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1 with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).
2 than the previously described small molecule suberoylanilide hydroxamic acid.
3  FDA-approved histone deacetylase inhibitor, suberoylanilide hydroxamic acid.
4 one deacetylase inhibitors trichostatin A or suberoylanilide hydroxamic acid.
5 ere we demonstrate that treatment with SAHA (suberoylanilide hydroxamic acid), a known inhibitor of h
6 by treatment with the proteostasis regulator suberoylanilide hydroxamic acid, a histone deacetylase i
7 etylase activity by using trichostatin A and suberoylanilide hydroxamic acid alone or in combination
8 hough histone deacetylase inhibitors such as suberoylanilide hydroxamic acid (also known as vorinosta
9 microM, comparable to or better than that of suberoylanilide hydroxamic acid, an inhibitor of histone
10       Treatment with the pan-HDAC inhibitor, suberoylanilide hydroxamic acid and HDAC3 siRNA resulted
11 o the histone deacetylase inhibitors (HDACi) suberoylanilide hydroxamic acid and LAQ824.
12  has important implications for the study of suberoylanilide hydroxamic acid and other HDAC inhibitor
13 eal that the histone deacetylase inhibitors, suberoylanilide hydroxamic acid and trichostatin A, fit
14 deacetylase inhibitors (HDACIs): vorinostat (suberoylanilide hydroxamic acid) and valproic acid (VPA)
15 e targets, such as bortezomib, depsipeptide, suberoylanilide hydroxamic acid, and a host of other com
16 inhibitors of HDAC activity, trichostatin A, suberoylanilide hydroxamic acid, and apicidin, induced a
17 he effects of the chemical HDACis PCI-24781, suberoylanilide hydroxamic acid, and MS-275 on a panel o
18 that deacetylase inhibitors (trichostatin A, suberoylanilide hydroxamic acid, and sodium butyrate) pr
19 d was abrogated by butyrate, trichostatin A, suberoylanilide hydroxamic acid, and STAT1 small interfe
20 tone deacetylase inhibitors (trichostatin A, suberoylanilide hydroxamic acid, and tributyrin).
21  enhances the affinity of the HDAC inhibitor suberoylanilide hydroxamic acid by 5-fold.
22 stance to HDAC inhibitors (trichostatin A or suberoylanilide hydroxamic acid), despite induction of g
23               In comparison, the hydroxamate suberoylanilide hydroxamic acid does not discriminate be
24  histone deacetylase inhibitors butyrate and suberoylanilide hydroxamic acid, followed by culture in
25                       Indeed, treatment with suberoylanilide hydroxamic acid greatly reduced the expr
26 induced by the histone deacetylase inhibitor suberoylanilide hydroxamic acid has strikingly distinct
27 sed to the novel hybrid polar compound SAHA (suberoylanilide hydroxamic acid) have been examined.
28 gized with the histone deacetylase inhibitor suberoylanilide hydroxamic acid in induction of the hype
29 s in constitutive expression and response to suberoylanilide hydroxamic acid in levels of antiapoptot
30 d HDAC inhibitors 5-Aza-2'-deoxycytidine and suberoylanilide hydroxamic acid in vitro, and proved ver
31 he histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid) in persistent, progress
32 eness of HDAC inhibitors, valproic acid, and suberoylanilide hydroxamic acid, in models of pulmonary
33 e show that low micromolar concentrations of suberoylanilide hydroxamic acid induce the expression of
34 oxamic acid-based HDACIs such as vorinostat (suberoylanilide hydroxamic acid) induce the differentiat
35            The broad-spectrum HDAC inhibitor suberoylanilide hydroxamic acid induced AQP3 mRNA and pr
36  15-lipoxygenase-1 significantly reduced the suberoylanilide hydroxamic acid-induced effects.
37 ression of 15-lipoxygenase-1 correlates with suberoylanilide hydroxamic acid-induced increase in 13-S
38                       Both valproic acid and suberoylanilide hydroxamic acid inhibited the imprinted
39                                      Because suberoylanilide hydroxamic acid is already approved to t
40                 Because of its low toxicity, suberoylanilide hydroxamic acid is currently in clinical
41                              One such agent, suberoylanilide hydroxamic acid, is a potent inhibitor o
42                        Combining b-AP15 with suberoylanilide hydroxamic acid, lenalidomide, or dexame
43 ellular mechanisms by which HDAC inhibitors (suberoylanilide hydroxamic acid, m-carboxycinnamic acid
44  cells with HDAC inhibitors (trichostatin A, suberoylanilide hydroxamic acid, MS-275, and OSU-HDAC42)
45                     Four HDAI (depsipeptide, suberoylanilide hydroxamic acid, MS-275, and trichostati
46 that histone deacetylase inhibitors, such as suberoylanilide hydroxamic acid, not only inhibit deacet
47 coordinate activation of Akt/p300 pathway by suberoylanilide hydroxamic acid occurs at the chromatin
48 th camptothecin and sodium butyrate (NaB) or suberoylanilide hydroxamic acid on the day of, the day b
49                        HDAC inhibition using suberoylanilide hydroxamic acid or MS-275 significantly
50 peat (LTR), subsequent exposure to the HDACi suberoylanilide hydroxamic acid or vorinostat (VOR) resu
51 optosis following treatment with bortezomib, suberoylanilide hydroxamic acid, or the combination, sho
52 DAC) activity, butyrate, trichostatin A, and suberoylanilide hydroxamic acid, prevented IFNgamma-indu
53 c therapy, the histone deacetylase inhibitor suberoylanilide hydroxamic acid, restored miR-200a expre
54 ne deacetylase inhibitors, valproic acid and suberoylanilide hydroxamic acid, restored the expression
55        A clinically approved HDAC inhibitor (suberoylanilide hydroxamic acid) reverses the dysregulat
56 pares cyclosporin A (CyA) with the pan-HDACi suberoylanilide hydroxamic acid (SAHA) and a novel HDAC6
57    These dual-acting agents are derived from suberoylanilide hydroxamic acid (SAHA) and anthracycline
58 e mechanisms of action of 2 HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA) and ITF 2357, on
59 he development of the second-generation HPCs suberoylanilide hydroxamic acid (SAHA) and m-carboxycinn
60        In this study we found that the HDACi suberoylanilide hydroxamic acid (SAHA) and MS-275, a ben
61 fferential sensitivity to the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) and PARP inhibito
62  for cancer, and two HDAC inhibitors, namely suberoylanilide hydroxamic acid (SAHA) and romidepsin, h
63  the histone deacetylase inhibitors (HDACIs) suberoylanilide hydroxamic acid (SAHA) and sodium butyra
64 d osteoblasts, MC3T3 cells were treated with suberoylanilide hydroxamic acid (SAHA) and subjected to
65 nces both the affinity of the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) and the Michaelis
66                                    Pan-HDACi suberoylanilide hydroxamic acid (SAHA) and/or ITF2357 (g
67 istone deacetylase (HDAC) inhibitors such as suberoylanilide hydroxamic acid (SAHA) are known to indu
68 nt with histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) corrected the VLC
69          Here, we present new functionalized suberoylanilide hydroxamic acid (SAHA) derivatives that
70 ith 250 nM imatinib mesylate and 2.0 micro M suberoylanilide hydroxamic acid (SAHA) for 24 h, exposur
71                                              Suberoylanilide hydroxamic acid (SAHA) has been approved
72 nhibitors (HDACIs) sodium butyrate (NaB) and suberoylanilide hydroxamic acid (SAHA) have been examine
73 nd that histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) increased AQP5 ex
74                                              Suberoylanilide hydroxamic acid (SAHA) is a histone deac
75                                              Suberoylanilide hydroxamic acid (SAHA) is a novel histon
76                                              Suberoylanilide hydroxamic acid (SAHA) is a potent inhib
77                                              Suberoylanilide hydroxamic acid (SAHA) is a prototype of
78                                              Suberoylanilide hydroxamic acid (SAHA) is an HDAC inhibi
79     The histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) is being evaluate
80 lammation, the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) is currently in c
81                                              Suberoylanilide hydroxamic acid (SAHA) is currently in c
82 rodrug of the canonical broad-spectrum HDACi suberoylanilide hydroxamic acid (SAHA) is described.
83                                    The HDACi suberoylanilide hydroxamic acid (SAHA) is in phase I/II
84                                              Suberoylanilide hydroxamic acid (SAHA) is the first HDAC
85                                              Suberoylanilide hydroxamic acid (SAHA) is the prototype
86 ith the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) led to a dramatic
87 sought to study the effect of HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) on experimental f
88 tivated by the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) only after DNMT-1
89  toxic concentrations of bortezomib + either suberoylanilide hydroxamic acid (SAHA) or sodium butyrat
90 o additional classes of HDAC inhibitors, and suberoylanilide hydroxamic acid (SAHA) reactivated EBV i
91           In this study, we demonstrate that suberoylanilide hydroxamic acid (SAHA) reactivates HIV f
92 ator STAT6 and that inhibition of STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease
93 s sodium butyrate (NaB), valproate (VPA) and suberoylanilide hydroxamic acid (SAHA) were tested for t
94 hesis of N-hydroxy-N(1)-phenyloctanediamide (suberoylanilide hydroxamic acid (SAHA)), providing the p
95 By chemical library screening, we identified suberoylanilide hydroxamic acid (SAHA), a Food and Drug
96         In this study, we determined whether suberoylanilide hydroxamic acid (SAHA), a histone deacet
97  effect that is amplified when combined with suberoylanilide hydroxamic acid (SAHA), a histone deacet
98          Here, we tested the hypothesis that suberoylanilide hydroxamic acid (SAHA), a histone deacet
99      To this end, it is also noteworthy that suberoylanilide hydroxamic acid (SAHA), a polar compound
100                                              Suberoylanilide hydroxamic acid (SAHA), a potent differe
101 ith the histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA), acting in part t
102                                              Suberoylanilide hydroxamic acid (SAHA), an orally admini
103 ne-N,N-dimethylcarboxamide) malonate (EMBA), suberoylanilide hydroxamic acid (SAHA), and m-carboxycin
104 s such as hexamethylene bisacetamide (HMBA), suberoylanilide hydroxamic acid (SAHA), and other histon
105     For the binding of trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA), and two other SA
106 tural elements of the general HDAC inhibitor suberoylanilide hydroxamic acid (SAHA), as well as benzo
107  Finally, we demonstrate that prostratin and suberoylanilide hydroxamic acid (SAHA), but not hexameth
108                                   One HDACi, suberoylanilide hydroxamic acid (SAHA), exhibits off-tar
109 inhibitors, such as trichostatin A (TSA) and suberoylanilide hydroxamic acid (SAHA), have anti-tumour
110 lase (HDAC) inhibitor, OSU-HDAC42, vis-a-vis suberoylanilide hydroxamic acid (SAHA), in in vitro and
111       Hybrid polar compounds (HPCs), such as suberoylanilide hydroxamic acid (SAHA), induce different
112 t two distinct HDAC inhibitors, butyrate and suberoylanilide hydroxamic acid (SAHA), induced caspase-
113 c acid-based hybrid polar compounds, such as suberoylanilide hydroxamic acid (SAHA), induces differen
114                  One of the HDAC inhibitors, suberoylanilide hydroxamic acid (SAHA), is currently bei
115         Coadministration of sodium butyrate, suberoylanilide hydroxamic acid (SAHA), or trichostatin
116 ecently showed that HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), potently induce
117        Histone deacetylase (HDAC) inhibitor, suberoylanilide hydroxamic acid (SAHA), restored Ogg1 ex
118 eveloped a class of HDAC inhibitors, such as suberoylanilide hydroxamic acid (SAHA), that were initia
119 n this study, we characterized the effect of suberoylanilide hydroxamic acid (SAHA), the prototype of
120 rtial chemical scaffolds of enzalutamide and suberoylanilide hydroxamic acid (SAHA), with weakened in
121 cally promising drugs-namely, prostratin and suberoylanilide hydroxamic acid (SAHA)-overcomes the lim
122 NA induced by the class I/IIb HDAC inhibitor suberoylanilide hydroxamic acid (SAHA).
123 bitors trichostatin (TSA, 1), MS-275 (2) and suberoylanilide hydroxamic acid (SAHA, 3) arrest growth
124 -characterized histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA, a.k.a. Vorinostat
125                 The path to the discovery of suberoylanilide hydroxamic acid (SAHA, vorinostat) began
126 oad-spectrum HDACi, Trichostatin A (TSA) and Suberoylanilide Hydroxamic Acid (SAHA, Vorinostat), alon
127 5-aza-2'-deoxycytidine [5azaD]), followed by suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or t
128 , we followed a path that led us to discover suberoylanilide hydroxamic acid (SAHA; vorinostat (Zolin
129 tration of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA; vorinostat) show
130                               We showed that suberoylanilide hydroxamic acid (SAHA; vorinostat), one
131 e treated with trichostatin A or vorinostat (suberoylanilide hydroxamic acid [SAHA]) to evaluate the
132                                  Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deac
133 -PP-F11N with the HDAC inhibitor vorinostat (suberoylanilide hydroxamic acid, SAHA) significantly red
134                   HDAC inhibitor vorinostat (suberoylanilide hydroxamic acid, SAHA) was used to exami
135 he histone deacetylase inhibitor vorinostat (suberoylanilide hydroxamic acid, SAHA) were evaluated in
136 ibitors trichostatin A (TSA) and vorinostat (suberoylanilide hydroxamic acid, SAHA), although largazo
137    Here, we show that the HDACi, vorinostat (Suberoylanilide hydroxamic acid, SAHA), induces DNA doub
138 PAD4 inhibitor Cl-amidine and HDAC inhibitor suberoylanilide hydroxamic acid show additive effects in
139  mice with the histone deacetylase inhibitor suberoylanilide hydroxamic acid significantly decreased
140  site-directed mutant proteins, we find that suberoylanilide hydroxamic acid stimulates Akt activity,
141                Here we provide evidence that suberoylanilide hydroxamic acid stimulates NF-kappaB tra
142 d by HDAC inhibitors valproic acid (VPA) and suberoylanilide hydroxamic acid than SW620 or HT-29 cell
143 n of the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) to animals reared in a
144 ells were downregulated by valproic acid and suberoylanilide hydroxamic acid treatment.
145                           Trichostatin A and suberoylanilide hydroxamic acid, two broad spectrum HDAC
146                           Trichostatin A and suberoylanilide hydroxamic acid, two structurally relate
147                                    The HDACi suberoylanilide hydroxamic acid (vorinostat [VOR]) has b
148                       FK228 (romidepsin) and suberoylanilide hydroxamic acid (vorinostat) are histone
149 sponse to the histone deacetylase inhibitor, suberoylanilide hydroxamic acid (vorinostat), a new anti
150 valproic acid, a class I HDAC inhibitor, and suberoylanilide hydroxamic acid (vorinostat), an inhibit
151  the clinically approved prototypical HDACi, suberoylanilide hydroxamic acid (vorinostat).
152 f Dnmt1 by the histone deacetylase inhibitor suberoylanilide hydroxamic acid was associated with decr
153 n by the HDAC inhibitors (HDACIs) MS-275 and suberoylanilide hydroxamic acid was associated with hype
154                Exposure to valproic acid and suberoylanilide hydroxamic acid was associated with incr
155  in down-regulating phospho-Akt, followed by suberoylanilide hydroxamic acid, whereas MS-275 shows on
156                 When cells were treated with suberoylanilide hydroxamic acid, which releases P-TEFb f
157 mbination with histone deacetylase inhibitor suberoylanilide hydroxamic acid, WIF1 promoter activity

 
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