Relevant bibliographies by topics / IIIa (GP IIb/IIIa) complex

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Academic literature on the topic 'IIIa (GP IIb/IIIa) complex'

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Published: 3 June 2025
Last updated: 31 July 2025

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Journal articles on the topic "IIIa (GP IIb/IIIa) complex"

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Parise, L. V., B. Steiner, L. Nannizzi, A. B. Criss, and D. R. Phillips. "Evidence for novel binding sites on the platelet glycoprotein IIb and IIIa subunits and immobilized fibrinogen." Biochemical Journal 289, no. 2 (1993): 445–51. http://dx.doi.org/10.1042/bj2890445.

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The present study was designed to examine the interaction of the purified platelet glycoprotein IIb-IIIa complex (GP IIb-IIIa or integrin alpha IIb beta 3) and the individual subunits of the complex with immobilized fibrinogen. Although 125I-GP IIb-IIIa binding to fibrinogen immobilized on Sepharose was specific, this interaction exhibited properties distinct from those of reversible fibrinogen binding to platelets: 125I-GP IIb-IIIa binding appeared irreversible, but non-covalent, Ca(2+)-independent, and was inhibited only weakly, or not at all, by the anti-(GP IIb-IIIa) monoclonal antibodies
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Royo, Teresa, Matilde Vidal, and Lina Badimon. "Purification of the Porcine Platelet GP IIb-IIIa Complex and the Propolypeptide of von Willebrand Factor." Thrombosis and Haemostasis 80, no. 08 (1998): 302–9. http://dx.doi.org/10.1055/s-0037-1615192.

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SummaryPlatelet membrane glycoproteins (GP) are involved in platelet adhesion and aggregation. The glycoprotein IIb-IIIa complex (GP IIbIIIa) is a Ca2+-dependent heterodimer that binds fibrinogen and other adhesive proteins, thereby mediating platelet aggregation and adhesion. We have purified two major glycoproteins from pig platelets by Concanavalin A-Sepharose, Heparin-Sepharose and Sephacryl S-300 HR chromatography (Fitzgerald et al. Anal Biochem, 1985): i) the GP IIb-IIIa complex, GP IIb Mr = 140,000 and GP IIIa a single chain of Mr = 95,000-100,000; and ii) a predominant glycoprotein of
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Kieffer, N., JL Wautier, L. Coulombel, et al. "Uncoupling in the expression of platelet GP IIb/IIIa in human endothelial cells and K562 cells: absence of immunologic crossreactivity between platelet GP IIb and the vitronectin receptor alpha chain [see comments]." Blood 72, no. 4 (1988): 1209–15. http://dx.doi.org/10.1182/blood.v72.4.1209.1209.

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Abstract Platelet glycoproteins (GP) IIb and IIIa exist as noncovalently associated Ca++-dependent heterodimer complexes within the platelet membrane and express the major platelet alloantigens Leka (Baka) and PIA1 (Zwa), which are genetic markers of GP IIb and GP IIIa, respectively. Since heterodimers immunologically related to platelet GP IIb/IIIa have been identified in a number of nucleated cell types, we tested anti-Leka and anti-PIA1 antiserum, polyclonal anti-platelet GP IIb/IIIa IgG, as well as a panel of 28 monoclonal anti-GP IIb, GP IIIa, or complex dependent anti-GP IIb/IIIa antibod
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Kieffer, N., JL Wautier, L. Coulombel, et al. "Uncoupling in the expression of platelet GP IIb/IIIa in human endothelial cells and K562 cells: absence of immunologic crossreactivity between platelet GP IIb and the vitronectin receptor alpha chain [see comments]." Blood 72, no. 4 (1988): 1209–15. http://dx.doi.org/10.1182/blood.v72.4.1209.bloodjournal7241209.

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Platelet glycoproteins (GP) IIb and IIIa exist as noncovalently associated Ca++-dependent heterodimer complexes within the platelet membrane and express the major platelet alloantigens Leka (Baka) and PIA1 (Zwa), which are genetic markers of GP IIb and GP IIIa, respectively. Since heterodimers immunologically related to platelet GP IIb/IIIa have been identified in a number of nucleated cell types, we tested anti-Leka and anti-PIA1 antiserum, polyclonal anti-platelet GP IIb/IIIa IgG, as well as a panel of 28 monoclonal anti-GP IIb, GP IIIa, or complex dependent anti-GP IIb/IIIa antibodies on en
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Meyer, M., C. M. Kirchmaier, A. Schirmer, P. Spangenberg, Ch Ströhl, and K. Breddin. "Acquired Disorder of Platelet Function Associated with Autoantibodies against Membrane Glycoprotein IIb-IIIa Complex - 1. Glycoprotein Analysis." Thrombosis and Haemostasis 65, no. 05 (1991): 491–96. http://dx.doi.org/10.1055/s-0038-1648178.

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SummaryA patient with idiopathic thrombocytopenic purpura developed after splenectomy a thrombasthenia-like severe haemor-rhagic diathesis characterized by a normal or subnormal platelet count, prolonged bleeding time, strongly reduced platelet adhesion to glass and defective platelet aggregation in response to ADP and collagen. In contrast to hereditary thrombasthenia membrane glycoproteins (GP) lib and Ilia were normally present in the patient’s platelets. Immunoelectrophoretic analysis revealed an abnormal behaviour of the patient’s GP IIb-IIIa complex. Autoantibodies against GP IIb-IIIa we
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Fournier, Dominique J., Arnold Kabral, Peter A. Castaldi, and Michael C. Berndt. "A Variant of Glanzmann's Thrombasthenia Characterized by Abnormal Glycoprotein IIb/IIIa Complex Formation." Thrombosis and Haemostasis 62, no. 03 (1989): 977–83. http://dx.doi.org/10.1055/s-0038-1651038.

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SummaryGlanzmann's thrombasthenia is a congenital bleeding abnormality characterized by absent platelet aggregation due to the failure of fibrinogen to bind to activated thrombasthenic platelets. In the majority of cases, this defect is caused by the absence or marked reduction of a specific fibrinogen-binding aggregation receptor, the GP IIb/IIIa complex. E.T., an 18-year-old female with a life-long history of bleeding and easy bruising, had the normal clinical features of Glanzmann's thrombasthenia. Surprisingly, sodium dodecyl sulphate-polyacrylamide gel electrophoresis of her platelets sho
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Pidard, D., D. Didry, TJ Kunicki, and AT Nurden. "Temperature-dependent effects of EDTA on the membrane glycoprotein IIb- IIIa complex and platelet aggregability." Blood 67, no. 3 (1986): 604–11. http://dx.doi.org/10.1182/blood.v67.3.604.604.

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Abstract In agreement with previous studies, we observed that incubation of washed human platelets with EDTA at 37 degrees C for short periods caused an irreversible loss of their aggregation response to adenosine diphosphate and markedly diminished their capacity to bind fibrinogen. AP-2 is a monoclonal antibody that reacts with a determinant specific to the glycoprotein (GP) IIb-IIIa complex. We now report that in a direct binding assay, the number of sites for AP-2 on platelets incubated with EDTA at 37 degrees C fell to approximately 30% of those present on control platelets. This effect o
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Pidard, D., D. Didry, TJ Kunicki, and AT Nurden. "Temperature-dependent effects of EDTA on the membrane glycoprotein IIb- IIIa complex and platelet aggregability." Blood 67, no. 3 (1986): 604–11. http://dx.doi.org/10.1182/blood.v67.3.604.bloodjournal673604.

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In agreement with previous studies, we observed that incubation of washed human platelets with EDTA at 37 degrees C for short periods caused an irreversible loss of their aggregation response to adenosine diphosphate and markedly diminished their capacity to bind fibrinogen. AP-2 is a monoclonal antibody that reacts with a determinant specific to the glycoprotein (GP) IIb-IIIa complex. We now report that in a direct binding assay, the number of sites for AP-2 on platelets incubated with EDTA at 37 degrees C fell to approximately 30% of those present on control platelets. This effect of EDTA wa
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Hiraiwa, A., A. Matsukage, H. Shiku, T. Takahashi, K. Naito, and K. Yamada. "Purification and partial amino acid sequence of human platelet membrane glycoproteins IIb and IIIa." Blood 69, no. 2 (1987): 560–64. http://dx.doi.org/10.1182/blood.v69.2.560.560.

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Abstract The glycoprotein (GP) IIb-IIIa complex was isolated from human platelet membranes by immunoaffinity chromatography using a monoclonal antibody specific for GP IIb-IIIa. GP IIb and IIIa were further separated in the presence of sodium dodecyl sulfate (SDS) by gel filtration high- performance liquid chromatography (HPLC). Two cycles of this procedure yielded almost complete separation of homogeneous preparations of GP IIb and IIIa. Each protein was then digested with lysyl endopeptidase (Achromobacter protease I), which cleaves at the carboxyl side of lysine residues, and the resulting
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Hiraiwa, A., A. Matsukage, H. Shiku, T. Takahashi, K. Naito, and K. Yamada. "Purification and partial amino acid sequence of human platelet membrane glycoproteins IIb and IIIa." Blood 69, no. 2 (1987): 560–64. http://dx.doi.org/10.1182/blood.v69.2.560.bloodjournal692560.

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The glycoprotein (GP) IIb-IIIa complex was isolated from human platelet membranes by immunoaffinity chromatography using a monoclonal antibody specific for GP IIb-IIIa. GP IIb and IIIa were further separated in the presence of sodium dodecyl sulfate (SDS) by gel filtration high- performance liquid chromatography (HPLC). Two cycles of this procedure yielded almost complete separation of homogeneous preparations of GP IIb and IIIa. Each protein was then digested with lysyl endopeptidase (Achromobacter protease I), which cleaves at the carboxyl side of lysine residues, and the resulting oligopept
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Dissertations / Theses on the topic "IIIa (GP IIb/IIIa) complex"

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MOREL-KOPP, MARIE-CHRISTINE. "Anticorps monoclonaux anti-complexe gp iib/iiia : outils pour l'etude de thrombopathies." Paris 6, 1991. http://www.theses.fr/1991PA066247.

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Les anticorps monoclonaux murins (moabs) sont devenus un outil indispensable pour l'etude structurale et fonctionnelle des proteines et glycoproteines. Nous avons produit des moabs diriges contre le complexe glycoproteique (gp) iib/iiia plaquettaire afin d'une part d'etudier certains aspects de la regulation de l'activation plaquettaire et d'autre part de caracteriser differentes thrombopathies dont la thrombasthenie de glanzmann. Parmi les moabs obtenus, nous avons selectionne un moab inducteur de l'activation et de l'agregation plaquettaire: le pl2-49 (anti-gp iib) et deux inhibiteurs: le pl
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Jallu, Vincent. "Contribution à l'étude de l'immunologie du complexe GP IIb-IIIa : caractérisation d'anticorps humains et de la souris." Bordeaux 2, 1993. http://www.theses.fr/1993BOR28268.

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McCaslin, James. "Platelet function in patients with polymorphisms of GP IIb/IIIa and cyclooxygenase." Thesis, University of Newcastle Upon Tyne, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.493079.

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Platelets contribute to the progression of atherosclerotic disease by adhering to the subendothelial matrix at sites of shear-induced mechanical injury to the vessel. The understanding that genetic factors play a role in the development of atheroma led to recent interest in polymorphisms of platelet receptors as a possible basis for this. Furthermore, there is a growing body of evidence to link these polymorphisms with resistance to antiplatelet agents, the implications of which are not yet fully appreciated.
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Kulle, Konrad. "Thrombozyteninhibition und Glykoprotein-IIb/IIIa- Rezeptorbesetzung bei intrakoronarer versus intravenöser Bolusgabe von Abciximab bei Patienten mit ST-Hebungs- Infarkt." Doctoral thesis, Universitätsbibliothek Leipzig, 2015. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-160129.

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Bei Patienten mit ST-Strecken-Elevations-Myokardinfarkt (STEMI) ist die direkte intrakoronare Bolusverabreichung des Glykoprotein-IIb/IIIa-Rezeptorantagonist Abciximab, im Gegensatz zur periphervenösen Bolusinjektion, mit einer Reduktion von Infarktgröße und mikrovaskulärer Obstruktion sowie mit einem höheren Anteil geretteten Myokards assoziiert, vermutlich ausgelöst durch eine höhere lokale Arzneimittelkonzentration und der dadurch gesteigerten Hemmung der Plättcheninhibition. Ziel der Arbeit war es herauszufinden, ob es Unterschiede gibt bezüglich der GP-IIb/IIIa Rezeptorbesetzung und der T
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Croizet, François. "Modélisation et conception d'antagonistes du récepteur plaquettaire du fibrinogène (αIIb/ß3 - GP IIb/IIIa)". Bordeaux 2, 1997. http://www.theses.fr/1997BOR2B006.

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Troesch, Alain. "Biosynthèse et maturation de la glycoprotéine plaquettaire IIb/IIIa, récepteur du fibrinogène." Université Joseph Fourier (Grenoble), 1990. http://www.theses.fr/1990GRE10120.

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Les intégrines constituent une famille de récepteurs membranaires présents a la surface de nombreux types cellulaires et qui interviennent dans un grand nombre de phénomènes biologiques nécessitant des réactions d'adhérence (embryogénèse, prolifération et différenciation cellulaire, réponse hémostatique, angiogénèse, réponse immunitaire. . . ). Ces récepteurs sont des hétérodimères non covalents de type alpha-beta. La glycoprotéine plaquettaire IIb/IIIa (GPIIb/IIIa) et le récepteur de la vitronectine (VNR) sont deux intégrines qui possèdent la même sous unité beta et font partie du groupe des
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Vetter, Christian. "Langzeitresultate nach PTCA mit - ohne Stentimplantation in Abhängigkeit vom Genotyp des Gp-IIb-IIIa-Rezeptors." [S.l.] : [s.n.], 2002. http://www.diss.fu-berlin.de/2002/122/index.html.

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Carteaux, Jean-Philippe. "Circulation extra-corporelle, thrombose artérielle : modèles expérimentaux : rôle de l'inhibition des récepteurs plaquettaires GP IIb-IIIa." Nancy 1, 1996. http://www.theses.fr/1996NAN10340.

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La thrombose artérielle et les troubles de l'hémostase induits par la circulation extra corporelle (C. E. C. ) sont des préoccupations majeures du chirurgien cardio-vasculaire. Les plaquettes sanguines ont un rôle déterminant dans l'intrication des facteurs impliqués dans la physiopathologie des désordres cardio-vasculaires d'origine thrombotique ainsi que dans. La survenue des troubles hémobiologiques associés à la circulation extra-corporelle. La liaison du récepteur plaquettaire, la glycoprotéine IIb-IIIa (GP IIb-IIIa) au facteur Willebrand participe aux phénomènes d'adhésion plaquettaire ;
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Thon, Jonathan Noah. "Application of proteomics to the study of protein translation in stored platelet units." Thesis, University of British Columbia, 2008. http://hdl.handle.net/2429/2346.

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Platelet products have a short shelf life (5 to 7 days) owing in part to the deterioration of the quality of platelets stored at 22°C. This creates significant inventory challenges, and blood banks may suffer shortages and high wastage as a result. Proteomics offers a global quantitative approach to investigate changes occurring in stored blood products. These data sets can identify processes leading to storage-associated losses of blood component quality such as the platelet storage lesion (PSL). Changes to the platelet proteome between days 1 and 7 of storage were analysed with 3 complementa
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Jaminet, Patrick. "Bifunktionale Fusionsproteine Kombination hochselektiver, direkter Faktor-Xa-Inhibition mit aktivationsspezifischer GP IIb/IIIa-Blockade einerseits, und zielgerichtetem Fibrin-Targeting andererseits /." [S.l.] : [s.n.], 2006. http://www.freidok.uni-freiburg.de/volltexte/2466/index.html.

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Books on the topic "IIIa (GP IIb/IIIa) complex"

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Michael, Lincoff A., and Topol Eric J. 1954-, eds. Platelet glycoprotein IIb/IIIa receptor inhibitors in cardiovascular disease. Humana Press, 1999.

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1934-, Brown Allan, and Canadian Coordinating Office for Health Technology Assessment., eds. Economic evaluation of glycoprotein IIb/IIIa inhibitors in patients undergoing percutaneous coronary intervention with stenting. Canadian Coordinating Office for Health Technology Assessment, 2005.

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Chuong, Ho, and Canadian Coordinating Office for Health Technology Assessment., eds. Glycoprotein IIb/IIIa antagonists: A systematic review of randomized clinical trials in patients undergoing percutaneous coronary intervention. Canadian Coordinating Office for Health Technology Assessment, 2005.

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Pharand, Chantal. The use of platelet glycoprotein IIB/IIIA receptor antagonists in the management of unstable angina and non-st-elevation myocardial infarction: A critical evaluation. s.n., 2000.

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Platelet glycoprotin IIb/IIIa inhibitors in cardiovascular disease. 2nd ed. Humana Press, 2003.

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Lincoff, A. Michael. Platelet Glycoprotein IIb/IIIa Inhibitors in Cardiovascular Disease (Contemporary Cardiology). 2nd ed. Humana Press, 2003.

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Fröhlich, Jürgen Frank. Einfluss parenteraler GP IIb/IIIa -Antagonisten auf Migration und Proliferation glatter Muskelzellen in vitro. 2005.

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Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199687039.003.0070.

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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, an
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Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_001.

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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, an
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Mannucci, Pier Mannuccio. Bleeding and haemostasis disorders. Oxford University Press, 2017. http://dx.doi.org/10.1093/med/9780199687039.003.0070_update_002.

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The main cause of haemostasis defects and related bleeding complications in patients with acute coronary syndromes admitted to the intensive cardiac care unit is the use of multiple antithrombotic drugs, alone or concomitantly with invasive procedures such as percutaneous coronary intervention with stent deployment and coronary artery bypass surgery. These drugs, that act upon several components of haemostasis (platelet function, coagulation, fibrinolysis), are associated with bleeding complications, particularly in elderly patients (more so in women than in men), those who are underweight, an
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Book chapters on the topic "IIIa (GP IIb/IIIa) complex"

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Timson, David J., Richard J. Reece, James B. Thoden, et al. "GT Platelet Glycoprotein IIb–IIIa Deficiency GP IIb–IIIa Complex." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8590.

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Metze, Dieter, Tam Nguyen, Birgit Haack, et al. "Deficiency of Glycoprotein Complex IIb–IIIa." In Encyclopedia of Molecular Mechanisms of Disease. Springer Berlin Heidelberg, 2009. http://dx.doi.org/10.1007/978-3-540-29676-8_8592.

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Ranjan, Shraddha, and Gagandeep Singh Wander. "Intravenous anti-platelet therapy—GP IIb/IIIa blockers and cangrelor." In Acute Coronary Syndromes. CRC Press, 2020. http://dx.doi.org/10.1201/9780429025396-19.

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Cazenave, J. P., C. Gachet, and F. Lanza. "Pharmacological Inhibition of the ADP-GP IIb/IIIa-Fibrinogen Pathway of Platelet Aggregation." In Developments in Cardiovascular Medicine. Springer Netherlands, 1991. http://dx.doi.org/10.1007/978-94-011-3484-2_5.

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Calvete, Juan José. "Elements for a Structural/Functional Model of Human Platelet Plasma Membrane Fibrinogen Receptor, the Glycoprotein IIb/IIIa Complex (Integrin αIIb/β3)." In Cell Adhesion Molecules. Springer US, 1993. http://dx.doi.org/10.1007/978-1-4615-2830-2_6.

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Berliner, Shlomo A., Richard A. Houghten, James R. Roberts, and Zaverio M. Ruggeri. "Multiple Epitope Specificity of Monoclonal Antibodies to a Single Synthetic Peptide: Use in the Characterization of the GP IIb-IIIa Binding Domain of Von Willebrand Factor." In Advances in Experimental Medicine and Biology. Springer US, 1990. http://dx.doi.org/10.1007/978-1-4615-3806-6_13.

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"GP IIb/IIIa receptor antagonists." In Drug Therapy in Cardiology. CRC Press, 2001. http://dx.doi.org/10.3109/9780203213476-35.

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Abrams, Charles, and Sanford J. Shattil. "The Platelet Integrin, GP IIb-IIIa (αIIbß3)." In The Platelet. Elsevier, 1997. http://dx.doi.org/10.1016/s1569-2558(08)60411-7.

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Lockie, Tim, and Simon Redwood. "Current status of GP IIb/IIIa inhibitors." In Oxford Textbook of Interventional Cardiology. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199569083.003.023.

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The process of atheromatous plaque rupture is thought to underlie most acute coronary syndromes (ACS) and thus is a major cause of overall morbidity and mortality. As a result, the costs in terms of healthcare expenditure of the consequences of acute plaque rupture are considerable. The immediate and often catastrophic result of plaque rupture is intracoronary thrombosis resulting in vessel occlusion and myocardial infarction (MI). Over the last 20 years there has been a steady decline in the mortality rates from ACS that has resulted from the successful implementation of therapies to attenuat
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Lockie, Tim. "Current status of glycoprotein IIb/IIIa inhibitors." In Oxford Textbook of Interventional Cardiology, edited by Simon Redwood, Nick Curzen, and Adrian Banning. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780198754152.003.0025.

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Atheromatous plaque rupture is the crucial event that underlies most acute coronary syndromes (ACS). The immediate and often catastrophic result of plaque rupture is intracoronary thrombosis resulting in vessel occlusion and myocardial infarction. Over the past 30 years there has been a steady decline in the mortality rates from ACS. This has resulted from the successful implementation of therapies to attenuate the effects of plaque rupture that include antiplatelet drugs, fibrinolysis, percutaneous coronary intervention (PCI), antithrombotic therapy, and plaque stabilization. Glycoprotein (GP
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Conference papers on the topic "IIIa (GP IIb/IIIa) complex"

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Phillips, David R., Laurence A. Fitzgerald, Leslie V. Parise, and Israel F. Charo. "The Platelet Membrane Glycoprotein IIb-III a Complex: Member of a Superfamily of Adhesive Protein Receptors." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643727.

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The glycoprotein (GP) IIb-IIIa complex isthe receptor for fibrinogen,fibronectin and von Willebrand factor on the surface of activated platelets that mediates platelet aggregation.The GP IIb-IIIa complex contains two subunits; an a subunit, GP IIb, and a smaller 8 subunit, GP IIIa. To identify the subunits of GP IIb-IIIa responsible for fibrinogen binding, we examined the ability of purified subunitsto bind to immobilized fibrinogen. Both the GP IIb and the GP III a subunits have fibrinogen binding activity, suggesting that fibrinogen binds to multiple sites onthe GP I Ib-IIIa complex.A GP Ilb
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Steiner, B., and D. R. Phillips. "CA2+-INDUCED STRUCTURAL TRANSITIONS OF THE PLATELET GP IIb-IIIa COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643956.

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Previous studies have shown that the membrane glycoprotein (GP) IIb-IIIa complex can be reversibly dissociated by incubating platelets for 5 min at 37°C in an EDTA-containing buffer. Prolonged incubations (30 min) with EDTA, however, result in the formation of high molecular weight aggregates of GP IIb and GP IIIa. These aggregates of individual GP's neither bind fibrinogen nor support platelet aggregation, indicating that chelation of Ca2+ can affect the functional activity of GP IIb-IIIa. The present study was designed to identify conditions for the generation of functionally active GP IIb a
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Tanoue, K., and H. Yamazaki. "DIFFERENT INTEGRITIES OF GP Ilb/Ilia COMPLEX ARE REQUIRED FOR ADP- OR THROMBIN-INDUCED AGGREGATIONS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644882.

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A relation between the integrity of platelet GP IIb/IIIa complex and aggregability by ADP or thrombin was studied on intact platelets with EDTA-induced irreversibly dissociated GP IIb/IIIa complex. Human platelets were washed once and suspended in Ca-, Mg-free HEPES-Tyrode's solution (pH 7d). Aliquots of the suspensions were incubated with 2mM EDTA at 37°C for 2 to 60 min. Control platelets were incubated at 22°C. Then, kwM CaCl2 were added to the samples, which were incubated for another 30 min at 37°C. The platelets were washed twice with HEPES-Tyrode1s solution (pH 6.7). For the measurement
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Parise, L. V., B. Steiner, L. Nannizzi, and D. A. Phillips. "PEPTIDES FROM FIBRINOGENAND FIBRONECTIN CHANGE THE CONFORMATIONOF PURIFIED PLATELET GLYCOPROTEIN IIb-IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643697.

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Specific amino acid sequences in fibrinogen and fibronectin appear to mediate the binding of these ligands to the glycoprotein (GP) IIb-IIIacomplex in platelets. Thesesequences include LGGAKQAGDV from the y chain of fibrinogen, and RGD(S) from the a chain of fibrinogenand the cell-binding domain of fibronectin. Several recent reports suggest thatfibrinogen and/or peptides with these sequences cause clustering of GPIIb-IIIa on the platelet surface and Na+/H+ exchange in epinephrine-stimulated platelets. Thus, it is possible that occupancy of specific sites on GP Ilb-IIIa affects its conformatio
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Giltay, J. C., O. C. Leeksma, C. Breederveld, and J. A. van Mourik. "NORMAL SYNTHESIS AND EXPRESSION OF ENDOTHELIAL GP IIb/IIIa IN GLANZMANN'S THROMBASTENIA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642817.

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In Glanzmann’s thrombastenia (GT), an autosomal recessive inherited hemorrhagic disease, the platelet membrane glycoprotein (GP) IIb/IIIa complex is absent or reduced. Recently we and others demonstrated that cultured human umbilical vein endothelial cells synthesize a membrane protein complex that is structurally closely related to GP IIb/IIIa. Endothelial cells of thrombasthénie patients could, therefore be deficient in GP IIb/IIIa. We had the opportunity to culture endothelial cells isolated from the umbilical cord of a newborn with GT and to examine the plasma membrane composition of these
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Charo, I. F., L. A. Fitzgerald, D. Meyer, L. S. Bekeart, and D. R. Phillips. "PLATELET GLYCOPROTEIN IIb-IIIa-LIKE PROTEINS MEDIATE ENDOTHELIAL CELL ATTACHMENT TO ADHESIVE MATRIX PROTEINS AND ARE UP-REGULATED BY PHORBOL ESTERS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642816.

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Human endothelial cells (EC) express glycoproteins that are similar to the platelet glycoprotein IIb-IIIa complex (GP IIb-IIIa), the platelet receptor for adhesive proteins. Although GP IIb—IIIa is abundant in both platelets and EC, its only known function is to mediate platelet aggregation. The present study tests the hypotheses that EC attachment to adhesive proteins in the extracellular matrix is mediated by the GP IIb-IIIa-1ike proteins. Endothelial cells attached well to glass slides that were previously coated with adhesive proteins, but not albumin. To determine whether GP IIb-IIIa was
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Pidard, D., A. Fischer, C. Bouillot, F. Ledeist, and A. T. Nurden. "INHERITED DEFICIENCIESCAN AFFECT SEPARATELY THE PLATELET MEMBRANE GLYCOPROTEIN Ilb-IIIa COMPLEX AND THE LEUKOCYTE LFA-1, Mac-1 and pl50,95 COMPLEXES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643704.

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The human platelet membrane glycoprotein (GP) IIb-IIIa complex and a family of functional leukocyte cell membrane antigens, LFA-1 (L), Mac-1 (M) andpl50,95 (X), possess knownstructural analogies. Similaritiesinclude a heterodimeric structure with a high mol. wt. αsubunit (Mr∽ 145-180 kDa) , associated nonconvalently with a lower mol. wt.β-subunit (Mr ∽ 90-95 kDa),anda partial amino acid sequence hommology between GP lib and αL or CKM. Furthermore, GP lib, α L and αM were reported to be co-expressed in murine cells transfected with a 20 kilobase human DNA fragment.To address the question of a p
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Thorsen, L. I., B. Hessel, F. Brosstad, G. Gogstad та N. O. Solum. "THE N-DSK γ-CHAIN BINDS TO IMMUNOPRECIPITATED GP IIBIIIa". У XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643774.

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We have previously demonstrated binding of the CNBr-split N-terminal disulphide knot of the fibrinogen molecule (N-DSK) to blood platelets and to their immunoprecipitated fibrinogen receptor, the glycoprotein IIb-IIIa complex. To further investigate which part of the N-DSK molecule that is responsible for its binding to GP IIb-IIIa, this fragment was split into its separate Aα (1-51), Bβ (1-118) and γ- (1-78) chains and carboxymethylated. GP IIb-IIIa was immunoprecipitated by crossed immunoelectrophoresis (CIE) of Triton X-100 extracts of platelets against rabbit antibodies to whole platelet p
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Lewis, J. C., R. R. Hantgan, N. Kieffer, A. Nurden, and J. Breton-Gorius. "DISTRIBUTION OF GLYCOPROTEINS (GP) lib AND Ilia AND THEIR COMPLEX ON ADHERENT/ACTIVATED PLATELETS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643707.

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Redistribution of GP Ilbllla has recentlybeen demonstrated for platelets activatedin suspension in the presence of either fibrinogen or specific monoclonal antibodies, and it has been suggested that redistribution is important for normal platelet function. Reported here is the distribution of GPIIb an GPIIIa following adhesion, and event focal to the hemostatic process. Human platelets isolated by centrifugation from heparinized blood and washed in Hank’s Salts, pH 6.5 with and without EDTA (3%) were activated by adhesion to carbon-stabilized formvar grids. Subsequent to activation/adhesion, G
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Andreas, Ruf, Eberhard Morgenstern, Heinrich Patscheke, Sentot Santoso, Christian Müller-Eckhardt, and Norbert Heimburger. "THE ROLE OF THE GP IIb/IIIa COMPLEX AND vWF IN PLATELET -COLLAGEN INTERACTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643518.

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Our recent studies showed that collagen fibrils (CF) are internalized by platelets in citrated plasm. This phenomenon was not observed in EDTA-PRP. In order to investigate whether collagen internalization is mediated by a receptor we studied the effect of monoclonal antibodies against the receptor molecules GP IIb/IIIa (Gi5) and GP Ib (AN51, Da-kopatts GmbH, Hamburg). Washed human platelets from healthy donors were incubated with lOμg of Gi5 or 4μg of AN51 per ml of platelet suspension (2 × 108 platelets per ml). After 10 min. at 37° C we added AOpg collagen (Hormonchemie, München) per ml of p
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