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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                                  Despite all HDACIs having a similar mechanism of action, their uniqu
15                  In combination with RA, all HDACIs tested overcame the transcriptional repression ex
16                       We have established an HDACI-inducible, p21-driven reporter system that has the
17  the combination of an anthracycline with an HDACI should have significant clinical activity in patie
18 istone acetylation are activated by ATRA and HDACI, induce MDR1 in APL cells, and point to the critic
19 utic effect by combined treatment of GCV and HDACI.
20 iting BCL-2 family function on sorafenib and HDACI lethality.
21                             However, VDA and HDACI when combined were successful in de-repressing VDR
22 nvestigation of strategies combining CFZ and HDACIs in DLBCL.
23 xtent to the combination of flavopiridol and HDACIs.
24 hich antileukemic synergism between 2-ME and HDACIs stems primarily from induction of oxidative damag
25 l of animals carrying orthotopic tumors, and HDACIs enhanced survival further.
26 t with SB and sodium phenylbutyrate, another HDACI, recovered cell viability and overall mitochondria
27 gomyelinase inhibitor desipramine attenuated HDACI/perifosine-mediated ceramide and ROS production as
28                        Hydroxamic acid-based HDACIs such as vorinostat (suberoylanilide hydroxamic ac
29 CAP region of a set of triazolylphenyl-based HDACIs, and show that the nature of substitution on the
30 Inhibition of JNK1 activation attenuated Bay/HDACI lethality without affecting NF-kappaB inactivation
31 dramatically protected cells against the Bay/HDACI regimen but failed to prevent ROS production and J
32  L-cysteine blocked apoptosis induced by Bay/HDACIs by abrogating ROS generation.
33 e investigation whether associations between HDACIs' ADR profiles and their physicochemical and pharm
34 f reactive oxygen species and Ca(2+) blocked HDACI and MDA-7/IL-24 killing.
35  kinase (MEK) 1 or myristoylated Akt blocked HDACI/perifosine-mediated ceramide production and cell d
36 icantly, siRNA NEMO or ATM knockdown blocked HDACI-mediated NF-kappaB activation, resulting in dimini
37                                         Both HDACIs were effective against both Rb cell lines, induci
38 e accumulation; this effect was abrogated by HDACI coadministration, which suggests that cells underg
39     In contrast, genes that are activated by HDACI are moderately expressed.
40 V)-mediated anticancer effect contributed by HDACI-induced and p21-driven truncated herpes simplex vi
41 ber genes are more likely to be repressed by HDACI than non-amplified genes.
42 es markedly potentiated apoptosis induced by HDACIs, and this was accompanied by enhanced reactive ox
43  to 15-LOX-1 transcriptional reactivation by HDACIs in colon cancer cells.
44 dings indicate that in human leukemia cells, HDACIs activate the cytoprotective NF-kappaB pathway thr
45 lucidate the pharmacodynamics of combination HDACIs and endocrine therapy.
46 ls using a chemical approach that correlates HDACI isoform specificity with their ability to reactiva
47 uper-repressor transfected cells) diminished HDACI-mediated Mn-SOD2 induction and increased ROS accum
48 typical ATM/NEMO nuclear pathway can enhance HDACI antileukemic activity.
49 6 phosphorylation and significantly enhanced HDACI susceptibility.
50                                 All explored HDACIs in combination with decitabine produced a synergi
51  was also unable to prevent the flavopiridol/HDACI regimen from inducing a conformational change in a
52 n with respect to the nuclear pore following HDACI treatment, including the recruitment of promoter r
53                                 Furthermore, HDACI-induced OX40L inhibited the generation of IL-10-pr
54                           Uncertainty of how HDACI-induced protein acetylation leads to cell death, h
55  human SH-SY5Y neuroblastoma cells, however, HDACIs were not able to prevent p53-dependent cell death
56  we herein report the development of class I HDACIs, including information regarding their structure,
57 RelA acetylation and NF-kappaB activation in HDACI-treated cells.
58 enetic means leads to a dramatic increase in HDACI-mediated lethality through enhanced oxidative dama
59 orylation sites also significantly increased HDACI lethality.
60 and the novel histone deacetylase inhibitor (HDACI) depsipeptide (FK228) induced P-gp expression and
61  by the novel histone deacetylase inhibitor (HDACI) LAQ824 were examined in human leukemia cells (U93
62  flavopiridol/histone deacetylase inhibitor (HDACI) regimen, arguing against the involvement of the r
63 riazole-based histone deacetylase inhibitor (HDACI), octanedioic acid hydroxyamide[3-(1-phenyl-1H-[1,
64 rate (NaB), a histone deacetylase inhibitor (HDACI), or by hexamethylene bisacetamide (HMBA), a non-H
65 ms underlying histone deacetylase inhibitor (HDACI)-mediated NF-kappaB activation were investigated i
66 e of a potent histone deacetylase inhibitor (HDACI).
67 r a VDR agonist (VDA) nor an HDAC inhibitor (HDACI) nor a demethylating agent (DAC) individually coul
68              Histone deacetylase inhibitors (HDACI) are promising antitumor agents.
69 orafenib and histone deacetylase inhibitors (HDACI) interact to kill pancreatic carcinoma cells and d
70 eatment with histone deacetylase inhibitors (HDACI) results in potent cytotoxicity of a variety of ca
71 ign selective histone deactylase inhibitors (HDACI), we discovered that the aryl urea 1 is a modestly
72                    As such, HDAC inhibitors (HDACI) could be used to deplete reservoirs of persistent
73              Histone deacetylase inhibitors (HDACIs) activate the prosurvival nuclear factor-kappaB (
74 ions between histone deacetylase inhibitors (HDACIs) and decitabine were investigated in models of di
75 ions between histone deacetylase inhibitors (HDACIs) and the alkyl-lysophospholipid perifosine were e
76 ions between histone deacetylase inhibitors (HDACIs) and the novel proteasome inhibitor carfilzomib (
77 esistance of histone deacetylase inhibitors (HDACIs) are not well understood.
78              Histone deacetylase inhibitors (HDACIs) are therapeutic drugs that inhibit deacetylase a
79 velopment of histone deacetylase inhibitors (HDACIs) as anticancer agents.
80              Histone deacetylase inhibitors (HDACIs) can disrupt the viability of prostate cancer (PC
81 we show that histone deacetylase inhibitors (HDACIs) can inhibit apoptosis of CD4(+) T cells within t
82 nstrate that histone deacetylase inhibitors (HDACIs) enhance toxicity of melanoma differentiation-ass
83 l (2-ME) and histone deacetylase inhibitors (HDACIs) have been investigated in human leukemia cells.
84 ietic cells, histone deacetylase inhibitors (HDACIs) induced RelA hyperacetylation and NF-kappaB acti
85              Histone deacetylase inhibitors (HDACIs) inhibit the growth of a variety of transformed c
86              Histone deacetylase inhibitors (HDACIs) may overcome endocrine resistance in estrogen re
87 ggested that histone deacetylase inhibitors (HDACIs) may reduce apoptotic cell death in various model
88              Histone deacetylase inhibitors (HDACIs) produce a marked inhibition of HIF-1alpha expres
89 idol and the histone deacetylase inhibitors (HDACIs) sodium butyrate (NaB) and suberoylanilide hydrox
90  between the histone deacetylase inhibitors (HDACIs) suberoylanilide hydroxamic acid (SAHA) and sodiu
91 sly that the histone deacetylase inhibitors (HDACIs) trichostatin A and sodium butyrate (SB) ameliora
92 erability of histone deacetylase inhibitors (HDACIs) were always a matter of concern.
93      Several histone deacetylase inhibitors (HDACIs) were used in vitro to promote the preferential d
94 on (e.g. via histone deacetylase inhibitors (HDACIs)) is essential for restoring terminal cell differ
95 ple, through histone deacetylase inhibitors (HDACIs)) restores apoptosis to cancer cells.
96 ility of the histone deacetylase inhibitors (HDACIs), depsipeptide, sodium butyrate (NaB) and trichos
97 mpounds were histone deacetylase inhibitors (HDACIs).
98 ntrations of histone deacetylase inhibitors (HDACIs).
99 with several histone deacetylase inhibitors (HDACIs).
100  2 different histone deacetylase inhibitors (HDACIs): vorinostat (suberoylanilide hydroxamic acid) an
101                             HDAC inhibitors (HDACIs) are currently being explored as anti-cancer agen
102 ing AUD and the efficacy of HDAC inhibitors (HDACIs) in different animal models of AUD may involve cl
103 investigated the effects of HDAC inhibitors (HDACIs) in vitro and in these animal models.
104 NF-kappaB activation by the HDAC inhibitors (HDACIs) MS-275 and suberoylanilide hydroxamic acid was a
105 53 accumulation, Class I/II HDAC inhibitors (HDACIs) protected neurons from p53-dependent cell death
106  inducing NF-kappaB activation, and limiting HDACI lethality in human multiple myeloma (MM) cells.
107      Enforced activation of Akt blocked 2-ME/HDACI-mediated mitochondrial injury, caspase activation,
108                 Notably, treatment with 2-ME/HDACIs resulted in down-regulation of thioredoxin, MnSOD
109 hairpin RNA Sirt1 knockdown failed to modify HDACI sensitivity, which suggests that factors other tha
110                                    Moreover, HDACIs also prevented caspase-3 cleavage in postnatal co
111                            Lastly, these new HDACIs were studied for both their anticancer and antima
112  by hexamethylene bisacetamide (HMBA), a non-HDACI tRA-differentiation inducer, as determined by nitr
113 kappaB activation, blocked TNFalpha- but not HDACI-mediated NF-kappaB activation and lethality.
114 t PCa cells with weakened effects on nuclear HDACI targets.
115  (JNK) and p38MAPK activation, abrogation of HDACI-mediated nuclear factor-kappaB activation, AKT ina
116 erapy to optimize the therapeutic benefit of HDACI.
117                  However, the development of HDACI to purge latent HIV-1 requires knowledge of the HD
118  system (p21-3H) to evaluate the efficacy of HDACI and the ganciclovir (GCV)-mediated anticancer effe
119 ght explain the cancer-specific lethality of HDACI, and may represent a general therapeutic strategy
120 is also a molecular target for the action of HDACIs, and in this context, a mediator of NB cell death
121 ntly, we found that the co-administration of HDACIs and anti-CTLA4 could further enhance the infiltra
122                                  The ADRs of HDACIs were curated from the World Health Organisation (
123 e findings indicate that coadministration of HDACIs with perifosine in human leukemia cells leads to
124 FZ) with marginally lethal concentrations of HDACIs (vorinostat, SNDX-275, or SBHA) synergistically i
125 h mutation in FasL, the beneficial effect of HDACIs on AICD of infiltrating CD4(+) T cells is not see
126 tial for evaluating the anticancer effect of HDACIs on cancer cells by multiple molecular imaging mod
127  In this work, we investigated the effect of HDACIs on the regulation of PDH activity in striatal cel
128  FasL regulation in the anti-tumor effect of HDACIs.
129 echanism underlying the anti-tumor effect of HDACIs.
130 raft model were used to study the effects of HDACIs and decitabine in this system.
131 omponent underlying the antitumor effects of HDACIs.
132 s could contribute to the ineffectiveness of HDACIs in PCa treatment.
133 , pharmacokinetics, and toxicity profiles of HDACIs to achieve a better understanding of their effica
134 linical evaluation of depsipeptide and other HDACIs in patients with primary and metastatic UM.
135 ulation of a series of antioxidants in a pan-HDACI-resistant leukemia cell line HL60/LR.
136 mic acid (SAHA), with weakened intrinsic pan-HDACI activities, to target HSP90 and AR in enzalutamide
137     Interactions between resveratrol and pan-HDACIs (vorinostat and panobinostat) were examined in hu
138 azol-4-ylphenyl bearing hydroxamates are pan-HDACIs like SAHA.
139                          Exposure to the pan-HDACIs vorinostat or LBH-589 induced phosphorylation of
140 imately ineffective in preventing perifosine/HDACI-mediated apoptosis.
141 emonstrated previously that the hybrid-polar HDACI m-carboxycinnamic acid bis-hydroxamide (CBHA) indu
142 ions (25-50 muM) synergistically potentiated HDACI lethality in AML cell lines and primary AML blasts
143 tetrakis 4-benzoic acid porphyrin) prevented HDACI-induced ROS and NF-kappaB activation while dramati
144 uption of the NF-kappaB cascade in promoting HDACI-mediated lethality.
145 analysis, we identified genes induced by RA, HDACIs, or both together.
146 ere substantially protected from resveratrol/HDACI treatment, which suggests a significant functional
147 o Sirt1 activation contribute to resveratrol/HDACI interactions.
148 = 12,779 ADRs were reported for the selected HDACIs, with n = 15/27 of the system organ class (SOC)-r
149                     Conclusion: Simultaneous HDACIs and AI dosing in patients with cancer resistant t
150                                  Sorafenib + HDACI exposure generated a CD95- and Beclin1-dependent p
151 the sorafenib/HDACI combination (sorafenib + HDACI).
152 -2 family antagonist facilitates sorafenib + HDACI killing via autophagy and the intrinsic pathway.
153 ssing c-FLIP-s, the lethality of sorafenib + HDACI exposure was abolished and was restored when cells
154              The potentiation of sorafenib + HDACI killing by GX15-070 was suppressed by knockdown of
155  of BAX and BAK modestly reduced sorafenib + HDACI lethality but abolished the effects of GX15-070 tr
156 c tumor cells are susceptible to sorafenib + HDACI lethality and that in tumor cells unable to signal
157 95 suppressed the lethality of the sorafenib/HDACI combination (sorafenib + HDACI).
158                          Our results suggest HDACIs alone or combined with retinoids may have therape
159  measure nascent transcription, we find that HDACI cause transcriptional repression by blocking RNA p
160  was similar in both groups, indicating that HDACI-induced p21 promoter activation is independent of
161                           Our data show that HDACI preferentially repress the transcription of highly
162 nal silencing in colon cancer cells and that HDACIs can activate gene transcription via KDM3A demethy
163 n suppression in colon cancer cells and that HDACIs can inhibit NuRD recruitment to a promoter to act
164               These results demonstrate that HDACIs block Bax-dependent cell death by two distinct me
165       Collectively our data demonstrate that HDACIs enhance MDA-7/IL-24 lethality, and adenoviral del
166                 These findings indicate that HDACIs increase CFZ activity in GC- and ABC-DLBCL cells
167                 These findings indicate that HDACIs induce Ser-536 phosphorylation of the NF-kappaB s
168        Here, we present data indicating that HDACIs induce the proteasomal degradation of HIF-1alpha
169         Although it has been postulated that HDACIs affect HIF-1alpha expression by enhancing its int
170                   These results suggest that HDACIs may be potentially neuroprotective against DA cel
171            Together, these data suggest that HDACIs promote the accumulation of acetylated RelA/p65 i
172                   These results suggest that HDACIs, particularly SB, promote the activity of PDH in
173 rve to validate the superior activity of the HDACI 10c.
174                                          The HDACIs sodium butyrate (NaB), valproate (VPA) and subero
175 -2 and CREB1 phosphorylation mediated by the HDACIs in K562 cells, in conjunction with histone H4 hyp
176 d FDA new drug application documents for the HDACIs studied.
177     The authors evaluated the effects of the HDACIs vorinostat and m-carboxycinnamic acid bis-hydroxa
178 cologically achievable concentrations of the HDACIs vorinostat or sodium valproate.
179  adverse drug reaction (ADR) profiles of the HDACIs: vorinostat, belinostat, panobinostat, pracinosta
180                                        These HDACIs were evaluated for their ability to inhibit the g
181              The protective effects of these HDACIs coincided with significant increases in histone a
182                                    All three HDACIs at least partially prevented MPP(+)-mediated apop
183  mechanisms may be involved in resistance to HDACI therapy in leukemia.
184  synthesis may be particularly vulnerable to HDACI lethality.
185 ment of NF-kappaB DNA binding in response to HDACIs and a significant although modest increase in apo
186 failed to undergo acetylation in response to HDACIs, impaired NF-kappaB activation and increased cell
187 Here, we show that NB cells are sensitive to HDACIs, and that the mechanism by which HDACIs induce ap
188 modulating compound increases sensitivity to HDACIs and also overcomes vorinostat resistance.
189                                         Upon HDACI treatment, acetylated Ku70 releases Bax, allowing
190 D of tumor-infiltrating CD4(+) T cells using HDACIs can enhance anti-tumor immune responses, uncoveri
191                                     In vivo, HDACIs induced accumulation of acetylated histones in ta
192 ts, the exact mechanism and targets by which HDACIs achieve their antitumor effects remain poorly und
193  degradation, the actual mechanisms by which HDACIs decrease HIF-1alpha levels are not clear.
194 e to HDACIs, and that the mechanism by which HDACIs induce apoptosis involves Bax.
195                 Exposure to resveratrol with HDACI induced sustained reactive oxygen species (ROS) ge
196        Coadministration of flavopiridol with HDACIs down-regulated the X-linked inhibitor of apoptosi
197 ontributes to antileukemic interactions with HDACIs, other NF-kappaB-independent flavopiridol actions
198 t resveratrol interacts synergistically with HDACIs in AML cells through multiple ROS-dependent actio

 
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