Gotowe bibliografie tematyczne / Phosphatidic acid

Gotowa bibliografia na temat „Phosphatidic acid”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 25 maja 2024

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Artykuły w czasopismach na temat "Phosphatidic acid"

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ENGLISH, Denis, Margaret MARTIN, Kevin A. HARVEY, Luke P. AKARD, Ruth ALLEN, Theodore S. WIDLANSKI, Joe G. N. GARCIA i Rafat A. SIDDIQUI. "Characterization and purification of neutrophil ecto-phosphatidic acid phosphohydrolase". Biochemical Journal 324, nr 3 (15.06.1997): 941–50. http://dx.doi.org/10.1042/bj3240941.

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Phosphatidic acid and its derivatives play potentially important roles as extracellular messengers in biological systems. An ecto-phosphatidic acid phosphohydrolase (ecto-PAPase) has been identified which effectively regulates neutrophil responses to exogenous phosphatidic acid by converting the substrate to diacylglycerol. The present study was undertaken to characterize this ecto-enzyme on intact cells and to isolate the enzyme from solubilized neutrophil extracts. In the absence of detergent, short chain phosphatidic acids were hydrolysed most effectively by neutrophil plasma membrane ecto-PAPase; both saturated and unsaturated long chain phosphatidic acids were relatively resistant to hydrolysis. Both long (C18:1) and short (C8) chain lyso-phosphatidic acids were hydrolysed at rates comparable with those observed for short chain (diC8) phosphatidic acid. Activity of the ecto-enzyme accounted for essentially all of the N-ethylmaleimide-insensitive, Mg2+-independent PAPase activity recovered from disrupted neutrophils. At 37 °C and pH 7.2, the apparent Km for dioctanoyl phosphatidic acid (diC8PA) was 1.4×10-3 M. Other phosphatidic acids and lysophosphatidic acids inhibited hydrolysis of [32P]diC8PA in a rank order that correlated with competitor solubility, lysophosphatidic acids and unsaturated phosphatidic acids being much more effective inhibitors than long chain saturated phosphatidic acids. Dioleoyl (C18:1) phosphatidic acid was an unexpectedly strong inhibitor of activity, in comparison with its ability to act as a direct substrate in the absence of detergent. Other inhibitors of neutrophil ecto-PAPase included sphingosine, dimethyl- and dihydro-sphingosine, propranolol, NaF and MgCl2. Of several leucocyte populations isolated from human blood by FACS, including T cells, B cells, NK lymphocytes and monocytes, ecto-PAPase was most prevalent on neutrophils; erythrocytes were essentially devoid of activity. A non-hydrolysable, phosphonate analogue of phosphatidic acid, phosphonate 1, efficiently solubilized catalytic activity from intact neutrophils without causing cell disruption or increasing permeability. Enzyme activity in solubilized extracts was purified in the absence of detergent by successive heparin–Sepharose, gel filtration and anion exchange chromatography. By assaying activity in renatured SDS/polyacrylamide gel slices, the molecular mass of neutrophil ecto-PAPase was estimated to be between 45 and 52 kDa, similar to the molecular mass of previously purified plasma membrane PAPases. Since a large portion of neutrophil plasma membrane PAPase is available for hydrolysis of exogenous substrates, ecto-PAPase may play an important role in regulating inflammatory cell responses to extracellular phosphatidic acid in biological systems.
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Kaszkin, M., L. Seidler, R. Kast i V. Kinzel. "Epidermal-growth-factor-induced production of phosphatidylalcohols by HeLa cells and A431 cells through activation of phospholipase D". Biochemical Journal 287, nr 1 (1.10.1992): 51–57. http://dx.doi.org/10.1042/bj2870051.

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In response to epidermal growth factor (EGF), HeLa cells and A431 cells rapidly accumulate substantial amounts of phosphatidic acid (up to 0.16 and 0.2 micrograms/10(6) cells respectively), which represents approx. 0.17% of total phospholipid. Phosphatidic acid may be a potential product of diacylglycerol kinase and/or of phospholipase D. To evaluate the contribution of phospholipase D, the phosphatidyl-transfer reaction to a primary alcohol (mostly butan-1-ol; 0.2%) was measured; this reaction is known to be mediated exclusively by phospholipase D in intact cells. In HeLa and in A431 cells prelabelled with [1-14C]oleic acid, EGF (10 and 100 nM respectively) caused a 3-fold increase in radioactive phosphatidylbutanol within 5 min at the expense of labelled phosphatidic acid. Dose-response relationships showed 10 nM- and 100 nM-EGF to be maximally effective in HeLa cells and A431 cells respectively. Mass determinations showed that the phosphatidylbutanol formed within 5 min represented only part of the phosphatidic acid. Depletion of protein kinase C by pretreatment of A431 cells for 17 h with the phorbol ester phorbol 12-myristate 13-acetate (0.1 microM) did not impair EGF-induced formation of phosphatidylbutanol, thus indicating that the reaction was independent of this enzyme. Since phosphatidic acid is suggested to exert second-messenger functions as well as to induce biophysical changes in cellular membranes, its formation, including that via the phospholipase D pathway, may represent an important link between extracellular signals and intracellular targets.
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Altin, J. G., i F. L. Bygrave. "Phosphatidic acid and arachidonic acid each interact synergistically with glucagon to stimulate Ca2+ influx in the perfused rat liver". Biochemical Journal 247, nr 3 (1.11.1987): 613–19. http://dx.doi.org/10.1042/bj2470613.

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The administration of phosphatidic acid to rat livers perfused with media containing either 1.3 mM- or 10 microM-Ca2+ was followed by a stimulation of Ca2+ efflux, O2 uptake and glucose output. The responses elicited by 100 microM-phosphatidic acid were similar to those induced by the alpha-adrenergic agonist phenylephrine. Contrary to suggestions that phosphatidic acid acts like a Ca2+-ionophore, no net influx of Ca2+ was detected until the phosphatidic acid was removed. Sequential infusions of phenylephrine and phosphatidic acid indicate that the two agents release Ca2+ from the same intracellular source. The co-administration of glucagon (or cyclic AMP) and phosphatidic acid, and also of glucagon and arachidonic acid, led to a synergistic stimulation of Ca2+ uptake of the liver, a feature similar to that observed after the co-administration of glucagon and other Ca2+-mobilizing hormones [Altin & Bygrave (1986) Biochem. J. 238, 653-661]. A notable difference, however, is that the synergistic stimulation of Ca2+ uptake induced by the co-administration of glucagon and arachidonic acid was inhibited by indomethacin, whereas that induced by glucagon and phosphatidic acid, or glucagon and other Ca2+-mobilizing agents, was not. The results suggest that the synergistic action of glucagon and arachidonic acid in stimulating Ca2+ influx is mediated by prostanoids, but that of glucagon and phosphatidic acid is evoked by a mechanism similar to that of Ca2+-mobilizing agents.
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Raben, Daniel M., i Casey N. Barber. "Phosphatidic acid and neurotransmission". Advances in Biological Regulation 63 (styczeń 2017): 15–21. http://dx.doi.org/10.1016/j.jbior.2016.09.004.

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Fraser, T., A. Waters, S. Chatrattanakunchai i K. Stobart. "Does triacylglycerol biosynthesis require diacylglycerol acyltransferase (DAGAT)?" Biochemical Society Transactions 28, nr 6 (1.12.2000): 698–700. http://dx.doi.org/10.1042/bst0280698.

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Microsomal membrane preparations from the developing seeds of sunflower (Helianthus annuus L.) catalyse the conversion of sn-glycerol-3-phosphate and acyl-CoA to triacylglycerol via phosphatidic acid and diacylglycerol. The formation of diacylglycerol from phosphatidic acid was Mg2+ dependent and in the presence of EDTA phosphatidic acid accumulated. This property was used to generate large quantities of endogenous radioactive phosphatidic acid in the membranes. On addition of Mg2+ the phosphatidic acid was used in triacylglycerol formation. Acyl-CoA had little effect on the label which accumulated in triacylglycerol from phosphatidic acid. Diacylglycerol acyltransferase, therefore, may not play a major role in oil formation as originally envisaged and other enzymes, including diacylglycerol: diacylglycerol transacylase [Stobart, Mancha, Lenman, Dahlqvist and Stymne (1997) Planta 203, 58–66] may have important biosynthetic functions.
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Bodachivska, L. Yu. "Biodegradable surfactants from side streams of the vegetable oils production in technical systems". Voprosy Khimii i Khimicheskoi Tekhnologii, nr 6 (grudzień 2022): 3–11. http://dx.doi.org/10.32434/0321-4095-2022-145-6-3-11.

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This work reports the structure of surfactants synthesized from by-products of the vegetable oil production. These are raw materials that do not compete with food products; they are low-cost phosphatidic sludge that can be used directly for chemical transformation. Fatty acid monoetanolamides derived from side streams of the vegetable oils production do not have residues of the original phosphatides or acylglycerols as determined by spectral methods. There are clearly reflected cross-peaks between the amide group and the adjacent methylene group. This indicates a high conversion of substrate and further confirms the amidation reaction. The main acyl residue of the synthesized surfactants are hydrocarbon chain of linoleic acid however, while the detection of methylene groups near double bonds indicates the presence of other fatty acids (oleic, linolenic and gadolein), this corresponds to the fatty acid composition of the original phosphatidic sludge. Synthesized surfactants are effective emulsifiers-stabilizers for dispersed systems. The use of environmentally friendly components in the composition of surfactants improves their biodegradability to 83–86%.
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Andringa, Ruben L. H., Marijn Jonker i Adriaan J. Minnaard. "Synthesis of phosphatidic acids via cobalt(salen) catalyzed epoxide ring-opening with dibenzyl phosphate". Organic & Biomolecular Chemistry 20, nr 11 (2022): 2200–2204. http://dx.doi.org/10.1039/d2ob00168c.

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Sakane, Fumio, Fumi Hoshino i Chiaki Murakami. "New Era of Diacylglycerol Kinase, Phosphatidic Acid and Phosphatidic Acid-Binding Protein". International Journal of Molecular Sciences 21, nr 18 (16.09.2020): 6794. http://dx.doi.org/10.3390/ijms21186794.

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Diacylglycerol kinase (DGK) phosphorylates diacylglycerol (DG) to generate phosphatidic acid (PA). Mammalian DGK consists of ten isozymes (α–κ) and governs a wide range of physiological and pathological events, including immune responses, neuronal networking, bipolar disorder, obsessive-compulsive disorder, fragile X syndrome, cancer, and type 2 diabetes. DG and PA comprise diverse molecular species that have different acyl chains at the sn-1 and sn-2 positions. Because the DGK activity is essential for phosphatidylinositol turnover, which exclusively produces 1-stearoyl-2-arachidonoyl-DG, it has been generally thought that all DGK isozymes utilize the DG species derived from the turnover. However, it was recently revealed that DGK isozymes, except for DGKε, phosphorylate diverse DG species, which are not derived from phosphatidylinositol turnover. In addition, various PA-binding proteins (PABPs), which have different selectivities for PA species, were recently found. These results suggest that DGK–PA–PABP axes can potentially construct a large and complex signaling network and play physiologically and pathologically important roles in addition to DGK-dependent attenuation of DG–DG-binding protein axes. For example, 1-stearoyl-2-docosahexaenoyl-PA produced by DGKδ interacts with and activates Praja-1, the E3 ubiquitin ligase acting on the serotonin transporter, which is a target of drugs for obsessive-compulsive and major depressive disorders, in the brain. This article reviews recent research progress on PA species produced by DGK isozymes, the selective binding of PABPs to PA species and a phosphatidylinositol turnover-independent DG supply pathway.
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Kolesnikov, Y. S., S. V. Kretynin, V. S. Kravets i Y. K. Bukhonska. "Phosphatidic acid formation and signaling in plant cells". Ukrainian Biochemical Journal 96, nr 1 (23.02.2024): 5–21. http://dx.doi.org/10.15407/ubj96.01.005.

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This review conteins updated information on the structure, localization and regulation of phosphatidic acid (PA)-producing enzymes phospholipase D, phosphoinositide-specific and non-specific phospholipases C and diacylglycerol kinases is analyzed. The specific role of PA and PA-producing enzymes in plant stress signaling is discussed.
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Singh, Ram Raj, Priti Prasad, Cynthia Tran i Ramesh Halder. "A self-glycerophospholipid suppresses immunity and inflammation via recruitment of Ly6C+ myeloid cells". Journal of Immunology 198, nr 1_Supplement (1.05.2017): 221.19. http://dx.doi.org/10.4049/jimmunol.198.supp.221.19.

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Abstract Membrane lipids function as essential components of biological membranes, as signaling molecules, and as energy storage molecules. Phosphatidic acid is a vital membrane lipid that serves as a precursor for the synthesis of all acylglycerol lipids in the cell. Phosphatidic acid participates in a wide range of cellular processes, including cytoskeletal organization, secretion, endocytosis, and cell proliferation. Here, we examined the effect of phosphatidic acid on myeloid cells and its ability to modulate tumor immunity and inflammatory disease. We found that in vivo administration of phosphatidic acid protected against immune mediated liver inflammation induced by concanavalin A, but worsened tumor spread in the B16F10 melanoma lung metastasis model. Phosphatidic acid reduced pro-inflammatory cytokines but increased anti-inflammatory cytokine interleukin-10 in the liver. Phosphatidic acid did so by inducing the mobilization and migration from the bone marrow to peripheral organs of Ly6C+ myeloid cells that upon adoptive transfer protected against autoimmune liver inflammation. Our novel observations indicating immune suppressive functions of phosphatidic acid may have wide implications for a variety of conditions with altered lipid metabolism and inflammation such as atherosclerosis and autoimmune disease and conditions with local or systemic alterations in phosphatidic acid such as osteoarthritis and Alzheimer’s disease.
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Rozprawy doktorskie na temat "Phosphatidic acid"

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Lee, Sue Chin. "Spatial signalling of phosphatidic acid". Thesis, University of Strathclyde, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.510804.

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Fleming, Ian Neil. "Purification and properties of phosphatidic acid phosphohydrolase". Thesis, University of Newcastle Upon Tyne, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.260059.

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Stace, Catherine Lucy. "Functional studies of phosphatidic acid production by phospholipase D1". Thesis, University of Cambridge, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.612984.

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Jakobson, Katherine. "The role of phosphatidic acid in astrocyte intracellular signalling". Thesis, Open University, 1990. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.293615.

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Han, Eun Hyang. "Phosphatidic Acid Mediation of Environmentally Induced Adaptive Growth Responses". The Ohio State University, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=osu1492678342062212.

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Buckland, Andrew G. "Anionic phospholipids, annexins and the activity of phospholipases A2". Thesis, University of Southampton, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.246259.

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Heyward, Catherine Anne. "Investigation of potential phosphatidic acid target proteins in intracellular signalling pathways". Thesis, Birmingham City University, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.479113.

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Williams, David. "Phosphatidic Acid Increases Lean Body Tissue and Strength In Resistance Trained Men". Master's thesis, University of Central Florida, 2012. http://digital.library.ucf.edu/cdm/ref/collection/ETD/id/5575.

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Phosphatidic Acid (PA) is a natural phospholipid compound derived from lecithin which is commonly found in egg yolk, grains, fish, soybeans, peanuts and yeast. It has been suggested that PA is involved in several intracellular processes associated with muscle hypertrophy. Specifically, PA has been reported to activate protein synthesis through the mammalian target of rapamycin (mTOR) signaling pathway and thereby may enhance the anabolic effects of resistance training. To our knowledge, no one has examined the effect of PA supplementation in humans while undergoing a progressive resistance training program. To examine the effect of PA supplementation on lean soft tissue mass (LM) and strength after 8 weeks of resistance training. Fourteen resistance-trained men (mean [plus or minus] SD; age 22.7 [plus or minus] 3.3 yrs; height: 1.78 [plus or minus] 0.10m; weight: 89.3 [plus or minus] 16.3 kg) volunteered to participate in this randomized, double-blind, placebo-controlled, repeated measures study. The participants were assigned to a PA group (750mg/day; Mediator, ChemiNutra, MN, n=7) or placebo group (PL; rice flower; n=7), delivered in capsule form that was identical in size, shape and color. Participants were tested for 1RM strength in the bench press (BP) and squat (SQ) exercise. LM was measured using dual-energy X-ray absorptiometry. After base line testing, the participants began supplementing PA or PL for 8 weeks during a progressive resistance training program intended for muscular hypertrophy. Data was analyzed using magnitude-based inferences on mean changes for BP, SQ and LM. Furthermore, the magnitudes of the inter-relationships between changes in total training volume and LM were interpreted using Pearson correlation coefficients, which had uncertainty (90% confidence limits) of approximately +0.25. In the PA group, the relationship between changes in training volume and LM was large (r=0.69, [plus or minus] 0.27; 90%CL), however, in the PL group the relationship was small (r=0.21, [plus or minus] 0.44; 90%CL). PA supplementation was determined to be likely beneficial at improving SQ and LM over PL by 26% and 64%, respectively. The strong relationship between changes in total training volume and LM in the PA group suggest that greater training volume most likely lead to the greater changes in LM, however, no such relationship was found with PL group. For the BP data, the PA group resulted in a 42% greater increase in strength over PL, although the effect was considered unclear. While more research is needed to elucidate mechanism of action; the current findings suggest that in experienced resistance trained men supplementing 750mg PA per day for 8 weeks may likely benefit greater changes in muscle mass and strength compared with resistance training only.
M.S.
Masters
Child, Family and Community Sciences
Education and Human Performance
Sport and Exercise Sciences; Applied Exercise Physiology
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Yu, Changhua. "Phospholipase D/phosphatidic acid phosphatase signal transduction pathway in post-infarction congestive heart failure". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23565.pdf.

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Urs, Aarti N. "Reciprocal binding of sphingosine and phosphatidic acid to steroidogenic factor 1 regulates the transcription of CYP17". Thesis, Available online, Georgia Institute of Technology, 2005, 2005. http://etd.gatech.edu/theses/available/etd-11212005-102620/.

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Thesis (M. S.)--Biology, Georgia Institute of Technology, 2006.
Donald Doyle, Committee Member ; Harish Radhakrishna, Committee Member ; Alfred Merrill, Committee Member ; Marion Sewer, Committee Chair Includes bibliographical references.
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Książki na temat "Phosphatidic acid"

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Attiogbevi-Somado, Eklou. The use of phosphate rock in a rice-legume rotation system on acid soil in the humid forest zone of West Africa. Göttingen: Goltze, 2000.

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Yang, Lu Ying *. A comparative study of triacylglycerol biosynthesis via the monocylglyerol and phosphatidic acid pathways in rat small intestine. 1991.

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Części książek na temat "Phosphatidic acid"

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Bocckino, Stephen B., i John H. Exton. "Phosphatidic Acid". W Lipid Second Messengers, 75–123. Boston, MA: Springer US, 1996. http://dx.doi.org/10.1007/978-1-4899-1361-6_3.

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Liu, Yu, Yuan Su i Xuemin Wang. "Phosphatidic Acid-Mediated Signaling". W Advances in Experimental Medicine and Biology, 159–76. Dordrecht: Springer Netherlands, 2013. http://dx.doi.org/10.1007/978-94-007-6331-9_9.

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Yin, C. C., B. Z. Lin i H. Hauser. "Phase Behavior of Phosphatidic Acid". W Progress in Membrane Biotechnology, 30–39. Basel: Birkhäuser Basel, 1991. http://dx.doi.org/10.1007/978-3-0348-7454-0_3.

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Nakamura, Yuki, i Hiroyuki Ohta. "Phosphatidic Acid Phosphatases in Seed Plants". W Lipid Signaling in Plants, 131–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_9.

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Nakamura, Yuki. "Assaying Plant Phosphatidic Acid Phosphatase Activity". W Methods in Molecular Biology, 233–40. Totowa, NJ: Humana Press, 2013. http://dx.doi.org/10.1007/978-1-62703-401-2_21.

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Ischebeck, Till. "Phosphatidic Acid in Plants: Functional Diversity". W Encyclopedia of Lipidomics, 1–4. Dordrecht: Springer Netherlands, 2017. http://dx.doi.org/10.1007/978-94-007-7864-1_148-1.

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Kooijman, Edgar Eduard, i Christa Testerink. "Phosphatidic Acid: An Electrostatic/Hydrogen-Bond Switch?" W Lipid Signaling in Plants, 203–22. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_14.

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Distéfano, Ayelen M., M. Luciana Lanteri, Arjen ten Have, Carlos García-Mata, Lorenzo Lamattina i Ana M. Laxalt. "Nitric Oxide and Phosphatidic Acid Signaling in Plants". W Lipid Signaling in Plants, 223–42. Berlin, Heidelberg: Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-642-03873-0_15.

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Fleming, Ian N., i Stephen J. Yeaman. "Phosphatidic Acid Phosphohydrolase: Its Role in Cell Signalling". W Signalling Mechanisms — from Transcription Factors to Oxidative Stress, 57–64. Berlin, Heidelberg: Springer Berlin Heidelberg, 1995. http://dx.doi.org/10.1007/978-3-642-79675-3_6.

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Wang, Xuemin, Yuan Su, Yu Liu, Sang-Chul Kim i Brian Fanella. "Phosphatidic Acid as Lipid Messenger and Growth Regulators in Plants". W Signaling and Communication in Plants, 69–92. Berlin, Heidelberg: Springer Berlin Heidelberg, 2013. http://dx.doi.org/10.1007/978-3-642-42011-5_4.

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Streszczenia konferencji na temat "Phosphatidic acid"

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Sokornova, S. V., A. L. Shavarda, E. A. Gusenkov, D. A. Emelianov i G. M. Frolova. "Biochemical features of phoma-like fungi". W 2nd International Scientific Conference "Plants and Microbes: the Future of Biotechnology". PLAMIC2020 Organizing committee, 2020. http://dx.doi.org/10.28983/plamic2020.233.

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Biochemical analysis of phoma-like fungi showed significant differences in the phosphatidic acid and glycoceramides levels and close values of phosphatidylcholine / phosphatidylethanolamine, trehalose, arabitol, mannitol, sorbitol levels.
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Cascar, J. M., i J. L. Kavarro. "ARACHIDGIIC ACID METABOLISM II PLATELETS STORED FOR FIVE DAYS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644685.

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Arachidonlc acid (AA) netabolisn has been extensively studied in fresh platelets, but there Is little infomation available for stored platelets . we stored platelets in CLI bags far five days at 22+/-2°C and, on days 0, 3 and 5, six si of platelet concentrate were revved from the container and platelets were labeled with (C-14J-AA. Both incorporation and distribution of radiotracer sere studied in rest and thrcnfcln stivlated platelets.Total uptake of, (C-14)-AA dropped fron day 0 to 5 (p 0.01). Distribution oh day 0 was sinilar to fresh platelets. Incorporation of (C-14)-AA on phosphatidyl inositol (FI) decayed fron 12.4+/-1.5 on day 0, to 7.9+/-0.9 on day 3 (p 0.001), While the percentage attached on phosphatidylserine (PS),increased fron 5.3+/-0.9 to 8.8+/-1.5 (p 0.001). There were not any changes fron day 3 to 5.On day 0,17.7+/-5.2X of radiactlvity was released fron phospholipids by thronbin. This anount decreased to 7.3+/-2.5X (p 0.01) on day 5. I^xaiment in breakdown of both PI and phosphatidylcholine (PC) was detected. Generation of phosphatidic acid (PA) by thronbin, decreased fron 2.6+/-0.4X of total radiactlvity on day 0 to 1.4+/-0.3X on day 3 (p 0.001) and 0.9+/-0.2X on day 5 (p 0.01). Ve did not find changes in TxB2 and HHT, but HETE decayed fron 7.2+/-2.9X on day 0, to 2.3t/-0.9% on day 5 (p 0.01).We concluded that both activities of phospholipases A-2 and C are affected by storage.
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Haji, K., S. Sato, H. Ogawa, Y. Isomura, N. Bando, R. Suzue, T. T. Hong Phuong i in. "The Effect of Novel Autotaxin Inhibitor, 2-carba Cyclic Phosphatidic Acid, in Lung Fibrosis". W American Thoracic Society 2024 International Conference, May 17-22, 2024 - San Diego, CA. American Thoracic Society, 2024. http://dx.doi.org/10.1164/ajrccm-conference.2024.209.1_meetingabstracts.a2463.

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Setty, B. N. Y., M. Berger i M. J. Stuart. "13-HYDROXY-9,11-OCTADECADIENOIC ACID (13-HOD) INCREASES PROSTACYCLIN PRODUCTION IN ENDOTHELIAL CELLS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643948.

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Recently, endothelial cells (ECs) have been shown to generate a potent vascular chemorepellant factor. This metabolite, 13-HOD is reported to be the major lipoxygenase product produced in microgram amounts in ECs (JBC 260:16056, 1985). We have studied the effect of 13-HOD on EC arachidonic acid (AA) metabolism, and report modulation of both AA release and conversion to prostacyclin. Using fetal bovine aortic ECs, 13-HOD stimulated prostacyclin production (RIA for 6KPGF1α ) by 40±13% (1SE), and 51±09% at 10 and 30μM (P<0.05; n=5). When the time-course of this effect was evaluated, 13-HOD (30μM) significantly enhanced the time-dependent release of 6KPGF1α by 31 to 51% between 5 and 120 min. (P<0.05 to 0.01; n=5). In [14C]AA labeled cells, this compound modulated both AA release and its subsequent conversion. In 5 paired experiments, 13-HOD (30μM) enhanced the release of AA from membrane phospholipids (9065±0553 cpm/well in controls vs 10738±1725 in 13-HOD treated cells; PC0.01). Analysis of cellular phospholipids revealed a significant decrease in [14C]phosphatidylethanolamine (62312±3963 cpm/well in controls vs 56959±4104 in 13-HOD treated cells; P<0.02). No significant changes were seen in the levels of phosphatidyl-choline, -serine, -inositol, or phosphatidic acid. Production of [14C]prostacyclin was stimulated by 56±16% (P<0.01 ), while total cyclooxygenase metabolites increased by 28±8% (P<0.01), suggesting effects on both cyclooxygenase and prostacyclin synthetase. 13-HOD, the major vascular product of linoleic acid enhances both AA release and metabolism, thus demonstrating an intimate hemostatic interaction between the metabolic products of these two polyunsaturated fatty acids in endothelial cells.
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Myers, Amanda, Hitham Aldharee, Shimpi Bedi i Weiwen Long. "Abstract 4308: Phosphatidic acid binds to ERK3 and stimulates phosphorylation of the ERK3 activation loop". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.sabcs18-4308.

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Myers, Amanda, Hitham Aldharee, Shimpi Bedi i Weiwen Long. "Abstract 4308: Phosphatidic acid binds to ERK3 and stimulates phosphorylation of the ERK3 activation loop". W Proceedings: AACR Annual Meeting 2019; March 29-April 3, 2019; Atlanta, GA. American Association for Cancer Research, 2019. http://dx.doi.org/10.1158/1538-7445.am2019-4308.

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Tysnes, O.-B., AJ M. Verhoeven i H. Holmsen. "Thrombin stimulation of human platelets:Phosphoinositides as the only source of the diacylglycerol moiety in phosphatidic acid". W 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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Crouch, Michael F., i Eduardo G. Lapetina. "PHOSPHOLIPASE A2 ACTIVATION BY A MECHANISM SEPARATE TO THAT RESPONSIBLE FOR PHOSPHOLIPASE C STIMULATION IN ALPHA-THROMBIN-STIMULATED HUMAN PLATELETS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644470.

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The ability of cell surface receptor occupation to increase the activity of phospholipase A2 has been thought to be due to the prior activation of phospholipase C and an increase in the intracellular Ca2+ concentration. However, recent evidence from our and other laboratories has suggested that this may not be the case, but rather stimulation of phospholipase A2 may be under the control of separate receptor-activated events. We have investigated this further by comparing the ability of prostacyclin (PGI2) and epinephrine to alter platelet responses to thrombin and examining the resulting phospholipase A2 activities.Alpha-thrombin stimulated aggregation of human platelets, the formation of inositol phosphates and phosphatidic acid, mobilizaton of Ca2+ from internal stores and Ca2+ influx, protein phosporylation (47 kDa and 20 kDa) and arachidonic acid (AA) release. Each of these responses was partially inhibited by prostacyclin (PGI2) except that of AA release, which was abolished. In combination with epinephrine and PGI2, alpha-thrombin-induced aggregation, phosphatidic acid formation and protein phosphorylation were restored, but the release of AA only reached 50% of its control value. Epinephrine alone had no effect on any of these responses, either in the presence or absence of PGI2. Thus, alpha-thrombin-induced activation of phospholipase A2 is more sensitive to the effects of PGI2 than is phospholipase C, and supports the possibility that there are distinct control mechanisms for receptor activation of these enzymes. We are presently examining the role of Gs in the inhibition by PGI2 of platelet phospholipase A2 and of Gi in the thrombin stimulation of this enzyme
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Pengo, V., M. J. Heine, P. Thiagarajan i s. s. Shapiro. "A GENERAL MECHANISM FOR LUPUS ANTICOAGULANTS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643660.

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Although- a number of observations have implied that lupus anticoagulants have immunologic specificity towards anionic. phospholipids, thereby prolonging phospholipid-dependent coagulation tests, this assumption has been directly demonstrated in only one patient with a monoclonal IgM paraprotein. We have tested the generality of this hypothesis directly by isolating five IgG lupus anticoagulants from patients with lupus-like syndromes and/or thrombosis. IgG lupus anticoagulant fractions were isolated free of other plasma proteins and free of contaminating phospholipid by adsorption to and elution from cardiolipin-cholesterol-dicetylphosphate liposomes , followed by chromatography on protein A-Sepharose. Cardiolipin liposomes, but not phosphatidylcholine liposomes, were capable of removing all, or nearly all, lupus anticoagulant activity from patient plasma. Anticardiolipin and lupus anticoagulant activity were both present in acidic fractions on isoelectric focusing. F(ab’)2 fragments retained lupus anti coagulant activity and bound to cardiolipin in an ELISA assay. The affinity-purified IgG preparations reacted with cardiolipin, phosphatidyl serine , phosphatidylinositol and phosphatidic acid, but not with phosphatidylcholine or phosphatidyl ethanol amine, and inhibited calcium-dependent binding of prothrombin and of factor X to phosphatidy1serine-coated surfaces. These data demonstrate a general mechanism for the action of lupus anticoagulants: antibodies that have immunologic specificity towards anionic phospholipids, thereby blocking the calcium-mediated binding of vitamin K-dependent coagulation factors to coagulation-active phospholipid surfaces.
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Crouch, Michael F., Roger D. Nolan i Eduardo G. Lapetina. "THROMBIN-INDUCED RELEASE OF INTRA-PLATELET CA2+ STORES IS INHIBITED BY PROSTACYCLIN, BUT GTP- AND IP3-INDUCED RELEASE IS UNAFFECTED". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644515.

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Alpha-thrombin induced the release of internal Ca2+ stores and the influx of Ca2+ in human platelets, as measured by quin-2 fluorescence. This was accompanied by a stimulated formation of inositol phosphates and phosphatidic acid. The Ca2+ responses were inhibited almost totally by pretreatment of cells with prostacyclin (PGI2). Epinephrine was able to restore the influx of Ca2+ from the external medium, but not the alpha-thrombin-induced release of internal Ca2+ stores. This was despite epinephrine restoring phosphatidic acid formation and, at least partially, the generation of inositol trisphosphate (IP3). This suggested that PGI2 was inhibiting the actions of IP3 in inducing release of Ca2+ from the dense tubular system. Since the effects of PGI2 are thought to be mediated by formation of cAMP, we examined whether cAMP could modulate the release of 45Ca2+ induced by IP3 from permeabilized platelets. IP3 induced about a 30% release of cellular 45Ca2+ over a 4 min period. However, neither pretreatment of cells with PGI2 nor the direct application of dibutyryl cAMP had any effect on the IP3-stimulated 45Ca2+ release. GTP, which released about 10% of total cell 45Ca2+, also was not affected by these agents. These results suggest either that permeabilization of platelets dilutes cytoplasmic components which are necessary for cAMP action, or that PGI2 is inhibiting the release of Ca2+ stores induced by thrombin, presumably via IP3, by a mechanism which is separate to the elevation of intracellular cAMP levels.
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