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1                                              SAHA at 1-5 microM for 24 and 48 h induced apoptosis in
2                                              SAHA at 1-5 muM for 48 h also induced more apoptosis of
3                                              SAHA can cause growth arrest and death of a broad variet
4                                              SAHA can cause growth arrest and death of a broad variet
5                                              SAHA decreased phosphorylation of insulin receptor beta,
6                                              SAHA dose-dependently increased GRN mRNA and protein lev
7                                              SAHA downregulated Bcl-XL and upregulated proapoptotic B
8                                              SAHA enhanced acetylation of histone H3 in Bim promoter
9                                              SAHA has demonstrated therapeutic potential in other neu
10                                              SAHA has many protein targets whose structure and functi
11                                              SAHA induced higher Smad7 levels and inhibited transloca
12                                              SAHA is a potent inhibitor of histone deacetylase, induc
13                                              SAHA is approved for human use, and molecules similar to
14                                              SAHA is in clinical trials and has significant anticance
15                                              SAHA plasma concentrations were similar to those achieve
16                                              SAHA reacts with and blocks the catalytic site of these
17                                              SAHA reduced infarct size and partially rescued systolic
18                                              SAHA restored cyclophosphamide-induced bladder pathology
19                                              SAHA significantly ameliorated the impaired growth, bone
20                                              SAHA treatment caused an accumulation of acetylated hist
21                                              SAHA-mediated correction restores Z-alpha1AT secretion a
22                                              SAHA-TAP demonstrates cytotoxicity activity against vari
23 tronger antiproliferative activities than 1 (SAHA) with GI(50) values ranging from 0.36 to 1.21 muM a
24 ffect occurs in H/H mice treated with 17DMAG+SAHA and in H/H and Q/- mice treated with the potent Hsp
25 signed to 3 groups: (1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3)
26 tment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only.
27 suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulted in a highe
28  1005) or more potently than (compound 2-75) SAHA.
29 oups known to interact with IMPDH afforded a SAHA analogue 14, which inhibits IMPDH (Ki=1.7 microM) a
30                          In addition, 17-AAG/SAHA abrogated the DNA binding and the transcriptional a
31 TG5, essential autophagy proteins, abolished SAHA's cardioprotective effects.
32 e pan-HDACi suberoylanilide hydroxamic acid (SAHA) and a novel HDAC6-specific inhibitor (KA1010) in m
33 erived from suberoylanilide hydroxamic acid (SAHA) and anthracycline daunorubicin, prototypical histo
34 inhibitors, suberoylanilide hydroxamic acid (SAHA) and ITF 2357, on mouse DC responses.
35 t the HDACi suberoylanilide hydroxamic acid (SAHA) and MS-275, a benzamide, cause an accumulation of
36 C inhibitor suberoylanilide hydroxamic acid (SAHA) and PARP inhibitor olaparib, and identified one pa
37 ors, namely suberoylanilide hydroxamic acid (SAHA) and romidepsin, have been recently approved for ca
38 nhibitors suberanoylanilide hydroxamic acid (SAHA) and sodium butyrate (SB) and the heat shock protei
39 reated with suberoylanilide hydroxamic acid (SAHA) and subjected to microarray gene expression profil
40 C inhibitor suberoylanilide hydroxamic acid (SAHA) and the Michaelis constant, with Fe(II)- and Co(II
41 ors such as suberoylanilide hydroxamic acid (SAHA) are known to induce apoptosis of cancer cells and
42 ) inhibitor suberoylanilide hydroxamic acid (SAHA) corrected the VLCFA derangement both in vitro and
43             Suberoylanilide hydroxamic acid (SAHA) has been approved as a drug to treat cutaneous T c
44 e (NaB) and suberoylanilide hydroxamic acid (SAHA) have been examined in human leukemia cells in rela
45 ) inhibitor suberoylanilide hydroxamic acid (SAHA) increased AQP5 expression and Sp1-mediated transcr
46             Suberoylanilide hydroxamic acid (SAHA) is a histone deacetylase inhibitor used in the tre
47             Suberoylanilide hydroxamic acid (SAHA) is an HDAC inhibitor which is in phase I/II clinic
48 ) inhibitor suberoylanilide hydroxamic acid (SAHA) is being evaluated for imatinib-resistant chronic
49             Suberoylanilide hydroxamic acid (SAHA) is currently in clinical trials as an antitumor ag
50 e inhibitor suberoylanilide hydroxamic acid (SAHA) is currently in clinical trials.
51 ctrum HDACi suberoylanilide hydroxamic acid (SAHA) is described.
52             Suberoylanilide hydroxamic acid (SAHA) is the first HDAC inhibitor to be approved for cli
53 e inhibitor suberoylanilide hydroxamic acid (SAHA) only after DNMT-1 dissociation from the 15-LOX-1 p
54 bitors, and suberoylanilide hydroxamic acid (SAHA) reactivated EBV in HH514-16 cells; this activity w
55 strate that suberoylanilide hydroxamic acid (SAHA) reactivates HIV from latency in chronically infect
56  STAT6 with suberoylanilide hydroxamic acid (SAHA) restores protease expression and reverses cytokine
57 e (VPA) and suberoylanilide hydroxamic acid (SAHA) were tested for their ability to prevent MPP(+)-me
58 anediamide (suberoylanilide hydroxamic acid (SAHA)), providing the product in 79.8% yield.
59  identified suberoylanilide hydroxamic acid (SAHA), a Food and Drug Administration-approved histone d
60 thesis that suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor approved for canc
61 mbined with suberoylanilide hydroxamic acid (SAHA), a histone deacetylase inhibitor.
62 worthy that suberoylanilide hydroxamic acid (SAHA), a polar compound that was initially developed as
63             Suberoylanilide hydroxamic acid (SAHA), a potent differentiation agent acting through inh
64 ) inhibitor suberoylanilide hydroxamic acid (SAHA), acting in part through HDAC7 silencing and involv
65             Suberoylanilide hydroxamic acid (SAHA), an orally administered inhibitor of histone deace
66 ide (HMBA), suberoylanilide hydroxamic acid (SAHA), and other histone deacetylase inhibitors lead to
67 in A (TSA), suberoylanilide hydroxamic acid (SAHA), and two other SAHA derivatives to HDAH, two diffe
68 C inhibitor suberoylanilide hydroxamic acid (SAHA), as well as benzophenone and alkyne moieties to ef
69 stratin and suberoylanilide hydroxamic acid (SAHA), but not hexamethylene bisacetamide (HMBA) or 5-az
70 , vis-a-vis suberoylanilide hydroxamic acid (SAHA), in in vitro and in vivo models of human HCC.
71 inhibitors, suberoylanilide hydroxamic acid (SAHA), is currently being used for treating cutaneous T-
72 m butyrate, suberoylanilide hydroxamic acid (SAHA), or trichostatin with perifosine synergistically i
73  inhibitor, suberoylanilide hydroxamic acid (SAHA), restored Ogg1 expression in cells treated with ac
74 utamide and suberoylanilide hydroxamic acid (SAHA), with weakened intrinsic pan-HDACI activities, to
75 stratin and suberoylanilide hydroxamic acid (SAHA)-overcomes the limitations of single-agent approach
76 275 (2) and suberoylanilide hydroxamic acid (SAHA, 3) arrest growth in transformed cells and in human
77 iscovery of suberoylanilide hydroxamic acid (SAHA, vorinostat) began over three decades ago with our
78 followed by suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulte
79 to discover suberoylanilide hydroxamic acid (SAHA; vorinostat (Zolinza)), which is a histone deacetyl
80 e inhibitor suberoylanilide hydroxamic acid (SAHA; vorinostat) show increases in unspliced cellular H
81 showed that suberoylanilide hydroxamic acid (SAHA; vorinostat), one of the histone deacetylase inhibi
82 ent HDACi, suberoylanilide hydroxyamic acid (SAHA), had minimal effects.
83 inhibitor, suberoylanilide hydroxyamic acid (SAHA).
84 effects of suberoylanilide hydroxyamic acid (SAHA, a specific inhibitor of Zn-HDAC activity) on hepat
85 h IGF-1, and suberoylanilidehydroxamic acid (SAHA) or halofuginone +/- IGF-1.
86 C) inhibitor suberoylanilidehydroxamic acid (SAHA, also known as vorinostat) potently reactivates KSH
87 vorinostat (suberoylanilide hydroxamic acid [SAHA]) to evaluate the activation of p21 promoter-driven
88 Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinical
89 vorinostat (suberoylanilide hydroxamic acid, SAHA) were evaluated in patients with refractory cutaneo
90 vorinostat (suberoylanilide hydroxamic acid, SAHA), although largazole upregulated endogenous E-cadhe
91 vorinostat (Suberoylanilide hydroxamic acid, SAHA), induces DNA double-strand breaks (DSBs) in normal
92 ematologic toxicities resolved shortly after SAHA was stopped.
93      To characterize the UGTs active against SAHA, homogenates from HEK293 cell lines overexpressing
94 nalyzed for glucuronidation activity against SAHA and compared with UGT2B17 genotype.
95 hibited the highest overall activity against SAHA as determined by V(max)/K(M) (16+/-6.5, 7.1+/-2.2,
96 decrease in glucuronidation activity against SAHA compared with wild-type UGT1A8, the UGT1A8p.Cys277T
97 ing the lowest K(M) (300 micromol/L) against SAHA of any UGT in vitro.
98 ndividuals could potentially exhibit altered SAHA clearance rates with differences in overall respons
99                      Notably, the TSA analog SAHA (suberoylanilide hydroxaminc acid) that is already
100                  Cotreatment with 17-AAG and SAHA or SB synergistically induced mitochondrial dysfunc
101  In addition, conditioning with anti-CD3 and SAHA allows donor CD8(+) T cell-mediated GVA activity to
102               Conditioning with anti-CD3 and SAHA allows induction of chimerism with lower doses of d
103 ppressive effect of KA1010 over both CyA and SAHA, in the models of allotransplantation adopted.
104 death induced by etoposide, doxorubicin, and SAHA.
105 e been evaluated side-by-side with FK228 and SAHA for inhibition of HDACs 1, 2, 3, and 6.
106    Daily oral treatments with OSU-HDAC42 and SAHA, both at 25 mg/kg, suppressed the growth of orthoto
107 values of 82.0 nM and 13.4 nM for KA1010 and SAHA).Mice treated with KA1010 displayed no significant
108               The HDAC inhibitors LAQ824 and SAHA increase phosphocholine (PC) levels in human colon
109 ated side-by-side with FK228, largazole, and SAHA for inhibition of the class I HDACs 1, 2, 3, and 6.
110  marginally toxic concentrations of 2-ME and SAHA or sodium butyrate in diverse human leukemia-cell t
111              Both MAHA (IC50=4.8 microM) and SAHA analogue 14 (IC50=7.7 microM) were more potent than
112 eas the pan-HDAC inhibitors panobinostat and SAHA significantly induced GAS5-AS1 in a dose-dependent
113 , or latency reversing agents prostratin and SAHA, yielded increased phosphorylation of IkappaBalpha,
114 wed that combination of E1A gene therapy and SAHA showed high therapeutic efficacy with low toxicity
115 roxamic acid-based vorinostat (also known as SAHA and Zolinza) inhibits classes I, II and IV, but not
116 properties of other HDAC inhibitors, such as SAHA and MS-275, in the tail suspension test and social
117 of SAHA to Btz treatment was synergistic, as SAHA induced early acetylation of p53 and reduced intera
118 when apoptosis is pharmacologically blocked, SAHA-induced nonapoptotic cell death can also be potenti
119 allowed 15-LOX-1 transcription activation by SAHA.
120 lity of cyclin D1 were minimally affected by SAHA over 8 hours.
121 t of IL-1beta stimulation and was blocked by SAHA, suggesting that SAHA inhibits IL-6 signaling in OA
122 AC-associated proteins were also enriched by SAHA-BPyne, even after denaturation of probe-labeled pro
123 appaB-regulated gene expression inhibited by SAHA can enhance apoptosis and inhibit invasion and oste
124 ble NO synthase expression were inhibited by SAHA.
125 associated proteins are directly modified by SAHA-BPyne, placing them in close proximity to HDAC acti
126 that can be transcriptionally reactivated by SAHA or T-cell activation.
127                                         BZ + SAHA-mediated stimulation of apoptosis includes the indu
128 ty may be particularly sensitive to the BZ + SAHA combination.
129 esome formation and thus sensitivity to BZ + SAHA, and these responses required de novo protein synth
130 , induction of Noxa, and sensitivity to BZ + SAHA-induced apoptosis.
131 cant roles in Myc-driven sensitivity to BZ + SAHA-induced apoptosis.
132 ivity of multiple myeloma (MM) cells to BZ + SAHA-induced cell death.
133 -positive cells, and the sensitivity to BZ + SAHA-induced cell death.
134  reduced the sensitivity of MM cells to BZ + SAHA-mediated apoptosis.
135  (lambda(ex)=325 nm, lambda(em)=400 nm) of c-SAHA due to its competitive binding against other HDAC i
136 e-consuming, we synthesized coumarin-SAHA (c-SAHA) as a fluorescent probe for determining the binding
137 ite wide distribution of HDACs in chromatin, SAHA alters the expression of few genes in transformed c
138 effects of SAHA or TRAIL alone and combining SAHA with TRAIL on the expression of a number of apoptos
139 sion synthesis (TLS) under these conditions, SAHA and cisplatin cotreatment promoted focal accumulati
140 been time-consuming, we synthesized coumarin-SAHA (c-SAHA) as a fluorescent probe for determining the
141                       This probe, designated SAHA-BPyne, contains structural elements of the general
142                   Administration of low-dose SAHA reduces cytokine production and ameliorates the cyt
143 is essential for autophagy activation during SAHA treatment.
144 e molecular mechanisms may facilitate either SAHA or TRAIL targeted use and the selection of suitable
145  autophagy by chloroquine treatment enhances SAHA-induced superoxide generation, triggers relocalizat
146                                 As expected, SAHA induced differentiation and matrix calcification of
147 g anti-CD3/CD28 treatment, but not following SAHA treatment (rho = 0.21, P = 0.99).
148 A new drug application has been approved for SAHA (vorinostat) treatment of cutaneous T-cell lymphoma
149                       HDAC is the target for SAHA, but the mechanisms of the consequent induced death
150 t strikingly different cellular effects from SAHA and have the potential for use in combination antit
151                                 Furthermore, SAHA inhibited the NF-kappaB-dependent reporter gene exp
152                                  Within 1 h, SAHA caused modifications in acetylation and methylation
153 anol-withdrawn mice incubated with the HDACi SAHA (vorinostat) or trichostatin A (TSA) for 2 h, the h
154                         Using a known HDACi (SAHA) and a unique small-molecule HDACi (LB-205), GCase
155 , two histone deacetylase inhibitors (HDIs), SAHA and Depsipeptide, are FDA approved for single-agent
156                       We conclude that HMBA, SAHA, and JQ1 affect transcription elongation by a simil
157                                          How SAHA mediates its effects is poorly understood.
158  of chromatin structure, we investigated how SAHA may affect DNA replication and integrity to gain de
159     We focused our molecular analyses on how SAHA improved the impaired adipogenesis leading to the l
160  Treatment with suberoylanilide hydroxamide (SAHA), a histone deacetylase (HDAC) inhibitor, causes do
161                                 Importantly, SAHA activates HIV replication in peripheral blood monon
162 elated with increased autophagic activity in SAHA-treated cells.
163 vels and glomerular IgG and C3 deposition in SAHA-treated mice were similar to controls.
164 glioblastoma cells results in an increase in SAHA-induced apoptosis.
165 one deacetylase (HDAC) inhibitors, including SAHA (vorinostat) and LBH589, which are currently being
166 matin immunoprecipitation analyses indicated SAHA increased the extent of acetylation of nucleosomal
167 tration of the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) to animals reared
168            The histone deacetylase inhibitor SAHA enhances cell death stimulated by the proteasome in
169 e and doxorubicin and the pan-HDAC inhibitor SAHA (vorinostat) in transformed cells (LNCaP, MCF-7), a
170 ide a proof-of principle that HDAC inhibitor SAHA may have a therapeutic potential for X-ALD.
171  show that treatment with the HDAC inhibitor SAHA restores sensitivity to prednisolone in TBL1XR1-dep
172 ning P5091 with lenalidomide, HDAC inhibitor SAHA, or dexamethasone triggers synergistic anti-MM acti
173 ith the histone deacetylase (HDAC) inhibitor SAHA led to detectable clusters of DNA-Pt that colocaliz
174     The histone deacetylase (HDAC) inhibitor SAHA synergizes with JQ1 to augment cell death and more
175 ed anticancer histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal
176                               Interestingly, SAHA rescued the COL2A1 and ACAN expression in OA chondr
177 matologic malignancy were enrolled (14 on IV SAHA and 25 on oral SAHA), of whom 35 were treated.
178 nyl bearing hydroxamates are pan-HDACIs like SAHA.
179 und that in several human cancer cell lines, SAHA potentiated the apoptosis induced by tumor necrosis
180   In Thra1(PV/+)Ncor1(DeltaID/DeltaID) mice, SAHA improved these abnormalities even further.
181 tions as a prosurvival mechanism to mitigate SAHA-induced apoptotic and nonapoptotic cell death, sugg
182  In this study, we determined the ability of SAHA and TRAIL as single agents or in combination to inh
183 ase-3 may underlie the therapeutic action of SAHA in CTCL patients.
184 agy would augment the anticancer activity of SAHA.
185                              The addition of SAHA to Btz treatment was synergistic, as SAHA induced e
186  cells at the time of BMT, administration of SAHA did not impair GVL activity and resulted in signifi
187                       More potent analogs of SAHA have shown unacceptable toxicity.
188                          Coadministration of SAHA and olaparib synergistically inhibited the growth o
189                           The combination of SAHA with other compounds inhibited cell proliferation o
190                         At concentrations of SAHA achieved clinically, only 0.079% of proviruses in r
191 e found that pharmacologic concentrations of SAHA induce replication-mediated DNA damage with activat
192              The cardioprotective effects of SAHA during ischemia/reperfusion occur, at least in part
193 ically augment the antineoplastic effects of SAHA in CML cell lines and primary CML cells expressing
194 y, we investigated the anti-tumor effects of SAHA in CTCL cell lines and freshly isolated peripheral
195       Thus, this study identifies effects of SAHA on p21(WAF1)-associated proteins that explain, at l
196  further determined the different effects of SAHA or TRAIL alone and combining SAHA with TRAIL on the
197 lts demonstrate that the distinct effects of SAHA or TRAIL individually and in combination on the pro
198 agy might improve the therapeutic effects of SAHA.
199                          After incubation of SAHA-TAP with an HDAC, the thiol of a conserved HDAC cys
200 reated MRL/lpr mice with daily injections of SAHA from age 10 to 20 wk.
201  cell lymphomas (CTCL), but the mechanism of SAHA action is unknown.
202  play an important role in the metabolism of SAHA and that UGT2B17-null individuals could potentially
203                              A major mode of SAHA metabolism is by glucuronidation via the UDP-glucur
204                            A modification of SAHA with groups known to interact with IMPDH afforded a
205   Interestingly, the enhanced performance of SAHA-BPyne as an in situ activity-based probe could not
206                    We developed a prodrug of SAHA by appending a promoiety, sensitive to thiols, to t
207 y, sensitivity, and inhibitory properties of SAHA-BPyne and related potential activity-based probes f
208 ascade reaction that leads to the release of SAHA.
209             The development of senescence of SAHA-induced polyploidy cells was similar in all colon c
210 HDACs were identified as specific targets of SAHA-BPyne in proteomes.
211 tylases was substantially lower than that of SAHA in cell-free and in situ assays.
212 nstrated that the combinatorial treatment of SAHA and TRAIL may target multiple pathways and serve as
213 UGT2B17 gene deletion variant (UGT2B17*2) on SAHA glucuronidation phenotype, human liver microsomes (
214          On treatment with trichostatin A or SAHA, H1299 cells carrying p21-3H showed a significant i
215  enhances DNA damage induced by etoposide or SAHA as indicated by increased accumulation of gammaH2AX
216      Finally, the effects of JQ1 and HMBA or SAHA on the P-TEFb equilibrium were cooperative.
217                There was no effect of TSA or SAHA on GABA sensitivity of pDAergic VTA neurons from sa
218 tment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).
219 sponse to CerS6 knockdown and tunicamycin or SAHA treatment.
220                                         Oral SAHA had linear pharmacokinetics from 200 to 600 mg, wit
221                                         Oral SAHA has linear pharmacokinetics and good bioavailabilit
222 acokinetic profile and bioavailibity of oral SAHA were determined.
223 etylated histones from 200 to 600 mg of oral SAHA.
224  were enrolled (14 on IV SAHA and 25 on oral SAHA), of whom 35 were treated.
225 atologic malignancies were treated with oral SAHA administered once or twice a day on a continuous ba
226 eventy-three patients were treated with oral SAHA and major dose-limiting toxicities were anorexia, d
227 nilide hydroxamic acid (SAHA), and two other SAHA derivatives to HDAH, two different modes of action,
228                        GATA6 overexpression, SAHA treatment or HDAC3 knockdown increased histone H3 (
229 components in native proteomic preparations, SAHA-BPyne was markedly superior for profiling HDAC acti
230 hibition of caspase activity did not prevent SAHA and butyrate-induced cell death.
231 developed a photoreactive "clickable" probe, SAHA-BPyne, to report on HDAC activity and complex forma
232 subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%.
233                               Significantly, SAHA-mediated RI regeneration restored the TGF-beta resp
234                              Here we studied SAHA-induced changes in the p21(WAF1) promoter of ARP-1
235 iols, to the hydroxamic acid warhead (termed SAHA-TAP).
236 acies that were comparable to or better than SAHA.
237 uppresses tumor growth more effectively than SAHA (1, N-hydroxy-N'-phenyloctanediamide) and is theref
238 showed higher antiproliferative effects than SAHA.
239 about 1 order of magnitude more potency than SAHA in both enzymatic and cellular assays.
240 U937 leukemia cells, 2t was more potent than SAHA in inducing apoptosis, and 3i displayed cell differ
241 SU-HDAC42 was several times more potent than SAHA in suppressing the viability of PLC5, Huh7, and Hep
242 d found to be about 10-fold more potent than SAHA.
243 nfluence Z-alpha1AT protein traffic and that SAHA may represent a potential therapeutic approach for
244 protein phosphorylation, we demonstrate that SAHA activates this pathway in several subpopulations of
245                Our findings demonstrate that SAHA produces profound alterations in DNA replication th
246 inositol (PI) kinase assay demonstrated that SAHA directly inhibited kinase activity of PI 3' kinase.
247                       It was discovered that SAHA inhibits the activity of histone deacetylases (HDAC
248                           We also found that SAHA had no effect on direct binding of NF-kappaB to the
249                                We found that SAHA is a potent suppressor of IL-1beta-induced MMP-13,
250                                We found that SAHA reverted the impaired adipogenesis by de-repressing
251 fects by modulating NF-kappaB and found that SAHA suppressed NF-kappaB activation induced by TNF, IL-
252          Overall, our findings indicate that SAHA activates autophagy via inhibiting mTOR and up-regu
253              Pathway analysis indicated that SAHA increased the expression of insulin signaling modul
254 e regulated by NF-kappaB, we postulated that SAHA mediates its effects by modulating NF-kappaB and fo
255                In this study, we report that SAHA induced polyploidy in human colon cancer cell line
256                         Here, we report that SAHA inhibits the proliferative and cytotoxic activity o
257              ChIP-Seq analysis revealed that SAHA increased histone H4 acetylation genome-wide and in
258                           Here, we show that SAHA increases the expression of the autophagic factor L
259                         We further show that SAHA-BPyne can be used to measure differences in HDAC co
260              Further examination showed that SAHA blunted hepatic expression and activation of cell c
261 trast, metabolic labeling assays showed that SAHA decreased incorporation of [(35)S]methionine into c
262                      The results showed that SAHA treatment suppressed the effects of PH on histone d
263     Taken together, our results suggest that SAHA could be used as a therapeutic agent for the manage
264                   These results suggest that SAHA has activity in hematologic malignancies including
265                              We suggest that SAHA possibly could provide true, multimodality, salubri
266 ion and was blocked by SAHA, suggesting that SAHA inhibits IL-6 signaling in OA chondrocytes.
267                                          The SAHA-induced increase in AQP3 levels resulted in enhance
268                                          The SAHA-induced increase in Trx activity in normal cells is
269 g this HDAC member as a likely target in the SAHA response.
270 in 1, which increased levels of P-TEFb, then SAHA once again reactivated HIV.
271                                         Thus SAHA, which is a Food and Drug Administration-approved d
272                                        Thus, SAHA induces genome-wide H4 acetylation and modulates th
273 tudies were done along the path from DMSO to SAHA.
274 levels of cyclin D1 after 8-hour exposure to SAHA (5 muM) in MCL lines (SP49, SP53, Jeko1).
275                              With respect to SAHA, OSU-HDAC42 exhibited greater apoptogenic potency,
276 ng pathways are involved in cell response to SAHA and olaparib treatment.
277 f dormant replication origins in response to SAHA.
278 iferation, and an increase in sensitivity to SAHA-induced cell death.
279                                   Similar to SAHA, compounds 2-75 and 1005 decreased the level of HSP
280 uggested that NK-HDAC-1 might be superior to SAHA in bioavailability and in vivo half-life.
281                              Taken together, SAHA caused a rapid decrease of cyclin D1 in MCL by bloc
282                          In clinical trials, SAHA has shown significant anticancer activity against b
283    The in vivo efficacy of OSU-HDAC42 versus SAHA was assessed in orthotopic and subcutaneous xenogra
284 ylase (HDAC) inhibitors, such as vorinostat (SAHA), have shown promise as therapeutic agents.
285 onse to the broad-spectrum HDACi Vorinostat (SAHA) in A549 cells, we find that combination with ATXN3
286 by histone deacetylase inhibitor vorinostat (SAHA).
287 tivity with greater potency than vorinostat (SAHA), erlotinib, lapatinib, and combinations of vorinos
288 srupting compounds such as JQ1 or vorinostat/SAHA, the CARM1 inhibitor achieved synergistic effects o
289 ll lines including Jurkat J.gamma1 for which SAHA and the previously disclosed 3HPT-derived HDACi wer
290                                        While SAHA was found to be unselective for the inhibition of c
291 ts was assessed by daily administration with SAHA (100 mg/kg intraperitoneally) or GCV (20 mg/kg) for
292                  Tubacin in combination with SAHA or etoposide is more potent than either drug alone
293 ther increased when tubacin is combined with SAHA.
294                                Compared with SAHA, compound 2-75 induced greater hyperacetylation of
295                             In contrast with SAHA, neither hybrid molecule caused substantial hyperac
296 ity was inhibited by IGF-1, and further with SAHA in particular, and with halofuginone.
297  to the viral promoter upon stimulation with SAHA.
298 s and three healthy donors were treated with SAHA (1, 2.5, and 5 microM) for 24 and/or 48 h.
299 l therapy that were reactivated ex vivo with SAHA or antibodies to CD3/CD28.
300                  In the infarct border zone, SAHA increased autophagic flux, assayed in both rabbit m

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