 LTR.

214 Inhibiting HDAC6 led to hyperacetylation of Hsp90 and loss of complex formation

215 by a specific small interfering RNA leads to hyperacetylation of hsp90 and that the glucocorticoid re

216 ed that sulforaphane treatment would lead to hyperacetylation of HSP90 and that this would destabiliz

217 te that HDAC6 is an hsp90 client protein and hyperacetylation of hsp90 augments the anti-hsp90 and an

218 Hyperacetylation of hsp90 increased its binding to 17-AA

219 Hyperacetylation of Hsp90 is a predictor and causal mole

220 to HA-HDIs is associated with loss of HDAC6, hyperacetylation of hsp90, aggressive leukemia phenotype

221 o reduced HDAC6 binding to hsp90 and induced hyperacetylation of hsp90.

222 is lower level of expression correlated with hyperacetylation of IDH2 and SOD2 mitochondrial proteins

223 Cardiac Sirt1 deficiency in mice induces hyperacetylation of K1479 in Nav1.5, decreases expressio

224 th cambinol during genotoxic stress leads to hyperacetylation of key stress response proteins and pro

225 tions and by SIRT3 in vitro and in vivo; and hyperacetylation of LCAD reduces its enzymatic activity.

226 pression by small interfering RNA causes the hyperacetylation of Lys-9 in histone H3 on the gdf11 pro

227 c location of the epigenetic disturbances to hyperacetylation of lysine 27 of histone H3, showing dyn

228 Specifically, the authors report that hyperacetylation of microtubules in mesenchymal cells in

229 Hyperacetylation of mitochondrial malate-aspartate shutt

230 e analysis of the origins revealed that both hyperacetylation of nucleosomes and binding of the origi

231 mouse models of FRDA, we demonstrate marked hyperacetylation of numerous cardiac mitochondrial prote

232 We further show that HDAIs induce hyperacetylation of p300 and repress the HIF-1alpha.p300

233 vealed that HDACi is associated with histone hyperacetylation of Pax2/Pax8, Gdnf, Sfrp1, and p21.

234 level of PEPCK1, and was accompanied by the hyperacetylation of PEPCK1 as well as decreased glucose

235 ssion of a genetic domain is correlated with hyperacetylation of promoters and other regulatory eleme

236 rmal under basal conditions, but show marked hyperacetylation of several mitochondrial proteins.

237 Sirt1 deacetylase activity, which results in hyperacetylation of Sirt1 substrates such as forkhead bo

238 inhibiting HDAC complexes, resulting in the hyperacetylation of specific genes.

239 that activating E2F species are required for hyperacetylation of target chromatin in human cells.

240 l line upon costimulation is associated with hyperacetylation of the chromatin at the variable region

241 red with SAHA, compound 2-75 induced greater hyperacetylation of the HDAC6 substrate alpha-tubulin.

242 ells to VPA resulted in rapid dose-dependent hyperacetylation of the histones H3 and H4.

243 Lastly, we show cellular hyperacetylation of the hSirt2 targeted tubulin caused b

244 sor effector cells, and this correlated with hyperacetylation of the Il7ra promoter.

245 ective Sirt2 degradation that results in the hyperacetylation of the microtubule network coupled with

246 P) assays revealed that localized histone H3 hyperacetylation of the P2 promoter was observed on the

247 reversed glucose-induced hypomethylation and hyperacetylation of the p66(Shc) promoter in podocytes.

248 irt3 knockdown in myoblasts in vitro induced hyperacetylation of the PDH E1alpha subunit, altering it

249 atin immunoprecipitation assays demonstrated hyperacetylation of the promoter region and occupancy by

250 nes H3 and H4 from the quiescent genome, and hyperacetylation of the remaining histones.

251 d Hdac2 in the UB epithelium leads to marked hyperacetylation of the tumor suppressor protein p53 on

252 3 and antihistone H4 antibodies demonstrated hyperacetylation of this core promoter region.

253 atin immunoprecipitation assays demonstrated hyperacetylation of this region and occupancy by GATA-1

254 iated repression of nuclear receptors led to hyperacetylation of thousands of genomic sites and assoc

255 hypoacetylation across the locus compared to hyperacetylation of wild-type chromatin.

256 his study, we determined the effect of hsp90 hyperacetylation on the anti-hsp90 and antileukemia acti

257 p domain and an inhibitory affect of histone hyperacetylation on the MENT-induced chromatin remodelin

258 enes are enriched with K4 trimethylation and hyperacetylation on the N-terminal tail of histone H3.

259 treatment appear to be secondary to histone hyperacetylation or other effects of butyrate since depl

260 ibit covalent histone modifications, such as hyperacetylation, over broad regions of 10 kb or more ha

261 Alcohol exposure induced histone 3 hyperacetylation owing to inhibition of histone deacetyl

262 iation programs establish long-range histone hyperacetylation patterns that extend at least 50 kb in

263 tionally, TNFalpha induced localized histone hyperacetylation, phosphorylation, and methylation in th

264 se SIRT3 and resultant mitochondrial protein hyperacetylation play a critical role in the pathogenesi

265 because of proteasomal dysfunction and that hyperacetylation plays a key role in dopaminergic neuron

266 We found that H4 hyperacetylation preceded Brg1 binding in a MyoD-depende

267 Increased NADH/NAD(+) and protein hyperacetylation, previously observed in genetic models

268 We propose that nucleosome hyperacetylation promotes pre-RC assembly onto adjacent

269 a model in which BRD4-NUT-stimulated histone hyperacetylation recruits additional BRD4 and interactin

270 , that RNA polymerase II distribution and H3 hyperacetylation reflect the transcriptional activity of

271 The hyperacetylation renders H3.3 resistant to proteasomal d

272 that SIRT3 inhibition and consequent protein hyperacetylation represents a negative feedback mechanis

273 In contrast, promoter hyperacetylation requires the promoter GATA-1, and CACC-

274 y preventing p300 recruitment and histone H4 hyperacetylation, resulting in the inhibition of TGF-bet

275 er, whereas id1 function promotes histone H3 hyperacetylation, SD induction is associated with increa

276 of histone deacetylases can lead to histone hyperacetylation, selective up-regulation of interferon-

277 Hyperacetylation shifts its equilibrium from a predomina

278 The Athda7-2 mutation that induces histone hyperacetylation significantly increases the transcripti

279 mmunoprecipitation was used to determine the hyperacetylation status of histones independent of the l

280 unoprecipitation was used to determine their hyperacetylation status when associated with RNAPII.

281 region of ap-uch was accompanied by histone hyperacetylation, suggesting that CREB2 cannot only inhi

282 imals exhibit striking mitochondrial protein hyperacetylation, suggesting that SIRT3 is a major mitoc

283 ns of histone modifications, such as histone hyperacetylation, that are normally associated with acti

284 t to the CD4 enhancer and causing histone H3-hyperacetylation to this regulatory region.

285 the CAF-I chromatin assembly pathway, H3K56 hyperacetylation, together with the nucleosome remodeler

286 The hyperacetylation was attributed to dieldrin-induced prot

287 In these promoters, H3K9/14 hyperacetylation was closely associated with NF-kappaB o

288 In contrast, no mitochondrial hyperacetylation was detectable in mice lacking the two

289 No effect of histone hyperacetylation was detectable in this system.

290 duced by chronic, but not acute, cocaine, H3 hyperacetylation was observed with chronic cocaine only.

291 As expected, histone hyperacetylation was readily induced in all PEL cells ex

292 of DNA methyltransferase enzyme, and histone hyperacetylation were also observed.

293 ated fibroblasts was associated with histone hyperacetylation, whereas p300 depletion, or selective p

294 ef1-deficient CD8(+) T cells exhibit histone hyperacetylation, which can be ascribed to intrinsic his

295 with covalent histone modifications, such as hyperacetylation, which can modulate chromatin structure

296 double bromodomains also stimulates histone hyperacetylation, which causes BRD4 to bind tighter to c

297 g together with TPPP/p25 provoke microtubule hyperacetylation, which is coupled with process elongati

298 vate HIV-1 transcription by inducing histone hyperacetylation within a regulatory nucleosome, nuc-1,

299 chromatin environment containing histone H3 hyperacetylation within heterochromatic tandem repeats.

300 s to the cytoplasm, a process dependent upon hyperacetylation within two HMGB1 nuclear localization s