1d-1-O-tert-Butyl-diphenyl-silyl-2,3,6-O-tris-(meth-oxy-methyl-ene)-myo-inositol 4,5-bis-(dibenzyl-phosphate).
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ABSTRACT:
SUBMITTER: Anderson RJ
PROVIDER: S-EPMC3297945 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:IN THE TITLE COMPOUND [SYSTEMATIC NAME: (tert-butyl-dimethyl-silyl)methane-triyl tris-(4-methyl-benzene-sulfonate)], C(32)H(44)O(10)S(3)Si, the central C atom and the Si(IV) center are in a tetra-hedral configuration. The inter-planar angles between pairs of the three benzene rings of the 4-methyl-phenyl-sulfonyl units are 41.15?(10), 18.11?(10) and 44.09?(10)°. C-H?? inter-actions are observed in the crystal structure. Mol-ecules are linked into screw chains along the b axis by weak C-H?O inter-actions. Weak intramolecular C-H?O hydrogen bonds are also present.
| S-EPMC2962104 | biostudies-literature
Project description:The title centrosymmetric mol-ecule, C(46)H(42)Si(2), is composed of a central benzene ring with buta-1,3-diynyl chains at positions 1 and 4. These chains are terminated by tert-butyl-diphenyl-silyl groups, hence the molecule is dumbbell in shape. The mol-ecules are connected via C-H?? inter-actions in the structure, so forming an undulating two-dimensional network in the bc plane. There is also a weak ?-? inter-action involving centrosymmetrically related phenyl rings with a centroid-centroid distance of 3.8359?(11)?Å.
| S-EPMC2983810 | biostudies-other
Project description:Dephosphorylation of 1D-myo-inositol 1,4-bisphosphate [Ins(1,4)P2] in rat liver is catalysed by a cytosolic phosphatase that removes the 1-phosphate group. The Km for Ins(1,4)P2 is approx. 17 microM. Li+ (100 mM) causes 50% inhibition of Ins(1,4)P2 phosphatase activity when activity is measured at the very low substrate concentration of 10 nM, but on raising the substrate concentration to 100 microM there is a greater than 10-fold increase in sensitivity to Li+, suggesting that Li+ acts mainly, but not entirely, as an uncompetitive inhibitor of Ins(1,4)P2 phosphatase. In addition, rat liver cytosol shows Li+-sensitive phosphatase activity against 1D-myo-inositol 1-,3- and 4-monophosphates. The Ins(1,4)P2 1-phosphatase and inositol monophosphatase activities all share an apparent Mr of 47 x 10(3), as determined by gel-filtration chromatography. However, the Ins(1,4)P2 1-phosphatase is more sensitive to inactivation by heat, and can be separated from inositol monophosphatase activity by anion-exchange chromatography. We conclude that rat liver cytosol contains an Ins(1,4)P2 1-phosphatase that is distinct from, but in many ways similar to, inositol monophosphatase.
| S-EPMC1135135 | biostudies-other
Project description:BACKGROUNDMyo-inositol (MI), successfully used in polycystic ovary syndrome (PCOS), was administered with ?-LA to exploit its action of favouring the passage of other molecules through biological barriers, and also considering its anti-inflammatory effect.METHODSPCOS patients, according to the Rotterdam ESHRE-ASRM criteria, with anovulation and infertility >?1 year, were included in this open and prospective study. The preliminary phase was aimed at determining a set of MI-resistant PCOS patients. This treatment involved 2 g MI, taken twice per day by oral route, for three months. The Homeostasis Model Assessment (HOMA) index and MI plasma levels were measured. In the main phase, previously selected MI-resistant patients received the same daily amount of MI plus 50 mg ?-LA twice a day, for a further three months. Ovulation was assessed using ultrasound examination on days 12, 14 and 20 of the cycle. The HOMA index, lipid, hormone and MI plasma levels were detected at baseline and at the end of this phase.RESULTSThirty-seven anovulatory PCOS subjects were included in the study. Following MI treatment, 23 of the 37 women (62%) ovulated, while 14 (38%) were resistant and did not ovulate. In the latter group, MI plasma levels did not increase. These MI-resistant patients underwent treatment in the main phase of the study, receiving MI and ?-LA. After this combined treatment, 12 (86%) of them ovulated. Their MI plasma levels were found to be significantly higher than at baseline; also, a hormone and lipid profile improvement was recorded.CONCLUSIONThe combination of MI with ?-LA allowed us to obtain significant progress in the treatment of PCOS MI-resistant patients. Therefore, this new formulation was able to re-establish ovulation, greatly increasing the chances of desired pregnancy.TRIAL REGISTRATIONClinical trial registration number: NCT03422289 ( ClinicalTrials.gov registry).
| S-EPMC5944130 | biostudies-literature
Project description:In the title compound, C(15)H(26)O(6)Si, the dioxa six-membered ring bonded to the myo-inositol skeleton is in a boat conformation while the rest of the six-membered rings adopt chair conformations.
| S-EPMC3006906 | biostudies-other
Project description:The mol-ecule of the title compound, C(22)H(26)Si(2), is centrosymmetric. The dihedral angle between the central benzene ring and its phenyl substituents is 67.7?(2)°. The crystal packing is stabilized by van der Waals forces.
| S-EPMC2983822 | biostudies-literature
Project description:AIM:To assess dietary myo-inositol in reducing stem cell activation in colitis, and validate p?-cateninS552 as a biomarker of recurrent dysplasia. METHODS:We examined the effects of dietary myo-inositol treatment on inflammation, p?-cateninS552 and pAkt levels by histology and western blot in IL-10-/- and dextran sodium sulfate-treated colitic mice. Additionally, we assessed nuclear p?-cateninS552 in patients treated with myo-inositol in a clinical trial, and in patients with and without a history of colitis-induced dysplasia. RESULTS:In mice, p?-cateninS552 staining faithfully reported the effects of myo-inositol in reducing inflammation and intestinal stem cell activation. In a pilot clinical trial of myo-inositol administration in patients with a history of low grade dysplasia (LGD), two patients had reduced numbers of intestinal stem cell activation compared to the placebo control patient. In humans, p?-cateninS552 staining discriminated ulcerative colitis patients with a history of LGD from those with benign disease. CONCLUSION:Enumerating crypts with increased numbers of p?-cateninS552 - positive cells can be utilized as a biomarker in colitis-associated cancer chemoprevention trials.
| S-EPMC5537179 | biostudies-literature
Project description:The enzyme myo-inositol oxygenase is the key enzyme of a pathway leading from myo-inositol to UDP-glucuronic acid. In Arabidopsis, myo-inositol oxygenase is encoded by four genes. All genes are strongly expressed in syncytia induced by the beet cyst nematode Heterodera schachtii in Arabidopsis roots. Here, we studied the effect of a quadruple myo-inositol oxygenase mutant on nematode development. We performed metabolite profiling of syncytia induced in roots of the myo-inositol oxygenase quadruple mutant. The role of galactinol in syncytia was studied using Arabidopsis lines with elevated galactinol levels and by supplying galactinol to wild-type seedlings. The quadruple myo-inositol oxygenase mutant showed a significant reduction in susceptibility to H. schachtii, and syncytia had elevated myo-inositol and galactinol levels and an elevated expression level of the antimicrobial thionin gene Thi2.1. This reduction in susceptibility could also be achieved by exogenous application of galactinol to wild-type seedlings. The primary function of myo-inositol oxygenase for syncytium development is probably not the production of UDP-glucuronic acid as a precursor for cell wall polysaccharides, but the reduction of myo-inositol levels and thereby a reduction in the galactinol level to avoid the induction of defence-related genes.
| S-EPMC4285123 | biostudies-literature
Project description:Myo-inositol is a ubiquitous metabolite of plants. It is synthesized by a highly conserved enzyme L-myo-inositol phosphate synthase (MIPS; EC 5.5.1.4). Myo-inositol is well characterized during abiotic stress tolerance but its role during growth and development is unclear. In this study, we demonstrate that the apical hook maintenance and hypocotyl growth depend on myo-inositol. We discovered the myo-inositol role during hook formation and its maintenance via ethylene pathway in Arabidopsis by supplementation assays and qPCR. Our results suggest an essential requirement of myo-inositol for mediating the ethylene response and its interaction with brassinosteroid to regulate the skotomorphogenesis. A model is proposed outlining how MIPS regulates apical hook formation and hypocotyl growth.
| S-EPMC7567114 | biostudies-literature
Project description:Growth of Salmonella enterica serovar Typhimurium strain 14028 with myo-inositol (MI) as the sole carbon and energy source is characterized by a bistable phenotype that manifests in a growth phenotype with an extraordinarily long and length-variable lag phase. However, in the presence of hydrogen carbonate, in the absence of IolR that represses the MI degradation pathway, or if cells are already adapted to minimal medium (MM) with MI, the lag phase is drastically shortened, and the bistable phenotype is abolished. We hypothesized that memory development or hysteresis is a further characteristic of MI degradation by S. Typhimurium; therefore, we investigated the transition from a short to a long lag phase in more detail. Growth experiments demonstrated that memory on the population level is successively lost within approximately 8 hr after cells, which had been adapted to MI utilization, were transferred to lysogeny broth (LB) medium. Flow cytometry (FC) analysis using a chromosomal fusion to PiolE , a promoter controlling the expression of the enzymatic genes iolE and iolG involved in MI degradation, indicated a gradual reversion within a few hours from a population in the "ON" status with respect to iolE transcription to one that is mainly in the "OFF" status. Growth and FC experiments revealed that IolR does not affect hysteresis.
| S-EPMC5387303 | biostudies-literature