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Relevant bibliographies by topics / Thy-1 glycoprotein

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Academic literature on the topic 'Thy-1 glycoprotein'

Author: Grafiati

Published: 4 June 2021

Last updated: 12 February 2022

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Journal articles on the topic "Thy-1 glycoprotein"

1

Perkins, Stephen J., Alan F. Williams, Thomas W. Rademacher, and Raymond A. Dwek. "The Thy-1 glycoprotein: a three-dimensional model." Trends in Biochemical Sciences 13, no. 8 (August 1988): 302–3. http://dx.doi.org/10.1016/0968-0004(88)90124-7.

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El Amir, A., S. El Deeb, A. F. Wahby, and R. El Ridi. "Isolation and characterization of lizard Thy-1 glycoprotein." Developmental & Comparative Immunology 10, no. 1 (December 1986): 115. http://dx.doi.org/10.1016/0145-305x(86)90087-x.

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Conzelmann, A., A. Spiazzi, and C. Bron. "Glycolipid anchors are attached to Thy-1 glycoprotein rapidly after translation." Biochemical Journal 246, no. 3 (September 15, 1987): 605–10. http://dx.doi.org/10.1042/bj2460605.

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The attachment of glycolipid anchors to the Thy-1 glycoprotein during biosynthesis was followed by the change of detergent-binding properties of biosynthetically labelled Thy-1 precursors upon phospholipase C treatment in the murine thymoma lines BW5147 and S1A. In S1A, 80% of the Thy-1 molecules were phospholipase-C-sensitive after a 2 min pulse with [35S]methionine, indicating that these molecules were already anchored via a glycolipid tail. In BW5147, 47% of the Thy-1 molecules had phospholipase-C-sensitive anchors attached after a 1.5 min labelling and, with longer pulses, this percentage rose to 76%. Tunicamycin did not block the addition of glycolipid anchors, and glycolipid attachment also occurred at 21 degrees C. The findings suggest that the attachment of glycolipid anchors occurs in the rough endoplasmic reticulum.

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French, P. W., and P. L. Jeffrey. "Partial characterization of chicken Thy-1 glycoprotein by monoclonal antibodies." Journal of Neuroscience Research 16, no. 3 (1986): 479–89. http://dx.doi.org/10.1002/jnr.490160304.

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Low, Martin G., and Paul W. Kincade. "Phosphatidylinositol is the membrane-anchoring domain of the Thy-1 glycoprotein." Nature 318, no. 6041 (November 1, 1985): 62–64. http://dx.doi.org/10.1038/318062a0.

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Williams, Alan F., and Albert G. D. Tse. "A glycophospholipid covalently attached to the C-terminus of the Thy-1 glycoprotein." Bioscience Reports 5, no. 10-11 (January 1, 1985): 999–1005. http://dx.doi.org/10.1007/bf01119912.

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The Thy-1 glycoprotein is a very abundant cell surface molecule of rat thymocytes and neuronal cells with the properties of a molecule that inserts into the lipid bilayer. The hydrophobicity is due to a glycophospholipid component covalently attached to the carboxy group of the C-terminal cysteine residue. The mature glycoprotein does not contain a stretch of hydrophobic amino acids that could traverse the membrane bilayer. These findings present a new mode of membrane attachment for a cell surface molecule that can mediate lymphokine release and cell division after cross-linking by antibodies.

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Dowsing, Bruce J., A. A. Gooley, P. Gunning, A. Cunningham, and P. L. Jeffrey. "Molecular cloning and primary structure of the avian Thy-1 glycoprotein." Molecular Brain Research 14, no. 3 (July 1992): 250–60. http://dx.doi.org/10.1016/0169-328x(92)90180-j.

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Turner, C. E., M. R. Newton, and D. M. Shotton. "Cytoskeletal involvement in the sequential capping of rat thymocyte surface glycoproteins." Journal of Cell Science 89, no. 3 (March 1, 1988): 309–19. http://dx.doi.org/10.1242/jcs.89.3.309.

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The independent capping of the three major rat thymocyte glycoproteins, the leucocyte-common (L-C) antigen, the leucocyte sialoglycoprotein (LSGP) and Thy-1, was investigated using specific monoclonal antibodies. The capping of each antigen did not require redistribution of the other major surface glycoproteins, and was accompanied by a partial co-capping of the cytoskeletal proteins fodrin and actin, but not of tubulin. A study of the ability of a cell that already possesses one glycoprotein cap to cap a second different glycoprotein showed that this was possible in all cases to varying degrees, the second cap always forming at the same position on the cell surface as the first. Colchicine failed to perturb this observed sequential capping polarity, indicating that microtubules did not direct this second capping event.

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Conzelmann, A., A. Spiazzi, C. Bron, and R. Hyman. "No glycolipid anchors are added to Thy-1 glycoprotein in Thy-1-negative mutant thymoma cells of four different complementation classes." Molecular and Cellular Biology 8, no. 2 (February 1988): 674–78. http://dx.doi.org/10.1128/mcb.8.2.674.

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Recent evidence shows that the mature Thy-1 surface glycoprotein lacks the C-terminal amino acids 113 to 143 predicted from the cDNA sequence and is anchored in the plasma membrane by a complex, phosphatidylinositol-containing glycolipid attached to the alpha-carboxyl group of amino acid 112. Here we studied the biosynthesis of Thy-1 in two previously described and two newly isolated Thy-1-deficient mutant cell lines. Somatic cell hybridization indicated that their mutations affected some processing step rather than the Thy-1 structural gene. The Thy-1 made by mutants of classes C, F, and H bound detergent but, in contrast to wild-type Thy-1, their detergent-binding moieties could not be removed by phospholipase C. In addition, tryptophan, which only occurs in position 124, was incorporated into Thy-1 of these mutants but not of wild-type cells. Last, the Thy-1 of wild-type but not mutant cells could be radiolabeled with [3H]palmitic acid. Together, these findings strongly suggest that mutants of classes C, F, and H accumulate a biosynthetic intermediate of Thy-1 which retains at least part of the hydrophobic C-terminal peptide. The Thy-1 of these mutants remained endoglycosidase H sensitive, suggesting that it accumulated in the rough endoplasmic reticulum or the Cis-Golgi. A different Thy-1 intermediate was found in a class B mutant cell line: the Thy-1 of this mutant was 2 kilodaltons smaller than the Thy-1 of other cell lines, did not bind detergent, and was rapidly secreted via a normal secretory pathway.

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Conzelmann, A., A. Spiazzi, C. Bron, and R. Hyman. "No glycolipid anchors are added to Thy-1 glycoprotein in Thy-1-negative mutant thymoma cells of four different complementation classes." Molecular and Cellular Biology 8, no. 2 (February 1988): 674–78. http://dx.doi.org/10.1128/mcb.8.2.674-678.1988.

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Recent evidence shows that the mature Thy-1 surface glycoprotein lacks the C-terminal amino acids 113 to 143 predicted from the cDNA sequence and is anchored in the plasma membrane by a complex, phosphatidylinositol-containing glycolipid attached to the alpha-carboxyl group of amino acid 112. Here we studied the biosynthesis of Thy-1 in two previously described and two newly isolated Thy-1-deficient mutant cell lines. Somatic cell hybridization indicated that their mutations affected some processing step rather than the Thy-1 structural gene. The Thy-1 made by mutants of classes C, F, and H bound detergent but, in contrast to wild-type Thy-1, their detergent-binding moieties could not be removed by phospholipase C. In addition, tryptophan, which only occurs in position 124, was incorporated into Thy-1 of these mutants but not of wild-type cells. Last, the Thy-1 of wild-type but not mutant cells could be radiolabeled with [3H]palmitic acid. Together, these findings strongly suggest that mutants of classes C, F, and H accumulate a biosynthetic intermediate of Thy-1 which retains at least part of the hydrophobic C-terminal peptide. The Thy-1 of these mutants remained endoglycosidase H sensitive, suggesting that it accumulated in the rough endoplasmic reticulum or the Cis-Golgi. A different Thy-1 intermediate was found in a class B mutant cell line: the Thy-1 of this mutant was 2 kilodaltons smaller than the Thy-1 of other cell lines, did not bind detergent, and was rapidly secreted via a normal secretory pathway.

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Dissertations / Theses on the topic "Thy-1 glycoprotein"

1

Li, Lei. "The regulation of stanniocalcin-1 gene expression in rat sertoli and leydig cells." HKBU Institutional Repository, 2006. http://repository.hkbu.edu.hk/etd_ra/784.

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Kemp, Pauline Anne. "The glycosylation of human alpha-1-antitrypsin expressed in transgenic mouse milk." Thesis, University of Kent, 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.298167.

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Edmonds, Judith Helen Clinical School St Vincent's Hospital Faculty of Medicine UNSW. "Functional characterisation of the HIV-1 glycoprotein-41 cytoplasmic tail." Publisher:University of New South Wales. Clinical School - St Vincent's Hospital, 2009. http://handle.unsw.edu.au/1959.4/44099.

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The unusually long Cytoplasmic tail (CT) of Human Immunodeficiency Virus Type-1 (HIV-1) glycoprotein-41 (gp41) is highly conserved and engineered large truncations often render the virus non-infectious in a cell-type dependent manner. While large CT truncations occur infrequently in natural isolates, little is known about the mechanisms involved in infectious virions harbouring a large CT truncation. This thesis characterises RFgp34, a replication competent laboratory HIV-1 isolate with an acquired 100 amino acid CT truncation, and how it diverged from wildtype RF. The CT truncation and two possible compensatory mutations in Matrix (E40K and F44I) were introduced into the HIV-1 isolate NL4-3. These mutants were tested for infectivity, syncytia formation and glycoprotein incorporation into virions, alternative co-receptor usage and sensitivity to the fusion inhibitor T-20. Compared with RFwt, RFgp34-infected cultures displayed delayed viral replication kinetics in all cell types. Similar sized (MT-4 cells, PBMC) or larger and more numerous syncytia (Hut78 cells) were detected in RFgp34-infected cultures. Similar (Hut78 cells) or decreased (MT-4 cells, PBMC) amounts of glycoprotein was incorporated into RFgp34 virions, compared with RFwt virions. The increased syncytia in RFgp34-infected Hut78 cultures and the reduced glycoprotein incorporation into RFgp34 virions from MT-4 cells and PBMCs may explain the delayed RFgp34 replication kinetics. The Matrix E40K and F44I mutations were not able to directly compensate for the CT truncation to restore infectivity in Hut78 and MT-4 cells, as secondary mutations or the reversion of the CT truncation to a full-length CT were observed. In PBMCs the Matrix mutations alone were able to partially restore infectivity, suggesting specific mutations may compensate for the CT truncation in different cell types. None of the viruses utilised alternative HIV-1 co-receptors, nor were more resistant to T-20 than wildtype HIV-1 suggesting that the CT does not directly play a role in these viral functions. This thesis suggests that the sequence of mutations acquired by RFgp34 to compensate for the CT truncation and restore infectivity in multiple cell types may have occurred in a specific order and the evolution of RFgp34 to out-compete RFwt occurred over many passages.

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Bruce, Rachel S. "The structural heterogeneity of alpha-1-acid glycoprotein in asthma." Thesis, University of Strathclyde, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.401354.

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Stewart, Yvonne M. "The characterisation of alpha 1 acid glycoprotein in rheumatoid arthritis." Thesis, University of Strathclyde, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248709.

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Lai, Pei-Jen. "HIV-1 neutralisation and other aspects of the envelope glycoprotein." Thesis, Imperial College London, 2009. http://hdl.handle.net/10044/1/5472.

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The absence of an effective humoral response contributes to the failure of controlling HIV-1 infection. Methods to elicit a potent neutralising antibody response is still underway and this thesis explores three aspects that can affect neutralisation. The pseudovirus-based assay is now recommended as the standard assay for assessing neutralising antibody response. However, recent studies have reported discrepancies between pseduovirus-based assay and conventional PBMCs or other cell-based assays. The first aim is to investigate possible causes behind this difference. The effect of virus producer cell type and virus platform (pseudovirus vs. replication-competent) was examined and both parameters can affect neutralisation. The second aim was to study the the neutralising antibody response in patients with primary HIV-1 infection. A panel of 6 patients were selected from the SPARTAC clinical trial. Pseudoviruses were constructed with the env gene derived from patient samples at week 0 (baseline) and week 52. The evolutionary history and the neutralisation sensitivity of these primary isolates against a panel of broadly neutralising antibodies and heterologous and autologous sera were studied. The week 52 isolates escaped from antisera neutralisation rapidly, most likely at the glycan level. In addition, viral load was found to correlate directly with intra-patient viral diversity and evolutionary divergence over time. Finally, the effect of Nef on HIV-1 neutralisation was investigated. Recent reports suggest that Nef modifies HIV-1 envelope glycoprotein. Hence, neutralising antibody response might also be modified in the absence of Nef. When subjected to neutralisation with a panel of monoclonal antibodies, the Nef-deleted (ΔNef) HIV-1 was more readily neutralised than the wild-type (WT) virus. Immunoprecipitation assays showed that neutralising antibodies can capture ΔNef virus more efficiently than WT virus. However, the enhanced neutralisation of ΔNef virus was neither due to CD4-down regulation nor difference in glycosylation.

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Anwar, Mohammad Arif. "Analysis of the fowlpox virus homologue of mammalian PC-1 glycoprotein." Thesis, University College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.321939.

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Ueno, Shohta. "Functional analysis of the herpes simplex virus type-1 glycoprotein H." Thesis, University of Cambridge, 2010. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608640.

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Cardy, Caroline Maria. "The structure and function of calcium binding epidermal growth factor-like domains in human fibrillin-1." Thesis, University of Oxford, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360210.

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Sheppard, Neil Christopher. "The serology of HIV-1 envelope glycoproteins for vaccine use." Thesis, University of Oxford, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.436954.

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Books on the topic "Thy-1 glycoprotein"

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The HIV-1 envelope glycoproteins: Folding, function and vaccin design. Amsterdam University Press, 2004.

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Downey, Laura A., and Nina A. Guzzetta. Von Willebrand Disease. Edited by Kirk Lalwani, Ira Todd Cohen, Ellen Y. Choi, and Vidya T. Raman. Oxford University Press, 2018. http://dx.doi.org/10.1093/med/9780190685157.003.0059.

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Von Willebrand disease (vWD) is the most common bleeding disorder in humans. It is the result of an abnormality in the amount, structure, or function of von Willebrand factor (vWF), a glycoprotein important in maintaining normal hemostasis.. In children with vWD, the most frequent presentation is easy bruising and epistaxis. Other symptoms include hematomas, menorrhagia, and bleeding from minor wounds. Although intraarticular bleeding may occur, especially in certain subtypes, it is much more commonly seen with hemophilia. There are several subtypes of vWD based on the underlying defect in vWF, but, in general, they may be categorized as quantitative (types 1 and 3) or qualitative (all types 2). If vWD is suspected, consultation with a hematologist to establish the correct diagnosis and perioperative approach to hemostasis is essential. Avoidance of medications that interfere with coagulation, anticipation of intraoperative and postoperative bleeding, and an appropriate hemostatic treatment plan should be addressed.

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Abhishek, Abhishek, and Michael Doherty. Pathophysiology of calcium pyrophosphate deposition. Oxford University Press, 2016. http://dx.doi.org/10.1093/med/9780199668847.003.0049.

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Calcium pyrophosphate (CPP) dihydrate crystals form extracellularly. Their formation requires sufficient extracellular inorganic pyrophosphate (ePPi), calcium, and pro-nucleating factors. As inorganic pyrophosphate (PPi) cannot cross cell membranes passively due to its large size, ePPi results either from hydrolysis of extracellular ATP by the enzyme ectonucleotide pyrophosphatase/phosphodiesterase 1 (also known as plasma cell membrane glycoprotein 1) or from the transcellular transport of PPi by ANKH. ePPi is hydrolyzed to phosphate (Pi) by tissue non-specific alkaline phosphatase. The level of extracellular PPi and Pi is tightly regulated by several interlinked feedback mechanisms and growth factors. The relative concentration of Pi and PPi determines whether CPP or hydroxyapatite crystal is formed, with low Pi/PPi ratio resulting in CPP crystal formation, while a high Pi/PPi ratio promotes basic calcium phosphate crystal formation. CPP crystals are deposited in the cartilage matrix (preferentially in the middle layer) or in areas of chondroid metaplasia. Hypertrophic chondrocytes and specific cartilage matrix changes (e.g. high levels of dermatan sulfate and S-100 protein) are related to CPP crystal deposition and growth. CPP crystals cause inflammation by engaging with the NALP3 inflammasome, and with other components of the innate immune system, and is marked with a prolonged neutrophilic inflitrate. The pathogenesis of resolution of CPP crystal-induced inflammation is not well understood.

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Alchi, Bassam, and David Jayne. The patient with antiphospholipid syndrome with or without lupus. Edited by Giuseppe Remuzzi. Oxford University Press, 2015. http://dx.doi.org/10.1093/med/9780199592548.003.0164.

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Antiphospholipid syndrome (APS) is an autoimmune disorder characterized by recurrent arterial or venous thrombosis and/or pregnancy loss, accompanied by laboratory evidence of antiphospholipid antibodies (aPL), namely anticardiolipin antibodies (aCL), lupus anticoagulant (LA), and antibodies directed against beta-2 glycoprotein 1 (β‎‎‎2GP1). APS may occur as a ‘primary’ form, ‘antiphospholipid syndrome,’ without any known systemic disease or may occur in the context of systemic lupus erythematosus (SLE), ‘SLE-related APS’. APS may affect any organ system and displays a broad spectrum of thrombotic manifestations, ranging from isolated lower extremity deep vein thrombosis to the ‘thrombotic storm’ observed in catastrophic antiphospholipid syndrome. Less frequently, patients present with non-thrombotic manifestations (e.g. thrombocytopaenia, livedo reticularis, pulmonary hypertension, valvular heart disease, chorea, and recurrent fetal loss).The kidney is a major target organ in both primary and SLE-related APS. Renal involvement is typically caused by thrombosis occurring at any location within the renal vasculature, leading to diverse effects, depending on the size, type, and site of vessel involved. The renal manifestations of APS include renal artery stenosis and/or renovascular hypertension, renal infarction, APS nephropathy (APSN), renal vein thrombosis, allograft vasculopathy and vascular thrombosis, and thrombosis of dialysis access.Typical vascular lesions of APSN may be acute, the so-called thrombotic microangiopathy, and/or chronic, such as arteriosclerosis, fibrous intimal hyperplasia, tubular thyroidization, and focal cortical atrophy. The spectrum of renal lesions includes non-thrombotic conditions, such as glomerulonephritis. Furthermore, renal manifestations of APS may coexist with other pathologies, especially proliferative lupus nephritis.Early diagnosis of APS requires a high degree of clinical suspicion. The diagnosis requires one clinical (vascular thrombosis or pregnancy morbidity) and at least one laboratory (LA, aCL, and/or anti-β‎‎‎2GP1) criterion, positive on repeated testing.The aetiology of APS is not known. Although aPL are diagnostic of, and pathogenic in, APS, a ‘second hit’ (usually an inflammatory event) may trigger thrombosis in APS. The pathogenesis of the thrombotic tendency in APS remains to be elucidated, but may involve a combination of autoantibody-mediated dysregulation of coagulation, platelet activation, and endothelial injury.Treatment of APS remains centred on anticoagulation; however, it has also included the use of corticosteroids and other immunosuppressive therapy. The prognosis of patients with primary APS is variable and unpredictable. The presence of APS increases morbidity (renal and cerebral) and mortality of SLE patients.

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Book chapters on the topic "Thy-1 glycoprotein"

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Dráberová, Lubica, and Petr Dráber. "Aggregation of Thy-1 Glycoprotein Induces Tyrosine Phosphorylation of Different Proteins in Isolated Rat Mast Cells and Rat Basophilic Leukemia Cells." In Advances in Experimental Medicine and Biology, 297–301. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1941-6_62.

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Clapham, Paul, Mohan Somasundaran, and Katherine Luzuriaga. "Tropism and Properties of the HIV-1 Envelope Glycoprotein in Transmission." In Encyclopedia of AIDS, 1–12. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9610-6_149-1.

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Clapham, Paul, Mohan Somasundaran, and Katherine Luzuriaga. "Tropism and Properties of the HIV-1 Envelope Glycoprotein in Transmission." In Encyclopedia of AIDS, 2081–91. New York, NY: Springer New York, 2018. http://dx.doi.org/10.1007/978-1-4939-7101-5_149.

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Doms, Robert W., Patricia L. Earl, and Bernard Moss. "The Assembly of the HIV-1 Env Glycoprotein into Dimers and Tetramers." In Mechanisms and Specificity of HIV Entry into Host Cells, 203–21. Boston, MA: Springer US, 1991. http://dx.doi.org/10.1007/978-1-4684-5976-0_13.

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Levine, Myron, Alexandra Krikos, Joseph C. Glorioso, and Fred L. Homa. "Regulation of Expression of the Glycoprotein Genes of Herpes Simplex Virus Type 1 (HSV-1)." In Immunobiology and Prophylaxis of Human Herpesvirus Infections, 151–64. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5853-4_16.

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Laal, Suman, and Susan Zolla-Pazner. "Epitopes of HIV-1 Glycoproteins Recognized by the Human Immune System." In Chemical Immunology and Allergy, 91–111. Basel: KARGER, 1993. http://dx.doi.org/10.1159/000319158.

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Campadelli-Fiume, Gabriella, and Franca Serafini-Cessi. "Processing of the Oligosaccharide Chains of Herpes Simplex Virus Type 1 Glycoproteins." In The Herpesviruses, 357–82. Boston, MA: Springer US, 1985. http://dx.doi.org/10.1007/978-1-4613-2383-9_8.

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Pipkorn, R., J. Blomberg, A. Lawoko, S. Moyo, B. E. Malmvall, J. Shao, R. Dasch, and S. Tswana. "Structural requirements for geographically selective serological reactivity in the envelope glycoprotein of HIV-1." In Peptide Chemistry 1992, 525–28. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1474-5_153.

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Seta, N., G. Durand, J. Agneray, J. Féger, and M. Corbic. "VARIATIONS IN THE PROPORTIONS OF MICROHETEROGENEOUS FORMS OF HUMAN ALPHA 1-ACID GLYCOPROTEIN IN ALCOHOLIC CIRRHOSIS." In Proceedings of the Third Symposium, Lyon, France, June 26–28, 1985, edited by Jacques Bienvenu, J. A. Grimaud, and Philippe Laurent, 673–78. Berlin, Boston: De Gruyter, 1986. http://dx.doi.org/10.1515/9783110860757-083.

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Markert, R., A. Schreiber, U. Eggenberger, E. Lichte, and C. Griesinger. "Synthesis, conformational and ELISA study of the immunodominant region of the HIV-1 and HIV-2 glycoprotein gp120." In Peptides 1992, 567–68. Dordrecht: Springer Netherlands, 1993. http://dx.doi.org/10.1007/978-94-011-1470-7_255.

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Conference papers on the topic "Thy-1 glycoprotein"

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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 possible genomic linkage between these related glycoproteins of different cells, we have examined patients with either ‘LFA-1 immunodeficiency disease’ or with Glanzmann's thrombasthenia (GT). S.Bo. and P.Ce. are children affected by recurrent bacterial infections since birth. Cytofluorimetric analysis using monoclonal antibodies (MAbs) for the αL, αM,αX and β subunits demonstrated that the surface expression of LFA-1, Mac-1 and pl50,95 intheir leukocytes was ≤1% of the normal values. Platelets from both patients aggregated normally and readily bound the MAbs AP-2 (anti-GP IIb-IIIa) or Tab (anti-GP IIb). Crossed immunoelectrophoresis confirmed the presenceof GP IIb-IIIa complexes, whileSDS-polyacrylamide gel electrophoresis showed a normal migration of GP IIb and GP IIIa. Patients C. Bl. and M.Ca.are typical of the type I subgroupofGT. Their platelets are unable toaggregate and contain < 1% of the normal platelet content of GP liband GP Ilia.Cytofluoro-graphy showed a normal expression of LFA-1, Mac-1 and 150,95 on the surface of lymphocytes, polymorphonuclear cells and/or monocytes of both patients. Our data thus show that despite sequence homologies and a potential genomic linkage, the cellular expression of the platelet GP IIb-IIIa complex and of the LFA-1 related leukocyte antigens may be dissociated in genetic disorders where anabnormal glycoprotein distribution may be restricted to one type of cell.

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McGregor, J. L., L. McGregor, M. Hans, A. Sayegh, M. C. Trzeeiak, and M. Dechavanne. "PLATELETS OF A PATIENT LACKING GLYCOPROTEINS lib AND Ilia AGGREGATE TO HIGH CONCENTRATIONS OF THROMBIN OR COLLAGEN." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643863.

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The aim of this study was to investigate the platelets of a patient having bleeding episodes that began in infancy. The patient’s platelets in citrated-PRP did not aggregate when stimulated with ADP (5 and 10 uM), collagen (2.5 ug/ml), or sodium arachidonate (1 uM). However, washed patient platelets, in the presence of 2mM calcium, aggregated and secreted when stimulated with high concentrations of thrombin (0.36, 0.72 and lU/ml) or collagen (2, 4, 10 ug/ml). Monoclonal antibodies (Mab) LYP18 (directed against the IIb-IIIa glycoprotein complex) and LYP8 (anti-thrombospondin) inhibited thrombin and collagen induced aggregation of control but not the patient platelets. Patient thrombin -stimulated platelets did not bind 125I-labelled fibrinogen (40 to 320 ug/ml). Moreover, stimulating the washed patient's platelets with ADP (10-100 uM), in the presence of fibrinogen (2mg/ml), did not result in aggregation. Binding studies using Mab 125I-LYP2 (directed against the IIb-IIIa glycoprotein complex) showed the absence of the complex on the patient's platelets. The absence of the IIb-IIIa complex on the patient's platelets was also observed using crossed immunoelectro -phoresis and Mab 125I-LYP2 or 125I-LYP18. Individual glycoproteins (lib or Ilia) were not detected on silver stained two-dimensional (non-reduced/reduced) SDS-PAGE. Moreover, Western blots of |he patients platelets used in combination with anti-PLA or anti-LEK polyclonal antibodies failed to detect the presence of these two glycoproteins. These results indicate that this patient has Glanzmann's thrombasthenia or a variant of this disease. Moreover, this study shows that platelets lacking the IIb-IIIa glycoprotein complex can aggregate in responseto collagen or thrombin in the presence of physiological concentrations of calcium.

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Bruce, Rachel S., John M. McGuire, and Kevin D. Smith. "THE IMMUNOMODULATORY ROLE OF ALPHA-1 ACID GLYCOPROTEIN IN ASTHMA." In XXIst International Carbohydrate Symposium 2002. TheScientificWorld Ltd, 2002. http://dx.doi.org/10.1100/tsw.2002.662.

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Rawi, Reda, Khalid Kunji, Abdelali Haoudi, and Halima Bensmail. "Residue-residue contact prediction in the HIV-1 envelope glycoprotein complex." In 2015 IEEE International Conference on Bioinformatics and Biomedicine (BIBM). IEEE, 2015. http://dx.doi.org/10.1109/bibm.2015.7359933.

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Horváth, Péter, Zsófia Lázár, Martina Mészáros, Gabriella Gálffy, Rita Puskás, György Losonczy, László Kunos, and András Bikov. "The role of P- selectin glycoprotein ligand-1 (PSGL-1) in the pathogenesis of obstructive sleep apnea." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa2536.

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Lam, Fong, Alan Burns, C. W. Smith, and Rolando Rumbaut. "Platelets Enhance Neutrophil Transmigration Across Endothelium: The Role Of P-selectin Glycoprotein Ligand-1." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a5719.

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MARA PEREIRA BEZERRA, CYNTHIA, and CARMEN SILVIA BERTUZZO. "As the deficiency of alpha-1 antitrypsin glycoprotein affects the severity of lung disease among patients with Cystic Fibrosis." In XXIV Congresso de Iniciação Científica da UNICAMP - 2016. Campinas - SP, Brazil: Galoa, 2016. http://dx.doi.org/10.19146/pibic-2016-51997.

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Vigh, Zs, and I. Scharrer. "INVESTIGATIONS ON MULTIMERIC STRUCTURE OF PLATELET VON WILLE-BRAND FACTOR IN PATIENTS WITH HEREDITARY DISORDERS OF PLATELET FUNCTION." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644087.

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Abstract:

Von Willebrand factor (vWF), a multimeric glycoprotein, plays an essential and multifunctional role in the hemostatic process. It is well known that platelet glycoproteins IB, IIB and IIIA contain receptors for vWF. Von Willebrand factor was also found in alpha granules of platelets. Therefore we investigated the multimeric structure of platelet vWF in 12 patients with different inherited disorders of platelet function. The patients had the following diagnosis: Hermansky Pudlak syndrome, Thrombasthenia and up to new undefined hereditary disorders of platelet function. The method is based upon:1) washing of platelets 2) release of platelet vWF 3) separation of vWF multimers by SDS-agarose electrophoresis 4) subsequent blotting of vWF mul timers onto nitrocellulose 5) staining by peroxidase conjugated antibodies.The investigations were repeated 3 times and compared to those of normal platelets. In 2 patients with Hermansky-Pudlak syndrane no multimeric structure could be detected in platelets whereas the multimeric pattern of plasma of these patients was normal. Also in one patient with the tentative diagnosis: thrombasthenia we couldn't find any multimeric structure in platelets compared to the normal multimeric composition of plasma. In 2 patients with giant platelets the multimeric distribution was normal. In the remaining 6 patients we observed multimeric structure which was different from that seen in vWd variants and in healthy volunteers. In 1 patient we found normal multimeric pattern in plasma and platelets.Based on our findings it can be assumed that the analysis of multimeric structure of platelet vWF can be helpful for the diagnostic approach and for the insight in pathogenesis of inherited disorders of platelet function.

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Farache Trajano, Luiza, Rebecca Moore, and Quentin Sattentau. "The Presence of Chemical Cross-Linking Stabilises HIV-1 Envelope Glycoprotein Trimer Antigens in a Model of Intramuscular Immunisation." In Building Bridges in Medical Science 2021. Cambridge Medicine Journal, 2021. http://dx.doi.org/10.7244/cmj.2021.03.001.4.

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Background: The HIV-1 envelope glycoprotein (Env) is the target of antigen design for antibody- based vaccination. In 2019, four trimeric Env vaccines entered an experimental trial: ConM, ConS, and their cross-linked counterparts. The trimers were formulated with MPLA adjuvant. Studies have demonstrated that adjuvants trigger neutrophil infiltration. Neutrophils activate and degranulate releasing proteases, namely elastase and cathepsinG. Aims: To assess the stability and immunogenicity of these vaccines in the presence of adjuvant- recruited neutrophils and their proteolytic enzymes. Methods: Trimers were incubated with commercially-sourced proteases. To analyse stability, samples were reduced, denatured and separated using gel electrophoresis. To assess antibody binding, a trimer-protease incubation was followed by an ELISA. To establish more physiologically relevant conditions, harvested neutrophils were exposed to various adjuvants. The supernatant, shown to contain elastase, was incubated alongside the vaccines. The reducing and denaturing gels, as well as the ELISA, was repeated. Results: Gel analysis revealed that un-crosslinked trimers underwent significant digestion whereas cross-linking conferred enhanced stability. In the presence of neutrophil-sourced protease-containing-supernatant, trimers displayed resistance to digestion. The differential stability profile of Env trimers when exposed to commercially sourced compared to supernatant- derived proteases may be due to the inhibitory effect of human serum on elastase. Antibody epitopes were maintained in vitro. Conclusion: The vaccine antigens are sensitive to enzymatic degradation. This is reduced by cross-linking and human serum.

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Yamamoto, N., H. Kitagawa, K. Tanoue, and H. YAmazaki. "AN EPITOPE OF A MONOCLONAL ANTIBODY (TM83) AGAINST GLYCOPROTEIN lib/Ilia COMPLEX." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644881.

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GPIIb/lIIa is forming a heterodimer complex on the human platelet membrane.Many monoclonal antibodiesagainst GPIIb/IIIa complex obtained elsewhere react with neither GPIIb nor GPIIIa separately when GPIIb/IIIa is blotted to filter after SDS-PAGE. Therefore the epitope of GPIIb/IIIa complex is not identified actually. Our attemption is to clarify the epitope recognized by a monoclonal antibody against GPIIb/IIIa designated TM83. TM83 (30 yg/ml) inhibited collagen-, ADP-, or thrombin-induced aggregation, but it did not inhibit ATP-secretion induced by 0.01 U/ml of thrombin. TM83 also inhibited fibrinogen-binding approximately to 50 % of total binding. The binding of 125 I- TM83 to platelets decreased to b0% of controlwhen platelets were incubated in the presence of 1 mM EDTA at 37°C for 30 min. However the incubation at25°C for 30 min did not change any binding capacity of 125 I-TM83 to platelets. Thus thebinding of TM83to platelets was dependent on both temperature and calcium concentration in surrouding medium, suggesting that TM83 bound to GPIIb/IIIa complex.If the small amounts of epitope of GPIIb/IIIa complex is not injured during SDS-PAGE and blotting, we may identify clearly the epitope of GPIIb/IIIa complex. For this aim, GPIIb/IIIa complex was extracted carefully in the presence of 1 mM calcium by the phase separationusing Triton X-11U, and was run on SDS-PAGE in the presence of 100 yM calcium. Western-blot of the membrane preparation showed that 125 I-TM83 was incorporated into both GPIIb and GPIIIa on Durapore filter. Further radio-crossed immunoelectrophoresis showed that I-TM83 was incorporated only into immunoprecipitin of GPIIb/IIIa complex in the presenceof 1 mM calcium. While after addition of 25 mM EDTA to the membrane preparation containing 1 mM calcium,125i-tm83 wasmainly incorporated into GPIIb/IIIa complex as well, however very faint radioactivity fromthe immunoprecipitin corresponding to GPIIIa was observed, but the radioactivity from GPIIb was not identified. While there is a discrepancy inour result, it must be further studied whether one monoclonal antibody can recognize or not two kinds of GPs, GPIIb and Ilia, which are formed in complex in physiological condition.

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