ライフサイエンスコーパス: DCA

1 DCA (10-150 microM) stimulated the release of both Hbeta

2 DCA (50-250 micromol/L) caused profound Ca2+ release fro

3 DCA activated the ERK1/2 pathway in HuH7 human hepatoma

4 DCA also caused dramatic translocation of PH-PLCdelta-GF

5 DCA and taurodeoxycholic acid (TDCA) (100 micromol/L) ca

6 DCA can accurately infer spatial adjacencies between res

7 DCA caused activation of the ERK1/2 and JNK1/2 pathways.

8 DCA did not activate the ERK1/2 pathway in mitochondria-

9 DCA did not affect RPP but normalized dP/dt in HYP.

10 DCA forces CSCs into oxidative phosphorylation but does

11 DCA had no effect on localization of a novel (PKCdelta)

12 DCA induced cAMP formation at the plasma membrane and cy

13 DCA induced mild, transient colonic inflammation within

14 DCA induces mild, transient colitis, resulting in persis

15 DCA involvement in these disease processes results partl

16 DCA is based on three features, primarily the previously

17 DCA is currently not approved for cancer treatment in th

18 DCA is shown to yield a large number of correctly predic

19 DCA rapidly (30 to 60 seconds) increased phosphorylation

20 DCA showed minimal net benefit.

21 DCA stimulated JNK activation and the JNK inhibitor SP60

22 DCA stimulated phosphorylation of the p65 subunit of NF-

23 DCA stimulated TGR5 redistribution to plasma membrane mi

24 DCA storage reduces ACC (1-aminocyclopropane-1-carboxyla

25 DCA treatment restored cardiac mitochondrial membrane po

26 DCA was also found to induce tyrosine phosphorylation an

27 DCA, taurolithocholic acid, and oleanolic acid did not s

28 DCA- and TDCA-induced receptor and signaling pathway act

29 DCA-CF is efficient in quality maintenance of 'Royal Gal

30 DCA-induced activation of the insulin receptor correlate

31 DCA-induced ERK1/2 activation was responsible for increa

32 DCA-induced JNK activation was independent of either the

33 DCA-RQ1.5 is the most suited for the storage of 'Fuji Su

34 ) day(-1) simvastatin + 30 mg kg(-1) day(-1) DCA (n = 9) or 88 mg kg(-1) day(-1) simvastatin + 40 mg

35 ) day(-1) simvastatin + 40 mg kg(-1) day(-1) DCA (n = 9).

36 ane (1,1,1-TCA); and 1,1-dichloroethane (1,1-DCA), range from -26.5 per thousand to -1.8 per thousand

37 Unlike 1,1,1-TCA and 1,1-DCA, reductive dechlorination of CF by the Dehalobacter-

38 /MEL also shown to degrade 1,1,1-TCA and 1,1-DCA.

39 icroarray analyses revealed a cluster of 142 DCA- and INA-responsive genes that show a pattern of dif

40 When aseptic root cultures were fed [14C]-DCA, compared with wild types, the ugt72B1 plants showed

41 Isotopic fractionation of 1,2-DCA (epsilonbulk(C) and epsilonbulk(Cl)) for Dehalococco

42 nisms controlling natural attenuation of 1,2-DCA and to design appropriate strategies to enhance biod

43 sed to characterize dihaloelimination of 1,2-DCA by different bacteria, which needs to be confirmed i

44 rination are the proposed mechanisms for 1,2-DCA degradation by coupled nZVI-dithionite treatment.

45 tterns allow for the first time reliable 1,2-DCA degradation pathway identification in the field, whi

46 e potential of this approach to identify 1,2-DCA degradation pathways in the field.

47 of the dual isotope approach to identify 1,2-DCA degradation pathways in the field.

48 and anaerobic biodegradation pathways of 1,2-DCA in the field and suggests that this approach might a

49 t coupling nZVI with dithionite to treat 1,2-DCA is proposed in this work.

50 nZVI-dithionite was able to degrade >90% 1,2-DCA over the course of a year.

51 lcitrance toward abiotic dechlorination, 1,2-DCA remains a challenging compound for the remediation c

52 nd-specific chlorine isotope analysis of 1,2-DCA was performed for the first time, and isotope fracti

53 Lambda values of 1,2-DCA were, for the first time, determined in two field si

54 rachloroethene (PCE)/1,2-dichloroethane (1,2-DCA) completely to ethene.

55 1,2-Dichloroethane (1,2-DCA) is a chlorinated solvent classified as a probable h

56 ic biodegradation of 1,2-dichloroethane (1,2-DCA) using five microbial cultures.

57 ic biodegradation of 1,2-dichloroethane (1,2-DCA) via dihaloelimination by Dehalococcoides and Dehalo

58 ic biodegradation of 1,2-dichloroethane (1,2-DCA) via oxidative cleavage of a C-H bond (Pseudomonas s

59 tepwise removed halogens from 2,4,6-TCP, 1,2-DCA, PCE, PBDEs, and PCBs.

60 o achieve nearly complete degradation of 1,2-DCA.

61 etallic) has been unable to dechlorinate 1,2-DCA.

62 phere monitored by respiratory quotient 1.3 (DCA-RQ 1.3) showed lower ethylene production, respiratio

63 and its metabolite 3,4-dichloroaniline (3,4-DCA) on thyroid function and metamorphosis in tadpoles o

64 phere monitored by respiratory quotient 1.5 (DCA-RQ 1.5) increased the acetaldehyde, ethanol and ethy

65 ative IGF-1 receptor (K1003R) also abolished DCA-induced AKT activation.

66 ck-out or knockdown of p53 or CD95 abolished DCA + MEK1/2 inhibitor-induced PERK phosphorylation and

67 ific bile acids, and the secondary bile acid DCA in particular, in the regulation of hepatic LCFA upt

68 ) enhanced the toxicity of deoxycholic acid (DCA) + MEK1/2 inhibitor.

69 the mechanism(s) by which deoxycholic acid (DCA) activates the JNK pathway were examined.

70 vestigating the effects of deoxycholic acid (DCA) and ursodeoxycholic acid on the expression and rele

71 Secondary bile acids like deoxycholic acid (DCA) are well-established tumor promoters that may exert

72 eoxycholic acid (UDCA) and deoxycholic acid (DCA) as the two most potent inhibitors of the liver-spec

73 Deoxycholic acid (DCA) is an endogenous secondary bile acid implicated in

74 ry bile acids (BA) such as deoxycholic acid (DCA) promote the development of several gastrointestinal

75 trated in hepatocytes that deoxycholic acid (DCA) promotes inactivation of protein tyrosine phosphata

76 a-linolenic acid (DGLA) to deoxycholic acid (DCA) species (DCAS) was significantly increased in obese

77 Deoxycholic acid (DCA) was instilled into the rat colon daily for 3 days a

78 d DR5/TRAIL-R2 expression, deoxycholic acid (DCA) was the most potent.

79 Second, CDCA, deoxycholic acid (DCA), and other synthetic FXR agonists, such as GW4064,

80 y bile acids, particularly deoxycholic acid (DCA), are implicated in promoting colon cancer growth an

81 atment of hepatocytes with deoxycholic acid (DCA), chenodeoxycholic acid (CDCA) or ursodeoxycholic ac

82 Deoxycholic acid (DCA), chenodeoxycholic acid (CDCA), taurodeoxycholic aci

83 BAs (deoxycholic acid (DCA), taurolithocholic acid) and the selective agonists

84 ta-cyclodextrin suppressed deoxycholic acid (DCA)-induced apoptosis, and staining for cholesterol wit

85 usly, we demonstrated that deoxycholic acid (DCA)-induced ERK1/2 and AKT signaling in primary hepatoc

86 we have demonstrated that deoxycholic acid (DCA)-induced signaling of extracellular signal-regulated

87 sulfoxide (DMSO) and 5% dichloroacetic acid (DCA) and successive heteronuclear (1)H-(15)N HSQC spectr

88 o-compartment model for dichloroacetic acid (DCA).

89 epresentative, 3,5-dichloroanthranilic acid (DCA), efficiently induced defense reactions to the phyto

90 Bile acids (deoxycholic acid, DCA; taurocholic acid, TCA) activated AKT and glycogen s

91 Genera previously associated with aerobic DCA biodegradation (Xanthobacter, Ancylobacter, Azoarcus

92 as early as 2 min and peaked at 10 min after DCA treatment.

93 a difference of convex functions algorithm (DCA).

94 )-alkylmethylammonium dicyanamide ([Aliquat][DCA]) and 1-n-octyl-3-methylimidazolium dicyanamide ([Om

95 Decision curve analyses (DCA) showed improvements of the clinical usefulness and

96 nalysis (RFA) and damping capacity analysis (DCA).

97 Dynamic cluster analysis (DCA) is an automated, unbiased technique which can ident

98 consC3 outperforms direct coupling analysis (DCA) methods significantly independent on family size, s

99 cts estimated from direct coupling analysis (DCA) of co-evolving genomic sequences.

100 based entirely on Direct Coupling Analysis (DCA) of correlated mutations in multiple sequence alignm

101 t constraints from direct coupling analysis (DCA) to determine the dominant docked conformation of th

102 d this model using direct coupling analysis (DCA), a powerful statistical inference method that has b

103 ecently introduced direct-coupling analysis (DCA).

104 global statistical direct coupling analysis (DCA).

105 sequent VLRAF using decision-curve analysis (DCA).

106 ic (ROC) curves and Decision Curve Analysis (DCA).

107 ated (-53+/-3% from 3.27+/-0.22 mm, n=9) and DCA (-51+/-3% from 3.08+/-0.15 mm, n=5) groups.

108 cid (50-200 microM) inhibited both basal and DCA-induced defensin release.

109 xycholic acid in unconjugated (CDCA, CA, and DCA) and tauro-conjugated (t-CDCA, t-CA, t-DCA) form on

110 ing ClustalW, Probcons, Muscle, T-Coffee and DCA.

111 FXR, whereas CA partially activated FXR and DCA and UDCA had negligible activities.

112 ty related to the values obtained by RFA and DCA devices, which could create disagreements and miscom

113 is had been made in various regions; RFA and DCA should have been applied in the same implants and pe

114 Both UDCA and DCA were able to inhibit LCFA uptake by primary hepatocy

115 which specific bile acids, such as UDCA and DCA, can impact hepatic triglyceride metabolism and may

116 al cases of a few protein families and apply DCA to a systematic large-scale study of nearly 2,000 Pf

117 en (ULO) with dynamic controlled atmosphere (DCA) and controlled atmosphere (CA) on the post storage

118 he effects of dynamic controlled atmosphere (DCA) storage based on chlorophyll fluorescence (DCA-CF)

119 a' apples, in dynamic controlled atmosphere (DCA), treated with or without 1-methylcyclopropene (1-MC

120 TACE inhibition was sufficient to attenuate DCA-induced AREG, but not TGF-alpha shedding.

121 n and cell-cycle progression, and attenuated DCA-induced colorectal cancer or PDAC tumorigenicity.

122 ine ACR was measured by nurses using a Bayer DCA 2000 analyzer and expressed in mg/mmol (reference ra

123 However, brefeldin A failed to block DCA-mediated JNK activation in wild-type hepatocytes.

124 Expression of dominant negative PERK blocked DCA + MEK1/2 inhibitor-induced expression of ATG5, GRP78

125 ation and the JNK inhibitor SP600125 blocked DCA-induced DR5/TRAIL-R2 mRNA and protein expression.

126 TILs) [emim][BF(4)], [emim][DCA], and [bmim][DCA] at 25 degrees C from below 1 GHz to 10 THz by ultra

127 th butylmethylpyrrolidinium-dicyanamide (BMP-DCA) IL shows high sensitivity toward ascorbic acid (AA)

128 did not alter AKT or GS activation caused by DCA.

129 ding to one of the two sites was enhanced by DCA treatment as evaluated by electrophoretic mobility s

130 patocytes prevented the activation of ERK by DCA.

131 (approximately 81%) the activation of ERK by DCA.

132 ocytes abolished activation of AKT and GS by DCA and TCA.

133 large interfaces are commonly identified by DCA.

134 t alter ERK1/2 and AKT activation induced by DCA or CDCA but abolished pathway activations by conjuga

135 findings suggest that contacts predicted by DCA can be used as a reliable guide to facilitate comput

136 aluate the accuracy of contact prediction by DCA for a large number of protein domains, based purely

137 pite the partial induction of BSEP mRNA, CA, DCA, and UDCA effectively repressed expression of choles

138 A simple hybrid method, called DCA-fold, integrating DCA contacts with an accurate know

139 e older group, FMT signal in dorsal caudate (DCA) and dorsal putamen was greater with age, suggesting

140 ilities to activate the BSEP promoter: CDCA, DCA, CA, and UDCA increased luciferase activity by 25-,

141 In hepatocytes and HuH7 cells, DCA inhibited PTPase activity.

142 nd the lowest by fruits stored under DCA-CF (DCA based on chlorophyll fluorescence).

143 ibitors, our findings suggest that combining DCA with a DNA methylation inhibitor would offer a means

144 In conclusion, DCA and TDCA cause ROS generation in hepatocytes that is

145 yme shown to be highly active in conjugating DCA and 2,4,5-trichlorophenol, as well as several other

146 Correspondingly, DCA increased cytoplasmic Ca2+ to levels that were appro

147 ystem based on chlorophyll fluorescence DCA (DCA-CF), and static controlled atmosphere.

148 ids, chenodeoxycholate (CDCA), deoxycholate (DCA), cholate (CA), and ursodeoxycholate (UDCA), act as

149 Dichloroacetate (DCA) is an anticancer agent that can reverse the Warburg

150 Dichloroacetate (DCA), a compound capable of shifting metabolism from gly

151 se complex (PDC) activator, dichloroacetate (DCA), would blunt activation of FOXO gene targets and re

152 and its synthetic analogue dichloroacetate (DCA).

153 Inhibiting PDK3 activity by dichloroacetate (DCA) or siRNA-mediated attenuation was sufficient to inc

154 inhibition of human PDK2 by dichloroacetate (DCA).

155 e effect of the orphan drug dichloroacetate (DCA) on survival in an animal model of hemorrhagic shock

156 he public and scientists in dichloroacetate (DCA) as a potential anticancer drug.

157 ochondrial kinase inhibitor dichloroacetate (DCA) has recently received attention in oncology due to

158 ed the potential neurotoxin dichloroacetate (DCA) was investigated using an intermediate-pressure mat

159 ained untreated or received dichloroacetate (DCA) to activate PDH and increase substrate competition

160 of PDH by cell exposure to dichloroacetate (DCA) increased production of hyperpolarized 5-(13)C-glut

161 Herein, it is shown that dichloroacetone (DCA) enhances helical secondary structures when introduc

162 e persistent pollutants 3,4-dichloroaniline (DCA) and 2,4,5-trichlorophenol (TCP).

163 The pollutant 3,4-dichloroaniline (DCA) was rapidly detoxified by glucosylation in Arabidop

164 ed for bioremediation of 1,2-dichloroethane (DCA) in groundwater.

165 Inhibition of either DCA-induced ERK1/2 or DCA-induced JNK1/2 signaling enhan

166 ionic liquids (RTILs) [emim][BF(4)], [emim][DCA], and [bmim][DCA] at 25 degrees C from below 1 GHz t

167 nduced LC3-GFP vesicularization and enhanced DCA + MEK1/2 inhibitor-induced toxicity.

168 or of C/EBPbeta and c-Jun function enhanced DCA-induced apoptosis above the levels resulting from th

169 pression of p21 or p27(Kip-1) (p27) enhanced DCA + MEK1/2 inhibitor toxicity in primary hepatocytes t

170 expression of p21 or p27 profoundly enhanced DCA + MEK1/2 inhibitor-induced expression of ATG5 and GR

171 thesis of enantiomeric deoxycholic acid (ent-DCA) from achiral 2-methyl-1,3-cyclopentanedione.

172 c acid (ent-CDCA), and deoxycholic acid (ent-DCA) to induce toxicity and apoptosis in HT-29 and HCT-1

173 ve completed the successful synthesis of ent-DCA in 25 steps with a yield of 0.3% with all stereochem

174 critical micelle concentration (cmc) of ent-DCA, determined by a dye solubilization method, was iden

175 olon cancer cell lines demonstrated that ent-DCA had similar effects on proliferation, yet showed a m

176 To further explore DCA induced changes in cell signaling, we completed a to

177 , a system based on chlorophyll fluorescence DCA (DCA-CF), and static controlled atmosphere.

178 ) storage based on chlorophyll fluorescence (DCA-CF) and respiratory quotient (DCA-RQ) on the quality

179 c-Jun function promoted apoptosis following DCA treatment, and the level of apoptosis was further in

180 lues for DCA, whereas binding affinities for DCA are comparable with wild-type PDK2.

181 range), although the uncertainty bounds for DCA exceeded the predicted variability.

182 CA and MEK1/2 inhibitor to that observed for DCA and MEK1/2 inhibitor.

183 stic increases in apparent IC(50) values for DCA, whereas binding affinities for DCA are comparable w

184 Furthermore, DCA treatment also abrogated the clonogenic advantage co

185 onexpresser of Pathogenesis-Related genes1), DCA acts transiently and is only partially dependent on

186 t cultures, with the N-beta-d-glucopyranosyl-DCA exported into the medium.

187 In primary hepatocytes, DCA activated ERBB1 (the epidermal growth factor recepto

188 In HuH7 cells and primary hepatocytes, DCA enhanced the production of ROS, an effect that was a

189 Here DCA is applied on (i) simulated isotope patterns of the

190 HFD+DCA activated PDC throughout and restored whole-body CHO

191 saline (CD and HFD) or dichloroacetate (HFD+DCA).

192 However, DCA molecule exhibits poor bioavailability and cellular

193 However, DCA, associated with etoposide or irradiation, induced a

194 petition from PDH reduced anaplerosis in HYP+DCA by 18%.

195 Interestingly, reduced anaplerosis in HYP+DCA corresponded with normalized TAG (14.9+/-0.6 micromo

196 ation: HYP=1419+/-220 nmol/g dry weight; HYP+DCA=343+/-56 nmol/g dry weight.

197 In contrast, in DCA pigs, myocardial stunning was ameliorated (P<0.05).

198 rast, ASM(-/-) hepatocytes were defective in DCA-induced ceramide generation.

199 cifically, we show that AREG participates in DCA-induced EGFR and STAT3 signaling, cell-cycle progres

200 1 plays a facilitating, proapoptotic role in DCA-induced apoptosis.

201 In younger adults, FMT signal in DCA was lower with age, likely related to ongoing develo

202 Storage in DCA-CF reduces fruit ester production, especially 2-meth

203 commended for 'Fuji Suprema' apple stored in DCA conditions.

204 The apples were stored in DCA-RQ, a new technology for storing fruits, and were co

205 amined a role for the BA transporter TGR5 in DCA-mediated EGFR and STAT3 signaling.

206 7 day initial adaptation phase of increasing DCA concentration.

207 mediated silencing of TGR5 or AREG inhibited DCA-induced EGFR, MAPK, and STAT3 signaling, blunted cyc

208 aB inhibitor, BMS-345541 (25 muM), inhibited DCA-induced HbetaD2, but not HbetaD1, release.

209 hybrid method, called DCA-fold, integrating DCA contacts with an accurate knowledge of local informa

210 Likewise, DCA was found to affect membrane distribution of caveoli

211 alogenase gene dhlA was developed to monitor DCA-degrading bacteria in the MBR, and a positive correl

212 tively, these data demonstrate that multiple DCA-induced signaling pathways and transcription factors

213 zed compounds, we have selected the multiple DCA-loaded compound 10, characterized by a tertiary amin

214 method, was identical to the cmc of natural DCA.

215 y to induce apoptosis as compared to natural DCA.

216 TCA, but not DCA, activated Galpha(i) proteins in primary rat hepatoc

217 Notably, DCA potentiated the antitumor effects of elesclomol, a p

218 come these biases, we have synthesized novel DCA-loaded compounds.

219 In the absence of DCA, myocardial stunning was observed; ie, wall thickeni

220 cells resistant to the antitumor activity of DCA.

221 Administration of DCA in vivo via injection or as part of a high-fat diet

222 gene abundance and the cumulative amount of DCA that had entered the MBR.

223 n studies together with a new application of DCA to the eukaryotic proteins NAF-1 and Bcl-2 provided

224 Biodegradation of DCA in the MBR began after 26 days, and was sustained fo

225 Our results show that low concentrations of DCA (5 and 50 microM) significantly increase tyrosine ph

226 rapid and sensitive method for detection of DCA-degrading bacteria.

227 r would offer a means to reduce the doses of DCA to avoid detrimental effects associated with high do

228 kinase resistant to the inhibitory effect of DCA, thereby uncoupling the active site from the alloste

229 We evaluated the effects of DCA on Ca2+ signaling in BHK-21 fibroblasts using fura-2

230 lls also abolished the inhibitory effects of DCA on PTPase activity.

231 Effects of DCA were mimicked by the Takeda GPCR 5 agonist, INT-777

232 es for ADP and ATP, mimicking the effects of DCA.

233 ack of effective mechanisms for the entry of DCA into tumor cells may underlie this phenomenon.

234 n, a Pt(II) compound, and two equivalents of DCA.

235 s it was concluded that the glucosylation of DCA may not be as effective in xenobiotic detoxification

236 ne cholesterol content observed after 4 h of DCA treatment of HCT116 cells.

237 computationally efficient implementation of DCA, which allows us to evaluate the accuracy of contact

238 l expression coinciding with the kinetics of DCA-mediated disease resistance.

239 ar differential effects on the metabolism of DCA and TCP were obtained in whole plant studies with wi

240 The potentiation of DCA- and CDCA-induced apoptosis by MEK1/2 inhibitors cor

241 alogous to wild-type PDK2 in the presence of DCA and ADP.

242 Rs can be an effective method for removal of DCA from groundwater, and that the dhlA qPCR is a rapid

243 ctyl-3-methylimidazolium dicyanamide ([Omim][DCA]) inside the porous structure of ceramic membranes.

244 Inhibition of either DCA-induced ERK1/2 or DCA-induced JNK1/2 signaling enhanced the apoptotic resp

245 In vitro studies using Leptin or DCA-treatment suggested causal significance of obesity-i

246 hepatocytes with either CsA or BKA prevented DCA-induced inhibition of PTPase activity.

247 which block lipid raft formation, prevented DCA stimulation of ERK1/2.

248 N-benzyl-3-(3,4 dihydroxyphenyl)propanamide (DCA) and phosphatidylcholine (PC) was explored in a 6-da

249 orescence (DCA-CF) and respiratory quotient (DCA-RQ) on the quality and volatile profile of 'Royal Ga

250 tmosphere monitored by respiratory quotient (DCA-RQ) with three fruit maturity stages at harvest (ear

251 small interfering RNA significantly reduced DCA-induced uPAR and cyclin D1 expression.

252 Regret-DCA showed that for physicians with Pt values of 3-year

253 Regret-based decision curve analysis (Regret-DCA) was performed on a Cox's regression model developed

254 function showed greater FMT signal in right DCA, independent of age effects.

255 biotic and very little metabolism to soluble DCA-glucose or associated polar conjugates.

256 ethyladenine or knockdown of ATG5 suppressed DCA + MEK1/2 inhibitor-induced LC3-GFP vesicularization

257 utralizing antibody significantly suppressed DCA-induced colon cancer cell proliferation and invasive

258 d DCA) and tauro-conjugated (t-CDCA, t-CA, t-DCA) form on human ENaC in its alphabetagamma- and delta

259 ction were less variable (2-fold range) than DCA production (5-fold range), although the uncertainty

260 In conclusion we demonstrate that DCA can be successfully used in the treatment of hemorrh

261 We further demonstrate that DCA can differentiate between subfamilies with different

262 Further analyses demonstrated that DCA-induced JNK2 signaling was cytoprotective whereas DC

263 cell lines under BA treatment revealed that DCA and its conjugated form, TDCA, significantly inhibit

264 nally, fluorescence anisotropy revealed that DCA causes a decrease in membrane fluidity consistent wi

265 In conclusion, these results show that DCA activates JNK and represses CYP7A1 mRNA levels in pr

266 In conclusion, these results show that DCA activates the Raf-1/MEK/ERK signaling cascade in pri

267 We show that DCA is able to shift the pyruvate metabolism in rat glio

268 ing for cholesterol with filipin showed that DCA caused a marked rearrangement of this lipid in the m

269 otif in mediating communications between the DCA-, the nucleotide-, and the lipoyl domain-binding sit

270 he absence of fluid resuscitation; therefore DCA may be a good candidate in prolonged field care foll

271 osure of colorectal cancer and PDAC cells to DCA resulted in colocalization of Src and TACE to the ce

272 d sciatic nerve tissues from rats exposed to DCA.

273 The former phenomenon is related to DCA-induced Foxo3 and p53 expression, resulting in the o

274 ASM)-deficient hepatocytes were resistant to DCA-induced activation of the JNK pathway.

275 in vitro antitumor activity with respect to DCA and increased in vivo stability.

276 singly, the knockouts were less sensitive to DCA.

277 dically reduced conjugating activity towards DCA and TCP and the absence of immunodetectable UGT72B1

278 Here we show that SLC5A8 transports DCA very effectively with high affinity.

279 )CHCl(2))(2)Cl(2)], mitaplatin, in which two DCA units are appended to the axial positions of a six-c

280 Contacts were predicted with two DCA methods (gplmDCA and PSICOV).

281 The storage of 'Galaxy' apple under DCA-RQ 1.3 is efficient in keeping quality regardless of

282 r ULO; and the lowest by fruits stored under DCA-CF (DCA based on chlorophyll fluorescence).

283 h firmness was higher in fruits stored under DCA-CF and ULO differing from CA, in the year 2012, but

284 acetate), as compared to fruit stored under DCA-CF, but fruit stored under DCA-RQ 1.5 and RQ 2.0 als

285 ar quality maintenance to those stored under DCA-CF.

286 stored under DCA-CF, but fruit stored under DCA-RQ 1.5 and RQ 2.0 also showed higher amounts of key

287 When DCA-induced MAPK activation was blocked using MEK1/2 inh

288 SEP mRNA by 750-fold in HepG2 cells, whereas DCA, CA, and UDCA induced BSEP mRNA by 250-, 75-, and 15

289 ed JNK2 signaling was cytoprotective whereas DCA-induced JNK1 signaling was cytotoxic.

290 Whether DCA modulates beta-catenin and promotes colon cancer cel

291 ion, and metastasis, we investigated whether DCA activates beta-catenin signaling and promotes colon

292 Data are consistent with a model in which DCA directly induces both Ca2+ release from internal sto

293 Cotreatment of melanomas with DCA and elesclomol in vivo achieved a more durable respo

294 ear DNA with cisplatin and mitochondria with DCA selectively in cancer cells.

295 Simvastatin with DCA maintained body mass gain and food intake, abrogated

296 to hemorrhagic injury (HI) when treated with DCA.

297 Treatment with DCA resulted in movement of FAS-R to the cell surface, w

298 Treatment with DCA resulted in normalization of several metabolic and m

299 mitochondria following HI and treatment with DCA.

300 um with the active open conformation without DCA and ADP.