ライフサイエンスコーパス: ADH

1 ADH (alcohol dehydrogenase) gene expression, enzyme acti

2 ADH and its cofactor nicotinamide adenine dinucleotide (

3 ADH is caused by mutations in the low-density lipoprotei

4 ADH peptides induced the production of interferon-gamma

5 ADH-1 enhancement of response to melphalan was associate

6 ADH-1 improved responses to regional LPAM but had variab

7 ADH-1 in combination with LPAM ILI improved antitumor re

8 ADH-1 increased vascular permeability without effecting

9 ADH-1 is a cyclic pentapeptide that disrupts N-cadherin

10 ADH-41 targets Abeta in a sequence and structure-specifi

11 ADH-41 was also effective at inhibiting the seed-catalyz

12 ADH-specific peripheral T-cell responses were assessed b

13 ADH-specific T-cell responses have not been characterize

14 tion and results in disinhibition of Class 1 ADH transcription.

15 tabolizing enzymes alcohol dehydrogenase 1B (ADH-1B; rs1229984) and alcohol dehydrogenase 1c (ADH-1C;

16 1B; rs1229984) and alcohol dehydrogenase 1c (ADH-1C; rs698).

17 odococcus ruber (ADH-A), whereas evo-1.1.200 ADH led to their counterpart (R)-enantiomers also with c

18 gical excision was performed in 66 of the 72 ADH cases and in 117 of 118 DCIS cases.

19 Similar to PBMCs in abstinents, ADH peptides induced weak T-cell proliferation and a sim

20 no-3,7-dideoxy-d-threo-hept-6-ulosonic acid (ADH) synthase, the product of the Mj0400 gene, catalyzes

21 arison of the enzyme with related aldolases, ADH synthase is classified as a new member of the class

22 ehydrogenase (either metagenomic ADH-150, an ADH from Sphingobium yanoikuyae (SyADH), or a variant of

23 Ten years after an ADH diagnosis, an estimated 5.7% (95% CI, 4.3%-10.1%) of

24 eved claudin-14 gene silencing and caused an ADH-like phenotype.

25 vating mutation in this region, V836L, in an ADH patient, we studied the remaining residues in this r

26 the absolute protein expression level of an ADH isoenzyme, ADH1C1, in human liver.

27 We propose that an ADH-independent mechanism is responsible for the downreg

28 obility shift assays were conducted using an ADH-specific SRE site.

29 rate specificity compared with the ancestral ADH.

30 This imbalance between gene expression and ADH activity at 10 degrees C, as well as the unexpected

31 ng that ChREBP regulates EtOH metabolism and ADH activity through its direct control of sirtuin 1 exp

32 administration of the N-cadherin antagonist, ADH-1, or saline.

33 irected to alcohol dehydrogenase (ADH), anti-ADH titers being associated with disease severity and ac

34 We aimed to define anti-ADH cellular immune responses and their association with

35 Proliferative anti-ADH immune responses in alcoholic hepatitis focused on i

36 ial hypercholesterolemia 4 (FH4), defined as ADH in absence of mutations in these genes and thereafte

37 ment of highly homologous isoenzymes such as ADHs where multiple signature peptides can be examined b

38 ressed genes between DCIS-HN and 447 between ADH-HN, with >90% of the ADH-HN genes also present among

39 Only 61 genes were identified between ADH-DCIS.

40 1 (E-47 cells) were exposed to ethanol, both ADH- and CYP2E1-generated products reduced STAT1 phospho

41 and bienzymatic (anchoring sequentially both ADH and aldehyde dehydrogenase) systems were tested.

42 Employing Lactobacillus brevis ADH, it was possible to achieve the synthesis of enantio

43 ction of alpha-helicity in Abeta mediated by ADH-41.

44 Inhibition of Candida ADH enzyme using disulfiram and 4-methylpyrazole resulte

45 ce that: (a) class I ADH is the medium-chain ADH that is expressed in human breast parenchyma, specif

46 IV alcohol dehydrogenase (ADH), medium chain ADHs that can catalyze oxidation of ethanol, are express

47 For the first time among characterized ADHs, the high-resolution structures of all reaction ste

48 1 to catalysis was studied by characterizing ADH with His-51 substituted with Gln (H51Q).

49 d to assess for calcifications and confirmed ADH in 101 cases with subsequent surgical excision.

50 uct or terminal duct-lobular unit containing ADH was considered a focus and counted.

51 used the mouse hepatocyte cell line (CYP2E1/ADH-transfected HepB5 cells) or primary mouse hepatocyte

52 because inhibition of alcohol dehydrogenase (ADH) activity blunted ChREBP EtOH-induced acetylation in

53 ionships between some alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) genes and alcohol

54 e catabolism in which alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH) play central role

55 cells), which express alcohol dehydrogenase (ADH) and CYP2E1.

56 betaL crystallin and alcohol dehydrogenase (ADH) and significantly less effective than wt alphaB cry

57 e dismutase (SOD) and alcohol dehydrogenase (ADH) as protein models] showed the integrity of the Zn-b

58 (OECT) modified with alcohol dehydrogenase (ADH) as the sensor.

59 tigated bioanode with alcohol dehydrogenase (ADH) catalysing oxidation of glycerol and glyceraldehyde

60 enetically dissecting alcohol dehydrogenase (ADH) enzyme activity.

61 ns in hepatic Class 1 alcohol dehydrogenase (ADH) expression in ethanol-fed rats correspondent with r

62 solutely quantify the alcohol dehydrogenase (ADH) expression level in a human liver sample.

63 The alcohol dehydrogenase (ADH) family of enzymes catalyzes the reversible oxidatio

64 trameric Zn-dependent alcohol dehydrogenase (ADH) from Cupriavidus necator JMP134.

65 ombinant medium chain alcohol dehydrogenase (ADH) from the hyperthermophilic archaeon Aeropyrum perni

66 aimed to test whether alcohol dehydrogenase (ADH) gene variants were associated with alcohol use befo

67 in the region of the alcohol dehydrogenase (ADH) genes, affected risk for alcoholism.

68 ions of AD with seven alcohol dehydrogenase (ADH) genes.

69 l (PBMC) responses to alcohol dehydrogenase (ADH) in patients with alcohol-related cirrhosis, associa

70 s to demonstrate that alcohol dehydrogenase (ADH) is downregulated in Candida biofilms.

71 ine-51 in horse liver alcohol dehydrogenase (ADH) is part of a hydrogen-bonded system that appears to

72 yde produced from the alcohol dehydrogenase (ADH) reaction was shown to improve the linearity of NAD(

73 ll extant short-chain alcohol dehydrogenase (ADH) through retroposition, provides an opportunity to e

74 the immobilization of alcohol dehydrogenase (ADH) via Nafion entrapment, with excellent analytical ch

75 mammals catalyzed by alcohol dehydrogenase (ADH), aldehyde dehydrogenase (ALDH), flavin-containing m

76 zyme, hepatic Class I alcohol dehydrogenase (ADH), and this mechanism involves regulated CCAAT/enhanc

77 ntibodies directed to alcohol dehydrogenase (ADH), anti-ADH titers being associated with disease seve

78 nzyme family) with an alcohol dehydrogenase (ADH), applying the in situ substrate feeding product rem

79 a potent inhibitor of alcohol dehydrogenase (ADH), decreased the conversion of [3H]20-HETE to 20-COOH

80 the coenzyme bound to alcohol dehydrogenase (ADH), may facilitate hydride transfer and hydrogen tunne

81 her class I and/or IV alcohol dehydrogenase (ADH), medium chain ADHs that can catalyze oxidation of e

82 the CYP71 clan and an alcohol dehydrogenase (ADH).

83 arboxylases (KDC) and alcohol dehydrogenase (ADH).

84 relation of maternal alcohol dehydrogenase (ADH)1B genotype (rs1229984) with these outcomes (the A a

85 zing a single enzyme, alcohol dehydrogenase (ADH)] and bienzymatic (anchoring sequentially both ADH a

86 ependent alcohol and aldehyde dehydrogenase (ADH and AldDH) enzymes for biofuel cell applications.

87 ude any genes of the arginine dehydrogenase (ADH) pathway.

88 latinum) and enzymes (alcohol dehydrogenase, ADH; lactate dehydrogenase, LDH; xanthine oxidase, XOx;

89 haeal homotetrameric alcohol dehydrogenases (ADHs) and also to the mammalian dimeric ADHs.

90 y of metal-dependent alcohol dehydrogenases (ADHs).

91 s encoding zebrafish alcohol dehydrogenases (ADHs).

92 s obtained here, DET using the PQQ-dependent ADH and AldDH still lacks high current density, while th

93 entiate between the methods used to diagnose ADH, which may be related to the size of the ADH focus.

94 e the risk in women with presently diagnosed ADH.

95 methods, involving adipic acid dihydrazide (ADH) as a linker, were used.

96 roups of the CWP to adipic acid dihydrazide (ADH)-derivatized protein, and (ii) binding of the carbod

97 ses (ADHs) and also to the mammalian dimeric ADHs.

98 When cells expressing either ADH (VA-13 cells) or CYP2E1 (E-47 cells) were exposed to

99 (21%), the diagnosis was upgraded to either ADH or DCIS (exact two-sided 95% CI = 11.4%, 36.4%).

100 new architecture can up-regulate endogenous ADH activity by > 20-fold in transgenic Arabidopsis.

101 on the coupled alcohol dehydrogenase enzyme(ADH).

102 First, ADH was bound to GAMP activated with cyanogen bromide (C

103 CI: 1.2, 10) more likely in mass (n = 20 for ADH and n = 20 for DCIS) than in non-mass (n = 46 for AD

104 = 20 for DCIS) than in non-mass (n = 46 for ADH and n = 97 for DCIS), compared with nonunderestimati

105 ears, met modified Simon-Broome criteria for ADH and were screened for mutations in the exons and con

106 demonstrated these sites to be essential for ADH transcription.

107 Ten variants in four ADH genes were genotyped in women from South-West Englan

108 The Lactobacillus gasseri ADH beta-glucuronidase gene, gusA, was cloned previously

109 mans have seven alcohol dehydrogenase genes (ADH) falling into five classes.

110 On the other hand, ADH-A mediated bioreduction of 4,9-dihydro-1H-carbazol-3

111 oncentration, the antiparallel double helix (ADH) conformation was observed to be most abundant for G

112 patient-matched histologically normal (HN), ADH, and DCIS from 12 patients with estrogen receptor po

113 of a thermophilic alcohol dehydrogenase (ht-ADH): Y25A (at the dimer interface) and V260A (at the co

114 tant thermophilic alcohol dehydrogenases (ht-ADH), presenting evidence for Arrhenius prefactor values

115 Arrhenius curves previously reported for ht-ADH are proposed to arise, at least in part, from a chan

116 dynamical transition at 30 degrees C for ht-ADH, the temperature dependence of the KIE is seen to in

117 The reciprocal mutation in ht-ADH, ht-Y25A, results in kinetic behavior similar to tha

118 esidues in the cofactor-binding pocket of ht-ADH (Leu176 and V260) have been mutated to a series of h

119 a thermolabile psychrophilic homologue of ht-ADH, ps-A25Y, leads to a more thermostable enzyme and a

120 ogenase from Bacillus stearothermophilus (ht-ADH) has been mutated at an aromatic side chain in the a

121 ation of normal Arrhenius behavior in the ht-ADH reaction occurs at elevated temperatures.

122 ced temperature alters the ability of the ht-ADH variants to sample the catalytically relevant region

123 lapping peptides representing the full human ADH protein (beta 1 subunit).

124 25 overlapping peptides, spanning the human ADH beta1 subunit, were constructed.

125 Autosomal-dominant hypercholesterolemia (ADH) is characterized by elevated low-density lipoprotei

126 ND- Autosomal dominant hypercholesterolemia (ADH), characterized by elevated plasma levels of low-den

127 a diagnosis of atypical ductal hyperplasia (ADH) (75 of 6,081 [1.2%]) were reviewed; these patients

128 erestimation of atypical ductal hyperplasia (ADH) and ductal carcinoma in situ (DCIS) at magnetic res

129 djacent foci of atypical ductal hyperplasia (ADH) in eight, and well-differentiated papillary ductal

130 Atypical ductal hyperplasia (ADH) is a known risk factor for breast cancer.

131 ), one focus of atypical ductal hyperplasia (ADH), and one atypical lobular hyperplasia.

132 plasia (SH) and atypical ductal hyperplasia (ADH), are candidate precursors to ductal carcinoma in si

133 tients with autosomal dominant hypocalcemia (ADH) repressed the transcription of miR-9 and miR-374 ge

134 bjects with autosomal dominant hypocalcemia (ADH), five appear at the junction of TM helices 6 and 7

135 The antigenic distance hypothesis (ADH) predicts that negative interference from prior seas

136 The one property of class I ADH fitting this designation is its potential to catalyz

137 Products of the three class I ADH genes that share 95% sequence identity are believed

138 virtual abrogation of expression of class I ADH in invasive breast cancer suggests that the enzyme h

139 Expression of class I ADH in normal human breast parenchyma was confirmed by p

140 f ethanol; and (c) the expression of class I ADH is dramatically reduced or abrogated in invasive bre

141 findings provide evidence that: (a) class I ADH is the medium-chain ADH that is expressed in human b

142 Ethanol induces rat Class I ADH mRNA and activity by an as yet unknown mechanism.

143 a classical competitive inhibitor of class I ADH, failed to inhibit ADH8A.

144 ction of optimal codons led to a decrease in ADH activity.

145 eated hepatocytes, a significant decrease in ADH protein content and/or acetylation was observed.

146 (Adh) gene led to a significant decrease in ADH protein expression.

147 We observed a significant decrease in ADH protein production with number of unpreferred codons

148 ated genes and pathways were dysregulated in ADH and maintained in DCIS.

149 optimal leucine codons led to an increase in ADH activity in third-instar larvae.

150 DCIS), compared with nonunderestimation, in ADH and DCIS respectively.

151 Conclusion The rates of underestimation in ADH and DCIS diagnosed at MR imaging-guided vacuum-assis

152 the molecular mechanism for ethanol-induced ADH expression during the UEC pulse in adult male rats f

153 Insulin inhibited ADH gene expression, and this was abolished by LY294002

154 e specimens were examined for class I and IV ADH mRNA by reverse transcription-PCR, for protein by im

155 her these results indicate that class I-like ADH is conserved in zebrafish, albeit with mixed functio

156 phy of doubly substituted His51Gln:Lys228Arg ADH complexed with NAD(+) and 2,3- or 2,4-difluorobenzyl

157 le alcohol dehydrogenase (either metagenomic ADH-150, an ADH from Sphingobium yanoikuyae (SyADH), or

158 times higher than the risk in women with no ADH.

159 We mapped a novel ADH locus at 4p13 and identified 4 variants in STAP1 tha

160 the other pathway leads to the activation of ADH and ACS9.

161 paucity of data about the molecular basis of ADH among ethnic groups other than those of European or

162 Here, we examined the molecular basis of ADH in a multiethnic patient cohort from lipid clinics i

163 binding of most of the substrate classes of ADH, ALDH, and CYP.

164 Combination of ADH-1 with TMZ ILI did not improve tumor response in A37

165 hen catalyzes deamination and cyclization of ADH, resulting in DHQ, which is fed into the canonical p

166 at NPS 2143 corrects the molecular defect of ADH mutations for treatment of this disease are also dis

167 included 955331 women with 1727 diagnoses of ADH, 1058 (61.3%) of which were diagnosed by core biopsy

168 ALH at CNB and in those with a diagnosis of ADH at CNB was performed (Pearson chi(2) test).

169 invasive breast cancer after a diagnosis of ADH may be lower than those previously reported.

170 Diagnosis of ADH on core needle biopsy or excisional biopsy in women

171 ted with underestimation when a diagnosis of ADH was made at MR imaging-guided biopsy.

172 A diagnosis of ADH was obtained after biopsy in 72 cases, and a diagnos

173 Ten years following a diagnosis of ADH, the cumulative risk of invasive breast cancer was 2

174 mammography with and without a diagnosis of ADH.

175 Cell-based assays to assess the effect of ADH-41 on Abeta are underway and will be presented in du

176 ranscription) reduced in vitro expression of ADH mRNA by 2-fold.

177 tly higher in cases of three or more foci of ADH (15 [28%] of 53 cases) than in cases of fewer than t

178 2] or amorphous [n = 2]), and seven foci of ADH manifested as amorphous calcifications.

179 the direct electron exchange between heme of ADH and modified AuNPs.

180 ing proteins to mediate ethanol induction of ADH in vivo.

181 the phenotypes of cell and animal models of ADH.

182 From 1996 to 2012, the proportion of ADH diagnosed by core needle biopsy increased from 21% t

183 to ethanol vapor, the enzymatic reaction of ADH and ethanol transforms NAD(+) into NADH, which cause

184 The reversible oxidation and reduction of ADH heme proceeded at around -0.05V vs. SCE.

185 Three crystal structures of ADH synthase were determined in this work: a complex wit

186 pattern of regulation is similar to that of ADH that encodes alcohol dehydrogenase, which we have re

187 No other parameters were associated with of ADH or DCIS upgrade at surgery.

188 tudied the effects of insulin and ethanol on ADH gene expression in a highly differentiated rat hepat

189 ional biopsy is supported when LCIS, ALH, or ADH is diagnosed at CNB.

190 en it was placed under anoxia; the two other ADH homologs encoded on the Chlamydomonas genome do not

191 We hypothesized that the novel pentapeptide (ADH-1), which disrupts N-cadherin adhesion, could sensit

192 e enhanced thermal stability of the A.pernix ADH is thought to arise primarily from increased ionic a

193 The 1.62 A resolution A.pernix ADH structure is that of the holo form, with the cofacto

194 Unlike BvADHbeta and other plant ADHs that are strongly inhibited by Tyr, BvADHalpha exhi

195 tion of OYE2 with a Prelog or an anti-Prelog ADH allowed the preparation of the secondary alcohols wi

196 EtOH metabolism as a consequence of reduced ADH activity.

197 lcohol dehydrogenase from Rhodococcus ruber (ADH-A), whereas evo-1.1.200 ADH led to their counterpart

198 Second, ADH was bound to BSA with EDC to form AHBSA.

199 Seven ADH genes exist in a segment of ~370 kb on 4q21.

200 eotide polymorphisms (SNPs) across the seven ADH genes and analyzed their association with alcoholism

201 We also found that several ADH genes and the ALDH2 gene were susceptibility loci fo

202 ] showed the integrity of the Zn-binding SOD/ADH under the OFFGEL electrophoretic conditions.

203 xpression system for Sulfolobus solfataricus ADH-10 (Alcohol Dehydrogenase isozyme 10) and its use in

204 he overall fold similar to previously solved ADH structures.

205 ium; (b) human breast parenchyma can support ADH-mediated oxidation of ethanol; and (c) the expressio

206 -to-matrix adhesion molecules in human SW480-ADH colon carcinoma cells.

207 Systemic ADH-1 was associated with increased growth and activatio

208 In a preclinical animal model, systemic ADH-1 given with regional melphalan demonstrated synergi

209 ssels convert 20-HETE to 20-COOH-AA and that ADH catalyzes the reaction.

210 We conclude that ADH and DCIS share highly similar gene expression and ar

211 These data provide genetic evidence that ADH (but not SH) are often precursors to cancer and sugg

212 and atomic force microscopy (AFM) show that ADH-41 wholly suppresses the aggregation of Abeta at a s

213 Overall, we speculate that ADH-41 directs Abeta into off-pathway structures, and th

214 two peaks in the ADH region suggesting that ADH populations are composed of two distinct conformers.

215 The ADH and DCIS underestimation rates were 25.8% (17 of 66)

216 The ADH monomer is formed from a catalytic and a cofactor-bi

217 The ADH-ALDH pathway also governs the metabolism of retinol

218 e-nucleotide polymorphisms (SNPs) across the ADH clusters in a global sampling of 42 populations.

219 Because the ADH promoter contains two canonical sterol response elem

220 Chaperoning abilities, as determined by the ADH assay and the betaL-crystallin heat denaturation ass

221 At 30 degrees C, the ADH activity (ethanol to acetaldehyde direction), increa

222 At 10 degrees C, the ADH activity increased at 20%wl and continued to rise ev

223 The limit of detection for the ADH, LDH, XOx, and GOx was equal to 0.18, 0.14, 0.0031,

224 has the highest F(st) of the 54 SNPs in the ADH cluster, and it is significantly above the mean F(st

225 -95 and other discontinuous sequences in the ADH peptide, whereas only one sequence was targeted in a

226 spectrometry data revealed two peaks in the ADH region suggesting that ADH populations are composed

227 Although the sequence identity of the ADH family members is relatively low (34-37%), in vitro

228 ADH, which may be related to the size of the ADH focus.

229 bium yanoikuyae (SyADH), or a variant of the ADH from Thermoanaerobacter ethanolicus (TeSADH W110A))

230 that SREBP-1 is a negative regulator of the ADH gene and may work in concert with the CCAAT/enhancer

231 s within the proximal promoter region of the ADH gene were studied by electrophoretic mobility shift

232 lin-induced transcriptional repressor of the ADH gene.

233 genes, including the two known genes of the ADH pathway, kauB and gbuA, were found to be inducible b

234 encode enzymes for the initial steps of the ADH pathway, the potential physiological functions of th

235 tOH attenuates the antiviral function of the ADH-ALDH pathway, which suggests the possibility that Et

236 -HN and 447 between ADH-HN, with >90% of the ADH-HN genes also present among the DCIS-HN genes.

237 Functional analysis of the ADH-SREs demonstrated these sites to be essential for AD

238 mic amperometric detection of ethanol on the ADH-Nafion/NiOxNPs/GC modified electrode gives linear re

239 In this study, we defined that the ADH-ALDH pathway serves as a potent antiviral host facto

240 nd identified novel risk loci mapping to the ADH gene cluster on chromosome 4 and extending centromer

241 g protein-beta expression and binding to the ADH promoter.

242 pecificity of nuclear protein binding to the ADH-SRE site was confirmed using antibody and UV cross-l

243 In hypophysectomized rats, in which the ADH protein increased by approximately 6-fold, the nucle

244 s C already at 10%wl in a synchrony with the ADH activity, indicating a rapid response likely due to

245 y during dehydration in combination with the ADH activity.

246 fluenza vaccination were consistent with the ADH and may have contributed to findings of low VE acros

247 significantly by season, consistent with the ADH.

248 three genes are tandemly arrayed within the ADH cluster on chromosome 4 and have very high nucleotid

249 cination effects were interpreted within the ADH framework.

250 nt study, we genotyped 16 markers within the ADH gene cluster (including the ADH1A, ADH1B, ADH1C, ADH

251 We genotyped 16 markers within the ADH gene cluster and 38 unlinked ancestry-informative ma

252 Further, sequence analysis shows that these ADHs form a monophyletic group along with additional fam

253 7 cases in which there were fewer than three ADH foci and all calcifications were removed.

254 alcoholic hepatitis recognised one to three ADH peptides (SI </=5.7).

255 The in vivo binding status of SREBP-1 to ADH-SRE sites, as measured by the chromatin immunoprecip

256 ggest that additional loci may contribute to ADH, especially in understudied populations such as blac

257 vated terminal phosphate group of the CWP to ADH-derivatized protein.

258 Proliferation to ADH peptides (1 x 10(5) cells per well, cultured with 10

259 This suggests that Th 1 responses to ADH in ARC are induced by alcohol consumption.

260 ucture is in an open conformation similar to ADH structures without the bound cofactor.

261 bstantial number of lesions were upgraded to ADH and DCIS at excision.

262 A tripyridylamide, ADH-41, was identified as one of the most potent antagon

263 In turn, ADH acetylation was reduced, suggesting that ChREBP regu

264 e dehydrogenases (TyrAa /ADH) encoded by two ADH genes (BvADHalpha and BvADHbeta).

265 Wild-type ADH binds 2,3,4,5,6-pentafluorobenzyl alcohol in one pos

266 of the V292T ADH-NAD+-pyrazole and wild-type ADH-NAD+-4-iodopyrazole ternary complexes are very simil

267 a plastidic arogenate dehydrogenases (TyrAa /ADH) encoded by two ADH genes (BvADHalpha and BvADHbeta)

268 N(tz)AD(+) and N(tz)ADH serve as substrates for NADase, which selectively cl

269 tored in real time, show N(tz)AD(+) and N(tz)ADH to be substrates for yeast alcohol dehydrogenase and

270 e is seen as N(tz)AD(+) is converted to N(tz)ADH, reflecting a complementary photophysical behavior t

271 remaining 60 patients (65%) had unexplained ADH.

272 tes (57%) or Hispanics (53%) had unexplained ADH.

273 s with LDLR variants, those with unexplained ADH had lower levels of LDL-cholesterol (292 +/- 47 mg/d

274 These unique ADHs have exquisite substrate specificity, unusual metal

275 Chaperone activity was determined by using ADH, insulin, and betaL-crystallin as the target protein

276 cestor with mammalian class I, II, IV, and V ADHs.

277 3-fold (for V292T ADH) to 16-fold (for V203A ADH).

278 enzyl alcohol oxidation by 3-fold (for V292T ADH) to 16-fold (for V203A ADH).

279 The structures of the V292T ADH-NAD+-pyrazole and wild-type ADH-NAD+-4-iodopyrazole

280 37, blocked activation of the CaR by various ADH mutations.

281 We then compared the in vivo ADH activities imparted by the wild-type and mutant alle

282 Surgical excision is recommended even when ADH involves fewer than three foci and all mammographic

283 most effective bioanode was fabricated when ADH was immobilized on gold nanoparticles (AuNPs) modifi

284 he upgrade rate is significantly higher when ADH involves at least three foci.

285 We aimed to define whether ADH-specific cellular immunity is present in alcoholic h

286 e based on cohorts that included women whose ADH was diagnosed before widespread use of screening mam

287 d with ADH is slightly lower for women whose ADH was diagnosed by needle core biopsy compared with ex

288 fied 4 variants in STAP1 that associate with ADH.

289 the risk of invasive cancer associated with ADH diagnosed using core needle biopsy vs excisional bio

290 The risk associated with ADH is slightly lower for women whose ADH was diagnosed

291 port here that melphalan in combination with ADH-1 significantly reduced tumor growth up to 30-fold o

292 %) of 75 (95% CI: 7.7%, 24.3%) patients with ADH, lesions were upgraded.

293 similar to the upgrade rate in patients with ADH.

294 When the bioreductions were performed with ADH-A from Rhodococcus ruber overexpressed in E. coli, n

295 95% CI, 3.0%-12.8%) compared with those with ADH diagnosed via core needle biopsy (5%; 95% CI, 2.2%-8

296 ents with LCIS or ALH and that in those with ADH was not significant (P =.88).

297 Women with ADH diagnosed on excisional biopsy had a slightly higher

298 sphate and l-aspartate semialdehyde to yield ADH.

299 The genes encoding these zebrafish ADHs have been named Adh8a and Adh8b by the nomenclature

300 Phylogenetic analysis of these zebrafish ADHs indicates that they share a common ancestor with ma