ライフサイエンスコーパス: TSA

1 TSA also impaired ASGP-R endocytic trafficking, but to a

2 TSA also increases the expression of transcription facto

3 TSA also increases the stability of NAG-1 mRNA.

4 TSA also restored Friend leukemia virus integration 1, a

5 TSA caused significant differentiation and neuritogenesi

6 TSA concentrations of 250 nM or less were noncytotoxic a

7 TSA down regulates 9 of 15 genes in this pathway in the

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

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

10 TSA indirectly increases NAG-1 promoter activity and inc

11 TSA induced caspase-mediated apoptotic pathways; caspase

12 TSA inhibits TGF-beta1-induced accumulation of extracell

13 TSA initiates a mechanism whereby the phosphatidylinosit

14 TSA is undergoing clinical trials as a prostate cancer t

15 TSA nearly abolishes TF-kappaB binding without affecting

16 TSA specifically inhibits LPS-dependent genes of seconda

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

18 TSA treatment did not restore CXCR4 expression.

19 TSA treatment of male gametophytes is associated with th

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

21 TSA upregulated DeltaNp63-EGFP plasmid expression; this

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

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

24 TSA-induced NAG-1 expression involves multiple mechanism

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

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

27 5azaD/TSA treatment led to a dramatic reduction in the number

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

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

30 Exposure of IM CD34(+) cells to 5azaD/TSA resulted in a reduction of the proportion of JAK2V61

31 Unlike normal CD34(+) cells where 5azaD/TSA treatment leads to the expansion of CD34(+) cells an

32 Treatment of IM CD34(+) cells with 5azaD/TSA resulted in the up-regulation of CXCR4 expression by

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

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

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

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

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

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

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

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

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

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

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

44 peritoneal doses of 10 mg/kg trichostatin A (TSA) in nontransgenic and SMA model mice resulted in inc

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) induces GFP activation in GFP(-) cells and can also

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

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

49 6 (miR-1296), genistein, and trichostatin A (TSA) on the MCM complex.

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

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

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

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

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

55 We investigated whether trichostatin A (TSA) would alter the expression of NAG-1 in glioblastoma

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

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

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

59 Treatment of the cells with trichostatin A (TSA), a histone deacetylase inhibitor, induced changes i

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

61 d F9 cell lines treated with Trichostatin A (TSA), a potent histone deacetylase inhibitor.

62 Addition of trichostatin A (TSA), an HDAC6 inhibitor, induced microtubule acetylatio

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

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

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

66 2'-deoxycytidine (5azaD) and trichostatin A (TSA), but not treatment with small molecule inhibitors o

67 inhibitors (HDACi), such as trichostatin A (TSA), can regulate gene expression by promoting acetylat

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

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

70 stone deacetylase inhibitor, trichostatin A (TSA), induces derepression of the human luteinizing horm

71 eacetylase (HDAC) inhibitor, trichostatin A (TSA), on neuronal mu-opioid receptor (MOR) gene expressi

72 line RGC-5 was treated with trichostatin A (TSA), other HDAC inhibitors, and staurosporine; differen

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

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

75 eacetylase (HDAC) inhibitors trichostatin A (TSA), sodium butyrate, and scriptaid was observed in all

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

77 itor of histone deacetylase, trichostatin A (TSA), to activate GFP expression from nonexpressing cell

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

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

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

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

82 f histone deacetylation with trichostatin A (TSA).

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

84 comparison to vorinostat or trichostatin A (TSA).

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

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

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

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

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

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

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

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

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

94 Systemically administered TSA protected cartilage in the DMM model.

95 , also forms embryogenic cell clusters after TSA treatment.

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

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

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

99 tion involves tyramide signal amplification (TSA).

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

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

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

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

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

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

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

107 tween binding of transition state analogues (TSAs) and catalysis is an open problem.

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

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

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

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

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

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

114 a restriction enzyme accessibility assay and TSA-stimulated uPA promoter activity through the inhibit

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

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

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

118 Similarly, both ethanol and TSA impaired transcytosis of the single-spanning apical

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

120 Genistein and TSA significantly downregulated the expression of all MC

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

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

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

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

125 In HH514-16 cells, NaB and TSA strongly activated the EBV lytic cycle and caused hy

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

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

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

129 ion was impaired in both ethanol-treated and TSA-treated cells, indicating that increased microtubule

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

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

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

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

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

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

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

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

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

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

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

141 its the same spectrum of biologic effects as TSA.

142 ulation of oxtr and avpr1a gene promoters as TSA.

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

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

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

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

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

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

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

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

151 n patterns of specific genes induced by both TSA and LIF withdrawal.

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

153 za-dC did not increase NAG-1 expression, but TSA up-regulated NAG-1 expression and acted synergistica

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

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

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

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

158 owed that the induction of uPA expression by TSA was accompanied by a remarkable increase of acetylat

159 Changes in chromatin structure induced by TSA cause the release of PP2A in JAR cells or of PP1 in

160 ink NAG-1 expression to apoptosis induced by TSA.

161 re powerfully and significantly inhibited by TSA.

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

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

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

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

166 In human umbilical vein endothelial cells, TSA attenuates by approximately 70% TNF-alpha stimulatio

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

168 ertoire are not controlled by Aire-dependent TSAs.

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

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

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

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

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

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

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

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

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

178 Finally, TSA treatment did not support the maintenance or progres

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

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

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

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

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

184 Database(http://www.ncbi.nlm.nih.gov/genbank/TSA.html) under accession numbers JI163767-JI182837 and

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

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

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

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

189 e signal amplification immunohistochemistry (TSA-IHC).

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

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

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

193 assays indicate that Egr-1 and Sp-1 mediate TSA-induced NAG-1 expression.

194 PP2A and PP1 from the LHR promoter mediates TSA-induced activation of LHR gene transcription in a ce

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

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

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

198 We determined that exposure to 50 nM TSA for 30 minutes induced microtubule acetylation ( app

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

200 pared to suspicious colonies on nonselective TSA II.

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

202 abundant collaterals showed neither TTP nor TSA time delay.

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

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

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

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

207 Repeated daily doses of TSA caused increases in both SMN2-derived transcript and

208 A time course study on the effect of TSA on gene expression of various enzymes and transcript

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

210 ted with a reduction in p53 independently of TSA.

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

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

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

214 populations, we found that after removal of TSA, GFP silencing was reestablished in a subset of cell

215 Upon removal of TSA, the cells reverted to the undifferentiated phenotyp

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

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

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

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

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

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

222 er, when Raji cells were treated with NaB or TSA, neither of which is sufficient to activate the lyti

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

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

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

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

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

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

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

230 A recent study of the binding of phenolate TSAs to ketosteroid isomerase (KSI) found a small change

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

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

233 t the structure of TraI translocation signal TSA.

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

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

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

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

238 ogenous E-cadherin levels more strongly than TSA.

239 oter-luciferase reporter system confirm that TSA inhibits TF-kappaB but not NF-kappaB activation.

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

241 We find that TSA and four other HDACi (apicidin, MS-275, sodium butyr

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

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

244 RT-PCR analysis further revealed that TSA also decreased the steady-state level of MOR mRNA in

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

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

247 These experiments show that TSA treatment results in clear repression of genes invol

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

249 Thus, data suggest that TSA, an epigenetic regulator, affects neuronal MOR gene

250 Taken together, these results suggested that TSA enhanced neuronal MOR gene expression at the transcr

251 ChIP analysis further suggested that TSA enhanced the recruitment of Sp1/Sp3 and PCBP to the

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

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

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

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 activity, was identified as critical for the TSA effect.

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

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

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

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

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

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

267 It is found that the binding of the TSA and the chemical catalysis represent different therm

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 SH2 domain that is highly homologous to the TSAd protein and ALX SH2 domains and that shares other s

277 ith a change in charge delocalization of the TSAs.

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

279 total proteins were observed in response to TSA using Western blot analysis.

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

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

282 We conclude that in contrast to TSAd and ALX proteins, SH2D4A is dispensable for TCR sig

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.