ライフサイエンスコーパス: myo-inositol

1 r (MDD) is reduced cerebral concentration of myo-Inositol.

2 -di-O-triisopropylsilyl-1,2-O-isopropylidene-myo-inositol.

3 fects in homozygotes were rescued by dietary myo-inositol.

4 at the IatP-IatA transporter is specific for myo-inositol.

5 of glycerophosphocholine (GPC), taurine, and myo-inositol.

6 -fold while completely abolishing binding to myo-inositol.

7 een achieved starting from readily available myo-inositol.

8 but their expression was strongly induced by myo-inositol.

9 pathway leading from glucose 6-phosphate via myo-inositol.

10 -acetamido-2-deoxy-alpha-D-glucopyranosyl)-D-myo-inositol.

11 and transportation of food that contains the myo-inositol.

12 s found to share similarities with that of a myo-inositol 1 phosphate synthase mutant that is also se

13 Di-myo-inositol 1,1'-phosphate (DIP) is a major osmoprotect

14 d highly specific PDK1 inhibitor, 2-O-benzyl-myo-inositol 1,3,4,5,6-pentakisphosphate (2-O-Bn-InsP5),

15 tudies showed that the K(m) for ZmIPK1 using myo-inositol 1,3,4,5,6-pentakisphosphate as a substrate

16 he ZmIPK1 enzyme catalyzes the conversion of myo-inositol 1,3,4,5,6-pentakisphosphate to phytic acid.

17 yl inositol 1,3,4,5,6-pentakisphosphates and myo-inositol 1,3,4,5,6-pentakisphosphate with biological

18 s established utilizing the novel orthoester myo-inositol 1,3,5-orthobutyrate as an example.

19 n acid mediated hydrolysis of enol ethers of myo-inositol 1,3,5-orthoesters giving a synthetically ve

20 Acid hydrolysis of myo-inositol 1,3,5-orthoesters, apart from orthoformates

21 erentiate the enantiotopic hydroxy groups of myo-inositol 1,3,5-orthoformate in the presence of a chi

22 d via Yb(OTf)3-catalyzed desymmetrization of myo-inositol 1,3,5-orthoformate using a proline-based ch

23 ylation of myo-inositol 1,4,6-trisphosphate, myo-inositol 1,4,5,6-tetrakisphosphate, and myo-inositol

24 e Ca(2+)-releasing intracellular messenger d-myo-inositol 1,4,5-trisphosphate [1, Ins(1,4,5)P(3)] are

25 Ca(2+)-mobilizing intracellular messenger d-myo-inositol 1,4,5-trisphosphate [Ins(1,4,5)P(3)].

26 phostin A (AdA) is a potent agonist of the d-myo-inositol 1,4,5-trisphosphate receptor (Ins(1,4,5)P3R

27 hostin A (AdA), the most potent agonist of d-myo-inositol 1,4,5-trisphosphate receptors (IP(3)R), is

28 ates, in particular via the second messenger myo-inositol 1,4,5-trisphosphate, and phosphoinositides

29 A variety of inositol phosphates including myo-inositol 1,4,5-trisphosphate, which is a secondary m

30 e of large cholangiocytes by activation of D-myo-inositol 1,4,5-trisphosphate/Ca(2+) /calmodulin-depe

31 ndicates that the phosphorylation product of myo-inositol 1,4,6-trisphosphate is inositol 1,2,4,6-tet

32 capable of catalyzing the phosphorylation of myo-inositol 1,4,6-trisphosphate, myo-inositol 1,4,5,6-t

33 magnitude greater than those determined for myo-inositol 1-phosphate (IMP) and fructose 1,6-bisphosp

34 novel insights into the architecture of the myo-inositol 1-phosphate binding site and the involvemen

35 l-myo-inositol 1-phosphate synthase (MIPS; EC 5.5.1.4) cat

36 activity was obtained with myo-inositol, 1D-myo-inositol 1-phosphate, or myo-inositol 2-phosphate as

37 l transporter and a kinase that generates 1L-myo-inositol 1-phosphate.

38 ermined complex structure in the presence of myo-inositol-1,2,3,4,5,6-hexakisphosphate (InsP6 or phyt

39 degradation of adenosine-5'-triphosphate and myo-inositol-1,2,3,4,5,6-hexakisphosphate by (31)P NMR.

40 ng which 4,6-di-O-(methoxy-diethyleneglycol)-myo-inositol-1,2,3,5-tetrakis(phosphate), (OEG(2))(2)-IP

41 renergic agonist stimulating intracellular D-myo-inositol-1,4,5-triphosphate (IP(3) )/Ca(2+) levels,

42 nnosylated GPI intermediate D-GlcNalpha1-6-D-myo-inositol-1-HPO4-sn-lipid precedes mannosylation.

43 uM (determined by measuring A7r5 cell line D-myo-inositol-1-phosphate accumulation).

44 cosamine from UDP-N-acetylglucosamine to 1-L-myo-inositol-1-phosphate in the first committed step of

45 Myo-inositol-1-phosphate synthase (MIPS) catalyzes the c

46 de occurrence in all eukaryotes, the role of myo-inositol-1-phosphate synthase and de novo inositol b

47 ulation of tobacco Alternative oxidase1a and Myo-inositol-1-phosphate synthase in PsAP2 overexpressin

48 myo-Inositol-1-phosphate synthase is a conserved enzyme

49 philic attack of the 3-hydroxyl group of 1-L-myo-inositol-1-phosphate while at the same time promotin

50 the enzyme to distinguish between HOLP and d-myo-inositol-1-phosphate).

51 inorganic phosphate from HOLP but not from d-myo-inositol-1-phosphate, the main substrate of IMPases.

52 zes the conversion of glucose-6-phosphate to myo-inositol-1-phosphate.

53 UDP and generating the binding site for 1-L-myo-inositol-1-phosphate.

54 n binding of UDP-N-acetylglucosamine and 1-L-myo-inositol-1-phosphate.

55 substrates and in a complex with UDP and 1-L-myo-inositol-1-phosphate.

56 ssential inositol tetraphosphate molecule--D-myo-inositol-(1,4,5,6)-tetrakisphosphate (Ins(1,4,5,6)P(

57 -p-methoxybenzyl-1,2:4,5-di-O-isopropylidene-myo-inositol 11.

58 mc(2)155, little activity was obtained with myo-inositol, 1D-myo-inositol 1-phosphate, or myo-inosit

59 yo-inositol, 1D-myo-inositol 1-phosphate, or myo-inositol 2-phosphate as the N-acetylglucosamine acce

60 e (11% lower, P < 0.001), N-acetyl-aspartate:myo-inositol (24% lower, P < 0.001), and myo-inositol:cr

61 o find alternative molecules and predicted d-myo-inositol 3,4,5,6-tetrakisphosphate (TMI) to strongly

62 myo-inositol 1,4,5,6-tetrakisphosphate, and myo-inositol 3,4,5,6-tetrakisphosphate.

63 ly expressing an antisense gene sequence for myo-inositol 3-phosphate synthase (IPS, catalysing the f

64 (2-acetamido-2-deoxy-alpha-glucopyranosyl)-D-myo-inositol 3-phosphate to produce 1-O-(2-acetamido-2-d

65 irst time that GSK-3 is required for optimal myo-inositol-3 phosphate synthase activity and de novo i

66 Activity of myo-inositol-3 phosphate synthase, the rate-limiting enz

67 t is synthesized from glucose 6-phosphate by myo-inositol-3-phosphate synthase (IP synthase), a homot

68 myo-Inositol-3-phosphate synthase (MIPS) plays a crucial

69 o the structures reported for the GlcNAc-1-d-myo-inositol-3-phosphate synthase (MshA) apo and ternary

70 proate (VPA) depletes inositol by inhibiting myo-inositol-3-phosphate synthase, the enzyme that catal

71 ease in transcription of INO1, which encodes myo-inositol-3-phosphate synthase.

72 Uncaging of glycerophosphoryl-myo-inositol 4,5-bisphosphate (gPIP2), a poorly metaboli

73 s the key step in a streamlined synthesis of myo-inositol-6-phosphate.

74 ), creatine (a marker of energy metabolism), myo-inositol (a marker of glial cells), and N-acetylaspa

75 s the rate-limiting step in the synthesis of myo-inositol, a critical compound in the cell.

76 bpA with these mutant alleles unable to bind myo-inositol abolishes C. crescentus growth in medium co

77 However, whether myo-inositol accumulation during osmoregulation affects

78 p-methoxy-benzyl-1,2:4,5-di-O-isopropylidene-myo-inositol allowed the preparation of 11.

79 bisphosphate (PIP2), which is generated from myo-inositol, an osmolyte transported into cells by sodi

80 and diesters of 1,2:5,6-di-O-isopropylidene-myo-inositol and 1,2:5,6-di-O-cyclohexylidene-myo-inosit

81 es utilizations of the existing framework of myo-inositol and a regioselective esterification.

82 r using RNA interference inhibited uptake of myo-inositol and blocked the synthesis of the myo-inosit

83 es of increased Glutamate/glutamine, reduced myo-inositol and choline are hyperammonemia-associated a

84 Glx (as well as N-acetylaspartate, choline, myo-inositol and creatine) group contrasts from all indi

85 f IbpA with inverted binding specificity for myo-inositol and D-ribose.

86 rations characteristic of AD (i.e. increased myo-inositol and decreased N-acetylaspartate (NAA)).

87 antimicrobial activity, was synthesized from myo-inositol and dimethyl d-camphor acetal in 14 steps.

88 in 25 steps in an overall yield of 6% using myo-inositol and ethyl propiolate as the starting materi

89 It also quantifies myo-inositol and galactinol making it suitable both for

90 and fivefold increases in specific titers of myo-inositol and glucaric acid, respectively.

91 changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-i

92 o-inositol oxygenase (RSOR/MIOX) catabolizes myo-inositol and is implicated in the pathogenesis of di

93 showed significantly higher ipsilesional PMd myo-inositol and lower SMA N-acetylaspartate.

94 ue to a specific lack of de novo synthesized myo-inositol and not a general inositol-less death.

95 amino acid accumulation and the synthesis of myo-inositol and raffinose during plant adaptation to lo

96 Efflux of uncharged osmolytes (myo-inositol and taurine) was suppressed by deletion of

97 is a distinction between de novo synthesized myo-inositol and that from the extracellular environment

98 r concentrations of N-acetylaspartate (NAA), myo-inositol, and glutamate as measured by magnetic reso

99 Alterations in NAA, myo-inositol, and glutamate progressively worsened and w

100 l and glial compartments: N-acetylaspartate, myo-inositol, and glutamate/glutamine, were quantified b

101 lycerol 3- and 2-phosphate, malate, alanine, myo-inositol, and linoleic acid.

102 pseudouridine, N-acetylalanine, erythronate, myo-inositol, and N-acetylcarnosine.

103 ile gs was related to sugars, organic acids, myo-inositol, and shikimate, gm showed a more complex pa

104 ps from the cheap and commercially available myo-inositol, and this common intermediate has been used

105 tylaspartate, choline, glutamate, glutamine, myo-inositol, and total creatine).

106 T. maritima is unable to grow on myo-inositol as a single carbon source.

107 es C. crescentus growth in medium containing myo-inositol as the sole carbon source.

108 f Y247S/Y251S in the absence and presence of myo-inositol as well as Y246S/Y247S/Y248S/Y251S indicate

109 The mips1 mutants have lower myo-inositol, ascorbic acid, and phosphatidylinositol le

110 ture of Caulobacter crescentus IbpA bound to myo-inositol at 1.45 A resolution.

111 Ibuprofen protected the increase of myo-inositol at six months of age in the hippocampus, bu

112 -peptidoglycan complex, and the phosphatidyl-myo-inositol-based lipoglycans are key features of the m

113 ng protein (PBP) IbpA mediates the uptake of myo-inositol by the IatP-IatA ATP-binding cassette trans

114 These findings, coupled with the fact the myo-inositol can serve as a sole carbon source for growt

115 sociated with active disease, with the urine myo-inositol:citrate ratio being tightly correlated with

116 tes (L-serine, L-leucine, glucose, fructose, myo-inositol, citric acid and 2, 3-hydroxypropanoic acid

117 major depressive episode had lower levels of myo-Inositol compared with schizophrenia patients withou

118 myo-Inositol-containing compounds may provide informatio

119 are important intermediates for higher order myo-inositol-containing compounds.

120 yo-inositol and blocked the synthesis of the myo-inositol-containing phospholipids, phosphatidylinosi

121 We found that overexpression of the Na(+)/myo-inositol cotransporter (SMIT1) and myo-inositol supp

122 Higher concentrations of glutamate, taurine, myo-inositol, creatine and inosine were present in aqueo

123 n metabolites, including N-acetyl-aspartate, myo-inositol, creatine/phosphocreatine and choline-conta

124 ad significantly higher choline/creatine and myo-inositol/creatine ratios than APOE E3 homozygotes.

125 tylaspartate (NAA)/Choline, NAA/Creatine and myo-inositol/Creatine ratios were measured.

126 ging normal population, choline/creatine and myo-inositol/creatine ratios were significantly increase

127 Lower myo-inositol/creatine values, suggesting astrocytic dama

128 n (1)H-MRS metabolites (choline/creatine and myo-inositol/creatine).

129 ate:myo-inositol (24% lower, P < 0.001), and myo-inositol:creatine/phosphocreatine (17% higher, P < 0

130 ning compounds:creatine/phosphocreatine, and myo-inositol:creatine/phosphocreatine were measured usin

131 d for the downregulation of the idhA-encoded myo-inositol dehydrogenase activity in the presence and

132 a starts as the conventional route using the myo-inositol dehydrogenase IolG followed by three novel

133 Orthogonally protected chiral myo-inositol derivatives are important intermediates for

134 Amino-myo-inositol derivatives have been found to be potent in

135 step to generate a suitably protected chiral myo-inositol derivatives is described here as a unified

136 o access both enantiomers of 4,5-di-O-benzyl-myo-inositol, derived from the same set of starting mate

137 h as channel regulation by SMIT-transported, myo-inositol-derived phosphatidylinositol 4,5-bisphospha

138 ion ensures KCNQ2/3 exposure to locally high myo-inositol-derived PIP2 concentrations.

139 while syntheses of triacylated-phosphatidyl-myo-inositol dimannoside (Ac(1)PIM(2)) and Man(1)GlcAGro

140 cid, palmitoleic acid, L-serine, oleic acid, myo-inositol, dodecanoic acid, L-methionine, hypoxanthin

141 The optimised method within 20min separated myo-inositol, galactinol, glucose, fructose, sucrose, ra

142 The composite neurochemical measure, myo-inositol+glycine/creatine, was consistently increase

143 here-like self-exclusion; urea, taurine, and myo-inositol have a tendency toward self-association; so

144 ntains a monoester phosphate attached to its myo-inositol headgroup, also supported enhanced enzymati

145 Selenomonas ruminantium PhyA in complex with myo-inositol hexa- and pentakisphosphate.

146 * Myo-inositol hexakisphosphate (InsP(6)), abundant in ani

147 ds produce large amounts of their precursor, myo-inositol hexakisphosphate (InsP6 ).

148 Myo-inositol hexakisphosphate (IP6) is a natural product

149 We subsequently demonstrate that a myo-inositol hexakisphosphate (IP6) noncovalent adduct c

150 Myo-inositol hexakisphosphate (IP6), is the main iron ch

151 This Bifidobacterium strain contributed to myo-inositol hexakisphosphate (phytate) hydrolysis, resu

152 In these habitats, myo-inositol hexakisphosphate (phytate) is prevalent and

153 Phytic acid (myo-inositol hexakisphosphate, InsP6) is an important ph

154 SNF472, intravenous myo-inositol hexaphosphate, selectively inhibits the for

155 ne, total choline, glycerophosphorylcholine, myo-inositol, imidazole, uridine diphosphate glucose, is

156 hieved from (+/-)-1,2:4,5-diisopropylidene-D-myo-inositol in 16 steps in 3% overall yield.

157 ed 3-O-allyl-6-O-benzyl-1,2-O-isopropylidene-myo-inositol in a convergent synthesis.

158 that metabolism of endogenous and exogenous myo-inositol in T. brucei is strictly segregated.

159 Myo-Inositol in the ACC was negatively correlated with M

160 rticipants, acute oral ebselen reduced brain myo-inositol in the anterior cingulate cortex, consisten

161 ice at 6 months of age showed an increase in myo-inositol in the hippocampus at a time when the Abeta

162 05), and pons (P < .01) and higher levels of myo-inositol in the motor cortex (P < .001) and subcorti

163 -(11Z-octadecenoyl)-sn-glycero-3-phospho-(1'-myo-inositol), in which the sn-1 position contains an et

164 yo-inositol and 1,2:5,6-di-O-cyclohexylidene-myo-inositol, in both solid and solution states.

165 in Escherichia coli, resulting in titers of myo-inositol increased 5.5-fold and titers of glucaric a

166 Myo-inositol increased as a function of age in the amygd

167 Pretreatment with exogenous myo-inositol inhibited synapse formation, demonstrating

168 phocreatinine, choline-containing compounds, myo-inositol (Ins) and glutamate+glutamine (Glx) were de

169 The cellular myo-inositol (Ins) pool is important to many metabolic a

170 ty is essential for the de novo synthesis of myo-Inositol (Ins), and for recycling of Ins in Ins(1,4,

171 The first 2-keto-myo-inositol intermediate is oxidized by another, previo

172 ible osmolytes such as betaine, taurine, and myo-inositol is a protective response shared by all euka

173 myo-Inositol is an essential biomolecule that is synthes

174 myo-Inositol is an essential precursor for the productio

175 Myo-inositol is an important cellular osmolyte in autore

176 Myo-inositol is an important constituent of membrane pho

177 Since reduced brain myo-Inositol is associated with MDD, myo-Inositol may be

178 Intracellular myo-inositol is generated by de novo synthesis from gluc

179 e nine 1,2,3,4,5,6-cyclohexanehexol isomers, myo-inositol is pre-eminent, with "other" inositols (cis

180 ing sickness and nagana in domestic animals, myo-inositol is taken up via a specific proton-coupled e

181 Myo-inositol is the precursor of phosphoinositides, key

182 Therefore, myo-inositol is thought to have an important role in the

183 It also showed that the de novo synthesized myo-inositol is utilized to form PI, which is preferenti

184 From differentially protected D-myo-inositol key intermediates, a versatile phosphoramid

185 glutamate (Glu), Gln/Glu, N-acetylaspartate, myo-Inositol, lactate, and alanine.

186 n magnetic resonance spectroscopy to examine myo-Inositol levels in the anterior cingulate cortex (AC

187 We examined whether myo-Inositol levels provide a potential marker for depre

188 Thus, MIPS1 has a significant impact on myo-inositol levels that is critical for maintaining lev

189 In contrast, high myo-inositol levels were observed prior to nodule format

190 et positioned between the lobes contains the myo-inositol ligand, which binds with submicromolar affi

191 ) (7.5 +/- 0.2 vs 8.3 +/- 0.3; P < .01), and myo-inositol (m-Ins) (3.8 +/- 0.3 vs 5.6 +/- 0.4; P < .0

192 Cho), creatine plus phosphocreatine (Cr) and myo-Inositol (m-Ins), were quantified at C1-C3.

193 tes the biosynthetic pathway of phosphatidyl-myo-inositol mannoside, lipomannan, and lipoarabinomanna

194 Phosphatidyl-myo-inositol mannosides (PIMs) are key glycolipids of th

195 involved in the biosynthesis of phosphatidyl-myo-inositol mannosides (PIMs), which are key components

196 e biosynthesis of mycobacterial phosphatidyl-myo-inositol mannosides (PIMs).

197 arked reduction of higher order phosphatidyl-myo-inositol mannosides and the presence of dimycocerosa

198 ManLAM and reduced higher order phosphatidyl-myo-inositol mannosides in strains HN885 and HN1554 resu

199 e is stimulated in part through phosphatidyl-myo-inositol mannosides that are present in the cell wal

200 tes the biosynthetic pathway of phosphatidyl-myo-inositol mannosides, lipomannan, and lipoarabinomann

201 ipomannan, and the higher-order phosphatidyl-myo-inositol mannosides.

202 Phosphatidyl-myo-inositol mannosyltransferase A (PimA) is an essentia

203 Phosphatidyl-myo-inositol mannosyltransferase A (PimA) is an essentia

204 Phosphatidyl-myo-inositol mannosyltransferase A (PimA) is an essentia

205 d brain myo-Inositol is associated with MDD, myo-Inositol may be a biochemical marker of depressive m

206 Therefore, the in vivo quantification of myo-inositol may distinguish NMO from MS.

207 red with controls only in N-acetyl-aspartate:myo-inositol (mean: 3.6%/year; 95% confidence interval:

208 ce interval: 0.9-3.5) and N-acetyl-aspartate:myo-inositol (mean: 3.7%/year; 95% confidence interval:

209 nderlying the clinical effect of lithium and myo-inositol-mediated skeletal development.

210 show a new thermal event associated to beta myo-inositol melting at 221.43 degrees C, suggesting tha

211 rs from T. maritima in its genes involved in myo-inositol metabolism.

212 Baseline N-acetylaspartate (NAA) level, myo-inositol (mI) in normal-appearing white and gray mat

213 myo-inositol (MI) is a key sugar alcohol component of va

214 r the enzyme catalyzing the limiting step of myo-inositol (MI) synthesis.

215 nase (MIOX) catalyzes the 4e(-) oxidation of myo-inositol (MI) to D-glucuronate using a substrate act

216 A) and N-acetylaspartylglutamate (NAAG), and myo-inositol (MI), an osmolyte linked to Alzheimer disea

217 mpounds, creatine-containing compounds (Cr), myo-inositol (mI), and glutamate (Glu) levels in the ant

218 partate (NAA), choline (Cho), creatine (Cr), myo-inositol (mI), and glutamine plus glutamate (Glx) in

219 se in the levels of N-acetylaspartate (NAA), myo-inositol (mI), scyllo-inositol (sI), glycine, taurin

220 ntrations of total N-acetylaspartate (tNAA), myo-inositol (mI), total choline-containing compounds (t

221 used to measure N-Acetyl-aspartate (NAA) and myo-inositol (mI).

222 ated with scaling and root planing (SRP) and myo-inositol (MI).

223 dle than the younger group were observed for myo-inositol (mIns) in DLPFC and hippocampus and total c

224 The separation of myo-inositol mono-, di-, tri-, tetra-, pentakis-, and he

225 essential biomolecule that is synthesized by myo-inositol monophosphatase (IMPase) from inositol mono

226 st abundant transcript in axons was mRNA for myo-inositol monophosphatase-1 (Impa1), a key enzyme tha

227 nown previously in prokaryotes and resembles myo-inositol monophosphatases (IMPases).

228 in a beta-bulge that is conserved in related myo-inositol monophosphatases.

229 lute concentrations of glutamate, glutamine, myo-inositol, NAA, creatine and choline.

230 After adjustment for N-acetyl-aspartate:myo-inositol, none of the other variables differed signi

231 ese data show the following: the increase in myo-inositol occurs before the decrease in NAA in hippoc

232 ays, by feeding cells with either [(13)C(6)]-myo-inositol or [(13)C(6)]-D-glucose.

233 -expression, in the absence of extracellular myo-inositol or other SMIT1 substrates, on fundamental f

234 tate, alanine, glycerol 3-phosphate, malate, myo-inositol, or stearic acid tissue concentrations were

235 Reductive cleavage of myo-inositol orthoformate to the corresponding 1,3-aceta

236 myo-Inositol oxygenase (MIOX) catalyzes the 4e(-) oxidat

237 However, myo-inositol oxygenase (MIOX) exemplifies a second, very

238 verexpression of the proximal tubular enzyme myo-inositol oxygenase (MIOX) induces oxidant stress in

239 Conceivably, upregulation of myo-inositol oxygenase (MIOX) is associated with altered

240 The catabolic enzyme myo-inositol oxygenase (MIOX) is expressed in proximal t

241 Myo-inositol oxygenase (MIOX), a tubular-specific enzyme

242 se phosphorylase (OsGGP) by 80%, while KO of myo-inositol oxygenase (OsMIOX) did not affect foliar As

243 Renal-specific oxidoreductase/myo-inositol oxygenase (RSOR/MIOX) catabolizes myo-inosi

244 s methods and was also applied to assays for myo-inositol oxygenase activity.

245 r to the carbon-carbon bond cleaving enzyme, myo-inositol-oxygenase.

246 Inositol pyrophosphates, such as diphospho-myo-inositol pentakisphosphates (InsP7), are an importan

247 mutants of protein-tyrosine phosphatase-like myo-inositol phosphatases (PTPLPs) from the non-pathogen

248 f the InoEFGK (TM0418-TM0421) transporter to myo-inositol-phosphate suggests that the novel pathway i

249 1-L-myo-inositol-phosphate synthase (mIPS) catalyzes the fir

250 The analysis of myo-inositol phosphates (InsPs) and myo-inositol pyropho

251 myo-Inositol phosphates (IPs) are important bioactive mo

252 Diphospho-myo-inositol phosphates (PP-InsP(y)) are an important cl

253 nd PimB' (MSMEG_4253) recognize phosphatidyl-myo-inositol (PI) as a lipid acceptor, PimA specifically

254 ite for the acceptor substrate, phosphatidyl-myo-inositol (PI).

255 T cells by the hexamannosylated phosphatidyl-myo-inositol (PIM(6)), a family of mycobacterial antigen

256 gates the thermal behavior of alpha and beta myo-inositol polymorphs.

257 se structures provide the first glimpse of a myo-inositol polyphosphatase-ligand complex consistent w

258 The myo-inositol polyphosphate 5-phosphatases (5PTases) (E.C

259 By labeling the endogenous myo-inositol pool in 5ptase11 mutants, we correlated the

260 d enantiomer of racemic 1,2-O-isopropylidene-myo-inositols possessing chemically and sterically diver

261 t affects desymmetrization of an appropriate myo-inositol precursor.

262 equired for potentiation of SMIT activity by myo-inositol preincubation.

263 clusively affords the corresponding 2-O-acyl myo-inositol products via a 1,2-bridged five-membered ri

264 lysis of myo-inositol phosphates (InsPs) and myo-inositol pyrophosphates (PP-InsPs) is a daunting cha

265 Motor cortex total N-acetylaspartate to myo-inositol ratio (tNAA:mIns) significantly declined in

266 served was that between N-acetylaspartate-to-myo-inositol ratio and Braak stage (R(N)(2) = 0.47, P <

267 The N-acetylaspartate-to-myo-inositol ratio proved to be the strongest predictor

268 oftware (PROBE-Q) and the N-acetyl-aspartate:myo-inositol ratio was derived.

269 Hypocitraturia and elevated urinary myo-inositol remained associated with active disease, wi

270 r of a Manp residue to the 2-position of the myo-inositol ring of PI, whereas PimB' exclusively trans

271 osphorylated IP binding differed in both the myo-inositol ring position and orientation when compared

272 lly binds to negatively charged phosphatidyl-myo-inositol substrate and non-substrate membrane model

273 Na(+)/myo-inositol cotransporter (SMIT1) and myo-inositol supplementation enlarged intracellular PI(4

274 suggested that PI(4)P levels increased after myo-inositol supplementation with SMIT1 expression.

275 tracellular stores also were augmented after myo-inositol supplementation.

276 ere validated by rescuing the phenotype with myo-inositol supplemented media during differentiation o

277 hate or is provided from the environment via myo-inositol symporters.

278 ults reveal critical roles for intracellular myo-inositol synthesis in craniofacial development and t

279 Concentrations of neurochemicals choline and myo-inositol that were higher pretransplant compared wit

280 myo-Inositol, the precursor of all inositol compounds, h

281 ible to determine the transition lifetime of myo-inositol to occur 5% of solid-solid transition at 20

282 ndex of neuronal integrity, and increases in myo-inositol-to-creatine ratio were associated with high

283 In contrast, myo-inositol (transported through SMIT1) reproduced the

284 of the M813 receptor murine sodium-dependent myo-inositol transporter 1 (mSMIT1) allowed previously n

285 This demonstrates the presence of a myo-inositol transporter and a kinase that generates 1L-

286 ther with the unexpected localization of the myo-inositol transporter in both the plasma membrane and

287 Down-regulation of the myo-inositol transporter using RNA interference inhibite

288 e transported into cells by sodium-dependent myo-inositol transporters (SMITs).

289 ium-dependent solute transporters, including myo-inositol transporters SMIT1 and SMIT2, potentially f

290 myo-Inositol trispyrophosphate (ITPP) is a recently iden

291 iation of KCNQ2/3 currents by SMIT1-mediated myo-inositol uptake, suggesting close channel-transporte

292 r more phosphates from highly phosphorylated myo-inositols via a relatively ordered pathway.

293 ct standard deviation for N-acetyl-aspartate:myo-inositol was 0% for controls and 3.5%/year for patie

294 Myo-inositol was also moderately predictive.

295 The putative gliosis marker myo-inositol was higher than controls in the vermis and

296 5-Azido-5-deoxy-d-myo-inositol was inaccessible due to an unusual beta-eli

297 t frontal gyri (19 voxels, CCLAV = 0.05) and myo-inositol was reduced in the left cerebellum (34 voxe

298 tegy, 3-azido-3-deoxy- and 4-azido-4-deoxy-d-myo-inositol were efficiently synthesized.

299 line and sphingomyelin with inflammation and myo-inositol with cellular proliferation.

300 ion of 2,3,6-O-tribenzyl- and 2,6-O-dibenzyl-myo-inositols with beta-primary, secondary, and tertiary