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Relevant bibliographies by topics / Phosphatidylinositols

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Academic literature on the topic 'Phosphatidylinositols'

Author: Grafiati

Published: 4 June 2021

Last updated: 21 February 2023

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Journal articles on the topic "Phosphatidylinositols"

1

Morisaki, Naoko, Koji Morita, Asuka Nishikawa, Noriyuki Nakatsu, Yasuhisa Fukui, Yuichi Hashimoto, and Ryuichi Shirai. "Phosphorylation of Unnatural Phosphatidylinositols with Phosphatidylinositol 3-Kinase." Tetrahedron 56, no. 17 (April 2000): 2603–14. http://dx.doi.org/10.1016/s0040-4020(00)00161-7.

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Shirai, Ryuichi, Koji Morita, Asuka Nishikawa, Noriyuki Nakatsu, Yasuhisa Fukui, Naoko Morisaki, and Yuichi Hashimoto. "The structural requirement of phosphatidylinositols as substrate of phosphatidylinositol 3-kinase." Tetrahedron Letters 40, no. 9 (February 1999): 1693–96. http://dx.doi.org/10.1016/s0040-4039(99)00004-0.

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3

Fan, Zheng, Lizhi Gao, and Wenxia Wang. "Phosphatidic acid stimulates cardiac KATPchannels like phosphatidylinositols, but with novel gating kinetics." American Journal of Physiology-Cell Physiology 284, no. 1 (January 1, 2003): C94—C102. http://dx.doi.org/10.1152/ajpcell.00255.2002.

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Membrane-bound anionic phospholipids such as phosphatidylinositols have the capacity to modulate ATP-sensitive potassium (KATP) channels through a mechanism involving long-range electrostatic interaction between the lipid headgroup and channel. However, it has not yet been determined whether the multiple effects of phosphatidylinositols reported in the literature all result from this general electrostatic interaction or require a specific headgroup structure. The present study investigated whether phosphatidic acid (PA), an anionic phospholipid substantially different in structure from phosphatidylinositols, evokes effects similar to phosphatidylinositols on native KATP channels of rat heart and heterogeneous Kir6.2/SUR2A channels. Channels treated with PA (0.2–1 mg/ml applied to the cytoplasmic side of the membrane) exhibited higher activity, lower sensitivity to ATP inhibition, less Mg2+-dependent nucleotide stimulation, and poor sulfonylurea inhibition. These effects match the spectrum of phosphatidylinositols' effects, but, in addition, PA also induced a novel pattern in gating kinetics, represented by a decreased mean open time (from 12.2 ± 2.0 to 3.3 ± 0.7 ms). This impact on gating kinetics clearly distinguishes PA's effects from those of phosphatidylinositols. Results indicate that multiple effects of anionic phospholipids on KATP channels are related phenomena and can likely be attributed to a common mechanism, but additional specific effects due to other mechanisms may also coincide.

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Shirai, Ryuichi, Koji Morita, Asuka Nishikawa, Noriyuki Nakatsu, Yasuhisa Fukui, Naoko Morisaki, and Yuichi Hashimoto. "ChemInform Abstract: The Structural Requirement of Phosphatidylinositols as Substrate of Phosphatidylinositol 3-Kinase." ChemInform 30, no. 21 (June 15, 2010): no. http://dx.doi.org/10.1002/chin.199921219.

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Garigapati, Venkata R., and Mary F. Roberts. "Synthesis of short chain phosphatidylinositols." Tetrahedron Letters 34, no. 5 (January 1993): 769–72. http://dx.doi.org/10.1016/0040-4039(93)89007-d.

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Raper, J., T. L. Doering, L. U. Buxbaum, and P. T. Englund. "Glycosyl Phosphatidylinositols in Trypanosoma brucei." Experimental Parasitology 76, no. 2 (March 1993): 216–20. http://dx.doi.org/10.1006/expr.1993.1026.

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MCCONVILLE, M. "Glycosylated-phosphatidylinositols as virulence factors in." Cell Biology International Reports 15, no. 9 (September 1991): 779–98. http://dx.doi.org/10.1016/0309-1651(91)90033-f.

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EKHOLM, S. E., T. W. MORRIS, and G. V. MARINETTI. "Effects of Contrast Media on Synaptosomal Phosphatidylinositols." Investigative Radiology 25 (September 1990): S84—S85. http://dx.doi.org/10.1097/00004424-199009001-00039.

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Sandelius, Anna Stina, and Marianne Sommarin. "Phosphorylation of phosphatidylinositols in isolated plant membranes." FEBS Letters 201, no. 2 (June 9, 1986): 282–86. http://dx.doi.org/10.1016/0014-5793(86)80624-x.

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D'Souza, Kenneth, and Richard M. Epand. "Enrichment of phosphatidylinositols with specific acyl chains." Biochimica et Biophysica Acta (BBA) - Biomembranes 1838, no. 6 (June 2014): 1501–8. http://dx.doi.org/10.1016/j.bbamem.2013.10.003.

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Dissertations / Theses on the topic "Phosphatidylinositols"

1

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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Dyer, Blake S., and n/a. "The synthesis and characterisation of phosphatidylinositol mannans." University of Otago. Department of Chemistry, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080415.142001.

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Mycobacterial cell wall components have been shown to elicit a range of immunological responses in mammalian hosts. A family of cell wall antigens, the phosphatidylinositol mannans (PIMs), have been shown to reduce allergic response in a murine model of allergic airway disease and have been suggested as potential therapeutic agents. Isolation and characterisation of these compounds is not facile. To confirm the structure of PIMs a number of phosphatidylinositols (PIs), 1a-c, PIM1s 2a, 2d and 2e, and AcPIM1s, 2g and 2f, were prepared to allow assignment of the acylation pattern of natural products and for evaluation in immunological assays. As the natural products include 19:0 acylation in the form of (R)-tuberculostearoyl residues, a source of (R)-tuberculostearic acid was needed. To this end, an efficient synthesis of (R)-tuberculostearic acid from (S)-citronellol, utilising a copper-catalysed cross-coupling reaction and a modified Julia olefination, was developed. This material was incorporated into diacylglycerols prepared from (R)-benzyl glycidol. A protected myo-inositol derivative, 188, and two protected pseudo-disaccharides, 10 and 241, were prepared from myo-inositol via desymmetrisation utilising a camphylidene acetal. These were coupled with diacylglycerols via a phosphate ester and deprotected to give PIs, PIM1s and AcPIM1s. Mass spectrometry studies were undertaken on the PIs, 1a-c, PIM1s 2a, 2d and 2e, and AcPIM1s, 2g and 2f which structures that have been established by chemical synthesis. Comparison of these data with those reported for natural PIs and PIMs containing 19:0 ((R)-tuberculostearoyl) and 16:0 (palmitoyl) acyl groups unequivocally established that the 19:0 residue was located at the sn-1 and the 16:0 at the sn-2 position of the glycerol moiety in nature.

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Kawashima, Masahiro. "High-resolution imaging mass spectrometry reveals detailed spatial distribution of phosphatidylinositols in human breast cancer." Kyoto University, 2014. http://hdl.handle.net/2433/188666.

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Riggs, Bridget May. "Phosphatidylinositol synthase of tetrahymena utilization of inositol isomers in the headgroup exchange reaction /." [Pensacola, Fla.] : University of West Florida, 2006. http://purl.fcla.edu/fcla/etd/WFE0000030.

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Hartley, David Alan. "Dissection of Lymphocyte Activation: Defining a Role for PI-3 Kinase." eScholarship@UMMS, 1996. http://escholarship.umassmed.edu/gsbs_diss/212.

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This dissertation was intended to identify potential roles for phosphatidylinositol-3 kinase (PI-3 kinase) in the responses of lymphocytes to activation. To understand what functions PI-3 kinase is performing in lymphocytes, experiments were performed to identify proteins that will stably associate with the p85 subunit of PI-3 kinase. Co-precipitation revealed an activation dependent association of p85 with two different phosphotyrosine containing proteins. One protein, pp36-38, is a membrane protein that interacts with PI-3 kinase, PLCγ1, and Grb2/S0S. The other associated protein was identified as the proto-oncogene c-Cbl. The interaction of p85 with cbl was shown to be mediated through the SH2 domains of p85. More importantly, the interactions of p85 with p36-38 and cbl were found to be specific for p85 isoforms. Although the SH2 domains of the α and β isoforms are highly similar in amino acid sequence, they are shown to establish distinct protein interactions in intact cells. Experiments on the cbl/PI-3 kinase complex revealed a stimulation dependent translocation into membrane and insoluble/cytoskeletal fractions of wild type, but not mutant cells. The movement of cbl did not require tyrosine phosphorylation or PI-3 kinase activity. The cbl/PI-3 kinase complex was greatly enhanced in the membrane fraction in contrast to the cytosol, where the largest concentration of cbl can be found. In addition, these complexes were found to form at the membrane in the absence of the tyrosine kinase, p56lck.

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Malaby, Andrew W. "An Integrated Structural Mechanism for Relief of Autoinhibition and Membrane Targeting in Cytohesin Family Guanine Nucleotide Exchange Factors: A Dissertation." eScholarship@UMMS, 2014. https://escholarship.umassmed.edu/gsbs_diss/703.

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Guanine nucleotide exchange factors (GEFs) regulate and organize diverse cellular processes through their role in converting GTPases from the inactive GDP bound state to the active GTP bound state. An increasing number of GEFs undergo autoregulatory mechanisms through complex intramolecular interactions. Relief of autoinhibition involves specific phosphorylation or binding to lipid and/or effector proteins at sites distal from the catalytic domain, and is often coupled to membrane recruitment. In Cytohesin Arf GEFs, the catalytic Sec7 domain is autoinhibited by a linker region and C-terminal helix flanking a Pleckstrin Homology (PH) domain. Upon binding of the PH domain to low abundance phosphoinositides, the GTPase Arf6-GTP can both relieve autoinhibition and recruit Cytohesins to the plasma membrane. This thesis focuses on determining the molecular mechanism underlying both these functions. The structural mechanisms by which Arf6-GTP binding relieves autoinhibition were studied using biochemical and crystallographic studies. The crystal structure of the Grp1 PH domain in complex with Arf6 revealed that Arf6-GTP binding relieves autoinhibition through competitive sequestration of the inhibitory elements into grooves formed at the periphery of the interface. Importantly, the interaction orients all known membrane targeting components to a common surface. Detailed biochemical studies showed a common mode of binding among Cytohesin family members in which phosphoinositide head group binding primes the interaction with Arf6, and membrane recruitment of both stimulatory and substrate Arf enhances the effect. To assess changes in the Sec7 domain conformation upon activation, Size Exclusion Chromatography in line with Small Angle X-Ray Scattering (SEC-SAXS) was performed. The unique nature of this data led to the development of a novel data analysis and processing strategy. A graphically based, python-extensible software package was created for data normalization, buffer correction, Guinier Analysis, and constant background subtraction. As an unbiased substitute for traditional buffer subtraction, a method to reconstruct the protein scattering through singular value decomposition (SVD) and linear combination of the basis vectors was developed. These methods produced exceptional data quality and allowed versatility for application to other data collection techniques or systems, especially those lacking confident buffer matching or low signal. SEC-SAXS confirmed the overall structure of autoinhibited Grp1 in solution and showed only slight overall changes upon activation by deletion of the autoinhibitory Cterminal helix. Fusion of Arf6 with Grp1 produced a consistently elongated shape in the active state that was incompatible with the autoinhibited or theoretical active positions of the Sec7 domain. Monte Carlo and rigid body modeling using known structural domains revealed a requirement for Sec7-PH linker flexibility in addition to Sec7 domain mobility. These data support an integrated structural model whereby phosphoinositides and Arf-GTP support nucleotide exchange at membranes through allosteric activation, membrane recruitment, and large-scale rearrangement of the Sec7 domain. Overall, these findings offer insight into Cytohesin function that can be applied to assess relief of autoinhibition in the context of other GEFs and GTPases.

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Malaby, Andrew W. "An Integrated Structural Mechanism for Relief of Autoinhibition and Membrane Targeting in Cytohesin Family Guanine Nucleotide Exchange Factors: A Dissertation." eScholarship@UMMS, 2004. http://escholarship.umassmed.edu/gsbs_diss/703.

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Guanine nucleotide exchange factors (GEFs) regulate and organize diverse cellular processes through their role in converting GTPases from the inactive GDP bound state to the active GTP bound state. An increasing number of GEFs undergo autoregulatory mechanisms through complex intramolecular interactions. Relief of autoinhibition involves specific phosphorylation or binding to lipid and/or effector proteins at sites distal from the catalytic domain, and is often coupled to membrane recruitment. In Cytohesin Arf GEFs, the catalytic Sec7 domain is autoinhibited by a linker region and C-terminal helix flanking a Pleckstrin Homology (PH) domain. Upon binding of the PH domain to low abundance phosphoinositides, the GTPase Arf6-GTP can both relieve autoinhibition and recruit Cytohesins to the plasma membrane. This thesis focuses on determining the molecular mechanism underlying both these functions. The structural mechanisms by which Arf6-GTP binding relieves autoinhibition were studied using biochemical and crystallographic studies. The crystal structure of the Grp1 PH domain in complex with Arf6 revealed that Arf6-GTP binding relieves autoinhibition through competitive sequestration of the inhibitory elements into grooves formed at the periphery of the interface. Importantly, the interaction orients all known membrane targeting components to a common surface. Detailed biochemical studies showed a common mode of binding among Cytohesin family members in which phosphoinositide head group binding primes the interaction with Arf6, and membrane recruitment of both stimulatory and substrate Arf enhances the effect. To assess changes in the Sec7 domain conformation upon activation, Size Exclusion Chromatography in line with Small Angle X-Ray Scattering (SEC-SAXS) was performed. The unique nature of this data led to the development of a novel data analysis and processing strategy. A graphically based, python-extensible software package was created for data normalization, buffer correction, Guinier Analysis, and constant background subtraction. As an unbiased substitute for traditional buffer subtraction, a method to reconstruct the protein scattering through singular value decomposition (SVD) and linear combination of the basis vectors was developed. These methods produced exceptional data quality and allowed versatility for application to other data collection techniques or systems, especially those lacking confident buffer matching or low signal. SEC-SAXS confirmed the overall structure of autoinhibited Grp1 in solution and showed only slight overall changes upon activation by deletion of the autoinhibitory Cterminal helix. Fusion of Arf6 with Grp1 produced a consistently elongated shape in the active state that was incompatible with the autoinhibited or theoretical active positions of the Sec7 domain. Monte Carlo and rigid body modeling using known structural domains revealed a requirement for Sec7-PH linker flexibility in addition to Sec7 domain mobility. These data support an integrated structural model whereby phosphoinositides and Arf-GTP support nucleotide exchange at membranes through allosteric activation, membrane recruitment, and large-scale rearrangement of the Sec7 domain. Overall, these findings offer insight into Cytohesin function that can be applied to assess relief of autoinhibition in the context of other GEFs and GTPases.

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8

Xiang, Hong. "Alpha₁-adrenoceptor-mediated phosphoinositide breakdown and inotropic responses in right ventricles of streptozotocin-diabetic rats." Thesis, University of British Columbia, 1990. http://hdl.handle.net/2429/31036.

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The morbidity of and the mortality from cardiac disease are higher in diabetic patients. Clinical and experimental evidence suggests that diabetes-induced changes at the level of myocardium can, at least partially, contribute to these cardiac problems. The mechanism(s) involved in this diabetic cardiomyopathy is still unclear, but one defect appears to occur in the alpha₁-adrenoceptor system. Altered myocardial sensitivity and responsiveness to alpha₁-adrenoceptor agonists have been reported in experimental diabetes mellitus. Stimulation of alpha₁-adrenoceptors is known to produce a positive inotropic effect and has been recently shown to stimulate the hydrolysis of phosphoinositides. To evaluate the possibility that the changes in the inotropic responsiveness to alpha₁-adrenoceptor stimulation in the diabetic heart could be linked to altered alpha₁-adrenoceptor-stimulated phosphoinositide turnover and further to the development of diabetic cardiomyopathy, we studied contractility and receptor-stimulated phosphoinositide turnover following norepinephrine (in the presence of propranolol) stimulation in right ventricles from male Wistar rats (200-225 g) which were made diabetic with streptozotocin (55 mg/kg, i.v.). Rats were sacrificed six weeks after the induction of diabetes. Diabetic rats were characterized by decreased body weight gain, hypoinsulinemia, hyperglycemia and hyperlipidemia. Stimulation of alpha₁-adrenoceptors by norepinephrine (in the presence of propranolol) in right ventricles resulted in the formation of inositol monophosphate (measured with a radioisotope method) and inositol 1,4,5-trisphosphate (measured with an inositol 1,4,5-trisphosphate protein binding assay kit) in a time- and concentration-dependent manner in both control and diabetic rats. The increase in inositol 1,4,5-trisphosphate levels preceded the increase in the alpha₁-adrenoceptor-mediated positive inotropic effect. Diabetic hearts showed a greater maximum inotropic response to norepinephrine stimulation and also had a higher inositol 1,4,5-trisphosphate levels. However, with the radioisotope method, a decreased inositol monophosphate formation was shown in diabetic hearts compared with controls. Omega-3 fatty acids supplementation (Promega[symbol omitted], 0.5 ml/kg/day) had no significant effect on the changes in norepinephrine-stimulated inositol monophosphate formation in diabetic hearts. In the presence of the cyclooxygenase inhibitor indomethacin or the thromboxane synthetase inhibitor imidazole, the norepinephrine-stimulated positive inotropic effect and inositol 1,4,5-trisphosphate formation were significantly increased in control hearts, but were unaltered in the hearts from diabetics. The addition of the prostacyclin synthetase inhibitor tranylcypromine reduced the norepinephrine-stimulated positive inotropic effect and inositol 1,4,5-trisphosphate formation only in diabetic hearts and had no effect in the controls. While inositol 1,4,5-trisphosphate may be able to mediate only transient inotropic effects produced by alpha₁-adrenoceptor stimulation, diacylglycerol may provoke a sustained positive inotropic effect by activating slow Ca²⁺ channels through stimulation of protein kinase C. Our results showed that the diabetic hearts had a higher protein kinase C activity in the membrane fraction compared with controls and this was accompanied by a decrease in cytosolic protein kinase C activity. The present study suggests that the increases in inositol 1,4,5-trisphosphate levels and the membrane fraction protein kinase C activity may be implicated in the increased inotropic responsiveness to alpha₁-adrenoceptor stimulation in the hearts of the streptozotocin-diabetic rats. The increases in inositol 1,4,5-trisphosphate level and protein kinase C activity could induce Ca²⁺ overload in the diabetic heart which might be involved in the development of diabetic cardiomyopathy. The results from the omega-3 fatty acid study indicate that the changes in cardiac alpha₁-adrenoceptor-mediated inositol phosphates formation cannot contribute to the previously described improved cardiac function of omega-3 fatty acid-treated streptozotocin-diabetic rats. The nature and physiological significance of the enhanced positive inotropic effect and inositol 1,4,5-trisphosphate formation in the control heart with the addition of indomethacin and imidazole is still unclear. The effect of tranylcypromine may indicate the participation of prostaglandins in mediating the enhanced alpha₁-inotropic effect of norepinephrine in the diabetic heart.
Pharmaceutical Sciences, Faculty of
Graduate

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9

Pesesse, Xavier. "Clonage moléculaire et caractérisation de SHIP2, une nouvelle inositols et phosphatidylinositols polyphosphates 5-phosphatase qui contrôle la voie de signalisation de la PI 3-kinase." Doctoral thesis, Universite Libre de Bruxelles, 2000. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/211771.

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10

Walker, Valerie Glynis. "Pl3-kinase mediates cSrc activation and podosome formation through the adaptor protein, AFAP-110, in response to PKC[alpha] activation." Morgantown, W. Va. : [West Virginia University Libraries], 2007. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=5191.

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Thesis (Ph. D.)--West Virginia University, 2007.
Title from document title page. Document formatted into pages; contains viii, 306 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.

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Books on the topic "Phosphatidylinositols"

1

Inositol phosphates and lipids: Methods and protocols. New York: Humana Press, 2010.

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N.Y.) Inositol Phospholipid Signaling in Physiology and Disease (Conference) (2012 New York. Inositol phospholipid signaling in physiology and disease. Edited by Fernandes, Sandra (Sandra R.), Kerr William G, and New York Academy of Sciences. Hoboken, NJ: New York Academy of Sciences, 2012.

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H, Stenmark, ed. Phosphoinositides in subcellular targeting and enzyme activation. Berlin: Springer, 2004.

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McDermott, Mark Ian. Phospholipase D2 regulation by ADP-ribosylation factor-6 and phosphatidylinositol 4-phosphate 5-kinase. Birmingham: University of Birmingham, 2002.

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Mei, Yu. Functional Characterization of Arabidopsis Phosphatidylinositol Monophosphate 5-kinase 2 in Lateral Root Development, Gravitropism and Salt Tolerance. Dordrecht: Springer Netherlands, 2014. http://dx.doi.org/10.1007/978-94-017-9373-5.

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Falcioni, Lisa. The role of the phosphatidylinositol-3 kinase-Akt pathway in determining radiation sensivity in the breast cancer cell line MDA-MB 231. Sudbury, Ont: Laurentian University, School of Graduate Studies, 2005.

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GPI-Anchored Membrane Proteins and Carbohydrates. LANDES BIOSCIENCE PUBLISHERS, 1999.

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(Editor), A. Lahiri Majumder, and B. B. Biswas (Editor), eds. Biology of Inositols and Phosphoinositides (Subcellular Biochemistry). Springer, 2006.

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Majumder, A. Lahiri, and B. B. Biswas. Biology of Inositols and Phosphoinositides. Springer, 2006.

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Barker, Christopher J. Inositol Phosphates and Lipids: Methods and Protocols. Humana Press, 2012.

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Book chapters on the topic "Phosphatidylinositols"

1

Mak, Lok Hang. "Lipid Signaling and Phosphatidylinositols." In Encyclopedia of Biophysics, 1286–89. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-16712-6_537.

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Varela, Isabel, Jose F. Alvarez, Jose Puerta, Rosa Clemente, Ana Guadaño, Matias Avila, Francisco Estevez, Susana Alemany, and Jose M. Mato. "Role of Glycosyl-Phosphatidylinositols in Insulin Signalling." In Activation and Desensitization of Transducing Pathways, 167–79. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-83618-3_10.

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Ischebeck, Till. "Phosphatidylinositols and Derivatives in Plants: Overview Of." In Encyclopedia of Lipidomics, 1–4. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7864-1_150-1.

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Hale, Andrew T., Bradley P. Clarke, and John D. York. "Metabolic Labeling of Inositol Phosphates and Phosphatidylinositols in Yeast and Mammalian Cells." In Methods in Molecular Biology, 83–92. New York, NY: Springer US, 2019. http://dx.doi.org/10.1007/978-1-0716-0167-9_7.

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Schomburg, Dietmar, and Margit Salzmann. "Phosphatidylinositol deacylase." In Enzyme Handbook 3, 219–21. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76463-9_48.

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Schomburg, Dietmar, and Margit Salzmann. "Phosphatidylinositol-bisphosphatase." In Enzyme Handbook 3, 459–63. Berlin, Heidelberg: Springer Berlin Heidelberg, 1991. http://dx.doi.org/10.1007/978-3-642-76463-9_97.

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Schomburg, Dietmar, and Dörte Stephan. "Phosphatidylinositol N-acetylglucosaminyltransferase." In Enzyme Handbook 12, 893–95. Berlin, Heidelberg: Springer Berlin Heidelberg, 1996. http://dx.doi.org/10.1007/978-3-642-61117-9_198.

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Schomburg, Dietmar, and Dörte Stephan. "Phosphatidylinositol 3-phosphatase." In Enzyme Handbook 15, 151–53. Berlin, Heidelberg: Springer Berlin Heidelberg, 1998. http://dx.doi.org/10.1007/978-3-642-58948-5_35.

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Donato, Dominique M., Steven K. Hanks, Kenneth A. Jacobson, M. P. Suresh Jayasekara, Zhan-Guo Gao, Francesca Deflorian, John Papaconstantinou, et al. "Phosphatidylinositol 3-Kinase." In Encyclopedia of Signaling Molecules, 1369. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_101025.

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Burke, John E., and Roger L. Williams. "Phosphatidylinositol 3-Kinases." In Encyclopedia of Metalloproteins, 1686–92. New York, NY: Springer New York, 2013. http://dx.doi.org/10.1007/978-1-4614-1533-6_53.

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Conference papers on the topic "Phosphatidylinositols"

1

Ni, Qiang, Matthew Fosbrink, and Jin Zhang. "Illuminating the phosphatidylinositol 3-kinase/Akt pathway." In Biomedical Optics (BiOS) 2008, edited by Alexander P. Savitsky, Robert E. Campbell, and Robert M. Hoffman. SPIE, 2008. http://dx.doi.org/10.1117/12.765524.

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Suga, K., Y. Uemura, T. Tsuijinaka, M. Sakon, J. Kambayashi, and T. Mori. "PROPERTIES OF PHOSPHATIDYLINOSITOL KINASE IN HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643807.

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We have reported the specific 32P-labelling in phosphatidyl-inositol-4-monophosphate(PIP) of intact platelets upon addition of the agents which elevate intracellular cAMP (Thrombos.Res.44, 155,1986).This event may be catalyzed by the action of Pl-kinase, the properties of which has not been elucidatedyet.Thereby, attempts were made to assay and to characterize PI-kinase of human platelets.Fresh lysed platelets prelabelled with 32P in cold Tris-HCl buffer containing 2mM EGTA were incubated at 37 C in the presence of MgCl2 for designated times and the phospholipids were extracted and analyzed by thin layer chromatography.32P-labelling in PIP was gradually increased in consort with the decreased labelling in PI-4,5-bisphosphate.As the changes in the labelling was not affected by the presence of apyrase and as the radioactive inositol trisphosphate was not detected,it was suggested that the changes is due to the action of phoshomono-esterase rather than PI-kinase or phospholipase C.When 32P-ATP was added to non-labelled lysed platelets upon incubation, 32P was labelled only into PIP and the amount was markedly increased until 5min. after incubation.Since the labelling was strongly inhibited by apyrase,it likely reflects the activity of Pl-kinase. The activity of PI-kinase thus measured required Mg2+ strictly for the activity and the maximal activity was obtained in the presence of 30mM Mg2+ .In contrast,it was markedly inhibited in the presence of Ca2+ (as low as 2mM Ca2+ in the presence of 2mM EGTA),which was compatible.with our previous findings with intact platelets. The activity of A-kinase was not inhibited by a low concentration of Ca2+ .Furthermore,the activity was inhibited by cAMP or dbcAMP in a dose related manner and no enhancement of the activity Was obtained by the addition of catalytic subunit of A-kinase,though a significant reduction in the activity was observed in the presence of inhibitor protein to A-kinase. From these observations,the following conclusions were obtained; l)The activity of Pl-kinase in lysed platelets may be determined by pulse labelling with 32P-ATP. 2)It requires Mg2+ absolutely and is inhibited by a very low concentration of Ca2+. 3)Pl-kinase is activated by A-kinase but the activated enzyme is inhibited by cAMP, suggesting the presence of feedback mechanism.

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Morita, Yasu S., Svetozar Kovacevic, Helen Billman-Jacobe, and Malcolm J. McConville. "RECONSTITUTION OF PHOSPHATIDYLINOSITOL MANNOSIDE BIOSYNTHESIS IN MYCOBACTERIUM SMEGMATIS." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.453.

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Holmsen, Holm, Adrie J. M. Verhoeven, Ole-Bjørn Tysnes, Grethe M. Aarbakke, and Carol A. Cook. "TURNOVER OF THE PHOSPHOMONOESTER GROUPS OF POLYPHOSPHOINOSITIDES IN UNSTIMULATED HUMAN PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643808.

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The metabolic activity of the polyphosphoinositides in unstimulated human platelets was studied by 1) short-term labelling with 32P-Pi, 2) by replacement of PP. from pre-labelled platelets with unlabelled phosphate and 3) by depriving the cells of metabolic ATP. Under short-term labelling conditions, the 4- and 5-phosphates of phosphatidylinositol-4-phosphate (PIP2) and phosphatidylinositol 4,5-bisphosphate (PIP2) had the same specific radioactivity as the γ-phosphate of metabolic ATP. The specific radioactivity of the 1-phosphates of phosphatidylinositol, PIP and PIP2 was similar but only 4-13 % as compared to the γ phosphate of ATP. When 32P-Pi. pre-labelled platelets were incubated with up to 25 mA of unlabelled phosphate, the displacement of the P-label from PIP, PIP2 and metabolic ATP followed similar kinetics. Inhibition of ATP regeneration in 32P-Pi pre-labelled platelets resulted in a rapid fall in metabolic ATP with much slower fall in 32P-PIP. 32P-PIP increased initially and decreased thereafter in parallel with PIP2. However, ATP turnover was not abolished, as indicated by the marked (25 % of the control) incorporation of extracellular 32P-Pi. into PIP and PIP2 in metabolically inhibited platelets. This low phosphate turnover may explain the relative resistance of PIP and PIP2 to metabolic inhibition.We conclude that PIP and PIP2 are present as a single metabolic pool in human platelets. Turnover of the 4- and 5-phosphates of PIP and PIP2 in unstimulated platelets is as rapid as that of the γ- Phosphate of metabolic ATP, and accounts for about 7 % of basal ATP consumption.

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Bryckaert, M. C., A. Wasteson, G. Tobelem, F. Rendu, and J. P. Caen. "PLATELET DERIVED GROWTH FACTOR (PDGF) BINDS TO HUMAN PLATELETS AND MODULATES PLATELET ACTIVATION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643493.

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PDGF which is released during platelet activation like the other ∝ granule components (fibrinogen, F VIII/vWF, PF4) could bind to platelet membrane Following this hypothesis, we have studied the binding of 125I pure human PDGF to washed human platelets activated by collagen. This binding was specific and time dependent and reached a plateau with 20 μg/ml of collagen. With 200 fold excess of unlabeled PDGF, the binding of 125I-PDGF decreased progressively to 10 .whereas unlabeled Epidermal Growth Factor did not compete with 125I-PDGF. Saturation curve and scatchard analysis have shown one class of sites 3,000 sites/cell with an apparent Kd = 10-8 M. The demonstration of PDGF binding to platelets led us to investigate the effects of PDGF on platelet function. PDGF inhibited the aggregation and 14C serotonin release induced by thrombin or collagen. This inhibition was dose dependent and more effective with human PDGF. A total inhibition of collagen-induced platelet aggregation was obtained with 50 ng/ml of human PDGF and 200 ng/ml of porcine PDGF. The aggregation and 14C serotonin release induced by arachidonic acid were not inhibited by PDGF. The metabolism of phosphoinositide was also investigated on washed human platelets prelabeled with 32P orthophosphate. We found that PDGF (200 ng/ml) induced a decrease of 32P associated with phosphatidylinositol 4 biphosphate (72 %) after 3 min, with a parallel increase of 32P-phosphatidylinositol 4 Phosphate (120 %) and 32P-phosphatidylinositol (120 %).In conclusion i) PDGF binds to activated platelets, ii) PDGF inhibits platelet aggregation and secretion, iii) PDGF modifies phosphoinositide metabolism. These results are in favour of a role of PDGF in a negative feed back control of platelet activation.

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Govindarajan, Barani, Sreenivasa Chinni, and Diego Sbrissa. "Abstract 2293: Role of phosphatidylinositol 4-kinase IIIα in chemokine signaling." In Proceedings: AACR Annual Meeting 2021; April 10-15, 2021 and May 17-21, 2021; Philadelphia, PA. American Association for Cancer Research, 2021. http://dx.doi.org/10.1158/1538-7445.am2021-2293.

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Wu, Lingzhi, Lihua Tang, Xiaofei Hu, and Dong Hu. "Thermodynamic studies of the interaction of phosphatidylinositol phosphate with aminoglycosides antibiotics." In 2011 International Conference on Remote Sensing, Environment and Transportation Engineering (RSETE). IEEE, 2011. http://dx.doi.org/10.1109/rsete.2011.5966304.

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Numata-Nakamura, Mari, Yoji Nagashima, Janelle Posey, James R. Mitchell, Karin Z. Berry, Robert C. Murphy, and Dennis R. Voelker. "Phosphatidylinositol Is A New Anionic Lipid Antagonist Of Respiratory Syncytial Virus Infections." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a3291.

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Sbrissa, Diego, Louie Semaan, Li Yanfeng, Assia Shisheva, and Sreenivasa R. Chinni. "Abstract 5162: Phosphatidylinositol 4-Kinase type IIIa (PI4KA) expression in prostate cancer." In Proceedings: AACR 106th Annual Meeting 2015; April 18-22, 2015; Philadelphia, PA. American Association for Cancer Research, 2015. http://dx.doi.org/10.1158/1538-7445.am2015-5162.

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Trautmann, Marcel, Magdalene Cyra, Christian Bertling, Ilka Isfort, Bianca Altvater, Claudia Rossig, Susanne Hafner, et al. "Abstract 3939: Activation of phosphatidylinositol-3′-kinase/Akt signaling in myxoid liposarcoma." In Proceedings: AACR Annual Meeting 2018; April 14-18, 2018; Chicago, IL. American Association for Cancer Research, 2018. http://dx.doi.org/10.1158/1538-7445.am2018-3939.

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Reports on the topic "Phosphatidylinositols"

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Hutchinson, John N., and William Muller. The Role of Phosphatidylinositol 3' -OH Kinase Signaling in Mammary Tumorigenesis. Fort Belvoir, VA: Defense Technical Information Center, July 2001. http://dx.doi.org/10.21236/ada396742.

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Balajee, A. S., J. A. Meador, and Y. Su. Cellular response to low dose radiation: Role of phosphatidylinositol-3 kinase like kinases. Office of Scientific and Technical Information (OSTI), March 2011. http://dx.doi.org/10.2172/1009811.

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Parker, Amanda P., Barbara S. Beckman, and Matthew Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2002. http://dx.doi.org/10.21236/ada409382.

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Parker, Amanda, Barbara Beckman, and Matthew E. Burow. Phosphatidylinositol 3-Kinase and Protein Kinase C as Molecular Determinants of Chemoresistance in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, July 2004. http://dx.doi.org/10.21236/ada431891.

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Hansen, Peter J., and Amir Arav. Embryo transfer as a tool for improving fertility of heat-stressed dairy cattle. United States Department of Agriculture, September 2007. http://dx.doi.org/10.32747/2007.7587730.bard.

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The overall objective of the current proposal is to develop procedures to improve the pregnancy rate achieved following transfer of fresh or cryopreserved embryos produced in the laboratory into heat-stress recipients. The overall hypothesis is that pregnancy rate in heat-stressed lactating cows can be improved by use of embryo transfer and that additional gains in pregnancy rate can be achieved through development of procedures to cryopreserve embryos, select embryos most likely to establish and maintain pregnancy after transfer, and to enhance embryo competence for post-transfer survival through manipulation of culture conditions. The original specific objectives were to 1) optimize procedures for cryopreservation (Israel/US), 2) develop procedures for identifying embryos with the greatest potential for development and survival using the remote monitoring system called EmbryoGuard (Israel), 3) perform field trials to test the efficacy of cryopreservation and the EmbryoGuard selection system for improving pregnancy rates in heat-stressed, lactating cows (US/Israel), 4) test whether selection of fresh or frozen-thawed blastocysts based on measurement of group II caspase activity is an effective means of increasing survival after cryopreservation and post-transfer pregnancy rate (US), and 5) identify genes in blastocysts induced by insulin-like growth factor-1 (IGF-1) (US). In addition to these objectives, additional work was carried out to determine additional cellular determinants of embryonic resistance to heat shock. There were several major achievements. Results of one experiment indicated that survival of embryos to freezing could be improved by treating embryos with cytochalasin B to disrupt the cytoskeleton. An additional improvement in the efficacy of embryo transfer for achieving pregnancy in heat-stressed cows follows from the finding that IGF-1 can improve post-transfer survival of in vitro produced embryos in the summer but not winter. Expression of several genes in the blastocyst was regulated by IGF-1 including IGF binding protein-3, desmocollin II, Na/K ATPase, Bax, heat shock protein 70 and IGF-1 receptor. These genes are likely candidates 1) for developing assays for selection of embryos for transfer and 2) as marker genes for improving culture conditions for embryo production. The fact that IGF-1 improved survival of embryos in heat-stressed recipients only is consistent with the hypothesis that IGF-1 confers cellular thermotolerance to bovine embryos. Other experiments confirmed this action of IGF-1. One action of IGF-1, the ability to block heat-shock induced apoptosis, was shown to be mediated through activation of the phosphatidylinositol 3-kinase pathway. Other cellular determinants of resistance of embryos to elevated temperature were identified including redox status of the embryo and the ceramide signaling pathway. Developmental changes in embryonic apoptosis responses in response to heat shock were described and found to include alterations in the capacity of the embryo to undergo caspase-9 and caspase-3 activation as well as events downstream from caspase-3 activation. With the exception of IGF-1, other possible treatments to improve pregnancy rate to embryo transfer were not effective including selection of embryos for caspase activity, treatment of recipients with GnRH.and bilateral transfer of twin embryos. In conclusion, accomplishments achieved during the grant period have resulted in methods for improving post-transfer survival of in vitro produced embryos transferred into heat-stressed cows and have lead to additional avenues for research to increase embryo resistance to elevated temperature and improve survival to cryopreservation. In addition, embryo transfer of vitrified IVF embryos increased significantly the pregnancy rate in repeated breeder cows.

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