ライフサイエンスコーパス: SAHA

1 SAHA (25 mg/kg) (n = 30) or vehicle (DMSO) (n = 30) was

2 SAHA at 1-5 microM for 24 and 48 h induced apoptosis in

3 SAHA at 1-5 muM for 48 h also induced more apoptosis of

4 SAHA can cause growth arrest and death of a broad variet

5 SAHA can cause growth arrest and death of a broad variet

6 SAHA decreased phosphorylation of insulin receptor beta,

7 SAHA dose-dependently increased GRN mRNA and protein lev

8 SAHA downregulated Bcl-XL and upregulated proapoptotic B

9 SAHA enhanced acetylation of histone H3 in Bim promoter

10 SAHA has demonstrated therapeutic potential in other neu

11 SAHA has many protein targets whose structure and functi

12 SAHA induced higher Smad7 levels and inhibited transloca

13 SAHA is a potent inhibitor of histone deacetylase, induc

14 SAHA is approved for human use, and molecules similar to

15 SAHA is in clinical trials and has significant anticance

16 SAHA plasma concentrations were similar to those achieve

17 SAHA reacts with and blocks the catalytic site of these

18 SAHA reduced infarct size and partially rescued systolic

19 SAHA restored cyclophosphamide-induced bladder pathology

20 SAHA significantly ameliorated the impaired growth, bone

21 SAHA treatment caused an accumulation of acetylated hist

22 SAHA was able to inhibit experimental fungal keratitis i

23 SAHA-mediated correction restores Z-alpha1AT secretion a

24 SAHA-TAP demonstrates cytotoxicity activity against vari

25 tronger antiproliferative activities than 1 (SAHA) with GI(50) values ranging from 0.36 to 1.21 muM a

26 ffect occurs in H/H mice treated with 17DMAG+SAHA and in H/H and Q/- mice treated with the potent Hsp

27 signed to 3 groups: (1) vehicle control, (2) SAHA pretreatment (1 day before and at surgery), and (3)

28 tment (1 day before and at surgery), and (3) SAHA treatment at the time of reperfusion only.

29 suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulted in a highe

30 1005) or more potently than (compound 2-75) SAHA.

31 oups known to interact with IMPDH afforded a SAHA analogue 14, which inhibits IMPDH (Ki=1.7 microM) a

32 TG5, essential autophagy proteins, abolished SAHA's cardioprotective effects.

33 e pan-HDACi suberoylanilide hydroxamic acid (SAHA) and a novel HDAC6-specific inhibitor (KA1010) in m

34 erived from suberoylanilide hydroxamic acid (SAHA) and anthracycline daunorubicin, prototypical histo

35 inhibitors, suberoylanilide hydroxamic acid (SAHA) and ITF 2357, on mouse DC responses.

36 t the HDACi suberoylanilide hydroxamic acid (SAHA) and MS-275, a benzamide, cause an accumulation of

37 C inhibitor suberoylanilide hydroxamic acid (SAHA) and PARP inhibitor olaparib, and identified one pa

38 ors, namely suberoylanilide hydroxamic acid (SAHA) and romidepsin, have been recently approved for ca

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 Pan-HDACi suberoylanilide hydroxamic acid (SAHA) and/or ITF2357 (givinostat) significantly reduced

42 ors such as suberoylanilide hydroxamic acid (SAHA) are known to induce apoptosis of cancer cells and

43 ) inhibitor suberoylanilide hydroxamic acid (SAHA) corrected the VLCFA derangement both in vitro and

44 Suberoylanilide hydroxamic acid (SAHA) has been approved as a drug to treat cutaneous T c

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 e inhibitor suberoylanilide hydroxamic acid (SAHA) is currently in clinical trials.

50 ctrum HDACi suberoylanilide hydroxamic acid (SAHA) is described.

51 Suberoylanilide hydroxamic acid (SAHA) is the first HDAC inhibitor to be approved for cli

52 C inhibitor suberoylanilide hydroxamic acid (SAHA) on experimental fungal keratitis in mice.

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 One HDACi, suberoylanilide hydroxamic acid (SAHA), exhibits off-target effects on host gene expressi

71 , vis-a-vis suberoylanilide hydroxamic acid (SAHA), in in vitro and in vivo models of human HCC.

72 inhibitors, suberoylanilide hydroxamic acid (SAHA), is currently being used for treating cutaneous T-

73 m butyrate, suberoylanilide hydroxamic acid (SAHA), or trichostatin with perifosine synergistically i

74 inhibitor, suberoylanilide hydroxamic acid (SAHA), restored Ogg1 expression in cells treated with ac

75 utamide and suberoylanilide hydroxamic acid (SAHA), with weakened intrinsic pan-HDACI activities, to

76 stratin and suberoylanilide hydroxamic acid (SAHA)-overcomes the limitations of single-agent approach

77 C inhibitor suberoylanilide hydroxamic acid (SAHA).

78 275 (2) and suberoylanilide hydroxamic acid (SAHA, 3) arrest growth in transformed cells and in human

79 iscovery of suberoylanilide hydroxamic acid (SAHA, vorinostat) began over three decades ago with our

80 followed by suberoylanilide hydroxamic acid (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulte

81 to discover suberoylanilide hydroxamic acid (SAHA; vorinostat (Zolinza)), which is a histone deacetyl

82 e inhibitor suberoylanilide hydroxamic acid (SAHA; vorinostat) show increases in unspliced cellular H

83 showed that suberoylanilide hydroxamic acid (SAHA; vorinostat), one of the histone deacetylase inhibi

84 ent HDACi, suberoylanilide hydroxyamic acid (SAHA), had minimal effects.

85 inhibitor, suberoylanilide hydroxyamic acid (SAHA).

86 effects of suberoylanilide hydroxyamic acid (SAHA, a specific inhibitor of Zn-HDAC activity) on hepat

87 n fatty acids and suberanilohydroxamic acid (SAHA), could individually or in combination induce miR-2

88 etylase inhibitor suberanilohydroxamic acid (SAHA).

89 h IGF-1, and suberoylanilidehydroxamic acid (SAHA) or halofuginone +/- IGF-1.

90 C) inhibitor suberoylanilidehydroxamic acid (SAHA, also known as vorinostat) potently reactivates KSH

91 vorinostat (suberoylanilide hydroxamic acid [SAHA]) to evaluate the activation of p21 promoter-driven

92 Vorinostat (suberoylanilide hydroxamic acid, SAHA) is a histone deacetylase inhibitor active clinical

93 vorinostat (suberoylanilide hydroxamic acid, SAHA) were evaluated in patients with refractory cutaneo

94 vorinostat (suberoylanilide hydroxamic acid, SAHA), although largazole upregulated endogenous E-cadhe

95 vorinostat (Suberoylanilide hydroxamic acid, SAHA), induces DNA double-strand breaks (DSBs) in normal

96 ematologic toxicities resolved shortly after SAHA was stopped.

97 To characterize the UGTs active against SAHA, homogenates from HEK293 cell lines overexpressing

98 nalyzed for glucuronidation activity against SAHA and compared with UGT2B17 genotype.

99 hibited the highest overall activity against SAHA as determined by V(max)/K(M) (16+/-6.5, 7.1+/-2.2,

100 decrease in glucuronidation activity against SAHA compared with wild-type UGT1A8, the UGT1A8p.Cys277T

101 ing the lowest K(M) (300 micromol/L) against SAHA of any UGT in vitro.

102 ndividuals could potentially exhibit altered SAHA clearance rates with differences in overall respons

103 Notably, the TSA analog SAHA (suberoylanilide hydroxaminc acid) that is already

104 In addition, conditioning with anti-CD3 and SAHA allows donor CD8(+) T cell-mediated GVA activity to

105 Conditioning with anti-CD3 and SAHA allows induction of chimerism with lower doses of d

106 ppressive effect of KA1010 over both CyA and SAHA, in the models of allotransplantation adopted.

107 death induced by etoposide, doxorubicin, and SAHA.

108 e been evaluated side-by-side with FK228 and SAHA for inhibition of HDACs 1, 2, 3, and 6.

109 Daily oral treatments with OSU-HDAC42 and SAHA, both at 25 mg/kg, suppressed the growth of orthoto

110 values of 82.0 nM and 13.4 nM for KA1010 and SAHA).Mice treated with KA1010 displayed no significant

111 The HDAC inhibitors LAQ824 and SAHA increase phosphocholine (PC) levels in human colon

112 ated side-by-side with FK228, largazole, and SAHA for inhibition of the class I HDACs 1, 2, 3, and 6.

113 marginally toxic concentrations of 2-ME and SAHA or sodium butyrate in diverse human leukemia-cell t

114 Both MAHA (IC50=4.8 microM) and SAHA analogue 14 (IC50=7.7 microM) were more potent than

115 eas the pan-HDAC inhibitors panobinostat and SAHA significantly induced GAS5-AS1 in a dose-dependent

116 , or latency reversing agents prostratin and SAHA, yielded increased phosphorylation of IkappaBalpha,

117 wed that combination of E1A gene therapy and SAHA showed high therapeutic efficacy with low toxicity

118 -1-deficient Caenorhabditis elegans animals, SAHA was shown to counteract the defective KDM5C/rbr-2-H

119 roxamic acid-based vorinostat (also known as SAHA and Zolinza) inhibits classes I, II and IV, but not

120 properties of other HDAC inhibitors, such as SAHA and MS-275, in the tail suspension test and social

121 of SAHA to Btz treatment was synergistic, as SAHA induced early acetylation of p53 and reduced intera

122 when apoptosis is pharmacologically blocked, SAHA-induced nonapoptotic cell death can also be potenti

123 allowed 15-LOX-1 transcription activation by SAHA.

124 lity of cyclin D1 were minimally affected by SAHA over 8 hours.

125 t of IL-1beta stimulation and was blocked by SAHA, suggesting that SAHA inhibits IL-6 signaling in OA

126 AC-associated proteins were also enriched by SAHA-BPyne, even after denaturation of probe-labeled pro

127 appaB-regulated gene expression inhibited by SAHA can enhance apoptosis and inhibit invasion and oste

128 associated proteins are directly modified by SAHA-BPyne, placing them in close proximity to HDAC acti

129 enes, SMARCB1 and PARP1, whose modulation by SAHA and RMD is predicted to inhibit HIV reactivation, w

130 that can be transcriptionally reactivated by SAHA or T-cell activation.

131 2) was established, which was upregulated by SAHA.

132 BZ + SAHA-mediated stimulation of apoptosis includes the indu

133 ty may be particularly sensitive to the BZ + SAHA combination.

134 esome formation and thus sensitivity to BZ + SAHA, and these responses required de novo protein synth

135 , induction of Noxa, and sensitivity to BZ + SAHA-induced apoptosis.

136 cant roles in Myc-driven sensitivity to BZ + SAHA-induced apoptosis.

137 ivity of multiple myeloma (MM) cells to BZ + SAHA-induced cell death.

138 -positive cells, and the sensitivity to BZ + SAHA-induced cell death.

139 reduced the sensitivity of MM cells to BZ + SAHA-mediated apoptosis.

140 (lambda(ex)=325 nm, lambda(em)=400 nm) of c-SAHA due to its competitive binding against other HDAC i

141 e-consuming, we synthesized coumarin-SAHA (c-SAHA) as a fluorescent probe for determining the binding

142 effects of SAHA or TRAIL alone and combining SAHA with TRAIL on the expression of a number of apoptos

143 sion synthesis (TLS) under these conditions, SAHA and cisplatin cotreatment promoted focal accumulati

144 been time-consuming, we synthesized coumarin-SAHA (c-SAHA) as a fluorescent probe for determining the

145 This probe, designated SAHA-BPyne, contains structural elements of the general

146 Administration of low-dose SAHA reduces cytokine production and ameliorates the cyt

147 is essential for autophagy activation during SAHA treatment.

148 e molecular mechanisms may facilitate either SAHA or TRAIL targeted use and the selection of suitable

149 autophagy by chloroquine treatment enhances SAHA-induced superoxide generation, triggers relocalizat

150 As expected, SAHA induced differentiation and matrix calcification of

151 g anti-CD3/CD28 treatment, but not following SAHA treatment (rho = 0.21, P = 0.99).

152 A new drug application has been approved for SAHA (vorinostat) treatment of cutaneous T-cell lymphoma

153 e deacetylases (HDACs) as the key target for SAHA.

154 t strikingly different cellular effects from SAHA and have the potential for use in combination antit

155 Furthermore, SAHA inhibited the NF-kappaB-dependent reporter gene exp

156 anol-withdrawn mice incubated with the HDACi SAHA (vorinostat) or trichostatin A (TSA) for 2 h, the h

157 Using a known HDACi (SAHA) and a unique small-molecule HDACi (LB-205), GCase

158 , two histone deacetylase inhibitors (HDIs), SAHA and Depsipeptide, are FDA approved for single-agent

159 We conclude that HMBA, SAHA, and JQ1 affect transcription elongation by a simil

160 How SAHA mediates its effects is poorly understood.

161 of chromatin structure, we investigated how SAHA may affect DNA replication and integrity to gain de

162 We focused our molecular analyses on how SAHA improved the impaired adipogenesis leading to the l

163 Treatment with suberoylanilide hydroxamide (SAHA), a histone deacetylase (HDAC) inhibitor, causes do

164 Importantly, SAHA activates HIV replication in peripheral blood monon

165 elated with increased autophagic activity in SAHA-treated cells.

166 glioblastoma cells results in an increase in SAHA-induced apoptosis.

167 one deacetylase (HDAC) inhibitors, including SAHA (vorinostat) and LBH589, which are currently being

168 matin immunoprecipitation analyses indicated SAHA increased the extent of acetylation of nucleosomal

169 tration of the histone deacetylase inhibitor SAHA (suberoylanilide hydroxamic acid) to animals reared

170 The histone deacetylase inhibitor SAHA enhances cell death stimulated by the proteasome in

171 e and doxorubicin and the pan-HDAC inhibitor SAHA (vorinostat) in transformed cells (LNCaP, MCF-7), a

172 tration of the class I and II HDAC inhibitor SAHA (vorinostat) preserved the antipsychotic profile of

173 ide a proof-of principle that HDAC inhibitor SAHA may have a therapeutic potential for X-ALD.

174 show that treatment with the HDAC inhibitor SAHA restores sensitivity to prednisolone in TBL1XR1-dep

175 ning P5091 with lenalidomide, HDAC inhibitor SAHA, or dexamethasone triggers synergistic anti-MM acti

176 ith the histone deacetylase (HDAC) inhibitor SAHA led to detectable clusters of DNA-Pt that colocaliz

177 The histone deacetylase (HDAC) inhibitor SAHA synergizes with JQ1 to augment cell death and more

178 ed anticancer histone deacetylase inhibitor, SAHA, reduces myocardial infarct size in a large animal

179 Interestingly, SAHA rescued the COL2A1 and ACAN expression in OA chondr

180 matologic malignancy were enrolled (14 on IV SAHA and 25 on oral SAHA), of whom 35 were treated.

181 nyl bearing hydroxamates are pan-HDACIs like SAHA.

182 In Thra1(PV/+)Ncor1(DeltaID/DeltaID) mice, SAHA improved these abnormalities even further.

183 tions as a prosurvival mechanism to mitigate SAHA-induced apoptotic and nonapoptotic cell death, sugg

184 In Arx-KO murine ES-derived neurons, SAHA was able to rescue KDM5C depletion, recover H3K4me3

185 In this study, we determined the ability of SAHA and TRAIL as single agents or in combination to inh

186 ase-3 may underlie the therapeutic action of SAHA in CTCL patients.

187 agy would augment the anticancer activity of SAHA.

188 The addition of SAHA to Btz treatment was synergistic, as SAHA induced e

189 e fungal inoculation, and the same amount of SAHA injection or DMSO was followed at day 2.

190 More potent analogs of SAHA have shown unacceptable toxicity.

191 Coadministration of SAHA and olaparib synergistically inhibited the growth o

192 The combination of SAHA with other compounds inhibited cell proliferation o

193 At concentrations of SAHA achieved clinically, only 0.079% of proviruses in r

194 e found that pharmacologic concentrations of SAHA induce replication-mediated DNA damage with activat

195 The inhibitory effect of SAHA on mice fungal keratitis was revealed by GMS and H&

196 RNA-Seq, we sought to compare the effects of SAHA and RMD on gene expression in primary CD4(+) T cell

197 The cardioprotective effects of SAHA during ischemia/reperfusion occur, at least in part

198 ically augment the antineoplastic effects of SAHA in CML cell lines and primary CML cells expressing

199 y, we investigated the anti-tumor effects of SAHA in CTCL cell lines and freshly isolated peripheral

200 further determined the different effects of SAHA or TRAIL alone and combining SAHA with TRAIL on the

201 lts demonstrate that the distinct effects of SAHA or TRAIL individually and in combination on the pro

202 agy might improve the therapeutic effects of SAHA.

203 After incubation of SAHA-TAP with an HDAC, the thiol of a conserved HDAC cys

204 cell lymphomas (CTCL), but the mechanism of SAHA action is unknown.

205 play an important role in the metabolism of SAHA and that UGT2B17-null individuals could potentially

206 A major mode of SAHA metabolism is by glucuronidation via the UDP-glucur

207 A modification of SAHA with groups known to interact with IMPDH afforded a

208 Interestingly, the enhanced performance of SAHA-BPyne as an in situ activity-based probe could not

209 We developed a prodrug of SAHA by appending a promoiety, sensitive to thiols, to t

210 y, sensitivity, and inhibitory properties of SAHA-BPyne and related potential activity-based probes f

211 ascade reaction that leads to the release of SAHA.

212 The development of senescence of SAHA-induced polyploidy cells was similar in all colon c

213 HDACs were identified as specific targets of SAHA-BPyne in proteomes.

214 tylases was substantially lower than that of SAHA in cell-free and in situ assays.

215 nstrated that the combinatorial treatment of SAHA and TRAIL may target multiple pathways and serve as

216 across a number of NDDs for whom the use of SAHA may be considered a potential therapeutic strategy.

217 UGT2B17 gene deletion variant (UGT2B17*2) on SAHA glucuronidation phenotype, human liver microsomes (

218 On treatment with trichostatin A or SAHA, H1299 cells carrying p21-3H showed a significant i

219 enhances DNA damage induced by etoposide or SAHA as indicated by increased accumulation of gammaH2AX

220 Finally, the effects of JQ1 and HMBA or SAHA on the P-TEFb equilibrium were cooperative.

221 There was no effect of TSA or SAHA on GABA sensitivity of pDAergic VTA neurons from sa

222 tment with ER stress inducers tunicamycin or SAHA (suberoylanilide hydroxamic acid).

223 sponse to CerS6 knockdown and tunicamycin or SAHA treatment.

224 Oral SAHA had linear pharmacokinetics from 200 to 600 mg, wit

225 etylated histones from 200 to 600 mg of oral SAHA.

226 were enrolled (14 on IV SAHA and 25 on oral SAHA), of whom 35 were treated.

227 atologic malignancies were treated with oral SAHA administered once or twice a day on a continuous ba

228 nilide hydroxamic acid (SAHA), and two other SAHA derivatives to HDAH, two different modes of action,

229 GATA6 overexpression, SAHA treatment or HDAC3 knockdown increased histone H3 (

230 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

232 subjected to simulated ischemia/reperfusion, SAHA pretreatment reduced cell death by 40%.

233 different potencies and HDAC specificities, SAHA and RMD modulate an overlapping set of genes, impli

234 iols, to the hydroxamic acid warhead (termed SAHA-TAP).

235 acies that were comparable to or better than SAHA.

236 uppresses tumor growth more effectively than SAHA (1, N-hydroxy-N'-phenyloctanediamide) and is theref

237 showed higher antiproliferative effects than SAHA.

238 about 1 order of magnitude more potency than SAHA in both enzymatic and cellular assays.

239 U937 leukemia cells, 2t was more potent than SAHA in inducing apoptosis, and 3i displayed cell differ

240 SU-HDAC42 was several times more potent than SAHA in suppressing the viability of PLC5, Huh7, and Hep

241 d found to be about 10-fold more potent than SAHA.

242 nfluence Z-alpha1AT protein traffic and that SAHA may represent a potential therapeutic approach for

243 protein phosphorylation, we demonstrate that SAHA activates this pathway in several subpopulations of

244 Our findings demonstrate that SAHA produces profound alterations in DNA replication th

245 inositol (PI) kinase assay demonstrated that SAHA directly inhibited kinase activity of PI 3' kinase.

246 It was discovered that SAHA inhibits the activity of histone deacetylases (HDAC

247 We also found that SAHA had no effect on direct binding of NF-kappaB to the

248 We found that SAHA is a potent suppressor of IL-1beta-induced MMP-13,

249 We found that SAHA reverted the impaired adipogenesis by de-repressing

250 fects by modulating NF-kappaB and found that SAHA suppressed NF-kappaB activation induced by TNF, IL-

251 Overall, our findings indicate that SAHA activates autophagy via inhibiting mTOR and up-regu

252 Pathway analysis indicated that SAHA increased the expression of insulin signaling modul

253 e regulated by NF-kappaB, we postulated that SAHA mediates its effects by modulating NF-kappaB and fo

254 In this study, we report that SAHA induced polyploidy in human colon cancer cell line

255 Here, we report that SAHA inhibits the proliferative and cytotoxic activity o

256 ChIP-Seq analysis revealed that SAHA increased histone H4 acetylation genome-wide and in

257 Here, we show that SAHA increases the expression of the autophagic factor L

258 We further show that SAHA-BPyne can be used to measure differences in HDAC co

259 Further examination showed that SAHA blunted hepatic expression and activation of cell c

260 trast, metabolic labeling assays showed that SAHA decreased incorporation of [(35)S]methionine into c

261 The results showed that SAHA treatment suppressed the effects of PH on histone d

262 Taken together, our results suggest that SAHA could be used as a therapeutic agent for the manage

263 We suggest that SAHA possibly could provide true, multimodality, salubri

264 ion and was blocked by SAHA, suggesting that SAHA inhibits IL-6 signaling in OA chondrocytes.

265 The SAHA-induced increase in AQP3 levels resulted in enhance

266 The SAHA-induced increase in Trx activity in normal cells is

267 g this HDAC member as a likely target in the SAHA response.

268 in 1, which increased levels of P-TEFb, then SAHA once again reactivated HIV.

269 Thus SAHA, which is a Food and Drug Administration-approved d

270 Thus, SAHA induces genome-wide H4 acetylation and modulates th

271 tudies were done along the path from DMSO to SAHA.

272 levels of cyclin D1 after 8-hour exposure to SAHA (5 muM) in MCL lines (SP49, SP53, Jeko1).

273 With respect to SAHA, OSU-HDAC42 exhibited greater apoptogenic potency,

274 ng pathways are involved in cell response to SAHA and olaparib treatment.

275 f dormant replication origins in response to SAHA.

276 iferation, and an increase in sensitivity to SAHA-induced cell death.

277 Similar to SAHA, compounds 2-75 and 1005 decreased the level of HSP

278 uggested that NK-HDAC-1 might be superior to SAHA in bioavailability and in vivo half-life.

279 Taken together, SAHA caused a rapid decrease of cyclin D1 in MCL by bloc

280 In clinical trials, SAHA has shown significant anticancer activity against b

281 The in vivo efficacy of OSU-HDAC42 versus SAHA was assessed in orthotopic and subcutaneous xenogra

282 ylase (HDAC) inhibitors, such as vorinostat (SAHA), have shown promise as therapeutic agents.

283 is found in the anticancer drug vorinostat (SAHA).

284 onse to the broad-spectrum HDACi Vorinostat (SAHA) in A549 cells, we find that combination with ATXN3

285 by histone deacetylase inhibitor vorinostat (SAHA).

286 tivity with greater potency than vorinostat (SAHA), erlotinib, lapatinib, and combinations of vorinos

287 srupting compounds such as JQ1 or vorinostat/SAHA, the CARM1 inhibitor achieved synergistic effects o

288 ll lines including Jurkat J.gamma1 for which SAHA and the previously disclosed 3HPT-derived HDACi wer

289 While SAHA was found to be unselective for the inhibition of c

290 ts was assessed by daily administration with SAHA (100 mg/kg intraperitoneally) or GCV (20 mg/kg) for

291 Tubacin in combination with SAHA or etoposide is more potent than either drug alone

292 ther increased when tubacin is combined with SAHA.

293 Compared with SAHA, compound 2-75 induced greater hyperacetylation of

294 In contrast with SAHA, neither hybrid molecule caused substantial hyperac

295 ity was inhibited by IGF-1, and further with SAHA in particular, and with halofuginone.

296 to the viral promoter upon stimulation with SAHA.

297 been achieved with RMD use ex vivo than with SAHA; however, reduction of viral reservoir size has not

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