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1 th suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor.
2 tructurally unique, potent class 1 selective histone deacetylase inhibitor.
3 ght potentially benefit from the use of this histone deacetylase inhibitor.
4 lation and mimicked by trichostatin A, a pan-histone deacetylase inhibitor.
5 n as chidamide) is an oral subtype-selective histone deacetylase inhibitor.
6       Panobinostat (pano) is an FDA-approved histone deacetylase inhibitor.
7 howcased by the formal synthesis of a potent histone deacetylase inhibitor.
8  disruption of the human Sin3 network with a histone deacetylase inhibitor.
9 bination of PI3K-alpha/delta inhibitors with histone deacetylase inhibitors.
10 -1beta in the absence or presence of various histone deacetylase inhibitors.
11 ated transcription factor regulators such as histone deacetylase inhibitors.
12 ensitivity to epigenetic modulators, such as histone deacetylase inhibitors.
13 fied these seleno-alpha-keto acids as potent histone deacetylase inhibitors.
14  hydroxamates (2) and 2-aminoanilides (3) as histone deacetylase inhibitors.
15 otypes can be partially rescued with certain histone deacetylase inhibitors.
16  agents, including ultraviolet radiation and histone deacetylase inhibitors.
17 sor effects are globally similar to those of histone deacetylase inhibitors.
18 gene expression alone or in combination with histone deacetylase inhibitors.
19 ndoles has been identified as a new class of histone deacetylase inhibitors.
20  death in CTCL especially when combined with histone deacetylase inhibitors.
21 ions had the highest level of sensitivity to histone deacetylase inhibitors.
22 d increased sensitivity of leukemia cells to histone deacetylase inhibitors.
23 that RAE-1 is transcriptionally repressed by histone deacetylase inhibitor 3 (HDAC3) in healthy cells
24                      These molecules include histone deacetylase inhibitors, 4-phenylbutyrate (4PBA)
25 that uses low-dose DNA methyltransferase and histone deacetylase inhibitors, 5-azacytidine and entino
26                 Indeed, treatment with novel histone deacetylase inhibitors abolished hypoxia-induced
27 using Bruton's tyrosine kinase inhibitor and histone deacetylase inhibitor abrogated refractory B-1b
28  SAMHD1-dependent antiretroviral activity of histone deacetylase inhibitors acting via p53 activation
29 in A, and two small molecules without direct histone deacetylase inhibitor activity, hydroxyurea (HU)
30 ed to virus production by a combination of a histone deacetylase inhibitor and a protein kinase C act
31 nt epigenetic modulators and identified four histone deacetylase inhibitors and a bromodomain and ext
32   We further observed strong synergy between histone deacetylase inhibitors and EZH2 inhibitors.
33 menable to pharmacological intervention with histone deacetylase inhibitors and help to explain the b
34               Based on the synergism between histone deacetylase inhibitors and hypomethylating agent
35 , combinations of proteasome inhibitors with histone deacetylase inhibitors and ixabepilone and MK177
36 azole and its analogues are isoform-targeted histone deacetylase inhibitors and potent LRAs.
37 and can be re-activated with Trichostatin A (histone deacetylase inhibitor) and/or 5-aza-dC (an inhib
38 erferon alpha, extracorporeal photopheresis, histone deacetylase inhibitors, and antibody therapies s
39 poptotic triggers, including glucocorticoid, histone deacetylase inhibitors, and overexpression of th
40 at suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for cancer treatm
41                              Romidepsin is a histone deacetylase inhibitor approved for the treatment
42                          Belinostat (BEL), a histone deacetylase inhibitor approved for the treatment
43                                              Histone deacetylase inhibitors are currently approved to
44 st HDACi pharmacological activity.IMPORTANCE Histone deacetylase inhibitors are widely studied HIV la
45  with Akt, mammalian target of rapamycin, or histone deacetylase inhibitors, are active even in borte
46 ted in humans, provides proof-of-concept for histone deacetylase inhibitors as a therapeutic class, a
47 cacy and tolerability of belinostat, a novel histone deacetylase inhibitor, as a single agent in rela
48 HA), a Food and Drug Administration-approved histone deacetylase inhibitor, as an enhancer of GRN exp
49 cells could be induced into lytic phase with histone deacetylase inhibitors, as is known for latently
50  identifies cell types that are sensitive to histone deacetylase inhibitors based on their metabolic
51 ng histone acetylation via administration of histone deacetylase inhibitors before or after a learnin
52 beta receptor II (TGFbetaRII) induced by the histone deacetylase inhibitor belinostat, we observed re
53 her known P-TEFb-releasing agents, including histone deacetylase inhibitors, bromodomain and extrater
54 redict that combinations of standard agents, histone deacetylase inhibitors, bromodomain inhibitors,
55 sting primed hESC lines by preculture in the histone deacetylase inhibitors butyrate and suberoylanil
56  intact high-H3K27me3 levels; treatment with histone deacetylase inhibitors can relieve chromatin com
57 by a variety of anti-cancer drugs, including histone deacetylase inhibitors, confers chemoresistance
58 at the combination of an ACE inhibitor and a histone deacetylase inhibitor could have therapeutic pot
59 agents (IMiDs), proteasome inhibitors (PIs), histone deacetylase inhibitors (DACIs), and monoclonal a
60                              Panobinostat, a histone deacetylase inhibitor, demonstrated potent activ
61 d 3' genetic elements and sublethal doses of histone deacetylase inhibitors demonstrates that while t
62                                              Histone deacetylase inhibitors (DIs) are promising drugs
63  been proposed for DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi), primar
64  relevant doses of DNA methyltransferase and histone deacetylase inhibitors (DNMTi and HDACi, respect
65                       Here, we show that the histone deacetylase inhibitor drug, vorinostat, in addit
66 fic overexpression of Ascl1, together with a histone deacetylase inhibitor, enables adult mice to gen
67           Previously known functions include histone deacetylase inhibitor, endoplasmic reticulum str
68                      Trichostatin A (TSA), a histone deacetylase inhibitor, enhanced ENaC acetylation
69 s reason, we investigated the ability of the histone deacetylase inhibitor entinostat (ENT) to trigge
70 eage of origin, which led us to identify the histone deacetylase inhibitor entinostat as a pharmacolo
71 of the retinoic acid receptor (RAR)-beta The histone deacetylase inhibitor entinostat is emerging as
72 ved by combining EHMT1/2 inhibition with the histone deacetylase inhibitor entinostat or hypomethylat
73            Here we report that combining the histone deacetylase inhibitor entinostat with the demeth
74 al organs, whereas a combination of PAD4 and histone deacetylase inhibitors further decreases tumor g
75 n line with this finding, treatment with the histone deacetylase inhibitor givinostat caused a signif
76         The development of clinically useful histone deacetylase inhibitors has expanded greatly.
77    In some cases, the therapeutic effects of histone deacetylase inhibitors have been attributed to a
78                                              Histone deacetylase inhibitors have been demonstrated to
79                  For more than a decade now, histone deacetylase inhibitors have been investigated fo
80                                              Histone deacetylase inhibitors have shown some activity
81                   Treatment of mice with the histone deacetylase inhibitor (HDAC-I) vorinostat restor
82 molecular response to one such intervention, histone deacetylase inhibitor (HDACi) administration.
83 n agent that promotes chromatin opening, the histone deacetylase inhibitor (HDACi) AR-42, ameliorates
84 olated from ART-suppressed patients with the histone deacetylase inhibitor (HDACi) panobinostat toget
85 that treatment with the anticancer compounds histone deacetylase inhibitor (HDACi) results in a profo
86                                          The histone deacetylase inhibitor (HDACi) sodium butyrate pr
87                 The therapeutic potential of histone deacetylase inhibitor (HDACi) treatment has attr
88            We now show that the FDA-approved histone deacetylase inhibitor (HDACi) valproic acid (VPA
89           In this study romidepsin, a potent histone deacetylase inhibitor (HDACi), induced apoptosis
90    Treating differentiating osteoblasts with histone deacetylase inhibitors (HDACi) abrogated their a
91                   Finally, we discovered how histone deacetylase inhibitors (HDACi) alone, when admin
92 ased on the well-established synergy between histone deacetylase inhibitors (HDACi) and alkylating ag
93 roylanilide hydroxamic acid (vorinostat) are histone deacetylase inhibitors (HDACi) approved by the U
94                                              Histone deacetylase inhibitors (HDACi) are being evaluat
95                             Controversially, histone deacetylase inhibitors (HDACi) are in clinical t
96                                              Histone deacetylase inhibitors (HDACi) are largely ineff
97                                              Histone deacetylase inhibitors (HDACi) are the most wide
98 ing a chemical library screen, we identified histone deacetylase inhibitors (HDACi) as agents reducin
99 egulated upon treatment with pan- or class I histone deacetylase inhibitors (HDACi) as well as after
100                   We describe a set of novel histone deacetylase inhibitors (HDACi) equipped with eit
101 an TTNT of 8.7 months (95% CI 6.0-18.0), and histone deacetylase inhibitors (HDACi) gave a median TTN
102                                              Histone deacetylase inhibitors (HDACi) have been propose
103                                              Histone deacetylase inhibitors (HDACi) have been shown t
104                                              Histone deacetylase inhibitors (HDACi) have been suggest
105 s, we identified miR-31 as a novel target of histone deacetylase inhibitors (HDACi) in breast cancer
106 previously showed that 2-aminobenzamide-type histone deacetylase inhibitors (HDACi) increase FXN mRNA
107                         Clinical response to histone deacetylase inhibitors (HDACi) is strongly assoc
108 estigate this notion, we tested 24 different histone deacetylase inhibitors (HDACi) on colon cancer c
109  reactivation of dormant HIV-1 proviruses by histone deacetylase inhibitors (HDACi) represents a poss
110                               Treatment with histone deacetylase inhibitors (HDACI) results in potent
111                                              Histone deacetylase inhibitors (HDACi) target abnormal e
112 ing group (ZBG) have been the most effective histone deacetylase inhibitors (HDACi) to date.
113                Clinical trials investigating histone deacetylase inhibitors (HDACi) to reverse HIV-1
114      By using a "drug repurposing" strategy, histone deacetylase inhibitors (HDACi), which are presen
115  efforts has been on a class of drugs called histone deacetylase inhibitors (HDACi), which have the p
116 ch as molecularly targeted agents, including histone deacetylase inhibitors (HDACi).
117  that these were similar to those induced by histone deacetylase inhibitors (HDACi).
118 proposed as the major antitumor responses to histone deacetylase inhibitors (HDACi).
119 s inhibited by valproic acid (VPA) and other histone deacetylase inhibitors (HDACi).
120 5) inhibited tail regeneration, including 18 histone deacetylase inhibitors (HDACi).
121  to fitness of the individual in response to histone deacetylases inhibitors (HDACi).
122                                              Histone deacetylase inhibitors (HDACIs) activate the pro
123 ies include PKC and MAPK agonists as well as histone deacetylase inhibitors (HDACis) and bromodomain
124                         Interactions between histone deacetylase inhibitors (HDACIs) and decitabine w
125 s on CD8+ T cell phenotype and function: the histone deacetylase inhibitors (HDACis) and protein kina
126 one methyltransferase inhibitors (HMTis) and histone deacetylase inhibitors (HDACis) are reported to
127 d progression that prompt the development of histone deacetylase inhibitors (HDACIs) as anticancer ag
128                                              Histone deacetylase inhibitors (HDACIs) can disrupt the
129                  In this study, we show that histone deacetylase inhibitors (HDACIs) can inhibit apop
130                We presently demonstrate that histone deacetylase inhibitors (HDACIs) enhance toxicity
131                                              Histone deacetylase inhibitors (HDACis) have been shown
132  methyltransferase inhibitors [DNMTis]) with histone deacetylase inhibitors (HDACis) holds promise fo
133 rated that in malignant hematopoietic cells, histone deacetylase inhibitors (HDACIs) induced RelA hyp
134 n the present study, we investigated whether histone deacetylase inhibitors (HDACis) may induce a fav
135                                              Histone deacetylase inhibitors (HDACIs) may overcome end
136                   It has been suggested that histone deacetylase inhibitors (HDACis) may purge HIV in
137                     Recent evidence suggests histone deacetylase inhibitors (HDACis) may represent a
138 merous studies have looked at the effects of histone deacetylase inhibitors (HDACis) on HIV reactivat
139                                We found that histone deacetylase inhibitors (HDACis) significantly in
140                   In vivo studies have shown histone deacetylase inhibitors (HDACis) to be neuroprote
141                We showed previously that the histone deacetylase inhibitors (HDACIs) trichostatin A a
142 ced by AML1-ETO-targeting drugs, such as the histone deacetylase inhibitors (HDACis) valproic acid (V
143                                      Several histone deacetylase inhibitors (HDACIs) were used in vit
144  SDHB protein increased after treatment with histone deacetylase inhibitors (HDACis), implicating the
145      Among the most effective compounds were histone deacetylase inhibitors (HDACIs).
146 dividing CB CD34+ cells ex vivo with several histone deacetylase inhibitors (HDACIs).
147 0 antibodies and confirmed with nonselective histone deacetylase inhibitors (HDACis).
148        To identify molecular determinants of histone deacetylase inhibitor (HDI) resistance, we selec
149                                              Histone deacetylase inhibitors (HDI) have exhibited some
150                                              Histone deacetylase inhibitors (HDIs) promote terminal o
151 ndicating a potential therapeutic benefit of histone deacetylase inhibitors (HDIs), and preclinical d
152                                 In fact, two histone deacetylase inhibitors (HDIs), SAHA and Depsipep
153 rogression is suppressed by treatment with a histone deacetylase inhibitor; however, this treatment h
154  histone deacetylases; a screen for suitable histone deacetylase inhibitors identified belinostat as
155 ected pharmaceutical residues in water, is a histone deacetylase inhibitor in mammals, and is reporte
156 on, which can be reactivated by a mixture of histone deacetylase inhibitors in combination with TNF.
157  used for measurement of cellular potency of histone deacetylase inhibitors in intact cells.
158 ne perturbations could reduce sensitivity to histone deacetylase inhibitors in SS patients.
159                                              Histone deacetylase inhibitors, including valproic acid,
160  identified the molecular mechanism by which histone deacetylase inhibitors increase the quantity and
161                                              Histone deacetylase inhibitors induce apoptosis and re-e
162 sing a high-throughput screen, we found that histone deacetylase inhibitors induce Id2 expression by
163             We also showed that AR-42, a pan-histone deacetylase inhibitor, inhibited proliferation o
164       We found that bilateral infusions of a histone deacetylase inhibitor into the CeA attenuated an
165                          Panobinostat (a pan histone deacetylase inhibitor) is approved in combinatio
166                      Valproic acid (VPA), an histone deacetylase inhibitor, is emerging as a promisin
167                          Upon treatment with histone deacetylase inhibitors, KSHV-infected murine cel
168 atment of BALB/c murine macrophages with the histone deacetylase inhibitor LAQ824 induces chromatin c
169                                          The histone deacetylase inhibitor largazole 1 was synthesize
170  A number of analogues of the marine-derived histone deacetylase inhibitor largazole incorporating ma
171 A2, or suppressing HMGA2 expression with the histone deacetylase inhibitor LBH589, inhibits epithelia
172 ed with treatment of melanoma cells with the histone deacetylase inhibitor LBH589.
173 oylanilide hydroxamic acid (SAHA), and other histone deacetylase inhibitors lead to a rapid release o
174  Nevertheless, derepression of frataxin by a histone deacetylase inhibitor leads to a decrease in miR
175 combination of a demethylating reagent and a histone deacetylase inhibitor led to rapid activation of
176                                 Notably, pan-histone deacetylase inhibitors lift promoter-specific re
177              We show that the small-molecule histone deacetylase inhibitor M344 reduces beta-amyloid
178 etic changes and that valproic acid (VPA), a histone deacetylase inhibitor, may reverse such changes.
179                           The selectivity of histone deacetylase inhibitor-mediated silencing of AICD
180 are a prerequisite during the cell cycle and histone deacetylase inhibitor-mediated therapeutics.
181 compound identified from this screen was the histone deacetylase inhibitor methyl-4-(phenylthio)butan
182 ities incorporating antifolates, conjugates, histone deacetylase inhibitors, monoclonal antibodies, n
183 genes and prevented by administration of the histone deacetylase inhibitor MS-275.
184                                            A histone deacetylase inhibitor, MS-275, resulted in upreg
185  with extinction enhancements induced by the histone deacetylase inhibitor NaB.
186                                          One histone deacetylase inhibitor, NCH-51, was validated as
187      Preclinical studies have shown that the histone deacetylase inhibitor nicotinamide (vitamin B3)
188 NS and has several advantages over available histone deacetylase inhibitors now in clinical trials, o
189 egulation and demonstrate a direct effect of histone deacetylase inhibitors on the SS18-SSX complex c
190                                 Accordingly, histone deacetylase inhibitors or BET inhibitors, the la
191                               Treatment with histone deacetylase inhibitors or depletion of the polyc
192 ination with other epigenetic drugs, such as histone deacetylase inhibitors or differentiation induce
193 scent HSPCs are resistant to reactivation by histone deacetylase inhibitors or P-TEFb activation but
194    Cotreatment with BA and panobinostat (pan-histone deacetylase inhibitor) or palbociclib (CDK4/6 in
195  compared with interferon-alpha (P = .0067), histone deacetylase inhibitors (P = .0003), novel immuno
196                                    The multi-histone deacetylase inhibitor panobinostat demonstrated
197  to determine the safety and activity of the histone deacetylase inhibitor panobinostat in patients w
198 e CDK7/super-enhancer inhibitor THZ1 and the histone deacetylase inhibitor panobinostat synergistical
199               We assessed the ability of the histone deacetylase inhibitor panobinostat to disrupt HI
200  organotypic cultures with trichostatin A, a histone deacetylase inhibitor, partially restored differ
201 Treatment with trichostatin A, but not other histone deacetylase inhibitors, partially restored reeli
202 r of small molecules, we have found that the histone deacetylase inhibitor phenylbutyrate increases D
203  how the effector molecule HC-toxin (HCT), a histone deacetylase inhibitor produced by the fungal pat
204  with TEPP-46 and shikonin or treatment with histone deacetylase inhibitors produced similar results.
205 ibitors, and cell culture in the presence of histone deacetylase inhibitors, promote development to t
206 hput sequencing (ATAC-seq), we show that the histone deacetylase inhibitor promotes accessibility at
207 e further amplified by DNA demethylation and histone deacetylase inhibitors providing an exquisite th
208 amine-based Pt(IV) derivative containing the histone deacetylase inhibitor rac-2-(2-propynyl)octanoat
209 f REST was blocked by cycloheximide; and (c) histone deacetylase inhibitors reactivated the WT parent
210 lly, growth of Salmonella in the presence of histone deacetylases inhibitors reduced expression of SP
211                        Romidepsin (RMD) is a histone deacetylase inhibitor reported to reverse HIV-1
212                               Treatment with histone deacetylase inhibitors rescued IR-induced ATM si
213 ecitabine (demethylating agent) or butyrate (histone deacetylase inhibitor) restored hOCT1 expression
214                                              Histone deacetylase inhibitors reversed the effects of c
215 ombination with bromodomain inhibitor JQ1 or histone deacetylase inhibitors robustly induce HIV-1 tra
216                        Administration of the histone deacetylase inhibitor SAHA (suberoylanilide hydr
217  and Drug Administration-approved anticancer histone deacetylase inhibitor, SAHA, reduces myocardial
218 ns using a combination of the checkpoint and histone deacetylase inhibitors.See related article by Fu
219 ion in aging and AD models and suggests that histone deacetylase inhibitors should be further explore
220                    DNA methyltransferase and histone deacetylase inhibitors similarly reset the trans
221 dial prefrontal cortex administration of the histone deacetylase inhibitor sodium butyrate (NaB) afte
222                           In particular, the histone deacetylase inhibitor sodium butyrate (SB) may i
223  inhibitor N-omega-hydroxy-l-norarginine and histone deacetylase inhibitor sodium valproate.
224 ting pair-bond regulation and found that the histone deacetylase inhibitors sodium butyrate and trich
225 C, we studied the effect of the FDA-approved histone deacetylase inhibitor suberanilohydroxamic acid
226 e and resveratrol) and were increased by the histone deacetylase inhibitor, suberolylanilide hydroxam
227  (Dznep) either alone or in combination with histone deacetylase inhibitor suberoylanilide hydroxamic
228 cal studies of in vivo administration of the histone deacetylase inhibitor suberoylanilide hydroxamic
229 ow that the chromatin opening induced by the histone deacetylase inhibitor suberoylanilide hydroxamic
230  that treatment with epigenetic therapy, the histone deacetylase inhibitor suberoylanilide hydroxamic
231                  Degradation of Dnmt1 by the histone deacetylase inhibitor suberoylanilide hydroxamic
232 olecules, both of which were reversed by the histone deacetylase inhibitor suberoylanilide hydroxanic
233 orated in mice treated with the FDA-approved histone deacetylase inhibitor, suberoylanilide hydroxami
234                                     Although histone deacetylase inhibitors such as suberoylanilide h
235              In particular, our results with histone deacetylase inhibitors support the view that chr
236 ression induced by LAC, whereas the use of a histone deacetylase inhibitor supported the epigenetic c
237     Combined treatment with MAPK-pathway and histone-deacetylase inhibitors suppressed MITF expressio
238 ethyltransferase inhibitor decitabine or the histone deacetylase inhibitor tacedinaline on NET cells
239                    While butyrate is a known histone deacetylase inhibitor that activates expression
240                              Vorinostat is a histone deacetylase inhibitor that changes gene expressi
241                              Entinostat is a histone deacetylase inhibitor that has been combined wit
242  in Cpt2M(-/-) hearts, but trichostatin A, a histone deacetylase inhibitor that improves cardiac remo
243 Modulation of chromatin conformation using a histone deacetylase inhibitor that increases transcripti
244      Pretreatment with trichostatin A, a pan-histone deacetylase inhibitor that renders chromatin dec
245                                            A histone deacetylase inhibitor that suppresses neurodegen
246      Entinostat is an oral isoform selective histone deacetylase inhibitor that targets resistance to
247                   Moreover, valproic acid, a histone deacetylase inhibitor that we previously showed
248                                              Histone deacetylase inhibitors that increased the acetyl
249 ignature-relevant drug candidates, including histone deacetylase inhibitors that specifically reduced
250 ted with both calcitriol and trichostatin A (histone deacetylase inhibitor), the level of IL-9 reache
251 ic assessments of response and resistance to histone deacetylase inhibitor therapy.
252            Treatment of mammalian cells with histone deacetylase inhibitors to increase euchromatin o
253                                              Histone deacetylase inhibitor treatment significantly re
254 that all functional NKG2D ligands induced by histone deacetylase inhibitor treatment were abolished b
255 ivation of HDAC9 expression and sensitive to histone deacetylase inhibitor treatment.
256 inhibited surface expression of MICA/B after histone deacetylase inhibitor treatment; the inhibition
257 intensity in the nucleus increased following histone-deacetylase inhibitor treatment.
258 nsferase inhibitor 5-Aza 2-deoxycytidine and histone deacetylase inhibitor trichostatin A (herein ref
259 ces of acute intra-CA1 administration of the histone deacetylase inhibitor Trichostatin A (TSA) on cu
260  a combination regimen of bortezomib and the histone deacetylase inhibitor trichostatin A abolished H
261 of skin repair we found that the class I-IIa histone deacetylase inhibitor trichostatin A accelerated
262 t did inhibit the relaxation produced by the histone deacetylase inhibitor trichostatin A, an effect
263 n agent 5'-aza-2'-deoxycytidine, but not the histone deacetylase inhibitor trichostatin A, drasticall
264 trodifferentiation process is blocked by the histone deacetylase inhibitor trichostatin A, opening ne
265 versal of endotoxin tolerance exerted by the histone deacetylase inhibitor trichostatin A.
266  (THLE-2 and THLE-3) were incubated with the histone deacetylase inhibitor trichostatin A.
267 ration and angiogenesis were reversed by the histone deacetylase inhibitor trichostatin A.
268 (SIRT) inhibitor nicotinamide but not by the histone deacetylase inhibitor trichostatin A.
269 IGF-1(NEG) and mIGF-1(POS) SMA mice with the histone deacetylase inhibitor, trichostatin A (TSA), res
270                        When treated with the histone deacetylase inhibitor, Trichostatin A, genes nea
271 eased the sensitivity of cancer cells to the histone deacetylase inhibitor, trichostatin A, in C42B,
272  anti-microtubule drug thiabendazole and the histone deacetylase inhibitor tricostatin A when a histo
273     Treatment of cells with phorbol ester or histone deacetylase inhibitors triggered the expression
274                                            A histone deacetylase inhibitor, TSA, stimulated Rgs16::GF
275  (3C) consisting of sodium butyrate (a broad histone deacetylase inhibitor), UNC0646 (a histone methy
276 ormal cells, by DNA-demethylating agents and histone deacetylase inhibitors using clinically achievab
277  conducted to investigate the effects of the histone deacetylase inhibitor valproate and all-trans re
278 uciferase activity assay, we found that both histone deacetylase inhibitor valproic acid (VPA) and DN
279                                          The histone deacetylase inhibitor valproic acid (VPA) is kno
280 vated levels of hTdp1 were more sensitive to histone deacetylase inhibitors valproic acid (VPA) and t
281                                 We show that histone deacetylase inhibitors valproic acid and butyrat
282 th all-trans retinoic acid combined with the histone-deacetylase inhibitor valproic acid.
283 tion is further promoted by treatment with a histone deacetylase inhibitor, valproic acid (VPA).
284                             Importantly, the histone deacetylase inhibitor, valproic acid, blocked ME
285 d) obtained by conjugation to valproic acid (histone deacetylase inhibitor) via an ester bond, exhibi
286 gated the mechanism of MMP-13 suppression by histone deacetylase inhibitor vorinostat (SAHA).
287 o receive ART-only (control) or ART plus the histone deacetylase inhibitor vorinostat (the kick) and
288                         A single dose of the histone deacetylase inhibitor vorinostat (VOR) up-regula
289       We performed two phase I trials of the histone deacetylase inhibitor vorinostat combined with e
290 n the present study, we demonstrate that the histone deacetylase inhibitor vorinostat not only reprog
291 al administration of the clinically approved histone deacetylase inhibitor vorinostat not only restor
292 lowed to devise an inactive precursor of the histone deacetylase inhibitor vorinostat that was effici
293                       Notably, combining the histone deacetylase inhibitor vorinostat with a PI3K inh
294          Epigenetic modifiers, including the histone deacetylase inhibitor vorinostat, may sensitize
295 nergistically increased upon exposure to the histone deacetylase inhibitor vorinostat.
296        Combining a demethylation agent and a histone deacetylase inhibitor was sufficient to reexpres
297                                  As a class, histone deacetylase inhibitors were greatly overrepresen
298                                              Histone deacetylase inhibitors were used to treat cells.
299 vity relationship for designing novel potent histone deacetylase inhibitors, which can be applied tow
300 nsin-converting enzyme (ACE) inhibitor and a histone deacetylase inhibitor would maximally reverse th

 
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