ライフサイエンスコーパス: suberoylanilide hydroxamic acid

1 with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).

2 FDA-approved histone deacetylase inhibitor, suberoylanilide hydroxamic acid.

3 one deacetylase inhibitors trichostatin A or suberoylanilide hydroxamic acid.

4 ere we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of h

5 etylase activity by using trichostatin A and suberoylanilide hydroxamic acid alone or in combination

6 hough histone deacetylase inhibitors such as suberoylanilide hydroxamic acid (also known as vorinosta

7 microM, comparable to or better than that of suberoylanilide hydroxamic acid, an inhibitor of histone

8 Treatment with the pan-HDAC inhibitor, suberoylanilide hydroxamic acid and HDAC3 siRNA resulted

9 o the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.

10 has important implications for the study of suberoylanilide hydroxamic acid and other HDAC inhibitor

11 eal that the histone deacetylase inhibitors, suberoylanilide hydroxamic acid and trichostatin A, fit

12 deacetylase inhibitors (HDACIs): vorinostat (suberoylanilide hydroxamic acid) and valproic acid (VPA)

13 e targets, such as bortezomib, depsipeptide, suberoylanilide hydroxamic acid, and a host of other com

14 inhibitors of HDAC activity, trichostatin A, suberoylanilide hydroxamic acid, and apicidin, induced a

15 he effects of the chemical HDACis PCI-24781, suberoylanilide hydroxamic acid, and MS-275 on a panel o

16 that deacetylase inhibitors (trichostatin A, suberoylanilide hydroxamic acid, and sodium butyrate) pr

17 d was abrogated by butyrate, trichostatin A, suberoylanilide hydroxamic acid, and STAT1 small interfe

18 tone deacetylase inhibitors (trichostatin A, suberoylanilide hydroxamic acid, and tributyrin).

19 enhances the affinity of the HDAC inhibitor suberoylanilide hydroxamic acid by 5-fold.

20 stance to HDAC inhibitors (trichostatin A or suberoylanilide hydroxamic acid), despite induction of g

21 In comparison, the hydroxamate suberoylanilide hydroxamic acid does not discriminate be

22 histone deacetylase inhibitors butyrate and suberoylanilide hydroxamic acid, followed by culture in

23 Indeed, treatment with suberoylanilide hydroxamic acid greatly reduced the expr

24 induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid has strikingly distinct

25 sed to the novel hybrid polar compound SAHA (suberoylanilide hydroxamic acid) have been examined.

26 gized with the histone deacetylase inhibitor suberoylanilide hydroxamic acid in induction of the hype

27 s in constitutive expression and response to suberoylanilide hydroxamic acid in levels of antiapoptot

28 he histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid) in persistent, progress

29 eness of HDAC inhibitors, valproic acid, and suberoylanilide hydroxamic acid, in models of pulmonary

30 e show that low micromolar concentrations of suberoylanilide hydroxamic acid induce the expression of

31 oxamic acid-based HDACIs such as vorinostat (suberoylanilide hydroxamic acid) induce the differentiat

32 The broad-spectrum HDAC inhibitor suberoylanilide hydroxamic acid induced AQP3 mRNA and pr

33 15-lipoxygenase-1 significantly reduced the suberoylanilide hydroxamic acid-induced effects.

34 ression of 15-lipoxygenase-1 correlates with suberoylanilide hydroxamic acid-induced increase in 13-S

35 Both valproic acid and suberoylanilide hydroxamic acid inhibited the imprinted

36 Because suberoylanilide hydroxamic acid is already approved to t

37 Because of its low toxicity, suberoylanilide hydroxamic acid is currently in clinical

38 One such agent, suberoylanilide hydroxamic acid, is a potent inhibitor o

39 Combining b-AP15 with suberoylanilide hydroxamic acid, lenalidomide, or dexame

40 ellular mechanisms by which HDAC inhibitors (suberoylanilide hydroxamic acid, m-carboxycinnamic acid

41 cells with HDAC inhibitors (trichostatin A, suberoylanilide hydroxamic acid, MS-275, and OSU-HDAC42)

42 Four HDAI (depsipeptide, suberoylanilide hydroxamic acid, MS-275, and trichostati

43 that histone deacetylase inhibitors, such as suberoylanilide hydroxamic acid, not only inhibit deacet

44 coordinate activation of Akt/p300 pathway by suberoylanilide hydroxamic acid occurs at the chromatin

45 th camptothecin and sodium butyrate (NaB) or suberoylanilide hydroxamic acid on the day of, the day b

46 HDAC inhibition using suberoylanilide hydroxamic acid or MS-275 significantly

47 peat (LTR), subsequent exposure to the HDACi suberoylanilide hydroxamic acid or vorinostat (VOR) resu

48 optosis following treatment with bortezomib, suberoylanilide hydroxamic acid, or the combination, sho

49 DAC) activity, butyrate, trichostatin A, and suberoylanilide hydroxamic acid, prevented IFNgamma-indu

50 c therapy, the histone deacetylase inhibitor suberoylanilide hydroxamic acid, restored miR-200a expre

51 ne deacetylase inhibitors, valproic acid and suberoylanilide hydroxamic acid, restored the expression

52 A clinically approved HDAC inhibitor (suberoylanilide hydroxamic acid) reverses the dysregulat

53 pares cyclosporin A (CyA) with the pan-HDACi suberoylanilide hydroxamic acid (SAHA) and a novel HDAC6

54 These dual-acting agents are derived from suberoylanilide hydroxamic acid (SAHA) and anthracycline

55 e mechanisms of action of 2 HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA) and ITF 2357, on

56 he development of the second-generation HPCs suberoylanilide hydroxamic acid (SAHA) and m-carboxycinn

57 In this study we found that the HDACi suberoylanilide hydroxamic acid (SAHA) and MS-275, a ben

58 fferential sensitivity to the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) and PARP inhibito

59 for cancer, and two HDAC inhibitors, namely suberoylanilide hydroxamic acid (SAHA) and romidepsin, h

60 the histone deacetylase inhibitors (HDACIs) suberoylanilide hydroxamic acid (SAHA) and sodium butyra

61 d osteoblasts, MC3T3 cells were treated with suberoylanilide hydroxamic acid (SAHA) and subjected to

62 nces both the affinity of the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) and the Michaelis

63 istone deacetylase (HDAC) inhibitors such as suberoylanilide hydroxamic acid (SAHA) are known to indu

64 nt with histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) corrected the VLC

65 ith 250 nM imatinib mesylate and 2.0 micro M suberoylanilide hydroxamic acid (SAHA) for 24 h, exposur

66 Suberoylanilide hydroxamic acid (SAHA) has been approved

67 nhibitors (HDACIs) sodium butyrate (NaB) and suberoylanilide hydroxamic acid (SAHA) have been examine

68 nd that histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) increased AQP5 ex

69 Suberoylanilide hydroxamic acid (SAHA) is a histone deac

70 Suberoylanilide hydroxamic acid (SAHA) is a novel histon

71 Suberoylanilide hydroxamic acid (SAHA) is a potent inhib

72 Suberoylanilide hydroxamic acid (SAHA) is a prototype of

73 Suberoylanilide hydroxamic acid (SAHA) is an HDAC inhibi

74 The histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) is being evaluate

75 lammation, the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) is currently in c

76 Suberoylanilide hydroxamic acid (SAHA) is currently in c

77 rodrug of the canonical broad-spectrum HDACi suberoylanilide hydroxamic acid (SAHA) is described.

78 The HDACi suberoylanilide hydroxamic acid (SAHA) is in phase I/II

79 Suberoylanilide hydroxamic acid (SAHA) is the first HDAC

80 Suberoylanilide hydroxamic acid (SAHA) is the prototype

81 ith the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) led to a dramatic

82 tivated by the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) only after DNMT-1

83 toxic concentrations of bortezomib + either suberoylanilide hydroxamic acid (SAHA) or sodium butyrat

84 o additional classes of HDAC inhibitors, and suberoylanilide hydroxamic acid (SAHA) reactivated EBV i

85 In this study, we demonstrate that suberoylanilide hydroxamic acid (SAHA) reactivates HIV f

86 ator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease

87 s sodium butyrate (NaB), valproate (VPA) and suberoylanilide hydroxamic acid (SAHA) were tested for t

88 hesis of N-hydroxy-N(1)-phenyloctanediamide (suberoylanilide hydroxamic acid (SAHA)), providing the p

89 By chemical library screening, we identified suberoylanilide hydroxamic acid (SAHA), a Food and Drug

90 In this study, we determined whether suberoylanilide hydroxamic acid (SAHA), a histone deacet

91 Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacet

92 effect that is amplified when combined with suberoylanilide hydroxamic acid (SAHA), a histone deacet

93 To this end, it is also noteworthy that suberoylanilide hydroxamic acid (SAHA), a polar compound

94 Suberoylanilide hydroxamic acid (SAHA), a potent differe

95 ith the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA), acting in part t

96 Suberoylanilide hydroxamic acid (SAHA), an orally admini

97 ne-N,N-dimethylcarboxamide) malonate (EMBA), suberoylanilide hydroxamic acid (SAHA), and m-carboxycin

98 s such as hexamethylene bisacetamide (HMBA), suberoylanilide hydroxamic acid (SAHA), and other histon

99 For the binding of trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA), and two other SA

100 tural elements of the general HDAC inhibitor suberoylanilide hydroxamic acid (SAHA), as well as benzo

101 Finally, we demonstrate that prostratin and suberoylanilide hydroxamic acid (SAHA), but not hexameth

102 inhibitors, such as trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA), have anti-tumour

103 lase (HDAC) inhibitor, OSU-HDAC42, vis-a-vis suberoylanilide hydroxamic acid (SAHA), in in vitro and

104 Hybrid polar compounds (HPCs), such as suberoylanilide hydroxamic acid (SAHA), induce different

105 t two distinct HDAC inhibitors, butyrate and suberoylanilide hydroxamic acid (SAHA), induced caspase-

106 c acid-based hybrid polar compounds, such as suberoylanilide hydroxamic acid (SAHA), induces differen

107 One of the HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA), is currently bei

108 Coadministration of sodium butyrate, suberoylanilide hydroxamic acid (SAHA), or trichostatin

109 ecently showed that HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), potently induce

110 Histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), restored Ogg1 ex

111 eveloped a class of HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), that were initia

112 n this study, we characterized the effect of suberoylanilide hydroxamic acid (SAHA), the prototype of

113 rtial chemical scaffolds of enzalutamide and suberoylanilide hydroxamic acid (SAHA), with weakened in

114 cally promising drugs-namely, prostratin and suberoylanilide hydroxamic acid (SAHA)-overcomes the lim

115 bitors trichostatin (TSA, 1), MS-275 (2) and suberoylanilide hydroxamic acid (SAHA, 3) arrest growth

116 The path to the discovery of suberoylanilide hydroxamic acid (SAHA, vorinostat) began

117 5-aza-2'-deoxycytidine [5azaD]), followed by suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or t

118 , we followed a path that led us to discover suberoylanilide hydroxamic acid (SAHA; vorinostat (Zolin

119 tration of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA; vorinostat) show

120 We showed that suberoylanilide hydroxamic acid (SAHA; vorinostat), one

121 e treated with trichostatin A or vorinostat (suberoylanilide hydroxamic acid [SAHA]) to evaluate the

122 Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deac

123 he histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid, SAHA) were evaluated in

124 ibitors trichostatin A (TSA) and vorinostat (suberoylanilide hydroxamic acid, SAHA), although largazo

125 Here, we show that the HDACi, vorinostat (Suberoylanilide hydroxamic acid, SAHA), induces DNA doub

126 PAD4 inhibitor Cl-amidine and HDAC inhibitor suberoylanilide hydroxamic acid show additive effects in

127 mice with the histone deacetylase inhibitor suberoylanilide hydroxamic acid significantly decreased

128 site-directed mutant proteins, we find that suberoylanilide hydroxamic acid stimulates Akt activity,

129 Here we provide evidence that suberoylanilide hydroxamic acid stimulates NF-kappaB tra

130 d by HDAC inhibitors valproic acid (VPA) and suberoylanilide hydroxamic acid than SW620 or HT-29 cell

131 n of the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) to animals reared in a

132 ells were downregulated by valproic acid and suberoylanilide hydroxamic acid treatment.

133 Trichostatin A and suberoylanilide hydroxamic acid, two broad spectrum HDAC

134 Trichostatin A and suberoylanilide hydroxamic acid, two structurally relate

135 sponse to the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (vorinostat), a new anti

136 valproic acid, a class I HDAC inhibitor, and suberoylanilide hydroxamic acid (vorinostat), an inhibit

137 n by the HDAC inhibitors (HDACIs) MS-275 and suberoylanilide hydroxamic acid was associated with hype

138 Exposure to valproic acid and suberoylanilide hydroxamic acid was associated with incr

139 in down-regulating phospho-Akt, followed by suberoylanilide hydroxamic acid, whereas MS-275 shows on

140 When cells were treated with suberoylanilide hydroxamic acid, which releases P-TEFb f

141 mbination with histone deacetylase inhibitor suberoylanilide hydroxamic acid, WIF1 promoter activity