Relevant bibliographies by topics / Membrane cofactor protein; Glycoproteins

Contents

  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers

Academic literature on the topic 'Membrane cofactor protein; Glycoproteins'

Author: Grafiati
Published: 4 June 2021
Last updated: 12 February 2022

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Journal articles on the topic "Membrane cofactor protein; Glycoproteins"

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Herbert, A., J. O'Leary, M. Krych-Goldberg, J. P. Atkinson, and P. N. Barlow. "Three-dimensional structure and flexibility of proteins of the RCA family — a progress report." Biochemical Society Transactions 30, no. 6 (2002): 990–96. http://dx.doi.org/10.1042/bst0300990.

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Members of the regulator of complement activation (RCA) protein family perform a vital role in health and disease. In this report we describe our efforts to solve the structures of human membrane cofactor protein (CD46), the vaccinia virus complement control protein, which mimics mammalian RCA proteins, and human complement receptor type 1 (CD35). These examples illustrate that, despite good progress over the last decade, the regulators of complement, as extracellular multiple domain glycoproteins, still pose formidable problems to structural biologists. Many important questions remain unanswe
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Wu, Eugene, Sunia A. Trauger, Lars Pache, et al. "Membrane Cofactor Protein Is a Receptor for Adenoviruses Associated with Epidemic Keratoconjunctivitis." Journal of Virology 78, no. 8 (2004): 3897–905. http://dx.doi.org/10.1128/jvi.78.8.3897-3905.2004.

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ABSTRACT Subgroup D adenovirus (Ad) types 8, 19, and 37 (Ad8, -19, and -37, respectively) are causative agents of epidemic keratoconjunctivitis and genital tract infections. Previous studies showed that Ad37 binds to a 50-kDa membrane glycoprotein expressed on human ocular (conjunctival) cells. To identify and characterize the role of the 50-kDa glycoprotein in Ad37 infection, we partially purified this molecule from solubilized Chang C conjunctival cell membranes by using lentil lectin chromatography and preparative sodium dodecyl sulfate-polyacrylamide gel electrophoresis. Liquid chromatogra
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Seya, T., J. R. Turner, and J. P. Atkinson. "Purification and characterization of a membrane protein (gp45-70) that is a cofactor for cleavage of C3b and C4b." Journal of Experimental Medicine 163, no. 4 (1986): 837–55. http://dx.doi.org/10.1084/jem.163.4.837.

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Based on preliminary evidence indicating that a cell-associated protein of U937 (a human monocyte-like cell line) possessed cofactor activity and was not the C3b/C4b receptor, we sought to further characterize this protein. A sequential four-column purification procedure was devised that includes C3(H2O) affinity chromatography to isolate in reasonable yields and purity a cell-associated protein of U937 and several other human cell lines. Based on its pattern and Mr on SDS-PAGE, acidic pI, and ligand specificity, it is identical to a recently described C3(H2O) or C3b-binding membrane glycoprot
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Kraus, Damian, M. Edward Medof, and Carolyn Mold. "Complementary Recognition of Alternative Pathway Activators by Decay-Accelerating Factor and Factor H." Infection and Immunity 66, no. 2 (1998): 399–405. http://dx.doi.org/10.1128/iai.66.2.399-405.1998.

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ABSTRACT The alternative complement pathway (ACP) functions as a surveillance mechanism by which microorganisms are opsonized with C3b in the absence of specific antibodies. The effectiveness of the ACP relies on its ability to distinguish self from non-self. This recognition function is mediated by C3 regulatory proteins including serum factor H, membrane cofactor protein (MCP), and membrane decay-accelerating factor (DAF). H activity against bound C3b can be increased by host components such as sialic acid and decreased by microbial polysaccharides. DAF and MCP may also recognize cell surfac
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Pfueller, Sharron L., Margaret A. Howard, James G. White, Chandrasekhara Menon, and Elizabeth W. Berry. "Shortening of Bleeding Time by 1-Deamino-8-Arginine Vasopressin (DDAVP) in the Absence of Platelet von Willebrand Factor in Gray Platelet Syndrome." Thrombosis and Haemostasis 58, no. 04 (1987): 1060–63. http://dx.doi.org/10.1055/s-0038-1646056.

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SummaryThe Gray platelet syndrome is a rare disorder characterised by the absence of platelet a-granules and their contents. We describe a new patient and the effects of infusions of l-deainino-8-aiginine vasopressin (DDAVP). The patient had a prolonged skin bleeding time and his platelets had reduced numbers of a-granules, increased vacuolation and reduced retention on glass beads. Flatelet von Willebrand factor antigen (vWf:Ag) was undetectable and levels of platelet fibrinogen, p-thioniboglobulin, platelet factor 4 and thrombospondin were reduced. All tests of plasma coagulation factors wer
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Zhou, Quansheng, Peter J. Sims, and Therese Wiedmer. "Expression of Proteins Controlling Transbilayer Movement of Plasma Membrane Phospholipids in the B Lymphocytes From a Patient With Scott Syndrome." Blood 92, no. 5 (1998): 1707–12. http://dx.doi.org/10.1182/blood.v92.5.1707.417k15_1707_1712.

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Scott syndrome is a rare inherited bleeding disorder in which platelets and other blood cells fail to promote normal assembly of the membrane-stabilized proteases of the plasma coagulation system. The defect in Scott blood cells is known to reflect inability to mobilize phosphatidylserine from inner plasma membrane leaflet to the cell surface in response to an elevation of Ca2+ at the endofacial surface. To gain insight into the molecular basis of this membrane defect, we examined the expression in Scott cells of plasma membrane proteins that have been implicated to participate in the accelera
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Bora, N. S., D. M. Lublin, B. V. Kumar, R. D. Hockett, V. M. Holers, and J. P. Atkinson. "Structural gene for human membrane cofactor protein (MCP) of complement maps to within 100 kb of the 3' end of the C3b/C4b receptor gene." Journal of Experimental Medicine 169, no. 2 (1989): 597–602. http://dx.doi.org/10.1084/jem.169.2.597.

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The structural gene for membrane cofactor protein (MCP), a widely distributed C3b/C4b binding regulatory glycoprotein of the complement system, has been mapped to the same locus as the structural genes for CR1, CR2, DAF, and C4bp. The order of the genes within an approximately 800-kb DNA fragment on the long arm of chromosome 1 is MCP-CR1-CR2-DAF-C4bp. Further, the MCP gene maps to within 100 kb of 3' end of the CR1 gene.
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Wijnen, Merel van, Jeanette G. Stam, Cornells van't Veer, et al. "The Interaction of Protein S with the Phospholipid Surface Is Essential for the Activated Protein C-independent Activity of Protein S." Thrombosis and Haemostasis 76, no. 03 (1996): 397–403. http://dx.doi.org/10.1055/s-0038-1650590.

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SummaryProtein S is a vitamin-K dependent glycoprotein involved in the regulation of the anticoagulant activity of activated protein C (APC). Recent data showed a direct anticoagulant role of protein S independent of APC, as demonstrated by the inhibition of prothrombinase and tenase activity both in plasma and in purified systems. This anticoagulant effect of protein S can be explained either by a direct interaction of protein S with one of the components of the complexes and/or by the interference with the binding of these components to phospholipid surfaces.During our investigation we noted
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Zhou, Quansheng, Peter J. Sims, and Therese Wiedmer. "Expression of Proteins Controlling Transbilayer Movement of Plasma Membrane Phospholipids in the B Lymphocytes From a Patient With Scott Syndrome." Blood 92, no. 5 (1998): 1707–12. http://dx.doi.org/10.1182/blood.v92.5.1707.

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Abstract Scott syndrome is a rare inherited bleeding disorder in which platelets and other blood cells fail to promote normal assembly of the membrane-stabilized proteases of the plasma coagulation system. The defect in Scott blood cells is known to reflect inability to mobilize phosphatidylserine from inner plasma membrane leaflet to the cell surface in response to an elevation of Ca2+ at the endofacial surface. To gain insight into the molecular basis of this membrane defect, we examined the expression in Scott cells of plasma membrane proteins that have been implicated to participate in the
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Post, T. W., M. K. Liszewski, E. M. Adams, I. Tedja, E. A. Miller, and J. P. Atkinson. "Membrane cofactor protein of the complement system: alternative splicing of serine/threonine/proline-rich exons and cytoplasmic tails produces multiple isoforms that correlate with protein phenotype." Journal of Experimental Medicine 174, no. 1 (1991): 93–102. http://dx.doi.org/10.1084/jem.174.1.93.

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Membrane cofactor protein (MCP) is a complement regulatory protein that is expressed on human cells and cell lines as two relatively broad species with Mr of 58,000-68,000 and 48,000-56,000. The structure of a previously reported cDNA clone indicated that MCP was a type 1 membrane glycoprotein and a member of the regulators of complement activation gene/protein cluster. However, it did not provide an explanation for the unusual phenotypic pattern of MCP. Therefore, in parallel with an analysis of the gene, additional cDNAs were cloned and characterized. Six different MCP cDNA classes were iden
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Dissertations / Theses on the topic "Membrane cofactor protein; Glycoproteins"

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Pollard, Alison Jane. "Characterisation of CD46 isoforms in human peripheral blood cells : localisation of complement regulatory proteins throughout the male reproductive tract." Thesis, University of Liverpool, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.365911.

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Richards, Anna. "Genetic factors predisposing to the haemolytic uraemic syndrome." Thesis, University of Newcastle Upon Tyne, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.289212.

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Simpson, Karen Lesley. "Expression of complement regulatory proteins in human development and reproduction." Thesis, University of Bristol, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.294904.

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Turner, C. E. "Capping of the major rat thymocyte glycoproteins : Their interactions with other membrane proteins and the cytoskeleton." Thesis, University of Oxford, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.376955.

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Crombie, Andrea Rene. "Lysosomal integral membrane protein II, a member of the CD36 gene family : comparative analysis of structure-function relationships /." Access full-text from WCMC, 1998. http://proquest.umi.com/pqdweb?did=733079741&sid=9&Fmt=2&clientId=8424&RQT=309&VName=PQD.

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Holmlund, Camilla. "Identification and investigations of leucine-rich repeats and immunoglobulin-like domains protein 2 (LRIG2)." Doctoral thesis, Umeå : Department of Radiation Sciences, Oncology, Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-33784.

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Alvares, Stacy M. "The role of membrane microdomains in the phosphorylation of the epithelial transmembrane protein, GP140/CDCP1 /." Thesis, Connect to this title online; UW restricted, 2007. http://hdl.handle.net/1773/5022.

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Oran, Alp E. "Defining sites of interaction in the Ã-chain of C3 for factor H, membrane cofactor protein (MCP), and complement receptor 1 (CR1)." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ29260.pdf.

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Chang, Eddie. "The role of perforin and chemokines in the pathogenesis of chronic corneal inflammation induced by herpes simplex virus type-1 infection." free to MU Campus, others may purchase, 2003. http://wwwlib.umi.com/cr/mo/fullcit?p3091911.

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Wilson, Cheryl Anne. "The Membrane Integration of the Hemagglutinin-Neuraminidase Glycoprotein of Newcastle Disease Virus: A Thesis." eScholarship@UMMS, 1989. http://escholarship.umassmed.edu/gsbs_diss/295.

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The hemagglutinin-neuraminidase (HN) molecule of Newcastle disease virus (NDV) is an integral membrane glycoprotein that is oriented with its N-terminus in the cytoplasm and its C-terminus external to the infected cell. Single spanning membrane proteins with this type of topology (N-terminus in, C-terminus out) have been classified as Type II glycoproteins, in contrast to the more common Type I glycoproteins, which are oriented in the opposite direction. (C-terminus in, N-terminus out). The membrane integration of HN protein was investigated using a wheat germ translation system to synthesize
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Books on the topic "Membrane cofactor protein; Glycoproteins"

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Oran, Alp Eren. Definging sites of interaction in the A-chain of C3 for factor H, membrane cofactor protein (MCP), and complement receptor 1 (CR1). National Library of Canada, 1997.

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Alexander, D. J., N. Phin, and M. Zuckerman. Influenza. Edited by I. H. Brown. Oxford University Press, 2011. http://dx.doi.org/10.1093/med/9780198570028.003.0037.

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Influenza is a highly infectious, acute illness which has affected humans and animals since ancient times. Influenza viruses form the Orthomyxoviridae family and are grouped into types A, B, and C on the basis of the antigenic nature of the internal nucleocapsid or the matrix protein. Infl uenza A viruses infect a large variety of animal species, including humans, pigs, horses, sea mammals, and birds, occasionally producing devastating pandemics in humans, such as in 1918 when it has been estimated that between 50–100 million deaths occurred worldwide.There are two important viral surface glyc
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E, Vance Dennis, and Vance Jean E, eds. Biochemistry of lipids, lipoproteins, and membranes. Elsevier, 1991.

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Book chapters on the topic "Membrane cofactor protein; Glycoproteins"

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Liszewski, M. K., and J. P. Atkinson. "Membrane Cofactor Protein." In Membrane Defenses Against Attack by Complement and Perforins. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77014-2_4.

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Lublin, D. M., and J. P. Atkinson. "Decay-Accelerating Factor and Membrane Cofactor Protein." In Current Topics in Microbiology and Immunology. Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-74977-3_7.

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White, D. J. G., T. Oglesby, M. K. Liszewski, et al. "Expression of human decay accelerating factor or membrane cofactor protein genes on mouse cells inhibits lysis by human complement." In Transplant International Official Journal of the European Society for Organ Transplantation. Springer Berlin Heidelberg, 1992. http://dx.doi.org/10.1007/978-3-642-77423-2_190.

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Liszewski, M. Kathryn, and John P. Atkinson. "Membrane Cofactor Protein." In The Complement FactsBook. Elsevier, 2018. http://dx.doi.org/10.1016/b978-0-12-810420-0.00026-2.

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Liszewski, M. Kathryn, and John P. Atkinson. "Membrane cofactor protein." In The Complement FactsBook. Elsevier, 2000. http://dx.doi.org/10.1016/b978-012733360-1/50027-0.

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Mohammed Ali Jassim, Marwa, Majid Mohammed Mahmood, and Murtada Hafedh Hussein. "Human Herpetic Viruses and Immune Profiles." In Innate Immunity in Health and Disease. IntechOpen, 2021. http://dx.doi.org/10.5772/intechopen.96340.

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Herpesviruses are large, spherical, enveloped viral particles with linear double-stranded DNA genome. Herpesvirus virion consists of an icosahedral capsid containing viral DNA, surrounded by a protein layer called tegument, and enclosed by an envelope consisting of a lipid bilayer with various glycoproteins. Herpesviruses persist lifelong in their hosts after primary infection by establishing a latent infection interrupted recurrently by reactivations. The Herpesviridae family is divided into three subfamilies; α-herpesviruses, β-herpesviruses, and γ-herpesviruses based on the genome organization, sequence homology, and biological properties. There are eight human herpes viruses: Herpes simplex virus type 1 and 2 (HSV-1, −2) andVaricella-zoster virus (VZV), which belong to the α-herpesvirus subfamily; Human cytomegalovirus (HCMV), and Human herpesvirus type 6 and 7 (HHV-6,HHV-7), which belong to the β-herpesvirus subfamily; and Epstein–Barr virus (EBV) and Kaposi’s sarcoma-associated herpesvirus (KSHV) or Human herpesvirus 8 (HHV-8), which belong to the γ-herpesvirus subfamily. Within this chapter, we summarize the current knowledge about EBV and CMV, regarding their genome organization, structural characteristics, mehanisms of latency, types of infections, mechanisms of immune escape and prevention. Epstein–Barr Virus (EBV) genome encodes over 100 proteins, of which only (30) proteins are well characterized, including the proteins expressed during latent infection and lytic cycle proteins. Based on major variation in the EBNA-2 gene sequence, two types of EBV are recognized, EBV type 1 and 2. Epstein–Barr virus types occur worldwide and differ in their geographic distribution depending on the type of virus. EBV spreads most commonly through bodily fluids, especially saliva. However, EBV can also spread through blood, blood transfusions, and organ transplantations. The EBV is associated with many malignant diseases such as lymphomas, carcinomas, and also more benign such as infectious mononucleosis, chronic active infection. The EBV has also been suggested as a trigger/cofactor for some autoimmune diseases. Overall, 1–1.5% of the cancer burden worldwide is estimated to be attributable to EBV The latently infected human cancer cells express the most powerful monogenic proteins, LMP-1 and LMP-2(Latent Membrane Protein-1,-2), as well as Epstein–Barr Nuclear Antigens (EBNA) and two small RNAs called Epstein–Barr Encoded Small RNAs (EBERs). The EBV can evade the immune system by its gene products that interfering with both innate and adaptive immunity, these include EBV-encoded proteins as well as small noncoding RNAs with immune-evasive properties. Currently no vaccine is available, although there are few candidates under evaluation. Human cytomegalovirus (HCMV) is a ubiquitous beta herpesvirus type 5 with seroprevalence ranges between 60 to 100% in developing countries. CMV is spread from one person to another, usually by direct and prolonged contact with bodily fluids, mainly saliva, but it can be transmitted by genital secretions, blood transfusion and organ transplantation. In addition, CMV can be transmitted vertically from mother to child. CMV infection can result in severe disease for babies, people who receive solid organ transplants or bone marrow/stem cell transplants and people with severe immune suppression such as advanced human immunodeficiency virus (HIV) infection. The HCMV has several mechanisms of immune system evasion. It interferes with the initiation of adaptive immune responses, as well as prevent CD8+ and CD4+ T cell recognition interfering with the normal cellular MHC Class I and MHC Class II processing and presentation pathways. Challenges in developing a vaccine include adeptness of CMV in evading the immune system. Though several vaccine candidates are under investigation.
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"MCP (membrane cofactor protein, CD46)." In Encyclopedia of Genetics, Genomics, Proteomics and Informatics. Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_10005.

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Liszewski, M. Kathryn, and John P. Atkinson. "CD46 (Membrane Cofactor Protein, MCP)." In Encyclopedia of Immunology. Elsevier, 1998. http://dx.doi.org/10.1006/rwei.1999.0130.

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HUNTER, ERIC. "Membrane Insertion and Transport of Viral Glycoproteins: A Mutational Analysis." In Protein Transfer and Organelle Biogenesis. Elsevier, 1988. http://dx.doi.org/10.1016/b978-0-12-203460-2.50007-x.

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Parmelee, David C., Timothy Benjamin, Chien-Hua Niu, and Snorri S. Thorgeirsson. "DIRECT SEQUENCE ANALYSIS OF RAT LIVER MEMBRANE GLYCOPROTEINS SEPARATED BY 2D-PAGE." In Techniques in Protein Chemistry. Elsevier, 1989. http://dx.doi.org/10.1016/b978-0-12-682001-0.50011-7.

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Conference papers on the topic "Membrane cofactor protein; Glycoproteins"

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Aihara, M., S. Morimoto, Y. Sawada, A. Kimura, Y. Chiba, and Y. Yoshida. "A ROLE OF PLATELET MEMBRANE COMPONENTS IN THE INTERACTION OF PLATELET-COLLAGEN-VON WILLEBRAND FACTOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644480.

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To determine a role of platelet membrane components on the interaction of platelet-collagen-von Willebrand factor(vWF), several experimental approaches were used. The adhesion of human fixed washed platelets(FWP) to collagen was decreased after the treatment with Serratia marcescens protease(100 ug/ml), but the collagen cofactor activity(COo) of vWF that enhances the adhesion of FWP to collagen was still present after the digestion. Although the platelet adhesion in the absence of normal plasma was not changed by the addition of monoclonal antibody(M-ab) against platelet membrane glycoprotein(
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Colman, R. W., A. Gewirtz, D. L. Wang, et al. "BIOSYNTHESIS AND EXPRESSION OF FACTOR V IN MAGAKARYOCYTES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1642955.

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Coagulation factor V (FV), is a single chain, multifunctional glycoprotein of Mr 350,000 which interacts with a variety of hemostatic proteins such as factor Xa, prothrombin, thrombin and protein C, on the surface of platelets and vascular endothelial cells. FV serves as both a cofactor and substrate in the generation of thrombin and plays a critical regulatory role in both physiologic hemostasis and pathologic thrombosis. The biosynthesis of FV and its subsequent expression are therefore expected to be precisely controlled and may differ in the three sites of synthesis - hepatocytes, endothel
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Bienz, D., T. Wager, and K. J. Clemetson. "ISOLATION AND CHARACTERIZATION OF HUMAN PLATELET MEMBRANE GLYCOPROTEINS Ia AND IIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643910.

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Glycoproteins (GP) Ia and IIa are relatively minor components of the platelet surface with similar molecular properties. Nieuwenhuis et al. (Nature 319, 470-72, 1985) described a patient whose platelets show no response to collagen. The correlating lack of GPIa in the platelets of this patient suggests this glycoprotein being the receptor for collagen. Santoro (Cell, 46, 913-20, 1986) described a 160 kDa glycoprotein that binds to collagen in the presence of MG2 + and is possibly identical with GPIa. The role of GPIIa is still unknown but a similar molecule has also been found on endothelial c
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Butler-Zimrin, A. E., J. S. Bennett, M. Poncz, et al. "ISOLATION AND CHARACTERIZATION OF cDNA CLONES FOR THE PLATELET MEMBRANE GLYCOPROTEINS IIb and IIIa." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643961.

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The platelet membrane GPIIb/GPIIIa complex on activated platelets contains receptors for fibrinogen, von Willebrand factor, and fibronectin. GPIIb and GPIlia also appear to be members of a family of membrane receptors involved in cell-cell and cell-matrix interactions. To study the structure of GPIIb and GPIIIa, we have constructed an expression library in the vector lambda gtll using mRNA from the HEL cell line and screened it with polyclonal antibody against each platelet protein. HEL cells constitutively express proteins similar to platelet GPIIb and GPIIIa. A 3.2kb GPIIb cDNA clone was ide
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Wilkinson, J. M., N. Hack, L. I. Thorsen, and J. A. Thomas. "MONOCLONAL ANTIBODIES RECOGNISING PROTEINS OF THE OUTER AND INNER SURFACE OF THE PLATELET PLASMA MEMBRANE." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644493.

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Platelet membrane preparations can be fractionated into two major subpopulations by free flow electrophoresis and these have been shown to correspond to the plasma membrane and the endoplasmic reticulum of the platelet. The plasma membrane fraction can be shown, by two-dimensional electrophoresis, to contain the major surface glycoproteins together with considerable amounts of actin and actin-associated proteins such as the 250 kDa actin-binding protein (filamin), P235 (talin), myosin, α-actinin and tropomyosin (Hack, N. … Crawford, N., Biochem. J. 222, 235 (1984). These cytoskeletal proteins
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Wicki, A. N., A. Walz, and K. J. Clemetson. "IDENTIFICATION OF GLYCOPROTEIN lb IN “IN VITRO” TRANSLATES FROM ISOLATED HUMAN PLATELET mRNA." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643628.

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Platelet membrane glycoproteins play a crucial role in platelet adhesion and activation. To understand how they function it is of great importance to know their amino acid sequences and structures. It is rather difficult to purify membrane glycoproteins in amounts that are sufficient to determine their amino acid sequences by protein sequencing techniques. The easier way seems to be molecular cloning of the genes for these proteins.Metabolically stable mRNA derived from nucleated megakaryocytes is known to be present in the anuclear human platelets. We have developed a purification method for
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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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Ruan, C., X. Du, H. Wan, X. Hu, X. Xi, and P. Li. "CHARACTERIZATION OF THE FIBRINOGEN BINDING SITES USING MONOCLONAL ANTIBODIES TO HOMAN PLATELET MEMBRANE GLYCOPROTEINS IIb/IIIa*." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643700.

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Two new murine monoclonal antibodies, SZ-21 and SZ-22, (both IgG1 subclass), were produced by the hybridoma technique using washed human platelets as the immunogen. Both SZ-21 and SZ-22 reanted specifically with normal platelets and megakaryocytes but not with Glanzmann's thrombasthenic platelets which lack the membrane glycoprotein(GP)IIb/IIIa complex. Platelets from 10 normal donors bound 64,500±20,300(x+SD) SZ-21 molecules/platelet with KD4.4±1.5nM and 61,000±19,900 SZ-22 molecules/platelet with KD18.8±6.7nM respectively.Affinity chromatography confirmedthat SZ-21 and SZ-22 reacted with the
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9

Zafar, Rasheeda, and Daniel A. Walz. "PURIFICATION AND PROPERTIES OF HUMAN PLATELET MEMBRANE GLYCOPROTEIN V (GP-V)." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643907.

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Platelet membrane glycoproteins function as specific ligand receptors or substrates for selected platelet agonists and antagonists. GP-V is the only such membrane glycoprotein known to be a thrombin substrate. We have purified GP-V to homogeneity in order to better characterize the nature and specificity of this thrombin proteolysis. GP-V was extracted from fresh human platelets and purified through a combination of gel filtration, hydroxylapatite, DEAE and mono S chromatographies. The resulting protein had a molecular mass of 80 kDa by both non-reduced and reduced SDS electrophoresis. Aminort
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10

Kalyan, N. K., S. G. Lee, W.-T. Hum, R. Hartzell, M. Levner, and P. P. Hung. "IN VITRO STUDIES ON THE BINDING OF TISSUE-TYPE PLASMINOGEN ACTIVATOR (t-PA) AND UROKINASE (u-PA) TO LIVER MEMBRANES." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643603.

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The plasminogen activators, t-PA and u-PA, are glycoproteins known to be involved in homeostasis of the blood clotting system, and thus are of potential clinical use in the treatment of thrombosis. Several in vivo studies have shown that both t-PA and u-PA are quickly removed from the blood circulation, predominantly by the liver. The mechanism by which the liver removes these proteins is not understood. To delineate this, we conducted in vitro studies of binding of PAs or their derivatives to isolated mouse liver membranes utilizing a functional assay developed in our laboratory. The assay co
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