ライフサイエンスコーパス: SAHA

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