ライフサイエンスコーパス: threo

1 N-oleoylethanolamine or D-L-threo 1-phenyl-2-decanoylamino-3-morpholino-1-propanol (

2 -8(9)-epoxy-12(Z)-octadecenoic acid (erythro/threo, 1-4:1) and/or shifted ferryl oxygen insertion fro

3 Those containing both threo-1,2- and 1,3-syn diol motifs showed high affinity

4 [threo-1,2-Diamino-1-(4-fluorophenyl)propan]dichloridopla

5 , and xylitol revealed that diols containing threo-1,2-diol units have higher affinity for BBVs relat

6 Treatment of these cells with D-threo-1-(3',4'-ethylenedioxy)phenyl-2-palmitoylamino-3-p

7 UGCG inhibition with the ceramide analog d-threo-1-(3,4,-ethylenedioxy)phenyl-2-palmitoylamino-3-py

8 of 2 are (4-methoxyphenyl)acetone (73%) and threo-1-(4-methoxyphenyl)-1,2-propanediol (ca. 3%).

9 A series of threo-1-aza-3 or 4-substituted-5-phenyl[4.4.0]decanes (q

10 6 mice treated twice daily for 3 days with D-threo-1-ethylendioxyphenyl-2-palmitoylamino-3-pyrrolidi

11 iates included (-)-threo-isohomocitrate [(-)-threo-1-hydroxy-1,2, 4-butanetricarboxylic acid], (-)-th

12 cid], and (-)-threo-iso(homo)(3)citrate [(-)-threo-1-hydroxy-1,2, 6-hexanetricarboxylic acid].

13 ic acid], (-)-threo-iso(homo)(2)citrate [(-)-threo-1-hydroxy-1,2,5-pentanetricarboxylic acid], and (-

14 reversible CerGlc transferase inhibitor, DL-threo-1-phenyl-2-(palmitoylamino)-3-morpholino-1-propano

15 Treatment of NB cells with 10 microM DL-threo-1-phenyl-2-decanolylamine-3-morpholino-1-propanol

16 Surprisingly, a third inhibitor, d,l-threo-1-phenyl-2-decanoylamino-3-morpholino- 1-propanol

17 c cells with the GCS-specific inhibitor, D,L-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (

18 AN-5 cells exposed for 6 days to 10 microM D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (

19 this end, we studied a ceramide analogue, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (

20 inhibitor of glycosphingolipid synthesis, D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (

21 Mice fed D- threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (

22 istration of the synthetic ceramide analog L-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (

23 and glucosylceramide synthase inhibitors (dl-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol a

24 glucosylceramide synthase inhibitors PDMP (d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol),

25 h the glucosylceramide synthase inhibitor, d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol,

26 ivities were inhibited 50-60% by 20 microM D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol,

27 is, including N-butyldeoxyno jirimycin and d-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol-H

28 D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol.H

29 d-Threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol.H

30 synthase by a new specific inhibitor of d-l-threo-1-phenyl-2-hexadecanoylamino-3 -pyrrolidino-1-prop

31 On the other hand, D-threo-1-phenyl-2-palmitoylamino-3-morpholino-1-propanol

32 motility cells by depletion of GM3 by P4 (D-threo-1-phenyl-2-palmitoylamino-3-pyrrolidino-1-propanol

33 e they were enhanced by GM3 depletion with d-threo-1-phenyl-2-palmitoylamino-3-pyrrolidino-1-propanol

34 on of GM2 in HCV29 cells by treatment with D-threo-1-phenyl-2-palmitoylamino-3-pyrrolidino-1-propanol

35 er potency and efficacy of erythro, ( )-9 vs threo, ( )-10 constitutes the first demonstration of dia

36 unit was needed to arrive at diastereomeric threo-11-aminomefloquine and to introduce diversity.

37 orophenyl)propan]dichloridoplatinum(II) and [threo-2,3-diamino-3-(4-fluorophenyl)propan-1-ol]dichlori

38 ng Btn1p, btn1-delta, are resistant to D-(-)-threo-2-amino-1-[p-nitrophenyl]-1,3-propanediol (ANP) in

39 sulted in a pH-dependent resistance to D-(-)-threo-2-amino-1-[p-nitrophenyl]-1,3-propanediol (ANP).

40 on yeast strains are more resistant to D-(-)-threo-2-amino-1-[p-nitrophenyl]-1,3-propanediol (denoted

41 (D)-glucarate and (L)-idarate to 3-deoxy-(L)-threo-2-hexulosarate as well as their epimerization.

42 wo gemini analogues indicated that the 17,20 threo (20S) compound, UG-480, is the most active one and

43 The l-threo (2S, 3S) beta-OHAsp residues of alterobactin arise

44 D-threo-3', 4'-Ethylenedioxy-P4-inhibited glucosylceramide

45 ression were reversed by pretreatment with L-threo-3, 4-dihydroxyphenylserine, which partially restor

46 administration of the synthetic amino acid L-threo-3,4-dihydroxyphenylserine (L-DOPS), which is decar

47 Restoration of NE by using L-threo-3,4-dihydroxyphenylserine reinstated the behaviora

48 Threo-3-hydroxy-aspartate (THA), an inhibitor of glutama

49 D,L-Threo-3-hydroxyaspartate (THA), a glutamate-transport bl

50 ated by the glutamate uptake inhibitor L-(-)-threo-3-hydroxyaspartic acid.

51 DP-dependent oxidative decarboxylation of DL-threo-3-isopropylmalic acid, threo-isocitrate, erythro-i

52 various concentrations of L-glutamate and L-threo-3-methylaspartate and with use of stopped-flow spe

53 ar no molecules other than L-glutamate and L-threo-3-methylaspartate have been found to be substrates

54 ersible interconversion of L-glutamate and L-threo-3-methylaspartate via a radical-based mechanism.

55 with deuterated L-glutamate and deuterated L-threo-3-methylaspartate, respectively.

56 reversible isomerization of L-glutamate to L-threo-3-methylaspartate.

57 erization, that of L-2-hydroxyglutarate to L-threo-3-methylmalate, involving the migration of the car

58 oselective oxidation of racemic erythro- and threo-3-methyloctane-1,4-diols (1a and 1b).

59 The hydroxylation gives the anticipated L- threo-3-OH-Asp diastereomer found in syringomycin.

60 This compound, D-threo-4'-hydroxy-P4, inhibited glucosylceramide synthase

61 The enzyme product is 2-keto-d-threo-4,5-dihydroxyadipate, the enantiomer of the produc

62 el [6 + 4] "concerted" ene transition state (threo-4TS, DeltaH(double dagger)(UB3LYP(0K)) = 28.3 kcal

63 the monophosphate of dihydroxy stearic acid (threo-910-phosphonoxy-hydroxy-octadecanoic acid) with K(

64 allosteric modulator was discovered to be l-threo-alpha-d-galacto-octopyranoside, methyl-7-chloro-6,

65 Unlike the D-erythro-LacCer analog, the L-threo analog did not cluster in membrane microdomains wh

66 methyl)-(2S,3S)-1,4-benzodiox in-6-propanol, threo and erythro 3-methoxy-8,4'-oxyneolignan-3',4,7,9,9

67 Cupriachelin contains both l-threo and l-erythro beta-OHAsp, consistent with the pres

68 .11, 0.21, and 0.26 mol % for the L-threo, D-threo, and L-erythro isomers, respectively; (2) all ster

69 nd HPLC comigration identified the HEETAs as threo- and erythro-diastereomers of 13-H-trans-14,15-EET

70 The Cope elimination reactions for threo- and erythro-N,N-dimethyl-3-phenyl-2-butylamine ox

71 diastereoisomers of D-erythroC18-ceramide, D-threo-, and L-threo-C18-ceramide, as well as the enantio

72 vailable 1,2:3,5-di-O-isopropylidene-alpha-D-threo-apiofuranose (7) by a very effective spirolactoniz

73 urce of energy for the human body, whereas l-threo-ascorbic acid (vitamin C) is an essential nutrient

74 of all glutamate transporters with TBOA (DL-threo-b-benzyloxyaspartic acid) increased mGluR1 EPSCs >

75 blockers, dihydrokainic acid (500 muM) or DL-threo-beta-benzyloxyaspartate (250 muM), or saline.

76 release of glutamate and aspartate using DL-threo-beta-benzyloxyaspartate (DL-TBOA), a newly develop

77 s and that in the absence of glutamate or dl-threo-beta-benzyloxyaspartate (dl-TBOA), A395C in the hi

78 We recently synthesized novel analogs of threo-beta-benzyloxyaspartate (TBOA) and reported that t

79 portable glutamate transporter antagonist sc-threo-beta-benzyloxyaspartate (TBOA) but was insensitive

80 non-selective glutamate reuptake antagonist, threo-beta-benzyloxyaspartate (TBOA), was bilaterally mi

81 of Na(+)-dependent glutamate uptake with dl-threo-beta-benzyloxyaspartate (TBOA).

82 ed by DL-threo-beta-hydroxyaspartic acid, DL-threo-beta-benzyloxyaspartate or dihydrokainate, glutama

83 sites for aspartate, two sodium ions and d,l-threo-beta-benzyloxyaspartate, an inhibitor.

84 nd blocked by the transporter antagonist D,L-threo-beta-benzyloxyaspartate.

85 excitatory amino acid transporter blocker DL-threo-beta-benzyloxyaspartic acid (TBOA) and significant

86 inhibition of glutamate transporters with DL-threo-beta-benzyloxyaspartic acid (TBOA) increased the f

87 in individual astrocytes, using internal DL-threo-beta-benzyloxyaspartic acid (TBOA) or dissipating

88 d by the glutamate transporter antagonist DL-threo-beta-benzyloxyaspartic acid (TBOA), indicating tha

89 nia, the glutamate transporter inhibitor, DL-threo-beta-benzyloxyaspartic acid (TBOA), or the combina

90 excitatory amino acid reuptake inhibitor d,l-threo-beta-benzyloxyaspartic acid (TBOA), significantly

91 glutamate by the glutamate reuptake blocker threo-beta-benzyloxyaspartic acid (TBOA).

92 eceptor agonist; (2) application of TBOA (dl-threo-beta-benzyloxyaspartic acid), a selective inhibito

93 by the glutamate transport blocker TBOA (dl-threo-beta-benzyloxyaspartic acid), suggesting that mGlu

94 y the high-affinity EAAT antagonist TBOA (dl-threo-beta-benzyloxyaspartic acid), whereas the remainin

95 inhibition of astrocytic Glu uptake with dl-threo-beta-benzyloxyaspartic acid, but not by the ionotr

96 stration of a glutamate reuptake blocker, DL-threo-beta-benzyloxyaspartic acid, revealed increased ex

97 icked by the glutamate reuptake inhibitor dl-threo-beta-benzyloxyaspartic acid.

98 expedient synthesis of enantiomerically pure threo-beta-hydroxy-alpha-amino acid derivatives of pheny

99 ses might be useful for the preparation of L-threo-beta-hydroxy-alpha-amino acids.

100 inistration of a glutamate uptake inhibitor, threo-beta-hydroxy-aspartate (50 mM), increased extracel

101 nhibitory concentrations (0.1 and 0.5 mM) of threo-beta-hydroxy-aspartate (THA), a specific inhibitor

102 as two hydroxamic acid groups and an unusual threo-beta-hydroxy-l-histidine available for Fe(III) che

103 The presence of threo-beta-hydroxy-l-histidine gives rise to a unique mo

104 The required L-threo-beta-hydroxyamino acid components were constructed

105 g FmocNHCl was used for the preparation of d-threo-beta-hydroxyasparagine and d-threo-beta-methoxyasp

106 ric synthesis of an orthogonally protected l-threo-beta-hydroxyasparagine and the development of effe

107 ric synthesis of an orthogonally protected L-threo-beta-hydroxyasparagine and the development of effe

108 ate = L-CCG-III = L-cysteate = L-aspartate = threo-beta-hydroxyaspartate > trans-PDC > D-aspartate =

109 with confluent RMG cells were exposed to D,L-threo-beta-hydroxyaspartate (THA), a blocker of glutamat

110 by either removal of Na+ or addition of D,L-threo-beta-hydroxyaspartate.

111 When transporters were blocked by D,L-threo-beta-hydroxyaspartic acid (THA) or Li+, the mEPSC

112 Pyrrolidine-2,4-dicarboxylic acid and threo-beta-hydroxyaspartic acid caused relatively less i

113 dition of the glutamate reuptake blocker D,L-threo-beta-hydroxyaspartic acid or unlabeled L- glutamat

114 -induced neuroprotection was abolished by DL-threo-beta-hydroxyaspartic acid, DL-threo-beta-benzyloxy

115 related nonribosomal peptides contain an L- threo-beta-hydroxyaspartyl residue at the eighth positio

116 Yyy(8) being Trp/DTrp/D-threo-beta-Me2Nal/L-threo-beta-Me2Nal, and Zzz(11) being Phe/Ala, exhibit po

117 Cys(3) in 5 and 6 yielded H-c[DCys-Phe-Tyr-D-threo-beta-Me2Nal-Lys-Thr-Phe-Cys]-OH (11) and H-c[DCys-

118 -Thr-Phe-Cys]-OH (11) and H-c[DCys-Phe-Tyr-L-threo-beta-Me2Nal-Lys-Thr-Phe-Cys]-OH (12), with biologi

119 ectivity for human sst(3), H-c[Cys-Phe-Tyr-D-threo-beta-Me2Nal-Lys-Thr-Phe-Cys]-OH (5) has high affin

120 l sst's except for sst(1); H-c[Cys-Phe-Tyr-L-threo-beta-Me2Nal-Lys-Thr-Phe-Cys]-OH (6) has high affin

121 ity for human sst(4), that H-c[Cys-Phe-Tyr-D-threo-beta-Me2Nal-Lys-Thr-Phe-Cys]-OH had high affinity

122 xcept for sst(1), and that H-c[Cys-Phe-Tyr-L-threo-beta-Me2Nal-Lys-Thr-Phe-Cys]-OH had high affinity

123 by Tyr at position 11 in H-c[DCys-Phe-Phe-L-threo-beta-Me2Nal-Lys-Thr-Phe-Cys]-OH yielded 18 (IC(50)

124 ) being Phe/Ala/Tyr, Yyy(8) being Trp/DTrp/D-threo-beta-Me2Nal/L-threo-beta-Me2Nal, and Zzz(11) being

125 tion of d-threo-beta-hydroxyasparagine and d-threo-beta-methoxyaspartate, suitably protected for Fmoc

126 tion 25 of HIV-1 protease indicated that the threo-beta-methyl moiety may partially obstruct the adja

127 present in the modified proteins containing threo-beta-methylaspartate and beta,beta-dimethylasparta

128 analogues erythro-beta-methylaspartic acid, threo-beta-methylaspartic acid, or beta,beta-dimethylasp

129 e substitutions at positions 2 and 7, with l-threo-beta-MeTrp at position 8, yielded a much less sele

130 hr-Phe-Cys]-OH (OLT-8, 2), H-c[Cys-Phe-Phe-L-threo-beta-MeTrp-Lys-Thr-Phe-Cys]-OH (4) and H-c[Cys-Phe

131 ys-Thr-Phe-Cys]-OH (4) and H-c[Cys-Phe-Phe-D-threo-beta-MeTrp-Lys-Thr-Phe-Cys]-OH (5) to have very hi

132 ot reversed by pretreatment with MK801 or DL-threo-betabenzyloxyaspartate (DL-TBOA), suggesting that

133 s 6) were obtained with trans-alkenes, while threo bisadducts (compounds 7) were obtained with cis-al

134 us, cis alkenes gave erythro monoadducts and threo bisadducts, whereas trans alkenes gave threo monoa

135 rs of D-erythroC18-ceramide, D-threo-, and L-threo-C18-ceramide, as well as the enantiomeric L-erythr

136 -1,2-dideuterioethylene furnished Au(OAc(F))(threo-CHDCHDOAc(F))(tpy), consistent with an overall ant

137 Examination of erythro/ threo combinations shows that GC/MS/MS has the ability t

138 ide 2'-O-tosyl derivatives gave the 2'-deoxy-threo compounds in good yields.

139 lds the erythro diastereomer rather than the threo configuration that is found in syringomycin.

140 bioactivity differentials where the C17-C20 threo configuration usually imparts higher activity than

141 er products formed at alkyl centers have the threo configuration.

142 uted aziridine silanols give products with a threo configuration.

143 and 3'-deoxynucleoside analogues with beta-D-threo configurations.

144 d furanosyl-selective prebiotic synthesis of threo-cytidine 3, an essential component of TNA.

145 IC50 of 0.11, 0.21, and 0.26 mol % for the L-threo, D-threo, and L-erythro isomers, respectively; (2)

146 CDP-6-deoxy-L-threo-D-glycero-4-hexulose 3-dehydrase (E1), along with

147 CDP-6-deoxy-L-threo-D-glycero-4-hexulose 3-dehydrase (E1), together wi

148 The C-3 deoxygenation of CDP-6-deoxy-L-threo-D-glycero-4-hexulose is a critical reaction in the

149 CDP-6-deoxy-L-threo-D-glycero-4-hexulose-3-dehydrase (E(1)) catalyzes

150 CDP-6-deoxy-l-threo-d-glycero-4-hexulose-3-dehydrase (E1), which catal

151 n is catalyzed by two enzymes: CDP-6-deoxy-L-threo-D-glycero-4-hexulose-3-dehydrase (E1), which conta

152 lved in this transformation is CDP-6-deoxy-L-threo-D-glycero-4-hexulose-3-dehydrase (E1), which is a

153 is a dehydration catalyzed by CDP-6-deoxy-L-threo-D-glycero-4-hexulose-3-dehydrase (E1), which is PM

154 cyl-CoA dehydrogenases (ACDs), CDP-6-deoxy-l-threo-d-glycero-4-hexulose-3-dehydrase reductase (E3), C

155 center, and an NADH-dependent CDP-6-deoxy-L-threo-D-glycero-4-hexulose-3-dehydrase reductase (E3), w

156 requires an additional enzyme, CDP-6-deoxy-L-threo-D-glycero-4-hexulose-3-dehydrase reductase (E3, fo

157 The second catalyst, CDP-6-deoxy-L-threo-D-glycero-4-hexulose-3-dehydrase reductase, formal

158 hro-beta-Me2Nal instead of the corresponding threo derivatives at position 8, are essentially inactiv

159 Threo derivatives with m- or p-halo substituents were mo

160 acids (EETs) and their hydrolysis products (threo-DHETs) have been proposed to be endothelial-depend

161 istent with stereochemical assignment as the threo diastereomer (5'S,6'S)-GlyU.

162 reoselectivities up to 4.5:1 in favor of the threo-diastereomer.

163 Erythro- and threo-diastereomers of 13-H-trans-14,15-EETA relaxed end

164 We report herein that DL-threo-dihydrosphingosine (DHS), a competitive inhibitor

165 The sphingosine analogue, D-L-threo-dihydrosphingosine (DHS), inhibits the SK enzyme c

166 ; (d) whether cytotoxicity was enhanced by l-threo-dihydrosphingosine (safingol); (e) whether physiol

167 tidylinositol, diacylglycerol, ceramide, D,L-threo-dihydrosphingosine or N, N-dimethylsphingosine.

168 Surprisingly, d, l-threo-dihydrosphingosine was also phosphorylated by SPHK

169 Another SphK inhibitor, D,L-threo-dihydrosphingosine, also induced apoptosis and pro

170 atidylinositol, diacylglycerol, ceramide, DL-threo-dihydrosphingosine, or N,N-dimethylsphingosine.

171 with the inhibitor of sphingosine kinase, DL-threo-dihydrosphingosine, significantly increased the pe

172 fractions) and much stronger than that by DL-threo-dihydrosphingosine, which had been considered to b

173 tested whether systemic administration of L-threo-dihydroxyphenylserine (L-DOPS), a drug used succes

174 3,4-dihydroxyphenylalanine at 100 mg/kg or l-threo-dihydroxyphenylserine at 5 mg/kg) or a selective s

175 e enhanced memory function, the NE prodrug l-threo-dihydroxyphenylserine was administered in Ts65Dn a

176 ed by treatment with the NA precursor drug L-threo-dihydroxyphenylserine.

177 d, the core mannitol is cleaved at the C3-C4 threo-diol bond and in the absence of a threo-diol cleav

178 3-C4 threo-diol bond and in the absence of a threo-diol cleavage occurs to a lesser extent at erythro

179 Threo diols preferentially associate with the boronic ac

180 e the absolute configurations of erythro and threo diols, amino alcohols, and diamines is reported.

181 excess of chiral vicinal diols, specifically threo diols, has been developed.

182 Acute pharmacological replacement of NA by L-threo-DOPS partially restored phosphorylation of beta-Ca

183 sylceramide synthase inhibitors, including d-threo-ethylendioxyphenyl-2-palmitoylamino-3-pyrrolidinop

184 h recombinant human alpha-Gal A protein or d-threo-ethylenedioxyphenyl-P4, an inhibitor of glucosylce

185 qual amounts of (2R,3R)-erythro- and (2R,3S)-threo-fluoromalate are formed.

186 ,4-lactone conversion is in both cases the L-threo form of 3-deoxy-2-keto-hexarate.

187 L-threo-gamma-fluoromethotrexate (1t) and L-threo-gamma-fluorofolic acid (3t) are reported.

188 The stereospecific syntheses of L-threo-gamma-fluoromethotrexate (1t) and L-threo-gamma-fl

189 idative deamination to produce 3,7-dideoxy-d-threo-hept-2,6-diulosonic acid which cyclizes to 3-dehyd

190 2-Amino-3,7-dideoxy-d-threo-hept-6-ulosonic acid (ADH) synthase, the product o

191 e semialdehyde to form 2-amino-3,7-dideoxy-D-threo-hept-6-ulosonic acid.

192 tive 2,3,4-trideoxy-2,2,3,3,4,4-hexafluoro-l-threo-heptopyranose.

193 , producing the final product 4-deoxy-beta-l-threo-hex-4-enepyranosyl-uronic acid.

194 S-GlcNS6S (where Delta UA is 4-deoxy-alpha-L-threo-hex-4-enopyranosyluronic acid, GlcN is D-glucosami

195 -GlcNpS6S (where DeltaUAp is 4-deoxy-alpha-L-threo-hex-enopyranosyluronic acid, GlcNp is 2-amino-2-de

196 yranose 3, 2,3-dideoxy-2,2,3,3-tetrafluoro-d-threo-hexofuranose 4, and 2,3-dideoxy-2,2,3,3-tetrafluor

197 hreo-isomer, 5-O-tetradecanoyl-2,3-dideoxy-L-threo-hexono-1,4-lactone (2) was a good PK-C ligand (Ki

198 ork correspond to 2,3-dideoxy-L-erythro- or -threo-hexono-1,4-lactone (template III) and 2-deoxyapiol

199 constructed with the dideoxy-L-erythro- or -threo-hexono-1,4-lactone template were synthesized stere

200 y reported 2,3-dideoxy-2,2,3,3-tetrafluoro-d-threo-hexopyranose 3, 2,3-dideoxy-2,2,3,3-tetrafluoro-d-

201 rivatives, 3,4-dideoxy-3,3,4,4-tetrafluoro-d-threo-hexopyranose 6 and 3,4-dideoxy-3,3,4,4-tetrafluoro

202 (4-dimethylamino)-2,3,4,6-tetradeoxy-beta-D-threo-hexopyranose) is a highly deoxygenated sugar compo

203 re preexposed to the EAA transport inhibitor threo-hydroxy beta-aspartic acid (THBA).

204 initial current was inhibited by 300 microM threo-hydroxyaspartate (THA) and did not reverse as the

205 y inhibitors of glutamate transporters (beta-threo-hydroxyaspartate, dihydrokainate, and L-trans-pyrr

206 n = 18), NR2B-selective (ifenprodil, n = 6; threo-ifenprodil, n = 4; Ro25-6985, n = 13), and NR2C/D-

207 ydroxy-1,2, 4-butanetricarboxylic acid], (-)-threo-iso(homo)(2)citrate [(-)-threo-1-hydroxy-1,2,5-pen

208 xy-1,2,5-pentanetricarboxylic acid], and (-)-threo-iso(homo)(3)citrate [(-)-threo-1-hydroxy-1,2, 6-he

209 oxylation of DL-threo-3-isopropylmalic acid, threo-isocitrate, erythro-isocitrate, and homologs of th

210 citrate, erythro-isocitrate, and homologs of threo-isocitrate.

211 sarcoma cell line RD to the L-erythro and DL-threo isoforms of sphingosine did not induce apoptosis.

212 These intermediates included (-)-threo-isohomocitrate [(-)-threo-1-hydroxy-1,2, 4-butanet

213 ration of the cis-homoaconitate produces (-)-threo-isohomocitrate [(2R,3S)-1-hydroxy-1,2, 4-butanetri

214 s of cis-homoaconitate, homocitrate, and (-)-threo-isohomocitrate serve as intermediates.

215 (2R,3R)-erythro-Fluoromalate, but not the threo isomer, is a slow substrate for chicken liver mali

216 or reduction of the S enantiomer to give the threo isomer.

217 The erythro, but not the threo, isomer blocked angiotensin II-stimulated aortic S

218 ibutyrate to PK-C alpha showed that only the threo-isomer, 5-O-tetradecanoyl-2,3-dideoxy-L-threo-hexo

219 ous purification of the genetically relevant threo-isomer.

220 The threo isomers are potent and selective inhibitors of the

221 ependent decarboxylation of one isomer of DL-threo-isopropylmalate to 2-ketoisocaproate; thus, it is

222 e delta-opioid receptor it may be the 2S,3R (threo-L) configuration.

223 ized mainly via caveolae, the non-natural (L-threo) LacCer analog is taken up via clathrin-, RhoA-, a

224 ant unilamellar vesicles demonstrated that L-threo-LacCer did not undergo a concentration-dependent e

225 tereochemistry of the sphingosine group in L-threo-LacCer results in a perturbed structure, which is

226 he sphingosine hydrocarbon chain, while in L-threo-LacCer the carbohydrate group is nearly perpendicu

227 y scans following administration of [(11)C]d-threo-methylphenidate (a dopamine transporter ligand) me

228 ng positron emission tomography and [(11)C]d-threo-methylphenidate (DA transporter radioligand).

229 ing positron emission tomography with [11C]d-threo-methylphenidate (MP).

230 dly less potent than the corresponding (+/-)-threo-methylphenidate (TMP; Ritalin) derivatives.

231 ratio of the distribution volume for [11C]d-threo-methylphenidate in striatum to that in cerebellum

232 dopaminergic deficits assessed with (11)C-d-threo-methylphenidate PET were not detected.

233 l as multitracer PET with (18)F-FDG, (11)C-d-threo-methylphenidate, and (11)C-raclopride.

234 s demonstrated by a very direct synthesis of threo-methylphenidate.

235 rs (age range 20-74 yr) using PET and [11C]d-threo-methylphenidate.

236 A), erythro-methyltartaric acid (e-MTA), and threo-methyltartaric acid (t-MTA).

237 g the NMR signals of meso compound in a meso-threo mixture of cyclic molecules is first discussed.

238 nes) gave (E)-(5-thianthreniumyl)alkenes and threo monoadducts (from trans alkenes) gave (Z)-(5-thian

239 threo bisadducts, whereas trans alkenes gave threo monoadducts and erythro bisadducts.

240 ed on the difference between the erythro and threo monodeuterated diastereomers ( trans/ cis = 2.0 fo

241 electivity for the Watson-Crick base-pairing threo-monomer, warrants further study of the role they c

242 ecane (12a), was equipotent to unconstrained threo-MP against [(3)H]WIN35,428 binding.

243 Positron-emission tomography and [11C]d-threo-MP were used to estimate DAT occupancies at differ

244 In contrast, a single activated threo-nucleotide at the end of an RNA primer or in an RN

245 is of noncanonical nucleotides including the threo-nucleotide building blocks of TNA.

246 Even a single activated threo-nucleotide in the presence of an activated downstr

247 '-hydroxyl and the phosphate of the incoming threo-nucleotide intermediate.

248 that primer extension by multiple sequential threo-nucleotide monomers is strongly disfavored relativ

249 for the effective exclusion of arabino- and threo-nucleotides from primordial oligonucleotides.

250 s of non-templated primer extension, whereas threo-nucleotides showed lower reactivity.

251 Here, we examine the ability of activated threo-nucleotides to participate in nonenzymatic templat

252 firmed the bias against the incorporation of threo-nucleotides.

253 des share a common pathway with arabino- and threo-nucleotides.

254 d-type ABDC with the disodium salt of either threo- or erythro-beta-hydroxy-dl-Asp at 50 mM resulted

255 roisomer but not the synthetic L-erythro-, D-threo-, or L-threosiomers of sphingosine can serve as a

256 of the protease, a beta-methyl group in the threo orientation, present in the modified proteins cont

257 r granule cells were treated in vitro with d-threo-P4 (P4).

258 an inhibitor of glycosylceramide synthase (d-threo-P4) led to a reduction of MNV-1 binding and infect

259 o pair of enantiomers (2S,3S, 2R,3R) and the threo pair of enantiomers (2S,3R, 2R,3S), which were the

260 shed that aliphatic polyols do not require a threo pair of hydroxy groups to form hypercoordinated Si

261 lutamate to the acceptor, uridine 5'-(beta-l-threo-pentapyranosyl-4"-ulose diphosphate), the intermed

262 P-glucuronic acid to form uridine 5'-(beta-l-threo-pentapyranosyl-4"-ulose diphosphate).

263 cA) to the UDP-4' '-ketopentose [UDP-beta-(l-threo-pentapyranosyl-4' '-ulose] and (2) the N-10-formyl

264 ''-ketopentose, uridine 5'-diphospho-beta-(L-threo-pentapyranosyl-4''-ulose), which is converted by A

265 no analogs of 9-(2,3-dideoxy-2-fluoro-beta-D-threo-pentofuranosyl) purines (F-ddN) has been synthesiz

266 osyladenosine gave 9-(5-O-TPS-2-deoxy-beta-D-threo-pentofuranosyl)adenine.

267 ti-HIV agent, 9-(2,3-dideoxy-2-fluoro-beta-D-threo-pentofuranosyl)hypoxanthine (F-ddI).

268 Interestingly, benzyl-beta-D-threo-pentopyranos-4-uloside (4-keto derivative) and ben

269 The second activity converts UDP-beta-l-threo-pentopyranosyl-4''-ulose and NADH to UDP-xylose an

270 arboxylate UDP-glucuronic acid to UDP-beta-l-threo-pentopyranosyl-4''-ulose in the presence of NAD(+)

271 degradation of the C(5) osone, D-xylosone (D-threo-pentose-2-ulose), showing that this transposition

272 mployed in the reaction, allowing erythro or threo products to be obtained selectively.

273 alysed coordination-insertion ROP results in threo-(R,R)-di-isotactic PHAs with chiral retention, whe

274 (4-methoxyphenyl)-1, 2-propanediols (erythro:threo ratio ca. 3:1).

275 LP)-dependent transaldolase that catalyzes a threo-selective aldol-type reaction to generate the thio

276 D-erythro-SPC and L-threo-SPC at the concentration of 100 microM increased t

277 coupled to bovine serum albumin), but not L-threo-SPC, was active extracellular; the former (at 10 m

278 nd its N-methyl derivatives, the effect of L-threo-Sph or its N-methyl derivatives is minimal, and no

279 be selectively reduced to either erythro- or threo-sphinganines.

280 latter is a useful synthon for assembly of L-threo-sphingoid bases: long-chain aminoalkanols and amin

281 tereochemistry, beta-D-lactosyl-N-octanoyl-L-threo-sphingosine, (1) selectively inhibits caveolar end

282 he DNA fragmentation-inducing ability of the threo stereoisomers and D-e-C8-Ceramine cannot be attrib

283 omers to be stereospecific with the D- and L-threo stereoisomers being severalfold more potent than t

284 (His)) hydroxylates histidyl residues with l-threo stereospecificity.

285 A variety of erythro and threo substrates were investigated to verify this chirop

286 erythro- and threo-(tBu3SiO)3HTaCHDCHDOEt (2-CHDCHDOEt) are staggered

287 The unsubstituted RRA, threo(trans)-1-aza-5-phenyl[4.4.0]decane (12a), was equi

288 hose with the stereochemistry of threo-trans-threo-trans-erythro (from C-15 to C-24) were the most po

289 etogenins, those with the stereochemistry of threo-trans-threo-trans-erythro (from C-15 to C-24) were

290 dihydroxylation generates either erythro or threo vicinal diols from cis or trans alkenes, depending