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Journal articles on the topic 'Inositol derive'

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Published: 4 June 2021

Last updated: 12 February 2022

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1

López-Gambero, Antonio J., Carlos Sanjuan, Pedro Jesús Serrano-Castro, Juan Suárez, and Fernando Rodríguez de Fonseca. "The Biomedical Uses of Inositols: A Nutraceutical Approach to Metabolic Dysfunction in Aging and Neurodegenerative Diseases." Biomedicines 8, no. 9 (2020): 295. http://dx.doi.org/10.3390/biomedicines8090295.

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Inositols are sugar-like compounds that are widely distributed in nature and are a part of membrane molecules, participating as second messengers in several cell-signaling processes. Isolation and characterization of inositol phosphoglycans containing myo- or d-chiro-inositol have been milestones for understanding the physiological regulation of insulin signaling. Other functions of inositols have been derived from the existence of multiple stereoisomers, which may confer antioxidant properties. In the brain, fluctuation of inositols in extracellular and intracellular compartments regulates ne

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2

Chattopadhyay, Ansuman, та Graham Carpenter. "PLC-γ1 is required for IGF-I protection from cell death induced by loss of extracellular matrix adhesion". Journal of Cell Science 115, № 10 (2002): 2233–39. http://dx.doi.org/10.1242/jcs.115.10.2233.

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Phospholipase C-γ1, a tyrosine kinase substrate, hydrolyses phosphatidylinositol 4,5-bisphosphate to produce inositol 1,4,5-trisphosphate and diacylglycerol, which act as second messenger moleculesto mobilize intracellular calcium and activate protein kinase C, respectively. We have investigated the role of phospholipase C-γ1 in anoikis, or cell death,induced by the loss of extracellular matrix adhesion. Spontaneously immortalized mouse embryonic fibroblasts nullizygous at the Plcg1locus (Plcg1-/-), referred to as Null cells, were derived from targeted gene disruption experiments. Subsequently

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3

Li, Xingyao, Chunfang Gu, Sarah Hostachy, et al. "Control of XPR1-dependent cellular phosphate efflux by InsP8 is an exemplar for functionally-exclusive inositol pyrophosphate signaling." Proceedings of the National Academy of Sciences 117, no. 7 (2020): 3568–74. http://dx.doi.org/10.1073/pnas.1908830117.

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Homeostasis of cellular fluxes of inorganic phosphate (Pi) supervises its structural roles in bones and teeth, its pervasive regulation of cellular metabolism, and its functionalization of numerous organic compounds. Cellular Pi efflux is heavily reliant on Xenotropic and Polytropic Retrovirus Receptor 1 (XPR1), regulation of which is largely unknown. We demonstrate specificity of XPR1 regulation by a comparatively uncharacterized member of the inositol pyrophosphate (PP-InsP) signaling family: 1,5-bis-diphosphoinositol 2,3,4,6-tetrakisphosphate (InsP8). XPR1-mediated Pi efflux was inhibited b

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4

Christophe, J. "Pancreatic tumoral cell line AR42J: an amphicrine model." American Journal of Physiology-Gastrointestinal and Liver Physiology 266, no. 6 (1994): G963—G971. http://dx.doi.org/10.1152/ajpgi.1994.266.6.g963.

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AR42J cells derive from azaserine-induced malignant nodules from the rat pancreas. They differ from normal acinar cells for at least three reasons: 1) they proliferate rapidly; 2) they synthesize, store, and secrete digestive enzymes but the regulation of their exocrine function is abnormal, from the emergence of atypical receptors (e.g., cholecystokinin octapeptide type B and pituitary adenylate cyclase-activating polypeptide type I receptors) to unusual inositol phosphate metabolism and cytoskeleton disorganization; and 3) they possess an added neuroendocrine-regulated pathway characterized

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5

Lin, Xiaobo, Lina Ma, Chaya Gopalan, and Richard E. Ostlund. "d-chiro-Inositol is absorbed but not synthesised in rodents." British Journal of Nutrition 102, no. 10 (2009): 1426–34. http://dx.doi.org/10.1017/s0007114509990456.

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d-chiro-inositol (DCI) and pinitol (1d-3-O-methyl-chiro-inositol) are distinctive inositols reported to possess insulin-mimetic properties. DCI-containing compounds are abundant in common laboratory animal feed. By GC–MS of 6 m-HCl hydrolysates, Purina Laboratory Rodent Diet 5001 (diet 5001) contained 0·23 % total DCI by weight with most found in the lucerne and soya meal components. In contrast, only traces of l-chiro-inositol were observed. The DCI moiety was present in a water-soluble non-ionic form of which most was shown to be pinitol. To measure the absorption of dietary inositols, rats

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6

Turner, Benjamin L., Michael J. Papházy, Philip M. Haygarth, and Ian D. Mckelvie. "Inositol phosphates in the environment." Philosophical Transactions of the Royal Society of London. Series B: Biological Sciences 357, no. 1420 (2002): 449–69. http://dx.doi.org/10.1098/rstb.2001.0837.

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The inositol phosphates are a group of organic phosphorus compounds found widely in the natural environment, but that represent the greatest gap in our understanding of the global phosphorus cycle. They exist as inositols in various states of phosphorylation (bound to between one and six phosphate groups) and isomeric forms (e.g. myo , D– chiro , scyllo , neo ), although myo –inositol hexakisphosphate is by far the most prevalent form in nature. In terrestrial environments, inositol phosphates are principally derived from plants and accumulate in soils to become the dominant class of organic p

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7

Loss, Omar, Chun Ting Wu, Antonella Riccio, and Adolfo Saiardi. "Modulation of inositol polyphosphate levels regulates neuronal differentiation." Molecular Biology of the Cell 24, no. 18 (2013): 2981–89. http://dx.doi.org/10.1091/mbc.e13-04-0198.

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The binding of neurotrophins to tropomyosin receptor kinase receptors initiates several signaling pathways, including the activation of phospholipase C-γ, which promotes the release of diacylglycerol and inositol 1,4,5-trisphosphate (IP3). In addition to recycling back to inositol, IP3 serves as a precursor for the synthesis of higher phosphorylated inositols, such as inositol 1,3,4,5,6-pentakisphosphate (IP5) and inositol hexakisphosphate (IP6). Previous studies on the effect of neurotrophins on inositol signaling were limited to the analysis of IP3 and its dephosphorylation products. Here we

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8

Guo, Dachuan, Alex Fong, Andy Lail, et al. "Simplifying Complex Microarray Data To Derive Gene Expression Profiles Which Identify Childhood Acute Lymphoblastic Leukaemia Patients at Risk of Relapse." Blood 106, no. 11 (2005): 4506. http://dx.doi.org/10.1182/blood.v106.11.4506.4506.

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Abstract The optimal treatment of patients with childhood acute lymphoblastic leukaemia (ALL) depends on establishing accurate diagnosis. Our investigations seek to strategically develop the application of microarray gene expression profiling to identify ALL patients with clinically homogenous presentations but which may respond differently to established treatment regimens. We have determined the gene expression profiles of ALL bone marrow (BM) samples taken from patients at diagnosis. Data analysis has focussed on the use of a novel and innovative statistical technology, Gene-RaVE. This seri

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9

Stephens, L., P. T. Hawkins, N. Carter, et al. "l-myo-inositol 1,4,5,6-tetrakisphosphate is present in both mammalian and avian cells." Biochemical Journal 249, no. 1 (1988): 271–82. http://dx.doi.org/10.1042/bj2490271.

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When myo-[3H]inositol-prelabelled primary-cultured murine bone-marrow-derived macrophages were challenged with platelet-activating factor (PAF; 200 ng/ml), there was a rapid (2.5-fold at 10 s) rise in the intracellular concentration of D-myo-[3H]inositol 1,4,5-trisphosphate, followed by a rise in myo-[3H]inositol tetrakisphosphate. myo-[3H]Inositol tetrakisphosphate fractions were isolated by high-performance anion-exchange chromatography from myo-[3H]inositol-prelabelled chick erythrocytes and primary-cultured macrophages. In both cases [3H]iditol and [3H]inositol were the only significant pr

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10

Balla, T., S. S. Sim, A. J. Baukal, S. G. Rhee, and K. J. Catt. "Inositol polyphosphates are not increased by overexpression of Ins(1,4,5)P3 3-kinase but show cell-cycle dependent changes in growth factor-stimulated fibroblasts." Molecular Biology of the Cell 5, no. 1 (1994): 17–27. http://dx.doi.org/10.1091/mbc.5.1.17.

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NIH 3T3 fibroblasts were stably transfected with rat brain inositol 1,4,5-trisphosphate (Ins(1,4,5)P3) 3-kinase to explore the relationship between increased production of Ins(1,3,4,5)P4 and the formation of InsP5 and InsP6. Mass measurements of InsP5 and InsP6 revealed no significant difference between kinase- and vector-transfected fibroblasts. However, such 3-kinase-transfected cells, when labeled with [3H]inositol for 48-72 h, showed lower levels of [3H]InsP5 and [3H]InsP6, as well as [3H]Ins(1,3,4,6)P4 and D/L[3H]Ins(1,4,5,6)P4, than their vector-transfected counterparts. Because Ins(1,4,

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11

Huang, S. J., P. N. Monk, C. P. Downes, and A. D. Whetton. "Platelet-activating factor-induced hydrolysis of phosphatidylinositol 4,5-bisphosphate stimulates the production of reactive oxygen intermediates in macrophages." Biochemical Journal 249, no. 3 (1988): 839–45. http://dx.doi.org/10.1042/bj2490839.

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To investigate the relationship between inositol lipid hydrolysis and reactive oxygen-intermediate (ROI) production in macrophages we have examined the effect of platelet-activating factor (PAF) on normal bone marrow-derived macrophages. Addition of PAF to macrophages prelabelled with [3H]inositol caused a marked and rapid increase in [3H]inositol trisphosphate levels. Similarly when PAF was added to [3H]-glycerol prelabelled macrophages there was a rapid increase in 1,2-diacyl[3H]glycerol levels. These events preceded any increase in the rate of PAF-stimulated ROI production by a discernible

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12

Batty, I. R., S. R. Nahorski, and R. F. Irvine. "Rapid formation of inositol 1,3,4,5-tetrakisphosphate following muscarinic receptor stimulation of rat cerebral cortical slices." Biochemical Journal 232, no. 1 (1985): 211–15. http://dx.doi.org/10.1042/bj2320211.

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Carbachol stimulation of muscarinic receptors in rat cortical slices prelabelled with myo-[2-3H]inositol caused the rapid formation of a novel inositol polyphosphate. Evidence derived from its chromatographic behaviour, and from the structure of the products formed in partial dephosphorylation experiments, suggests that it is probably D-myo-inositol 1,3,4,5-tetrakisphosphate. An enzyme in human red cell membranes specifically removes the 5-phosphate from it to form inositol 1,3,4-trisphosphate. It is suggested that inositol 1,3,4,5-tetrakisphosphate is likely to be a second messenger, and that

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13

Porfiri, E., AV Hoffbrand, and RG Wickremasinghe. "Retinoic acid-induced granulocytic differentiation of HL60 human promyelocytic leukemia cells is preceded by downregulation of autonomous generation of inositol lipid-derived second messengers." Blood 78, no. 4 (1991): 1069–77. http://dx.doi.org/10.1182/blood.v78.4.1069.1069.

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Abstract Inositol phosphates (InsPs) and diacyglycerol (DAG) are second messengers derived via the breakdown of inositol phospholipids, and which play important signalling roles in the regulation of proliferation of some cell types. We have studied the operation of this pathway during the early stages of retionic acid (RA)-induced granulocytic differentiation of HL60 myeloid leukemia cells. The autonomous breakdown of inositol lipids that occurred in HL60 cells labeled with [3H] inositol was completely abolished following 48 hours of RA treatment. The rate of influx of 45Ca2+ was also signific

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14

Porfiri, E., AV Hoffbrand, and RG Wickremasinghe. "Retinoic acid-induced granulocytic differentiation of HL60 human promyelocytic leukemia cells is preceded by downregulation of autonomous generation of inositol lipid-derived second messengers." Blood 78, no. 4 (1991): 1069–77. http://dx.doi.org/10.1182/blood.v78.4.1069.bloodjournal7841069.

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Inositol phosphates (InsPs) and diacyglycerol (DAG) are second messengers derived via the breakdown of inositol phospholipids, and which play important signalling roles in the regulation of proliferation of some cell types. We have studied the operation of this pathway during the early stages of retionic acid (RA)-induced granulocytic differentiation of HL60 myeloid leukemia cells. The autonomous breakdown of inositol lipids that occurred in HL60 cells labeled with [3H] inositol was completely abolished following 48 hours of RA treatment. The rate of influx of 45Ca2+ was also significantly dec

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15

Salazar-Pereda, Verónica, Laura Martínez-Martínez, Angelina Flores-Parra, María de Jesús Rosales-Hoz, Armando Ariza-Castolo, and Rosalinda Contreras. "New phenylboronic esters derived from inositol [1]." Heteroatom Chemistry 5, no. 2 (1994): 139–43. http://dx.doi.org/10.1002/hc.520050210.

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16

Stephens, L. R., P. T. Hawkins, C. J. Barker, and C. P. Downes. "Synthesis of myo-inositol 1,3,4,5,6-pentakisphosphate from inositol phosphates generated by receptor activation." Biochemical Journal 253, no. 3 (1988): 721–33. http://dx.doi.org/10.1042/bj2530721.

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myo-[3H]Inositol 1,3,4,5,6-pentakisphosphate can be made from myo-[3H]inositol 1,4,5-trisphosphate in a rat brain homogenate or soluble fraction. Although D-myo-inositol 3,4,5,6-tetrakisphosphate can be phosphorylated by a soluble rat brain enzyme to give myo-inositol 1,3,4,5,6-pentakisphosphate, it is not an intermediate in the pathway from myo-inositol 1,4,5-trisphosphate. The intermediates in the above pathway are myo-inositol 1,3,4,5-tetrakisphosphate, myo-inositol 1,3,4-trisphosphate and myo-inositol 1,3,4,6-tetrakisphosphate [Shears, Parry, Tang, Irvine, Michell & Kirk (1987) Biochem

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17

Florholmen, J., D. Malm, B. Vonen, and P. G. Burhol. "Effect of cholecystokinin on the accumulation of inositol phosphates in isolated pancreatic islets." American Journal of Physiology-Gastrointestinal and Liver Physiology 257, no. 6 (1989): G865—G870. http://dx.doi.org/10.1152/ajpgi.1989.257.6.g865.

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Sulfated cholecystokinin octapeptide (CCK-8S) potentiated glucose-induced secretion in isolated pancreatic islets with a maximal effect at 12 mM glucose, whereas no effect was observed at 3.3 and 25 mM glucose. This effect of CCK-8S was maximal at 10(-7) M. Anion-exchange fast-protein liquid chromatography analysis of [3H]inositol phosphates derived from islets prelabeled with myo-[3H]inositol showed that glucose induced accumulation of the 1,4,5-isomer of inositol trisphosphate and of inositol tetrakisphosphate. At 3.3 mM glucose, CCK-8S stimulated accumulation of inositol trisphosphate and i

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18

Turk, J., B. A. Wolf, and M. L. McDaniel. "Glucose-induced accumulation of inositol trisphosphates in isolated pancreatic islets. Predominance of the 1,3,4-isomer." Biochemical Journal 237, no. 1 (1986): 259–63. http://dx.doi.org/10.1042/bj2370259.

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Anion-exchange h.p.l.c. analysis of [3H]inositol phosphates derived from glucose-stimulated isolated pancreatic islets that had been prelabelled with myo-[3H]inositol revealed that the predominant inositol trisphosphate was the 1,3,4-isomer [Ins(1,3,4)P3]. The 1,4,5-isomer [Ins(1,4,5)P3] was also detectable, as was a more polar inositol phosphate with the chromatographic properties of inositol 1,3,4,5-tetrakisphosphate [Ins(1,3,4,5)P4]. Glucose-induced accumulation of Ins(1,3,4)P3 was augmented by Li+ and occurred after maximal accumulation of Ins(1,4,5)P3. These findings suggest a possible ro

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LEWIS, MALCOLM J., PETER COLLINS, and DEREK LANG. "Endothelium-derived relaxing factor, calcium and inositol phosphates." Biochemical Society Transactions 16, no. 4 (1988): 486–88. http://dx.doi.org/10.1042/bst0160486.

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20

Léo, Pierre-Marc, Christophe Morin, and Christian Philouze. "Design and synthesis of a cyclitol-derived scaffold with axial pyridyl appendages and its encapsulation of the silver(I) cation." Beilstein Journal of Organic Chemistry 6 (October 29, 2010): 1022–24. http://dx.doi.org/10.3762/bjoc.6.115.

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Conversion of a myo-inositol derivative into a scyllo-inositol-derived scaffold with C 3 v symmetry bearing three axial pyridyl appendages is presented. This pre-organized hexadentate ligand allows complexation of silver(I). The crystal structure of the complex was established.

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Stephens, L. R., P. T. Hawkins, A. J. Morris, and P. C. Downes. "l-myo-inositol 1,4,5,6-tetrakisphosphate (3-hydroxy)kinase." Biochemical Journal 249, no. 1 (1988): 283–92. http://dx.doi.org/10.1042/bj2490283.

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Homogenates of primary-cultured murine bone macrophages contain an enzyme capable of synthesizing myo-[3H]inositol pentakisphosphate from myo-[3H]inositol tetrakisphosphate fractions derived from myo-[3H]inositol-labelled mouse macrophages and chick erythrocytes. D-myo-inositol 1,3,4,5-tetrakis[32P]-phosphate present in the same incubations was not phosphorylated. Since the myo-[3H]inositol-labelled tetrakisphosphate fractions used as substrates consist of a mixture of L-myo-inositol 1,4,5,6-tetrakisphosphate (60-85%) and a periodate-resistant tetrakisphosphate(s) whose characteristics are con

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Biden, T. J., and C. B. Wollheim. "Active transport of myo-inositol in rat pancreatic islets." Biochemical Journal 236, no. 3 (1986): 889–93. http://dx.doi.org/10.1042/bj2360889.

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myo-Inositol transport by isolated pancreatic islets was measured with a dual isotope technique. Uptake was saturable with a half-maximal response at approx. 75 microM. With 50 microM-inositol, uptake was linear for at least 2 h during which time the free intracellular concentration rose to double that of the incubation medium. Inositol transport is therefore active and probably energized by electrogenic co-transport of Na+ down its concentration gradient as uptake was inhibited by ouabain, Na+ removal or depolarizing K+ concentrations. Inositol transport was abolished by cytochalasin B which

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Wakelam, M. J. O. "Amplification of fluoroaluminate-stimulated inositol phosphate generation in a cell line overexpressing the p21N-ras gene." Biochemical Journal 259, no. 3 (1989): 737–41. http://dx.doi.org/10.1042/bj2590737.

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The stimulation of inositol phosphate generation in NIH-3T3 cells and a derived transformant overexpressing the p21N-ras gene (T15+ cells) was examined. Incubation with NaF in the presence of Al3+ leads to the generation of inositol phosphates in each cell type, though the response in the T15+ cells is significantly amplified. The effect of fluoroaluminate is dose- and time-dependent. No differences were observed in fluoroaluminate-stimulated cyclic AMP accumulation among the cell types. In another NIH-3T3-derived cell line that expresses the transforming lys61 mutant of N-ras, no amplificatio

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Chanduri, Manasa, Ashim Rai, Aushaq Bashir Malla, et al. "Inositol hexakisphosphate kinase 1 (IP6K1) activity is required for cytoplasmic dynein-driven transport." Biochemical Journal 473, no. 19 (2016): 3031–47. http://dx.doi.org/10.1042/bcj20160610.

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Inositol pyrophosphates, such as diphosphoinositol pentakisphosphate (IP7), are conserved eukaryotic signaling molecules that possess pyrophosphate and monophosphate moieties. Generated predominantly by inositol hexakisphosphate kinases (IP6Ks), inositol pyrophosphates can modulate protein function by posttranslational serine pyrophosphorylation. Here, we report inositol pyrophosphates as novel regulators of cytoplasmic dynein-driven vesicle transport. Mammalian cells lacking IP6K1 display defects in dynein-dependent trafficking pathways, including endosomal sorting, vesicle movement, and Golg

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Tamboli, Majid I., Shobhana Krishanaswamy, Rajesh G. Gonnade, and Mysore S. Shashidhar. "Engineering crystals that facilitate the acyl-transfer reaction: insight from a comparison of the crystal structures ofmyo-inositol-1,3,5-orthoformate-derived benzoates and carbonates." Acta Crystallographica Section C Structural Chemistry 72, no. 11 (2016): 875–81. http://dx.doi.org/10.1107/s205322961601603x.

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Minor variations in the molecular structure of constituent molecules of reactive crystals often yield crystals with significantly different properties due to altered modes of molecular association in the solid state. Hence, these studies could provide a better understanding of the complex chemical processes occurring in the crystalline state. However, reactions that proceed efficiently in molecular crystals are only a small fraction of the reactions that are known to proceed (with comparable efficiency) in the solution state. Hence, for consistent progress in this area of research, investigati

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Herrera-Salgado, Yesenia, María Luisa Garduño-Ramírez, Lorena Vázquez, María Yolanda Rios, and Laura Alvarez. "Myo-inositol-Derived Glycolipids with Anti-inflammatory Activity fromSolanumlanceolatum†." Journal of Natural Products 68, no. 7 (2005): 1031–36. http://dx.doi.org/10.1021/np050054s.

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Palmer, S., P. T. Hawkins, R. H. Michell, and C. J. Kirk. "The labelling of polyphosphoinositides with [32P]Pi and the accumulation of inositol phosphates in vasopressin-stimulated hepatocytes." Biochemical Journal 238, no. 2 (1986): 491–99. http://dx.doi.org/10.1042/bj2380491.

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When hepatocytes were incubated with [32P]Pi, the kinetics for the labelling of the monoester phosphate groups of phosphatidylinositol 4-phosphate and phosphatidylinositol 4,5-bisphosphate were similar to each other and slightly slower than that for the labelling of the gamma-phosphate of ATP. Analysis of the water-soluble 3H-labelled materials derived from [3H]inositol-labelled hepatocytes revealed that, in addition to inositol and its mono-, bis- and tris-phosphates (Ins, InsP, InsP2 and InsP3), these cells contained two unidentified radioactive compounds which co-eluted with InsP on anion-e

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Lev, Sophie, Desmarini Desmarini, Cecilia Li, et al. "Phospholipase C of Cryptococcus neoformans Regulates Homeostasis and Virulence by Providing Inositol Trisphosphate as a Substrate for Arg1 Kinase." Infection and Immunity 81, no. 4 (2013): 1245–55. http://dx.doi.org/10.1128/iai.01421-12.

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ABSTRACTPhospholipase C (PLC) ofCryptococcus neoformans(CnPlc1) is crucial for virulence of this fungal pathogen. To investigate the mechanism of CnPlc1-mediated signaling, we established that phosphatidylinositol 4,5-bisphosphate (PIP2) is a major CnPlc1 substrate, which is hydrolyzed to produce inositol trisphosphate (IP3). InSaccharomyces cerevisiae, Plc1-derived IP3is a substrate for the inositol polyphosphate kinase Arg82, which converts IP3to more complex inositol polyphosphates. In this study, we show that inC. neoformans, the enzyme encoded byARG1is the major IP3kinase, and we further

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Stephens, L. R., P. T. Hawkins, A. F. Stanley, et al. "myo-inositol pentakisphosphates. Structure, biological occurrence and phosphorylation to myo-inositol hexakisphosphate." Biochemical Journal 275, no. 2 (1991): 485–99. http://dx.doi.org/10.1042/bj2750485.

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1. Standard and high-performance anion-exchange-chromatographic techniques have been used to purify myo-[3H]inositol pentakisphosphates from various myo-[3H]inositol-prelabelled cells. Slime mould (Dictyostelium discoideum) contained 8 microM-myo-[3H]inositol 1,3,4,5,6-pentakisphosphate, 16 microM-myo-[3H]inositol 1,2,3,4,6-pentakisphosphate and 36 microM-D-myo-[3H]inositol 1,2,4,5,6-pentakisphosphate [calculated intracellular concentrations; Stephens & Irvine (1990) Nature (London) 346, 580-583]; germinating mung-bean (Phaseolus aureus) seedlings contained both D- and L-myo-[3H]inositol 1

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Sultzman, L., C. Ellis, L. L. Lin, T. Pawson, and J. Knopf. "Platelet-derived growth factor increases the in vivo activity of phospholipase C-gamma 1 and phospholipase C-gamma 2." Molecular and Cellular Biology 11, no. 4 (1991): 2018–25. http://dx.doi.org/10.1128/mcb.11.4.2018.

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Upon binding to its cell surface receptor, platelet-derived growth factor (PDGF) causes the tyrosine phosphorylation of phospholipase C-gamma 1 (PLC-gamma 1) and stimulates the production of diacylglycerol and inositol 1,4,5-triphosphate. We showed that following stimulation by PDGF, rat-2 cells overexpressing PLC-gamma 1 display an increase in the levels of both tyrosine-phosphorylated PLC-gamma 1 and inositol phosphates compared with the parental rat-2 cells. This increased responsiveness to PDGF is a direct effect of PLC-gamma 1 overexpression, as a cell line expressing similar levels of an

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Sultzman, L., C. Ellis, L. L. Lin, T. Pawson, and J. Knopf. "Platelet-derived growth factor increases the in vivo activity of phospholipase C-gamma 1 and phospholipase C-gamma 2." Molecular and Cellular Biology 11, no. 4 (1991): 2018–25. http://dx.doi.org/10.1128/mcb.11.4.2018-2025.1991.

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Upon binding to its cell surface receptor, platelet-derived growth factor (PDGF) causes the tyrosine phosphorylation of phospholipase C-gamma 1 (PLC-gamma 1) and stimulates the production of diacylglycerol and inositol 1,4,5-triphosphate. We showed that following stimulation by PDGF, rat-2 cells overexpressing PLC-gamma 1 display an increase in the levels of both tyrosine-phosphorylated PLC-gamma 1 and inositol phosphates compared with the parental rat-2 cells. This increased responsiveness to PDGF is a direct effect of PLC-gamma 1 overexpression, as a cell line expressing similar levels of an

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Stenman, Katarina, Pär Stattin, Hans Stenlund, Katrine Riklund, Gerhard Gröbner, and Anders Bergh. "H HRMAS NMR Derived Bio-markers Related to Tumor Grade, Tumor Cell Fraction, and Cell Proliferation in Prostate Tissue Samples." Biomarker Insights 6 (January 2011): BMI.S6794. http://dx.doi.org/10.4137/bmi.s6794.

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A high-resolution magic angle spinning NMR spectroscopic approach is presented for evaluating the occurrence, amount and aggressiveness of cancer in human prostate tissue samples. Using this technique, key metabolites in malignant and non-malignant samples (n = 149) were identified, and patterns of their relative abundance were analyzed by multivariate statistical methods. Ratios of various metabolites – including (glycerophophorylcholine + phosphorylcholine)/creatine, myo-inositol/scyllo-inositol, scyllo-inositol/creatine, choline/creatine, and citrate/creatine – correlated with: i) for non-m

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Waite, Jerene J., and Paul A. Insel. "G–protein linked polyphosphoinositide phospholipase C activity in cell membranes from clonally derived and ras-transformed Madin–Darby canine kidney cells." Biochemistry and Cell Biology 68, no. 9 (1990): 1119–27. http://dx.doi.org/10.1139/o90-167.

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Membranes prepared from clone D1 of Madin–Darby canine kidney (MDCK) cells contain activity that can be attributed to Gp, a guanine nucleotide binding protein linked to phosphatidylinositol 4,5-bisphosphate dependent phospholipase C. Polyphosphoinositides are produced by addition of GTP, nonhydrolyzable GTP analogs, or fluoroaluminate. This production is inhibited by guanosine 5′-(β-thiodiphosphate). While Ca2+ at 1 μM or more can generate high yields of inositol phosphates, guanine nucleotide activation of Gp can potentiate this Ca2+-dependent yield at resting levels of the cation. Membranes

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34

Davis, J. S., L. L. Weakland, L. A. West, and R. V. Farese. "Luteinizing hormone stimulates the formation of inositol trisphosphate and cyclic AMP in rat granulosa cells. Evidence for phospholipase C generated second messengers in the action of luteinizing hormone." Biochemical Journal 238, no. 2 (1986): 597–604. http://dx.doi.org/10.1042/bj2380597.

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The following studies were conducted to determine whether luteinizing hormone (LH), a hormone which increases cellular levels of cyclic AMP, also provokes increases in ‘second messengers’ derived from inositol lipid metabolism (i.e. inositol phosphates and diacylglycerol). Rat granulosa cells isolated from mature Graafian follicles were prelabelled for 3 h with myo-[2-3H]inositol. LH provoked rapid (5 min) and sustained (up to 60 min) increases in the levels of inositol mono-, bis, and trisphosphates (IP, IP2 and IP3, respectively). Time course studies revealed that IP3 was formed more rapidly

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Rapoport, R. M., K. A. Stauderman, and R. F. Highsmith. "Effects of EDCF and endothelin on phosphatidylinositol hydrolysis and contraction in rat aorta." American Journal of Physiology-Cell Physiology 258, no. 1 (1990): C122—C131. http://dx.doi.org/10.1152/ajpcell.1990.258.1.c122.

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Endothelium-derived constricting factor (EDCF) and endothelin are peptidergic substances produced and released from endothelial cells that induce contraction of vascular smooth muscle. The purpose of the present study was to investigate possible mechanisms by which EDCF and endothelin elicit contraction. Exposure of rat aorta to EDCF or synthetic endothelin resulted in time- and concentration-dependent increases in tension and levels of inositol monophosphate, a breakdown product of the phosphatidylinositides. A 10-s exposure to endothelin elevated levels of inositol 1,4,5-trisphosphate. Tryps

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Porcellati, Francesca, Tommy Hlaing, Masaki Togawa, et al. "Human Na+-myo-inositol cotransporter gene: alternate splicing generates diverse transcripts." American Journal of Physiology-Cell Physiology 274, no. 5 (1998): C1215—C1225. http://dx.doi.org/10.1152/ajpcell.1998.274.5.c1215.

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Na+- myo-inositol cotransport activity generally maintains millimolar intracellular concentrations of myo-inositol and specifically promotes transepithelial myo-inositol transport in kidney, intestine, retina, and choroid plexus. Glucose-induced, tissue-specific myo-inositol depletion and impaired Na+- myo-inositol cotransport activity are implicated in the pathogenesis of diabetic complications, a process modeled in vitro in cultured human retinal pigment epithelium (RPE) cells. To explore this process at the molecular level, a human RPE cDNA library was screened with a canine Na+-dependent m

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Yorek, Mark A., Joyce A. Dunlap, Michael J. Thomas, Patrick R. Cammarata, Cheng Zhou та William L. Lowe. "Effect of TNF-α on SMIT mRNA levels andmyo-inositol accumulation in cultured endothelial cells". American Journal of Physiology-Cell Physiology 274, № 1 (1998): C58—C71. http://dx.doi.org/10.1152/ajpcell.1998.274.1.c58.

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Previously we have shown that hyperosmolarity increases Na+- myo-inositol cotransporter (SMIT) activity and mRNA levels in cultured endothelial cells. Because hyperosmolarity and cytokines, such as tumor necrosis factor-α (TNF-α), activate similar signal transduction pathways, we examined the effect of TNF-α on SMIT mRNA levels and myo-inositol accumulation. In contrast to the effect of hyperosmolarity, TNF-α caused a time- and concentration-dependent decrease in SMIT mRNA levels and myo-inositol accumulation. The effect of TNF-α on myo-inositol accumulation was found in large-vessel endotheli

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McAllister, G., P. Whiting, E. A. Hammond, et al. "cDNA cloning of human and rat brain myo-inositol monophosphatase. Expression and characterization of the human recombinant enzyme." Biochemical Journal 284, no. 3 (1992): 749–54. http://dx.doi.org/10.1042/bj2840749.

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Inositol monophosphatase (EC 3.1.3.25) is a key enzyme in the phosphoinositide cell-signalling system. Its role is to provide inositol required for the resynthesis of phosphatidylinositol and polyphosphoinositides. It is the probable pharmacological target for lithium action in brain. Using probes derived from the bovine inositol monophosphatase cDNA we have isolated cDNA clones encoding the human and rat brain enzymes. The enzyme is highly conserved in all three species (79% identical). The coding region of the human cDNA was inserted into a bacterial expression vector. The expressed recombin

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Stephens, L. R., and C. P. Downes. "Product-precursor relationships amongst inositol polyphosphates. Incorporation of [32P]Pi into myo-inositol 1,3,4,6-tetrakisphosphate, myo-inositol 1,3,4,5-tetrakisphosphate, myo-inositol 3,4,5,6-tetrakisphosphate and myo-inositol 1,3,4,5,6-pentakisphosphate in intact avian erythrocytes." Biochemical Journal 265, no. 2 (1990): 435–52. http://dx.doi.org/10.1042/bj2650435.

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Avian erythrocytes were incubated with myo-[3H]inositol for 6-7 h and with [32P]Pi for the final 50-90 min of this period. An acid extract was prepared from the prelabelled erythrocytes, and the specific radioactivities of the gamma-phosphate of ATP and of both the myo-inositol moieties (3H, d.p.m./nmol) and the individual phosphate groups (32P, d.p.m./nmol) of [3H]Ins[32P](1,3,4,6)P4,[3H]Ins[32P](1,3,4,5)P4, [3H]Ins[32P](3,4,5,6)P4 and [3H]Ins[32P](1,3,4,5,6)P5 were determined. The results provide direct confirmation that one of the cellular InsP4 isomers is Ins(1,3,4,5)P4 which is synthesize

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Aiba, Toshihiko, Masaki Sato, Daichi Umegaki, et al. "Regioselective phosphorylation of myo-inositol with BINOL-derived phosphoramidites and its application for protozoan lysophosphatidylinositol." Organic & Biomolecular Chemistry 14, no. 28 (2016): 6672–75. http://dx.doi.org/10.1039/c6ob01062h.

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Blakeley, D. M., A. N. Corps, and K. D. Brown. "Bombesin and platelet-derived growth factor stimulate formation of inositol phosphates and Ca2+ mobilization in Swiss 3T3 cells by different mechanisms." Biochemical Journal 258, no. 1 (1989): 177–85. http://dx.doi.org/10.1042/bj2580177.

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Highly purified platelet-derived growth factor (PDGF) or recombinant PDGF stimulate DNA synthesis in quiescent Swiss 3T3 cells. The dose-response curves for the natural and recombinant factors were similar, with half-maximal responses at 2-3 ng/ml and maximal responses at approx. 10 ng/ml. Over this dose range, both natural and recombinant PDGF stimulated a pronounced accumulation of [3H]inositol phosphates in cells labelled for 72 h with [3H]inositol. In addition, mitogenic concentrations of PDGF stimulated the release of 45Ca2+ from cells prelabelled with the radioisotope. However, in compar

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42

Rahman, Md Lutfor, Mashitah Mohd Yusoff, and Sandeep Kumar. "Synthesis and photoswitching properties of liquid crystals derived from myo-inositol." RSC Adv. 4, no. 66 (2014): 35089–98. http://dx.doi.org/10.1039/c4ra05568c.

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A new myo-inositol-based liquid crystal can be used for the creation of optical storage devices. The dark area is the UV-irradiated area forming a disordered isotropic phase, whereas the bright area protected from the light by using a mask remains in the ordered phase.

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43

Haines, K. A., J. Reibman, X. Y. Tang, M. Blake, and G. Weissmann. "Effects of protein I of Neisseria gonorrhoeae on neutrophil activation: generation of diacylglycerol from phosphatidylcholine via a specific phospholipase C is associated with exocytosis." Journal of Cell Biology 114, no. 3 (1991): 433–42. http://dx.doi.org/10.1083/jcb.114.3.433.

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Upon engagement of chemoattractant receptors, neutrophils generate inositol trisphosphate and diacylglycerol (DG) by means of a phosphatidylinositol-specific phospholipase C (PI-PLC) which is regulated by a GTP-binding protein(s). We have previously reported (Reibman, J., H. M. Korchak, L. B. Vosshall, K. A. Haines, A. M. Rich, and G. Weissmann. 1988. J. Biol. Chem. 263:6322-6328) a biphasic rise in DG after exposure of neutrophils to the chemoattractant FMLP: a rapid (less than or equal to 15 s) phase ("triggering") and a slow (greater than or equal to 30 s) phase ("activation"). These derive

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Martins, T. J., Y. Sugimoto, and R. L. Erikson. "Dissociation of inositol trisphosphate from diacylglycerol production in Rous sarcoma virus-transformed fibroblasts." Journal of Cell Biology 108, no. 2 (1989): 683–91. http://dx.doi.org/10.1083/jcb.108.2.683.

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The metabolism of phosphatidylinositol (PI) and related intermediates was studied in uninfected and Rous sarcoma virus-(RSV) infected chicken embryo fibroblasts (CEFs). Cells infected with wild-type RSV exhibited twofold increases in steady-state concentrations of inositol trisphosphate (IP3) and inositol bisphosphate (IP2) as compared to uninfected CEFs. In addition, increased concentrations of IP3 and IP2 were observed in CEFs infected with the RSV temperature-sensitive transformation mutant NY72-4 when maintained at the permissive temperature (35 degrees C) for greater than 24 h. Slight inc

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45

Hrbolich, J. K., M. Culty та R. J. Haslam. "Activation of phospholipase C associated with isolated rabbit platelet membranes by guanosine 5′-[γ-thio]triphosphate and by thrombin in the presence of GTP". Biochemical Journal 243, № 2 (1987): 457–65. http://dx.doi.org/10.1042/bj2430457.

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Rabbit platelets were labelled with [3H]inositol and a membrane fraction was isolated in the presence of ATP, MgCl2 and EGTA. Incubation of samples for 10 min with 0.1 microM-Ca2+free released [3H]inositol phosphates equivalent to about 2.0% of the membrane [3H]phosphoinositides. Addition of 10 microM-guanosine 5′-[gamma-thio]triphosphate (GTP[S]) caused an additional formation of [3H]inositol phosphates equivalent to 6.6% of the [3H]phosphoinositides. A half-maximal effect was observed with 0.4 microM-GTP[S]. The [3H]inositol phosphates that accumulated consisted of 10% [3H]inositol monophosp

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46

Slade, Angela T., Cornelis Lensink, Andrew Falshaw, George R. Clark, and L. James Wright. "Ruthenium and osmium complexes of hemilabile chiral monophosphinite ligands derived from 1D-pinitol or 1D-chiro-inositol as catalysts for asymmetric hydrogenation reactions." Dalton Trans. 43, no. 45 (2014): 17163–71. http://dx.doi.org/10.1039/c4dt02558j.

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Chiral monophosphinite ligands derived from 1D-pinitol or 1D-chiro-inositol coordinate to ruthenium as bidentate hemilabile ligands to produce ketone hydrogenation catalysts that give high conversions but low %ee values.

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47

TAKEUCHI, Hiroshi, Miho MATSUDA, Tada-aki YAMAMOTO, et al. "PTB domain of insulin receptor substrate-1 binds inositol compounds." Biochemical Journal 334, no. 1 (1998): 211–18. http://dx.doi.org/10.1042/bj3340211.

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We examined whether a phosphotyrosine binding (PTB) domain from the human insulin receptor substrate-1 (hIRS-1) is capable of binding inositol phosphates/phosphoinositides. The binding specificity was compared with that of the pleckstrin homology (PH) domain derived from the same protein because the three dimensional structure was found to be very similar to that of the PH domain, despite the lack of sequence similarity. We also attempted to locate the site of binding of the inositol compounds. The PTB domain bound [3H]Ins(1,4,5)P3, which was displaced most strongly by Ins(1,3,4,5,6)P5 and Ins

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48

McPhee, F., C. P. Downes, and G. Lowe. "Studies of inositol analogues as inhibitors of the phosphoinositide pathway, and incorporation of 2-deoxy-2-fluoro-myo-inositol to give analogues of phosphatidylinositol intermediates." Biochemical Journal 277, no. 2 (1991): 407–12. http://dx.doi.org/10.1042/bj2770407.

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The incorporation of [3H]Ins into PtdIns by exchange of free and lipid-bound inositol moieties occurs via the action of at least two types of Mg2+/Mn(2+)-dependent enzymes in turkey erythrocytes. One is a nucleotide-independent PtdIns/Ins exchange enzyme and its function is, as yet, unknown, whereas the other is CMP-dependent and appears to be an exchange reaction catalysed by PtdIns synthase. The effects of analogues with modifications of the substituent at the 1-, 2-, 3-, 4- and 5-positions on the incorporation of [3H]Ins into PtdIns under both synthase and exchange reaction conditions were

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Shin, Sun-H., Jong-S. Kim, Hak-R. Kim, Jin-K. Lim, Byung-K. Choi, and Young-K. Yeo. "Polyphosphoinositides Are Derived from Ether-linked Inositol Glycerophospholipids in Rat Brain." BMB Reports 38, no. 3 (2005): 360–65. http://dx.doi.org/10.5483/bmbrep.2005.38.3.360.

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Belmaker, RH, J. Shapiro, E. Vainer, L. Nemanov, RP Ebstein, and G. Agam. "Reduced inositol content in lymphocyte-derived cell lines from bipolar patients." Bipolar Disorders 4, no. 1 (2002): 67–69. http://dx.doi.org/10.1034/j.1399-5618.2002.00108.x.

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