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

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

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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

1

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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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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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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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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7

Levene, RB, and EM Rabellino. "Platelet glycoproteins IIb and IIIa associated with blood monocytes are derived from platelets." Blood 67, no. 1 (1986): 207–13. http://dx.doi.org/10.1182/blood.v67.1.207.207.

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Abstract Platelet glycoprotein IIb/IIIa (GP IIb/IIIa), the receptor complex for fibrinogen, has been regarded as a megakaryocyte/platelet lineage- restricted antigen. Recently, however, it has been reported that GP IIb/IIIa is expressed in blood monocytes. Studies were performed to establish the origin and immunological characteristics of monocyte- associated glycoproteins IIb and IIIa (GPs IIb and IIIa). Preparations of blood monocytes containing varying platelet-monocyte ratios were metabolically labeled with [35S]methionine with the expectation that any newly synthesized GPs IIb and IIIa wo

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Levene, RB, and EM Rabellino. "Platelet glycoproteins IIb and IIIa associated with blood monocytes are derived from platelets." Blood 67, no. 1 (1986): 207–13. http://dx.doi.org/10.1182/blood.v67.1.207.bloodjournal671207.

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Platelet glycoprotein IIb/IIIa (GP IIb/IIIa), the receptor complex for fibrinogen, has been regarded as a megakaryocyte/platelet lineage- restricted antigen. Recently, however, it has been reported that GP IIb/IIIa is expressed in blood monocytes. Studies were performed to establish the origin and immunological characteristics of monocyte- associated glycoproteins IIb and IIIa (GPs IIb and IIIa). Preparations of blood monocytes containing varying platelet-monocyte ratios were metabolically labeled with [35S]methionine with the expectation that any newly synthesized GPs IIb and IIIa would be mo

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Parise, LV, AB Criss, L. Nannizzi, and MR Wardell. "Glycoprotein IIIa is phosphorylated in intact human platelets." Blood 75, no. 12 (1990): 2363–68. http://dx.doi.org/10.1182/blood.v75.12.2363.2363.

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Abstract The glycoprotein IIb-IIIa complex (GP IIb-IIIa) is a multifunctional transmembrane protein on platelets. Its most completely described function is as a fibrinogen receptor that mediates platelet aggregation, but it is also involved in clot retraction, signal transduction, calcium transport, and other events. However, the mechanisms that regulate the functions of GP IIb-IIIa during platelet activation are largely unknown. One possible mechanism is phosphorylation, since several other receptors are regulated by this process. We found that GP IIIa, but not GP IIb, was phosphorylated in 3

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Parise, LV, AB Criss, L. Nannizzi, and MR Wardell. "Glycoprotein IIIa is phosphorylated in intact human platelets." Blood 75, no. 12 (1990): 2363–68. http://dx.doi.org/10.1182/blood.v75.12.2363.bloodjournal75122363.

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The glycoprotein IIb-IIIa complex (GP IIb-IIIa) is a multifunctional transmembrane protein on platelets. Its most completely described function is as a fibrinogen receptor that mediates platelet aggregation, but it is also involved in clot retraction, signal transduction, calcium transport, and other events. However, the mechanisms that regulate the functions of GP IIb-IIIa during platelet activation are largely unknown. One possible mechanism is phosphorylation, since several other receptors are regulated by this process. We found that GP IIIa, but not GP IIb, was phosphorylated in 32P-labele

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

1

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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4

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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5

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

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6

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

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7

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 "Glycoprotein IIb/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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3

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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4

"The Platelet Glycoprotein IIb-IIIa Complex." In Platelets, Thrombosis and the Vessel Wall. CRC Press, 2003. http://dx.doi.org/10.1201/9781482283433-12.

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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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Becker, Richard C., and Frederick A. Spencer. "Platelet Glycoprotein IIb/IIIa Receptor Antagonists." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0014.

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The glycoprotein (GP) IIb/IIIa (αIIb/β3) receptor totalling 50,000 to 70,000 copies per platelet represents a common pathway for platelet aggregation in response to a wide variety of biochemical and mechanical stimuli. Accordingly, it represents an attractive target for pharmacologic inhibition that can be applied to patients with acute coronary syndromes. The evolution of GPIIb/IIIa receptor antagonists began with murine monoclonal antibodies and subsequently expanded to include small peptide or nonpeptide molecules with structural similarities to fibrinogen. There are three intravenous GPIIb

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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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Massberg, Steffen, Julinda Mehilli, and Adnan Kastrati. "The role of bivalirudin in percutaneous coronary intervention." In Oxford Textbook of Interventional Cardiology. Oxford University Press, 2010. http://dx.doi.org/10.1093/med/9780199569083.003.025.

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Rapid progress has been made in interventional cardiology over the past years, and many patients with coronary artery disease, even those with complex lesions, are nowadays being treated with percutaneous coronary interventions (PCI). As a result, a major focus of current cardiovascular research is on reducing negative peri-procedural clinical events associated with PCI, particularly in high-risk patients. Among the most dangerous peri-procedural events are thrombotic complications, leading to recurrent myocardial or cerebral ischaemia, often with fatal outcome. Anticoagulant and antithromboti

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Becker, Richard C., and Frederick A. Spencer. "Clopidogrel." In Fibrinolytic and Antithrombotic Therapy. Oxford University Press, 2006. http://dx.doi.org/10.1093/oso/9780195155648.003.0013.

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Clopidogrel, a thienopyridine derivative, is a novel platelet antagonist that is several times more potent than ticlopidine but associated with fewer adverse effects. After repeated 75-mg oral doses of clopidogrel, plasma concentrations of the parent compound, which has no platelet-inhibiting effect, are very low. Clopidogrel is extensively metabolized in the liver. The main circulating metabolite is a carboxylic acid derivative with a plasma elimination half-life of 7.7 ± 2.3 hours. Approximately 50% of an oral dose is excreted in the urine and the remaining 50% in feces over the following 5

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Phillips, David R., and Lisa Nannizzi-Alaimo. "Platelet membrane glycoprotein (GP) IIb–IIIa antagonists and acute arterial thrombosis." In Platelets in Thrombotic and Non-Thrombotic Disorders. Cambridge University Press, 2002. http://dx.doi.org/10.1017/cbo9780511545283.064.

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Conference papers on the topic "Glycoprotein IIb/IIIa (GP IIb/IIIa) complex"

1

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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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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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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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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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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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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De Marco, L., M. Mazzucato, M. G. Del Ben, et al. "THE PLATELET AGGREGATING PROPERTIES OF TYPE IIB VON WILLEBRAND FACTOR (vWF): THE ROLE OF PLATELET ACTIVATION, FIBRINOGEN AND TWO DISTINCT MEMBRANE RECEPTORS." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644643.

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Three preparations of purified von Willebrand factor (vWF), obtained from unrelated patients affected by type IIB von Willebrand disease, were found to have normal sialic acid content (between 129-190 nmoles/mg of vWF, as compared to 158 ± 17 nmoles/mg in four normal preparations) and to induce platelet aggregation in the presence of physiologic levels of divalent cations and without addition of ristocetin. A monoclonal antibody that blocks the vWF binding domain of the platelet glycoprotein (GP) Ib caused complete inhibition of IIB vWF-induced aggregation. On the contrary, a monoclonal antibo

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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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Kiefel, V., S. Santoso, and C. Mueller-Eckhardt. "ANALYSIS OF PLATELET REACTIVE ANTIBODIES USING MONOCLONAL ANTIBODIES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643929.

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The characterization of platelet reactive alloantibodies and autoantibodies is mandatory for the diagnosis of posttransfusion purpura, neonatal alloimmune thrombocytopenia, autoimmune thrombocytopenia and for the selection of platelet donors prior to platelet transfusions in immunized polytransfused patients. The platelet immunofluorescence test is suitable for the detection of platelet reactive antibodies. In many cases, however, mixtures containing different platelet reactive antibodies have to be dissected.In order to analyze these sera, we have developed a novel enzyme immunoassay based up

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