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1 fects in homozygotes were rescued by dietary myo-inositol.
2 at the IatP-IatA transporter is specific for myo-inositol.
3 of glycerophosphocholine (GPC), taurine, and myo-inositol.
4 -fold while completely abolishing binding to myo-inositol.
5 een achieved starting from readily available myo-inositol.
6 but their expression was strongly induced by myo-inositol.
7 and transportation of food that contains the myo-inositol.
8 pathway leading from glucose 6-phosphate via myo-inositol.
9 -acetamido-2-deoxy-alpha-D-glucopyranosyl)-D-myo-inositol.
10 n compatible osmolytes, betaine, taurine and myo-inositol.
11 r (MDD) is reduced cerebral concentration of myo-Inositol.
12 -di-O-triisopropylsilyl-1,2-O-isopropylidene-myo-inositol.
13 s found to share similarities with that of a myo-inositol 1 phosphate synthase mutant that is also se
16 d highly specific PDK1 inhibitor, 2-O-benzyl-myo-inositol 1,3,4,5,6-pentakisphosphate (2-O-Bn-InsP5),
17 tudies showed that the K(m) for ZmIPK1 using myo-inositol 1,3,4,5,6-pentakisphosphate as a substrate
18 he ZmIPK1 enzyme catalyzes the conversion of myo-inositol 1,3,4,5,6-pentakisphosphate to phytic acid.
19 yl inositol 1,3,4,5,6-pentakisphosphates and myo-inositol 1,3,4,5,6-pentakisphosphate with biological
21 n acid mediated hydrolysis of enol ethers of myo-inositol 1,3,5-orthoesters giving a synthetically ve
23 erentiate the enantiotopic hydroxy groups of myo-inositol 1,3,5-orthoformate in the presence of a chi
24 d via Yb(OTf)3-catalyzed desymmetrization of myo-inositol 1,3,5-orthoformate using a proline-based ch
25 ylation of myo-inositol 1,4,6-trisphosphate, myo-inositol 1,4,5,6-tetrakisphosphate, and myo-inositol
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 pase C products, namely diacylglycerol and d-myo-inositol 1,4,5-trisphosphate, were identified as pro
30 A variety of inositol phosphates including myo-inositol 1,4,5-trisphosphate, which is a secondary m
31 e of large cholangiocytes by activation of D-myo-inositol 1,4,5-trisphosphate/Ca(2+) /calmodulin-depe
32 ndicates that the phosphorylation product of myo-inositol 1,4,6-trisphosphate is inositol 1,2,4,6-tet
33 capable of catalyzing the phosphorylation of myo-inositol 1,4,6-trisphosphate, myo-inositol 1,4,5,6-t
34 magnitude greater than those determined for myo-inositol 1-phosphate (IMP) and fructose 1,6-bisphosp
35 novel insights into the architecture of the myo-inositol 1-phosphate binding site and the involvemen
37 activity was obtained with myo-inositol, 1D-myo-inositol 1-phosphate, or myo-inositol 2-phosphate as
40 ermined complex structure in the presence of myo-inositol-1,2,3,4,5,6-hexakisphosphate (InsP6 or phyt
41 degradation of adenosine-5'-triphosphate and myo-inositol-1,2,3,4,5,6-hexakisphosphate by (31)P NMR.
42 , by both cyclic AMP/protein kinase A- and D-myo-inositol-1,4,5-thriphosphate/Ca(2+)-dependent pathwa
43 renergic agonist stimulating intracellular D-myo-inositol-1,4,5-triphosphate (IP(3) )/Ca(2+) levels,
44 nnosylated GPI intermediate D-GlcNalpha1-6-D-myo-inositol-1-HPO4-sn-lipid precedes mannosylation.
45 cosamine from UDP-N-acetylglucosamine to 1-L-myo-inositol-1-phosphate in the first committed step of
48 de occurrence in all eukaryotes, the role of myo-inositol-1-phosphate synthase and de novo inositol b
49 ulation of tobacco Alternative oxidase1a and Myo-inositol-1-phosphate synthase in PsAP2 overexpressin
51 gidus transcripts indicates that neither the myo-inositol-1-phosphate synthase, the first step in ino
52 philic attack of the 3-hydroxyl group of 1-L-myo-inositol-1-phosphate while at the same time promotin
54 inorganic phosphate from HOLP but not from d-myo-inositol-1-phosphate, the main substrate of IMPases.
60 ssential inositol tetraphosphate molecule--D-myo-inositol-(1,4,5,6)-tetrakisphosphate (Ins(1,4,5,6)P(
61 mc(2)155, little activity was obtained with myo-inositol, 1D-myo-inositol 1-phosphate, or myo-inosit
62 in the determination of the conformation of myo-inositol 2-monophosphate (Ins(2)P1), a member of the
63 yo-inositol, 1D-myo-inositol 1-phosphate, or myo-inositol 2-phosphate as the N-acetylglucosamine acce
64 e (11% lower, P < 0.001), N-acetyl-aspartate:myo-inositol (24% lower, P < 0.001), and myo-inositol:cr
65 o find alternative molecules and predicted d-myo-inositol 3,4,5,6-tetrakisphosphate (TMI) to strongly
67 ly expressing an antisense gene sequence for myo-inositol 3-phosphate synthase (IPS, catalysing the f
68 (2-acetamido-2-deoxy-alpha-glucopyranosyl)-D-myo-inositol 3-phosphate to produce 1-O-(2-acetamido-2-d
70 irst time that GSK-3 is required for optimal myo-inositol-3 phosphate synthase activity and de novo i
72 e inhibited activity of both yeast and human myo-inositol-3 phosphate synthase, the rate-limiting enz
74 t is synthesized from glucose 6-phosphate by myo-inositol-3-phosphate synthase (IP synthase), a homot
76 o the structures reported for the GlcNAc-1-d-myo-inositol-3-phosphate synthase (MshA) apo and ternary
77 proate (VPA) depletes inositol by inhibiting myo-inositol-3-phosphate synthase, the enzyme that catal
79 isomerization of glucose 6-phosphate to 1-D-myo-inositol-3-phosphate, catalysed by a 1-D-myo-inosito
81 olysis of caged IP3/GPIP2 (glycerophosphoryl-myo-inositol 4,5-bisphosphate) places the voltage sensor
83 ), creatine (a marker of energy metabolism), myo-inositol (a marker of glial cells), and N-acetylaspa
85 bpA with these mutant alleles unable to bind myo-inositol abolishes C. crescentus growth in medium co
87 bisphosphate (PIP2), which is generated from myo-inositol, an osmolyte transported into cells by sodi
88 and diesters of 1,2:5,6-di-O-isopropylidene-myo-inositol and 1,2:5,6-di-O-cyclohexylidene-myo-inosit
89 r using RNA interference inhibited uptake of myo-inositol and blocked the synthesis of the myo-inosit
90 es of increased Glutamate/glutamine, reduced myo-inositol and choline are hyperammonemia-associated a
92 rations characteristic of AD (i.e. increased myo-inositol and decreased N-acetylaspartate (NAA)).
95 changes are associated with altered cortical myo-inositol and glycine levels, suggesting sleep loss-i
96 o-inositol oxygenase (RSOR/MIOX) catabolizes myo-inositol and is implicated in the pathogenesis of di
99 amino acid accumulation and the synthesis of myo-inositol and raffinose during plant adaptation to lo
101 is a distinction between de novo synthesized myo-inositol and that from the extracellular environment
102 r concentrations of N-acetylaspartate (NAA), myo-inositol, and glutamate as measured by magnetic reso
104 l and glial compartments: N-acetylaspartate, myo-inositol, and glutamate/glutamine, were quantified b
107 ile gs was related to sugars, organic acids, myo-inositol, and shikimate, gm showed a more complex pa
108 ps from the cheap and commercially available myo-inositol, and this common intermediate has been used
109 ol monophosphatase (IMPase), which generates myo-inositol, are significantly upregulated upon thermal
113 f Y247S/Y251S in the absence and presence of myo-inositol as well as Y246S/Y247S/Y248S/Y251S indicate
117 -peptidoglycan complex, and the phosphatidyl-myo-inositol-based lipoglycans are key features of the m
118 -acetamido-2-deoxy-alpha-D-glucopyranosyl)-D-myo-inositol, but its substrates and immediate products
119 ng protein (PBP) IbpA mediates the uptake of myo-inositol by the IatP-IatA ATP-binding cassette trans
120 o show for the first time that extracellular myo-inositol can in fact be used in GPI formation althou
121 These findings, coupled with the fact the myo-inositol can serve as a sole carbon source for growt
122 sociated with active disease, with the urine myo-inositol:citrate ratio being tightly correlated with
123 tes (L-serine, L-leucine, glucose, fructose, myo-inositol, citric acid and 2, 3-hydroxypropanoic acid
124 major depressive episode had lower levels of myo-Inositol compared with schizophrenia patients withou
126 higher ratio of glutamate plus glutamine to myo-inositol-containing compounds than children with ADH
128 yo-inositol and blocked the synthesis of the myo-inositol-containing phospholipids, phosphatidylinosi
129 We found that overexpression of the Na(+)/myo-inositol cotransporter (SMIT1) and myo-inositol supp
130 Higher concentrations of glutamate, taurine, myo-inositol, creatine and inosine were present in aqueo
131 n metabolites, including N-acetyl-aspartate, myo-inositol, creatine/phosphocreatine and choline-conta
132 ad significantly higher choline/creatine and myo-inositol/creatine ratios than APOE E3 homozygotes.
134 ging normal population, choline/creatine and myo-inositol/creatine ratios were significantly increase
137 ate:myo-inositol (24% lower, P < 0.001), and myo-inositol:creatine/phosphocreatine (17% higher, P < 0
138 ning compounds:creatine/phosphocreatine, and myo-inositol:creatine/phosphocreatine were measured usin
139 d for the downregulation of the idhA-encoded myo-inositol dehydrogenase activity in the presence and
140 a starts as the conventional route using the myo-inositol dehydrogenase IolG followed by three novel
143 step to generate a suitably protected chiral myo-inositol derivatives is described here as a unified
144 h as channel regulation by SMIT-transported, myo-inositol-derived phosphatidylinositol 4,5-bisphospha
146 while syntheses of triacylated-phosphatidyl-myo-inositol dimannoside (Ac(1)PIM(2)) and Man(1)GlcAGro
147 novo synthesis was responsible for supplying myo-inositol for phosphatidylinositol (PI) destined for
148 The optimised method within 20min separated myo-inositol, galactinol, glucose, fructose, sucrose, ra
150 here-like self-exclusion; urea, taurine, and myo-inositol have a tendency toward self-association; so
151 ntains a monoester phosphate attached to its myo-inositol headgroup, also supported enhanced enzymati
156 This Bifidobacterium strain contributed to myo-inositol hexakisphosphate (phytate) hydrolysis, resu
159 ne, total choline, glycerophosphorylcholine, myo-inositol, imidazole, uridine diphosphate glucose, is
165 rticipants, acute oral ebselen reduced brain myo-inositol in the anterior cingulate cortex, consisten
166 ice at 6 months of age showed an increase in myo-inositol in the hippocampus at a time when the Abeta
167 05), and pons (P < .01) and higher levels of myo-inositol in the motor cortex (P < .001) and subcorti
168 -(11Z-octadecenoyl)-sn-glycero-3-phospho-(1'-myo-inositol), in which the sn-1 position contains an et
170 in Escherichia coli, resulting in titers of myo-inositol increased 5.5-fold and titers of glucaric a
173 phocreatinine, choline-containing compounds, myo-inositol (Ins) and glutamate+glutamine (Glx) were de
175 ty is essential for the de novo synthesis of myo-Inositol (Ins), and for recycling of Ins in Ins(1,4,
177 ible osmolytes such as betaine, taurine, and myo-inositol is a protective response shared by all euka
184 e nine 1,2,3,4,5,6-cyclohexanehexol isomers, myo-inositol is pre-eminent, with "other" inositols (cis
185 ing sickness and nagana in domestic animals, myo-inositol is taken up via a specific proton-coupled e
188 It also showed that the de novo synthesized myo-inositol is utilized to form PI, which is preferenti
191 n magnetic resonance spectroscopy to examine myo-Inositol levels in the anterior cingulate cortex (AC
193 Thus, MIPS1 has a significant impact on myo-inositol levels that is critical for maintaining lev
195 et positioned between the lobes contains the myo-inositol ligand, which binds with submicromolar affi
196 ) (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
198 tes the biosynthetic pathway of phosphatidyl-myo-inositol mannoside, lipomannan, and lipoarabinomanna
200 ope is highly mannosylated with phosphatidyl-myo-inositol mannosides (PIMs), lipomannan, and mannose-
201 involved in the biosynthesis of phosphatidyl-myo-inositol mannosides (PIMs), which are key components
203 arked reduction of higher order phosphatidyl-myo-inositol mannosides and the presence of dimycocerosa
204 ManLAM and reduced higher order phosphatidyl-myo-inositol mannosides in strains HN885 and HN1554 resu
205 e is stimulated in part through phosphatidyl-myo-inositol mannosides that are present in the cell wal
206 tes the biosynthetic pathway of phosphatidyl-myo-inositol mannosides, lipomannan, and lipoarabinomann
211 d brain myo-Inositol is associated with MDD, myo-Inositol may be a biochemical marker of depressive m
213 red with controls only in N-acetyl-aspartate:myo-inositol (mean: 3.6%/year; 95% confidence interval:
214 ce interval: 0.9-3.5) and N-acetyl-aspartate:myo-inositol (mean: 3.7%/year; 95% confidence interval:
216 show a new thermal event associated to beta myo-inositol melting at 221.43 degrees C, suggesting tha
218 Baseline N-acetylaspartate (NAA) level, myo-inositol (mI) in normal-appearing white and gray mat
221 nase (MIOX) catalyzes the 4e(-) oxidation of myo-inositol (MI) to D-glucuronate using a substrate act
222 e (MIOX) catalyzes the oxidative cleavage of myo-inositol (MI) to give d-glucuronic acid, a committed
223 A) and N-acetylaspartylglutamate (NAAG), and myo-inositol (MI), an osmolyte linked to Alzheimer disea
224 mpounds, creatine-containing compounds (Cr), myo-inositol (mI), and glutamate (Glu) levels in the ant
225 partate (NAA), choline (Cho), creatine (Cr), myo-inositol (mI), and glutamine plus glutamate (Glx) in
226 ctor and its interaction with the substrate, myo-inositol (MI), have been probed by electron paramagn
229 cyclohexan-(1,2,3,4,5,6-hexa)-ol substrate [myo-inositol (MI)] by four electrons to d-glucuronate.
232 essential biomolecule that is synthesized by myo-inositol monophosphatase (IMPase) from inositol mono
233 st abundant transcript in axons was mRNA for myo-inositol monophosphatase-1 (Impa1), a key enzyme tha
237 After adjustment for N-acetyl-aspartate:myo-inositol, none of the other variables differed signi
238 ese data show the following: the increase in myo-inositol occurs before the decrease in NAA in hippoc
239 -expression, in the absence of extracellular myo-inositol or other SMIT1 substrates, on fundamental f
240 tate, alanine, glycerol 3-phosphate, malate, myo-inositol, or stearic acid tissue concentrations were
247 verexpression of the proximal tubular enzyme myo-inositol oxygenase (MIOX) induces oxidant stress in
251 se phosphorylase (OsGGP) by 80%, while KO of myo-inositol oxygenase (OsMIOX) did not affect foliar As
255 Inositol pyrophosphates, such as diphospho-myo-inositol pentakisphosphates (InsP7), are an importan
256 mutants of protein-tyrosine phosphatase-like myo-inositol phosphatases (PTPLPs) from the non-pathogen
257 f the InoEFGK (TM0418-TM0421) transporter to myo-inositol-phosphate suggests that the novel pathway i
261 nd PimB' (MSMEG_4253) recognize phosphatidyl-myo-inositol (PI) as a lipid acceptor, PimA specifically
263 T cells by the hexamannosylated phosphatidyl-myo-inositol (PIM(6)), a family of mycobacterial antigen
265 se structures provide the first glimpse of a myo-inositol polyphosphatase-ligand complex consistent w
268 d enantiomer of racemic 1,2-O-isopropylidene-myo-inositols possessing chemically and sterically diver
271 clusively affords the corresponding 2-O-acyl myo-inositol products via a 1,2-bridged five-membered ri
272 served was that between N-acetylaspartate-to-myo-inositol ratio and Braak stage (R(N)(2) = 0.47, P <
276 r of a Manp residue to the 2-position of the myo-inositol ring of PI, whereas PimB' exclusively trans
277 osphorylated IP binding differed in both the myo-inositol ring position and orientation when compared
278 lly binds to negatively charged phosphatidyl-myo-inositol substrate and non-substrate membrane model
279 Na(+)/myo-inositol cotransporter (SMIT1) and myo-inositol supplementation enlarged intracellular PI(4
280 suggested that PI(4)P levels increased after myo-inositol supplementation with SMIT1 expression.
283 ults reveal critical roles for intracellular myo-inositol synthesis in craniofacial development and t
285 ible to determine the transition lifetime of myo-inositol to occur 5% of solid-solid transition at 20
286 ndex of neuronal integrity, and increases in myo-inositol-to-creatine ratio were associated with high
288 of the M813 receptor murine sodium-dependent myo-inositol transporter 1 (mSMIT1) allowed previously n
290 ther with the unexpected localization of the myo-inositol transporter in both the plasma membrane and
293 ium-dependent solute transporters, including myo-inositol transporters SMIT1 and SMIT2, potentially f
295 iation of KCNQ2/3 currents by SMIT1-mediated myo-inositol uptake, suggesting close channel-transporte
297 ct standard deviation for N-acetyl-aspartate:myo-inositol was 0% for controls and 3.5%/year for patie
301 ion of 2,3,6-O-tribenzyl- and 2,6-O-dibenzyl-myo-inositols with beta-primary, secondary, and tertiary
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