Relevant bibliographies by topics / Phosphoinositides

Academic literature on the topic 'Phosphoinositides'

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Published: 4 June 2021
Last updated: 25 May 2024

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Journal articles on the topic "Phosphoinositides"

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Min, Sang H., and Charles S. Abrams. "Regulation of platelet plug formation by phosphoinositide metabolism." Blood 122, no. 8 (August 22, 2013): 1358–65. http://dx.doi.org/10.1182/blood-2013-05-427716.

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Abstract Phosphatidylinositol and its phosphorylated derivatives, phosphoinositides, are minor constituents of phospholipids at the cellular membrane level. Nevertheless, phosphatidylinositol and phosphoinositides represent essential components of intracellular signaling that regulate diverse cellular processes, including platelet plug formation. Accumulating evidence indicates that the metabolism of phosphoinositides is temporally and spatially modulated by the opposing effects of specific phosphoinositide-metabolizing enzymes, including lipid kinases, lipid phosphatases, and phospholipases. Each of these enzymes generates a selective phosphoinositide or second messenger within precise cellular compartments. Intriguingly, phosphoinositide-metabolizing enzymes exist in different isoforms, which all produce the same phosphoinositide products. Recent studies using isoform-specific mouse models and chemical inhibitors have elucidated that the different isoforms of phosphoinositide-metabolizing enzymes have nonredundant functions and provide an additional layer of complexity to the temporo-spatial organization of intracellular signaling events. In this review, we will discuss recent advances in our understanding of phosphoinositide organization during platelet activation.
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Balla, Tamas, Zsofia Szentpetery, and Yeun Ju Kim. "Phosphoinositide Signaling: New Tools and Insights." Physiology 24, no. 4 (August 2009): 231–44. http://dx.doi.org/10.1152/physiol.00014.2009.

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Phosphoinositides constitute only a small fraction of cellular phospholipids, yet their importance in the regulation of cellular functions can hardly be overstated. The rapid metabolic response of phosphoinositides after stimulation of certain cell surface receptors was the first indication that these lipids could serve as regulatory molecules. These early observations opened research areas that ultimately clarified the plasma membrane role of phosphoinositides in Ca2+ signaling. However, research of the last 10 years has revealed a much broader range of processes dependent on phosphoinositides. These lipids control organelle biology by regulating vesicular trafficking, and they modulate lipid distribution and metabolism more generally via their close relationship with lipid transfer proteins. Phosphoinositides also regulate ion channels, pumps, and transporters as well as both endocytic and exocytic processes. The significance of phosphoinositides found within the nucleus is still poorly understood, and a whole new research concerns the highly phosphorylated inositols that also appear to control multiple nuclear processes. The expansion of research and interest in phosphoinositides naturally created a demand for new approaches to determine where, within the cell, these lipids exert their effects. Imaging of phosphoinositide dynamics within live cells has become a standard cell biological method. These new tools not only helped us localize phosphoinositides within the cell but also taught us how tightly phosphoinositide control can be linked with distinct effector protein complexes. The recent progress allows us to understand the underlying causes of certain human diseases and design new strategies for therapeutic interventions.
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Finkelstein, Stella, Sidney M. Gospe, Kai Schuhmann, Andrej Shevchenko, Vadim Y. Arshavsky, and Ekaterina S. Lobanova. "Phosphoinositide Profile of the Mouse Retina." Cells 9, no. 6 (June 7, 2020): 1417. http://dx.doi.org/10.3390/cells9061417.

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Phosphoinositides are known to play multiple roles in eukaryotic cells. Although dysregulation of phosphoinositide metabolism in the retina has been reported to cause visual dysfunction in animal models and human patients, our understanding of the phosphoinositide composition of the retina is limited. Here, we report a characterization of the phosphoinositide profile of the mouse retina and an analysis of the subcellular localization of major phosphorylated phosphoinositide forms in light-sensitive photoreceptor neurons. Using chromatography of deacylated phosphatidylinositol headgroups, we established PI(4,5)P2 and PI(4)P as two major phosphorylated phosphoinositides in the retina. Using high-resolution mass spectrometry, we revealed 18:0/20:4 and 16:0/20:4 as major fatty-acyl chains of retinal phosphoinositides. Finally, analysis of fluorescent phosphoinositide sensors in rod photoreceptors demonstrated distinct subcellular distribution patterns of major phosphoinositides. The PI(4,5)P2 reporter was enriched in the inner segments and synapses, but was barely detected in the light-sensitive outer segments. The PI(4)P reporter was mostly found in the outer and inner segments and the areas around nuclei, but to a lesser degree in the synaptic region. These findings provide support for future mechanistic studies defining the biological significance of major mono- (PI(4)P) and bisphosphate (PI(4,5)P2) phosphatidylinositols in photoreceptor biology and retinal health.
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Zhainazarov, Asylbek B., Richard Doolin, John-David Herlihy, and Barry W. Ache. "Odor-Stimulated Phosphatidylinositol 3-Kinase in Lobster Olfactory Receptor Cells." Journal of Neurophysiology 85, no. 6 (June 1, 2001): 2537–44. http://dx.doi.org/10.1152/jn.2001.85.6.2537.

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Two antagonists of phosphoinositide 3-OH kinases (PI3Ks), LY294002 and Wortmannin, reduced the magnitude of the receptor potential in lobster olfactory receptor neurons (ORNs) recorded by patch clamping the cells in vivo. An antibody directed against the c-terminus of human PI3K-P110β detected a molecule of predicted size in the outer dendrites of the ORNs. Two 3-phosphoinositides, PI(3,4)P2 (1–4 μM) and PI(3,4,5)P3 (1–4 μM) applied to the cytoplasmic side of inside-out patches taken from cultured lobster ORNs, reversibly activated a Na+-gated channel previously implicated in the transduction cascade in these cells. 3-Phosphoinositides were the most effective phosphoinositide (1 μM) in enhancing the open probability of the channel. Collectively, these results implicate 3-phosphoinositides in lobster olfactory transduction and raise the need to consider the 3-phosphoinositide pathway in olfactory transduction.
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Picas, Laura, Frederique Gaits-Iacovoni, and Bruno Goud. "The emerging role of phosphoinositide clustering in intracellular trafficking and signal transduction." F1000Research 5 (March 31, 2016): 422. http://dx.doi.org/10.12688/f1000research.7537.1.

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Phosphoinositides are master regulators of multiple cellular processes: from vesicular trafficking to signaling, cytoskeleton dynamics, and cell growth. They are synthesized by the spatiotemporal regulated activity of phosphoinositide-metabolizing enzymes. The recent observation that some protein modules are able to cluster phosphoinositides suggests that alternative or complementary mechanisms might operate to stabilize the different phosphoinositide pools within cellular compartments. Herein, we discuss the different known and potential molecular players that are prone to engage phosphoinositide clustering and elaborate on how such a mechanism might take part in the regulation of intracellular trafficking and signal transduction.
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Gandhi, C. R., K. Stephenson, and M. S. Olson. "A comparative study of endothelin- and platelet-activating-factor-mediated signal transduction and prostaglandin synthesis in rat Kupffer cells." Biochemical Journal 281, no. 2 (January 15, 1992): 485–92. http://dx.doi.org/10.1042/bj2810485.

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Endothelin-3 (ET-3) stimulated phosphoinositide metabolism and synthesis of prostaglandins in cultured rat Kupffer cells. ET-3-induced hydrolysis of phosphoinositides was characterized by the production of various inositol phosphates and of glycerophosphoinositol. The mechanism of ET-3-stimulated metabolism of phosphoinositides and synthesis of prostaglandins appeared to be distinct from the effect of platelet-activating factor (PAF) on these processes described previously [Gandhi, Hanahan & Olson (1990) J. Biol. Chem. 265, 18234-18241]. On a molar basis ET-3 was significantly more potent than PAF in stimulating phosphoinositide metabolism, e.g. ET-3-induced hydrolysis of phosphoinositides occurred at 1 pM, whereas PAF was ineffective at concentrations less than 1 nM. Upon challenging Kupffer cells with both ET-3 and PAF, an additive stimulation of phosphoinositide metabolism was observed, suggesting that the actions of these factors may be exerted on separate phosphoinositide pools. Treatment of Kupffer cells with pertussis toxin resulted in an inhibition of ET-3-induced phospholipase C activation; in contrast, cholera toxin treatment caused potentiation of ET-3-stimulated phospholipase C activity. Both toxins, however, inhibited PAF-stimulated phospholipase C activity. The present results suggest that the stimulatory effects of ET-3 and PAF on the phosphodiesteric metabolism of phosphoinositides in Kupffer cells require different guanine-nucleotide-binding proteins. Furthermore, the effects of bacterial toxins on ET-3- and PAF-induced phosphoinositide metabolism were not mediated by cyclic AMP. ET-3-induced metabolism of phosphoinositides was inhibited completely in Kupffer cells pretreated with ET-3, suggesting homologous ligand-induced desensitization of the ET-3 receptors. In contrast, similar experiments using PAF showed only a partial desensitization of subsequent PAF-induced phosphoinositide metabolism. In contrast to the increased production of prostaglandins E2 and D2 observed upon stimulation of Kupffer cells with PAF, ET-3 stimulated the biosynthesis of prostaglandin E2 only. Consistent with their additive effects on phosphoinositide metabolism, PAF and ET-3 exhibited an additive stimulation of the synthesis of prostaglandin E2.
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Conduit, Sarah E., and Bart Vanhaesebroeck. "Phosphoinositide lipids in primary cilia biology." Biochemical Journal 477, no. 18 (September 24, 2020): 3541–65. http://dx.doi.org/10.1042/bcj20200277.

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Primary cilia are solitary signalling organelles projecting from the surface of most cell types. Although the ciliary membrane is continuous with the plasma membrane it exhibits a unique phospholipid composition, a feature essential for normal cilia formation and function. Recent studies have illustrated that distinct phosphoinositide lipid species localise to specific cilia subdomains, and have begun to build a ‘phosphoinositide map’ of the cilium. The abundance and localisation of phosphoinositides are tightly regulated by the opposing actions of lipid kinases and lipid phosphatases that have also been recently discovered at cilia. The critical role of phosphoinositides in cilia biology is highlighted by the devastating consequences of genetic defects in cilia-associated phosphoinositide regulatory enzymes leading to ciliopathy phenotypes in humans and experimental mouse and zebrafish models. Here we provide a general introduction to primary cilia and the roles phosphoinositides play in cilia biology. In addition to increasing our understanding of fundamental cilia biology, this rapidly expanding field may inform novel approaches to treat ciliopathy syndromes caused by deregulated phosphoinositide metabolism.
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Ebner, Michael, Philipp Alexander Koch, and Volker Haucke. "Phosphoinositides in the control of lysosome function and homeostasis." Biochemical Society Transactions 47, no. 4 (August 5, 2019): 1173–85. http://dx.doi.org/10.1042/bst20190158.

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Abstract Lysosomes are the main degradative compartments of mammalian cells and serve as platforms for cellular nutrient signaling and sterol transport. The diverse functions of lysosomes and their adaptation to extracellular and intracellular cues are tightly linked to the spatiotemporally controlled synthesis, turnover and interconversion of lysosomal phosphoinositides, minor phospholipids that define membrane identity and couple membrane dynamics to cell signaling. How precisely lysosomal phosphoinositides act and which effector proteins within the lysosome membrane or at the lysosomal surface recognize them is only now beginning to emerge. Importantly, mutations in phosphoinositide metabolizing enzyme cause lysosomal dysfunction and are associated with numerous diseases ranging from neurodegeneration to cancer. Here, we discuss the phosphoinositides and phosphoinositide metabolizing enzymes implicated in lysosome function and homeostasis and outline perspectives for future research.
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Le Ma, Lewis C. Cantley, Paul A. Janmey, and Marc W. Kirschner. "Corequirement of Specific Phosphoinositides and Small GTP-binding Protein Cdc42 in Inducing Actin Assembly in Xenopus Egg Extracts." Journal of Cell Biology 140, no. 5 (March 9, 1998): 1125–36. http://dx.doi.org/10.1083/jcb.140.5.1125.

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Both phosphoinositides and small GTP-binding proteins of the Rho family have been postulated to regulate actin assembly in cells. We have reconstituted actin assembly in response to these signals in Xenopus extracts and examined the relationship of these pathways. We have found that GTPγS stimulates actin assembly in the presence of endogenous membrane vesicles in low speed extracts. These membrane vesicles are required, but can be replaced by lipid vesicles prepared from purified phospholipids containing phosphoinositides. Vesicles containing phosphatidylinositol (4,5) bisphosphate or phosphatidylinositol (3,4,5) trisphosphate can induce actin assembly even in the absence of GTPγS. RhoGDI, a guanine-nucleotide dissociation inhibitor for the Rho family, inhibits phosphoinositide-induced actin assembly, suggesting the involvement of the Rho family small G proteins. Using various dominant mutants of these G proteins, we demonstrate the requirement of Cdc42 for phosphoinositide-induced actin assembly. Our results suggest that phosphoinositides may act to facilitate GTP exchange on Cdc42, as well as to anchor Cdc42 and actin nucleation activities. Hence, both phosphoinositides and Cdc42 are required to induce actin assembly in this cell-free system.
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Coronas, Sophie, Damien Ramel, Caroline Pendaries, Frédérique Gaits-Iacovoni, Hélène Tronchère, and Bernard Payrastre. "PtdIns5P: a little phosphoinositide with big functions?" Biochemical Society Symposia 74 (January 12, 2007): 117–28. http://dx.doi.org/10.1042/bss2007c11.

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Phosphoinositides are minor constituents of cell membranes playing a critical role in the regulation of many cellular functions. Recent discoveries indicate that mutations in several phosphoinositide kinases and phosphatases generate imbalances in the levels of phosphoinositides, thereby leading to the development of human diseases. Although the roles of phosphoinositide 3-kinase products and PtdIns(4,5)P2 were largely studied these last years, the potential role of phosphatidylinositol monophosphates as direct signalling molecules is just emerging. PtdIns5P, the least characterized phosphoinositide, appears to be a new player in cell regulation. This review will summarize the current knowledge on the mechanisms of synthesis and degradation of PtdIns5P as well as its potential roles.
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Dissertations / Theses on the topic "Phosphoinositides"

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Coghlan, Samuel William. "Phosphoinositides : methodology, synthesis, application." Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612939.

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Bothmer, John. "Phosphoinositides, aging and Alzheimer's disease." Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1992. http://arno.unimaas.nl/show.cgi?fid=6504.

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Fang, Xiaoming. "Phosphoinositides in ciliary transport and ciliopathies." Thesis, University of Sheffield, 2018. http://etheses.whiterose.ac.uk/19194/.

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Cilia are finger-like protrusions that function in the detection and processing of a wide variety of signals. In vertebrates, they are intimately involved in early embryonic patterning, the differentiation and function of sensory neurons, morphogenesis and physiology of duct epithelia, cell motility and metabolism. Lipid composition of the ciliary membrane and its contribution to cilia function is one of the least studied areas of cilia biology. Here I use a collection of transgenic lines to determine the phosphoinositide content of the ciliary membrane and to test the role of phosphoinositides in cilia morphogenesis and function. My studies reveal that specific types of phosphoinositides are found in the ciliary membrane and that their content plays an important role in cilia morphology and function. Moreover, I generated a zebrafish model of a human ciliopathy to test whether some aspects of its mutant phenotype can be alleviated by manipulating the phosphoinositide content in the ciliary membrane. Finally, my studies developed a method that is generally applicable to the manipulation of ciliary content of other PIs in a living vertebrate using other enzymes.
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Blank, Jonathan Louis. "The phospholipase C specific for the phosphoinositides." Thesis, University of Nottingham, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252943.

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Zhang, Xuxiao. "How are class I phosphoinositide 3-kinases regulated?" Thesis, University of Cambridge, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.609245.

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Olsson, Henric. "Phosphatidylinositol 4-kinases in rat liver characterization of two forms with different subcellular distribution /." Lund : Biochemistry, Chemical Centre, University of Lund, 1994. http://books.google.com/books?id=L_xqAAAAMAAJ.

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Loovers, Harriët Maria. "Phosphoinositides and inositol 5-phosphatases in Dictyostelium discoideum /." Enschede : PrintPartners Ipskamp, 2005. http://www.gbv.de/dms/goettingen/479206880.pdf.

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Bernier, Louis-Philippe. "Functional regulation of P2X receptor channels by phosphoinositides." Thesis, McGill University, 2012. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=110361.

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Long after its initial discovery as part of DNA and as the main source of energy in the cell, the nucleotide adenosine-5'-triphosphate (ATP) is now rightfully considered as an important extracellular signalling molecule. It is now known that purinergic transmission plays significant physiological roles, notably in neuro- and gliotransmission, in the modulation of the innate and adaptive immune response, in smooth muscle constriction and in regulating blood clotting. It is also actively involved in the generation and maintenance of various pathological states, including chronic neuropathic and inflammatory pain.How purinergic signalling can be implicated in such a diverse array of mechanisms via only one signalling molecule comes from the variety of receptors that are activated by ATP. Two major types of ATP-sensitive receptors exist: the P2X ionotropic receptor channels and the metabotropic P2Y receptors. The P2X family of ATP-gated ion channels is composed of seven subunits that assemble as trimers to form receptors with various functional and pharmacological profiles. Like all ion channels, the activity of P2X receptor channels is tightly regulated by orthosteric and allosteric regulation mechanisms. This thesis provides evidence of a novel type of post-translational regulation mechanism where the levels of intracellular phosphoinositides (PIPn) modulate the channel activity of P2X receptors. The first article included in my thesis focuses on the P2X1 subtype, which is mainly involved in smooth muscle constriction in blood vessels and vas deferens, as well as in the control of platelet aggregation and blood clotting. We demonstrate that the activity of the P2X1 receptor channel is positively regulated by membrane PI(4,5)P2 (PIP2). Depleting the intracellular levels of PIP2 decreased the ATP-activated current carried through the P2X1 channel and had an inhibitory effect on ATP-mediated mesenteric artery constriction, a P2X1-dependent process. Direct binding between the P2X1 cytosolic tail and PIP2 is shown to be necessary for the full expression of P2X1 activity.The next article in this thesis describes the PIPn-dependent regulation of the P2X4 receptor channel, which is highly involved in the generation of neuropathic and inflammatory pain through its expression in spinal cord microglia. Results obtained show that complete P2X4 function is dependent on the levels of PIP2 and PI(3,4,5)P3 (PIP3). Both species of phospholipids potentiate the P2X4-mediated ionic current and calcium entry by directly binding to the C-terminal domain of P2X4 subunits. Activation of co-expressed microglial metabotropic receptors can trigger changes in PIP2 or PIP3 levels, which could affect the contribution of P2X4 in pain-inducing mechanisms.In the third report, we investigate the molecular characteristics of the interaction between membrane PIPn and the various P2X receptors that were shown to be directly modulated by the phospholipids. By analyzing the functional and PIPn-binding effects of various mutations performed on the C-terminal domain of the PIPn-sensitive P2X1, P2X4 and P2X7 subtypes as well as on the PIPn-insensitive P2X5 subtype, we identify the PIPn-binding regulatory motif of P2X receptors. The last article included in this thesis examines the dynamic changes in channel permeability brought by sustained activation of the microglial P2X4 receptor. We show that upon sustained ATP application, P2X4 channels form large conductance pores allowing the flux of large organic molecules. The large pore formation of co-expressed microglial P2X7 receptors has been extensively studied; we show here that P2X4-mediated permeation is mechanistically distinct and, in contrast with P2X7, does not induce membrane blebbing or cell death. Furthermore, we demonstrate that membrane PIPn potentiate the formation of this high-conductance P2X4 pore, suggesting that this property can be regulated by metabotropic changes in PIPn levels.
Longtemps après la découverte de sa présence dans l'ADN et de son rôle en tant que principale source d'énergie chimique dans la cellule, le nucléotide adenosine-5'-triphosphate (ATP) est maintenant considéré comme une importante molécule de signalisation extracellulaire. La transmission purinergique est activement impliquée dans plusieurs processus physiologiques, notamment dans la neuro- et glio-transmission, la modulation de la réponse immunitaire innée et adaptative, la constriction vasculaire et la coagulation sanguine. Elle participe aussi à la génération et au maintien de divers états pathologiques, tels la douleur chronique neuropathique et inflammatoire.La signalisation purinergique est impliquée dans des processus aussi diversifiés par l'entremise d'une seule molécule de signalisation grâce à une grande variété de récepteurs activés par l'ATP. Les deux principaux types de récepteurs sensibles à l'ATP sont les récepteurs ionotropiques P2X et les récepteurs métabotropiques P2Y. La famille P2X de canaux ioniques activés par l'ATP est composée de sept sous-unités qui s'assemblent comme trimères pour former des récepteurs possédant divers profils fonctionnels et pharmacologiques. Comme tous les canaux ioniques, l'activité des P2X est étroitement régulée par des mécanismes de régulation orthostériques et allostériques. Cette thèse démontre l'existence d'un nouveau type de mécanisme de régulation post-traductionnel, où les niveaux de phosphoinositides (PIPn) intracellulaires modulent l'activité de canal ionique des récepteurs P2X.Le premier article porte sur le sous-type P2X1, qui contribue à la contraction des muscles lisses dans les vaisseaux sanguins et le canal déférent, ainsi qu'à l'agrégation plaquettaire. Nous démontrons que l'activité du récepteur canal P2X1 est positivement régulée par les PI(4,5)P2 (PIP2) membranaires. La déplétion des niveaux intracellulaires de PIP2 diminue l'amplitude du courant ionique induit par P2X1. Nous montrons que le couplage direct entre le domaine C-terminal cytosolique de P2X1 et PIP2 est nécéssaire pour l'expression complète de l'activité de P2X1.Le second article de cette thèse décrit la régulation PIPn-dépendante du récepteur canal P2X4, qui joue un rôle majeur dans la génération et le maintien de la douleur neuropathique et inflammatoire par son expression dans les microglies de la moelle épinière. Nous démontrons que le fonctionnement de P2X4 dépend des niveaux de PIP2 et de PI(3,4,5)P3 (PIP3). Les deux types de phospholipides potentialisent le courant ionique ainsi que l'entrée de calcium par le canal P2X4 en se liant directement au domaine C-terminal des sous-unités P2X4. Dans le troisième rapport, nous étudions les caractéristiques moléculaires de l'interaction entre les PIPn membranaires et les récepteurs P2X directement modulés par ces phospholipides. En analysant les effets fonctionnels de diverses mutations effectuées sur le domaine C-terminal des sous-types PIPn-dépendant P2X1, P2X4 et P2X7 et sur le sous-type PIPn-indépendant P2X5, nous identifions le motif nécessaire à la liaison P2X-PIPn et à la régulation fonctionnelle du canal par les PIPn.Le dernier article de cette thèse examine les changements dynamiques de la perméabilité du canal ionique apportés par une activation soutenue des récepteurs microgliaux P2X4. Nous montrons que, lors d'une application soutenue d'ATP, les canaux P2X4 forment des pores à haute conductance permettant le flux de molécules organiques à haut poids moléculaire. La formation de larges pores par les récepteurs P2X7 a été étudiée intensivement; nous démontrons ici que la perméation induite par P2X4 est mécanistiquement distincte et, à l'opposé de P2X7, ne mène à aucun réarrangement de la structure membranaire ni à la mort cellulaire. Les PIPn membranaires potentialisent la formation de ces pores à haute conductance par P2X4, suggérant que cette propriété peut être régulée par des changements intracellulaires des niveaux de PIPn.
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Rutherford, Anna. "3-phosphoinositides and their effectors in endosomal sorting." Thesis, University of Bristol, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.434740.

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Hammond, Gerald Raymond Vere. "The role of phosphoinositides in mast cell exocytosis." Thesis, University College London (University of London), 2005. http://discovery.ucl.ac.uk/1445567/.

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The phosphoinositides (Pin) are a family of phospholipids that contain myo inositol as their headgroup. Despite being present in eukaryotic membranes with low abundance, their high rates of metabolic turnover allow them to control a plethora of cellular functions. In particular, phosphatidylinositol 4,5-&wphosphate (PtdIns(4,5)P2) regulates several processes, including preparing secretory organelles to undergo fusion with the plasma membrane in response to a stimulus (regulated exocytosis), budding and fission of vesicular cargo from the plasma membrane (endocytosis), and controlling the cortical actin cytoskeleton. In this thesis, the role of Pin in regulated exocytosis is examined in mast cells, since these undergo an acute, massive and rapid exocytosis, without any immediate endocytosis. Using a reconstitution approach, it was not possible to define which Pin are involved in exocytosis, although it was concluded that at least one Pin that is not PtdIns(4,5)P2 is required. In order to study PtdIns(4,5)P2 dynamics in primary mast cells, a novel quantitative immunofluoescence technique for Pin was established. Using this technique, PtdIns(4,5)P2 was identified at the plasma membrane of mast cells, but was depleted almost entirely during exocytosis the latter observation was confirmed using biochemical approaches. This depletion was blocked by inhibitors of phospholipase C (PLC), an enzyme that breaks down PtdIns(4,5)P2 into diacylglycerol (DAG) and the calcium mobilising messenger, inositol 1,4,5-frisphosphate (Ins(l,4,5)P3). Although PLC activity was required for initiation of calcium signalling in mast cells, experiments whereby the Ins(l,4,5)P3/calcium pathway was bypassed demonstrated further requirements for PLC activity. These were not precisely defined, but simple elimination of plasma membrane PtdIns(4,5)P2 or production of DAG were not sufficient. Both events may be required in conjunction, however. A model is proposed whereby elimination of plasma membrane PtdIns(4,5)P2 together with production of DAG may activate the protein machinery for membrane fusion during exocytosis.
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Books on the topic "Phosphoinositides"

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Bruzik, Karol S., ed. Phosphoinositides. Washington, DC: American Chemical Society, 1998. http://dx.doi.org/10.1021/bk-1999-0718.

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Botelho, Roberto J., ed. Phosphoinositides. New York, NY: Springer US, 2021. http://dx.doi.org/10.1007/978-1-0716-1142-5.

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FALASCA, MARCO, ed. Phosphoinositides and Disease. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8.

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Bleasdale, John E., Joseph Eichberg, and George Hauser, eds. Inositol and Phosphoinositides. Totowa, NJ: Humana Press, 1985. http://dx.doi.org/10.1007/978-1-4612-5184-2.

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Shamshad, Cockcroft, ed. Biology of phosphoinositides. Oxford: Oxford University Press, 2000.

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W, Putney James, ed. Phosphoinositides and receptor mechanisms. New York: A.R. Liss, 1986.

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Majumder, A. Lahiri, and B. B. Biswas, eds. Biology of Inositols and Phosphoinositides. Boston, MA: Springer US, 2006. http://dx.doi.org/10.1007/0-387-27600-9.

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Balla, Tamas, Matthias Wymann, and John D. York, eds. Phosphoinositides II: The Diverse Biological Functions. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-3015-1.

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S, Bruzik K., American Chemical Society. Division of Carbohydrate Chemistry., and American Chemical Society Meeting, eds. Phosphoinositides: Chemistry, biochemistry, and biomedical applications. Washington, DC: American Chemical Society, 1999.

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E, Bleasdale John, Eichberg Joseph 1935-, Hauser George, and Chilton Conference on Inositol and Phosphoinositides (1984 : Southwestern Medical School), eds. Inositol and phosphoinositides: Metabolism and regulation. Clifton, NJ: Humana Press, 1985.

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Book chapters on the topic "Phosphoinositides"

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D’Angelo, G., M. Vicinanza, A. Di Campli, and M. A. De Matteis. "The Phosphoinositides." In Handbook of Neurochemistry and Molecular Neurobiology, 269–88. Boston, MA: Springer US, 2009. http://dx.doi.org/10.1007/978-0-387-30378-9_11.

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Weiger, Michael C., and Carole A. Parent. "Phosphoinositides in Chemotaxis." In Subcellular Biochemistry, 217–54. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-3015-1_7.

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Maffucci, Tania. "An Introduction to Phosphoinositides." In Phosphoinositides and Disease, 1–42. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_1.

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Amoasii, Leonela, Karim Hnia, and Jocelyn Laporte. "Myotubularin Phosphoinositide Phosphatases in Human Diseases." In Phosphoinositides and Disease, 209–33. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_10.

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Mongiorgi, Sara, Matilde Y. Follo, Cristina Clissa, Roberto Giardino, Milena Fini, Lucia Manzoli, Giulia Ramazzotti, Roberta Fiume, Carlo Finelli, and Lucio Cocco. "Nuclear PI-PLC β1 and Myelodysplastic Syndromes: From Bench to Clinics." In Phosphoinositides and Disease, 235–45. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_11.

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Hakim, Sandra, Micka C. Bertucci, Sarah E. Conduit, David L. Vuong, and Christina A. Mitchell. "Inositol Polyphosphate Phosphatases in Human Disease." In Phosphoinositides and Disease, 247–314. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_12.

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Ghigo, Alessandra, Alessia Perino, and Emilio Hirsch. "Phosphoinositides and Cardiovascular Diseases." In Phosphoinositides and Disease, 43–60. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_2.

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Bridges, Dave, and Alan R. Saltiel. "Phosphoinositides in Insulin Action and Diabetes." In Phosphoinositides and Disease, 61–85. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_3.

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Wen, Peter J., Shona L. Osborne, and Frederic A. Meunier. "Phosphoinositides in Neuroexocytosis and Neuronal Diseases." In Phosphoinositides and Disease, 87–98. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_4.

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Larijani, Banafshé, and Dominic L. Poccia. "Effects of Phosphoinositides and Their Derivatives on Membrane Morphology and Function." In Phosphoinositides and Disease, 99–110. Dordrecht: Springer Netherlands, 2012. http://dx.doi.org/10.1007/978-94-007-5025-8_5.

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Conference papers on the topic "Phosphoinositides"

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Tysnes, O.-B., AJ M. Verhoeven, and H. Holmsen. "Thrombin stimulation of human platelets:Phosphoinositides as the only source of the diacylglycerol moiety in phosphatidic acid." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644505.

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Recent reports on various cell types including platelets have concluded in the heterogenous production of phosphatidic acid (PA) during the stimulus-response coupling. Human platelets were pulse-labelled simultaneously with [32P] P. and [32H]glycerol. Extracts were analyzed for masses and radioactivities of ATP and phosphoinositides. When the cells were stimulated with low concentrations of thrombin, the production of [32P] PA was evident without measurable production of [3H] PA. At higher doses of the agonist,[3H] PA was formed, but distinctly later than [32P] PA.This suggested a heterogenous production of PA upon thrombin stimulation of platelets. The specific H-radioactivity of PA in unstimulated cells was about 50% of that of the phosphoinositides. Upon l80 sec of stimulation with 0.5 U/ml of thrombin, the specific [3H] PA radioactivity increased to the level of the phosphoinositides which remained constant during platelet activation. Since other phospholipids incorporate [3H] glycerol much slower than the phosphoinositides, these latter remain the only possible source of the diacylglycerol moiety of PA. The specific 32P-radioactivity of PA in unstimulated cells was only 4% of that of α-ATP and similar to the specific 32P-radioactivity of phosphatidylinositol in unstimulated platelets. After Jyijin of stimulation with 0.5 U/ml of thrombin, specific [32P] PA was similar to that of γ-ATP. The descrepancy in [32P] Pi. and [3H] glycerol incorporation into PA upon thrombin stimulation of platelets is therefore mainly due to a thrombin-induced shift inspecific 32P-radioactivity in PA.
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Tysnes, Q.-B., A. J. M. Verhoeven, G. M. Aarbakke, and H. Holmsen. "Phosphoinositide metabolism in resting and thrombin-stimulated human platelets: Evidence for metabolic homogeneity." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644517.

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On the basis of differences in specific radioactivity (SA), separate pools of phosphoinositides have recently been proposed in platelets. Human platelets were labelled for 60 min with [32p]p- and subsequently transferred to a phosphate- and Ca2+free Tyrode’s solution by gel-filtration. Thereafter, the platelets were either incubated at 37°C for 120 min, a condition which induces increase in specific labelling of the diester phosphate of phosphatitylinositol (PI), or stimulated with 0.5 U/ml of thrombin. The changes in SA of both diester and monoester phosphates of the phosphoinositides were detrmined. Immediately after the gel filtration, the SA of the diester phosphate of phosphatidylinositol-4-phosphate (PIP) and phosphatidylinositol-4,5-bisphosphate (PIP2) were both similar to that of PI and amounted to 4% or the SA of the monoester groups of PIP and PIP2- Whereas the SA of the monoester phosphate essentially remained constant and the same for PIP and PIP2 during the entire incubation, the SA of their diester phosphates increased gradually in parallel to that of PI, and reached 20% of the monoster groups after 120 min. The effect of thrombin was studied at 15, 60 and 180 sec after the addition. The absolute radioactivity of both diester and monoester phosphates of all phosphoinositides increased conciderably after an initial decrease. However, for the monoester groups, the changes in radioactivity were parallelled by the changes in mass for both PIP and PIP2. Thrombin therefore induced no changes in SA of the monoester phosphates. In contrast, the SA of the diester phosphates increased 5-fold and remained similar for all three phosphoinositides during the 180 sec of stimulation.In conclusion, our results demonstrate close metabolic equilibrium between all three phosphoinositides.Thrombin-induced changes in SA of PIP and PIP2 are purely secondary to changes in specific labelling of the diester phosphate.
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Medini, L., P. Maderna, E. Tremoli, and C. Galli. "PLATELETS FROM TYPE IIA HYPERCHOLESTEROLEMIC PATIENTS GENERATE MORE INOSITOLPHOSPHATES AFTER THROMBIN STIMULATION IN COMPARISON WITH THOSE OF NORMAL SUBJECTS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643415.

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Functional and biochemical responses of platelets to stimulating agents have been reported to be amplified in several pathological conditions, including hyperlipidemia. Enhanced aggregation and thromboxane formation are, e.g. frequently observed in the presence of high plasma cholesterol levels (type Ila hypercholesterolemia). Stimulation of phosphoinositides breakdown through specific phosphohydrolases (phospholipase C) resulting in the formation of inositolphosphates (IPs), is one of the early events in platelet activation. A study was thus designed in order to investigate IPs generation in thrombin stimulated platelets from type Ila hypercholesterolemic patients in comparison with a group of normocholesterolemic subjects. Preparation of washed platelets, prelabelling with 2[3H] myo inositol and separation of lipid and water soluble inositides was carried out according to Watson et al (1). Product generation (inositoltrisphosphate, IP3; inositolbisphosphate, IP2; inositol mono phosphate, IP) in relation to the 2[3H) inositol incorporated in phosphoinositides was evaluated at 10 and 90 s after platelet stimulation with 1 U/ml NIH in the presence of 10 mM lithium chloride. The major differences found in platelets from type Ila patients in comparison with those of controls were the following:1) in non stimulated platelets a greater incorporation of myoinositol in phosphoinositides and lower levels of labelled IP2; 2) after stimulation, the levels of all labelled IPs were significantly greater, and those of IP2 were double than in controls. In particular the percent increment of IP2 over basal values in platelets of type Ila patients was more than two fold greater. It is concluded that the enhanced generation of IPs in platelets from type IIa patients, following thrombin stimulation, may contribute to the greater sensitivity to agonists of the aggregatory process in this pathological condition.1) Watson P.S., McConnell R.T. and Lapetina E.G., J. Biol. Chem.21:13199, 1984
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Lete, Marta, Hasna Ahyayauch, Jesús Sot, Felix Goni, and Alicia Alonso. "Histones Bind, Aggregate and Fuse Phosphoinositides Containing Bilayers." In MOL2NET, International Conference on Multidisciplinary Sciences. Basel, Switzerland: MDPI, 2015. http://dx.doi.org/10.3390/mol2net-1-b035.

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Mattson, C. J., and W. D. Estry. "EFFECTS OF 12-O-TETRADECANOYL PH0RB0L-13-ACETATE (TPA) ON PLATELET ADHESION-INDUCED SHAPE CHANGE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643552.

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Adherent platelets undergo changes in shape which involve conversion of the resting discoid platelet to a sphered or dentritic/pseudopodial form followed by cytoplasmic spreading to produce a fully spread cell with centralized organelles. Platelets from donors who have taken 10 gr aspirin (ASA) 4 hr prior to venipuncture show adequate pseudopod formation but defective spreading. Addition of 0.5 uM ADP is sufficient to reconstitute normal spreading suggesting that shape change is a two step process and that formation of spread platelets may require release of dense granule ADP. Since activation of platelets in suspension by ADP is associated with degradation of phosphoinositides and phosphorylation of a 40 KD protein, the potential role of this pathway in the formation of spread platelets was examined. Citrated platelets formed large aggregates when stimulated by TPA interfering with evaluation of adhesion and contact-activated shape change. When EGTA treated platelets were stimulated with TPA, aggregation was blocked but adhesion and spreading were unaffected by calcium chelation in the presence of magnesium. Therefore ASA-inhibited, EGTA-treated platelets were stimulated with 100 ng/ml TPA to activate protein kinase C, and platelet morphology was evaluated by whole mount transmission electron microscopy. TPA stimulated platelets underwent normal shape change to the fully spread stage despite endoperoxide inhibition by ASA. This data supports a role for ADP-trigqered phosphoinositide degradation in the spreading phase of adhesion induced shape change.
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Koutouzov, S., A. Remmal, P. Marche, and P. Meyer. "IMPAIRMENT OF PLATELET PHOSPHOINOSITIDE METABOLISM IN PRIMARY HYPERTENSION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643812.

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Blood platelets from hypertensive patients and spontaneously hypertensive rats (SHR) display multiple abnormalities when compared with cells from normotensive controls. The major features of the modified platelet profile are an enhanced rate of adhesion/aggregation in response to many stimuli, a greater sensitivity for thrombin and adrenaline to produce increases in cytoplasmic free Ca2+, and an exaggerated release reaction. Furthermore, the resting levels of cytosolic free Ca2+ ions are specifically and constantly increased. Since phosphoinositides are involved in the stimulus-response coupling mediated by intracellular Ca2+ mobilization, the metabolism of these lipids was investigated in platelets of SHR and compared with those of normotensive Wistar-Kyoto rats (WKY). Following 32P-labelling of quiescent platelets, labeled lipids were analyzed both in platelets at rest and after thrombin stimulation. In resting platelets, the 32P associated with each of the phosphoinositides and phosphatidic acid (PA) was similar in SHR and WKY indicating that both the pool size of the various lipids and their basal turnover did not differ between the two strains. By contrast, within the first seconds after thrombin stimulation (10-60 sec), the dose-response and time-course curves of agonist-induced increase in 32P-PA were markedly shifted to the left and reached higher equilibrium levels in SHR. Since thrombin-induced 32P-PA formation is held as the most sensitive index of phospholipase C activity, our results indicate that this enzyme displays hyperreactivity in SHR (vs WKY). It is therefore likely that in SHR, the enhanced physiological responses (serotonin secretion, aggregation) that we observed under the same experimental conditions may be related to an increased formation of Phospholipase C products (inosi-toltriphosphate and diacylglycerol) which are the two second messengers responsible for internal Ca2+ mobilization and activation of protein kinase C, respectively. Therefore, these data suggest that the hypersensitivity of Phospholipase C may be involved in the overall alteration of cell calcium handling and hence in the SHR platelet responses.
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Rendu, F., T. Hovig, P. Marche, M. Lebret, D. Tenza, J. Maclouf, J. P. Caen, and S. Levy-Toledano. "MEMBRANE SIGNAL TRANSDUCTION IN PLATELETS WITH ALTERED RELEASE REACTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644746.

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The process of signal transduction during thrombin-induced activation was studied in pathological platelets characterized by a defect in a specific storage granule, i.e. from Hermansky-Pudlak syndrome (HPS) and from Grey-Platelet Syndrome (GPS). HPS platelets exhibited an apparently normal ultrastructure except for a decreased number of dense bodies. Grey platelets showed marked vacuolization and an almost total absence of alpha-granules. During thrombin stimulation both types of platelets showed the same tendency of centralization of the organelles present indicating that neither type of granule is a prerequisite for this ring-like structure.However this granule centralization was clearly delayed in GPS where it occurred 15 sec after thrombin addition instead of 5 sec in normal platelets. The transducing system involving phosphoinositides specific phospholipase C was observed in platelets lacking dense bodies (HPS) but the phosphatidyl 4,5 bisphosphate(PIP2 )breakdown in 32P-prelabelled platelets was measurable at 202 sec instead of 10 sec in normal platelets. No ch activity was detectable at any time in grey platelets. 32P-phosphatidate (PA) formation was subnormal in HPS platelets and normal in grey platelets. Phosphorylation pattern of myosin light chain (P20) and of 43K protein (P43) were normal in HPS platelets and markedly reduced in grey platelets, being less than half of the normal during the first 15 sec and remaining subnormal even after complete aggregation. The release of constituents from the present granules and the thromboxane formation were lower than in normal platelets in all cases. In conclusions, (i) alpha-granules but not dense bodies may play a key role in the activation of the PIP2 specific phospholipase C,(ii) PA formation does not always correlate with phosphoinositide metabolism and could originate from another pool of diacylglycerol,(iii) complete phosphorylations of both P20 and P43 may not be sufficient to stimulate a normal release, and (iv) end products such as thromboxanes and released ADP accelerate and reinforce platelet responses.
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Huzoor-Akbar, H., and Khursheed Anwer. "EVIDENCE THAT ABNORMAL PLATELET AGGREGATION IN SPONTANEOUSLY HYPERTENSIVE RATS IS LINKED WITH PHOSPHOINOSITIDES TURNOVER AND PHOSPHORYLATION OF 47,000 DALTON PROTEIN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643810.

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We have shown earlier that abnormal platelet aggregation in spontaneously hypertensive rats (SHR) is not caused by prostaglandins (Thromb. Res. 41, 555-566, 1986). In this study platelets from SHR and normotensive (Wistar Kyoto, WKY) rats were used to examine the role of phosphoinositides (Pins) and protein phosphorylation in increased platelet activation in hypertension. Thrombin (0.05 U/ml) induced rapid hydrolysis of phosphatidylinositol-4,5-bis-phosphate (PIP2), phosphatidyl-inositol-4-phosphate (PIP), and phosphatidylinositol (PI) in (32p)-pO4 labeled platelets. However, significantly greater hydrolysis of PIP2 and PI was seen in SHR platelets than in WKY platelets (see Table). Thrombin also caused two- to three-fold increased accumulation of phosphatidic acid (PA) in SHR platelets than in WKY platelets (see Table).Thrombin caused phosphorylation of 18,000 Dalton (P18) and 47, Dalton (P47) proteins in SHR and WKY Platelets. Significantly increased phosphorylation of P47 was seen at 5, 15, 60 and 240 seconds of incubation with thrombin in SHR platelets (60%, 68%, 98% and 91%) than in WKY platelets (13%, 37%, 44% and 47%). The extent of P18 phosphorylation was same in both SHR and WKY platelets. Aspirin (500 uM) did not affect phosphorylation of P47 or P18 in SHR or WKY Platelets. These data lead us to suggest that increased turnover of Pins and increased phosphorylation of P47 are involved in abnormal platelet aggregation in SHR (Supported in part by the COHC grant #86-01-A and the Ohio University College of Osteopathic Medicine).
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Machado, Roberta Ismael Lacerda, Bruno de Mattos Lombardi Badia, Wladimir Bocca Vieira de Rezende Pinto, Igor Braga Farias, José Marcos Vieira de Albuquerque Filho, Paulo Victor Sgobbi de Souza, and Acary Souza Bulle Oliveira. "INPP5K-Related congenital muscular dystrophy: when juvenile cataracts give clues to a complex diagnosis." In XIII Congresso Paulista de Neurologia. Zeppelini Editorial e Comunicação, 2021. http://dx.doi.org/10.5327/1516-3180.511.

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Introduction: Congenital muscular dystrophies (CMDs) are a group of rare genetic muscle diseases that present at birth or during infancy with hypotonia and weakness. Multiple forms of CMDs are also associated with cerebral and ocular phenotypes. Recently, INPP5K mutations have been described associated with CMD, cataracts and cognitive impairment. The INPP5K gene, encodes SKIP, one of the enzymes that phosphorylate the 5-phosphate position of phosphoinositides and is highly expressed in developing and adult brain, eye and muscle. Methods: We performed a case report of three Brazilian patients with INPP5KCMD with cataracts and intellectual disability under clinical follow-up at our service. Results: Case 1: 39 years old, female, presenting with progressive leg weakness since childhood, mild intellectual disability and bilateral cataracts at 20 years. Her 35-yearold sister (Case 2) had a similar clinical picture with limb-girdle weakness since childhood, cognitive impairment and early- onset bilateral cataracts. Both with myopathic pattern in EMG, elevated creatine phosphokinase (CK) and dystrophic pattern in muscle biopsy. Brain MRI studies disclosed a large megacistern in the elderly and no abnormalities in the younger sister. Genetic testing: c.653_655del(p.(Ser218del) in homozygosity in INPP5K gene. Case 3: 20 years old, female, normal motor development but learning difficulties since childhood. Presented with progressive pelvic girdle weakness in childhood and bilateral cataracts in late adolescence. Exams disclosed elevated CK, brain MRI was normal and genetic testing with the following mutation in INPP5K gene:c.[881_883del];[1088T>C];p.[Ser294del];[Ile363Thr]. Conclusion: We describe patients with CMD, cataracts and intellectual disability, caused by mutation in the INPP5K gene. In literature few cases are reported.
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Winocour, P. P., P. D. Rand, J. D. Vickers, R. L. Kinlough-Rathbone, and J. F. Mustard. "ENHANCED THROMBIN-INDUCED AGGREGATION AND INOSITOL TRISPHOSPHATE FORMATION OF PLATELETS FROM SPONTANEOUSLY HYPERCHOLESTEROLEMIC RATS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643811.

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Platelets from rats with diet-induced hypercholesterolemia are hypersensitive to thrombin through a pathway independent of released ADP or thromboxane A2 (TXA2) formation. We examined if platelets from rats with spontaneous hypercholesterolemia (HC) are similarly hypersensitive. HC rats (plasma cholesterol: 130±4 mg/dl, n=15) were compared with their normocholesterolemic genetic controls (NC) (87±4 mg/dl, p<0.001, n=16). Total cholesterol/109 platelets was not different between the groups (HC: 0.314±0.032 μmole, n=7; NC: 0.357±0.046 ymole, n=7). Washed platelets were prelabelled with 14c-serotonin. In the presence of aspirin (to inhibit TXA2 formation) and creatine phosphate/creatine phosphokinase (CP/CPK) (to remove released ADP), HC platelets aggregated more (22±2%, n=ll) than NC platelets (10±4%, n=12, p<0.01) in response to thrombin (0.065 U/ml); 14C release was not different. Thrombin causes inositol mono-, bis-, and trisphosphate (IP, IP2, IP3) formation from phosphoinositides (PI, PIP, PIP2 respectively) in rabbit platelets; IP3 may be involved in Ca++ mobilization and the release of granule contents. We examined if enhanced inositol phosphate formation was associated with hypersensitivity of HC platelets. Platelets were prelabelled with 3H-inositol and stimulated with thrombin (0.057 U/ml) for 30 sec in the presence of aspirin and CP/CPK. Li+ (20 mM) was used to prevent degradation of inositol phosphates to inositol. 3H-IP, IP2 and IP3 were isolated by ion-exchange chromatography. The increase in radioactivity (dpm/109 platelets) in IP2 and IP3 following thrombin stimulation was greater in HC platelets (IP2: 2210±160, n=4; IP3: 1430±180, n=4) than in NC platelets (IP2: 660±150, n=4, p<0.001; IP3: 490±100, n=4, p<0.01); IP was not different.Thus platelets from spontaneously HC rats are hypersensitive to thrombin independently of released ADP or TXA2 formation. This hypersensitivity is associated with only moderate increases in plasma cholesterol and no detectable increase in total platelet cholesterol. Enhanced labelling of IP3 may indicate that enhanced activity of the pathways leading to IP3 formation is associated with this hypersensitivity.
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Reports on the topic "Phosphoinositides"

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Jerde, Travis J. Phosphoinositide-Driven Epithelial Proliferation in Prostatic Inflammation. Fort Belvoir, VA: Defense Technical Information Center, January 2008. http://dx.doi.org/10.21236/ada485294.

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Jerde, Travis J., and Wade Bushman. Phosphoinositide-Driven Epithelial Proliferation in Prostatic Inflammation. Fort Belvoir, VA: Defense Technical Information Center, April 2009. http://dx.doi.org/10.21236/ada510023.

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Jope, Richard S. Activation of Phosphoinositide Metabolism by Cholinergic Agents. Fort Belvoir, VA: Defense Technical Information Center, December 1990. http://dx.doi.org/10.21236/ada235299.

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Cheng, Jin Q. Phosphoinositide 3-Kinase/AKT1 Pathway and Human Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2001. http://dx.doi.org/10.21236/ada406214.

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Yuan, Tina. The Role of Phosphoinositide 3-Kinase in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, October 2010. http://dx.doi.org/10.21236/ada541781.

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Cheng, Jin Q. Phosphoinositide 3-Kinase/AKT1 Pathway and Human Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2002. http://dx.doi.org/10.21236/ada412768.

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Cheng, Jin Q. Phosphoinositide 3-Kinase/AKT1 Pathway and Human Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada420944.

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Cheng, Jin Q. AKT2 Oncogene and Phosphoinositide 3-Kinase in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2004. http://dx.doi.org/10.21236/ada430371.

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Cheng, Jin Q. AKT2 Oncogene and Phosphoinositide 3-Kinase in Human Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, September 2003. http://dx.doi.org/10.21236/ada421343.

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Sellers, William R. The Development of Novel Small Molecule Inhibitors of the Phosphoinositide-3-Kinase Pathway Through High-Throughput Cell-Based Screens. Fort Belvoir, VA: Defense Technical Information Center, February 2005. http://dx.doi.org/10.21236/ada435277.

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