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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)
27 suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulted in a highe
29 oups known to interact with IMPDH afforded a SAHA analogue 14, which inhibits IMPDH (Ki=1.7 microM) a
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
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
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
48 ) inhibitor suberoylanilide hydroxamic acid (SAHA) is being evaluated for imatinib-resistant chronic
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
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
62 worthy that suberoylanilide hydroxamic acid (SAHA), a polar compound that was initially developed as
64 ) inhibitor suberoylanilide hydroxamic acid (SAHA), acting in part through HDAC7 silencing and involv
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
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
84 effects of suberoylanilide hydroxyamic acid (SAHA, a specific inhibitor of Zn-HDAC activity) on hepat
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
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
98 ndividuals could potentially exhibit altered SAHA clearance rates with differences in overall respons
101 In addition, conditioning with anti-CD3 and SAHA allows donor CD8(+) T cell-mediated GVA activity to
103 ppressive effect of KA1010 over both CyA and SAHA, in the models of allotransplantation adopted.
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
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
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
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
125 associated proteins are directly modified by SAHA-BPyne, placing them in close proximity to HDAC acti
129 esome formation and thus sensitivity to BZ + SAHA, and these responses required de novo protein synth
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
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
148 A new drug application has been approved for SAHA (vorinostat) treatment of cutaneous T-cell lymphoma
150 t strikingly different cellular effects from SAHA and have the potential for use in combination antit
153 anol-withdrawn mice incubated with the HDACi SAHA (vorinostat) or trichostatin A (TSA) for 2 h, the h
155 , two histone deacetylase inhibitors (HDIs), SAHA and Depsipeptide, are FDA approved for single-agent
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
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
169 e and doxorubicin and the pan-HDAC inhibitor SAHA (vorinostat) in transformed cells (LNCaP, MCF-7), a
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
177 matologic malignancy were enrolled (14 on IV SAHA and 25 on oral SAHA), of whom 35 were treated.
179 und that in several human cancer cell lines, SAHA potentiated the apoptosis induced by tumor necrosis
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
186 cells at the time of BMT, administration of SAHA did not impair GVL activity and resulted in signifi
191 e found that pharmacologic concentrations of SAHA induce replication-mediated DNA damage with activat
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
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
202 play an important role in the metabolism of SAHA and that UGT2B17-null individuals could potentially
205 Interestingly, the enhanced performance of SAHA-BPyne as an in situ activity-based probe could not
207 y, sensitivity, and inhibitory properties of SAHA-BPyne and related potential activity-based probes f
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 (
215 enhances DNA damage induced by etoposide or SAHA as indicated by increased accumulation of gammaH2AX
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,
229 components in native proteomic preparations, SAHA-BPyne was markedly superior for profiling HDAC acti
231 developed a photoreactive "clickable" probe, SAHA-BPyne, to report on HDAC activity and complex forma
237 uppresses tumor growth more effectively than SAHA (1, N-hydroxy-N'-phenyloctanediamide) and is theref
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
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
246 inositol (PI) kinase assay demonstrated that SAHA directly inhibited kinase activity of PI 3' kinase.
251 fects by modulating NF-kappaB and found that SAHA suppressed NF-kappaB activation induced by TNF, IL-
254 e regulated by NF-kappaB, we postulated that SAHA mediates its effects by modulating NF-kappaB and fo
261 trast, metabolic labeling assays showed that SAHA decreased incorporation of [(35)S]methionine into c
263 Taken together, our results suggest that SAHA could be used as a therapeutic agent for the manage
283 The in vivo efficacy of OSU-HDAC42 versus SAHA was assessed in orthotopic and subcutaneous xenogra
285 onse to the broad-spectrum HDACi Vorinostat (SAHA) in A549 cells, we find that combination with ATXN3
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
291 ts was assessed by daily administration with SAHA (100 mg/kg intraperitoneally) or GCV (20 mg/kg) for
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