ライフサイエンスコーパス: TSA

1 TSA also restored Friend leukemia virus integration 1, a

2 TSA and the other small molecules identified here repres

3 TSA concentrations of 250 nM or less were noncytotoxic a

4 TSA exerted its anti-EMT effects by deactivating the mot

5 TSA increased the acetylation level of histone H3, inclu

6 TSA increases miRNA-143 production in a miRNA sensor ass

7 TSA indirectly increases NAG-1 promoter activity and inc

8 TSA induced caspase-mediated apoptotic pathways; caspase

9 TSA inhibits TGF-beta1-induced accumulation of extracell

10 TSA initiates a mechanism whereby the phosphatidylinosit

11 TSA is undergoing clinical trials as a prostate cancer t

12 TSA specifically inhibits LPS-dependent genes of seconda

13 TSA treatment did not alter the DNA-binding activity of

14 TSA treatment did not restore CXCR4 expression.

15 TSA treatment of male gametophytes is associated with th

16 TSA treatment showed 60% to 75% decreases in TGF-beta1-i

17 TSA upregulated DeltaNp63-EGFP plasmid expression; this

18 TSA was a potent inhibitor of tumor necrosis factor (TNF

19 TSA, valproic acid, and MS-275 repressed cytokine-induce

20 TSA-induced NAG-1 expression involves multiple mechanism

21 TSA-seq mapping suggests that gene distance to nuclear s

22 TSAd is required for normal TCR-induced synthesis of IL-

23 ctahedral geometry observed within AlF(4)(-) TSA complexes, which endorses the proposal that some of

24 (SAHA; 5azaD/SAHA), or trichostatin A (5azaD/TSA) resulted in a higher degree of apoptosis.

25 ncluding SHP1, were comparable between 5azaD/TSA and control cultures following extended culture.

26 Culturing 5azaD/TSA-expanded cord blood cells in extended cultures revea

27 Following 5azaD/TSA treatment, JAK2V617F-negative PMF hematopoietic prog

28 y, and the allostimulatory capacity of 5azaD/TSA-expanded cells as determined by MLC were both signif

29 he reduced allostimulatory capacity of 5azaD/TSA-expanded cells is likely because of reversible inhib

30 sults suggest that a graft composed of 5azaD/TSA-expanded cells possesses relatively less allostimula

31 uantitative PCR analysis revealed that 5azaD/TSA-expanded cells expressed more STAT3 transcript than

32 ed the allostimulatory capacity of the 5azaD/TSA-expanded grafts.

33 ikely indicative of STAT3 inactivity in 5azD/TSA-expanded grafts.

34 The HDAC inhibitor trichostatin A (TSA) acts on the gene 50 promoter to induce lytic replic

35 HDAC inhibitor trichostatin A (TSA) also significantly increased P-Rex1 promoter activi

36 y of HDAC6 was suppressed by trichostatin A (TSA) and by siRNA specific to HDAC6.

37 Deacetylase inhibitors trichostatin A (TSA) and nicotinamide (NIA) increase Drosha protein leve

38 riptional activators such as trichostatin A (TSA) and tumor necrosis factor alpha (TNF) only modulate

39 rm selective HDAC inhibitors trichostatin A (TSA) and vorinostat (suberoylanilide hydroxamic acid, SA

40 n of histone deacetylases by trichostatin A (TSA) enhances the expression of CYP24A1 in prostate canc

41 hibitors sodium butyrate and trichostatin A (TSA) facilitated partner preference formation in female

42 e HDACi SAHA (vorinostat) or trichostatin A (TSA) for 2 h, the hyposensitivity of pDAergic VTA neuron

43 deacetylase (HDAC) inhibitor trichostatin A (TSA) in a retinal ischemic model.

44 Blocking HDAC activity with trichostatin A (TSA) in cultured male gametophytes of Brassica napus lea

45 ssion in 75% of cells, while trichostatin A (TSA) induced less widespread lytic gene expression and i

46 istone deacetylase inhibitor trichostatin A (TSA) inhibited EMT; this was reflected by the preservati

47 istone deacetylase inhibitor Trichostatin A (TSA) on cue versus place learning strategy selection aft

48 6 (miR-1296), genistein, and trichostatin A (TSA) on the MCM complex.

49 ment with the HDAC inhibitor trichostatin A (TSA) prevented the pressure-overload-stimulated up-regul

50 nd the deacetylase inhibitor trichostatin A (TSA) restores axonal transport.

51 istone deacetylase inhibitor trichostatin A (TSA) resulted in a synergistic increase in SMN protein l

52 denervation was amendable by trichostatin A (TSA) treatment, which increased innervation in clinicall

53 a-2-deoxycytidine (5-Aza) or trichostatin A (TSA) was used to induce demethylation or inhibit histone

54 onents in cells treated with trichostatin A (TSA), a deacetylase inhibitor that leads to protein hype

55 Trichostatin A (TSA), a histone deacetylase inhibitor, enhanced ENaC ace

56 Trichostatin A (TSA), a histone deacetylase inhibitor, has been shown to

57 We identified trichostatin A (TSA), a pan-HDAC (histone deacetylase) inhibitor, as a c

58 s, sodium butyrate (NaB) and trichostatin A (TSA), and the DNA methyltransferase inhibitor azacytidin

59 DACi, sodium butyrate (NaB), trichostatin A (TSA), and valproic acid (VPA).

60 ical HDAC inhibitor (HDACi), trichostatin A (TSA), attenuated both load- and agonist-induced hypertro

61 2'-deoxycytidine (5azaD) and trichostatin A (TSA), but not treatment with small molecule inhibitors o

62 tion of the top scoring hit, Trichostatin A (TSA), demonstrated utrophin upregulation and functional

63 eacetylase (HDAC) inhibitor, trichostatin A (TSA), for efficacy in reducing endothelial activation.

64 l phorbol acetate (TPA), and trichostatin A (TSA), in U1 monocytic and J-Lat 10.6 lymphocytic latentl

65 tors valproic acid (VPA) and trichostatin A (TSA), recapitulating the SDL interaction in human cells

66 stone deacetylase inhibitor, trichostatin A (TSA), resulted in a further extension of survival and im

67 For the binding of trichostatin A (TSA), suberoylanilide hydroxamic acid (SAHA), and two ot

68 how that sodium butyrate and Trichostatin A (TSA), two structurally different and widely used HDAC in

69 2'-deoxycytidine (5azaD) and trichostatin A (TSA), which expands transplantable HSC 7- to 10-fold.

70 this paper, we describe that trichostatin A (TSA), which inhibits deacetylase activity, blocks LPS-de

71 basal promoter activity and trichostatin A (TSA)-induced gene transcriptional activation and express

72 comparison to vorinostat or trichostatin A (TSA).

73 tivity of the HDAC inhibitor trichostatin A (TSA).

74 f histone deacetylation with trichostatin A (TSA).

75 ng the global HDAC inhibitor trichostatin A (TSA).

76 The HDAC inhibitor, trichostatin A (TSA, 0.1 mg/kg), was intraperitoneally injected daily fo

77 Trichostatin-A (TSA; 3.31 muM) was used to induce cell death as measured

78 T cell-specific adapter (TSAd) protein and adapter protein in lymphocytes of unkn

79 omology 2-domain of T cell-specific adaptor (TSAd), which in turn regulates VEGF-induced activation o

80 s not bound after LPS stimulus when we added TSA.

81 In addition, TSA prevented vascular stasis in sickle mice, it exhibit

82 bular adenoma, traditional serrated adenoma (TSA), or sessile serrated adenoma (SSA) with villous cha

83 (SSA/Ps) and traditional serrated adenomas (TSAs) are now distinguished from hyperplastic polyps and

84 as (SSAs) and traditional serrated adenomas (TSAs) constituted 36.8% (137 of 372) and 4.3% (16 of 372

85 Systemically administered TSA protected cartilage in the DMM model.

86 , also forms embryogenic cell clusters after TSA treatment.

87 duction of tolerance to tissue-specific Ags (TSAs).

88 es and relevant cancers for each alternative TSA class, as well as discuss both current challenges pr

89 g the therapeutic application of alternative TSAs and potential solutions to aid in their clinical tr

90 nature of SNV neoantigens, some alternative TSAs may have the advantage of being widely shared by mu

91 ilable therapeutic TSA targets, 'alternative TSAs', defined here as high-specificity tumour antigens

92 Among these alternative TSAs are antigens derived from mutational frameshifts, s

93 Mediterranean (EUM), Tropical South America (TSA), and South Africa (SAF).

94 We used tyramide signal amplification (TSA) and label-free mass spectrometry (MS) to compare pr

95 n (FISH) with tyramide signal amplification (TSA) to achieve unequivocal detection of cell bodies of

96 y, we applied tyramide signal amplification (TSA) to fluorescence enzyme-linked immunosorbent assay (

97 tion involves tyramide signal amplification (TSA).

98 igand-bound UmpK, a transition state analog (TSA) complex was utilized to evaluate the extent to whic

99 eliver novel step 1 transition state analog (TSA) complexes for betaPGM, incorporating trifluoromagne

100 d with the dead end transition state analog (TSA) components taurocyamine-NO3 (2-)-MgADP.

101 this enzyme with a transition state analog (TSA) revealed that the TSA was bound in the active site,

102 ts in the MgF3(-) transition state analogue (TSA) complex as a spectroscopic reporter to indicate ele

103 taining ADP and a transition-state analogue (TSA) complex containing a 3PG-AlF(4)(-)-ADP moiety.

104 Transition state analogue (TSA) complexes formed by phosphoglycerate kinase (PGK) h

105 Total solvent-free analysis (TSA) by mass spectrometry (MS) of tissue sections is car

106 lity to perform total solvent-free analysis (TSA) consisting of solvent-free ionization and solvent-f

107 l clinical value of the time-shift analysis (TSA) approach for resting-state fMRI (rs-fMRI) blood oxy

108 behavior, but the combination of mIGF-1 and TSA treatment was not synergistic.

109 The detection of both Aire and TSA expression by cell populations outside of the thymus

110 electively and transiently depletes Aire and TSA expression in the thymus to create a window of defec

111 ral TSA-reactive CD4(+), CD8(+) T cells, and TSA-suppressive CD4(+) T cells can be detected and separ

112 arcoma cells were treated with cytokines and TSA, valproic acid, MS-275, or siRNA, and quantitative r

113 CR assay reveals that treatment with DAC and TSA increases the recruitment of vitamin D receptor to t

114 donor is more likely to result in a DSA and TSA of shared antibody specificities.

115 We determined that both ethanol and TSA impair internalization at a late stage before vesicl

116 correlation between claudin-1 expression and TSA-mediated regulation of invasion.

117 Genistein and TSA significantly downregulated the expression of all MC

118 anti-MCM effect by miR-1296, genistein, and TSA.

119 bovine insulin are examples in which LSI and TSA were combined to produce multiply charged ions, simi

120 the nonselective HDAC inhibitors (MI192 and TSA, respectively) were found to regulate cytokine produ

121 The integrated muFACS and TSA-FISH technologies provide a highly effective and low

122 n, and egr1, which were activated by NaB and TSA, were similar in HH514-16 cells treated with VPA.

123 f HIV-1 stimulating agents including PMA and TSA.

124 SSA and TSA tended to be large (mean size, 10.6 mm and 14.1 mm,

125 hinones, with the plasma AUC of CTS, TSI and TSA in GP 5-184, 4-619 and 5-130 times higher than TD.

126 n of HDAC4 and HDAC5, whereas vorinostat and TSA inhibit HDAC4 and HDAC5 in the higher micromolar ran

127 action in human cells and suggesting VPA and TSA as potential therapeutic agents for tumors with elev

128 ssels, was dependent on TSAd expression, and TSAd formed a complex with VE-cadherin, VEGFR2, and c-Sr

129 ment of HLA transfusion-specific antibodies (TSA) to blood donors of transfusions given posttransplan

130 f-tolerance through tissue-specific antigen (TSA) expression.

131 clonal expansion of tumor-specific antigen (TSA)-reactive T cells are critical to the success of che

132 peptides including tumor-specific antigens (TSAs) and minor histocompatibility antigens (MiHAs).

133 The study of tumour-specific antigens (TSAs) as targets for antitumour therapies has accelerate

134 of genes encoding tissue-specific antigens (TSAs) by thymic epithelial cells is critical for this pr

135 a-AChR and various tissue-specific antigens (TSAs) in human thymic epithelial cell (TEC) cultures.

136 th alloantigens and tumor-specific antigens (TSAs) initiate GVT responses.

137 erse repertoire of tissue-specific antigens (TSAs) that are also shared by tumors.

138 of a wide array of tissue-specific antigens (TSAs), particularly in the thymus.

139 f a diverse set of tissue-specific antigens (TSAs), which are presented and help tolerize self-reacti

140 artment, including tissue-specific antigens (TSAs).

141 an NBATS score for each trauma service area (TSA) as defined by the Pittsburgh Atlas.

142 its the same spectrum of biologic effects as TSA.

143 ulation of oxtr and avpr1a gene promoters as TSA.

144 Aza+TSA also significantly reduced mortality in the ALI mode

145 or trichostatin A (herein referred to as Aza+TSA) after endotoxemia-induced mouse lung injury.

146 first time the efficacy of combinatorial Aza+TSA therapy in preventing ALI in lipopolysaccharide-indu

147 ested the hypothesis that treatment with Aza+TSA after lipopolysaccharide induction of ALI through ep

148 Combinatorial treatment with Aza+TSA mitigated the increased endothelial permeability res

149 g Aire expression must be established before TSA expression can occur.

150 the beta-D-glucopyranose ring in the betaG1P TSA complexes (step 1) is flipped over and shifted relat

151 PC4 functions are beyond TSA-induced phosphatase release, PI3K-mediated Sp1 phosp

152 BBL Trypticase soy agar with 5% sheep blood (TSA II) and each chromogenic medium.

153 One SmTK monomer was observed with two bound TSAs and an asymmetric conformation, with the first lobe

154 in the Aire-expressing developmental branch, TSA expression peaked as Aire expression decreased, impl

155 he ultimate outcome of EMT, was abolished by TSA; this was indicated by the inhibition of type I coll

156 Inhibition of HDAC6 activity by TSA significantly suppressed EGF-induced cell migration

157 on of MMP-1 and MMP-3, which were blocked by TSA (100 nM).

158 s of retinal TNF-alpha, which was blocked by TSA treatment.

159 re powerfully and significantly inhibited by TSA.

160 TGFbeta1-induced EMT and its inhibition by TSA were replicated in human primary hepatocytes.

161 ilitate comparison of genome organization by TSA-seq, we reduced required cell numbers 10- to 20-fold

162 ne-induced extravasation was not affected by TSAd deficiency.

163 Here, we show that intra-CA1 TSA infusion administrated immediately post-training bia

164 indings suggest that post-training intra-CA1 TSA infusion promotes dynamic shift from striatum toward

165 less, using Sh2d2a knockout (KO; also called TSAd(-/-)) mice, we find that alloimmune CD4(+) Teff res

166 stulated that recognition of Aire-controlled TSAs by immature thymocytes results in the selection of

167 ertoire are not controlled by Aire-dependent TSAs.

168 and AMR (P = .02) compared with the DSA+ != TSA+ patients.

169 DSA+ = TSA+ patients had increased risk of allograft failure (P

170 with a DSA response in the recipient (DSA+ = TSA+).

171 e number of trauma centers allocated to each TSA and compared to the number of existing trauma center

172 ependent thymic expression of genes encoding TSAs, which underscores the importance of Aire's interac

173 mechanisms Aire uses to target loci encoding TSAs are unknown.

174 quired for Aire's targeting of loci encoding TSAs.

175 d APCs-CD8(+) dendritic cells (DCs)-enhances TSA responses and is required for optimal induction of G

176 hrough signal processing, was able to enrich TSA-FISH-labeled E. coli cells by 223-fold.

177 histochemical analyses were used to evaluate TSA-induced changes in histone-H3 acetylation and MMP se

178 ypan blue exclusion and MTT assays evaluated TSA cytotoxicity to the cornea.

179 The authors evaluated TSA cytotoxicity and its antifibrogenic activity on TGF-

180 ore-depleted Rho*e complexed with Gt and FAK*TSA peptide containing Lys(296) with the attached all-tr

181 led with tyramide signal amplification (FISH-TSA), that this gene is located in the distal region of

182 alled low-PTA conditions) was tested on five TSA-based media supplemented with anaerobic electron acc

183 ced required cell numbers 10- to 20-fold for TSA-seq by deliberately saturating protein-labeling whil

184 Furthermore, TSA core-like motifs are found in many other trans-splic

185 Furthermore, TSA-facilitated partner preference was prevented by OTR

186 The DeltaDeltaG() (G(TSA-TSD)) obtained in silico are consistent with the pre

187 flipped over and shifted relative to the G6P TSA complexes (step 2).

188 JQ1 cytotoxicity in cell culture, and Gem + TSA + JQ1 inhibited tumor initiation and progression in

189 Genistein, TSA, and small interfering RNA duplexes caused a signifi

190 lation of LPS-treated macrophages and on how TSA targets critical LPS-induced genes, such as nos2 and

191 fication fluorescence in situ hybridization (TSA-FISH) to address these two challenges.

192 CTS), tanshinone I (TSI) and tanshinone IIA (TSA) are the most widely-studied lipophilic ingredients,

193 e signal amplification immunohistochemistry (TSA-IHC).

194 In TSA, a 13-nucleotide (nt) core motif is conserved across

195 nnervation in clinically relevant muscles in TSA-treated SMNDelta7 mice.

196 ng a potential attribution of BMP pathway in TSA induced recovery of the hair inductive capacity of S

197 A histone deacetylase inhibitor, TSA, stimulated Rgs16::GFP expression in PDA primary cel

198 on-dependent labeling approach, intratumoral TSA-reactive CD4(+), CD8(+) T cells, and TSA-suppressive

199 quences in the middle of the last 5' intron, TSA and TSB, promote trans-splicing of mod(mdg4).

200 d on the structure of a RhoA/GAP-GDP-MgF3(-) TSA complex.

201 Moreover, TSA increased ENaC current in Fischer rat thyroid and ki

202 proteins ZEBRA and EA-D in response to NaB, TSA, or AzaCdR.

203 nsition state analogue AK:Arg:Mg.ADP:NO3(-) (TSA).

204 pared to suspicious colonies on nonselective TSA II.

205 t obvious MRA lesions showed neither TTP nor TSA time delay.

206 abundant collaterals showed neither TTP nor TSA time delay.

207 Notably, TSA treatment prevents p300 from being recruited to the

208 De novo TSA developed against 150/244 (61.5%) blood donors.

209 te responsible for translocation activity of TSA by targeting single residues for mutations.

210 ylases HDAC6 and Sirt2, or administration of TSA rescues both axonal transport and locomotor behavior

211 Deletions of TSA and TSB using the CRISPR/Cas9 system result in devel

212 There was no effect of TSA or SAHA on GABA sensitivity of pDAergic VTA neurons

213 ted with a reduction in p53 independently of TSA.

214 However, concomitant infusions of TSA with either PKA inhibitor, Rp-cAMPS, into CA1 or cAM

215 Re-introduction of TSA-treated wild type c-kit(+) CSCs into Kit(W)/Kit(W-v)

216 hat activation of the AAR in the presence of TSA led to specific changes in acetylation of histone H4

217 s to specifically identify the repertoire of TSA-reactive T cells due to their heterogeneous composit

218 changes in U1 snRNA rescue trans-splicing of TSA mutants, demonstrating that U1 recruitment is critic

219 Two-minute topical treatment of TSA on rabbit corneas subjected to -9 D PRK significantl

220 lysis demonstrated that the key mechanism of TSAd function in Tregs relates to its effects on cellula

221 The most commonly studied class of TSAs are those derived from non-synonymous single-nucleo

222 This ectopic expression of TSAs largely depends on autoimmune regulator (Aire), whi

223 MRSA on TSA II was confirmed by Gram staining, a coagulase test,

224 methicillin-susceptible S. aureus (MSSA) on TSA II was 12.4% (64/515) and 9.7% (50/515), respectivel

225 in mouse cremaster vessels, was dependent on TSAd expression, and TSAd formed a complex with VE-cadhe

226 When combined with NaB or TSA, VPA did not inhibit the activation of these cellula

227 gene expression in response to VPA, NaB, or TSA were globally similar as assessed by human genome ar

228 Patients with SSA/P or TSA are at increased risk for CRC; their level of risk i

229 ssion of alpha-AChR in TECs and not of other TSAs.

230 Our "TSA-MS ratio" approach successfully identified known nuc

231 timized to 30 mol% p-toluenesulfonic acid (p-TSA) in toluene using Dean-Stark apparatus, where the al

232 Metal-free, p-toluenesulfonic acid (p-TSA)-mediated, straightforward propargylation of beta-ke

233 Notably, in the presence of Bronsted acid p-TSA.H2O, the reaction afforded the hydrolyzed product pr

234 though exhibiting a dysfunctional phenotype, TSA-reactive CD8(+) TILs possess substantial capabilitie

235 The T cell-specific adaptor protein (TSAd), encoded by the SH2D2A gene, is an intracellular m

236 tion of PC4 expression significantly reduced TSA-induced recruitment of TFIIB and RNAP II, at the pro

237 Moreover, confocal images showed TSA-induced nuclear hot spots of endogenous PCBP in neur

238 t the structure of TraI translocation signal TSA.

239 A small angle x-ray scattering model of SmTK-TSA in solution with two closed active sites was generat

240 of VEGF receptor-2 (VEGFR-2), and subsequent TSAd-mediated activation of Src family kinases (SFKs), S

241 urfold amplified autophagic response to TAC, TSA abolished TAC-induced increases in autophagy and blu

242 and extended survival of SMA mice more than TSA alone.

243 ogenous E-cadherin levels more strongly than TSA.

244 Mutation analysis demonstrated that TSA response was mediated by both dsDNA (Sp1/Sp3 binding

245 In this study, we found that TSA markedly alleviated culture expansion induced SKP se

246 We also found that TSA reduces C/EBPbeta phosphorylation without affecting

247 These observations indicate that TSA and mating facilitate partner preference through epi

248 to known translocation signals we show that TSA is an independent folding unit and thus forms a bona

249 We also show that TSA is part of a larger vestigial helicase domain which

250 luciferase reporter gene system showed that TSA induced an approximately 3-fold increase of the prom

251 This observation suggests that TSA, and other related histone deacetylase inhibitors, m

252 Further analysis verified that TSA inhibited cyst formation in pkd2 knockdown animals.

253 We conclude that TSAd is required for VEGF-induced, c-Src-mediated regula

254 egion of KO versus WT Tregs, suggesting that TSAd, in part, promotes Treg stability.

255 Lastly, we found no evidence that TSAs presented by medullary thymic epithelial cells in A

256 The TSA approach was a promising alternative to DSC-PWI for

257 The TSA rescue of AAR activation in the absence of Atf4 also

258 The TSA-FISH protocol that was adapted for flow cytometry yi

259 n, overexpression of claudin-1 abrogated the TSA-induced inhibition of invasion in colon cancer cells

260 In 70/150 (46.7%) cases the TSA was of shared HLA antibody specificity with a DSA re

261 activity, was identified as critical for the TSA effect.

262 tions for the axial O-Mg-O alignment for the TSA of the phosphoryl group in the catalytic site differ

263 domain the changes induced upon forming the TSA complex are an intensification of those induced by b

264 ups were found to be remarkably rigid in the TSA complex, indicating that the enzyme has evolved to r

265 rt the possibility of a role for CREB in the TSA-mediated switch between these two memory systems.

266 human epidermal growth factor ELISA kit, the TSA method led to a >100-fold increase in fluorescence s

267 Notably, the TSA analog SAHA (suberoylanilide hydroxaminc acid) that

268 ly, relaxation dispersion experiments of the TSA reveal that it samples the structures of the Michael

269 l behavior shows that the free energy of the TSA, with all ligands bound, is lower by only about 8.9

270 a dominant excited state that resembles the TSA, as evidenced by the strong correlation between the

271 nsition state analog (TSA) revealed that the TSA was bound in the active site, interacted with the in

272 36 ms and the free energy difference to the TSA-like form is 8.5 kJ/mol.

273 ligands and an additional increase when the TSA complex is formed.

274 haelis or apo complex conformations with the TSA ligands present.

275 f the combination was also observed with the TSA mammary adenocarcinoma and MCA38 colon carcinoma tum

276 ease the repertoire of available therapeutic TSA targets, 'alternative TSAs', defined here as high-sp

277 Thus, TSAd serves as a critical cell-intrinsic molecule in CD4

278 Compared to bystander TILs, TSA-reactive TILs possess a distinct T cell receptor (TC

279 duced the most HIV activation, comparable to TSA activation.

280 Collaborative Grant 2018 (NNF18OC0052457, to TSA and MS), Heisenberg Professorship of the German Rese

281 VPA was only slightly superior to TSA in inducing histone acetylation of Rta's promoter, b

282 fic HDAC inhibitor structurally unrelated to TSA, or by knocking down hdac1, suppressed kidney cyst f

283 nalyses further indicated that post-training TSA infusion in aged mice rescued aging-associated dereg

284 By reducing ENaC ubiquitination, TSA decreased the rate of ENaC degradation.

285 ship between acetylation and ubiquitination; TSA reduced ENaC ubiquitination, whereas HDAC7 increased

286 PC4 at the LHR promoter that increased upon TSA treatment.

287 ontralateral hemisphere was calculated using TSA.

288 aric compositions were well-delineated using TSA by MS.

289 was activated in vivo and in vitro in a VEGF/TSAd-dependent manner, and was regulated via increased p

290 Weekly TSA treatment, between the ages of 6 and 10 months, was

291 itors prevented degradation of BNC, in which TSA and MS-275 repressed cytokine-induced MMP expression

292 nce (39.4%, 54 of 137 lesions) compared with TSA and HP.

293 FP(+) c-kit(+) CSCs were preconditioned with TSA (50 nmol/liter) for 24 h and re-introduced into infa

294 duce ischemic injury, rats were treated with TSA (2.5 mg/kg intraperitoneally) twice daily on days 0,

295 In rats treated with TSA, amplitudes of ERG a- and b-waves from ischemic eyes

296 , and p53 were assessed after treatment with TSA and siRNA.

297 Treatment with TSA increases H3K9ac and H3K4me2 and simultaneously decr

298 ereas Hdac5 heterozygosity or treatment with TSA, an HDAC inhibitor, reduced cyst formation in Pkd2(-

299 was 4.84 in the 14 cases vs 17 controls with TSAs (95% CI, 2.36-9.93), 2.51 in the 757 cases vs 1698

300 SSA/P with dysplasia, 4.5% for patients with TSAs, and 2.3% for patients with conventional adenomas.