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

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

9 6 mice treated twice daily for 3 days with D-threo-1-ethylendioxyphenyl-2-palmitoylamino-3-pyrrolidi

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

62 .11, 0.21, and 0.26 mol % for the L-threo, D-threo, and L-erythro isomers, respectively; (2) all ster

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

110 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-

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

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

113 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

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

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

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

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

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

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

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

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

122 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

123 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

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

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

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

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

128 -1,2-dideuterioethylene furnished Au(OAc(F))(threo-CHDCHDOAc(F))(tpy), consistent with an overall ant

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

164 3,4-dihydroxyphenylalanine at 100 mg/kg or l-threo-dihydroxyphenylserine at 5 mg/kg) or a selective s

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

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

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

168 3-C4 threo-diol bond and in the absence of a threo-diol cleavage occurs to a lesser extent at erythro

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

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

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

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

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

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

175 ,4-lactone conversion is in both cases the L-threo form of 3-deoxy-2-keto-hexarate.

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

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

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

179 2-Amino-3,7-dideoxy-d-threo-hept-6-ulosonic acid (ADH) synthase, the product o

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

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

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

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

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

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

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

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

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

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

190 (4-dimethylamino)-2,3,4,6-tetradeoxy-beta-D-threo-hexopyranose) is a highly deoxygenated sugar compo

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

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

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

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

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

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

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

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

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

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

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

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

203 (2R,3R)-erythro-Fluoromalate, but not the threo isomer, is a slow substrate for chicken liver mali

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

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

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

207 The threo isomers are potent and selective inhibitors of the

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

246 (4-methoxyphenyl)-1, 2-propanediols (erythro:threo ratio ca. 3:1).

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

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

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

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

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

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

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

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

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

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

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

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

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