ライフサイエンスコーパス: HDACI

1 HDACI was reported to be able to activate p21 promoter t

2 HDACIs also increased RA-induced differentiation.

3 HDACIs also synergize with phosphatidylinositol 3-kinase

4 HDACIs are potent inhibitors of primary and metastatic U

5 HDACIs have antineoplastic effects in preclinical and cl

6 HDACIs interacted with MDA-7/IL-24 prolonging generation

7 HDACIs potently inhibit survival of MYC-driven MB cells

8 HDACIs suppressed p53-dependent PUMA expression, a criti

9 HDACIs synergized with melanoma differentiation-associat

10 HDACIs, but not RA, induced accumulation of acetylated h

11 HDACIs, such as vorinostat, induce caspase-dependent apo

12 ransgenic mice and cells harboring t(15;17), HDACIs induced apoptosis and dramatic growth inhibition,

13 tment of CB CD34+ cells with the most active HDACI, valproic acid (VPA), following an initial 16-hour

14 In combination with RA, all HDACIs tested overcame the transcriptional repression ex

15 We have established an HDACI-inducible, p21-driven reporter system that has the

16 the combination of an anthracycline with an HDACI should have significant clinical activity in patie

17 istone acetylation are activated by ATRA and HDACI, induce MDR1 in APL cells, and point to the critic

18 utic effect by combined treatment of GCV and HDACI.

19 iting BCL-2 family function on sorafenib and HDACI lethality.

20 However, VDA and HDACI when combined were successful in de-repressing VDR

21 nvestigation of strategies combining CFZ and HDACIs in DLBCL.

22 xtent to the combination of flavopiridol and HDACIs.

23 hich antileukemic synergism between 2-ME and HDACIs stems primarily from induction of oxidative damag

24 l of animals carrying orthotopic tumors, and HDACIs enhanced survival further.

25 t with SB and sodium phenylbutyrate, another HDACI, recovered cell viability and overall mitochondria

26 gomyelinase inhibitor desipramine attenuated HDACI/perifosine-mediated ceramide and ROS production as

27 Hydroxamic acid-based HDACIs such as vorinostat (suberoylanilide hydroxamic ac

28 CAP region of a set of triazolylphenyl-based HDACIs, and show that the nature of substitution on the

29 Inhibition of JNK1 activation attenuated Bay/HDACI lethality without affecting NF-kappaB inactivation

30 dramatically protected cells against the Bay/HDACI regimen but failed to prevent ROS production and J

31 L-cysteine blocked apoptosis induced by Bay/HDACIs by abrogating ROS generation.

32 f reactive oxygen species and Ca(2+) blocked HDACI and MDA-7/IL-24 killing.

33 kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell d

34 icantly, siRNA NEMO or ATM knockdown blocked HDACI-mediated NF-kappaB activation, resulting in dimini

35 Both HDACIs were effective against both Rb cell lines, induci

36 e accumulation; this effect was abrogated by HDACI coadministration, which suggests that cells underg

37 In contrast, genes that are activated by HDACI are moderately expressed.

38 V)-mediated anticancer effect contributed by HDACI-induced and p21-driven truncated herpes simplex vi

39 ber genes are more likely to be repressed by HDACI than non-amplified genes.

40 es markedly potentiated apoptosis induced by HDACIs, and this was accompanied by enhanced reactive ox

41 to 15-LOX-1 transcriptional reactivation by HDACIs in colon cancer cells.

42 dings indicate that in human leukemia cells, HDACIs activate the cytoprotective NF-kappaB pathway thr

43 ls using a chemical approach that correlates HDACI isoform specificity with their ability to reactiva

44 uper-repressor transfected cells) diminished HDACI-mediated Mn-SOD2 induction and increased ROS accum

45 typical ATM/NEMO nuclear pathway can enhance HDACI antileukemic activity.

46 6 phosphorylation and significantly enhanced HDACI susceptibility.

47 All explored HDACIs in combination with decitabine produced a synergi

48 was also unable to prevent the flavopiridol/HDACI regimen from inducing a conformational change in a

49 n with respect to the nuclear pore following HDACI treatment, including the recruitment of promoter r

50 Furthermore, HDACI-induced OX40L inhibited the generation of IL-10-pr

51 Uncertainty of how HDACI-induced protein acetylation leads to cell death, h

52 human SH-SY5Y neuroblastoma cells, however, HDACIs were not able to prevent p53-dependent cell death

53 we herein report the development of class I HDACIs, including information regarding their structure,

54 RelA acetylation and NF-kappaB activation in HDACI-treated cells.

55 enetic means leads to a dramatic increase in HDACI-mediated lethality through enhanced oxidative dama

56 orylation sites also significantly increased HDACI lethality.

57 and the novel histone deacetylase inhibitor (HDACI) depsipeptide (FK228) induced P-gp expression and

58 by the novel histone deacetylase inhibitor (HDACI) LAQ824 were examined in human leukemia cells (U93

59 flavopiridol/histone deacetylase inhibitor (HDACI) regimen, arguing against the involvement of the r

60 riazole-based histone deacetylase inhibitor (HDACI), octanedioic acid hydroxyamide[3-(1-phenyl-1H-[1,

61 rate (NaB), a histone deacetylase inhibitor (HDACI), or by hexamethylene bisacetamide (HMBA), a non-H

62 ms underlying histone deacetylase inhibitor (HDACI)-mediated NF-kappaB activation were investigated i

63 e of a potent histone deacetylase inhibitor (HDACI).

64 r a VDR agonist (VDA) nor an HDAC inhibitor (HDACI) nor a demethylating agent (DAC) individually coul

65 Histone deacetylase inhibitors (HDACI) are promising antitumor agents.

66 orafenib and histone deacetylase inhibitors (HDACI) interact to kill pancreatic carcinoma cells and d

67 eatment with histone deacetylase inhibitors (HDACI) results in potent cytotoxicity of a variety of ca

68 ign selective histone deactylase inhibitors (HDACI), we discovered that the aryl urea 1 is a modestly

69 As such, HDAC inhibitors (HDACI) could be used to deplete reservoirs of persistent

70 Histone deacetylase inhibitors (HDACIs) activate the prosurvival nuclear factor-kappaB (

71 ions between histone deacetylase inhibitors (HDACIs) and decitabine were investigated in models of di

72 ions between histone deacetylase inhibitors (HDACIs) and the alkyl-lysophospholipid perifosine were e

73 ions between histone deacetylase inhibitors (HDACIs) and the novel proteasome inhibitor carfilzomib (

74 esistance of histone deacetylase inhibitors (HDACIs) are not well understood.

75 Histone deacetylase inhibitors (HDACIs) are therapeutic drugs that inhibit deacetylase a

76 velopment of histone deacetylase inhibitors (HDACIs) as anticancer agents.

77 Histone deacetylase inhibitors (HDACIs) can disrupt the viability of prostate cancer (PC

78 we show that histone deacetylase inhibitors (HDACIs) can inhibit apoptosis of CD4(+) T cells within t

79 nstrate that histone deacetylase inhibitors (HDACIs) enhance toxicity of melanoma differentiation-ass

80 l (2-ME) and histone deacetylase inhibitors (HDACIs) have been investigated in human leukemia cells.

81 ietic cells, histone deacetylase inhibitors (HDACIs) induced RelA hyperacetylation and NF-kappaB acti

82 Histone deacetylase inhibitors (HDACIs) inhibit the growth of a variety of transformed c

83 ggested that histone deacetylase inhibitors (HDACIs) may reduce apoptotic cell death in various model

84 Histone deacetylase inhibitors (HDACIs) produce a marked inhibition of HIF-1alpha expres

85 idol and the histone deacetylase inhibitors (HDACIs) sodium butyrate (NaB) and suberoylanilide hydrox

86 between the histone deacetylase inhibitors (HDACIs) suberoylanilide hydroxamic acid (SAHA) and sodiu

87 sly that the histone deacetylase inhibitors (HDACIs) trichostatin A and sodium butyrate (SB) ameliora

88 Several histone deacetylase inhibitors (HDACIs) were used in vitro to promote the preferential d

89 on (e.g. via histone deacetylase inhibitors (HDACIs)) is essential for restoring terminal cell differ

90 ple, through histone deacetylase inhibitors (HDACIs)) restores apoptosis to cancer cells.

91 ility of the histone deacetylase inhibitors (HDACIs), depsipeptide, sodium butyrate (NaB) and trichos

92 ntrations of histone deacetylase inhibitors (HDACIs).

93 with several histone deacetylase inhibitors (HDACIs).

94 mpounds were histone deacetylase inhibitors (HDACIs).

95 2 different histone deacetylase inhibitors (HDACIs): vorinostat (suberoylanilide hydroxamic acid) an

96 HDAC inhibitors (HDACIs) are currently being explored as anti-cancer agen

97 ing AUD and the efficacy of HDAC inhibitors (HDACIs) in different animal models of AUD may involve cl

98 investigated the effects of HDAC inhibitors (HDACIs) in vitro and in these animal models.

99 NF-kappaB activation by the HDAC inhibitors (HDACIs) MS-275 and suberoylanilide hydroxamic acid was a

100 53 accumulation, Class I/II HDAC inhibitors (HDACIs) protected neurons from p53-dependent cell death

101 inducing NF-kappaB activation, and limiting HDACI lethality in human multiple myeloma (MM) cells.

102 Enforced activation of Akt blocked 2-ME/HDACI-mediated mitochondrial injury, caspase activation,

103 Notably, treatment with 2-ME/HDACIs resulted in down-regulation of thioredoxin, MnSOD

104 hairpin RNA Sirt1 knockdown failed to modify HDACI sensitivity, which suggests that factors other tha

105 Moreover, HDACIs also prevented caspase-3 cleavage in postnatal co

106 Lastly, these new HDACIs were studied for both their anticancer and antima

107 by hexamethylene bisacetamide (HMBA), a non-HDACI tRA-differentiation inducer, as determined by nitr

108 kappaB activation, blocked TNFalpha- but not HDACI-mediated NF-kappaB activation and lethality.

109 t PCa cells with weakened effects on nuclear HDACI targets.

110 (JNK) and p38MAPK activation, abrogation of HDACI-mediated nuclear factor-kappaB activation, AKT ina

111 erapy to optimize the therapeutic benefit of HDACI.

112 However, the development of HDACI to purge latent HIV-1 requires knowledge of the HD

113 system (p21-3H) to evaluate the efficacy of HDACI and the ganciclovir (GCV)-mediated anticancer effe

114 ght explain the cancer-specific lethality of HDACI, and may represent a general therapeutic strategy

115 is also a molecular target for the action of HDACIs, and in this context, a mediator of NB cell death

116 ntly, we found that the co-administration of HDACIs and anti-CTLA4 could further enhance the infiltra

117 e findings indicate that coadministration of HDACIs with perifosine in human leukemia cells leads to

118 FZ) with marginally lethal concentrations of HDACIs (vorinostat, SNDX-275, or SBHA) synergistically i

119 h mutation in FasL, the beneficial effect of HDACIs on AICD of infiltrating CD4(+) T cells is not see

120 tial for evaluating the anticancer effect of HDACIs on cancer cells by multiple molecular imaging mod

121 In this work, we investigated the effect of HDACIs on the regulation of PDH activity in striatal cel

122 FasL regulation in the anti-tumor effect of HDACIs.

123 echanism underlying the anti-tumor effect of HDACIs.

124 raft model were used to study the effects of HDACIs and decitabine in this system.

125 omponent underlying the antitumor effects of HDACIs.

126 s could contribute to the ineffectiveness of HDACIs in PCa treatment.

127 , pharmacokinetics, and toxicity profiles of HDACIs to achieve a better understanding of their effica

128 linical evaluation of depsipeptide and other HDACIs in patients with primary and metastatic UM.

129 ulation of a series of antioxidants in a pan-HDACI-resistant leukemia cell line HL60/LR.

130 mic acid (SAHA), with weakened intrinsic pan-HDACI activities, to target HSP90 and AR in enzalutamide

131 Interactions between resveratrol and pan-HDACIs (vorinostat and panobinostat) were examined in hu

132 azol-4-ylphenyl bearing hydroxamates are pan-HDACIs like SAHA.

133 Exposure to the pan-HDACIs vorinostat or LBH-589 induced phosphorylation of

134 imately ineffective in preventing perifosine/HDACI-mediated apoptosis.

135 emonstrated previously that the hybrid-polar HDACI m-carboxycinnamic acid bis-hydroxamide (CBHA) indu

136 ions (25-50 muM) synergistically potentiated HDACI lethality in AML cell lines and primary AML blasts

137 tetrakis 4-benzoic acid porphyrin) prevented HDACI-induced ROS and NF-kappaB activation while dramati

138 uption of the NF-kappaB cascade in promoting HDACI-mediated lethality.

139 analysis, we identified genes induced by RA, HDACIs, or both together.

140 ere substantially protected from resveratrol/HDACI treatment, which suggests a significant functional

141 o Sirt1 activation contribute to resveratrol/HDACI interactions.

142 Sorafenib + HDACI exposure generated a CD95- and Beclin1-dependent p

143 the sorafenib/HDACI combination (sorafenib + HDACI).

144 -2 family antagonist facilitates sorafenib + HDACI killing via autophagy and the intrinsic pathway.

145 ssing c-FLIP-s, the lethality of sorafenib + HDACI exposure was abolished and was restored when cells

146 The potentiation of sorafenib + HDACI killing by GX15-070 was suppressed by knockdown of

147 of BAX and BAK modestly reduced sorafenib + HDACI lethality but abolished the effects of GX15-070 tr

148 c tumor cells are susceptible to sorafenib + HDACI lethality and that in tumor cells unable to signal

149 95 suppressed the lethality of the sorafenib/HDACI combination (sorafenib + HDACI).

150 Our results suggest HDACIs alone or combined with retinoids may have therape

151 measure nascent transcription, we find that HDACI cause transcriptional repression by blocking RNA p

152 was similar in both groups, indicating that HDACI-induced p21 promoter activation is independent of

153 Our data show that HDACI preferentially repress the transcription of highly

154 nal silencing in colon cancer cells and that HDACIs can activate gene transcription via KDM3A demethy

155 n suppression in colon cancer cells and that HDACIs can inhibit NuRD recruitment to a promoter to act

156 These results demonstrate that HDACIs block Bax-dependent cell death by two distinct me

157 Collectively our data demonstrate that HDACIs enhance MDA-7/IL-24 lethality, and adenoviral del

158 These findings indicate that HDACIs increase CFZ activity in GC- and ABC-DLBCL cells

159 These findings indicate that HDACIs induce Ser-536 phosphorylation of the NF-kappaB s

160 Here, we present data indicating that HDACIs induce the proteasomal degradation of HIF-1alpha

161 Although it has been postulated that HDACIs affect HIF-1alpha expression by enhancing its int

162 These results suggest that HDACIs may be potentially neuroprotective against DA cel

163 Together, these data suggest that HDACIs promote the accumulation of acetylated RelA/p65 i

164 These results suggest that HDACIs, particularly SB, promote the activity of PDH in

165 rve to validate the superior activity of the HDACI 10c.

166 The HDACIs sodium butyrate (NaB), valproate (VPA) and subero

167 -2 and CREB1 phosphorylation mediated by the HDACIs in K562 cells, in conjunction with histone H4 hyp

168 The authors evaluated the effects of the HDACIs vorinostat and m-carboxycinnamic acid bis-hydroxa

169 cologically achievable concentrations of the HDACIs vorinostat or sodium valproate.

170 These HDACIs were evaluated for their ability to inhibit the g

171 The protective effects of these HDACIs coincided with significant increases in histone a

172 All three HDACIs at least partially prevented MPP(+)-mediated apop

173 mechanisms may be involved in resistance to HDACI therapy in leukemia.

174 synthesis may be particularly vulnerable to HDACI lethality.

175 ment of NF-kappaB DNA binding in response to HDACIs and a significant although modest increase in apo

176 failed to undergo acetylation in response to HDACIs, impaired NF-kappaB activation and increased cell

177 Here, we show that NB cells are sensitive to HDACIs, and that the mechanism by which HDACIs induce ap

178 modulating compound increases sensitivity to HDACIs and also overcomes vorinostat resistance.

179 Upon HDACI treatment, acetylated Ku70 releases Bax, allowing

180 D of tumor-infiltrating CD4(+) T cells using HDACIs can enhance anti-tumor immune responses, uncoveri

181 In vivo, HDACIs induced accumulation of acetylated histones in ta

182 ts, the exact mechanism and targets by which HDACIs achieve their antitumor effects remain poorly und

183 degradation, the actual mechanisms by which HDACIs decrease HIF-1alpha levels are not clear.

184 e to HDACIs, and that the mechanism by which HDACIs induce apoptosis involves Bax.

185 Exposure to resveratrol with HDACI induced sustained reactive oxygen species (ROS) ge

186 Coadministration of flavopiridol with HDACIs down-regulated the X-linked inhibitor of apoptosi

187 ontributes to antileukemic interactions with HDACIs, other NF-kappaB-independent flavopiridol actions

188 t resveratrol interacts synergistically with HDACIs in AML cells through multiple ROS-dependent actio