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Articles de revues sur le sujet « Adenine nucleotides Receptors »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 10 février 2022

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1

Stone, Trevor W. "Receptors for adenosine and adenine nucleotides." General Pharmacology: The Vascular System 22, no. 1 (January 1991): 25–31. http://dx.doi.org/10.1016/0306-3623(91)90305-p.

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Newman, George C., Frank E. Hospod, Sean D. Trowbridge, Shilpa Motwani, and Yan Liu. "Restoring Adenine Nucleotides in a Brain Slice Model of Cerebral Reperfusion." Journal of Cerebral Blood Flow & Metabolism 18, no. 6 (June 1998): 675–85. http://dx.doi.org/10.1097/00004647-199806000-00010.

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Tissue adenine nucleotides are depleted during cerebral ischemia, impeding recovery after reperfusion. Although prior studies have attempted to prevent the initial loss of adenylates, the present study tests the hypothesis that stimulating synthesis of adenine nucleotides, through either adenosine kinase or adenine phosphoribosyltransferase, would result in significant cerebroprotection. To study the effects on neurons and glia directly while avoiding the influence of the cerebral vasculature, hippocampal brain slices were used for the model of transient ischemia with reperfusion. The standard

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3

Gorman, Mark W., Kayoko Ogimoto, Margaret V. Savage, Kenneth A. Jacobson, and Eric O. Feigl. "Nucleotide coronary vasodilation in guinea pig hearts." American Journal of Physiology-Heart and Circulatory Physiology 285, no. 3 (September 2003): H1040—H1047. http://dx.doi.org/10.1152/ajpheart.00981.2002.

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The role of P1 receptors and P2Y1 receptors in coronary vasodilator responses to adenine nucleotides was examined in the isolated guinea pig heart. Bolus arterial injections of nucleotides were made in hearts perfused at constant pressure. Peak increase in flow was measured before and after addition of purinoceptor antagonists. Both the P1 receptor antagonist 8-( p-sulfophenyl)theophylline and adenosine deaminase inhibited adenosine vasodilation. AMP-induced vasodilation was inhibited by P1 receptor blockade but not by adenosine deaminase or by the selective P2Y1 antagonist N6-methyl-2′-deoxya

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Murugappan, Swaminathan, Haripriya Shankar, and Satya P. Kunapuli. "Platelet Receptors for Adenine Nucleotides and Thromboxane A2." Seminars in Thrombosis and Hemostasis 30, no. 4 (August 2004): 411–18. http://dx.doi.org/10.1055/s-2004-833476.

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Eltzschig, Holger K., Linda F. Thompson, Jorn Karhausen, Richard J. Cotta, Juan C. Ibla, Simon C. Robson, and Sean P. Colgan. "Endogenous adenosine produced during hypoxia attenuates neutrophil accumulation: coordination by extracellular nucleotide metabolism." Blood 104, no. 13 (December 15, 2004): 3986–92. http://dx.doi.org/10.1182/blood-2004-06-2066.

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Abstract Hypoxia is a well-documented inflammatory stimulus and results in tissue polymorphonuclear leukocyte (PMN) accumulation. Likewise, increased tissue adenosine levels are commonly associated with hypoxia, and given the anti-inflammatory properties of adenosine, we hypothesized that adenosine production via adenine nucleotide metabolism at the vascular surface triggers an endogenous anti-inflammatory response during hypoxia. Initial in vitro studies indicated that endogenously generated adenosine, through activation of PMN adenosine A2A and A2B receptors, functions as an antiadhesive sig

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Williams, Wynford R. "Dampening of neurotransmitter action: molecular similarity within the melatonin structure." Endocrine Regulations 52, no. 4 (October 1, 2018): 199–207. http://dx.doi.org/10.2478/enr-2018-0025.

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AbstractObjectives. Melatonin initiates physiologic and therapeutic responses in various tissues through binding to poorly defined MT receptors regulated by G-proteins and purine nucleotides. Melatonin’s interaction with other G-protein regulated receptors, including those of serotonin, is unclear. This study explores the potential for the interaction of melatonin with nucleotide and receptor ligand structures. Methods. The study uses a computational program to investigate relative molecular similarity by the comparative superimposition and quantitative fitting of molecular structures to adeni

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Antos, Laura K., and Lincoln R. Potter. "Adenine nucleotides decrease the apparentKmof endogenous natriuretic peptide receptors for GTP." American Journal of Physiology-Endocrinology and Metabolism 293, no. 6 (December 2007): E1756—E1763. http://dx.doi.org/10.1152/ajpendo.00321.2007.

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Natriuretic peptide receptors A (NPR-A) and B (NPR-B) mediate most effects of natriuretic peptides by synthesizing cGMP. ATP increases the activity of these receptors by an unknown mechanism. We recently reported that a nonhydrolyzable form of ATP, adenylyl imidodiphosphate (AMPPNP), stabilizes but is not required for the activation of NPR-A and NPR-B in membranes from highly overexpressing cells. Here, we repeated these studies on receptors expressed in endogenous settings. Kinetic analysis indicated that both AMPPNP and ATP dramatically decrease the apparent Kmof both receptors for GTP but h

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Kawa, Kazuyoshi. "Discrete but simultaneous release of adenine nucleotides and serotonin from mouse megakaryocytes as detected with patch- and carbon-fiber electrodes." American Journal of Physiology-Cell Physiology 286, no. 1 (January 2004): C119—C128. http://dx.doi.org/10.1152/ajpcell.00014.2003.

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Using patch- and carbon-fiber electrodes, we studied release phenomena of adenine nucleotides and serotonin from megakaryocytes isolated from the bone marrow of the mouse. Megakaryocytes express ionotropic purinergic receptors on their surfaces. Under the condition of whole cell recording, the cells showed spikelike spontaneous inward currents. The spontaneous currents were carried by cations and had amplitudes of 30–800 pA at –43 mV and durations of 0.1–0.3 s. Pyridoxalphosphate-6-azophenyl-2′,4′-disulfonic acid (PPADS; 100 μM) and suramin (100 μM), purinoceptor-blocking agents, depressed the

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Puchałowicz, Kamila, Maciej Tarnowski, Marta Tkacz, Dariusz Chlubek, Patrycja Kłos, and Violetta Dziedziejko. "Extracellular Adenine Nucleotides and Adenosine Modulate the Growth and Survival of THP-1 Leukemia Cells." International Journal of Molecular Sciences 21, no. 12 (June 22, 2020): 4425. http://dx.doi.org/10.3390/ijms21124425.

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A new approach to improve the effectiveness of acute myeloid leukemia (AML) treatment is to use the properties of purinergic signaling molecules secreted into the bone marrow milieu in response to leukemic cell growth. Therefore, our study aimed to evaluate the effects of extracellular adenine nucleotides and adenosine on the growth and death parameters in the leukemic THP-1 cell line. Cells were exposed to ATP, ADP, AMP, adenosine and nonhydrolyzable analogues of ATP and ADP (ATPγS and ADPβS) in a 1–1000 μM broad concentration range. The basal mRNA expression of the P1 and P2 receptors was ev

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Cattaneo, M. "The platelet P2 receptors in inflammation." Hämostaseologie 35, no. 03 (2015): 262–66. http://dx.doi.org/10.5482/hamo-14-09-0044.

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SummaryIn addition to their well characterized and established role in haemostasis and thrombosis, platelets contribute to the pathogenesis of inflammation. Adenine nucleotides are signalling molecules that regulate the function of virtually every cell in the body, by interacting with P2 receptors. Their important role in inflammation is well established. In the last few years, the pro-inflammatory roles of adenine nucleotides interacting with their platelet P2 receptors has emerged. In particular, it was shown that the platelet P2Y12 receptor for ADP significantly contributed to the proinflam

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Guzman-Aranguez, Ana, Xavier Gasull, Yolanda Diebold, and Jesús Pintor. "Purinergic Receptors in Ocular Inflammation." Mediators of Inflammation 2014 (2014): 1–11. http://dx.doi.org/10.1155/2014/320906.

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Inflammation is a complex process that implies the interaction between cells and molecular mediators, which, when not properly “tuned,” can lead to disease. When inflammation affects the eye, it can produce severe disorders affecting the superficial and internal parts of the visual organ. The nucleoside adenosine and nucleotides including adenine mononucleotides like ADP and ATP and dinucleotides such as P1,P4-diadenosine tetraphosphate (Ap4A), and P1,P5-diadenosine pentaphosphate (Ap5A) are present in different ocular locations and therefore they may contribute/modulate inflammatory processes

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REES, D. Aled, Maurice F. SCANLON, and Jack HAM. "Novel insights into how purines regulate pituitary cell function." Clinical Science 104, no. 5 (May 1, 2003): 467–81. http://dx.doi.org/10.1042/cs20030053.

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Purine nucleosides and nucleotides are widely distributed substances that exhibit a diverse range of effects in a number of tissues, acting as important extracellular signalling molecules in addition to their more established roles in cellular metabolism. They mediate their effects via activation of distinct cell surface receptors, termed adenosine (or P1) and P2 purinergic receptors. Although roles for adenosine and adenine nucleotides have been described previously in the pituitary gland, the distribution of the receptor subtypes and the effects of their activation on pituitary function are

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Reddington, M. "Interactions of adenine nucleotides with A1 receptors in rat brain membranes." Japanese Journal of Pharmacology 52 (1990): 92. http://dx.doi.org/10.1016/s0021-5198(19)32966-x.

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Biffen, M., and D. R. Alexander. "Mobilization of intracellular Ca2+ by adenine nucleotides in human T-leukaemia cells: evidence for ADP-specific and P2y-purinergic receptors." Biochemical Journal 304, no. 3 (December 15, 1994): 769–74. http://dx.doi.org/10.1042/bj3040769.

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The expression of purinergic receptors on human T-cells was investigated and the receptors were shown to be functionally coupled to intracellular signals in two out of eight T-leukaemia cell-lines. Addition of adenine nucleotides resulted in mobilization of intracellular Ca2+ in HPB-ALL cells and a cell line (CB1) recently isolated from a patient with T-acute lymphoblastic leukaemia. Of a range of nucleotides tested only ADP and ATP elevated intracellular levels of Ca2+, with ADP being the more potent agonist. Ca2+ mobilization by ATP was accompanied by increased inositol phosphate production

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Nemeth, E. F., and L. M. Kosz. "Adenine nucleotides mobilize cellular Ca2+ and inhibit parathyroid hormone secretion." American Journal of Physiology-Endocrinology and Metabolism 257, no. 4 (October 1, 1989): E505—E513. http://dx.doi.org/10.1152/ajpendo.1989.257.4.e505.

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Measurements of the concentration of intracellular free calcium [( Ca2+]i) were used to screen for the presence of Ca2+-mobilizing receptors on dissociated and purified bovine parathyroid cells loaded with fura-2. Among a wide variety of agents known to mobilize cellular Ca2+ in other cells, only ATP and certain other nucleotides were capable of altering [Ca2+]i in parathyroid cells. The addition of ATP or adenosine 5'-O-(3-thiotriphosphate) (ATP gamma S) (10-200 microM) to parathyroid cells evoked a rapid and transient increase that was followed by a small, steady-state increase in [Ca2+]i. C

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Borowiec, Agnieszka, Katarzyna Lechward, Kinga Tkacz-Stachowska, and Andrzej C. Składanowski. "Adenosine as a metabolic regulator of tissue function: production of adenosine by cytoplasmic 5'-nucleotidases." Acta Biochimica Polonica 53, no. 2 (June 12, 2006): 269–78. http://dx.doi.org/10.18388/abp.2006_3339.

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Adenosine is a product of complete dephosphorylation of adenine nucleotides which takes place in various compartments of the cell. This nucleoside is a significant signal molecule engaged in regulation of physiology and modulation of the function of numerous cell types (i.e. neurons, platelets, neutrophils, mast cells and smooth muscle cells in bronchi and vasculature, myocytes etc.). As part a of purinergic signaling system, adenosine mediates neurotransmission, conduction, secretion, vasodilation, proliferation and cell death. Most of the effects of adenosine help to protect cells and tissue

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Schicker, Klaus, Simon Hussl, Giri K. Chandaka, Kristina Kosenburger, Jae-Won Yang, Maria Waldhoer, Harald H. Sitte, and Stefan Boehm. "A membrane network of receptors and enzymes for adenine nucleotides and nucleosides." BMC Pharmacology 8, Suppl 1 (2008): A40. http://dx.doi.org/10.1186/1471-2210-8-s1-a40.

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Schicker, Klaus, Simon Hussl, Giri K. Chandaka, Kristina Kosenburger, Jae-Won Yang, Maria Waldhoer, Harald H. Sitte, and Stefan Boehm. "A membrane network of receptors and enzymes for adenine nucleotides and nucleosides." Biochimica et Biophysica Acta (BBA) - Molecular Cell Research 1793, no. 2 (February 2009): 325–34. http://dx.doi.org/10.1016/j.bbamcr.2008.09.014.

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Buxton, D. B., S. M. Robertson, and M. S. Olson. "Stimulation of glycogenolysis by adenine nucleotides in the perfused rat liver." Biochemical Journal 237, no. 3 (August 1, 1986): 773–80. http://dx.doi.org/10.1042/bj2370773.

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Infusion of adenine nucleotides and adenosine into perfused rat livers resulted in stimulation of hepatic glycogenolysis, transient increases in the effluent perfusate [3-hydroxybutyrate]/[acetoacetate] ratio, and increased portal vein pressure. In livers perfused with buffer containing 50 microM-Ca2+, transient efflux of Ca2+ was seen on stimulation of the liver with adenine nucleotides or adenosine. ADP was the most potent of the nucleotides, stimulating glucose output at concentrations as low as 0.15 microM, with half-maximal stimulation at approx. 1 microM, and ATP was slightly less potent

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Mannix, R. J., T. Moatter, K. A. Kelley, and M. E. Gerritsen. "Cellular signaling responses mediated by a novel nucleotide receptor in rabbit microvessel endothelium." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 2 (August 1, 1993): H675—H680. http://dx.doi.org/10.1152/ajpheart.1993.265.2.h675.

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The adenine nucleotide, ATP, elicits an elevation in intracellular ionized calcium concentration ([Ca2+]i) and phospholipase C-mediated phosphatidylinositol hydrolysis and stimulates the synthesis of the prostaglandins E2 and I2 in cultured endothelial cells derived from rabbit cardiac muscle. Use of various ATP analogues indicated that these events did not fit the classical definition of P1 or P2 purinergic receptors and, furthermore, indicated that the receptor(s) mediating these activities was not specific for purines. The rank order of agonist potency on prostaglandin release, elevations i

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LEMMENS, Raf, Luc VANDUFFEL, Henri TEUCHY, and Ognjen CULIC. "Regulation of proliferation of LLC-MK2 cells by nucleosides and nucleotides: the role of ecto-enzymes." Biochemical Journal 316, no. 2 (June 1, 1996): 551–57. http://dx.doi.org/10.1042/bj3160551.

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1. Using the incorporation of [methyl-3H]thymidine as a proliferation marker, the effects of various nucleosides and nucleotides on endothelial LLC-MK2 cells were studied. We found that ATP, ADP, AMP and adenosine in concentrations of 10 μM or higher stimulate the proliferation of these cells. 2. Inhibition of ecto-ATPase (EC 3.6.1.15), 5´-nucleotidase (EC 3.1.3.5) or alkaline phosphatase (EC 3.1.3.1) significantly diminished the stimulatory effect of ATP, indicating that the effect is primarily caused by adenosine and not by adenine nucleotides. Also, the effect depends only on extracellular

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Salter, Kelli D., J. Gregory Fitz, and Richard M. Roman. "Domain-specific purinergic signaling in polarized rat cholangiocytes." American Journal of Physiology-Gastrointestinal and Liver Physiology 278, no. 3 (March 1, 2000): G492—G500. http://dx.doi.org/10.1152/ajpgi.2000.278.3.g492.

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In cholangiocytes, adenine nucleotides function as autocrine/paracrine signals that modulate ductular ion transport by activation of purinergic receptors. The purpose of these studies was to identify cellular signals that modulate ATP release and nucleotide processing in polarized normal rat cholangiocytes. In Ussing chamber studies, selective exposure of the apical and basolateral membranes to ATP or adenosine 5′- O-(3-thiotriphosphate) (ATPγS) stimulated increases in short-circuit current. Apical purinergic receptor agonist preference was consistent with the P2Y2subtype. In contrast, basolat

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Cote, S., J. Van Sande, and J. M. Boeynaems. "Enhancement of endothelial cAMP accumulation by adenine nucleotides: role of methylxanthine-sensitive sites." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 5 (May 1, 1993): H1498—H1503. http://dx.doi.org/10.1152/ajpheart.1993.264.5.h1498.

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ATP is a well-known inducer of prostacyclin and nitric oxide release from vascular endothelial cells. These responses are mediated by P2 receptors coupled to a phospholipase C. We have investigated the influence of ATP on the control of adenosine 3',5'-cyclic monophosphate (cAMP) in bovine aortic endothelial cells. ATP produced a slight increase in the cAMP content of unstimulated endothelial cells. A more impressive response to ATP (5-fold) was observed in forskolin-stimulated cells. The rank orders of potency of various ATP analogues were strikingly different for the increase in cAMP and the

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Kasztan, Małgorzata, Agnieszka Piwkowska, Ewelina Kreft, Dorota Rogacka, Irena Audzeyenka, Mirosława Szczepanska-Konkel, and Maciej Jankowski. "Extracellular purines' action on glomerular albumin permeability in isolated rat glomeruli: insights into the pathogenesis of albuminuria." American Journal of Physiology-Renal Physiology 311, no. 1 (July 1, 2016): F103—F111. http://dx.doi.org/10.1152/ajprenal.00567.2015.

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Purinoceptors (adrengeric receptors and P2 receptors) are expressed on the cellular components of the glomerular filtration barrier, and their activation may affect glomerular permeability to albumin, which may ultimately lead to albuminuria, a well-established risk factor for the progression of chronic kidney disease and development of cardiovascular diseases. We investigated the mechanisms underlying the in vitro and in vivo purinergic actions on glomerular filter permeability to albumin by measuring convectional albumin permeability ( Palb) in a single isolated rat glomerulus based on the v

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Park, Hyung Seo, Matthew J. Betzenhauser, Yu Zhang, and David I. Yule. "Regulation of Ca2+ release through inositol 1,4,5-trisphosphate receptors by adenine nucleotides in parotid acinar cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 302, no. 1 (January 2012): G97—G104. http://dx.doi.org/10.1152/ajpgi.00328.2011.

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Secretagogue-stimulated intracellular Ca2+ signals are fundamentally important for initiating the secretion of the fluid and ion component of saliva from parotid acinar cells. The Ca2+ signals have characteristic spatial and temporal characteristics, which are defined by the specific properties of Ca2+ release mediated by inositol 1,4,5-trisphosphate receptors (InsP3R). In this study we have investigated the role of adenine nucleotides in modulating Ca2+ release in mouse parotid acinar cells. In permeabilized cells, the Ca2+ release rate induced by submaximal [InsP3] was increased by 5 mM ATP.

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El-Moatassim, Chakib, Nicole Bernad, Jean-Claude Mani, and Jacques Dornand. "Extracellular ATP induces a nonspecific permeability of thymocyte plasma membranes." Biochemistry and Cell Biology 67, no. 9 (September 1, 1989): 495–502. http://dx.doi.org/10.1139/o89-080.

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We have previously demonstrated that extracellular ATP can give medullary thymocytes the calcium message required for the induction of their blastogenesis, without mobilization of intracellular calcium. We describe here the effects of extracellular nucleotides on membrane permeability to monovalent and divalent cations in mouse thymocytes. Among all nucleotides tested, under physiological conditions, only ATP and, to a lesser extent, 2-methylthio-ATP, adenosine 5′-O-(3-thio-triphosphate), and ADP were able to depolarize thymocyte plasma membranes and to induce Na+ and Ca2+ influxes into thymoc

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Dal Ben, D., M. Buccioni, C. Lambertucci, G. Marucci, R. Volpini, and G. Cristalli. "The Importance of Alkynyl Chain Presence for the Activity of Adenine Nucleosides/Nucleotides on Purinergic Receptors." Current Medicinal Chemistry 18, no. 10 (April 1, 2011): 1444–63. http://dx.doi.org/10.2174/092986711795328391.

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Fuentes-Martínez, Juan P., Diana Gutiérrez-Rodríguez, Edgar Rogel García, Karla I. Rivera-Márquez, Felipe Medrano, Oscar Torres-Ángeles, Evelin Castillo-Vargas, Blanca E. Duque Montaño, and Carolina Godoy-Alcántar. "Streptomycin Hydrazone Derivatives: Synthesis and Molecular Recognition in Aqueous Solution." Natural Product Communications 9, no. 10 (October 2014): 1934578X1400901. http://dx.doi.org/10.1177/1934578x1400901012.

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Five hydrazone derivatives of streptomycin were synthetized (D0h, D1ph, D2bt, D3dctf, D4ag) and characterized by IR, 1H and 13C NMR spectroscopy, mass spectrometry and elemental analysis. Protonation constants were determined by potentiometry for all derivatives. D1ph and D2bt derivatives were investigated as receptors of dicarboxylates and adenine nucleotides in aqueous solution by potentiometric and 1H NMR titrations. D1ph and D2bt derivatives have the highest affinity with AMP and ATP, respectively, which shows that electrostatic forces are not always the dominant factor in binding of strep

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Zhang, Xuejun, Jiayu Wen, Keshore R. Bidasee, Henry R. Besch, and Ronald P. Rubin. "Ryanodine receptor expression is associated with intracellular Ca2+ release in rat parotid acinar cells." American Journal of Physiology-Cell Physiology 273, no. 4 (October 1, 1997): C1306—C1314. http://dx.doi.org/10.1152/ajpcell.1997.273.4.c1306.

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The ryanodine receptor mediates intracellular Ca2+ mobilization in muscle and nerve, but its physiological role in nonexcitable cells is less well defined. Like adenosine 3′,5′-cyclic monophosphate and inositol 1,4,5-trisphosphate, cyclic ADP-ribose (0.3–5 μM) and ADP (1–25 μM) produced a concentration-dependent rise in cytosolic Ca2+ in permeabilized rat parotid acinar cells. Adenosine and AMP were less effective. Ryanodine markedly depressed the Ca2+-mobilizing action of the adenine nucleotides and forskolin in permeabilized cells and was likewise effective in depressing the action of forsko

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Ninomiya, Hideki, Hajime Otani, Kejie Lu, Takamichi Uchiyama, Masakuni Kido, and Hiroji Imamura. "Complementary role of extracellular ATP and adenosine in ischemic preconditioning in the rat heart." American Journal of Physiology-Heart and Circulatory Physiology 282, no. 5 (May 1, 2002): H1810—H1820. http://dx.doi.org/10.1152/ajpheart.00760.2001.

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Although adenosine is an important mediator of ischemic preconditioning (IPC), its relative contribution to IPC remains unknown. Because adenosine is formed through the hydrolysis of ATP, the present study investigated the role of ATP and adenosine in IPC. Isolated and buffer-perfused rat hearts underwent IPC by three cycles of 5-min ischemia and 5-min reperfusion before 25 min of global ischemia. The rate-pressure product (RPP) 30 min after reperfusion was taken as an endpoint of functional protection. Interstitial fluid (ISF) adenine nucleotides and adenosine were measured by cardiac microdi

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Vasconcellos, CA, and SE Lind. "Coordinated inhibition of actin-induced platelet aggregation by plasma gelsolin and vitamin D-binding protein." Blood 82, no. 12 (December 15, 1993): 3648–57. http://dx.doi.org/10.1182/blood.v82.12.3648.3648.

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Abstract Actin is an abundant intracellular protein that is released into the blood during tissue injury and its injection into rats causes microthrombi to form in the vasculature. This report and others have shown that actin filaments are able to aggregate platelets in an adenosine diphosphate (ADP)-dependent manner. The effects on this process of two plasma actin-binding proteins, vitamin D-binding protein (DBP) and gelsolin, were examined separately and together. The addition of DBP, a monomer-binding protein, to actin filaments did not affect their ability to induce platelet aggregation. H

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Vasconcellos, CA, and SE Lind. "Coordinated inhibition of actin-induced platelet aggregation by plasma gelsolin and vitamin D-binding protein." Blood 82, no. 12 (December 15, 1993): 3648–57. http://dx.doi.org/10.1182/blood.v82.12.3648.bloodjournal82123648.

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Actin is an abundant intracellular protein that is released into the blood during tissue injury and its injection into rats causes microthrombi to form in the vasculature. This report and others have shown that actin filaments are able to aggregate platelets in an adenosine diphosphate (ADP)-dependent manner. The effects on this process of two plasma actin-binding proteins, vitamin D-binding protein (DBP) and gelsolin, were examined separately and together. The addition of DBP, a monomer-binding protein, to actin filaments did not affect their ability to induce platelet aggregation. However, s

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Bagatini, Margarete Dulce, Alessandra Antunes dos Santos, Andréia Machado Cardoso, Aline Mânica, Cristina Ruedell Reschke, and Fabiano Barbosa Carvalho. "The Impact of Purinergic System Enzymes on Noncommunicable, Neurological, and Degenerative Diseases." Journal of Immunology Research 2018 (August 12, 2018): 1–21. http://dx.doi.org/10.1155/2018/4892473.

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Evidences show that purinergic signaling is involved in processes associated with health and disease, including noncommunicable, neurological, and degenerative diseases. These diseases strike from children to elderly and are generally characterized by progressive deterioration of cells, eventually leading to tissue or organ degeneration. These pathological conditions can be associated with disturbance in the signaling mediated by nucleotides and nucleosides of adenine, in expression or activity of extracellular ectonucleotidases and in activation of P2X and P2Y receptors. Among the best known

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Guarracino, Juan F., Alejandro R. Cinalli, Verónica Fernández, Liliana I. Roquel, and Adriana S. Losavio. "P2Y 13 receptors mediate presynaptic inhibition of acetylcholine release induced by adenine nucleotides at the mouse neuromuscular junction." Neuroscience 326 (June 2016): 31–44. http://dx.doi.org/10.1016/j.neuroscience.2016.03.066.

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Cunha, Rodrigo A., Paulo Correia-de-Sá, Ana M. Sebastião, and J. Alexandre Ribeiro. "Preferential activation of excitatory adenosine receptors at rat hippocampal and neuromuscular synapses by adenosine formed from released adenine nucleotides." British Journal of Pharmacology 119, no. 2 (September 1996): 253–60. http://dx.doi.org/10.1111/j.1476-5381.1996.tb15979.x.

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Song, L., SM Carter, Y. Chen, and R. Sitsapesan. "Diadenosine pentaphosphate is a potent activator of cardiac ryanodine receptors revealing a novel high-affinity binding site for adenine nucleotides." British Journal of Pharmacology 156, no. 5 (March 26, 2009): 857–67. http://dx.doi.org/10.1111/j.1476-5381.2008.00071.x.

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von Kügelgen, Ivar, Leni Späth, and Klaus Starke. "Stable adenine nucleotides inhibit [3H]-noradrenaline release in rabbit brain cortex slices by direct action at presynaptic adenosine A1-receptors." Naunyn-Schmiedeberg's Archives of Pharmacology 346, no. 2 (August 1992): 187–96. http://dx.doi.org/10.1007/bf00165300.

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Hung, C. T., F. D. Allen, K. D. Mansfield, and I. M. Shapiro. "Extracellular ATP modulates [Ca2+]i in retinoic acid-treated embryonic chondrocytes." American Journal of Physiology-Cell Physiology 272, no. 5 (May 1, 1997): C1611—C1617. http://dx.doi.org/10.1152/ajpcell.1997.272.5.c1611.

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When treated with low doses of retinoic acid (RA), cephalic chondrocytes of the chick embryonic sternum mature and express phenotypic characteristics of postmitotic hypertrophic cells. In concert with these maturation-dependent changes, cells release adenine nucleotides into the culture medium. To ascertain if these compounds modulate chondrocyte function, we challenged chondrocytes with nucleotides and measured one determinant of the signal transduction pathway, intracellular Ca2+ concentration ([Ca2+]i). In the presence of micromolar concentrations of ATP, there was a dose-dependent elevatio

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Murayama, Takashi, Nagomi Kurebayashi, and Yasuo Ogawa. "Role of Mg2+ in Ca2+-Induced Ca2+ Release through Ryanodine Receptors of Frog Skeletal Muscle: Modulations by Adenine Nucleotides and Caffeine." Biophysical Journal 78, no. 4 (April 2000): 1810–24. http://dx.doi.org/10.1016/s0006-3495(00)76731-2.

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Marteau, Frédéric, Didier Communi, Jean-Marie Boeynaems, and Nathalie Suarez Gonzalez. "Involvement of multiple P2Y receptors and signaling pathways in the action of adenine nucleotides diphosphates on human monocyte-derived dendritic cells." Journal of Leukocyte Biology 76, no. 4 (July 7, 2004): 796–803. http://dx.doi.org/10.1189/jlb.0104032.

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Weiss, Harvey, and Bruce Lages. "Secreted Dense Granule Adenine Nucleotides Promote Calcium Influx and the Maintenance of Elevated Cytosolic Calcium Levels in Stimulated Human Platelets." Thrombosis and Haemostasis 81, no. 02 (1999): 286–92. http://dx.doi.org/10.1055/s-0037-1614459.

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SummaryEvidence that secreted dense granule adenine nucleotides mediate part of the agonist-induced cytosolic calcium ([Ca2+]i) responses in human platelets was obtained from comparisons of fura-2-loaded platelets from normal subjects and from patients with a form of platelet storage pool deficiency (SPD) in which the secretory dense granules and their contents are virtually absent. SPD platelets had normal initial [Ca2+]i in creases induced by thrombin and the endoperoxide analog U46619, but a significantly enhanced decay of elevated [Ca2+]i levels following the initial increases. With thromb

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Santos, Karen Freitas, Jessié Martins Gutierres, Micheli Mainardi Pillat, Vitor Braga Rissi, Maria do Carmo dos Santos Araújo, Gustavo Bertol, Paulo Bayard Dias Gonçalves, Maria Rosa Chitolina Schetinger, and Vera Maria Morsch. "Uncaria tomentosa extract alters the catabolism of adenine nucleotides and expression of ecto-5′-nucleotidase/CD73 and P2X7 and A1 receptors in the MDA-MB-231 cell line." Journal of Ethnopharmacology 194 (December 2016): 108–16. http://dx.doi.org/10.1016/j.jep.2016.08.051.

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Laubinger, Werner, and Georg Reiser. "Differential characterization of binding sites for adenine and uridine nucleotides in membranes from rat lung as possible tools for studying P2 receptors in lung." Biochemical Pharmacology 55, no. 5 (March 1998): 687–95. http://dx.doi.org/10.1016/s0006-2952(97)00532-7.

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Catalfamo, JL, SL Raymond, JG White, and WJ Dodds. "Defective platelet-fibrinogen interaction in hereditary canine thrombopathia." Blood 67, no. 6 (June 1, 1986): 1568–77. http://dx.doi.org/10.1182/blood.v67.6.1568.bloodjournal6761568.

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A unique, intrinsic, hereditary canine platelet disorder attributable to abnormal fibrinogen receptor availability is described. Thrombopathic platelets from 13 severely affected basset hounds failed to aggregate in response to all agonists tested except thrombin. Normal platelet interaction with the various stimuli was inferred on the basis of their ability to elicit unimpaired shape change in thrombopathic platelets. No quantitative differences in major platelet membrane glycoproteins, intraplatelet fibrinogen, adenine nucleotides, or serotonin uptake were detected. Dense granule secretion w

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Chari, R. S., S. M. Schutz, J. E. Haebig, G. H. Shimokura, P. B. Cotton, J. G. Fitz, and W. C. Meyers. "Adenosine nucleotides in bile." American Journal of Physiology-Gastrointestinal and Liver Physiology 270, no. 2 (February 1, 1996): G246—G252. http://dx.doi.org/10.1152/ajpgi.1996.270.2.g246.

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Activation of purinergic receptors by ATP stimulates Cl- efflux in biliary epithelial cells. To determine whether purinergic agonists are present under physiological conditions, we have assayed mammalian bile for nucleotides and assessed whether hepatoma and cholangiocarcinoma cell lines are capable of nucleotide release. Bile samples were collected from human, rat, and pig donors and assayed for nucleotide concentrations by luminometry. ATP, ADP, and AMP were present in bile from each species, and the average total nucleotide concentration in human bile was 5.21 +/- 0.91 microM (n = 16). In a

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Catalfamo, JL, SL Raymond, JG White, and WJ Dodds. "Defective platelet-fibrinogen interaction in hereditary canine thrombopathia." Blood 67, no. 6 (June 1, 1986): 1568–77. http://dx.doi.org/10.1182/blood.v67.6.1568.1568.

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Abstract A unique, intrinsic, hereditary canine platelet disorder attributable to abnormal fibrinogen receptor availability is described. Thrombopathic platelets from 13 severely affected basset hounds failed to aggregate in response to all agonists tested except thrombin. Normal platelet interaction with the various stimuli was inferred on the basis of their ability to elicit unimpaired shape change in thrombopathic platelets. No quantitative differences in major platelet membrane glycoproteins, intraplatelet fibrinogen, adenine nucleotides, or serotonin uptake were detected. Dense granule se

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Kawashima, Yasuko, Toshiro Nagasawa, and Haruhiko Ninomiya. "Contribution of ecto-5′-nucleotidase to the inhibition of platelet aggregation by human endothelial cells." Blood 96, no. 6 (September 15, 2000): 2157–62. http://dx.doi.org/10.1182/blood.v96.6.2157.

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Abstract We studied the role of adenosine (Ado), which is generated from adenine nucleotides via the activity of ecto-5′-nucleotidase (ecto-5′-NT), in the inhibition of platelet aggregation by endothelial cells (ECs). The enzymatic activity of nucleotidases on human umbilical vein endothelial cells (HUVECs) was examined with regard to (1) the inhibition of adenosine diphosphate (ADP)–induced platelet aggregation and (2) the liberation of inorganic phosphate from adenine nucleotides. Adenosine 5′-monophosphate (AMP) preincubated with HUVECs significantly inhibited ADP-induced platelet aggregati

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Kawashima, Yasuko, Toshiro Nagasawa, and Haruhiko Ninomiya. "Contribution of ecto-5′-nucleotidase to the inhibition of platelet aggregation by human endothelial cells." Blood 96, no. 6 (September 15, 2000): 2157–62. http://dx.doi.org/10.1182/blood.v96.6.2157.h8002157_2157_2162.

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We studied the role of adenosine (Ado), which is generated from adenine nucleotides via the activity of ecto-5′-nucleotidase (ecto-5′-NT), in the inhibition of platelet aggregation by endothelial cells (ECs). The enzymatic activity of nucleotidases on human umbilical vein endothelial cells (HUVECs) was examined with regard to (1) the inhibition of adenosine diphosphate (ADP)–induced platelet aggregation and (2) the liberation of inorganic phosphate from adenine nucleotides. Adenosine 5′-monophosphate (AMP) preincubated with HUVECs significantly inhibited ADP-induced platelet aggregation. This

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Okajima, F., H. Tomura, and Y. Kondo. "Enkephalin activates the phospholipase C/Ca2+ system through cross-talk between opioid receptors and P2-purinergic or bradykinin receptors in NG 108–15 cells. A permissive role for pertussis toxin-sensitive G-proteins." Biochemical Journal 290, no. 1 (February 15, 1993): 241–47. http://dx.doi.org/10.1042/bj2900241.

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In an NG 108-15 neuroblastoma x glioma hybrid cell suspension, extracellular ATP (via P2-purinergic receptors) and bradykinin stimulated Ins(1,4,5)P3 formation, which was accompanied by an increase in the cytosolic Ca2+ concentration ([Ca2+]i). Leucine enkephalin (EK) also slightly increased [Ca2+]i in the absence, but not in the presence, of apyrase, which hydrolyses extracellular ATP and ADP to AMP. When the cells were stimulated by P2-agonists or bradykinin prior to the application of EK, EK induces a remarkable rise in [Ca2+]i. This P2-agonist- or bradykinin-assisted EK action was also obs

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MISSIAEN, Ludwig, Jan B. PARYS, Humbert DE SMEDT, Ilse SIENAERT, Henk SIPMA, Sara VANLINGEN, Karlien MAES, and Rik CASTEELS. "Effect of adenine nucleotides on myo-inositol-1,4,5-trisphosphate-induced calcium release." Biochemical Journal 325, no. 3 (August 1, 1997): 661–66. http://dx.doi.org/10.1042/bj3250661.

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The effects of a whole series of adenine nucleotides on Ins(1,4,5)P3-induced Ca2+ release were characterized in permeabilized A7r5 smooth-muscle cells. Several adenine nucleotides activated the Ins(1,4,5)P3 receptor. It was observed that 3′-phosphoadenosine 5′-phosphosulphate, CoA, di(adenosine-5′)tetraphosphate (Ap4A) and di(adenosine-5′)pentaphosphate (Ap5A) were more effective than ATP. Ap4A and Ap5A also interacted with a lower EC50 than ATP. In order to find out how these adenine nucleotides affected Ins(1,4,5)P3-induced Ca2+ release, we have measured their effect on the response of perme

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